tag:blogger.com,1999:blog-50026759507604888132024-03-12T20:25:06.772-07:00The Unsilenced Sciencenooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.comBlogger48125tag:blogger.com,1999:blog-5002675950760488813.post-79810640059165395782014-10-18T06:28:00.000-07:002014-10-18T07:56:38.407-07:00Merit’s Liquidity<div dir="ltr" style="text-align: left;" trbidi="on">
</div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-v2FiWPqRiic/VEJUrHW-4WI/AAAAAAAABDk/Wam6SMvA2u8/s1600/LiquidAssets.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://4.bp.blogspot.com/-v2FiWPqRiic/VEJUrHW-4WI/AAAAAAAABDk/Wam6SMvA2u8/s400/LiquidAssets.png" /></a></div>
Over the past year, multiple major media outlets and a powerful university president or two have been agitating about the correlation between parents’ income and SAT scores. Over that same time period, editors of various psychology journals were rejecting my regression study to determine the true influence of parents’ income on SAT scores while controlling for other possible factors because the study did not “make clear what the gap or problem is in the literature and exactly how the present study fills that gap.” If I cannot convince a journal that a lack of an examination on the influence of socioeconomic status in the entire 87-year history of America’s most important academic test is a gap in the literature, then what hope remains for my other project on the interplay of body-mass index and perspiration on navel lint accumulation?
<br><br>
Part of the problem resulted from my need to rely heavily on years of state averages, rather than the scores of individual students, but I am convinced that anyone who manages to gain access to individual data will merely corroborate my work at much greater expense. One editor conceded, “I agree that there is something we can learn from these data,” despite rejecting my work anyway. Ultimately, the new open-access journal, Open Differential Psychology published the <a href="http://openpsych.net/ODP/2014/07/parents-income-is-a-poor-predictor-of-sat-score/">study</a>.
<br><br>
Last week, the College Board released the latest year’s SAT results. The organization cleverly released its “benchmarks” report the day before their usual, more detailed report. Reporters were too lazy to report on the subject two days in a row, let alone do any analysis. Blasé headlines declared scores “flat,” as they would for any two-consecutive-year analysis. I found the numbers fascinating. They dovetail with my study and other <a href="http://theunsilencedscience.blogspot.com/2011/09/intelligence.html">previous writings</a> and flesh out some trends the media missed.
<br><br>
In my study I addressed the overlooked fact that correlations between parents’ education and (individual) SAT score and between parents’ income and SAT score have not been constant over time.
<blockquote>Family educational advantage seems to evince virtually undeviating growth as a predictor of SAT scores, but financial advantage seems to grow as the economy worsens. Rather than postulate that times of economic difficulty almost immediately make wealthy people smarter, one should focus on the exclusivity of the income category.</blockquote>
<br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-VCgT17zXLJA/VEJYC4ED6dI/AAAAAAAABD8/ksFhYv22ulQ/s1600/iq%2Bsat%2B2014%2Beducation%2Bgap.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://3.bp.blogspot.com/-VCgT17zXLJA/VEJYC4ED6dI/AAAAAAAABD8/ksFhYv22ulQ/s400/iq%2Bsat%2B2014%2Beducation%2Bgap.png" /></a></div>
<br>
2014 brought new record advantages to students whose parents have bachelor’s or graduate degrees on the critical-reading and mathematics subtests. This fact can inform discussion about the notion of an “education bubble.” The expansion of college access has raised concerns over indebtedness, falling standards, and underemployment, but, while these concerns are likely to grow, education appears increasingly to benefit the following generation as if to demonstrate that the ability of higher education to sift and inculcate basic skills remains intact, or at least it did one generation ago.
<br><br>
The difference between the yearly trends for the SAT-score benefit of education to a family compared to the benefit of coming from a home with a higher income startled me, especially given the sharp drop in income advantage coinciding with the 2008 economic downturn. So, I graphed income’s SAT advantage with US gross domestic product (GDP) growth rate. The graphs almost perfectly coincide when the income divide compares families above $100,000 to those below that.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-MRQX7KBhsVM/VEJWTCTzoUI/AAAAAAAABDw/soHsRAkoUdc/s1600/sat%2Badvantage%2B100k%2B%26%2Bgdp.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://2.bp.blogspot.com/-MRQX7KBhsVM/VEJWTCTzoUI/AAAAAAAABDw/soHsRAkoUdc/s400/sat%2Badvantage%2B100k%2B%26%2Bgdp.png" /></a></div>
<br>
My regression study included a control for year, but an even more detailed study of the influence of family income could benefit by controlling for the state of the economy, as I suggested in my concluding remarks.
<blockquote>Perhaps additional or alternative variables could be identified. For instance, year was significant in some regression iterations but had small β values. Perhaps year is a proxy variable for other factors like the state of the economy.</blockquote>
<br>
The graph provides convincing evidence that there is some kind of causal relationship between the economy and SAT scores despite the relatively low influence of parents’ income on scores in the regression analysis. Student stress or mood seems more plausible as a mechanism than radical yearly changes in educational quality, but my point about exclusivity concerned whether economic slowdown weeded out low test performers from higher economic strata due to the heritable component of cognitive ability shared between the parents and the student. However, for that to be the mechanism, one would expect GDP to look more like a leading indicator of test performance or for the slope of the growth rate to tend to be the negative of the slope of test scores over time. This graph actually seems to indicate that poor economies weed out <i>high</i> test performers from higher economic strata. In <u>The Bell Curve</u>, Richard Herrnstein and Charles Murray claimed that the twenty-first century would continue “the emergence of a cognitive elite.”
<blockquote>The isolation of the brightest from the rest of society is already extreme; the forces driving it are growing stronger rather than weaker.</blockquote>
Of course, the economy of the 1990’s, when they wrote that, usually appeared to be growing stronger rather than weaker.
<br><br>
I can imagine two mechanisms for economic contraction weeding out smart families from the upper class: circumstances cause the power elite to lose interest in the power of ideas, and some upstarts’ ideas were not that good from the start. I suspect both are at work. The first mechanism supports a leftist or Marxist vision of ensconced aristocracy holding the privileges of power and leisure. If recessions interspersed with periods of anemic growth are “the new normal,” then <u>The Bell Curve</u> was partly wrong, and economic populism should be of interest to the so-called cognitive elite. On the other hand, when bad ideas create bad economies, perhaps the cognitive elite receive their just desserts. Some people who are obsessed with IQ research engage in some paradoxically simplistic thinking. As anyone who has surveyed the differential psychology literature about liberals versus conservatives or even the results for the SAT Student Descriptive Questionnaire can attest, the best indicator of dimness is indifference. Wrong ideas also sometimes require intelligent formulation. Spectacularly wrong ideas receive their negative appraisal in retrospect because they were compelling enough to do damage. Moreover, misbegotten hype might serve as a more commonly available vehicle of upward mobility for smart upstarts than truly transformative ideas.
<br><br>
Wisdom and top-down analytic ability sadly receive fewer lauds than the clichés “street smarts” and “common sense.” To illustrate the distinctiveness of wisdom from intelligence so as to support the notion that smart people might promote unwise ideas, I would like to analogize with my personal experience working with engineers and doctors. Many of the engineers whom I have known work hard on mundane projects but like to engage in fascinating discussions about politics, metaphysics, and, of course, the possibility of alien life forms. They contrast with neurologists and neurosurgeons whom I have met who regularly work with cases of alexia without agraphia and amygdalectomy but remain willfully indifferent to any profound questions these phenomena raise about the soul or free will. If emphasis on analytic ability (as opposed to memory) is analogous to “wisdom,” then the engineers are the aristocrats in this analogy, although engineers often zealously advocate for their upstart ideas. I think most people assume that doctors are smarter than engineers because becoming a doctor is harder and better reimbursed, but I would say engineers are deeper conversationalists, which manifests a certain type of wisdom to me.
<br><br><br>
<center><b>Merit’s Mobility</b></center><br>
Though the 90’s are long gone, Bill Clinton might still point out that this is not “midnight in America.” The American economy usually does expand, and smart people disproportionately tend to be the proverbial movers and shakers. Hints of this appear as evidence for their geographical mobility based on yearly maps of SAT and ACT data. Racial demographics also relate to test scores and have their own trends of time and place.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-TJ6Pot2lNXo/VEJYxkPbiPI/AAAAAAAABEE/3rswo2fL9c0/s1600/iq%2Brace%2Bsat%2B2014%2Bincome%2Bstates.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://3.bp.blogspot.com/-TJ6Pot2lNXo/VEJYxkPbiPI/AAAAAAAABEE/3rswo2fL9c0/s400/iq%2Brace%2Bsat%2B2014%2Bincome%2Bstates.png" /></a></div>
<br>
<a href="http://theunsilencedscience.blogspot.com/2013/10/black-suits-gowns-skin-sat-scores-by.html">Last year</a>, I graphed all data from state SAT reports for SAT scores of different family income brackets according to the proportion of each state’s population that belongs to the two highest scoring racial groups, whites and Asians. As the updated version above shows, students from the wealthiest category have the lowest association between state racial demographics and SAT score. One reader considered this “evidence against a genetic explanation.” Of course, homes earning less than $80,000 per year are not all dealing with “typical environmental problems of poverty.” Part of my study’s regression analysis looked at the effects on SAT scores that were common to both income and race. These effects existed when the income cutoff was $100,000 but not $20,000. Without completely dismissing the environmental hypothesis, I pointed out alternative factors that could be at work. An alternative explanation for the graph could be that higher income families with good test performance are more likely to live in racially diverse states compared to other income levels, since the racial proportions pertain to the states, not the income brackets, themselves. It turns out that SAT data does offer some support for my previous contention that “racially diverse states like California have industries or attractions that pull in successful, educated whites.”
<br><br>
Before revealing the map that demonstrates this, I shall review the latest SAT and ACT data by race. Composite ACT-SAT scores by race are very similar to the year before.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-A-_5w-BKJhE/VEJY6on3tiI/AAAAAAAABEM/DxA90dIvsrk/s1600/iq%2Brace%2Bsat%2B2014%2Bsat-act%2Bcomposite.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://4.bp.blogspot.com/-A-_5w-BKJhE/VEJY6on3tiI/AAAAAAAABEM/DxA90dIvsrk/s400/iq%2Brace%2Bsat%2B2014%2Bsat-act%2Bcomposite.png" /></a></div>
<br>
Native-American scores remain just slightly above those of Hispanic Americans after a significant drop in Native-American ACT scores from 2010 to 2013.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-a8TG82SwW8w/VEJZGCPXLLI/AAAAAAAABEU/Qj9E9zEFda0/s1600/iq%2Bact%2Bcomposite%2B2014.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://3.bp.blogspot.com/-a8TG82SwW8w/VEJZGCPXLLI/AAAAAAAABEU/Qj9E9zEFda0/s400/iq%2Bact%2Bcomposite%2B2014.png" /></a></div>
<br>
Overall, Asian scores have continued their amazing progress. The Asian SAT mathematics subtest advantage over whites rose to 64 points.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-JSnJ2k4Mr-o/VEJZPVPUCHI/AAAAAAAABEc/YG02t3tXsNc/s1600/iq%2Brace%2Bsat%2B2014%2Bmath%2Braw.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-JSnJ2k4Mr-o/VEJZPVPUCHI/AAAAAAAABEc/YG02t3tXsNc/s400/iq%2Brace%2Bsat%2B2014%2Bmath%2Braw.png" /></a></div>
<br>
Asians are not closer to surpassing whites on the critical-reading subtest only because white scores rose by the same amount this year.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-wzhGmTPAQK4/VEJZW1ueBqI/AAAAAAAABEk/8gXErAWZR88/s1600/iq%2Brace%2Bsat%2B2014%2Bverbal%2Braw.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://4.bp.blogspot.com/-wzhGmTPAQK4/VEJZW1ueBqI/AAAAAAAABEk/8gXErAWZR88/s400/iq%2Brace%2Bsat%2B2014%2Bverbal%2Braw.png" /></a></div>
<br>
In contrast to all other groups, Asian SAT writing subtest scores rose in seven of the past nine years.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-M8BTyhzmVMc/VEJZeYnOdII/AAAAAAAABEs/UrFKEJ9wxVc/s1600/iq%2Brace%2Bsat%2B2014%2Bwriting%2Braw.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://2.bp.blogspot.com/-M8BTyhzmVMc/VEJZeYnOdII/AAAAAAAABEs/UrFKEJ9wxVc/s400/iq%2Brace%2Bsat%2B2014%2Bwriting%2Braw.png" /></a></div>
<br>
However, Asian progress on the ACT did appear to stop. Their scores on the reading and math subtests even slightly dropped. The average score drop for Pacific Islanders, for whom scores are available only in recent ACT data, was quite severe this year: almost a full composite ACT point. Fortunately for Pacific Islanders, this probably only resulted from a massive, 19-percent increase in ACT participation. Hawaiian students, who were 83 percent Asian-American, according to SAT numbers, bumped up their ACT participation from 40 percent to 90 percent, while their SAT participation rate barely budged at 63 percent. Asian students have been the one racial group who heavily favor taking the SAT rather than the ACT. This is likely due in large measure to foreign students. As the following graph shows, ACT participation surpassed that of the SAT, driven mostly by white students.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-osh_-dW0CRA/VEJZo086wgI/AAAAAAAABE0/vEKcMkyVQ2o/s1600/sat%2Bact%2Bparticipation%2Brace%2B2014.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" width="393" src="http://2.bp.blogspot.com/-osh_-dW0CRA/VEJZo086wgI/AAAAAAAABE0/vEKcMkyVQ2o/s400/sat%2Bact%2Bparticipation%2Brace%2B2014.png" /></a></div>
<br>
It would be tempting to surmise that foreign students are causing the continued progress of Asians on the SAT, but, as I <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">previously discussed</a>, the scores of foreign students (represented on the following graph as colored lines of a negative advantage for American students) still closely resemble Asian SAT scores (represented as gray lines for a negative white advantage), while the number of foreign students could not overwhelm the number of Asian students.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-WoHuHeB9Ouk/VEJZ_gK1QRI/AAAAAAAABE8/G1NE5dAdNXU/s1600/iq%2Brace%2Bsat%2B2014%2Bamerican-foreigner%2Bgap.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-WoHuHeB9Ouk/VEJZ_gK1QRI/AAAAAAAABE8/G1NE5dAdNXU/s400/iq%2Brace%2Bsat%2B2014%2Bamerican-foreigner%2Bgap.png" /></a></div>
<br>
Indeed, Asian progress has been so impressive that it calls into question some assumptions of experts in differential psychology and adherents to the philosophy behind so-called “human biodiversity.” Rather than reveal a unitary Asian-white general intelligence gap, Asians have always had a large mathematics advantage. Rather than maintain a constant mathematics gap as Asians improve their English skills, Asian mathematics, reading, and writing skills improved in tandem. Rather than have SAT scores that coincide with research on the secular IQ gains, known as the Flynn effect, Asian SAT gains have been large at the same time as their IQ gains have been small, and white SAT gains have been small, as large IQ gains in Western societies have continued unabated. Frey and Detterman famously called the SAT an IQ test in 2004, but they offered no explanation for why their IQ-estimation equation essentially eliminated the reading subtest. Murray <a href="http://www.aei-ideas.org/2014/10/the-bell-curve-20-years-later-a-qa-with-charles-murray/">recently defended</a> <u>The Bell Curve</u> by pointing out how little the black-white test score gap has changed. So, what is the precise meaning of that, given that the Asian-white gap has changed so greatly?
<br><br>
What should be clear from the preceding review of new data is that participation rates greatly matter. Hawaii’s ACT scores fell this year by almost two points on a scale from 11 to 36, following its participation increase. In order to appropriately map composite ACT-SAT scores, I must follow my <a href="http://theunsilencedscience.blogspot.com/2013/06/the-sat-act-score-map.html">previously described</a> methodology for adjusting scores according to state SAT and ACT participation rates.
<br><br>
For comparison, here is the map of the percentage of white and Asian SAT-taking students over the years:
<br><br>
<a href="http://s1087.photobucket.com/user/nooffensebut/media/sat%20aw%20map.gif.html" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat%20aw%20map.gif" border="0" alt=" photo sat aw map.gif"/></a>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-aN_35lMc3eA/VEJaK1Y4q1I/AAAAAAAABFE/C_ZuN3KV5Hg/s1600/sat%2Bmap%2Baw%2Blegend.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-aN_35lMc3eA/VEJaK1Y4q1I/AAAAAAAABFE/C_ZuN3KV5Hg/s400/sat%2Bmap%2Baw%2Blegend.png" /></a></div>
<br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>
Student diversity increased especially among coastal states. I previously <a href="http://theunsilencedscience.blogspot.com/2012/09/the-sat-zombie-apocalypse.html">claimed</a>, “Demographic changes correspond to falling test scores, and one can see it, at least in terms of a North-South divide, on these maps.” The most recent years of this participation-controlled composite SAT-ACT score map make me want to amend that assessment.
<br><br>
<a href="http://s1087.photobucket.com/user/nooffensebut/media/sat-act%20part%20cont.gif.html" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-act%20part%20cont.gif" border="0" alt=" photo sat-act part cont.gif"/></a>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-d3lnsicqScA/VEJaywi9FhI/AAAAAAAABFM/QKnEj5nJ254/s1600/sat%2Bmap%2Blegend.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-d3lnsicqScA/VEJaywi9FhI/AAAAAAAABFM/QKnEj5nJ254/s400/sat%2Bmap%2Blegend.png" /></a></div>
<br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>
One can more easily notice the change by just looking at the oldest and newest maps without animation.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-cVP9fGNMvc4/VEJa-3udV2I/AAAAAAAABFU/li6VFYudpdM/s1600/sat-act%2Bpart%2Bcont%2B1998.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" width="393" src="http://1.bp.blogspot.com/-cVP9fGNMvc4/VEJa-3udV2I/AAAAAAAABFU/li6VFYudpdM/s400/sat-act%2Bpart%2Bcont%2B1998.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-H03hTfn50k8/VEJbF7HBDjI/AAAAAAAABFc/B_4P88DFRyU/s1600/sat-act%2Bpart%2Bcont%2B2014.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" width="393" src="http://1.bp.blogspot.com/-H03hTfn50k8/VEJbF7HBDjI/AAAAAAAABFc/B_4P88DFRyU/s400/sat-act%2Bpart%2Bcont%2B2014.png" /></a></div>
<br>
The earliest year does suggest a North-South divide, but the coastal states of California, Georgia, South Carolina, and North Carolina improved, while some Mountain states declined. The trend could be a fluke, and a few states buck the trend, but it fits with my previous explanation of diverse states attracting relatively well scoring students from wealthy families. The upper class wishes to live near beaches and in high-status states with impressive cultural and educational institutions. Many of the cognitive elite actually might like some kinds of racial diversity. Southern states like Louisiana have not improved, or, in the case of Mississippi, scores improved but were already extremely low. Perhaps the cognitive elite would be attracted to this Southern coast but find Southern culture too alienating, and maybe such a feeling of alienation from otherwise attractive settings makes liberal condescension slightly more understandable.
<br><br>
In an era that made “big data” a catchphrase, the colossal data pool that describes the colossal sample who took these tests inspires elite news outlets to make bar graphs of simple correlations and reports of flat scores. I call that flat reporting.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Open+Differential+Psychology&rft_id=info%3Aother%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Parents%E2%80%99+Income+is+a+Poor+Predictor+of+SAT+Score&rft.issn=&rft.date=2014&rft.volume=&rft.issue=&rft.spage=1&rft.epage=19&rft.artnum=http%3A%2F%2Fopenpsych.net%2FODP%2F2014%2F07%2Fparents-income-is-a-poor-predictor-of-sat-score%2F&rft.au=nooffensebut&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">nooffensebut (2014). Parents’ Income is a Poor Predictor of SAT Score <span style="font-style: italic;">Open Differential Psychology</span>, 1-19</span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com10tag:blogger.com,1999:blog-5002675950760488813.post-7678941826288712512014-08-24T11:44:00.000-07:002014-12-10T14:55:40.812-08:00Correcting the Critics of Nicholas Wade & MAOA<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
Critics of Nicholas Wade’s latest book, A Troublesome Inheritance, have tried their best to pull discussion away from science and into the fluffy philosophy of racial semantics. They figure that if discussion never escapes the bog of racial constructivism, then no need exists for consideration of anything specific that would threaten or offend the modern paradigm. Wade deserves credit for effectively anticipating the critics’ points and blame for entertaining the critics’ points. However, Wade interrupted anthropological meanderings about the lack of perfect racial boundaries by introducing the subject of the warrior gene, monoamine oxidase A (MAOA). This is a specific gene with allele frequencies in a specific promoter sequence that differ tremendously by race.
<br><br>
Science reporter Fiona MacRae conveyed her alarm with the headline, “Author: Africans prone to violence.” The body of her <a href="http://www.iol.co.za/news/world/author-africans-prone-to-violence-1.1735354">article</a> offered no attempt to dispatch with the inconvenient gene, but I have collected all such attempts to put on display right here.
<br><br>
An unremarkable dismissal presumably became a centerpiece due to its placement in the pages of Wade’s employer, The New York Times. Science writer <a href="http://www.nytimes.com/2014/07/13/books/review/a-troublesome-inheritance-and-inheritance.html?_r=0">David Dobbs</a> provided glib assurance.
<blockquote> He tells, for instance, of specific gene variants that reputedly create less trust and more violence in African-Americans and, he says, explain their resistance to modern economic institutions and practices. Alas, the scientific literature he draws on is so uneven and disputed that many geneticists dismiss it outright.</blockquote>
One recurring motif of MAOA skeptics is stealing tactics from global-warming skeptics. After all, Dobbs is only a journalist. One must not expect him to conduct a thorough survey or even read a <a href="http://theunsilencedscience.blogspot.com/2014/07/the-warrior-gene-back-from-grave.html">meta-analysis</a> of 31 published studies on the gene. One should simply trust that the “many geneticists” he had in mind have some grasp of the evidence.
<br><br>
Many—143 to be exact—population geneticists published a <a href="http://cehg.stanford.edu/letter-from-population-geneticists/">five-sentence letter</a> in The New York Times Book Review. The brief letter explicitly thanked Dobbs and falsely accused Wade of claiming that natural selection “led to worldwide differences in IQ test results.” Columbia University biologist Molly Przeworski was one of the five geneticists who authored the letter. She told a <a href="http://www.cbc.ca/day6/blog/2014/08/15/a-scientist-disputes-book-on-race-and-genes/">Canadian radio program</a>, “We just don’t have any of the types of genetic variants that are associated with societal or social or behavioral changes that he’s speculating about.” So, not only do population geneticists object to Wade’s book and dismiss outright the scientific literature for MAOA, but they also categorically rule out having any knowledge of any behavioral genes. (I presume that she did not mean that no human has genes that influence behavior.) Ironically, Przeworski also wrote a study with two other signatories to the letter, Yoav Gilad and Karl Skorecki, that contributed to the outright dismissed MAOA scientific literature. Wade cited their study to suggest that natural selection had acted upon this gene. However, that is not a study of a behavioral phenotype. In fact, I did not recognize any names on the letter as having contributed to behavioral research on MAOA. Certainly none of the authors of the two studies on the MAOA-2R allele that Wade singled out (and pointed out was about fifty times more common in African-American men) signed the letter. Contrary to popular perceptions, geneticists are not the leading experts on behavioral genetics. I have been tabulating the academic backgrounds of authors of MAOA research studies. Out of 76 studies, 67 percent had psychiatrist authors. Only 43 percent of studies had a geneticist author. 20 percent had neuroscientist authors, and 18 percent had psychologist authors. One author, criminologist Kevin Beaver, writes on the subject of biosocial criminology. No one writes about “biosocial psychiatry” because the transition from Freudian psychotherapy to the management of psychotropic drugs has been nearly uniform. Psychiatrists understand that some behaviors reveal mental illnesses, and targeting the relevant neurotransmitters, as the MAOA enzyme does, can save lives. Indeed, criticism of MAOA research does <a href="http://scientiasalon.wordpress.com/2014/07/31/the-extreme-warrior-gene-a-reality-check/comment-page-1/#comment-5494">extend</a> to criticism of the relationship between neurotransmitters and behavior, which some scientists <a href="http://alandove.com/content/2012/11/single-molecule-determines-complex-behavior-say-scientists/">openly mock</a>.
<br><br>
Another letter signatory, University of Pennsylvania geneticist Sarah Tishkoff, seemed to be working from the same script as Przeworski when <a href="http://blogs.nature.com/news/2014/08/geneticists-say-popular-book-misrepresents-research-on-human-evolution.html">she told</a> science reporter Ewen Callaway, “We don’t have any strong candidates for playing a role in behaviour.” I wonder what standard of evidence Tishkoff awaits. Besides the aforementioned 31-study meta-analysis by Ficks and Waldman, a 27-study meta-analysis by Byrd and Manuck confirmed that MAOA has a powerful effect on antisocial behavior when coupled with childhood maltreatment. Both meta-analyses determined that the research did not show evidence of publication bias. This forest plot from the study just screams the words “uneven” and “disputed,” does it not?
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-6pL_g3y2WGM/U_ojhBxjZvI/AAAAAAAABC4/V8juofl7_yA/s1600/Byrd%26Manuck.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-6pL_g3y2WGM/U_ojhBxjZvI/AAAAAAAABC4/V8juofl7_yA/s400/Byrd%26Manuck.jpg" /></a></div>
<br>
University of North Carolina biologist Joseph Graves, Jr. signed the letter and reviewed Wade’s book, <a href="http://www.thisviewoflife.com/index.php/magazine/articles/book-review-great-are-wades-errors-in-a-troublesome-inheritance-genes-race">saying</a> “Similar just-so-stories appear throughout the text including his discussion of the MAO-A gene and aggression.” A “just-so story” is supposed to be unverifiable and unfalsifiable. Research on MAOA has verified its effect on behavior. If the evidence had failed to show an effect on behavior, it would have falsified the hypothesized role of MAOA. MAOA research has many facets, such as the purported stronger effect of MAOA-2R on violence than MAOA-4R or even MAOA-3R. Some facets are supported by evidence but not adequately replicated in multiple samples. The unwillingness of scientists to further replicate the effect of MAOA-2R since its discovery in 2008 or the interaction effect of MAOA-3R with low IQ in no way makes those findings legitimately unfalsifiable. Labeling scientific claims as “just-so stories” is a convenient way to dismiss scientific evidence without offering alternative hypotheses or evidence and has been used to describe the theory of <a href="https://www.beliefnet.com/Entertainment/Movies/2004/06/A-Modern-Day-Noah-Story-Without-The-Passion.aspx?p=4">evolution</a> and <a href="http://contracelsum.com/2013/09/28/gobal-warming/">global warming</a>.
<br><br>
Harvard geneticist Daniel MacArthur diligently covered all of his bases. He signed the letter and put out clear statements both <a href="http://theunsilencedscience.blogspot.com/2010/01/deus-ex-machina-genetics.html">for</a> (“[T]he evidence for an association between the [MAOA] VNTR variant and antisocial behavior is substantially more consistent than most of these associations. This may well be one of the rare cases of genuine associations.”) and <a href="http://genomesunzipped.org/2011/11/size-matters-and-other-lessons-from-medical-genetics.php">against</a> (“By historical analogy, most if not all of this [MAOA] literature is wrong and will soon be forgotten.”) the conclusions of MAOA research. Speaking of history, I wonder how perceptions of a connection between genetics research and reactionary ideas would impact genetics research funding.
<br><br>
Though University of North Carolina anthropologist Jonathan Marks could not sign the geneticists’ letter, he did <a href="http://inthesetimes.com/article/16674/the_genes_made_us_do_it">show</a> them that flippant dismissal of MAOA science need not be so lacking in flowery finesse.
<blockquote> Rather, he takes an enormous leap and speculates retrogressively that groups of people may simply differ in genes that affect personality and behavior. In his earlier book <u><i>Before the Dawn</i></u> (2007), Wade opined freely about the possible existence of ping-pong genes among the Chinese. Now he speculates about genetic propensities for violence among Africans, obedience in Chinese and capitalism in Jews. Mercifully, he stops short of inventing genes for basketball, laundry and stand-up comedy.</blockquote>
I am sure that he meant no implied insult of Chinese people’s ping-pong skills. Unlike ping-pong, violence is universal not only to humans but also to the entire animal kingdom and portions of the plant kingdom. Though none of these people mentioned it, scientists discovered <a href="http://theunsilencedscience.blogspot.com/2011/03/racial-controversy-of-violent-gene.html">Brunner syndrome</a>, which is marked by aggressive behavior apparently resulting from a completely nonfunctional MAOA gene, over twenty years ago. This lack of a functional MAOA gene also is present in some unusually aggressive mice. Scientists who attempted to interact with these MAOA-knockout mice found themselves in a real-life reenactment of Tom and Jerry.
<br><br>
Science writer Meredith Knight similarly <a href="http://www.geneticliteracyproject.org/2014/08/11/does-nicholas-wades-a-troublesome-inheritance-inaccurately-portray-evolution/">described</a> the twenty years of replicating the influence of MAOA on aggressiveness as a new, fragile overreach.
<blockquote> The scientific community largely agrees that Wade oversteps when making any claims about race, genetics and behavior, largely because evidence linking genetics and human behavior is so new and somewhat fragile. Even linking genes to major mental health disorders, like schizophrenia, is contentious. Relating genes to a more qualitative characteristic, like aggressiveness or social obedience seems rather an overreach.</blockquote>
Lest one think only liberal academics and reporters volunteer such brief, zero-substance slights of MAOA science, Charles Murray <a href="http://online.wsj.com/news/articles/SB10001424052702303380004579521482247869874">claimed</a> MAOA was a case in point of “tentative and often disputed” findings. Like the others, Murray’s brevity probably resulted from a lack of expertise that unfortunately did not accompany a more modest assertion. During Murray’s first public mention of Wade’s book (at the 45-minute mark), Harvard Professor of National Security and Military Affairs Stephen Peter Rosen brought up MAOA to Murray, confusing its gene-environment interaction with “epigenetics.” The environmental variable is measured in the environment, but that does not mean its mechanism of effect is nurture or epigenetics (which can also be influenced by genetics) rather than genetics.
<br><br>
<iframe width="393" height="259" src="http://www.youtube.com/embed/p_bFpmNSBiY?rel=0&start=2690&end=2958&autoplay=0" frameborder="0" allowfullscreen></iframe>
<br><br>
Reporter Robert VerBruggen <a href="http://www.realclearscience.com/articles/2014/05/06/race_is_real_what_does_that_mean_for_society_108642.html">questioned</a> whether Wade’s treatment of MAOA and other research relating to race was “suitable for a book aimed at the general public.” Apparently attacking MAOA science is suitable for the popular press, so why would defending it not be? I do not think most violent racists think about MAOA allele frequencies. Just as climate-change science belongs in many public policy discussions, well-reasoned and respectful discussion of MAOA can appropriately inform some social-justice debates and courtroom deliberations.
<br><br>
As Willamette University biologist <a href="http://theunsilencedscience.blogspot.com/2014/07/christopher-irwin-smith-is-idiot.html">Christopher Irwin Smith</a> and author <a href="http://theunsilencedscience.blogspot.com/2014/08/the-alondra-oubre-academic-fraud-exposed.html">Alondra Oubré</a> demonstrated, brief dismissals of MAOA research can make sense for a deluded scientist or writer because writing a lengthier composition will fill the Internet with more falsehoods and risk overspill. University of Maryland sociologist Philip Cohen wrote a somewhat <a href="http://www.bostonreview.net/books-ideas/philip-cohen-nicholas-wade-troublesome-inheritance">lengthy</a> <a href="http://familyinequality.wordpress.com/2014/06/25/wade-deeper-dive/">critique</a>, and it contains a number of mistakes, but perhaps these were honest mistakes.
<blockquote> Wade devotes considerable attention to MAO-A, the gene that encodes the enzyme monoamine oxidase A, which is related to aggression. He singles out studies showing that a rare version of the gene is associated with violence in U.S. male adolescents. Out of 1,200 young men surveyed in the National Longitudinal Study of Adolescent Health, eleven particularly violent young men carried the 2R version of MAO-A, subsequently known as the “warrior gene.” Nine of those eleven were African American, comprising 5 percent of the black male adolescents in the study…. Now Wade is off and running. He has a gene variant that is more common (though still rare) among black men and is associated with elevated rates of violence.</blockquote>
First, these basic facts need clarification. The National Longitudinal Study of Adolescent Health deliberately <a href="http://tools.nccor.org/css/system/37/">oversampled</a> African Americans with college-educated parents. Mixed racial ancestry is common among African Americans, so allele frequencies that are higher among African Americans than whites are probably even higher still among West Africans. The National Longitudinal Study of Adolescent Health contained nine African-American men with MAOA-2R based on interviewer-assessed race and ten based on self-reported race, constituting 5.2 percent or 5.5 percent of the African-American men, respectively. The term “warrior gene” dates back to a 2004 Science article by Ann Gibbons and explicitly refers to MAOA-3R, the most common allele of this VNTR promoter as providing a predisposition to violence, compared to MAOA-4R, which is the allele most common in white people. So, the relationship between MAOA and violence is already well-established in a large collection of research for a version that is not rare in any group.
<blockquote> This may be true. But it certainly overstates the strength of the case. Consider that, in the Adolescent Health data, black male adolescents were more than twice as likely as whites to report having committed an act of violence. If you found any gene that happened to be correlated with violence, chances are good it would also be correlated with race. Confirmation with more powerful genetic testing methods may strengthen this case in the future, but Wade’s inflated interpretation is not justified by the existing evidence.</blockquote>
This suggests that Cohen did not understand an extremely important fact about Beaver <i>et al</i>. That study compared African-American men with MAOA-2R to African-American men without MAOA-2R. Sociological inequities for African Americans could not confound a study that only included African Americans. The amount of African ancestry could confound, but that could result from genetic associations rather than class associations, since the percentage of African ancestry and class are probably not perfectly correlated.
<blockquote> Sometimes in genetics there is some gene or coding that produces some measureable effect, and that’s how most people seem to think about genetics most of the time – there is “a gene for” something. In the days before today’s genome-wide association (GWA) studies, before scientists had the means to investigate hundreds of thousands of genetic markers at a time, they often looked for effects of such “candidate” genes. This approach was valuable, especially when the role of specific genes was known (as in the case of the BRCA1 gene, associated with higher risk of breast cancer). However, with most diseases, and even more so with behavior, which is presumed to be more complicated than single-gene mechanisms, candidate gene studies were (are) often fishing expeditions, with a high risk of false-positive results, amplified by selective publication of positive findings. It is quite possible that’s at least part of what happened with MAO-A and aggression.</blockquote>
Genome-wide association studies on the genetics of violence and related mental illnesses have only used single-nucleotide polymorphism arrays, so far. Scientists can only study repeat polymorphisms like this promoter for MAOA with candidate-gene studies until whole-genome research technology becomes more advanced and widely available. However, the discovery of Brunner syndrome does not deserve to be called a “fishing expedition.” The rare missense mutation is virtually deterministic in its influence on behavior. Diseases like Norrie disease take out both MAOA and MAOB function and result in a severe set of morbidities. The standard GWAS attack on candidate-gene research that Cohen is repeating is flawed even for single-nucleotide polymorphisms but certainly lacks relevance for MAOA research. Meta-analyses for MAOA replicated the original findings, and the Byrd and Manuck meta-analysis found the effect was “no less likely to replicate in studies with sample sizes larger (or smaller)” than the original finding “or in studies published later.”
<blockquote>Most studies about MAOA have been gene-environment interaction studies, where some version of MAOA has a statistical association with a behavior only in the presence of a particular social factor, such as a history of child abuse.</blockquote>
No, they have not. Studies on the “main effect” of MAOA (the effect of MAOA on antisocial behavior without an interacting variable) began years earlier than the gene-environment interaction studies. The Ficks and Waldman meta-analysis of the main effect included 31 studies. The Byrd and Manuck meta-analysis of the gene-environment interaction only included 20 studies for the analysis of men.
<blockquote>First, that 2R version of MAO-A is very rare, and the two studies Wade cites about it … both used the same sample from Add Health – 11 boys with the variant. Two studies doesn’t mean two independent results. You could never get a drug approved based on that (I hope). Second, as far as I can tell there was no strong reason <i>a priori</i> to suspect that this 2R variant would be especially associated with violence. So that’s a caution. I have to say, as I did in the review, that it may be correct. But the evidence is not there (and you shouldn’t say “not there yet,” either). Those two studies are the entire evidentiary basis for Wade saying that genes that shape social behavior vary by race (“one behavioral gene … known to vary between races”.) I didn’t find any other studies that show MAO-A 2R varies by race (though maybe there are some).</blockquote>
No, research established the effect of MAOA in alleles that are not rare. When the Food and Drug Administration approves a drug, doctors receive wide leeway to prescribe it off-label and at dosages they deem appropriate. So, why should MAOA-2R not constitute a higher dosage of “warrior gene”? The strong <i>a priori</i> reason to suspect that MAOA-2R is especially associated with violence is that the study by Guo <i>et al</i> that Cohen reviewed also included an <i>in vitro</i> analysis of gene expression, which showed much lower expression for MAOA-2R. Brunner syndrome shows the effect of having an MAOA gene with zero gene expression. There are two additional studies on MAOA-2R and aggression in the Add Health sample. (I also would like to see more research on this in other samples.) However, the list of studies that establish differing allele frequencies for MAOA-2R, MAOA-3R, and MAOA-4R by race is long, and I have been attempting to tabulate them in a convenient <a href="http://theunsilencedscience.blogspot.com/2013/01/monoamine-oxidase-bibliography.html">table</a>.
<br><br>
In fairness, even Wade’s treatment of MAOA research was good but not perfect. He repeatedly referred to MAOA-2R as “two promoters.” It is actually two repeats of a DNA sequence within a single promoter. The distinction is important because MAOA actually does have multiple other promoters, including one other found to affect antisocial behavior in women more than this one, and this relates to Wade’s attempt to downplay the importance of MAOA.
<blockquote>Second, a large number of genes are evidently involved in controlling aggression, so even if African Americans are more likely to carry the violence-linked allele of MAO-A promoters than are Caucasians, Caucasians may carry the aggressive allele of other genes yet to be identified. Indeed a variant of a gene called HTR2B, an allele that predisposes carriers to impulsive and violent crimes when under the influence of alcohol, has been found in Finns. It is therefore impossible, by looking at single genes, to say on genetic grounds that one race is genetically more prone to violence than any other.</blockquote>
Determining the relative importance of MAOA compared to all other violence genes poses a significant challenge, but scientists have not even determined the importance of MAOA to overall aggression heritability, yet. Perhaps the controversy surrounding MAOA research or Wade’s book could convince the National Institutes of Health to fund a very large, international study to attempt to replicate and fully quantify the effects of every MAOA allele for every single-nucleotide polymorphism and promoter, every gene-environment interaction, every gene-drug interaction, every gene-hormone interaction, every gene-gene interaction, and every epigenetic effect together in the same study. Clues do exist that this single gene deserves all of the <a href="http://theunsilencedscience.blogspot.com/2011/08/genetics-of-violence.html">attention</a> that I have been giving it. The fact that MAOA research has discovered so many of these interaction effects could be evidence of the gene’s high importance. The other 2008 Guo <i>et al</i> study of MAOA-2R that Cohen did not review determined that the allele affected violent behavior more than two other candidate genes known for their effect on the neurotransmitter dopamine and that it had a large gene-environment interaction effect, as well. Brunner syndrome, itself, provides another clue. If MAOA is unimportant compared to unidentified functional alleles of other genes, why have scientists not discovered those through rare knockout polymorphisms?
<br><br>
Wade is pointing out such a knockout polymorphism syndrome for HTR2B. Like Brunner syndrome, only a small number of known cases exist, and that study claimed it was “apparently exclusive to Finns,” 1.2 percent of whom have it. Seven cases of the HTR2B knockout allele did not induce violent behavior, whereas Brunner syndrome research uncovered only four cases of MAOA knockout allele without accompanying antisocial behavior in men. HTR2B is on chromosome 2, and MAOA is on the X chromosome. So, men with an MAOA knockout allele have no MAOA enzyme. Men with the HTR2B knockout allele still have some HTR2B function except the one homozygote, and 1.2 percent is not the true allele frequency; 0.68 percent is. The hemizygosity of X-chromosome genes could increase their importance for behavior and help explain why men tend to commit more violent crime than women. Alcohol use precipitated 94 percent of violent crimes among these men with the HTR2B knockout allele. Follow-up research looked for personality effects of other alleles of the gene and came to contradicting conclusions.
<br><br>
Whatever evidentiary gaps exist should be taken to signify the need for more research, not an excuse for ignorant dismissals of the decades of existing research. I have good reason to interpret many of the listed errors and misjudgments as dishonest, politically motivated opposition to science. Oubré tried to pass off her work as a serious “reality check” for MAOA research. Her essay was full of careless errors, including completely wrong numbers taken from Wikipedia vandalism and attributed to the National Longitudinal Study of Adolescent Health. When I corrected the errors, her reply was complete denial (“I did not use Wikipedia for this article. Cheers.”), followed by admission with hysterical defensiveness against my unrealistic demand for correctness (“You imply that I should have a wider grasp of the literature on the MAOA gene, as though I am obligated to make this my raison d’etre…. Am I entitled to even have a life?”). When I suggested that the essay was a criticism of Wade’s book because she cited his book in a critical way, she responded that she had not even read it. Her editor’s response to me was initial denial, continued refusal to make a correction, and the statement, “I see not taking others seriously is your modus operandi.” Well, it is not simply a matter of an inability to take Alondra Oubré seriously. I am actually wondering whether anyone should take seriously anthropologists, sociologists, biologists, or population geneticists.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Psychiatric+quarterly&rft_id=info%3Apmid%2F24326626&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+2-Repeat+Allele+of+the+MAOA+Gene+Confers+an+Increased+Risk+for+Shooting+and+Stabbing+Behaviors.&rft.issn=0033-2720&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Beaver+KM&rft.au=Barnes+JC&rft.au=Boutwell+BB&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Beaver KM, Barnes JC, & Boutwell BB (2013). The 2-Repeat Allele of the MAOA Gene Confers an Increased Risk for Shooting and Stabbing Behaviors. <span style="font-style: italic;">The Psychiatric quarterly</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24326626">24326626</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Personality+and+Individual+Differences&rft_id=info%3Adoi%2F10.1016%2Fj.paid.2012.08.014&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Exploring+the+association+between+the+2-repeat+allele+of+the+MAOA+gene+promoter+polymorphism+and+psychopathic+personality+traits%2C+arrests%2C+incarceration%2C+and+lifetime+antisocial+behavior&rft.issn=01918869&rft.date=2013&rft.volume=54&rft.issue=2&rft.spage=164&rft.epage=168&rft.artnum=http%3A%2F%2Fwww.soc.iastate.edu%2Fstaff%2Fdelisi%2FMAOA%25202013.pdf&rft.au=Beaver%2C+K.&rft.au=Wright%2C+J.&rft.au=Boutwell%2C+B.&rft.au=Barnes%2C+J.&rft.au=DeLisi%2C+M.&rft.au=Vaughn%2C+M.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Beaver, K., Wright, J., Boutwell, B., Barnes, J., DeLisi, M., & Vaughn, M. (2013). Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior <span style="font-style: italic;">Personality and Individual Differences, 54</span> (2), 164-168 DOI: <a rev="review" href="http://dx.doi.org/10.1016/j.paid.2012.08.014">10.1016/j.paid.2012.08.014</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature&rft_id=info%3Apmid%2F21179162&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+population-specific+HTR2B+stop+codon+predisposes+to+severe+impulsivity.&rft.issn=0028-0836&rft.date=2010&rft.volume=468&rft.issue=7327&rft.spage=1061&rft.epage=6&rft.artnum=&rft.au=Bevilacqua+L&rft.au=Doly+S&rft.au=Kaprio+J&rft.au=Yuan+Q&rft.au=Tikkanen+R&rft.au=Paunio+T&rft.au=Zhou+Z&rft.au=Wedenoja+J&rft.au=Maroteaux+L&rft.au=Diaz+S&rft.au=Belmer+A&rft.au=Hodgkinson+CA&rft.au=Dell%27osso+L&rft.au=Suvisaari+J&rft.au=Coccaro+E&rft.au=Rose+RJ&rft.au=Peltonen+L&rft.au=Virkkunen+M&rft.au=Goldman+D&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Bevilacqua L, Doly S, Kaprio J, Yuan Q, Tikkanen R, Paunio T, Zhou Z, Wedenoja J, Maroteaux L, Diaz S, Belmer A, Hodgkinson CA, Dell'osso L, Suvisaari J, Coccaro E, Rose RJ, Peltonen L, Virkkunen M, & Goldman D (2010). A population-specific HTR2B stop codon predisposes to severe impulsivity. <span style="font-style: italic;">Nature, 468</span> (7327), 1061-6 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21179162">21179162</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+human+genetics&rft_id=info%3Apmid%2F8503438&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=X-linked+borderline+mental+retardation+with+prominent+behavioral+disturbance%3A+phenotype%2C+genetic+localization%2C+and+evidence+for+disturbed+monoamine+metabolism.&rft.issn=0002-9297&rft.date=1993&rft.volume=52&rft.issue=6&rft.spage=1032&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1682278%2Fpdf%2Fajhg00064-0013.pdf&rft.au=Brunner+HG&rft.au=Nelen+MR&rft.au=van+Zandvoort+P&rft.au=Abeling+NG&rft.au=van+Gennip+AH&rft.au=Wolters+EC&rft.au=Kuiper+MA&rft.au=Ropers+HH&rft.au=van+Oost+BA&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Brunner HG, Nelen MR, van Zandvoort P, Abeling NG, van Gennip AH, Wolters EC, Kuiper MA, Ropers HH, & van Oost BA (1993). X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. <span style="font-style: italic;">American journal of human genetics, 52</span> (6), 1032-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/8503438">8503438</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychiatry&rft_id=info%3Apmid%2F23786983&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA%2C+Childhood+Maltreatment%2C+and+Antisocial+Behavior%3A+Meta-analysis+of+a+Gene-Environment+Interaction.&rft.issn=0006-3223&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Byrd+AL&rft.au=Manuck+SB&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Byrd AL, & Manuck SB (2013). MAOA, Childhood Maltreatment, and Antisocial Behavior: Meta-analysis of a Gene-Environment Interaction. <span style="font-style: italic;">Biological psychiatry</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23786983">23786983</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft_id=info%3Apmid%2F7792602&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Aggressive+behavior+and+altered+amounts+of+brain+serotonin+and+norepinephrine+in+mice+lacking+MAOA.&rft.issn=0036-8075&rft.date=1995&rft.volume=268&rft.issue=5218&rft.spage=1763&rft.epage=6&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2Fpmc2844866%2F&rft.au=Cases+O&rft.au=Seif+I&rft.au=Grimsby+J&rft.au=Gaspar+P&rft.au=Chen+K&rft.au=Pournin+S&rft.au=M%C3%BCller+U&rft.au=Aguet+M&rft.au=Babinet+C&rft.au=Shih+JC&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, & Shih JC (1995). Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. <span style="font-style: italic;">Science (New York, N.Y.), 268</span> (5218), 1763-6 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/7792602">7792602</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+medical+genetics&rft_id=info%3Apmid%2F3162283&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Norrie+disease+resulting+from+a+gene+deletion%3A+clinical+features+and+DNA+studies.&rft.issn=0022-2593&rft.date=1988&rft.volume=25&rft.issue=2&rft.spage=73&rft.epage=8&rft.artnum=&rft.au=Donnai+D&rft.au=Mountford+RC&rft.au=Read+AP&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Donnai D, Mountford RC, & Read AP (1988). Norrie disease resulting from a gene deletion: clinical features and DNA studies. <span style="font-style: italic;">Journal of medical genetics, 25</span> (2), 73-8 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/3162283">3162283</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Behavior+genetics&rft_id=info%3Apmid%2F24902785&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Candidate+Genes+for+Aggression+and+Antisocial+Behavior%3A+A+Meta-analysis+of+Association+Studies+of+the+5HTTLPR+and+MAOA-uVNTR.&rft.issn=0001-8244&rft.date=2014&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Ficks+CA&rft.au=Waldman+ID&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. <span style="font-style: italic;">Behavior genetics</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24902785">24902785</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science&rft_id=info%3Adoi%2F10.1126%2Fscience.304.5672.818a&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=AMERICAN+ASSOCIATION+OF+PHYSICAL+ANTHROPOLOGISTS+MEETING%3A+Tracking+the+Evolutionary+History+of+a+%22Warrior%22+Gene&rft.issn=0036-8075&rft.date=2004&rft.volume=304&rft.issue=5672&rft.spage=818&rft.epage=818&rft.artnum=http%3A%2F%2Fwww.sciencemag.org%2Fcgi%2Fdoi%2F10.1126%2Fscience.304.5672.818a&rft.au=Gibbons%2C+A.&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Gibbons, A. (2004). AMERICAN ASSOCIATION OF PHYSICAL ANTHROPOLOGISTS MEETING: Tracking the Evolutionary History of a "Warrior" Gene <span style="font-style: italic;">Science, 304</span> (5672), 818-818 DOI: <a rev="review" href="http://dx.doi.org/10.1126/science.304.5672.818a">10.1126/science.304.5672.818a</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Sociological+Review&rft_id=info%3Adoi%2F10.1177%2F000312240807300402&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+Integration+of+Genetic+Propensities+into+Social-Control+Models+of+Delinquency+and+Violence+among+Male+Youths&rft.issn=0003-1224&rft.date=2008&rft.volume=73&rft.issue=4&rft.spage=543&rft.epage=568&rft.artnum=http%3A%2F%2Fandosciasociology.net%2Fresources%2FGenetics%2Band%2BSociology.pdf&rft.au=Guo%2C+G.&rft.au=Roettger%2C+M.&rft.au=Cai%2C+T.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Guo, G., Roettger, M., & Cai, T. (2008). The Integration of Genetic Propensities into Social-Control Models of Delinquency and Violence among Male Youths <span style="font-style: italic;">American Sociological Review, 73</span> (4), 543-568 DOI: <a rev="review" href="http://dx.doi.org/10.1177/000312240807300402">10.1177/000312240807300402</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=European+Journal+of+Human+Genetics&rft_id=info%3Adoi%2F10.1038%2Fsj.ejhg.5201999&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+VNTR+2+repeat+in+MAOA+and+delinquent+behavior+in+adolescence+and+young+adulthood%3A+associations+and+MAOA+promoter+activity&rft.issn=1018-4813&rft.date=2008&rft.volume=16&rft.issue=5&rft.spage=626&rft.epage=634&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2922855%2F&rft.au=Guo%2C+G.&rft.au=Ou%2C+X.&rft.au=Roettger%2C+M.&rft.au=Shih%2C+J.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Guo, G., Ou, X., Roettger, M., & Shih, J. (2008). The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity <span style="font-style: italic;">European Journal of Human Genetics, 16</span> (5), 626-634 DOI: <a rev="review" href="http://dx.doi.org/10.1038/sj.ejhg.5201999">10.1038/sj.ejhg.5201999</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychology&rft_id=info%3Apmid%2F21554924&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Gene+environment+interactions+with+a+novel+variable+Monoamine+Oxidase+A+transcriptional+enhancer+are+associated+with+antisocial+personality+disorder.&rft.issn=0301-0511&rft.date=2011&rft.volume=87&rft.issue=3&rft.spage=366&rft.epage=71&rft.artnum=&rft.au=Philibert+RA&rft.au=Wernett+P&rft.au=Plume+J&rft.au=Packer+H&rft.au=Brody+GH&rft.au=Beach+SR&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Philibert RA, Wernett P, Plume J, Packer H, Brody GH, & Beach SR (2011). Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder. <span style="font-style: italic;">Biological psychology, 87</span> (3), 366-71 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21554924">21554924</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Neuropsychobiology&rft_id=info%3Apmid%2F23774082&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=No+Association+between+a+polymorphism+in+the+serotonin+receptor+2B+%28HTR2B%29+gene+and+personality+traits+in+healthy+Japanese+subjects.&rft.issn=0302-282X&rft.date=2013&rft.volume=68&rft.issue=1&rft.spage=59&rft.epage=62&rft.artnum=&rft.au=Tsuchimine+S&rft.au=Taniguchi+T&rft.au=Sugawara+N&rft.au=Kaneda+A&rft.au=Yasui-Furukori+N&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Tsuchimine S, Taniguchi T, Sugawara N, Kaneda A, & Yasui-Furukori N (2013). No Association between a polymorphism in the serotonin receptor 2B (HTR2B) gene and personality traits in healthy Japanese subjects. <span style="font-style: italic;">Neuropsychobiology, 68</span> (1), 59-62 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23774082">23774082</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=New+Trends+in+Experimental+and+Clinical+Psychiatry&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Neuropsychiatric+and+biological+characteristics+of+X-linked+MAO-A+deficiency+syndrome.++A+single+case+intervention+study.&rft.issn=&rft.date=1995&rft.volume=95&rft.issue=&rft.spage=99&rft.epage=107&rft.artnum=&rft.au=Tuinier+S&rft.au=Verhoeven+WMA&rft.au=Scherders+MJWT&rft.au=Fekkes+D&rft.au=Pepplinkhuizen+L&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Tuinier S, Verhoeven WMA, Scherders MJWT, Fekkes D, & Pepplinkhuizen L (1995). Neuropsychiatric and biological characteristics of X-linked MAO-A deficiency syndrome. A single case intervention study. <span style="font-style: italic;">New Trends in Experimental and Clinical Psychiatry, 95</span>, 99-107</span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Personality+and+Individual+Differences&rft_id=info%3Adoi%2F10.1016%2Fj.paid.2012.07.026&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Association+between+the+HTR2B+gene+and+the+personality+trait+of+fun+seeking&rft.issn=01918869&rft.date=2012&rft.volume=53&rft.issue=8&rft.spage=1029&rft.epage=1033&rft.artnum=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0191886912003649&rft.au=Zhu+B&rft.au=Chen+C&rft.au=Moyzis+R&rft.au=Dong+Q&rft.au=Chen+C&rft.au=He+Q&rft.au=Li+J&rft.au=Lei+X&rft.au=Lin+C&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Zhu B, Chen C, Moyzis R, Dong Q, Chen C, He Q, Li J, Lei X, & Lin C (2012). Association between the HTR2B gene and the personality trait of fun seeking <span style="font-style: italic;">Personality and Individual Differences, 53</span> (8), 1029-1033 DOI: <a rev="review" href="http://dx.doi.org/10.1016/j.paid.2012.07.026">10.1016/j.paid.2012.07.026</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com13tag:blogger.com,1999:blog-5002675950760488813.post-59640610082913211492014-08-03T13:02:00.000-07:002014-08-03T15:23:57.333-07:00The Alondra Oubré Academic Fraud Exposed<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-2P8pIsra7z8/U962cDIqMMI/AAAAAAAABCo/aKG4hiTYw-g/s1600/Alondra+Oubr%C3%A9+Wikipedia+Scholar.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://4.bp.blogspot.com/-2P8pIsra7z8/U962cDIqMMI/AAAAAAAABCo/aKG4hiTYw-g/s400/Alondra+Oubr%C3%A9+Wikipedia+Scholar.jpg" /></a></div>
<b><center>Alondra Oubré</center>
<center>Wikipedia Scholar</center></b>
<br><br>
As further proof that a specific violence gene common to Africans threatens the worldview of fundamentalist anthropologists, Wikipedia scholar Alondra Oubré became the latest anthropologist to post an <a href="http://scientiasalon.wordpress.com/2014/07/31/the-extreme-warrior-gene-a-reality-check/">error-riddled Internet screed</a> against the warrior gene, monoamine oxidase A (MAOA). Oubré is the author of <i>Instinct and Revelation: Reflections on the Origins of Numinous Perception</i> and <i>Race, Genes and Ability: Rethinking Ethnic Differences</i>. She is also an expert at copying errors from Wikipedia into her writing. Her *Wikipedia* page lists her as a “newsmaker,” “prominent African American,” and an “African American achiever.” As an anti-science anthropologist, she joined her colleagues in writing another editorial against Nicholas Wade’s recent book, <i>A Troublesome Inheritance</i>, as well as the study of MAOA, a gene verified as causing violence in multiple meta-analyses. Unlike previous attacks on this science, no possibility exists that this is anything other than academic fraud. Oubré took false information from Wikipedia, for which I provide here the proof, and she deliberately lied about her source. I repeatedly requested an official correction from her editor, author and City University of New York professor Massimo Pigliucci, who refused to do so. What follows is a point-by-point refutation of Oubré’s work.
<br><br>
<blockquote>
Wow! What a poorly researched Internet post! I hope you don’t mind if I post the factual corrections here for you.
<br><br>
“The most common variant, MAOA-4R, has four repeats and is associated with high-activity breakdown of neurotransmitters.”
<br><br>
I guess it would be true that MAOA-4R is the most common variant if everyone in the world was white.
<br><br>
“Up to this point, all of the studies on the MAOA gene had been conducted in Caucasians. That changed when researchers started investigating this gene in the Maori of New Zealand.”
<br><br>
No, here is a list of studies that looked at non-whites prior to that study: Sabol <i>et al</i>, Kunugi <i>et al</i>, Balciuniene <i>et al</i>, Gilad <i>et al</i>, Ono <i>et al</i>, Williams <i>et al</i>, Koen <i>et al</i>, Huang <i>et al</i>, Yu <i>et al</i>, Young <i>et al</i>, Widom & Brzustowicz, and Rosenberg <i>et al</i>.
<br><br>
“For many experts, this ethnic gap is the result of numerous environmental causes, including poverty.”
<br><br>
I think you should revise this sentence.
<br><br>
“It turned out that while 3R was found in 56% of Maori males, it occurred in 58% of African American males and 34% of European males.”
<br><br>
Notice how the African-American number is slightly lower than the source? <a href="http://en.wikipedia.org/w/index.php?title=Monoamine_oxidase_A&diff=600804523&oldid=600683300 ">Someone in Wikipedia</a> has been tweaking the numbers at will. I don’t recommend that you rely so heavily on Wikipedia as your source for just this sort of reason. I also don’t recommend that you rely on that “study” by Lea and Chambers, which was the source of the “<a href="http://theunsilencedscience.blogspot.com/2013/12/the-stupid-stupidity-surrounding.html">idiot test</a>” copy-and-paste error that slandered Chinese men as having an MAOA-3R allele frequency of 77%.
<br><br>
“Interestingly, the press ignored studies indicating that the 3R variant occurred in 61% of Taiwanese males [15] and 56% of Chinese males [16].”
<br><br>
You switched your sources. Both samples were Taiwanese. You rounded 54.5% to 56%. That’s kind of sloppy.
<br><br>
“In the Add Health database, 5.5% of African American men, 0.9% of Caucasian men, and 0.00067% of Asian men have 2R.”
<br><br>
So, you took these numbers from Add Health, did you? No, you didn’t. I know because I calculated the number for Asian men and posted it on <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">my blog</a> and Wikipedia. Once again, the <a href="http://en.wikipedia.org/w/index.php?title=Monoamine_oxidase_A&diff=600804523&oldid=600683300 ">Wikipedia troll</a> screwed up your numbers for white men by a factor of 9. The Asian allele frequency was based on eight studies. I only found one Asian with MAOA-2R in those studies, but I have since looked at other studies and revised the number upwards. I have been maintaining a <a href="http://theunsilencedscience.blogspot.com/2013/01/monoamine-oxidase-bibliography.html">table</a> with my tabulated allele frequencies (without excluding any sample).
<br><br>
“This has led some popular writers to speculate that MAOA-2R might account for — or at least play a significant role in — the relatively higher rates of violent crime in African Americans. Not everyone agrees [21].”
<br><br>
If one writes, “Not everyone agrees,” it is good form to make sure that the source cited expresses some disagreement with what one wrote before “Not everyone agrees.”
<br><br>
“The rates of 2R are more than five times higher in African American males than in American white males, at least in the Add Health sample.”
<br><br>
Yeah, I guess 55 is more than 5. Damn that Wikipedia troll! Choe <i>et al</i>, which you cited, found it in 6% of black men and 0% of white men, so maybe it’s infinity times more common. Seriously, considering how rare it is in whites and Asians, why should we believe that those rare exceptions are actually genetically 100% white or Asian?
<br><br>
“Although genes affect individual differences in behavior, the effect of each individual gene is usually small.”
<br><br>
I think you meant to say “allele.” If the effects of individual genes are usually small, then missense mutations that completely shut off the gene and eliminate the protein should have little effect. Of course, you failed to mention the missense mutation specific to MAOA, which causes Brunner syndrome. The effect of Brunner syndrome on behavior is not small.
<br><br>
“The more common low-activity variant, 3R, interacts with adverse social effects such as childhood maltreatment. But other possible environmental factors, which conceivably could interact with the 2R, may not have been explored in-depth as yet.”
<br><br>
I think Fergusson <i>et al</i> did the most in-depth analysis of various environmental factors. Interestingly, the interaction effect of IQ on violence was more powerful than the interaction effect of childhood maltreatment. I’m afraid that you’ll have to look up for yourself whether African Americans differ from whites and Asians in average IQ because that is outside my area of expertise.
<br><br>
“Using PET imaging scans, these researchers found no correlation between MAOA brain levels and MAOA gene variants.”
<br><br>
However, Alia-Klein <i>et al</i> did find MAOA promoter effects on anger in an fMRI study. That study and Buckholtz <i>et al</i> found MAOA gene effects on the amygdala. Cerasa <i>et al</i> found that the gene influenced orbitofrontal cortical thickness with MRI. Buckholtz <i>et al</i> and Cerasa <i>et al</i> had much larger samples than the 34 men in Shumay <i>et al</i>. Shouldn’t you have mentioned those findings?
<br><br>
“Nonetheless, their results suggest that MAOA brain levels, which affect mood, are at least partially regulated by non-genetic factors — i.e., epigenetically.”
<br><br>
Of course, genes do influence epigenetics. In fact, the “environmental” interaction factors, like childhood maltreatment, might also have a component of heritability. Wong <i>et al</i> found that, compared to women, epigenetics of MAOA in men is minimal, low in variance, and high in hereditary influence. Pinsonneault <i>et al</i> was unable to detect any MAOA methylation in men. Philibert <i>et al</i> found less MAOA methylation in men and that MAOA methylation had no effect on antisocial personality disorder in men or women. That seems like a relevant finding.
<br><br>
“The jury is still out on whether 2R, the rare MAOA gene, acts independently of the environment (and independently of other genes) to shape antisocial personality traits.”
<br><br>
First of all, is MAOA-2R rare in Africans? A common definition of a rare allele is having an allele frequency less than 5%. It might not be rare in African-American men. We can extrapolate to the higher allele frequency in a population of Africans who are not racially mixed. All of the evidence we have on MAOA-2R, so far, suggests that it has a powerful effect independently of environment. The assumption is that this distinguishes MAOA-2R from MAOA-3R, which supposedly only has a gene-environment interaction effect. <a href="http://theunsilencedscience.blogspot.com/2014/07/the-warrior-gene-back-from-grave.html">A recent meta-analysis</a> of 31 studies actually disproved this and found that MAOA-3R has a slight effect on antisocial behavior independent of interaction factors.
</blockquote>
<br>
Pigliucci allowed me to post this comment only so that others could harass me with baseless <i>ad hominem</i>, but he censored all of my other responses.
<br><br>
Exposing falsehoods about the warrior gene is <a href="http://theunsilencedscience.blogspot.com/2011/08/genetics-of-violence.html">nothing new</a> for me, but this is different. It might be hard to believe that a respected scientist like <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html ">Steven Pinker</a> or an experienced writer like John Horgan would fall for the idiot test or that <a href="http://blogs.scientificamerican.com/cross-check/2011/04/26/code-rage-the-warrior-gene-makes-me-mad-whether-i-have-it-or-not/">Scientific American</a>, <a href="http://chronicle.com/article/Born-Outlaws-A-Criminally/128197/">The Chronicle of Higher Education</a>, and various journals and book publishers would reprint it. While one might not expect such incompetence from these sources, no evidence proves malfeasance. Also, Oubré’s mischaracterization of the science of MAOA epigenetics and brain imaging (also see Lei <i>et al</i>) is likely but not positively deceptive. In other words, she probably came across the evidence against her thesis and chose to keep it to herself, but one cannot absolutely demonstrate this as such. However, she unmistakingly lied when she attributed Wikipedia data to the Add Health subsample of the famous, widely used National Longitudinal Study of Adolescent Health database.
<br><br>
Interestingly, the idiot test almost constitutes a photographic negative of this fraud. The original copy-and-paste error by Rod Lea and Geoffrey Chambers first appeared in a scientific journal—perhaps not a highly respected journal, but a journal nonetheless—and subsequently spread to the public through mass media. This time, misinformation sprouted from the lowly, anonymously edited Wikipedia and traveled up the media food chain to scientific blogs. The Wikipedia page for MAOA originally contained correct information that I and other responsible agents copied correctly from peer-reviewed studies. Then, someone identified only by their Internet Protocol address, 76.78.226.57, began altering the data. One can observe from this person’s <a href="http://en.wikipedia.org/wiki/Special:Contributions/76.78.226.57">contributions page</a>, that he or she has a history of altering numbers in Wikipedia that relate to <a href="http://en.wikipedia.org/w/index.php?title=History_of_immigration_to_the_United_States&diff=599967864&oldid=598624275">immigration</a> and <a href="http://en.wikipedia.org/w/index.php?title=Mexicans_of_European_descent&diff=599631119&oldid=598802409">ethnicity</a> helter-skelter without providing new sources. On March 22nd, the offender made three unsourced edits to the same group of numbers on the MAOA page. At 2:25, the <a href="http://en.wikipedia.org/w/index.php?title=Monoamine_oxidase_A&diff=600683134&oldid=597682980">change</a> was as follows:
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-VxNaDQ5fOXc/U96Ov6z36XI/AAAAAAAABCA/EkF2PEQi4cg/s1600/maoa+wiki+3-22-2014+1.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://4.bp.blogspot.com/-VxNaDQ5fOXc/U96Ov6z36XI/AAAAAAAABCA/EkF2PEQi4cg/s400/maoa+wiki+3-22-2014+1.png" /></a></div>
<br>
Two minutes later, <a href="http://en.wikipedia.org/w/index.php?title=Monoamine_oxidase_A&diff=next&oldid=600683134">another change occurred</a>:
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-gI39waDilrQ/U96O12s6wzI/AAAAAAAABCI/sdEwRYASrrE/s1600/maoa+wiki+3-22-2014+2.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-gI39waDilrQ/U96O12s6wzI/AAAAAAAABCI/sdEwRYASrrE/s400/maoa+wiki+3-22-2014+2.png" /></a></div>
<br>
At 23:55, the offender <a href="http://en.wikipedia.org/w/index.php?title=Monoamine_oxidase_A&diff=next&oldid=600683300">changed</a> the same numbers, again:
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-Us-JO1BTGRo/U96O76f83kI/AAAAAAAABCQ/VYGq_2UrbC4/s1600/maoa+wiki+3-22-2014+3.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-Us-JO1BTGRo/U96O76f83kI/AAAAAAAABCQ/VYGq_2UrbC4/s400/maoa+wiki+3-22-2014+3.png" /></a></div>
<br>
This allowed for an error of an order of magnitude in Oubré’s numbers. So, who is 76.78.226.57? Is she Oubré? Is he Pigliucci? Who knows? Maybe he is Eric Holder. Nobody who knows is saying.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-8t7UiqXK4iA/U96PDehvO2I/AAAAAAAABCY/sT13SdpJvBs/s1600/massimo+pigliucci.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://1.bp.blogspot.com/-8t7UiqXK4iA/U96PDehvO2I/AAAAAAAABCY/sT13SdpJvBs/s400/massimo+pigliucci.jpg" /></a></div>
<b><center>Massimo Pigliucci</center>
<center>“Editor-in-Chief”</center></b>
<br><br>
To prevent confusion among the lay public, I politely asked Scientia Salon editor-in-chief Pigliucci for an official correction in this e-mail:
<br><br>
<blockquote>You posted my corrections for "The Extreme Warrior gene: a reality check" as a comment. However, the errors were quite serious, such as claiming that data from Wikipedia (which was false information) actually came from the National Longitudinal Study of Adolescent Health. Such errors should not only be addressed by an outsider's comment. As the editor-in-chief of Scientia Salon, you should see that someone actually investigates my claims and posts a complete correction, if true. Alternatively, you could direct me to the appropriate authority within your site who handles corrections.</blockquote>
<br>
Pigliucci could not bother himself with more than a curt reply.
<br><br>
<blockquote>your comment has been published, so I’m not sure what additional action you expect from me, or why.</blockquote>
<br>
I tried repeatedly.
<br><br>
<blockquote>Yes or no, did Alondra Oubré falsely claim on your site that information she took from Wikipedia had actually come from the Add Health subsample of the National Longitudinal Study of Adolescent Health? If yes, was the information from Wikipedia all accurate? If she falsely attributed false information from Wikipedia, why do you refuse to post an official correction at the end of her piece, as any reputable source of information would? I noted numerous other errors, but this one in particular seems especially egregious because it reveals a lack of integrity and provides a conduit for anyone to make up information on Wikipedia and disseminate it through disreputable blogs.</blockquote>
<br>
No reply came.
<br><br>
As shown by her citations, Oubré obviously intended her perversion of MAOA science as a rebuttal to Wade. Less than three weeks prior, Pigliucci spent forty-two minutes in a <a href="http://rationallyspeakingpodcast.org/show/rs112-race-just-a-social-construct.html">podcast</a> expatiating the standard semantic criticism that has amounted to basically the entirety of the fundamentalist anthropologist attack on Wade’s book. They call Wade a <a href="http://anthropomics2.blogspot.com/2014/06/nazis-love-nicholas-wade-shouldnt-that.html">racist</a>, and, in modern civilization, racists might be preferred to pedophiles but are considered far worse than necrophiliacs, cannibals, terrorists, zombies, Democrats, rapists, and even boy-band alumnae. Wade spent a good portion of his book criticizing white supremacy and called a book by JP Rushton racist in an interview. If idiotic anthropologists label every prestigious intellectual with whom they disagree a white supremacist, then the desire to be white supremacist among average white folks will grow like the tuition rates that young people pay to hear idiotic anthropologists bloviate. The colloquial definition of racism is the belief that average ability and tendency differences (stereotypes) exist between peoples grouped by place of origin. Heritability mathematics has nothing to do with it. Therefore, all anti-racists are racists. Actually, I would like to see the forces of good defeat white supremacy, which is why I know that the perceptual and strategic superiority lies with the recognition that the face of neo-Nazi white supremacy is the one covered in tattoos.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Emotion+%28Washington%2C+D.C.%29&rft_id=info%3Apmid%2F19485616&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Neural+mechanisms+of+anger+regulation+as+a+function+of+genetic+risk+for+violence.&rft.issn=1528-3542&rft.date=2009&rft.volume=9&rft.issue=3&rft.spage=385&rft.epage=96&rft.artnum=&rft.au=Alia-Klein+N&rft.au=Goldstein+RZ&rft.au=Tomasi+D&rft.au=Woicik+PA&rft.au=Moeller+SJ&rft.au=Williams+B&rft.au=Craig+IW&rft.au=Telang+F&rft.au=Biegon+A&rft.au=Wang+GJ&rft.au=Fowler+JS&rft.au=Volkow+ND&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Alia-Klein N, Goldstein RZ, Tomasi D, Woicik PA, Moeller SJ, Williams B, Craig IW, Telang F, Biegon A, Wang GJ, Fowler JS, & Volkow ND (2009). Neural mechanisms of anger regulation as a function of genetic risk for violence. <span style="font-style: italic;">Emotion (Washington, D.C.), 9</span> (3), 385-96 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19485616">19485616</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+molecular+evolution&rft_id=info%3Apmid%2F11231895&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+geographic+distribution+of+monoamine+oxidase+haplotypes+supports+a+bottleneck+during+the+dispersion+of+modern+humans+from+Africa.&rft.issn=0022-2844&rft.date=2001&rft.volume=52&rft.issue=2&rft.spage=157&rft.epage=63&rft.artnum=&rft.au=Balciuniene+J&rft.au=Syv%C3%A4nen+AC&rft.au=McLeod+HL&rft.au=Pettersson+U&rft.au=Jazin+EE&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Balciuniene J, Syvänen AC, McLeod HL, Pettersson U, & Jazin EE (2001). The geographic distribution of monoamine oxidase haplotypes supports a bottleneck during the dispersion of modern humans from Africa. <span style="font-style: italic;">Journal of molecular evolution, 52</span> (2), 157-63 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/11231895">11231895</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Molecular+psychiatry&rft_id=info%3Apmid%2F17519928&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genetic+variation+in+MAOA+modulates+ventromedial+prefrontal+circuitry+mediating+individual+differences+in+human+personality.&rft.issn=1359-4184&rft.date=2008&rft.volume=13&rft.issue=3&rft.spage=313&rft.epage=24&rft.artnum=&rft.au=Buckholtz+JW&rft.au=Callicott+JH&rft.au=Kolachana+B&rft.au=Hariri+AR&rft.au=Goldberg+TE&rft.au=Genderson+M&rft.au=Egan+MF&rft.au=Mattay+VS&rft.au=Weinberger+DR&rft.au=Meyer-Lindenberg+A&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Buckholtz JW, Callicott JH, Kolachana B, Hariri AR, Goldberg TE, Genderson M, Egan MF, Mattay VS, Weinberger DR, & Meyer-Lindenberg A (2008). Genetic variation in MAOA modulates ventromedial prefrontal circuitry mediating individual differences in human personality. <span style="font-style: italic;">Molecular psychiatry, 13</span> (3), 313-24 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/17519928">17519928</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Behavioural+brain+research&rft_id=info%3Apmid%2F20303364&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Morphological+correlates+of+MAO+A+VNTR+polymorphism%3A+new+evidence+from+cortical+thickness+measurement.&rft.issn=0166-4328&rft.date=2010&rft.volume=211&rft.issue=1&rft.spage=118&rft.epage=24&rft.artnum=&rft.au=Cerasa+A&rft.au=Cherubini+A&rft.au=Quattrone+A&rft.au=Gioia+MC&rft.au=Magariello+A&rft.au=Muglia+M&rft.au=Manna+I&rft.au=Assogna+F&rft.au=Caltagirone+C&rft.au=Spalletta+G&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Cerasa A, Cherubini A, Quattrone A, Gioia MC, Magariello A, Muglia M, Manna I, Assogna F, Caltagirone C, & Spalletta G (2010). Morphological correlates of MAO A VNTR polymorphism: new evidence from cortical thickness measurement. <span style="font-style: italic;">Behavioural brain research, 211</span> (1), 118-24 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20303364">20303364</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Behavior+genetics&rft_id=info%3Apmid%2F24902785&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Candidate+Genes+for+Aggression+and+Antisocial+Behavior%3A+A+Meta-analysis+of+Association+Studies+of+the+5HTTLPR+and+MAOA-uVNTR.&rft.issn=0001-8244&rft.date=2014&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Ficks+CA&rft.au=Waldman+ID&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. <span style="font-style: italic;">Behavior genetics</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24902785">24902785</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft_id=info%3Apmid%2F22297589&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Moderating+role+of+the+MAOA+genotype+in+antisocial+behaviour.&rft.issn=0007-1250&rft.date=2012&rft.volume=200&rft.issue=2&rft.spage=116&rft.epage=23&rft.artnum=&rft.au=Fergusson+DM&rft.au=Boden+JM&rft.au=Horwood+LJ&rft.au=Miller+A&rft.au=Kennedy+MA&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA (2012). Moderating role of the MAOA genotype in antisocial behaviour. <span style="font-style: italic;">The British journal of psychiatry : the journal of mental science, 200</span> (2), 116-23 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22297589">22297589</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft_id=info%3Apmid%2F11805333&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Evidence+for+positive+selection+and+population+structure+at+the+human+MAO-A+gene.&rft.issn=0027-8424&rft.date=2002&rft.volume=99&rft.issue=2&rft.spage=862&rft.epage=7&rft.artnum=&rft.au=Gilad+Y&rft.au=Rosenberg+S&rft.au=Przeworski+M&rft.au=Lancet+D&rft.au=Skorecki+K&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Gilad Y, Rosenberg S, Przeworski M, Lancet D, & Skorecki K (2002). Evidence for positive selection and population structure at the human MAO-A gene. <span style="font-style: italic;">Proceedings of the National Academy of Sciences of the United States of America, 99</span> (2), 862-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/11805333">11805333</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft_id=info%3Apmid%2F15150530&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=An+association+between+a+functional+polymorphism+in+the+monoamine+oxidase+a+gene+promoter%2C+impulsive+traits+and+early+abuse+experiences.&rft.issn=0893-133X&rft.date=2004&rft.volume=29&rft.issue=8&rft.spage=1498&rft.epage=505&rft.artnum=&rft.au=Huang+YY&rft.au=Cate+SP&rft.au=Battistuzzi+C&rft.au=Oquendo+MA&rft.au=Brent+D&rft.au=Mann+JJ&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Huang YY, Cate SP, Battistuzzi C, Oquendo MA, Brent D, & Mann JJ (2004). An association between a functional polymorphism in the monoamine oxidase a gene promoter, impulsive traits and early abuse experiences. <span style="font-style: italic;">Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 29</span> (8), 1498-505 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/15150530">15150530</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Australian+and+New+Zealand+Journal+of+Psychiatry&rft_id=info%3Adoi%2F10.1111%2Fj.1440-1614.2004.01338.x&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Violence+in+male+patients+with+schizophrenia%3A+risk+markers+in+a+South+African+population&rft.issn=0004-8674&rft.date=2004&rft.volume=38&rft.issue=4&rft.spage=254&rft.epage=259&rft.artnum=http%3A%2F%2Fwww.blackwell-synergy.com%2Flinks%2Fdoi%2F10.1111%252Fj.1440-1614.2004.01338.x&rft.au=Koen+L&rft.au=Kinnear+C&rft.au=Corfield+V&rft.au=Emsley+R&rft.au=Jordaan+E&rft.au=Keyter+N&rft.au=Moolman-Smook+J&rft.au=Stein+D&rft.au=Niehaus+D&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Koen L, Kinnear C, Corfield V, Emsley R, Jordaan E, Keyter N, Moolman-Smook J, Stein D, & Niehaus D (2004). Violence in male patients with schizophrenia: risk markers in a South African population <span style="font-style: italic;">Australian and New Zealand Journal of Psychiatry, 38</span> (4), 254-259 DOI: <a rev="review" href="http://dx.doi.org/10.1111/j.1440-1614.2004.01338.x">10.1111/j.1440-1614.2004.01338.x</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Molecular+psychiatry&rft_id=info%3Apmid%2F10483059&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+functional+polymorphism+in+the+promoter+region+of+monoamine+oxidase-A+gene+and+mood+disorders.&rft.issn=1359-4184&rft.date=1999&rft.volume=4&rft.issue=4&rft.spage=393&rft.epage=5&rft.artnum=&rft.au=Kunugi+H&rft.au=Ishida+S&rft.au=Kato+T&rft.au=Tatsumi+M&rft.au=Sakai+T&rft.au=Hattori+M&rft.au=Hirose+T&rft.au=Nanko+S&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Kunugi H, Ishida S, Kato T, Tatsumi M, Sakai T, Hattori M, Hirose T, & Nanko S (1999). A functional polymorphism in the promoter region of monoamine oxidase-A gene and mood disorders. <span style="font-style: italic;">Molecular psychiatry, 4</span> (4), 393-5 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/10483059">10483059</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=BioMed+research+international&rft_id=info%3Apmid%2F24971323&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+Functional+Polymorphism+of+the+MAOA+Gene+Modulates+Spontaneous+Brain+Activity+in+Pons.&rft.issn=2314-6133&rft.date=2014&rft.volume=2014&rft.issue=&rft.spage=243280&rft.epage=&rft.artnum=&rft.au=Lei+H&rft.au=Zhang+X&rft.au=Di+X&rft.au=Rao+H&rft.au=Ming+Q&rft.au=Zhang+J&rft.au=Guo+X&rft.au=Jiang+Y&rft.au=Gao+Y&rft.au=Yi+J&rft.au=Zhu+X&rft.au=Yao+S&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Lei H, Zhang X, Di X, Rao H, Ming Q, Zhang J, Guo X, Jiang Y, Gao Y, Yi J, Zhu X, & Yao S (2014). A Functional Polymorphism of the MAOA Gene Modulates Spontaneous Brain Activity in Pons. <span style="font-style: italic;">BioMed research international, 2014</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24971323">24971323</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+medical+genetics&rft_id=info%3Apmid%2F11920860&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=No+evidence+of+an+association+between+a+functional+monoamine+oxidase+a+gene+polymorphism+and+completed+suicides.&rft.issn=0148-7299&rft.date=2002&rft.volume=114&rft.issue=3&rft.spage=340&rft.epage=2&rft.artnum=&rft.au=Ono+H&rft.au=Shirakawa+O&rft.au=Nishiguchi+N&rft.au=Nishimura+A&rft.au=Nushida+H&rft.au=Ueno+Y&rft.au=Maeda+K&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Ono H, Shirakawa O, Nishiguchi N, Nishimura A, Nushida H, Ueno Y, & Maeda K (2002). No evidence of an association between a functional monoamine oxidase a gene polymorphism and completed suicides. <span style="font-style: italic;">American journal of medical genetics, 114</span> (3), 340-2 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/11920860">11920860</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+medical+genetics.+Part+B%2C+Neuropsychiatric+genetics+%3A+the+official+publication+of+the+International+Society+of+Psychiatric+Genetics&rft_id=info%3Apmid%2F18454435&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+methylation+is+associated+with+nicotine+and+alcohol+dependence+in+women.&rft.issn=1552-4841&rft.date=2008&rft.volume=147B&rft.issue=5&rft.spage=565&rft.epage=70&rft.artnum=&rft.au=Philibert+RA&rft.au=Gunter+TD&rft.au=Beach+SR&rft.au=Brody+GH&rft.au=Madan+A&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A (2008). MAOA methylation is associated with nicotine and alcohol dependence in women. <span style="font-style: italic;">American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B</span> (5), 565-70 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/18454435">18454435</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Human+molecular+genetics&rft_id=info%3Apmid%2F16893905&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Allelic+mRNA+expression+of+X-linked+monoamine+oxidase+a+%28MAOA%29+in+human+brain%3A+dissection+of+epigenetic+and+genetic+factors.&rft.issn=0964-6906&rft.date=2006&rft.volume=15&rft.issue=17&rft.spage=2636&rft.epage=49&rft.artnum=&rft.au=Pinsonneault+JK&rft.au=Papp+AC&rft.au=Sad%C3%A9e+W&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Pinsonneault JK, Papp AC, & Sadée W (2006). Allelic mRNA expression of X-linked monoamine oxidase a (MAOA) in human brain: dissection of epigenetic and genetic factors. <span style="font-style: italic;">Human molecular genetics, 15</span> (17), 2636-49 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/16893905">16893905</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Human+genetics&rft_id=info%3Apmid%2F16896926&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+association+of+DNA+sequence+variation+at+the+MAOA+genetic+locus+with+quantitative+behavioural+traits+in+normal+males.&rft.issn=0340-6717&rft.date=2006&rft.volume=120&rft.issue=4&rft.spage=447&rft.epage=59&rft.artnum=&rft.au=Rosenberg+S&rft.au=Templeton+AR&rft.au=Feigin+PD&rft.au=Lancet+D&rft.au=Beckmann+JS&rft.au=Selig+S&rft.au=Hamer+DH&rft.au=Skorecki+K&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Rosenberg S, Templeton AR, Feigin PD, Lancet D, Beckmann JS, Selig S, Hamer DH, & Skorecki K (2006). The association of DNA sequence variation at the MAOA genetic locus with quantitative behavioural traits in normal males. <span style="font-style: italic;">Human genetics, 120</span> (4), 447-59 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/16896926">16896926</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Human+Genetics&rft_id=info%3Adoi%2F10.1007%2Fs004390050816&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+functional+polymorphism+in+the+monoamine+oxidase+A+gene+promoter&rft.issn=0340-6717&rft.date=2014&rft.volume=103&rft.issue=3&rft.spage=273&rft.epage=279&rft.artnum=http%3A%2F%2Flink.springer.com%2F10.1007%2Fs004390050816&rft.au=Sabol+S&rft.au=Hu+S&rft.au=Hamer+D&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Sabol S, Hu S, & Hamer D (2014). A functional polymorphism in the monoamine oxidase A gene promoter <span style="font-style: italic;">Human Genetics, 103</span> (3), 273-279 DOI: <a rev="review" href="http://dx.doi.org/10.1007/s004390050816">10.1007/s004390050816</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychiatry&rft_id=info%3Apmid%2F16814261&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+and+the+%22cycle+of+violence%3A%22+childhood+abuse+and+neglect%2C+MAOA+genotype%2C+and+risk+for+violent+and+antisocial+behavior.&rft.issn=0006-3223&rft.date=2006&rft.volume=60&rft.issue=7&rft.spage=684&rft.epage=9&rft.artnum=&rft.au=Widom+CS&rft.au=Brzustowicz+LM&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Widom CS, & Brzustowicz LM (2006). MAOA and the "cycle of violence:" childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. <span style="font-style: italic;">Biological psychiatry, 60</span> (7), 684-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/16814261">16814261</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft_id=info%3Apmid%2F12629534&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Serotonin-related+gene+polymorphisms+and+central+nervous+system+serotonin+function.&rft.issn=0893-133X&rft.date=2003&rft.volume=28&rft.issue=3&rft.spage=533&rft.epage=41&rft.artnum=&rft.au=Williams+RB&rft.au=Marchuk+DA&rft.au=Gadde+KM&rft.au=Barefoot+JC&rft.au=Grichnik+K&rft.au=Helms+MJ&rft.au=Kuhn+CM&rft.au=Lewis+JG&rft.au=Schanberg+SM&rft.au=Stafford-Smith+M&rft.au=Suarez+EC&rft.au=Clary+GL&rft.au=Svenson+IK&rft.au=Siegler+IC&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Williams RB, Marchuk DA, Gadde KM, Barefoot JC, Grichnik K, Helms MJ, Kuhn CM, Lewis JG, Schanberg SM, Stafford-Smith M, Suarez EC, Clary GL, Svenson IK, & Siegler IC (2003). Serotonin-related gene polymorphisms and central nervous system serotonin function. <span style="font-style: italic;">Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 28</span> (3), 533-41 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/12629534">12629534</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Epigenetics+%3A+official+journal+of+the+DNA+Methylation+Society&rft_id=info%3Apmid%2F20505345&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+longitudinal+study+of+epigenetic+variation+in+twins.&rft.issn=1559-2294&rft.date=2010&rft.volume=5&rft.issue=6&rft.spage=516&rft.epage=26&rft.artnum=&rft.au=Wong+CC&rft.au=Caspi+A&rft.au=Williams+B&rft.au=Craig+IW&rft.au=Houts+R&rft.au=Ambler+A&rft.au=Moffitt+TE&rft.au=Mill+J&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, Moffitt TE, & Mill J (2010). A longitudinal study of epigenetic variation in twins. <span style="font-style: italic;">Epigenetics : official journal of the DNA Methylation Society, 5</span> (6), 516-26 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20505345">20505345</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+American+journal+of+psychiatry&rft_id=info%3Apmid%2F16741202&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Interaction+between+MAO-A+genotype+and+maltreatment+in+the+risk+for+conduct+disorder%3A+failure+to+confirm+in+adolescent+patients.&rft.issn=0002-953X&rft.date=2006&rft.volume=163&rft.issue=6&rft.spage=1019&rft.epage=25&rft.artnum=&rft.au=Young+SE&rft.au=Smolen+A&rft.au=Hewitt+JK&rft.au=Haberstick+BC&rft.au=Stallings+MC&rft.au=Corley+RP&rft.au=Crowley+TJ&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Young SE, Smolen A, Hewitt JK, Haberstick BC, Stallings MC, Corley RP, & Crowley TJ (2006). Interaction between MAO-A genotype and maltreatment in the risk for conduct disorder: failure to confirm in adolescent patients. <span style="font-style: italic;">The American journal of psychiatry, 163</span> (6), 1019-25 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/16741202">16741202</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft_id=info%3Apmid%2F15956990&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Association+study+of+a+monoamine+oxidase+a+gene+promoter+polymorphism+with+major+depressive+disorder+and+antidepressant+response.&rft.issn=0893-133X&rft.date=2005&rft.volume=30&rft.issue=9&rft.spage=1719&rft.epage=23&rft.artnum=&rft.au=Yu+YW&rft.au=Tsai+SJ&rft.au=Hong+CJ&rft.au=Chen+TJ&rft.au=Chen+MC&rft.au=Yang+CW&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Yu YW, Tsai SJ, Hong CJ, Chen TJ, Chen MC, & Yang CW (2005). Association study of a monoamine oxidase a gene promoter polymorphism with major depressive disorder and antidepressant response. <span style="font-style: italic;">Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 30</span> (9), 1719-23 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/15956990">15956990</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com21tag:blogger.com,1999:blog-5002675950760488813.post-43145775000431708232014-07-10T18:54:00.000-07:002014-07-10T19:04:17.820-07:00Christopher Irwin Smith is an Idiot<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-5KiRhU6neeE/U79BMgao-DI/AAAAAAAABBo/BZbWfGxjgDA/s1600/christopherirwinsmith.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://4.bp.blogspot.com/-5KiRhU6neeE/U79BMgao-DI/AAAAAAAABBo/BZbWfGxjgDA/s400/christopherirwinsmith.png" /></a></div>
<center><b>Poopy-Faced Idiot</b></center>
<br>
Deep inside an underground compound within the evil lair of the American Anthropological Association, Lord Skeletor summoned a scientist to spread falsehoods about the science of monoamine oxidase A, the warrior gene. That scientist was Christopher Irwin Smith, Associate Professor of Biology at Willamette University. Dr. Smith set about penning a <a href="http://nothinginbiology.org/2014/07/08/a-guide-to-the-science-and-pseudoscience-of-a-troublesome-inheritance-part-ii-has-natural-selection-favored-violent-behavior-in-some-human-populations/">diatribe</a> full of errors and misleading innuendo. “I shall post this on the Internet and not allow better-informed people to comment on it,” he muttered before mustering an evil cackle that echoed through his dark private chamber.
<br><br>
Our investigators have uncovered the following especially telling response comment:
<br><br>
<blockquote>
Dr. Smith,
<br><br>
Your impressive background prevents me from having any sympathy for you regarding the multiple egregious errors in this post. Probably the worst aspect of it is the timing because the last two years have produced two important meta-analyses confirming MAOA as an aggression and antisocial behavior gene. I’m guessing you have no awareness of either one.
<br><br>
“…Nielsen and Williamson’s studies were able to identify many regions in the genome that appear to have experienced recent natural selection, but MAO-A is not one of them.”
<br><br>
You neglected to mention that their study examined single-nucleotide polymorphisms, not repeat polymorphisms, like either of the functional MAOA-uVNTR promoters. The same is true for Voight <i>et al</i>.
<br><br>
“it is likely that these genetic variants are not –on their own– associated with violent or impulsive behavior… Simply carrying the ‘low expression’ allele in the MAO-A promoter does not have any effect at all on impulsivity or aggression.”
<br><br>
I doubt that you would have written this if you had been aware of the new meta-analysis by <a href="http://theunsilencedscience.blogspot.com/2014/07/the-warrior-gene-back-from-grave.html">Ficks and Waldman</a>, which came to the opposite conclusion.
<br><br>
“Instead, genetic variation in the MAO-A promoter seems to make some children less able to recover from abuse and childhood trauma, and therefore more likely to act out later in life (Caspi <i>et al</i>. 2002; Widom & Brzustowicz 2006).”
<br><br>
You are misrepresenting the findings of Caspi <i>et al</i>. It is MAOA-4R, not MAOA-3R that has the effect, which is a protective effect. According to Caspi <i>et al</i>, abuse could not affect those with MAOA-4R at all. Other studies have found the same protective effect against high testosterone levels and low IQ. Byrd and Manuck recently provided a meta-analysis verifying the abuse-MAOA interaction effect.
<br><br>
“Indeed, genetic variants associated with lower resilience to trauma are most common in Asian populations, not African ones (Sabol <i>et al</i>. 1998).”
<br><br>
Are you seriously saying that 61.0% is significantly higher than 59.1%? I think you must have been thinking about the copy-and-paste error by Lea and Chambers that claimed that 77% of Chinese men have MAOA-3R. I have labeled that the “<a href="http://theunsilencedscience.blogspot.com/2013/12/the-stupid-stupidity-surrounding.html">idiot test</a>” because it has caught many highly credentialed idiots who were trying to do the same thing that you are trying to do now: brush off decades of good research on MAOA. Ficks and Waldman only found a modest main effect of MAOA-3R, so you would need to argue not only that the gene is as common in Asians but also that the interacting factors (child abuse, high testosterone, an IQ less than 85) are as common in Asians, as well. Then, there is the issue of MAOA-2R….
<br><br>
“Note that Sabol study did not consider differences between populations in the frequencies of the ‘2-repeat’ alleles that Wade references…”
<br><br>
Did not consider? Gee, that is an interesting way of putting it. Of course, they tried to determine the allele frequency of each kind of allele in that VNTR, and they reported <a href="http://theunsilencedscience.blogspot.com/2010/01/deus-ex-machina-genetics.html">absolutely no instances of MAOA-2R</a> in any group out of a total sample of over 2,000 X-chromosomes. MAOA-2R had not been discovered until the next year by Kunugi <i>et al</i>. Ever since, we have known that MAOA-2R is rare in whites <i>but not that rare</i>. Something is seriously wrong with the Sabol <i>et al</i> allele frequencies.
<br><br>
“To my knowledge, the frequency of the 2-repeat allele across populations has not been extensively measured; studies that have looked at its incidence appear to have focused on specific cohorts in the US as part of epidemiological studies.”
<br><br>
Is this your way of trying to cast doubt upon the allele frequencies reported in the literature for MAOA-2R in African-American men? Establishing an allele frequency does not require a 31-study meta-analysis. We have consistent findings from multiple studies that MAOA-2R is <a href="http://theunsilencedscience.blogspot.com/2012/12/scientists-rediscover-violence-gene.html">many times</a> more common in African-American men than either white or Asian men. Would you like to read each study?
</blockquote>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com6tag:blogger.com,1999:blog-5002675950760488813.post-25095649573723831442014-07-08T22:14:00.000-07:002014-07-09T10:41:02.155-07:00The Warrior Gene, Back from the Grave<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-j0kM0EEG9T4/U7zGvXkHpLI/AAAAAAAABBY/pdJFZPUAF5Q/s1600/warrior+gene+bftg+1.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-j0kM0EEG9T4/U7zGvXkHpLI/AAAAAAAABBY/pdJFZPUAF5Q/s400/warrior+gene+bftg+1.jpg" /></a></div>
<br>
Recently I read a phenomenal book called A Troublesome Inheritance by Nicholas Wade. It has science and sociological “speculation,” but most of the speculation actually just cited the speculation of other writers. I would say the scholarship was relatively good compared to <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">other works of popular science</a>. I assumed that critical appraisal would universally approve, but I would like to report that this was not entirely true. The book was actually panned by a group of people called “anthropologists,” who are almost like real scientists with their own journals and everything. Anthropologists <a href="http://anthropomics2.blogspot.com/2014/05/wade-weighed.html">only had one criticism</a>: they wished Wade had scratched every use of the word “race” and written in “population,” which is ironic because a recent survey of anthropologists determined that “racist” was their second most commonly used word after “the.” It is troubling that while anthropologists have taken their courageous stand against racism, they are as of yet blind to the scourge of populationism. I think it was Confucius who said, “We have come so far but have so much farther to go.” I think “further” would have been more grammatically correct, but distance is a metaphor, and “farther” resembles a parallel construction.
<br><br>
Nicholas Wade took up <a href="http://theunsilencedscience.blogspot.com/2011/03/racial-controversy-of-violent-gene.html">my cause</a> of drawing attention to an allele of monoamine oxidase A, "the warrior gene," that is rare in non-Africans and thought to predispose one to violence. However, an anthropologist named <a href="http://violentmetaphors.com/2014/05/21/nicholas-wade-and-race-building-a-scientific-facade/comment-page-1/#comment-36547">Jennifer Raff</a> succeeded in invading the field of genetics, and she countered our claim by posting a study by Vassos et al.
<blockquote>"MAO-A’s effects (as well as those of any other candidate gene known at this point) appear to be very, very minor (if they even exist at all)…"</blockquote>
Good gravy! You mean to tell me that <a href="http://theunsilencedscience.blogspot.com/2013/01/monoamine-oxidase-bibliography.html">all that research</a> that I have been following all these years has been debunked by a single study?! Well, I decided that before I take the drastic step of erasing half of my blog, I should actually read the study. Then, I read the other study that was on basically the same subject and published at almost the same time but that came to the opposite conclusion. Then, I magnanimously offered up my very own blog as a moderated forum for a discussion with the correspondence authors of each study. They did not respond to my request, so I shall do <a href="http://theunsilencedscience.blogspot.com/2011/09/pulling-empty-chair-on-dr-kevin-beaver.html">what I usually do</a> and post the empty-chair interview questions.
<br><br>
Questions posed to Dr. Evangelos Vassos:
<ol>
<li>Your study mentions “increased aggressive behavior in … MAOA knockout mice.” Why does your study make no mention of the equivalent MAOA knockout condition, Brunner syndrome, in humans?</li>
<li>Your study concludes that “it is unlikely that few candidate genes explain a complex behavior like aggression” and “aggression and even violence are complex behaviors.” Does the existence of Brunner syndrome contradict your conclusions? </li>
<li>For MAOA in females, your study included Guo et al, “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity.” Unlike other studies on MAOA, that study obviously defined MAOA-2R as a distinct allele rather than another “low-activity allele” paired with MAOA-3R. How did your study account for this difference? Why did your study not note that Guo et al found a main effect of MAOA-2R, for which no attempt at replication with a different sample has been attempted? </li>
<li>Have you heard of the meta-analysis by Ficks and Waldman, “Candidate genes for aggression and antisocial behavior: A meta-analysis of association studies of the 5HTTLPR and MAOA-uVNTR”? Would you care to comment on how that study’s meta-analysis for MAOA differs from your meta-analysis? </li>
<li>Unlike Ficks and Waldman, your meta-analysis elected to include studies that used clinical psychiatric patients with mental illnesses and substance abuse problems. In fact, I count that 12 of the 17 studies on MAOA in males used such clinical patients. What is your rationale for this approach? </li>
<li>Supplementary Table 1 shows sample sizes for Gerra et al and Koller et al that suggest that your study did not consider the effects of MAOA on the aggression or hostility of each study’s control sample. It appears that you excluded the control samples and only considered the effects on the alcoholic or heroin-dependent subjects. Why is that? </li>
<li>Your meta-analysis found studies partly by scanning “reference lists of all included studies,” but these reference lists included multiple studies that Ficks and Waldman included but not your meta-analysis, specifically Manuck et al, Jacob et al, Beitchman et al, and Kim-Cohen et al. Manuck et al was listed in 4 of the 17 studies for MAOA in males. Ficks and Waldman were able to include 31 MAOA studies despite excluding studies of other psychiatric disorders, and neither meta-analysis included Williams et al (2003), Rosenberg et al (2006), Nilsson et al (2007), or Kuepper et al (2013). Why were these studies not included? </li>
<li>Like other negative studies of MAOA, your meta-analysis criticizes the entire project of candidate-gene behavioral genetics, saying “Our study provides evidence that the candidate gene approach has not succeeded in identifying genes associated with these outcomes. This is consistent with recent observations in the field that candidate gene studies of human characteristics and complex diseases at large have failed to produce consistent and clinically useful findings.” Ficks and Waldman included more studies for MAOA and found a modest positive effect, consistent with other lines of evidence (MAOA knockout mice, Brunner syndrome, gene-environment interaction, brain imaging, etc.). Should their meta-analysis have made just as strong of a judgment in favor of the usefulness of a candidate-gene approach to studying behavioral genetics? Why do only negative studies reflect upon this issue? </li>
<li>Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science? </li>
</ol>
<br>
Questions posed to Courtney Ficks:
<ol>
<li>For MAOA, your study included Guo et al, “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity.” Unlike other studies on MAOA, that study obviously defined MAOA-2R as a distinct allele rather than another “low-activity allele” paired with MAOA-3R. How did your study account for this difference? Why did your study not note that Guo et al found a main effect of MAOA-2R, for which no attempt at replication with a different sample has been attempted? </li>
<li>Have you heard of the meta-analysis by Vassos, Collier, and Fazel, “Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression”? Would you care to comment on how that study’s meta-analysis for MAOA differs from your meta-analysis? </li>
<li>It appears that their study was published by a journal with a higher impact factor than yours (15 versus 3 in 2012), but they elected to include studies that used clinical psychiatric patients with mental illnesses and substance abuse problems and included fewer studies on MAOA. Why is your study in a journal with a lower impact factor? Is it possible that the outcome of their study was ideologically favored over that of your study? </li>
<li>Did you consider including the studies by Williams et al (2003), Rosenberg et al (2006), Nilsson et al (2007), or Kuepper et al (2013)? If so, why were these studies not included? </li>
<li>Like other negative studies of MAOA, Vassos et al criticized the entire project of candidate-gene behavioral genetics, saying “Our study provides evidence that the candidate gene approach has not succeeded in identifying genes associated with these outcomes. This is consistent with recent observations in the field that candidate gene studies of human characteristics and complex diseases at large have failed to produce consistent and clinically useful findings.” Your study found a modest positive effect, consistent with other lines of evidence (MAOA knockout mice, Brunner syndrome, gene-environment interaction, brain imaging, etc.). Why didn’t your study conclude with just as strong of a judgment in favor of the usefulness of a candidate-gene approach to studying behavioral genetics? Why do only negative studies reflect upon this issue? </li>
<li>Your study claimed that “there is growing evidence that we must be wary of” gene-environment interaction findings. However, Byrd and Manuck published a meta-analysis last year that seemed to show a robust gene-environment interaction for MAOA and childhood maltreatment. Some GxE interaction studies for MAOA have had positive results for fairly common environmental factors, like an IQ less than 85, high cerebral spinal fluid free testosterone, and poverty. Is it possible that the totality of suspected environmental factors are so common that your finding of a modest main effect was actually picking up these effects, even though you didn’t try to isolate them? Should those factors be control variables in this type of research? </li>
<li>Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science? </li>
</ol>
<br>
I completely empathize with the decisions of Ficks and Vassos to ignore the interview requests. Ficks probably did not want to answer a question that would insult a prestigious journal, like Molecular Psychiatry. Dr. Vassos probably didn’t feel like answering because he must know that his study is complete garbage, and he doesn’t want to talk about it.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Behavior+genetics&rft_id=info%3Apmid%2F24902785&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Candidate+Genes+for+Aggression+and+Antisocial+Behavior%3A+A+Meta-analysis+of+Association+Studies+of+the+5HTTLPR+and+MAOA-uVNTR.&rft.issn=0001-8244&rft.date=2014&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Ficks+CA&rft.au=Waldman+ID&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. <span style="font-style: italic;">Behavior genetics</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24902785">24902785</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Molecular+psychiatry&rft_id=info%3Apmid%2F23546171&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Systematic+meta-analyses+and+field+synopsis+of+genetic+association+studies+of+violence+and+aggression.&rft.issn=1359-4184&rft.date=2014&rft.volume=19&rft.issue=4&rft.spage=471&rft.epage=7&rft.artnum=&rft.au=Vassos+E&rft.au=Collier+DA&rft.au=Fazel+S&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Vassos E, Collier DA, & Fazel S (2014). Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression. <span style="font-style: italic;">Molecular psychiatry, 19</span> (4), 471-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23546171">23546171</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com8tag:blogger.com,1999:blog-5002675950760488813.post-77496149122891750212014-07-04T07:37:00.000-07:002014-07-04T07:44:04.221-07:00Parents’ Income Poorly Predicts SAT Score
<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<b>Abstract</b>
<br>
Parents’ annual income lacks statistical significance as a predictor of state SAT scores when additional variables are well controlled. Spearman rank correlation coefficients reveal parents’ income to be a weaker predictor of average SAT scores for each income bracket within each state than parents’ education level as a predictor of average SAT scores for each education level within each state. Multiple linear regression of state SAT scores with covariates for sample size, state participation, year, and each possible combination of ordinal variables for parents’ income, parents’ education, and race shows income to lack statistical significance in 49% of the iterations with greater frequency of insignificance among iterations with higher explained variance. Cohen’s d comparisons of the yearly individual SAT advantage of having educated parents show a fairly consistently increasing positive relationship over time, whereas similar analysis of the yearly individual SAT advantage of having high-income parents shows variability somewhat coinciding with the business cycle.
<br><br>
Read the whole study at <a href="http://openpsych.net/ODP/2014/07/parents-income-is-a-poor-predictor-of-sat-score/">Open Differential Psychology</a>.
<br><br>
See below for important excerpts and extra super-awesome graphs.
<br><br>
“Sackett et al (2009) recounted a series of accusations that the SAT merely measures family wealth. The College Board’s announcement of 2016 SAT reforms has stirred anew claims that 'the only persistent statistical result from the SAT is the correlation between high income and high test scores' (Botstein, 2014). Thus, income as an important predictor of SAT scores somewhat fits a view critical of the SAT, which is that financial resources and class privilege unduly enable higher SAT achievement. If the education component of socioeconomic status dominates over the income component, then the relationship between socioeconomic status and scores might instead more accurately reflect a family’s values towards education and a hereditary influence shared between test performance and educability.”
<br><br>
“This study seeks to thoroughly parse the effects of multiple covariates, including family income, parents’ highest education level, and potential confounding variables specific to state or multiple-year comparisons. To do this, full advantage will be taken from all sixteen years of state data.”
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-7_IkmPqy3yQ/U7a9fyBxSZI/AAAAAAAABBA/H9Q-Pq6cqAY/s1600/Figure+2a.fig.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://1.bp.blogspot.com/-7_IkmPqy3yQ/U7a9fyBxSZI/AAAAAAAABBA/H9Q-Pq6cqAY/s400/Figure+2a.fig.png" /></a></div>
<br>
Income p-values without race as a covariate (p-values are shown on an inverse logarithmic scale)
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-GINgGCh8I9Q/U7a9o_O-fzI/AAAAAAAABBI/SYnGQdtDuw0/s1600/Figure+2b.fig.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://1.bp.blogspot.com/-GINgGCh8I9Q/U7a9o_O-fzI/AAAAAAAABBI/SYnGQdtDuw0/s400/Figure+2b.fig.png" /></a></div>
<br>
Income p-values with race as a covariate (p-values are shown on an inverse logarithmic scale)
<br><br>
“The racial variable was the most consistently significant variable of these three ordinal variables for composite scores and subtests, which speaks to its independence from socioeconomic status. Race also explained much of the SAT advantage that appeared to be attributable to parents’ income prior to the addition of the racial variable in iterations with low income thresholds simultaneous with the education cutoff being graduate degree.”
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-WBiEM7W1xoY/U7a8z0uW3nI/AAAAAAAABA4/0BCP_DD2z2c/s1600/Figure+3.tif" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-WBiEM7W1xoY/U7a8z0uW3nI/AAAAAAAABA4/0BCP_DD2z2c/s400/Figure+3.tif" /></a></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-sCz3BeQUc8Q/U7a6MsBWwzI/AAAAAAAABAk/EH7elkc-I_Y/s1600/Figure+3+legend.tif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-sCz3BeQUc8Q/U7a6MsBWwzI/AAAAAAAABAk/EH7elkc-I_Y/s320/Figure+3+legend.tif" /></a></div>
<br>
Critical-reading and mathematics standardized coefficients compared to adjusted R<sup>2</sup> values, organized by education first, race within each educational category, and income within each racial category
<br><br>
“Parents’ income has a significant association with SAT scores, but parents’ education is consistently stronger, and regression with effective controls for race, education, and other factors, usually suppresses the income variable to insignificance. The income variable achieved significance when the education threshold was high school diploma most likely because so few parents were dropouts that education was no longer effectively controlled, and parents’ income became a proxy variable for parents’ education…. Part of this dominance could result from heritability in test performance corresponding to parents’ educational attainment, given the high heritability estimates from twins studies for high-stakes standardized exams in the UK and the Netherlands (Bartels et al, 2002; Shakeshaft et al, 2013).”
<br><br>
“Figure 1 seems to contradict Dixon- Román et al in finding that the racial variable had its greatest influence at the highest education level and at high income levels.”
<br><br>
“Asian Americans have historically high average mathematics subtest scores but lower verbal/critical-reading average scores than the white majority…. Despite their likely small average verbal disadvantage and small population in many states, this study’s consistent regression results for Asian race match verifiable individual SAT-score phenomena. A study with fewer observations, a much smaller represented sample, or fewer or poorly chosen covariates might not have achieved that level of definition, but, fundamentally, states do not take the SAT; people do.”
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-2Y_AswYp19Q/U7a5thpeLAI/AAAAAAAABAc/dtSXDO8J1oc/s1600/Figure+7.tif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-2Y_AswYp19Q/U7a5thpeLAI/AAAAAAAABAc/dtSXDO8J1oc/s400/Figure+7.tif" /></a></div>
<br>
Cohen’s d SAT advantage of having parents’ annual income above $60,000
<br><br>
“Family educational advantage seems to evince virtually undeviating growth as a predictor of SAT scores, but financial advantage seems to grow as the economy worsens. Rather than postulate that times of economic difficulty almost immediately make wealthy people smarter, one should focus on the exclusivity of the income category…. The declining relative income advantage on the mathematics subtest compared to the critical-reading subtest also could be related to structural changes to the economy since the decline of the high-technology boom of the 1990’s, which also fits this interpretation of persistence within families.”
<br><br>
For those readers who <b>do not</b> have a heart condition, I recommend the spirited and colorful <i>statistics</i> debate in the <a href="http://www.openpsych.net/forum/showthread.php?tid=56">open peer-review forum</a>. One may also find there data supplements of state data that required many months of typing out the data from 816 state reports into a database, which makes a fun toy.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Open+Differential+Psychology&rft_id=info%3Aother%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Parents%E2%80%99+Income+is+a+Poor+Predictor+of+SAT+Score&rft.issn=&rft.date=2014&rft.volume=&rft.issue=&rft.spage=1&rft.epage=19&rft.artnum=http%3A%2F%2Fopenpsych.net%2FODP%2F2014%2F07%2Fparents-income-is-a-poor-predictor-of-sat-score%2F&rft.au=nooffensebut&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">nooffensebut (2014). Parents’ Income is a Poor Predictor of SAT Score <span style="font-style: italic;">Open Differential Psychology</span>, 1-19</span>
<br><br>
Ariel Investments. (2010). The Ariel Investments 2010 black investor survey: Saving and investing among higher income African-American and white Americans. Retrieved April 1, 2014 from http://www.arielinvestments.com/landmark-surveys/
<br><br>
Balf, T. (2014). The story behind the SAT overhaul. New York Times. Retrieved March 25, 2014 from http://www.nytimes.com/2014/03/09/magazine/the-story-behind-the-sat-overhaul.html.
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Twin+research+%3A+the+official+journal+of+the+International+Society+for+Twin+Studies&rft_id=info%3Apmid%2F12573186&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Heritability+of+educational+achievement+in+12-year-olds+and+the+overlap+with+cognitive+ability.&rft.issn=1369-0523&rft.date=2002&rft.volume=5&rft.issue=6&rft.spage=544&rft.epage=53&rft.artnum=&rft.au=Bartels+M&rft.au=Rietveld+MJ&rft.au=Van+Baal+GC&rft.au=Boomsma+DI&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Bartels M, Rietveld MJ, Van Baal GC, & Boomsma DI (2002). Heritability of educational achievement in 12-year-olds and the overlap with cognitive ability. <span style="font-style: italic;">Twin research : the official journal of the International Society for Twin Studies, 5</span> (6), 544-53 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/12573186">12573186</a></span>
<br><br>
Botstein, L. (2014). College president: SAT is part hoax, part fraud. Time. Retrieved March 25, 2014 from http://time.com/15199/college-president-sat-is-part-hoax-and-part-fraud/.
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Social+Forces&rft_id=info%3Adoi%2F10.1353%2Fsof.2010.0105&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Shadow+Education%2C+American+Style%3A+Test+Preparation%2C+the+SAT+and+College+Enrollment&rft.issn=0037-7732&rft.date=2010&rft.volume=89&rft.issue=2&rft.spage=435&rft.epage=461&rft.artnum=http%3A%2F%2Fsf.oxfordjournals.org%2Fcgi%2Fdoi%2F10.1353%2Fsof.2010.0105&rft.au=Buchmann%2C+C.&rft.au=Condron%2C+D.&rft.au=Roscigno%2C+V.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Buchmann, C., Condron, D., & Roscigno, V. (2010). Shadow Education, American Style: Test Preparation, the SAT and College Enrollment <span style="font-style: italic;">Social Forces, 89</span> (2), 435-461 DOI: <a rev="review" href="http://dx.doi.org/10.1353/sof.2010.0105">10.1353/sof.2010.0105</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Teachers+College+Record&rft_id=info%3Aother%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Race%2C+poverty+and+SAT+scores%3A+Modeling+the+influences+of+family+income+on+black+and+white+high+school+students%E2%80%99+SAT+performance.&rft.issn=&rft.date=2013&rft.volume=115&rft.issue=4&rft.spage=1&rft.epage=33&rft.artnum=http%3A%2F%2Fwww.tcrecord.org%2FContent.asp%3FContentId%3D16925&rft.au=Dixon-Rom%C3%A1n%2C+E.J.&rft.au=Everson%2C+H.T.&rft.au=McArdle%2C+J.J.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Dixon-Román, E.J., Everson, H.T., & McArdle, J.J. (2013). Race, poverty and SAT scores: Modeling the influences of family income on black and white high school students’ SAT performance. <span style="font-style: italic;">Teachers College Record, 115</span> (4), 1-33</span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft_id=info%3Apmid%2F21518867&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Role+of+test+motivation+in+intelligence+testing.&rft.issn=0027-8424&rft.date=2011&rft.volume=108&rft.issue=19&rft.spage=7716&rft.epage=20&rft.artnum=&rft.au=Duckworth+AL&rft.au=Quinn+PD&rft.au=Lynam+DR&rft.au=Loeber+R&rft.au=Stouthamer-Loeber+M&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Duckworth AL, Quinn PD, Lynam DR, Loeber R, & Stouthamer-Loeber M (2011). Role of test motivation in intelligence testing. <span style="font-style: italic;">Proceedings of the National Academy of Sciences of the United States of America, 108</span> (19), 7716-20 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21518867">21518867</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science&rft_id=info%3Adoi%2F10.1126%2Fscience.289.5478.457&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+Neural+Basis+for+General+Intelligence&rft.issn=00368075&rft.date=2000&rft.volume=289&rft.issue=5478&rft.spage=457&rft.epage=460&rft.artnum=http%3A%2F%2Fwww.sciencemag.org%2Fcgi%2Fdoi%2F10.1126%2Fscience.289.5478.457&rft.au=Duncan%2C+J.&rft.au=Seitz%2C+R.J.&rft.au=Kolodny%2C+J.&rft.au=Bor%2C+D.&rft.au=Herzog%2C+H.&rft.au=Ahmed%2C+A.&rft.au=Newell%2C+F.N.&rft.au=Emslie%2C+H.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Duncan, J., Seitz, R.J., Kolodny, J., Bor, D., Herzog, H., Ahmed, A., Newell, F.N., & Emslie, H. (2000). A Neural Basis for General Intelligence <span style="font-style: italic;">Science, 289</span> (5478), 457-460 DOI: <a rev="review" href="http://dx.doi.org/10.1126/science.289.5478.457">10.1126/science.289.5478.457</a></span>
<br><br>
Everson, H.T., and Millsap, R.E. (2004). Beyond individual differences: Exploring school effects on SAT scores. (RR-2004-3). New York: College Board.
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+bulletin&rft_id=info%3Apmid%2F8346326&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+problem+of+equivalent+models+in+applications+of+covariance+structure+analysis.&rft.issn=0033-2909&rft.date=1993&rft.volume=114&rft.issue=1&rft.spage=185&rft.epage=99&rft.artnum=&rft.au=MacCallum+RC&rft.au=Wegener+DT&rft.au=Uchino+BN&rft.au=Fabrigar+LR&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">MacCallum RC, Wegener DT, Uchino BN, & Fabrigar LR (1993). The problem of equivalent models in applications of covariance structure analysis. <span style="font-style: italic;">Psychological bulletin, 114</span> (1), 185-99 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/8346326">8346326</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Intelligence&rft_id=info%3Apmid%2F24944428&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Molecular+genetic+contributions+to+socioeconomic+status+and+intelligence.&rft.issn=0160-2896&rft.date=2014&rft.volume=44&rft.issue=100&rft.spage=26&rft.epage=32&rft.artnum=&rft.au=Marioni+RE&rft.au=Davies+G&rft.au=Hayward+C&rft.au=Liewald+D&rft.au=Kerr+SM&rft.au=Campbell+A&rft.au=Luciano+M&rft.au=Smith+BH&rft.au=Padmanabhan+S&rft.au=Hocking+LJ&rft.au=Hastie+ND&rft.au=Wright+AF&rft.au=Porteous+DJ&rft.au=Visscher+PM&rft.au=Deary+IJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Marioni RE, Davies G, Hayward C, Liewald D, Kerr SM, Campbell A, Luciano M, Smith BH, Padmanabhan S, Hocking LJ, Hastie ND, Wright AF, Porteous DJ, Visscher PM, & Deary IJ (2014). Molecular genetic contributions to socioeconomic status and intelligence. <span style="font-style: italic;">Intelligence, 44</span> (100), 26-32 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24944428">24944428</a></span>
<br><br>
Neter, J., Wasserman, W., and Kutner, M.H. (1983). Applied Linear Regression Models. Homewood, IL: Richard D. Irwin, Inc.
<br><br>
Prescott, B.T., and Bransberger, P. (2012). Knocking at the College Door: Projections of High School Graduates (eighth edition). Boulder, CO: Western Interstate Commission for Higher Education.
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+bulletin&rft_id=info%3Apmid%2F19210051&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Does+socioeconomic+status+explain+the+relationship+between+admissions+tests+and+post-secondary+academic+performance%3F&rft.issn=0033-2909&rft.date=2009&rft.volume=135&rft.issue=1&rft.spage=1&rft.epage=22&rft.artnum=&rft.au=Sackett+PR&rft.au=Kuncel+NR&rft.au=Arneson+JJ&rft.au=Cooper+SR&rft.au=Waters+SD&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Sackett PR, Kuncel NR, Arneson JJ, Cooper SR, & Waters SD (2009). Does socioeconomic status explain the relationship between admissions tests and post-secondary academic performance? <span style="font-style: italic;">Psychological bulletin, 135</span> (1), 1-22 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19210051">19210051</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+science&rft_id=info%3Apmid%2F22858524&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+role+of+socioeconomic+status+in+SAT-grade+relationships+and+in+college+admissions+decisions.&rft.issn=0956-7976&rft.date=2012&rft.volume=23&rft.issue=9&rft.spage=1000&rft.epage=7&rft.artnum=&rft.au=Sackett+PR&rft.au=Kuncel+NR&rft.au=Beatty+AS&rft.au=Rigdon+JL&rft.au=Shen+W&rft.au=Kiger+TB&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Sackett PR, Kuncel NR, Beatty AS, Rigdon JL, Shen W, & Kiger TB (2012). The role of socioeconomic status in SAT-grade relationships and in college admissions decisions. <span style="font-style: italic;">Psychological science, 23</span> (9), 1000-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22858524">22858524</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+applied+psychology&rft_id=info%3Apmid%2F19916657&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Prediction+of+4-year+college+student+performance+using+cognitive+and+noncognitive+predictors+and+the+impact+on+demographic+status+of+admitted+students.&rft.issn=0021-9010&rft.date=2009&rft.volume=94&rft.issue=6&rft.spage=1479&rft.epage=97&rft.artnum=&rft.au=Schmitt+N&rft.au=Keeney+J&rft.au=Oswald+FL&rft.au=Pleskac+TJ&rft.au=Billington+AQ&rft.au=Sinha+R&rft.au=Zorzie+M&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Schmitt N, Keeney J, Oswald FL, Pleskac TJ, Billington AQ, Sinha R, & Zorzie M (2009). Prediction of 4-year college student performance using cognitive and noncognitive predictors and the impact on demographic status of admitted students. <span style="font-style: italic;">The Journal of applied psychology, 94</span> (6), 1479-97 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19916657">19916657</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PloS+one&rft_id=info%3Apmid%2F24349000&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Strong+genetic+influence+on+a+UK+nationwide+test+of+educational+achievement+at+the+end+of+compulsory+education+at+age+16.&rft.issn=&rft.date=2013&rft.volume=8&rft.issue=12&rft.spage=&rft.epage=&rft.artnum=&rft.au=Shakeshaft+NG&rft.au=Trzaskowski+M&rft.au=McMillan+A&rft.au=Rimfeld+K&rft.au=Krapohl+E&rft.au=Haworth+CM&rft.au=Dale+PS&rft.au=Plomin+R&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Shakeshaft NG, Trzaskowski M, McMillan A, Rimfeld K, Krapohl E, Haworth CM, Dale PS, & Plomin R (2013). Strong genetic influence on a UK nationwide test of educational achievement at the end of compulsory education at age 16. <span style="font-style: italic;">PloS one, 8</span> (12) PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24349000">24349000</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Intelligence&rft_id=info%3Apmid%2F24489417&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genetic+influence+on+family+socioeconomic+status+and+children%27s+intelligence.&rft.issn=0160-2896&rft.date=2014&rft.volume=42&rft.issue=100&rft.spage=83&rft.epage=88&rft.artnum=&rft.au=Trzaskowski+M&rft.au=Harlaar+N&rft.au=Arden+R&rft.au=Krapohl+E&rft.au=Rimfeld+K&rft.au=McMillan+A&rft.au=Dale+PS&rft.au=Plomin+R&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Trzaskowski M, Harlaar N, Arden R, Krapohl E, Rimfeld K, McMillan A, Dale PS, & Plomin R (2014). Genetic influence on family socioeconomic status and children's intelligence. <span style="font-style: italic;">Intelligence, 42</span> (100), 83-88 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24489417">24489417</a></span>
<br><br>
US Census Bureau. (1990). Asians and Pacific Islanders in the United States. Retrieved March 23, 2014 from https://www.census.gov/prod/cen1990/cp3/cp-3-5.pdf.
<br><br>
US Census Bureau. (2013). Asian/Pacific American Heritage Month: May 2013. Retrieved March 24, 2014 from https://www.census.gov/newsroom/releases/pdf/cb13ff-09_asian.pdf.
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com2tag:blogger.com,1999:blog-5002675950760488813.post-54974228124666863722013-12-23T02:29:00.000-08:002013-12-23T03:10:16.186-08:00Dr. Kevin Beaver the Apostle<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-h4qbrzn8UEw/UrgNARNoBOI/AAAAAAAAA-Y/H_4Tb2js9Uo/s1600/Kevin_Beaver.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="http://3.bp.blogspot.com/-h4qbrzn8UEw/UrgNARNoBOI/AAAAAAAAA-Y/H_4Tb2js9Uo/s400/Kevin_Beaver.png" /></a></div>
<br>
In the discussion following my previous <a href="https://www.youtube.com/watch?v=4wPNnAn2MEo">video</a> about monoamine oxidase A, I noted a new study with lead author Dr. Kevin Beaver. The study closely resembles his previous study of the 2-repeat allele, <a href="http://theunsilencedscience.blogspot.com/2012/12/scientists-rediscover-violence-gene.html">my analysis</a> of which is well on its way to becoming my most popular blog essay. Once again, a small subset of African-American men from the National Longitudinal Study of Adolescent Health served as a comparison group for the eight African-American men, who possess this rare allele of the upstream promoter for MAOA and who had complete phenotype data. This time, the specific behaviors of shooting or stabbing replaced measures of psychopathic personality, arrests, and incarceration as the outcomes of interest. Despite the small sample size, the results were significant (odds ratio = 12.89, p < 0.05) because those with the allele had a fifty-percent chance of shooting or stabbing someone. For African-American men without this allele, the risk was only seven percent. Those with MAOA-2R were also more likely to have victimized multiple people based on their greater likelihood of admitting stabbing or shooting during multiple “waves” of study follow-up.
<br><br>
I still have concerns about population substructure. In a mixed population like African Americans, alleles associated with African ancestry like MAOA-2R might correlate with many other African alleles, and because MAOA-2R is so much more common in African Americans than whites and Asians, scientists have studied no other sample and no other race for behavioral phenotypes specifically for this allele. However, Guo <i>et al</i> previously demonstrated the functional differences between MAOA-2R and the other alleles <i>in vitro</i>.
<br><br>
This study bares the imprint of my influence. I <a href="http://theunsilencedscience.blogspot.com/2011/09/pulling-empty-chair-on-dr-kevin-beaver.html">previously</a> sent Beaver a list of questions that reflected beliefs of mine about the research on this gene. Here was one such question:
<blockquote>In your studies of MAOA, you used the convention of including the 2-repeat and 3-repeat alleles in the category MAOA-L, but Guo <i>et al</i> “The integration of genetic propensities into social-control models of delinquency and violence among male youths” and Guo <i>et al</i> “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity” found that the 2-repeat allele had twice as much effect on violent delinquency as either the 3-repeat or 4-repeat alleles and that the 2-repeat allele had more effect than the dopamine genes DAT1 and DRD2. How do you justify following the MAOA-L convention rather than studying the 2-repeat allele separately?</blockquote>
In this study, Beaver <i>et al</i> make the following similar remark:
<blockquote>[A]lmost all of the prior research examining the effects of MAOA on antisocial behaviors has pooled the 2-repeat allele together with the 3-repeat allele. As the results of this study indicate, however, this approach may be misguided as the most powerful effects may be found within the 2-repeat allele and combining the 2-repeat allele with the 3-repeat allele may attenuate the main effects of MAOA.</blockquote>
I raised another concern in a separate question:
<blockquote> A disproportionate number of studies on MAOA and antisocial personality disorder were negative (Saito et al, Koller et al, Parsian et al, Lu et al, and Prichard et al). Why should antisocial personality disorder be a focus of genetic research? Should not the aggression or impulsive criteria of antisocial personality disorder be considered separately in genetic studies?</blockquote>
Beaver <i>et al</i> echo my concern:
<blockquote>Using an additive scale of antisocial behaviors may mask important heterogeneity that exists between the individual behaviors and MAOA genotype such that MAOA may be related to certain types of antisocial behaviors, but not others. As a result, to further unpack the nexus between MAOA genotype and serious violence, the current study examines only extreme violence as measured by shooting and stabbing behaviors.</blockquote>
Neuroskeptic, who has been a <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html?showComment=1334300892391#c6350671525547839450">reader</a> of the Unsilenced Science, <a href="https://twitter.com/Neuro_Skeptic/status/412181501263237120">responded</a> to the study by saying, “Hmmm,” to which neurogeneticist Dr. Kevin Mitchell responded, “Grrrrr,” undoubtedly while pounding his chest. University of North Carolina geneticist Dr. Patrick Sullivan wrote, “I would have rejected wo review. Studies like these have not taught us much.” By “studies like these,” I assume he means the hundreds of corroborating studies pertaining to the MAOA gene, its enzyme, and its metabolites, but dismissive flippancy from genetics professors is the sign of the times. Mitchell passed along my recent video to his fellow <a href="http://theunsilencedscience.blogspot.com/2012/07/just-say-no-limit-trayvon.html">GWAS Jihadists</a> “based on the title,” which is clearly a Christmas miracle. I, for one, generally do not consider candidate-gene studies with large effect sizes to be evidence of no effect at all “<a href="http://www.genomesunzipped.org/2011/11/size-matters-and-other-lessons-from-medical-genetics.php">by historical analogy</a>.” In the past, interesting studies would lead to attempts to replicate the finding. Often some attempts would support, others would not, and a meta-analysis of all pertinent results would provide the final word. Now, some attempts support, and every attempt that does not support the original finding is evidence of a broader dysfunction in medicine or science, which are to blame for the media’s hype. Only a select few GWAS Jihadists have the moral courage to dismiss every positive finding with a self-righteous fist pound on the lectern. Nevertheless, Vimaleswaran <i>et al</i> determined that candidate-gene studies, which follow hypotheses about specific genes, show “evidence for enrichment” when compared to genome-wide association studies (for obesity) such that “the candidate gene approach retains some value.” Tielbeek <i>et al</i> attempted to test MAOA in a GWAS that only examined single nucleotide polymorphisms and found no effects for antisocial behavior. Of course, such a study could not directly examine the VNTR promoters that have drawn so much interest to this gene.
<br><br>
Eight is a small number of cases, but it is approximately the same as the number of cases of Brunner syndrome when that diagnosis was established in 1993, a diagnosis that only recently came into use for two additional families. When I <a href="http://theunsilencedscience.blogspot.com/2010/01/deus-ex-machina-genetics.html">first confronted</a> the GWAS Jihadists, I asked them if their disbelief in the gene-environment interaction for MAOA-3R extended to a disbelief in Brunner syndrome. They defensively denied reaching that conclusion. The lesson is obvious: in order to establish the effect of MAOA-2R on violence as a trustworthy scientific finding, this allele’s effect must have an eponym. But which scientist should the disease immortalize? Will it be Guo syndrome or Beaver syndrome? (How about nooffensebut syndrome?) We could follow the example of entomologists, <a href="http://www.livescience.com/6977-slime-mold-beetles-named-bush-cheney-rumsfeld.html">Quentin Wheeler and Kelly Miller</a>, and name this after the greatest president of my lifetime: George W. Bush syndrome. However, as any graduate of medical school can attest, eponyms are evil. The study of genetics as it pertains to social sciences might gain the respectability of physics if it follows physics naming conventions. Just as flavors of quarks have creative names like strange and charm, the disease with symptoms of shooting people and stabbing people caused by the allele MAOA-2R should be called sunshine syndrome.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Psychiatric+quarterly&rft_id=info%3Apmid%2F24326626&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+2-Repeat+Allele+of+the+MAOA+Gene+Confers+an+Increased+Risk+for+Shooting+and+Stabbing+Behaviors.&rft.issn=0033-2720&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Beaver+KM&rft.au=Barnes+JC&rft.au=Boutwell+BB&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Beaver KM, Barnes JC, & Boutwell BB (2013). The 2-Repeat Allele of the MAOA Gene Confers an Increased Risk for Shooting and Stabbing Behaviors. <span style="font-style: italic;">The Psychiatric quarterly</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/24326626">24326626</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+human+genetics&rft_id=info%3Apmid%2F23871722&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=XLID-causing+mutations+and+associated+genes+challenged+in+light+of+data+from+large-scale+human+exome+sequencing.&rft.issn=0002-9297&rft.date=2013&rft.volume=93&rft.issue=2&rft.spage=368&rft.epage=83&rft.artnum=&rft.au=Piton+A&rft.au=Redin+C&rft.au=Mandel+JL&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Piton A, Redin C, & Mandel JL (2013). XLID-causing mutations and associated genes challenged in light of data from large-scale human exome sequencing. <span style="font-style: italic;">American journal of human genetics, 93</span> (2), 368-83 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23871722">23871722</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PloS+one&rft_id=info%3Apmid%2F23077488&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Unraveling+the+genetic+etiology+of+adult+antisocial+behavior%3A+a+genome-wide+association+study.&rft.issn=&rft.date=2012&rft.volume=7&rft.issue=10&rft.spage=&rft.epage=&rft.artnum=&rft.au=Tielbeek+JJ&rft.au=Medland+SE&rft.au=Benyamin+B&rft.au=Byrne+EM&rft.au=Heath+AC&rft.au=Madden+PA&rft.au=Martin+NG&rft.au=Wray+NR&rft.au=Verweij+KJ&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Tielbeek JJ, Medland SE, Benyamin B, Byrne EM, Heath AC, Madden PA, Martin NG, Wray NR, & Verweij KJ (2012). Unraveling the genetic etiology of adult antisocial behavior: a genome-wide association study. <span style="font-style: italic;">PloS one, 7</span> (10) PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23077488">23077488</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Human+molecular+genetics&rft_id=info%3Apmid%2F22791748&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Candidate+genes+for+obesity-susceptibility+show+enriched+association+within+a+large+genome-wide+association+study+for+BMI.&rft.issn=0964-6906&rft.date=2012&rft.volume=21&rft.issue=20&rft.spage=4537&rft.epage=42&rft.artnum=&rft.au=Vimaleswaran+KS&rft.au=Tachmazidou+I&rft.au=Zhao+JH&rft.au=Hirschhorn+JN&rft.au=Dudbridge+F&rft.au=Loos+RJ&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Vimaleswaran KS, Tachmazidou I, Zhao JH, Hirschhorn JN, Dudbridge F, & Loos RJ (2012). Candidate genes for obesity-susceptibility show enriched association within a large genome-wide association study for BMI. <span style="font-style: italic;">Human molecular genetics, 21</span> (20), 4537-42 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22791748">22791748</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com20tag:blogger.com,1999:blog-5002675950760488813.post-82227651604327592242013-12-08T06:58:00.000-08:002013-12-08T06:58:19.983-08:00The Stupid Stupidity Surrounding the Warrior Gene, MAOA, is Stupid<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<br /><br /><iframe width="415" height="259" src="http://www.youtube.com/embed/4wPNnAn2MEo" frameborder="0" allowfullscreen></iframe>
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychiatry&rft_id=info%3Apmid%2F23786983&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA%2C+Childhood+Maltreatment%2C+and+Antisocial+Behavior%3A+Meta-analysis+of+a+Gene-Environment+Interaction.&rft.issn=0006-3223&rft.date=2013&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Byrd+AL&rft.au=Manuck+SB&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Byrd AL, & Manuck SB (2013). MAOA, Childhood Maltreatment, and Antisocial Behavior: Meta-analysis of a Gene-Environment Interaction. <span style="font-style: italic;">Biological psychiatry</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23786983">23786983</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com39tag:blogger.com,1999:blog-5002675950760488813.post-3723853710196575782013-10-24T01:03:00.001-07:002013-11-08T08:32:27.714-08:00Black Suits, Gowns, & Skin: SAT Scores by Income, Education, & Race<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
People with highly educated or wealthy parents score higher on the SAT than those from poor, uneducated families. Obvious statistic is obvious, but how important are dollars and degrees compared to race? The College Board, the organization that oversees the SAT, holds tight to its information on the subject, but incomplete leaks have occurred for <a href="http://www.lagriffedulion.f2s.com/testing.htm">1995</a>, <a href="http://www.jstor.org/stable/2999198">1997</a>, <a href="http://www.tcrecord.org/content.asp?contentid=16925">2003</a>, and <a href="http://lesacreduprintemps19.files.wordpress.com/2011/07/why-ses-does-not-explain.pdf">2008</a>. 1995’s top income bracket only started at $70,000, so the wealthiest African-American students that year did not outscore even the poorest white students. As shocking as that fact is, it provides no controls for confounding variables and neglects the currently largest minority, Hispanic Americans. Therefore, I decided to approach the question using multiple linear regression of state data. ("M" in the graph below stands for the math subtest. "V" stands for the critical reading or verbal subtest.)
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-1a52vkpjans/UmjAc5fGxtI/AAAAAAAAA6U/EmUPxCtOsXg/s1600/sat+race+income+1995.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-1a52vkpjans/UmjAc5fGxtI/AAAAAAAAA6U/EmUPxCtOsXg/s400/sat+race+income+1995.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-beHM3wvWXG0/UmjAnqgxfII/AAAAAAAAA6c/fkdStmOtOfM/s1600/sat+race+education+1995.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-beHM3wvWXG0/UmjAnqgxfII/AAAAAAAAA6c/fkdStmOtOfM/s400/sat+race+education+1995.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-lTIJiMUYPgU/UmjArdfT2UI/AAAAAAAAA6k/c7NfE3h4S74/s1600/sat+race+income+2003.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-lTIJiMUYPgU/UmjArdfT2UI/AAAAAAAAA6k/c7NfE3h4S74/s400/sat+race+income+2003.png" /></a></div>
<br>
First, I shall review the important news from this year’s SAT and ACT score reports. I used the <a href="http://theunsilencedscience.blogspot.com/2013/06/the-sat-act-score-map.html">ACT-to-SAT conversion equation</a> that I extracted from the conversion table to construct a summary graph of overall ACT-SAT scores for each race and gender. Asian scores continued to rise, despite the College Board’s <a href="http://blogs.wsj.com/korearealtime/2013/05/28/group-of-south-koreans-barred-from-sat/">South Korean crackdown</a>, which was based upon suspicions of widespread cheating. Meanwhile, overall scores fell, and whites, Native Americans, and men declined this year more than any of the previous sixteen available years.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-Myld998sNf0/UmjCOUAXHkI/AAAAAAAAA6w/vTAKdL__uLk/s1600/sat-act+race.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-Myld998sNf0/UmjCOUAXHkI/AAAAAAAAA6w/vTAKdL__uLk/s400/sat-act+race.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-yhVmwpGRlss/UmjCQwdJvOI/AAAAAAAAA64/c7cwrp1xUyI/s1600/sat-act+race+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-yhVmwpGRlss/UmjCQwdJvOI/AAAAAAAAA64/c7cwrp1xUyI/s400/sat-act+race+part.png" /></a></div>
<br>
Native Americans now barely score higher than Hispanic Americans. Native-American ACT scores slipped especially fast, and their average score on the optional ACT writing exam now equals those of African Americans. Since many white people have Native-American ancestry, and Canadian and US Native Americans tend to have high amounts of European ancestry, Native-American score trends could reflect changing cultural attitudes about racial identification, but their absolute number of test participants has not changed greatly.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-v_eTZt_OVas/UmjC_-2CvyI/AAAAAAAAA7A/M80049jE61E/s1600/act+race+w.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-v_eTZt_OVas/UmjC_-2CvyI/AAAAAAAAA7A/M80049jE61E/s400/act+race+w.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-o8em9Sa9pJo/UmjDER1OOwI/AAAAAAAAA7I/dOKMm53J3KE/s1600/sat-act+native+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-o8em9Sa9pJo/UmjDER1OOwI/AAAAAAAAA7I/dOKMm53J3KE/s400/sat-act+native+part.png" /></a></div>
<br>
I previously <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">commented</a> on evidence for possible white decline. So far, the evidence is subtle. If future scores demonstrate long-term decline, it could signify the “dumbing down” of education or culture, dysgenics, minority-centered education reforms, or low rates of whites taking test preparation services.
<br><br>
Because Asian score increases have been steady and measured, I believe that these represent genuine progress, even with or perhaps due to the same root causes as the reported cheating scandals among Asians. However, I suspect that Asian progress will eventually level off because most racial score gaps have stayed remarkably constant, and I think nature influences testing potential, especially among those of adequate means.
<br><br>
SAT annual reports provide scores of students grouped by their parents’ income and education levels. These graphs of that data should not surprise anyone.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-quRaRm8vOD8/UmjDnGvz_LI/AAAAAAAAA7Q/IkDiGWAMIIE/s1600/sat+income+v.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-quRaRm8vOD8/UmjDnGvz_LI/AAAAAAAAA7Q/IkDiGWAMIIE/s400/sat+income+v.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-N1zUQUSbikY/UmjDsPllXnI/AAAAAAAAA7Y/7TAxcCEDXHc/s1600/sat+income+m.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-N1zUQUSbikY/UmjDsPllXnI/AAAAAAAAA7Y/7TAxcCEDXHc/s400/sat+income+m.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-olo2vxPS8jU/UmjDxPxwarI/AAAAAAAAA7g/mYkgDkW6JQY/s1600/sat+income+w.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-olo2vxPS8jU/UmjDxPxwarI/AAAAAAAAA7g/mYkgDkW6JQY/s400/sat+income+w.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-Tcc4TkZRwwA/UmjD0pI_GyI/AAAAAAAAA7o/RgYcJWpNpxI/s1600/sat+education+v.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-Tcc4TkZRwwA/UmjD0pI_GyI/AAAAAAAAA7o/RgYcJWpNpxI/s400/sat+education+v.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-SD8-HtSiZgE/UmjD4Vo94mI/AAAAAAAAA7w/juagw1EEqLo/s1600/sat+education+m.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-SD8-HtSiZgE/UmjD4Vo94mI/AAAAAAAAA7w/juagw1EEqLo/s400/sat+education+m.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-q4b_XrCci-w/UmjD7GL1ZoI/AAAAAAAAA74/Y0ApMTJd-Kk/s1600/sat+education+w.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-q4b_XrCci-w/UmjD7GL1ZoI/AAAAAAAAA74/Y0ApMTJd-Kk/s400/sat+education+w.png" /></a></div>
<br>
The fluctuation of income categories tells an interesting story about the past two decades. The number of people with six-figure incomes took off not that long ago.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-LtEVUPy9PyM/UmjFa4ZnytI/AAAAAAAAA8Y/7sLM5aeEbPQ/s1600/sat+income+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-LtEVUPy9PyM/UmjFa4ZnytI/AAAAAAAAA8Y/7sLM5aeEbPQ/s400/sat+income+part.png" /></a></div>
<br>
Despite the fact that levels of (parents’) education have been trending upwards, coming from an educated family increasingly predicts obtaining a higher SAT score. This graph of educational advantage is a Cohen’s d graph with the vertical axis zoomed in. I defined those parents with a bachelor’s or graduate degree as “educated.” (This graph uses the older term for the critical reading subtest, verbal.)
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-mG4YT8OEAIY/UmjFoSVdExI/AAAAAAAAA8g/4FuyIG0J3tc/s1600/sat+educated.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-mG4YT8OEAIY/UmjFoSVdExI/AAAAAAAAA8g/4FuyIG0J3tc/s400/sat+educated.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-7V6XAnh3W3w/UmjFIX7nx-I/AAAAAAAAA8Q/ceXzZQo4PSk/s1600/sat+education+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-7V6XAnh3W3w/UmjFIX7nx-I/AAAAAAAAA8Q/ceXzZQo4PSk/s400/sat+education+part.png" /></a></div>
<br>
Parents’ education and income show clear links to SAT scores, but so do many other variables. When I mapped state SAT scores, I discovered that Midwestern states achieved higher scores than other states because a small percentage of studious Midwesterners took the SAT, and most other college-bound students in those states only took the ACT. Simple linear regression of state SAT scores with only participation rate as the predictor variable explains 78 percent of variance (P = 10<sup>-273</sup>). Usually psychology research conducts this kind of analysis with a sample population, but I cannot access the College Board’s raw data, obviously. I am trying to reverse-engineer an SAT database with 16 years of state data. However, a single data point for an income category could represent tens of thousands of people or as few as three. Plus, the year could potentially influence scores due to inflation or even societal changes in cognitive abilities, the so-called Flynn effect. I can appropriately control for those variables, but controlling for race would require estimation because racial group proportions are not broken down every year within each income bracket and educational degree. Therefore, I turned income and education levels into continuous variables for multiple linear regression.
<br><br>
For linear regression, I turned income into a continuous variable by dividing the number of students whose parents earn six-figure incomes by the number whose parents earn less than $20,000 per year. I compared results for this income “gap” to an income “divide” based on the number whose parents earn more than $60,000 per year divided by those whose parents earn less. I created a variable for education based on the number whose parents achieved at least a bachelor’s degree divided by the number whose parents did not. The racial variable was the number of whites and Asians divided by the number of another race. Simple linear regression for state population size showed that it was a significant predictor of SAT scores (P=4.3 x 10<sup>-47</sup>) that explained 22 percent of variance. However, it became insignificant with all further analysis except when the other predictor variables were either participation, year, and income gap or participation, year, education, and income divide with or without race. Year did not produce a significant P value for simple linear regression (P = 0.5) but always did in multiple linear regression of income or education, lowering scores over time like a reverse-Flynn effect. Both income gap and income divide were significant predictor variables in multiple linear regression, but income divide slightly better predicted SAT scores, explaining 86 percent of variance with year and participation variables, compared to 85 percent for income gap with year, size, and participation variables. Multiple linear regression with participation rate, year, income divide, and education explained 90 percent of variance with all variables achieving statistical significance, but the addition of education caused the P value of the income divide to worsen from 10<sup>-83</sup> to 10<sup>-3</sup>. <b>When I added race as an additional variable, the income divide was no longer a significant predictor of SAT scores (P = 0.4).</b> Most of the impact of income on SAT scores stems from its ability to predict parents’ education levels. Multiple linear regression with the remaining significant variables (state sample size, participation rate, year, education, and race) explained 92 percent of SAT variance.
<br><br>
Graphs of actual SAT scores for income brackets and education levels show the distinctiveness of children whose parents have graduate degrees. Trendlines are given with R-squared variances for the highest and lowest categories.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-2QMVTumgHIc/UmjF49fmF3I/AAAAAAAAA8o/odgquhuACQI/s1600/sat+income+state+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-2QMVTumgHIc/UmjF49fmF3I/AAAAAAAAA8o/odgquhuACQI/s400/sat+income+state+part.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-nijKxGNHxB0/UmjF-xyy_tI/AAAAAAAAA8w/hX3-FRm3v-g/s1600/sat+education+state+part.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-nijKxGNHxB0/UmjF-xyy_tI/AAAAAAAAA8w/hX3-FRm3v-g/s400/sat+education+state+part.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-xjC2HriPFBY/UmjGDl5L0BI/AAAAAAAAA84/npoQJjwSlLA/s1600/sat+income+state+size.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-xjC2HriPFBY/UmjGDl5L0BI/AAAAAAAAA84/npoQJjwSlLA/s400/sat+income+state+size.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://3.bp.blogspot.com/-qw9Sa5wI8eg/UmjGGJM_h0I/AAAAAAAAA9A/YJ0YnYnVKyw/s1600/sat+education+state+size.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-qw9Sa5wI8eg/UmjGGJM_h0I/AAAAAAAAA9A/YJ0YnYnVKyw/s400/sat+education+state+size.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://4.bp.blogspot.com/-pKc11G3Gh8Y/UmjGKpDQ1OI/AAAAAAAAA9I/OCD7j0BXUQk/s1600/sat+income+state+year.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-pKc11G3Gh8Y/UmjGKpDQ1OI/AAAAAAAAA9I/OCD7j0BXUQk/s400/sat+income+state+year.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://2.bp.blogspot.com/-OmYL7XsEMCc/UmjGNzHqBOI/AAAAAAAAA9Q/Cz6m_hlq1qk/s1600/sat+education+state+year.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-OmYL7XsEMCc/UmjGNzHqBOI/AAAAAAAAA9Q/Cz6m_hlq1qk/s400/sat+education+state+year.png" /></a></div>
<br>
<b>The graphs for income or education with race reach the provocative result that race affects scores more among the lower rungs of society.</b> As the data only represents <i>state</i> racial proportions, the results leave room for debate. For instance, the furthest left data in the graphs below represent Washington, DC, which I actually treated as a state. Higher-income families there are probably more likely to be white or Asian-American than are lower-income families. Many racially diverse states like California have industries or attractions that pull in successful, educated whites. Nevertheless, one could use these results to defend upper-class affirmative-action beneficiaries or to call for a new class-based system to benefit the many poor, but intelligent whites and Asian Americans.
<br><br>
<div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-uLFoEbC7bKs/UmjHdd0DMQI/AAAAAAAAA9c/X_qMHFlOg9M/s1600/sat+income+state+race.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-uLFoEbC7bKs/UmjHdd0DMQI/AAAAAAAAA9c/X_qMHFlOg9M/s400/sat+income+state+race.png" /></a></div><div class="separator" style="clear: both; text-align: center;"><a href="http://1.bp.blogspot.com/-cQonoAnocJo/UmjHgmYD4XI/AAAAAAAAA9o/AngxgHGUufE/s1600/sat+education+state+race.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-cQonoAnocJo/UmjHgmYD4XI/AAAAAAAAA9o/AngxgHGUufE/s400/sat+education+state+race.png" /></a></div>
<br>
Also of note is the fact that these graphs look totally awesome.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+Blacks+in+Higher+Education&rft_id=info%3Adoi%2F10.2307%2F2999198&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Why+Family+Income+Differences+Don%27t+Explain+the+Racial+Gap+in+SAT+Scores&rft.issn=&rft.date=1998&rft.volume=&rft.issue=20&rft.spage=6&rft.epage=8&rft.artnum=http%3A%2F%2Fwww.jstor.org%2Fdiscover%2F10.2307%2F2999198%3Fuid%3D2%26uid%3D4%26sid%3D21102808045857&rft.au=Anonymous&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Anonymous (1998). Why Family Income Differences Don't Explain the Racial Gap in SAT Scores <span style="font-style: italic;">The Journal of Blacks in Higher Education</span> (20), 6-8 DOI: <a rev="review" href="http://dx.doi.org/10.2307/2999198">10.2307/2999198</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+Blacks+in+Higher+Education&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Why+Family+Income+Differences+Don%27t+Explain+the+Racial+Gap+in+SAT+Scores&rft.issn=&rft.date=2008&rft.volume=&rft.issue=62&rft.spage=10&rft.epage=12&rft.artnum=&rft.au=Anonymous&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Anonymous (2008). Why Family Income Differences Don't Explain the Racial Gap in SAT Scores <span style="font-style: italic;">The Journal of Blacks in Higher Education</span> (62), 10-12</span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Teachers+College+Record&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Race%2C+Poverty+and+SAT+Scores%3A+Modeling+the+Influences+of+Family+Income+on+Black+and+White+High+School+Students%E2%80%99+SAT+Performance&rft.issn=&rft.date=2013&rft.volume=115&rft.issue=4&rft.spage=1&rft.epage=33&rft.artnum=http%3A%2F%2Fwww.tcrecord.org%2Fcontent.asp%3Fcontentid%3D16925&rft.au=Ezekiel+Dixon-Roman&rft.au=Howard+Everson&rft.au=John+McArdle&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CMedicine%2CMathematics%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Ezekiel Dixon-Roman, Howard Everson, & John McArdle (2013). Race, Poverty and SAT Scores: Modeling the Influences of Family Income on Black and White High School Students’ SAT Performance <span style="font-style: italic;">Teachers College Record, 115</span> (4), 1-33</span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com15tag:blogger.com,1999:blog-5002675950760488813.post-7176348137002313552013-06-10T00:53:00.000-07:002013-06-10T00:53:40.537-07:00The SAT-ACT Score Map<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<center>
<a href="http://s1087.photobucket.com/user/nooffensebut/media/sat-actpartcont.gif.html" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-actpartcont.gif" border="0" alt=" photo sat-actpartcont.gif"/></a>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://4.bp.blogspot.com/-FS6IHT5xhsQ/UGbBGZpGnuI/AAAAAAAAApI/8-tP8ARkpI8/s1600/sat%2Bmap%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="75" src="http://4.bp.blogspot.com/-FS6IHT5xhsQ/UGbBGZpGnuI/AAAAAAAAApI/8-tP8ARkpI8/s400/sat%2Bmap%2Blegend.png" /></a></div>
(Note: Following this post, I shall focus on finishing the <a href="http://theunsilencedscience.blogspot.com/2013/01/monoamine-oxidase-bibliography.html">MAOA bibliography</a> probably until it is up-to-date and until I can better quantify its data.)
<br><br>
In my <a href="http://theunsilencedscience.blogspot.com/2012/09/the-sat-zombie-apocalypse.html">last post</a> on college-entrance exams, I left incomplete the task of properly controlling for test participation a state map of combined SAT and ACT scores. I had already explored group average SAT gaps by <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">race</a> and <a href="http://theunsilencedscience.blogspot.com/2011/10/girls-versus-boys-final-battle.html">gender</a> and SAT <a href="http://theunsilencedscience.blogspot.com/2012/04/sat-bell-curve.html">score distributions</a>. Finally, I am posting above what I consider the definitive state map, which is properly controlled for test type and state participation levels.
<br><br>
The map demonstrates my contention that American demographic changes contribute to a North-South educational divide. Detailed mapping of potential academic decline can help inform discussion of policies like “immigration reform,” help extrapolate future global competitiveness of the American workforce, and delineate regional economic fault lines. In the explanation that follows, I compare the effects of state participation in the SAT and ACT and race with regression analysis. Then, I shall review an important study on the relative importance of these scores and what might augment or replace them.
<br><br>
Testing associations publish a standardized table to convert between ACT and SAT scores. The primary table converts between the composite ACT score and the combined SAT mathematics and critical-reading (formerly verbal) score. (I divided the scores in half for purposes of comparison with SAT subtest scores.) A separate table converts between the newer SAT writing score and the score for the optional ACT writing exam. However, I shall neglect the writing scores data at this time, but the <a href="http://theunsilencedscience.blogspot.com/2012/09/the-sat-zombie-apocalypse.html">previous post</a> maps raw SAT writing scores.
<br><br>
My last attempt at ACT-to-SAT score conversion amounted to a crude estimate that only accounted for the highest and lowest ACT scores with a line drawn between for all others. The tests follow different scales with several possible SAT scores coinciding with almost all ACT scores. Therefore, I created a new formula based on linear regression of the plot of average SAT scores for each ACT increment. Since state ACT averages tend to hover around 21, this graph illuminates how my previous formula unfairly underestimated states that emphasize the ACT over the SAT.
<br><br>
<a href="http://3.bp.blogspot.com/-CSjcZ_NXbdw/UbV90Ble3KI/AAAAAAAAA3M/bkPtPUee-p4/s1600/act+to+sat+conversion.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-CSjcZ_NXbdw/UbV90Ble3KI/AAAAAAAAA3M/bkPtPUee-p4/s320/act+to+sat+conversion.png" /></a>
<br>
As states increasingly have required the ACT for all high-school graduates, their average scores have declined. Plotting below each state’s yearly ACT and SAT score since 1998 by participation level confirms the association. All associations achieve statistical significance (P=9.54 x 10<sup>-27</sup> for the ACT, P=3.75 x 10<sup>-33</sup> for the weighted SAT-ACT scores) with the SAT, alone, achieving the greatest significance of any tested relationship in this entire effort (P=5.4 x 10<sup>-245</sup>) and the largest coefficient of determination (0.769). Midwestern states that strongly emphasize the ACT achieved impressive average SAT scores and seem to have an outsized impact on this finding. The combined SAT-ACT participation rates are out of a possible 200%, which would require all high-school graduates to take the SAT and the ACT.
<br><br>
<a href="http://4.bp.blogspot.com/-5eyKvtxwkLQ/UbV-En9-yOI/AAAAAAAAA3U/FsZrMDkCwqs/s1600/sat+participation+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-5eyKvtxwkLQ/UbV-En9-yOI/AAAAAAAAA3U/FsZrMDkCwqs/s320/sat+participation+scatter.png" /></a>
<a href="http://2.bp.blogspot.com/-wyK8-Fz5xsc/UbV-Lk9-44I/AAAAAAAAA3c/-v1o4ptFZgw/s1600/act+participation+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-wyK8-Fz5xsc/UbV-Lk9-44I/AAAAAAAAA3c/-v1o4ptFZgw/s320/act+participation+scatter.png" /></a>
<a href="http://2.bp.blogspot.com/-eJmgGNd5mqY/UbV-WZmWKHI/AAAAAAAAA3k/8O2vJSliJyM/s1600/sat-act+participation+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-eJmgGNd5mqY/UbV-WZmWKHI/AAAAAAAAA3k/8O2vJSliJyM/s320/sat-act+participation+scatter.png" /></a>
<br>
The comparison of score maps to demographic trends, which I presented with a map of the percentage of SAT examinees who are white or Asian, fits the familiar national racial group mean gaps. Simple linear regression better quantifies the effect of race, and multiple linear regression can tease apart the effect of state participation levels. Asians have the highest scores, but I lumped whites with Asians because Asians are a relatively small group. I would expect other racial gaps to be too confounding to separate Asians from the rest. The distinction I drew might seem arbitrary, but many institutions separate data on Asians and whites from that of “underrepresented minorities.” The graphs of scores by racial proportion appear to show that these are linear associations, all of which are significant (P=3.51 x 10<sup>-53</sup> for the SAT, P=1.33 x 10<sup>-41</sup> for the ACT, and P=1.48 x 10<sup>-40</sup> for the tests combined). Multiple regression shows that all associations remain significant. For the combined SAT-ACT score, participation had a P-value of 3.35 x 10<sup>-22</sup>, and race had a P-value of 1.29 x 10<sup>-29</sup>. The multiple regression model set score equal to 986 – 0.782 x participation (as a whole number) + 97.5 x the percentage white or Asian.
<br><br>
<a href="http://1.bp.blogspot.com/-B7i4giU18D0/UbV-x796UYI/AAAAAAAAA3s/Lzd3dkEMPX0/s1600/sat+w&a+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-B7i4giU18D0/UbV-x796UYI/AAAAAAAAA3s/Lzd3dkEMPX0/s320/sat+w&a+scatter.png" /></a>
<a href="http://1.bp.blogspot.com/-qXPzZt1jc24/UbV-4GD4kCI/AAAAAAAAA30/FR9hgv5taMc/s1600/act+w&a+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-qXPzZt1jc24/UbV-4GD4kCI/AAAAAAAAA30/FR9hgv5taMc/s320/act+w&a+scatter.png" /></a>
<a href="http://2.bp.blogspot.com/-yF49OoEltRI/UbWCSp-i5UI/AAAAAAAAA4U/zt9EFV6Y9t0/s1600/sat-act+a&w+scatter.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-yF49OoEltRI/UbWCSp-i5UI/AAAAAAAAA4U/zt9EFV6Y9t0/s320/sat-act+a&w+scatter.png" /></a>
<br>
The residuals from subtracting this model from the raw data fit a Gaussian distribution, as expected. So, I recalculated the SAT-ACT composite scores by adding the residuals back to the model under the assumption of 100% (out of a possible 200%) participation.
<br><br>
<a href="http://3.bp.blogspot.com/-tNWFujJIu_k/UbV_OejKqnI/AAAAAAAAA4E/EfJT8NgAIU8/s1600/sat-act+residuals.png" imageanchor="1" ><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-tNWFujJIu_k/UbV_OejKqnI/AAAAAAAAA4E/EfJT8NgAIU8/s320/sat-act+residuals.png" /></a>
<br>
While the score map might not appear identical to the map of demographic trends, one can make out a North-South gradient, and state efforts to adopt test requirements seem well-controlled. Further analysis could use ANCOVA for income categories or compare racial gaps within states. Composite writing scores could prove useful, despite the shorter timeframe for the SAT and the optional nature of the ACT written exam. In fact, the states of Texas, Nevada, and Florida might not seem to perform so badly in this map, given their diversity, but their raw SAT writing scores were especially low. Then again, immigration weighing down English writing skills could resolve with acculturation.
<br><br>
<center>
<a href="http://s1087.photobucket.com/user/nooffensebut/media/sat-actpartcont.gif.html" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-actpartcont.gif" border="0" alt=" photo sat-actpartcont.gif"/></a>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawmap.gif" border="0" alt="Photobucket"></a>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://3.bp.blogspot.com/-UStMdyxPfJM/UGbBoqGUG4I/AAAAAAAAApU/N5CkbQdi2rA/s1600/sat%2Bmap%2Baw%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="76" src="http://3.bp.blogspot.com/-UStMdyxPfJM/UGbBoqGUG4I/AAAAAAAAApU/N5CkbQdi2rA/s320/sat%2Bmap%2Baw%2Blegend.png" /></a></div>
<br>
Now, I wish to review a 2009 study on the relative relevance of SAT and ACT scores. <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdV9tTHR5VGItX1k/edit">Schmitt et al</a> compared the predictive value of those scores to high-school grades and twelve “noncognitive predictors”: knowledge, curiosity, adaptability, perseverance, ethics (“not cheating”), career orientation, healthy behaviors, interpersonal skills, “leadership,” community volunteer activities, “artistic and cultural appreciation,” and “appreciation for diversity” (“e.g. by culture, ethnicity, religion, or gender”). As the US Supreme Court revisits the issue of Affirmative Action in college admissions, universities might apply such predictors to lessen the influence of standardized tests. None of the “noncognitive predictors” could predict college grades even half as well as either high-school grades or the SAT/ACT scores, which had correlations of 0.531 and 0.539, respectively. Knowledge came closest, but I think knowledge is cognitive. Career orientation actually was alone in its statistically significant <i>negative</i> association with college grade-point average. The authors offered as their only explanatory hypothesis the poor performance of African Americans “for whom career mobility and a career orientation was a major reason for college attendance.” Indeed, career orientation was the strongest advantage for African Americans, who barely scored higher than whites on “appreciation for diversity.” Their only other advantage was perseverance. High-school grades underestimated African-American college grades, but not as much as SAT/ACT scores overestimated. Adding the “noncognitive” criteria to potential admissions selection would lower college grades, in general, but raise African-American and Hispanic-American admissions at the 15% most exclusive universities, at the expense of white and especially Asian-American applicants. However, African-American college graduation rates would fall eight percentage points at such institutions. SAT/ACT scores were significantly associated with higher college classroom absenteeism and lower “organizational citizenship behavior,” with which “appreciation for diversity” had a significant positive association. In other words, the more intelligent students were less inclined to go to all lectures, promote “the university to outsiders,” defend “it against criticism,” and participate “in student government or other clubs” to make the university “a better place.” The authors did not conclude that those are relatively unintelligent behaviors.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+applied+psychology&rft_id=info%3Apmid%2F19916657&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Prediction+of+4-year+college+student+performance+using+cognitive+and+noncognitive+predictors+and+the+impact+on+demographic+status+of+admitted+students.&rft.issn=0021-9010&rft.date=2009&rft.volume=94&rft.issue=6&rft.spage=1479&rft.epage=97&rft.artnum=https%3A%2F%2Fdocs.google.com%2Ffile%2Fd%2F0B4NGOBcoYImfdV9tTHR5VGItX1k%2Fedit&rft.au=Schmitt+N&rft.au=Keeney+J&rft.au=Oswald+FL&rft.au=Pleskac+TJ&rft.au=Billington+AQ&rft.au=Sinha+R&rft.au=Zorzie+M&rfe_dat=bpr3.included=1;bpr3.tags=Mathematics%2CPhilosophy%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Schmitt N, Keeney J, Oswald FL, Pleskac TJ, Billington AQ, Sinha R, & Zorzie M (2009). Prediction of 4-year college student performance using cognitive and noncognitive predictors and the impact on demographic status of admitted students. <span style="font-style: italic;">The Journal of applied psychology, 94</span> (6), 1479-97 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19916657">19916657</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com4tag:blogger.com,1999:blog-5002675950760488813.post-75513377914463128152013-03-13T04:53:00.000-07:002013-03-13T04:53:22.878-07:00Why YouTube Sucks Episode II – The Phantom Menace<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
I must apologize for taking a break from expanding the MAOA bibliography to interject myself into a YouTube debate about heredity.
<br /><br /><iframe width="415" height="259" src="http://www.youtube.com/embed/ftD0oyfecf0" frameborder="0" allowfullscreen></iframe>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com5tag:blogger.com,1999:blog-5002675950760488813.post-23089005086441743182013-01-13T06:01:00.001-08:002015-01-16T04:24:52.628-08:00Monoamine Oxidase A Bibliography<STYLE TYPE="text/css">
<!--
TD{font-family: Arial; font-size: 7pt;}
--->
</STYLE>
<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-TSE69LRp20U/UPK8E2FQtaI/AAAAAAAAA04/etezIu2zAGI/s1600/Under%2Bconstruction.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="126" width="400" src="http://4.bp.blogspot.com/-TSE69LRp20U/UPK8E2FQtaI/AAAAAAAAA04/etezIu2zAGI/s400/Under%2Bconstruction.jpg" /></a></div>
Last updated: 1-16-2015<br><br>
Bookmark this as a resource for research related to monoamine oxidase A (MAOA) or “the warrior gene.” New studies will appear as they become available. If a study is missing that belongs here, please email <a href="mailto:n00ffensebut@gmail.com">n00ffensebut@gmail.com</a>. Also, be sure to read my own detailed <a href="http://theunsilencedscience.blogspot.com/2011/08/genetics-of-violence.html">analyses</a>.
<br><br><br>
<div id="maoa study database_29124" align=center x:publishsource="Excel">
<h1 style='color:black;font-family:Calibri;font-size:14.0pt;font-weight:800;
font-style:normal'>MAOA Allele Frequencies</h1>
<table border=1 cellpadding=0 cellspacing=0 width=300 style='border-collapse:
collapse;table-layout:fixed;width:100pt'>
<col width=47 style='mso-width-source:userset;mso-width-alt:3291;width:47pt'>
<col width=37 style='width:37pt'>
<col width=37 style='mso-width-source:userset;mso-width-alt:3072;width:37pt'>
<col width=37 span=5 style='width:37pt'>
<tr height=37 style='height:15.0pt'>
<td class=xl6329124 width=60 align=right style='width:60pt'> </td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>2R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>2.5R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>3R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>3.5R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>4R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>5R</td>
<td class=xl6329124 width=30 align=right style='border-left:none;width:30pt'>6R</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>All Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>108</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>8769</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>173</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>11437</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>175</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>All %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.5226%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0097%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>42.4361%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.8372%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>55.3475%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.8469%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>White Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>26</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>4618</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>164</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>8032</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>146</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>White %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.2002%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0154%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>35.5559%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>1.2627%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>61.8417%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>1.1241%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Black Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>46</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>542</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>3</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>448</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>9</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Black %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>4.3893%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>51.7176%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.2863%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>42.7481%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.8588%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Asian Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>19</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2433</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>1</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>1559</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Asian %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.4733%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>60.6129%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0249%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>38.8391%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0498%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Hispanic Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>27</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>65</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Hispanic %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>29.3478%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>70.6522%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Native Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>220</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>1</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>354</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Native %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>38.1282%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.1733%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>61.3518%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.3466%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Jewish Raw</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>96</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>54</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>2</td>
<td class=xl6329124 align=right style='border-top:none;border-left:none'>0</td>
</tr>
<tr height=20 style='height:15.0pt'>
<td class=xl6329124 width=60 style='border-top:none'>Jewish %</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>1.2987%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>62.3377%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>35.0649%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>1.2987%</td>
<td class=xl6429124 align=right style='border-top:none;border-left:none'>0.0000%</td>
</tr>
<td width=60 style='width:60pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
<td width=30 style='width:30pt'></td>
</tr>
<![endif]>
</table>
</div>
<br><br>
<b>MAOA Gene Biochemistry</b>
<br><br>
Pintar <i>et al</i>. (2-1-1981). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZ1pfYkVCdzlXS00/edit">Gene for monoamine oxidase type A assigned to the human X chromosome.</a> Journal of Neuroscience 1(2): 166-175.
<br><br>
Kochersperger <i>et al</i>. (1986). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMjdQZEtFV0xJa1U/edit">Assignment of genes for human monoamine oxidase A and B to the X chromosome.</a> Journal of Neuroscience Research 16(4): 601-616.
<br><br>
Bach <i>et al</i>. (7-1-1988). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOHpPTXpBRVNBbzA/edit">cDNA cloning of human liver monoamine oxidase A and B: molecular basis of differences in enzymatic properties.</a> Proceedings of the National Academy of Sciences 85(13): 4934-4938.
<br><br>
Ozelius <i>et al</i>. (7-1988). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfR25OLWJhU1JkR00/edit">Human monoamine oxidase (MAOA): chromosome position (Xp21-Xp11) and DNA polymorphism.</a> Genomics 3(1): 53-58.
<br><br>
Black <i>et al</i>. (2-11-1991). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcE1WQ0VDbmVOcTA/edit">Dinucleotide repeat polymorphism at the MAOA locus.</a> Nucleic Acids Research 19(3): 689.
<br><br>
Grimsby <i>et al</i>. (5-1-1991). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfY0ktSjVMSkJaZUk/edit">Human monoamine oxidase A and B genes exhibit identical exon-intron organization.</a> Proceedings of the National Academy of Sciences 88(9): 3637-3641.
<br><br>
Chen <i>et al</i>. (8-25-1991). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMmxzUnBkclZOQ00/edit">Structure of the human gene for monoamine oxidase type A.</a> Nucleic Acids Research 19(16): 4537-4541.
<br><br>
Hinds <i>et al</i>. (7-1992). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUndxbkdwM0lqWEk/edit">Characterization of a highly polymorphic region near the first exon of the human MAOA gene containing a GT dinucleotide and a novel VNTR motif.</a> Genomics 13(3): 896-897.
<br><br>
Chen <i>et al</i>. (9-1992). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcHJhaEw3MVFlUjg/edit">Organization of the human monoamine oxidase genes and long-range physical mapping around them.</a> Genomics 14(1): 75-82.
<br><br>
Zhu <i>et al</i>. (11-1-1992). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfYVJkX195d0Ywd0U/edit">Promoter organization and activity of human monoamine oxidase (MAO) A and B genes.</a> Journal of Neuroscience 12(11): 4437-4446.
<br><br>
Shih <i>et al</i>. (1-1993). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbmhNUnNPVGs3SUk/edit">Structure and promoter organization of the human monoamine oxidase A and B genes.</a> Journal of Psychiatry & Neuroscience 18(1): 25-32.
<br><br>
Shih <i>et al</i>. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfei10eXhvYnJtNnc/">Identification of human monoamine oxidase (MAO) A and B gene promoters.</a> Journal of Neural Transmission. Supplementum 41:27-33.
<br><br>
Denney <i>et al</i>. (9-1994). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfaWlZU09MdnRkVUk/edit">A new look at the promoter of the human monoamine oxidase A: gene mapping, transcription initiation sites, and capacity to drive luciferase expression.</a> Journal of Neurochemistry 63(3): 843-856.
<br><br>
Denney <i>et al</i>. (1995). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSkFtanVNOWJrSlk/edit">The promoter of the human monoamine oxidase A gene.</a> Progress in Brain Research 106: 57-66.
<br><br>
Zhu <i>et al</i>. (10-1997). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeG0zdFRDcTdhSVE/edit">An extensive repeat structure down-regulates human monoamine oxidase A promoter activity independent of an initiator-like sequence.</a> Journal of Neurochemistry 69(4): 1368-1373.
<br><br>
Sabol <i>et al</i>. (9-1998). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQy1aZEp5ZEt5RzA/edit">A functional polymorphism in the monoamine oxidase A gene promoter.</a> Human Genetics 103(3): 273-279.
<br>
- P1 promoter discovery<br>
- Racial allele frequencies<br>
- Large sample with no MAOA-2R
<br><br>
Benjamin <i>et al</i>. (2-2000). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSWFLWGt5SkNMdFU/edit">A novel expression based approach for assessing the inactivation status of human X-linked genes.</a> European Journal of Human Genetics 8(2): 103-108.
<br><br>
Carrel and Willard. (3-17-2005). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTjdxUExVa2tpdjA/edit">X-inactivation profile reveals extensive variability in X-linked gene expression in females.</a> Nature 434(): 400-404.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTm1RLVBqbDR2Wmc/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeHdRZVFGWHZTSG8/edit">2</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZm82d0x5dXRMdnc/edit">3</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfWHF0RE16azRhanc/edit">4</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNW9SR2lCWmhVT0k/edit">5</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZGV3akE1MW5wT2M/edit">6</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSzc0VEhWcGs0Mm8/edit">7</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbmN1UThmSElmdGM/edit">8</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOGkwNkU2c0dPYkU/edit">9</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTXNsbFBBZnMyejg/edit">10</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfM0xyTWhIa1h5REU/edit">11</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfc1JvWTJkU050dWM/edit">12</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcktlNHBJZzJXVGc/edit">13</a>
<br><br>
Nordquist and Oreland. (9-22-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfY1J1dW40cTFPbVU/edit">Monoallelic expression of MAOA in skin fibroblasts.</a> Biochemical and Biophysical Research Communications 348(2): 763-767.
<br><br>
<b>Serotonin</b>
<br><br>
Tuinier and Verhoeven. (6-1995). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMDJ0RElsbVVRSFE/edit">Dimensional classification and behavioral pharmacology of personality disorders; a review and hypothesis.</a> European Neuropsychopharmacology 5(2): 135-146.
<br><br>
<b>MAOA Metabolites</b>
<br><br>
Nielsen <i>et al</i>. (1-1994). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMFZUY1NucXdJcWM/edit">Suicidality and 5-hydroxyindoleacetic acid concentration associated with a tryptophan hydroxylase polymorphism.</a> Archives of General Psychiatry 51(1): 34-38.
<br><br>
<b>MAOA Enzyme</b>
<br><br>
Bond <i>et al</i>. (10-15-1977). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfODJnTTNSVG5UVUE/edit">Properties of monoamine oxidase (MAO) in human blood platelets, plasma, lymphocytes and granulocytes.</a> Clinica Chimica Acta 80(2): 317-326.
<br><br>
Cawthon <i>et al</i>. (8-1981). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUklBNG5Xd3dSbWs/edit">Differences in the structure of A and B forms of human monoamine oxidase.</a> Journal of Neurochemistry 37(2): 363-372.
<br><br>
Weyler <i>et al</i>. (1990). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfV2R6UDhpLU1wak0/">Biochemistry and genetics of monoamine oxidase.</a> Pharmacology & Therapeutics 47(3): 391-417.
<br><br>
Ramsay <i>et al</i>. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfMFJJcmJ4WVhhbTQ/">Kinetic properties of cloned human liver monoamine oxidase A.</a> Journal of Neural Transmission. Supplementum 41: 17-26.
<br><br>
Fogel and Maslinski. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfc0IwTXU4OURWMlU/">The FAD dependent amine oxidases in relation to developmental state of enterocyte.</a> Journal of Neural Transmission. Supplementum 41: 95-99.
<br><br>
Fernandes and Soares-da-Silva. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfYmxXWFpOcGxFemc/">Role of monoamine oxidase and cathecol-O-methyltransferase in the metabolism of renal dopamine.</a> Journal of Neural Transmission. Supplementum 41:101-105.
<br><br>
Naoi <i>et al</i>. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfWHJtZnJmMTBSNlE/">Novel toxins and Parkinson’s disease: N-methylation and oxidation as metabolic bioactivation of neurotoxin.</a> Journal of Neural Transmission. Supplementum 41: 197-205.
<br><br>
Banchelli <i>et al</i>. (1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfcDMxcXg3WUNSLWc/">Histaminase activity of mesenteric artery of the rat.</a> Journal of Neural Transmission. Supplementum 41: 445-448.
<br><br>
Son <i>et al</i>. (4-15-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOHFEWEt6eVp4UEU/edit">Structure of human monoamine oxidase A at 2.2-A resolution: The control of opening the entry for substrates/inhibitors.</a> PNAS 105(15): 5739-5744.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSjZLREg1Z1A0bHM/edit">Supplement</a>
<br><br>
Alia-Klein <i>et al</i>. (5-7-2008). <a href="https://docs.google.com/open?id=0B4NGOBcoYImfc0w0MEFnRU51Nm8">Brain monoamine oxidase A activity predicts trait aggression.</a> The Journal of Neuroscience 28(19): 5099-5104.
<br>
- Subset of Fowler et al sample<br>
- Aggression as MPQ personality outcome
<br><br>
Meulendyke <i>et al</i>. (9-15-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfTEExSy03MllsT2M/">Elevated brain monoamine oxidase activity in SIV- and HIV-associated neurological disease.</a> Journal of Infectious Disease 210(6): 904-912.
<br>
- Supplement
<br><br>
<b>MAOA mRNA</b>
<br><br>
Grimsby <i>et al</i>. (10-1990). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZThPWHp4eVM1NGs/edit">Tissue distribution of human monoamine oxidase A and B mRNA.</a> The Journal of Neurochemistry 55(4): 1166-1169.
<br><br>
<b>Norrie Disease</b>
<br><br>
Lan <i>et al</i>. (5-1989). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeHk0YXlGNmdfdEE/edit">Human monoamine oxidase A and B genes map to Xp 11.23 and are deleted in a patient with Norrie disease.</a> Genomics 4(4): 552-559.
<br><br>
Levy <i>et al</i>. (8-1989). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQmgwUGdJY3IxOHc/edit">Localization of human monoamine oxidase-A gene to Xp11.23-11.4 by <i>in situ</i> hybridization: implications for Norrie disease.</a> Genomics 5(2): 368-370.
<br><br>
<b>MAOA/B Deletion Syndrome</b>
<br><br>
Whibley <i>et al</i>. (10-2010). <a href="">Deletion of MAOA and MAOB in a male patient causes severe developmental delay, intermittent hypotonia and stereotypical hand movements.</a> European Journal of Human Genetics 18(10): 1095-1099.
<br>
<br><br>
Saito <i>et al</i>. (2-13-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMEtuLVNRdEpDamM/edit">MAOA/B deletion syndrome in male siblings with severe developmental delay and sudden loss of muscle tonus.</a> Brain & Development: Epub ahead of print.
<br><br>
<b>Brunner Syndrome</b>
<br><br>
Brunner <i>et al</i>. (10-22-1993). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdDBhand4dlpYODA/edit">Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A.</a> Science 262(5133): 578-580.
<br><br>
Shih and Thompson. (9-1999). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfU3dUdENMUWdxeGc/view">Monoamine oxidase in neuropsychiatry and behavior.</a> American Journal of Human Genetics 65(3): 593-598.
<br>
- Review study<br>
- Describes unpublished finding by Hwang and Shih that “urine analysis of 119 inmates from a prison in Taiwan showed no evidence for altered monoamine metabolism, suggesting MAO A deficiency.”
<br><br>
Nelson and Trainor. (7-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNlZJWWRNOC0wdU0/edit">Neural mechanisms of aggression.</a> Nature Reviews Neuroscience 8(7): 536-546.
<br><br>
Craig and Halton. (7-2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeENWbHRuQ2IyS0E/edit">Genetics of human aggressive behaviour.</a> Human Genetics 126(1): 101-113.
<br><br>
<b>Knockout Mice</b>
<br><br>
<br><br>
<b>MAOA-2R</b>
<br><br>
Guo <i>et al</i>. (5-2008). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfTUFhd1NOOEpncGc/">The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: Associations and MAOA promoter activity.</a> European Journal of Human Genetics 16(5): 626-634.
<br><br>
Guo <i>et al</i>. (8-2008). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfcE9lMEFzVFRGMlU/">The integration of genetic propensities into social-control models of delinquency and violence among male youths.</a> American Sociological Review 73(4): 543-568.
<br>
- <a href="https://drive.google.com/file/d/0B4NGOBcoYImfUmttT1pUNUZ0UDA/ ">Supplement</a>
<br><br>
Beaver <i>et al</i>. (1-2013). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfb2JrOG5tZEVZSUk/">Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior.</a> Personality and Individual Differences 54(2): 164-168.
<br><br>
Roettger <i>et al</i>. (2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMW9BQURONDUzbEU/">MAOA genotype and longitudinal delinquency among males in the United States: the moderating role of parental incarceration and parental closeness.</a>
<br>
- National Longitudinal Study of Adolescent Health, Waves I and IV<br>
- Mother and father incarceration and closeness to child as environmental factors<br>
- Self-reported criminal delinquency outcome<br>
- Positive main effect (b=0.114, P < 0.036)<br>
- MAOA-2R interacts with father closeness such that closeness significantly decreases criminal delinquency in men with MAOA-2R (b=-0.086, P < 0.013)
<br><br>
Beaver <i>et al</i>. (9-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfLWFaY05rcFpmN2s/">The 2-repeat allele of the MAOA gene confers an increased risk for shooting and stabbing behaviors.</a> Psychiatric Quarterly 85(3): 257-265.
<br><br>
<b>MAOA-3R</b>
<br><br>
Manuck <i>et al</i>. (7-24-2000). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfdEVkdGxvbWlHWjQ/view ">A regulatory polymorphism of the monoamine oxidase-A gene may be associated with variability in aggression, impulsivity, and central nervous system serotonergic responsivity.</a> Psychiatry Research 95(1): 9-23.
<br>
<br><br>
Garpenstrand <i>et al</i>. (1-2003). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfTUZpLURPclpCbm8/view">A regulatory monoamine oxidase A promoter polymorphism and personality traits.</a> Neuropsychobiology 46(4): 190-193.
<br>
<br><br>
Williams <i>et al</i>. (3-2003). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZGVOMktFakxQTG8/">Serotonin-related gene polymorphisms and central nervous system serotonin function.</a> Neuropsychopharmacology 28(3): 533-541.
<br>
- Men with MAOA-3.5R or MAOA-4R averaged 17.70 ng/mL CSF 5-HIAA; men with MAOA-3R or MAOA-5R averaged 14.34 ng/mL<br>
- “Similar effects were found in separate analyses for” white men and African-American men<br>
- Negative finding for 5-HTTLPR epistasis (F=0.11, p=0.74)
<br><br>
Jacob <i>et al</i>. (9-2005). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfUnJFX0s1NVgxUlE/view">Cluster B personality disorders are associated with allelic variation of monoamine oxidase A activity.</a> Neuropsychopharmacology 30(9): 1711-1718.
<br>
<br><br>
Rosenberg <i>et al</i>. (11-2006). <a href="https://docs.google.com/open?id=0B4NGOBcoYImfbUJwV1prOHhIYzg">The association of DNA sequence variation at the MAOA genetic locus with quantitative behavioural traits in normal males.</a> Human Genetics 120(4): 447-459.
<br>
- Rare MAOA allele frequencies<br>
- NEO personality outcome
<br><br>
Fowler <i>et al</i>. (8-15-2007). <a href="https://docs.google.com/open?id=0B4NGOBcoYImfYmFuRWs2am9zb0E">Evidence that brain MAO A activity does not correspond to MAO A genotype in healthy male subjects.</a> Biological Psychiatry 62(4): 355-358.
<br>
- PET imaging<br>
- Does not control for race
<br><br>
Yang <i>et al</i>. (11-2007). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfUHR4bkU4YmtlOEk/">Association between monoamine oxidase A polymorphisms and anger-related personality traits in Korean women.</a> Neuropsychobiology 56(1): 19-23.
<br>
<br><br>
De Neve and Fowler. (11-18-2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUU5aLXNWazVqbkk/">The MAOA gene predicts credit card debt.</a>
<br>
- National Longitudinal Study of Adolescent Health<br>
- Positive main effect for credit card debt outcome
<br><br>
Fowler <i>et al</i>. (12-2009). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfZ1ZpczktOXVicEk/">Psychopathy trait scores in adolescents with childhood ADHD: the contribution of genotypes affecting MAOA, 5HTT and COMT activity.</a> Psychiatric Genetics 19(6): 312-319.
<br>
<br><br>
Zhong <i>et al</i>. (12-31-2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNkNyV013Q3p5Z0U/edit">Monoamine Oxidase A gene (MAOA) associated with attitude towards longshot risks.</a> PLOS One 4(12): e8516.
<br>
- Long-shot risk taking and insurance task outcomes<br>
- MAOA-4R significantly associated with long-shot risk taking (p=0.006)
<br><br>
Gong <i>et al</i>. (9-2010). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfMFJxZHBqdDBBbG8/view">Association analysis between 12 genetic variants of ten genes and personality traits in a young Chinese Han population.</a> Journal of Molecular Neuroscience 42(1): 120-126.
<br>
- Describes sample as being “324 females and 387 males,” but allele frequencies show 372 females and 293 males
<br><br>
Tikkanen <i>et al</i>. (2-28-2011). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfVUkzMHZQTHNpTjg/view">Psychopathy, PCL-R, and MAOA genotype as predictors of violent reconvictions.</a> Psychiatry Research 185(3): 382-386.
<br>
<br><br>
Stetler <i>et al</i>. (7-16-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfZjNDRGZzaUxVeVU/">Association of low-activity MAOA allelic variants with violent crime in incarcerated offenders.</a> Journal of Psychiatric Research 58: 69-75.
<br>
- Supplement
<br><br>
Ficks and Waldman. (9-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfVV9EVEdKV0dUMFU/">Candidate genes for aggression and antisocial behavior: A meta-analysis of association studies of the 5HTTLPR and MAOA-uVNTR.</a> Behavior Genetics 44(5): 427-44.
<br>
- <a href="https://drive.google.com/file/d/0B4NGOBcoYImfNnI3SC14enhfZ00/">Supplement</a>
<br><br>
<b>MAOA-3R Gene-Environment Interaction</b>
<br><br>
Caspi <i>et al</i>. (8-2-2002). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfWDNWN2J0ZzJFVm8/edit">Role of genotype in the cycle of violence in maltreated children.</a> Science 297(5582): 851-854.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeGZaTk1ELVZNM1k/edit">Supplement</a><br>
- Aged 26<br>
- Abuse during ages 3-11 as environmental factor<br>
- Conduct disorder, violent convictions, antisocial personality disorder, and Multidimensional Personality Questionnaire outcomes<br>
- Composite outcome index for males: beta=-0.36, t=2.53, P=0.01<br>
- MAOA-3R and MAOA-2R were 12% of the male group but 44% of violent convictions, 11% attributable risk fraction<br>
- Kim-Cohen meta-analysis equivalent: beta=0.29, 95% confidence interval 0.10-0.49, 17.4% weight<br>
- Byrd and Manuck meta-analysis equivalent for males: P=0.0050<br>
- Byrd and Manuck meta-analysis equivalent for females: P=0.1285
<br><br>
Huang <i>et al</i>. (5-19-2004). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSDNEUEE4ZXhPam8/edit">An association between a functional polymorphism in the monoamine oxidase A gene promoter, impulsive traits and early abuse experiences.</a> Neuropsychopharmacology 29(8): 1498-1505.
<br>
- MAOA-6R discovery
- “Early abuse” as environmental factor<br>
- Barratt Impulsivity Scale, Brown-Goodwin Aggression Scale, Buss-Durkee Hostility Inventory, major depressive disorder, bipolar disorder, and attempted suicide outcomes<br>
- Positive for male impulsivity (F(1, 24)=4.60, p=0.042) and female suicide (chi-squared=6.543, df=1, p=0.011)
<br><br>
Foley <i>et al</i>. (7-2004). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcWFKc0JXQUhlMU0/edit">Childhood adversity, monoamine oxidase A genotype, and risk for conduct disorder.</a> Archives of Psychiatry 61(7): 738-744.
<br>
- Aged 8-17<br>
- Neglect, interparental violence, and inconsistent parental discipline as environmental factors<br>
- Conduct disorder outcome<br>
- Odds ratio 5.84, 95% confidence interval 0.44-77.97, p=0.09<br>
- Negative finding incorrectly called “marginally significant”<br>
- Kim-Cohen meta-analysis equivalent: beta=0.14, 95% confidence interval -0.05-0.34, 17% weight<br>
- Byrd and Manuck meta-analysis equivalent: P=0.0200
<br><br>
Haberstick <i>et al</i>. (5-5-2005). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTDRjbG1ZZEd2eWM/edit">Monoamine oxidase A (MAOA) and antisocial behaviorsin the presence of childhood and adolescent maltreatment.</a> American Journal of Medical Genetics Part B 135B(1): 59-64.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbnMzdDM4S2RMZTg/edit">Supplement</a><br>
- Average age 22<br>
- National Longitudinal Study of Adolescent Health<br>
- Childhood abuse and neglect and adolescent victimization as environmental factors<br>
- Conduct disorder and violent convictions outcomes<br>
- Negative finding, P=0.109<br>
- Kim-Cohen meta-analysis equivalent: beta=0.14, 95% confidence interval -0.01-0.30, 28% weight<br>
- Byrd and Manuck meta-analysis equivalent: P=0.1423
<br><br>
Nilsson <i>et al</i>. (1-15-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNnpvZVdFcHVRYUk/edit">Role of monoamine oxidase A genotype and psychosocial factors in male adolescent criminal activity.</a> Biological Psychiatry 59(2): 121-127.
<br>
- Aged 16 and 19<br>
- Maltreatment or assault and multi-family household as environmental factors<br>
- Stealing, vandalism, violence, and total crime outcomes by self-report<br>
- Total criminality index: F=4.746, P=0.033, 1 degree of freedom<br>
- Violence index: not significant<br>
- Kim-Cohen meta-analysis equivalent: beta=0.51, 95% confidence interval 0.04-0.98, 3% weight<br>
- Byrd and Manuck meta-analysis equivalent: P=0.0078
<br><br>
Meyer-Lindenberg <i>et al</i>. (4-18-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTWZSNXBMWmdCS2c/edit">Neural mechanisms of genetic risk for impulsivity and violence in humans.</a> PNAS 103(16): 6269-6274.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfRlBqSUxybURNVWs/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfWUFUckJCUGxUY3c/edit">2</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdExRZ1QwMzUwc3M/edit">3</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOEg2bFQ2c09ELTA/edit">4</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcHNiTU5tVjJMMEE/edit">5</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeFYzRC03cm5MMVE/edit">6</a><br>
- Commentaries: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVExBa3A3OXFpVFU/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSUdUX2padHI5d2c/edit">2</a><br>
- angry and fearful face matching, aversive picture memory task, and inhibitory control flanker task as environmental factors<br>
- Positive fMRI activation outcomes for face matching (p<0.05), memory task (men only) (F(3,258)=3.0, p=0.03), and flanker task (men only)
<br><br>
Young <i>et al</i>. (6-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfN2RpUHB6V1cwSjA/edit">Interaction between MAO-A genotype and maltreatment in the risk for conduct disorder: failure to confirm in adolescent patients.</a> American Journal of Psychiatry 163(6): 1019-1025.
<br>
- Subjects selected for conduct and substance use problems without controls<br>
- Aged 12-18<br>
- Colorado Adolescent Rearing Inventory of abuse or neglect as environmental factor<br>
- Conduct disorder severity outcome<br>
- Negative finding
<br><br>
Huizinga <i>et al</i>. (10-1-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZ0sxQ2d3d0hpd0E/edit">Childhood maltreatment, subsequent antisocial behavior, and the role of monoamine oxidase A genotype.</a> Biological Psychiatry 60(7): 677-683.
<br>
- Abuse and violent victimization before age 17 as environmental factors<br>
- Conduct disorder, violent crime, violence disposition index, and antisocial personality disorder index, and antisocial behavior composite index outcomes<br>
- Negative finding (beta= -0.525, standard error=0.370, t/z=-1.419, P=0.157)<br>
- Byrd and Manuck meta-analysis equivalent: P=0.7794
<br><br>
Widom and Brzustowicz. (10-1-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVXQ5SVhTMWswd00/edit">MAOA and the “cycle of violence:” Childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior.</a> Biological Psychiatry 60(7): 684-689.
<br>
- Not controlled for gender<br>
- Cohort study used abuse cases (56-58% of cohort) and matched controls<br>
- Source of claim that MAOA only affects white people. “Given the differences in the allele frequencies in the white and non-white populations for the MAOA VNTR promoter polymorphism (observed in this study), as well as other polymorphisms within the MAOA gene and throughout the genome, it could be that there are substantially different frequencies of other MAOA modulating polymorphisms in white and non-white populations. This could lead to the situation where genotype at the promoter VNTR polymorphism is more highly correlated with expression levels in one population than the other. Thus, our failure to extend the findings of the protective effect of high MAOA expression to the non-white sample in this study could simply be a reflection of the inadequacy of the promoter VNTR polymorphism as a proxy for overall MAOA expression in non-whites.” “Non-whites” are not broken down by race. Whites with MAOA-3R were 24% female. Non-whites with MAOA-3R were 43% female.<br>
- Nikulina <i>et al</i> supposedly used the same sample. However, that study claimed non-Hispanic whites were 60.8% instead of 62.9% despite no change in the sample size listed. That study listed blacks as constituting 35.1% of the total and Hispanics as constituting the remaining 4.1%. Widom and Brzustowicz also listed Native Americans, Pacific Islanders, and “others.”<br>
- A subgroup of this study were previously studied by <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZWg2eGdxSDVZVlU/edit">Widom (1989)</a>. That study was 67% white and 31% black.
- White MAOA-2R allele frequency: 1.05%<br>
- Non-white MAOA-2R allele frequency: 4.17%<br>
- MAOA-2R, MAOA-3.5R, MAOA-5R, and heterozygous females excluded from analysis<br>
- Abuse before age 12 as environmental factor<br>
- Crime, self-reported violence, conduct disorder, antisocial personality disorder, juvenile violent and antisocial behavior index, and lifetime violent and antisocial behavior index outcomes<br>
- Abuse was not associated with non-white juvenile (beta=0.08, standard error=0.11, t=1.19, P “not significant”) or lifetime violent and antisocial behavior index (beta=0.13, standard error=0.12, t=1.86, P=0.06)<br>
- Positive for white juvenile violent and antisocial behavior index (beta=-0.16, standard error=15, t=-2.54, p < 0.01)<br>
- Negative finding for non-whites (juvenile: beta=0.06, standard error=0.28, t=0.67, P “not significant”; lifetime: beta=-0.01, standard error=0.29, t=-0.14, P “not significant”) and blacks (data not provided)<br>
- Byrd and Manuck meta-analysis equivalent: P=0.0143
<br><br>
Kim-Cohen <i>et al</i>. (10-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTXhTWFItSXlrY0U/edit">MAOA, maltreatment, and gene-environment interaction predicting children’s mental health: new evidence and a meta-analysis.</a> Molecular Psychiatry 11(10): 903-913.
<br>
- Also includes positive meta-analysis, using Caspi <i>et al</i>, Foley <i>et al</i>, Haberstick <i>et al</i>, Nilsson <i>et al</i>, and Kim-Cohen <i>et al</i> (beta=0.18, confidence interval 0.10-0.26, p < 0.001)<br>
- Aged 7<br>
- Abuse as environmental factor<br>
- Antisocial behavior, emotional problems, and ADHD outcomes<br>
- Significant opposite main effect for antisocial behavior (beta=0.19, t=2.34, p=0.019), ADHD (beta=0.18, t=2.23, p=0.026), and “composite mental health” (beta=0.19, t=2.40, p=0.017)<br>
- Only positive for ADHD outcome (beta=-0.78, t=2.26, p=0.024) and “composite mental health” (beta=-0.84, t=2.09, p=0.037)<br>
- Meta-analysis equivalent: beta=0.15, 95% confidence interval 0.01-0.28, 34.7% weight<br>
- Byrd and Manuck meta-analysis equivalent: P=0.0145
<br><br>
Sjöberg <i>et al</i>. (3-5-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTHJqcmQtTFNKTE0/edit">Adolescent girls and criminal activity: Role of MAOA-LPR genotype and psychosocial factors.</a> American Journal of Medical Genetics Part B (Neuropsychiatric Genetics) 144B(2): 159-164.
<br>
- Female subjects only<br>
- Aged 16 and 19<br>
- Multi-family house and sexual abuse as environmental factors<br>
- Violence index, stealing index, vandalism index, and total criminality index outcomes<br>
- MAOA-4R or MAOA-5R interact with sexual abuse to increase vandalism index (F=4.315, df=1, P=0.040) and total criminality index (F=2.732, df=1, P=0.036)<br>
- Byrd and Manuck meta-analysis equivalent: P=0.9082
<br><br>
Eisenberger <i>et al</i>. (5-1-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfYkNWb2JYYWR1UFk/edit">Understanding genetic risk for aggression: Clues from the brain’s response to social exclusion.</a> Biological Psychiatry 61(9): 1100-1108.
<br>
- Does not control for race<br>
- Cyberball social exclusion task as environmental factor<br>
- Spielberger Trait Anger scale and Brief Symptom Inventory for aggression and interpersonal hypersensitivity and fMRI dorsal anterior cingulated cortex activation outcomes<br>
- Positive main effects for aggression (F(2,29)=3.68, p<0.05) and for interpersonal hypersensitivity (excluding heterozygotes) (t(19)=2.32, p<0.05)<br>
- Positive interaction for dorsal anterior cingulated cortex activation outcome at 6,36,32 (F(2,28)=4.07, p<0.05)
<br><br>
Frazzetto <i>et al</i>. (5-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfWC1pTnBFNEx0Wk0/edit">Early trauma and increased risk for physical aggression during adulthood: the moderating role of MAOA genotype.</a> PLOS One 2(5): e486.
<br>
- Men and women assessed<br>
- Included psychiatric admits<br>
- Bandelow <i>et al</i> childhood traumatic life events questionnaire as environmental factor<br>
- Aggression questionnaire outcome<br>
- F = 7.04, p=0.009, 6.6% of variance explained
<br><br>
Oreland <i>et al</i>. (6-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVmVNMXVTcUo5MTA/edit">Monoamine oxidases – activities, genotypes and the shaping of behaviour.</a> Journal of Neural Transmission 114(6): 817-822.
<br><br>
Reif <i>et al</i>. (11-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfem1hUnRoSWJpRUE/edit">Nature and nurture predispose to violent behavior: serotonergic genes and adverse childhood environment.</a> Neuropsychopharmacology 32(11): 2375-2383.
<br>
- Childhood adverse environmental index as environmental factor<br>
- Compared violent criminals to criminals without violent offenses<br>
- Positive main effect (odds ratio = 2.3, 95% confidence interval 1.1-4.7, p=0.027)<br>
- Positive epistasis with 5-HTTLPR with adverse environment (p<0.0001)
<br><br>
Vanyukov <i>et al</i>. (12-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUDE3b0F2bWRfX2s/edit">The MAOA promoter polymorphism, disruptive behavior disorders, and early onset substance use disorder: Gene-environment interaction.</a> Psychiatric Genetics 17(6): 323-332.
<br>
- Aged 10 to 19<br>
- Child Assessment of Parental Involvement and Behavior scale as environmental factor<br>
- Attention deficit hyperactivity disorder, conduct disorder, oppositional defiant disorder, and substance use disorder outcomes<br>
- MAOA-4R interacts with father’s parental scale to decrease conduct disorder (odds ratio=0.380, 95% confidence interval: 0.179-0.805, P=0.011 for MAOA-4R alone) and increase ADHD (odds ratio=3.299, 95% confidence interval: 1.479-7.356, P=0.004 for MAOA-3R versus MAOA-4R and odds ratio=1.974, 95% confidence interval: 1.230-3.168, P=0.005 for MAOA-4R alone)
- Byrd and Manuck meta-analysis equivalent: P=0.6517
<br><br>
Ducci <i>et al</i>. (3-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQ1pxQktfeGZjSzQ/edit">Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women.</a> Molecular Psychiatry 13(3): 334-347.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfR0x4bHpUeDBrdnM/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfaGtaTS10T2dWdms/edit">2</a><br>
- All subjects have at least 25% Southwestern Native-American ancestry<br>
- Also examined MAOA SNPs<br>
- All 210 males excluded due to 90% having alcoholism and only 17% (of 126 asked) having experienced sexual abuse<br>
- One subject with a rare allele was unaccounted for<br>
- Sexual abuse before age 16 as environmental factor<br>
- Antisocial personality disorder, antisocial personality disorder symptom count, and alcohol use disorder outcomes<br>
- Positive main effect for antisocial personality disorder with alcohol use disorder (degrees of freedom=1, chi-squared=5.2, P=0.02), but not if sexually abused females were excluded<br>
- MAOA-3R interacts with sexual abuse to increase antisocial personality disorder with alcohol use disorder (degrees of freedom=1, chi-squared=7.17, P=0.007)<br>
- MAOA-3R interacts with sexual abuse to increase antisocial personality disorder symptom count (ANOVA: degrees of freedom=2, F=8.0, P=0.0006, regression model explained 22% of variance)<br>
- Identified 5 MAOA haplotypes with haplotype B (the most common MAOA-3R-associated haplotype) interacting with sexual abuse to increase alcohol use disorder (degrees of freedom=1, chi-squared=10.57, P=0.002) and antisocial personality disorder with alcohol use disorder (degrees of freedom=1, chi-squared=16.12, P=0.00001)<br>
- Byrd and Manuck meta-analysis equivalent: P=0.0002
<br><br>
Prichard <i>et al</i>. (3-5-2008). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfWEZlbVZET05oRkE/view">No evidence for interaction between MAOA and childhood adversity for antisocial behavior.</a> American Journal of Medical Genetics B (Neuropsychiatric Genetics) 147B(2): 228-232.
<br>
- Adversity exposures as environmental factor using the following criteria: lack of affection, anxiety or emotional trouble, parental drug or alcohol use, family conflict, parental divorce or separation, neglect, authoritarian parenting, psychological abuse, witnessing physical or sexual abuse, physical abuse, sexual abuse, poverty<br>
- Principle component factor as outcome using the following criteria: sex before age 15, leaving home before age 18, living with a partner before age 18, childbirth before age 18, smoking, past hazardous drinking, marijuana use before age 16, weekly or more marijuana use, frequent financial problems, less than 5 of secondary school education, unemployment, police problems or court appearance within last 6 months
<br><br>
Passamonti <i>et al</i>. (4-15-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZlpMUFQzYzF2VzA/edit">Genetically dependent modulation of serotonergic inactivation in the human prefrontal cortex.</a> NeuroImage 40(3): 1264-1273.
<br>
- Inhibitory control task as environmental factor<br>
- Anterior cingulate cortex and orbitofrontal cortex BOLD fMRI imaging outcomes<br>
- Non-significant MAOA effect for fMRI imaging of anterior cingulate cortex and orbitofrontal cortex<br>
- Positive anterior cingulated cortex imaging outcome for MAOA x 5-HTTLPR epistasis
<br><br>
McDermott <i>et al</i>. (2-17-2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbERXWk9xb0hVY2s/edit">Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation.</a> PNAS 106(7): 2118-2123.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVmZKcGNPZHFkUzg/edit">Supplement</a>
- College students, age unknown<br>
- Does not control for race<br>
- Amount of money taken from subject in game as environmental factor<br>
- Simulated hot sauce administration to opponents game outcome<br>
- Positive main effect (numbers not given)<br>
- Positive gene-environment interaction (Z=1.85, P=0.032)
<br><br>
Weder <i>et al</i>. (3-1-2009). <a href="https://docs.google.com/open?id=0B4NGOBcoYImfLTNsckx0UDhidlU">MAOA genotype, maltreatment, and aggressive behavior: the changing impact impact of genotype at varying levels of trauma.</a> Biological Psychiatry 65(5): 417-424.
<br>
- Aged 5-15<br>
- Does not control for gender<br>
- Positive for total group and for African Americans and biracial as a separate group<br>
- Total trauma exposure score (0 to 2) as environmental factor
- Aggression as Achenbach Teacher’s Report outcome
<br><br>
Van der Vegt <i>et al</i>. (8-2009). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfYll1VENPdWlHS28/view">High activity of monoamine oxidase A is associated with externalizing behaviour in maltreated and nonmaltreated adoptees.</a> Psychiatric Genetics 19(4): 209-211.
<br>
- Does not control for race, but does for country of origin<br>
- Race not identified
<br><br>
Hart and Marmorstein. (8-2009). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfLWxaemJ6QmpMVkk/">Neighborhoods and genes and everything in between: Understanding adolescent aggression in social and biological contexts.</a> Development and Psychopathology 21(3): 961-973.
<br>
-
<br><br>
Aslund <i>et al</i>. (3-2011). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVlplaHMtUzdFLXM/edit">Maltreatment, MAOA, and delinquency: Sex differences in gene-environment interaction in a large population-based cohort of adolescents.</a> Behavior Genetics 41(2): 262-272.
<br>
- Aged 17-18<br>
- Survey of Adolescent Life in Vestmanland (SALVe-2006)<br>
- Non-Scandinavian subjects not identified by race<br>
- MAOA-5R lumped with MAOA-3.5R and MAOA-4R as MAOA-L<br>
- Maltreatment summation index as environmental factor<br>
- Vandalism, stealing, violence, and total delinquency indices outcomes<br>
- Positive main effect of MAOA-3R (when not controlled for Scandinavian ethnicity) for total delinquency (degrees of freedom=2, F=3.78, P=0.023), stealing (degrees of freedom=2, F=5.40, P=0.005), and violence (degrees of freedom=2, F=4.68, P=0.009)<br>
- Positive gene-environment interaction for total delinquency (degrees of freedom=2, F=14.56, P<0.001), vandalism (degrees of freedom=2, F=4.97, P=0.007), stealing (degrees of freedom=2, F=19.66, P<0.001), and violence (degrees of freedom=2, F=21.27, P<0.001)<br>
- Positive gene-environment interaction in boys for total delinquency (degrees of freedom=3, chi-squared=57.21, P<0.001), vandalism (degrees of freedom=3, chi-squared =47.85, P<0.001), stealing (degrees of freedom=3, chi-squared =53.77, P<0.001), and violence (degrees of freedom=3, chi-squared=59.56, P<0.001)<br>
- Positive gene-environment interaction in girls for total delinquency (degrees of freedom=5, chi-squared =115.71, P<0.001), vandalism (degrees of freedom=5, chi-squared =108.01, P<0.001), stealing (degrees of freedom=5, chi-squared =51.98, P<0.001), and violence (degrees of freedom=5, chi-squared=57.40, P<0.001)
<br><br>
Takahashi <i>et al</i>. (2-2011). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdnNnU3lseDRtc1k/edit">Brain serotonin receptors and transporters: Initiation vs. termination of escalated aggression.</a> Psychopharmacology 213(2-3): 183-212.
<br><br>
Kieling <i>et al</i>. (3-2013). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfa1NXUzZnYjlvYTQ/edit">Gene-environment interaction in externalizing problems among adolescents: evidence from the Pelotas 1993 Birth Cohort Study.</a> The Journal of Child Psychology and Psychiatry: 54(3): 298-304.
<br>
- Aged 15<br>
- Skin color controlled<br>
- Pelotas 1993 Birth Cohort Study<br>
- Childhood maltreatment before age 15 as environmental factor<br>
- Negative finding for Strengths and Difficulties Questionnaire greater than 95% score for conduct disorder at age 15, P=0.823<br>
- Conduct disorder scores declined from age 11 (2.5) to age 15 (2.3)
<br><br>
Kuepper <i>et al</i>. (3-13-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUmEtaXExTjE5MzA/edit">MAOA-uVNTR genotype predicts interindividual differences in experimental aggressiveness as a function of the degree of provocation.</a> Behavioural Brain Research: epub ahead of print.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfa2xsS0s4NkZpYms/edit">Supplement</a><br>
- Noise aversive stimuli as environmental factor for reactive aggression<br>
- Competitive reaction time task (reactive aggression) and Freiburg Personality Inventory self-report general aggression scale outcomes<br>
- Positive for high (F(2,234)=3.883, P < 0.05) and extreme (F(2,235)=8.166, P < 0.001) provocation effects on reactive aggression<br>
- Not positive for gene interaction with gender
<br><br>
Ernst <i>et al</i>. (3-16-2013). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfNk1kOWJHOUFVUk0/">Genetic variation in MAOA modulates prefrontal cortical regulation of approach-avoidance reactions.</a> Neuropsychobiology 67(3): 168-180.
<br>
<br><br>
Haberstick <i>et al</i>. (5-28-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfamJIdlRhZjU1NU0/edit">MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors.</a> Biological Psychiatry: epub ahead of print.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfYzUzeUxQX1dXbVE/edit">Supplement</a>
- National Longitudinal Study of Adolescent Health Wave IV (excluded previous sample from Haberstick <i>et al</i> 2005)<br>
- White MAOA-2R allele frequency: 0.298%<br>
- Black MAOA-2R allele frequency: 4.79%<br>
- Abuse before age 18 as environmental factor<br>
- Childhood antisocial behavior, adult antisocial behavior, violent crime, Mini-International Personality Item Pool anger hostility scale, and composite antisocial index outcomes<br>
- In black males , abuse was not associated with composite antisocial index (beta=0.15, standard error=0.16, t=0.96, 95% confidence interval -0.16 to 0.47), childhood antisocial behavior (beta=0.44, standard error=0.31, t=1.43, P=0.15), adult antisocial behavior (beta=0.20, standard error=0.17, t=1.19, P=0.24), violent crime (beta=0.01, standard error=0.05, t=0.23, P=0.82), or anger hostility scale (beta=0.12, standard error=0.43, t=0.28, P=0.78)<br>
- Negative finding for composite antisocial index for white males (beta=-0.13, standard error=0.08, t=-1.67, 95% confidence interval -0.29 to 0.02, P=0.10) and black males (beta=-0.15, standard error=0.20, t=-0.76, 95% confidence interval -0.55 to 0.25, P=0.45)<br>
- Positive main effect for anger hostility scale in white males (95% confidence interval 0.15-0.87, P=0.006)<br>
- Positive main effect for violent crime in black males (95% confidence interval -0.11 to -0.02, P=0.006)
<br><br>
Byrd and Manuck. (6-17-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfY2FQWHBkT2RGeW8/edit">MAOA, childhood maltreatment, and antisocial behavior: meta-analysis of a gene-environment interaction.</a> Biological Psychiatry: epub ahead of print.
<br>
- Used Caspi <i>et al</i>, Foley <i>et al</i>, Haberstick <i>et al</i>, Huizinga <i>et al</i>, Kim-Cohen <i>et al</i>, Nilsson <i>et al</i>, Widom and Brzustowicz, Frazzetto <i>et al</i>, Sjoberg <i>et al</i>, Vanyukov <i>et al</i>, Ducci <i>et al</i>, Hart and Marmorstein, Prom-Wormley <i>et al</i>, van der Vegt <i>et al</i>, Weder <i>et al</i>, Beach <i>et al</i>, Beaver <i>et al</i>, Derringer <i>et al</i>, Edwards <i>et al</i>, Enoch <i>et al</i>, Waleschlag <i>et al</i>, Aslund <i>et al</i>, Lee, Reti <i>et al</i>, Cicchetti <i>et al</i>, Fergusson <i>et al</i>, and McGrath <i>et al</i><br>
- Total sample size: > 18,400 for all 27 studies, 11,064 subjects in studies with men, 7588 subjects in studies with women<br>
- Having MAOA-2R, MAOA-3R, or MAOA-5R with maltreatment as an environmental factor is significantly associated with male antisocial behavior (P=2 x 10<sup>-7</sup>, publication bias would require > 105 missing studies with 447 samples to explain away), male violent behavior (P=0.01), and male nonviolent antisocial behavior (P=4 x 10<sup>-4</sup>)<br>
- Negative findings for MAOA=2R, MAOA-3R, or MAOA-5R with maltreatment as an environmental factor significantly affecting female antisocial behavior (P=0.77)<br>
- Having MAOA-3.5R or MAOA-4R with childhood maltreatment as an environmental factor is significantly associated with female antisocial behavior (P=0.020)
<br><br>
Tiihonen <i>et al</i>. (10-28-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfSzBSLXhoTlY5d1E/">Genetic background of extreme violent behavior.</a> Molecular Psychiatry: epub ahead of print.
<br>
- <a href="https://drive.google.com/file/d/0B4NGOBcoYImfWjVweHJOV2VINlU/view?usp=sharing">Supplement</a><br>
- Allele frequencies of rare MAOA alleles are not given, but no copies of MAOA-2R are present<br>
- Violent crime, extremely violent crime (each committing 10 or more crimes of murder, manslaughter, attempted homicide, or battery), and homicide (in replication cohort) outcomes<br>
- Negative finding for HTR2B<br>
- GWAS identified CDH13 SNP rs11649622<br>
- Positive main effect for violent crime (P=2.93 x 10<sup>-5</sup>, odds ratio=1.708, 9% attributable risk fraction, 95% confidence interval: 4-15%) and extremely violent crime (P=1.6 x 10<sup>-4</sup>, odds ratio=2.662, 16% attributable risk fraction, 95% confidence interval: 8-24%)<br>
- Positive main effect in men for violent crime (P=4 x 10<sup>-4</sup>, odds ratio=1.661, 95% confidence interval: 1.252-2.204) and extremely violent crime (P=4 x 10<sup>-4</sup>, odds ratio=2.617, 95% confidence interval: 1.540-4.445)<br>
- Positive main effect in women for violent crime (P=0.0226, odds ratio=1.898, 95% confidence interval: 1.094-3.291) but not for extremely violent crime (P=0.2118, odds ratio=3.143, 95% confidence interval: 0.521-18.97)<br>
- Negative with childhood maltreatment as an environmental factor (odds ratio=1.62)
<br><br>
<b>MAOA-3R Gene-Hormone Interaction</b>
<br><br>
Zhu <i>et al</i>. (12-1994). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVElXc3RRTHNmcjQ/edit">Bidirectional promoter of human monoamine oxidase A (MAO A) controlled by transcription factor Sp1.</a> Journal of Neuroscience 14(12): 7393-7403.
<br><br>
Shih <i>et al</i>. (1995). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfeVdkVTRXOHEzUTg/edit">Expression of human monoamine oxidase (MAO) A gene controlled by transcription factor Sp1.</a> Progress in Brain Research 106: 49-56.
<br><br>
Sjöberg <i>et al</i>. (1-2008). <a href="https://docs.google.com/open?id=0B4NGOBcoYImfeV9xdjdSZERhdkE">A non-additive interaction of a functional MAO-A VNTR and testosterone predicts antisocial behavior.</a> Neuropsychopharmacology 33(): 425-430.
<br>
- Brown-Goodwin aggression scores and antisocial personality disorder outcomes
<br><br>
Romanuik <i>et al</i>. (9-24-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfb2U1T1pNdVYyTVE/edit">LNCaP Atlas: Gene expression associated with <i>in vivo</i> progression to castration-recurrent prostate cancer.</a> BMC Medical Genomics 3(43): 1-19.
<br><br>
<b>MAOA Epigenetics</b>
<br><br>
Wong <i>et al</i>. (8-16-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUWR3TEtwUGhNZ0k/edit">A longitudinal study of epigenetic variation in twins.</a> Epigenetics 5(6): 516-526.
<br>
- Male methylation lower, less variable, and more heritable than female methylation
<br><br>
Philibert <i>et al</i>. (7-2011). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVUNmOUxwd1ZmbmM/edit">Gene environment interactions with a novel variable monoamine oxidase A transcriptional enhancer are associated with antisocial personality disorder.</a> Biological Psychology 87: 366-371.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOW1nR1FqUHlOYnc/edit">Supplement</a><br>
- P2 promoter discovery<br>
- P2 9R allele had less methylation than 10R in women only (p < 0.03)<br>
- Abuse as environmental factor<br>
- Antisocial personality disorder outcome<br>
- Only positive results were in women for environment interaction with P2 (beta=-0.229, p=0.007) and environmental interaction with P1 and P2 (r(96)=0.458, p < 0.001)
<br><br>
<b>MAOA-3R Epistasis</b>
<br><br>
Strous <i>et al</i>. (7-1-2003). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMm9KOTNMU2NGbUk/edit">Aggressive behavior in schizophrenia is associated with the low enzyme activity COMT polymorphism: A replication study.</a> American Journal of Medical Genetics B (Neuropsychiatric Genetics) 120B(1): 29-34.
<br>
- Sample was 63% Sephardic Jew and 37% Ashkenazi Jew with allele frequencies: 1.3% MAOA-2R, 62.3% MAOA-3R, 35.1% MAOA-4R, 1.3% MAOA-5R<br>
- Subjects selected for schizophrenia without controls<br>
- Life History of Aggression Scale outcome<br>
- MAOA-3R or MAOA-5R x COMT Met/Met x female gender positive interaction (F(2,105)=3.6, p=0.031)
<br><br>
Qian <i>et al</i>. (6-18-2009). Association study of intelligence of attention deficit hyperactivity disorder children in China. Beijing Da Xue Xue Bao 41(3): 285-290.
<br><br>
Qian <i>et al</i>. (5-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUnpvZDNqTWJrdGc/edit">Gene-gene interaction between COMT and MAOA potentially predicts the intelligence of attention-deficit hyperactivity disorder boys in China.</a> Behavior Genetics 40(3): 357-365.
<br>
- COMT Val/Val x MAOA-3R average IQ=106.7, 95% confidence interval 103.7-109.8; COMT Val/Val x MAOA-4R average IQ=98.0, 95% confidence interval 93.5-102.6
<br><br>
Kang <i>et al</i>. (7-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbFEybmtKYWlONUk/edit">Association study between antipsychotic-induced restless legs syndrome and polymorphisms of monoamine oxidase genes in schizophrenia.</a> Human Psychopharmacology 25(5): 397-403.
<br>
- Subjects selected for schizophrenia without controls<br>
- International Restless Legs Syndrome Study Group rating scale outcome<br>
- MAOA-3R x MAOB A644G SNP x gender interaction (F=4.05 & p=0.047 for men, F=5.00 & p=0.028 for women but in opposite direction)
<br><br>
<b>MAOA Single-Nucleotide Polymorphisms</b>
<br><br>
Balciuniene <i>et al</i>. (2-2001). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQWRwTXVtQk1TRjg/edit">The geographic distribution of monoamine oxidase haplotypes supports a bottleneck during the dispersion of modern humans from Africa.</a> Journal of Molecular Evolution 52(2): 157-163.
<br>
- Haplotype frequency differences between Africans and non-Africans suggest a demographic bottleneck or positive selection.
<br><br>
Gilad <i>et al</i>. (1-22-2002). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfRnRpUGxFVnVadUk/edit">Evidence for positive selection and population structure at the human MAO-A gene.</a> PNAS 99(2): 862-867.
<br><br>
Eccles <i>et al</i>. (5-2012). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfS2x6NnB2SUtQaVU/edit">A unique demographic history exists for the MAO-A gene in Polynesians.</a> Journal of Human Genetics 57(5): 294-300.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVGt2Z3FGbmZNNWM/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMUpNV1lTcnRCZXM/edit">2</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQUtYdUxYOUxNMkE/edit">3</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQk0xUmpueUpoclk/edit">4</a><br>
- Supplementary figure 1 (supplement 1) has mislabeled bar graphs
<br><br>
Tielbeek <i>et al</i>. (10-15-2012). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcW02TURLMHdFOGM/edit">Unraveling the genetic etiology of adult antisocial behavior: A genome-wide association study.</a> PLOS One 7(10): e45086.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfQ1VjS0dnWkJWdVE/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfN2d3Y0pLS1BvVTQ/edit">2</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfM0ZjNkxwSk1Ld0E/edit">3</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfS3VXMHRpWl8yWVk/edit">4</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfblRfZjFWTXotQTA/edit">5</a><br>
- Genome-wide association study<br>
- Aged 18-81<br>
- Does not control for gender<br>
- Antisocial personality disorder outcome<br>
- No SNPs had genome-wide significance, including 7 MAOA SNPs.<br>
- All 278,570 SNPs collectively explained 55% of variance
<br><br>
Redin <i>et al</i>. (11-2014). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfcEM2VEw0Z3NnNnM/">Efficient strategy for the molecular diagnosis of intellectual disability using targeted high-throughput sequencing.</a> Journal of Medical Genetics 51(11): 724-736.
<br>
- Supplements: <a href="https://drive.google.com/file/d/0B4NGOBcoYImfN2VZcW1tS05Zbm8/">1</a>, <a href="https://drive.google.com/file/d/0B4NGOBcoYImfS1JEQ3p0UndvYms/">2</a><br>
<br><br>
<b>MAOA CA Repeat Polymorphisms</b>
<br><br>
Vanyukov <i>et al</i>. (11-29-1995). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfS3FiRlRQY1J4WDg/edit">A dinucleotide repeat polymorphism at the gene for monoamine oxidase A and measures of aggressiveness.</a> Psychiatry Research 59(1-2): 35-41.
<br>
- Negative finding
<br><br>
<b>MAOA Animal Models</b>
<br><br>
Gibbons. (5-7-2004). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfZlhtbzVXWnVOTGs/edit">Tracking the evolutionary history of a “warrior” gene.</a> Science 304(5672): 818.
<br>
- Origin of “warrior gene” label
<br><br>
<b>MAOA Research Criticism, Law, & “Ethics”</b>
<br><br>
Baker <i>et al</i>. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUGVGbFJyLVFKVUE/edit">Behavioral genetics: The science of antisocial behavior.</a> Law and Contemporary Problems 69(1-2): 7-46.
<br><br>
Kaplan. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfemxKamNGbEpoVlE/edit">Misinformation, misrepresentation, and misuse of human behavioral genetics research.</a> Law and Contemporary Problems 69(1-2): 47-80.
<br><br>
Garland and Frankel. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUlk1MTYwZEFjaUU/edit">Considering convergence: A policy dialogue about behavioral genetics, neuroscience, and law.</a> Law and Contemporary Problems 69(1-2): 101-113.
<br><br>
Denno. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOWNSODh5UGYwUU0/edit">Revisiting the legal link between genetics and crime.</a> Law and Contemporary Problems 69(1-2): 209-257.
<br><br>
Kaye. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSk51RUNPNjc3Y0k/edit">Behavioral genetics research and criminal DNA databases.</a> Law and Contemporary Problems 69(1-2): 259-299.
<br><br>
Beecher-Monas and Garcia-Rill. (Winter & Spring 2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfRENWLUd0N2hjdXM/edit">Genetic predictions of future dangerousness: Is there a blueprint for violence?</a> Law and Contemporary Problems 69(1-2): 301-341.
<br><br>
Bernet <i>et al</i>. (11-2007). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfakMyRHpBeGctb1U/edit">Bad nature, bad nurture, and testimony regarding MAOA and SLC6A4 genotyping at murder trials.</a> Journal of Forensic Sciences 52(6): 1362-1371.
<br><br>
Hunter. (9-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfd0dFNnJtNlZweXc/edit">The Psycho Gene.</a> EMBO Reports 11(9): 667-669.
<br>
- Falsely claimed “Brunner’s syndrome … having only been identified in five males…”<br>
- Falsely claimed “MAOA-L variant … occurs in about 40% of the population.”
<br><br>
Gillett & Tamatea. (2012). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfUGpVdzdJNUdJdEU/">The warrior gene: Epigenetic considerations.</a> New Genetics and Society 31(1): 41-53.
<br><br>
<b>Related Research on Antisocial Personality Disorder & Aggression</b>
<br><br>
<br><br>
<b>MAOA, Depression, Bipolar Disorder, & Suicide</b>
<br><br>
Craddock <i>et al</i>. (8-14-1995). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfaFVLXzhIOC0zNzQ/">No evidence for allelic association between bipolar disorder and monoamine oxidase A gene polymorphisms.</a> American Journal of Medical Genetics 60(4): 322-324.
<br><br>
Lim <i>et al</i>. (8-14-1995). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfZDFmbVhXV3dRVDQ/">Evidence for a genetic association between alleles of monoamine oxidase A gene and bipolar affective disorder.</a> American Journal of Medical Genetics 60(4): 325-331.
<br><br>
Muramatsu <i>et al</i>. (9-19-1997). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbHV2aTctblNLdnM/edit">Monoamine oxidase genes polymorphisms and mood disorder.</a> American Journal of Medical Genetics 74(5):494-496.
<br>
- Depression and bipolar outcomes<br>
- Negative findings for MAOA-CA, MAOA-VNTR (not P1 or P2), MAOA-RFLP, and MAOB-GT
<br><br>
Kunugi <i>et al</i>. (7-1999). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbUVrb3AzQW5RMUE/edit">A functional polymorphism in the promoter region of monoamine oxidase-A gene and mood disorders.</a> Molecular Psychiatry 4(4): 393-395.
<br>
- MAOA-2R discovery<br>
- Asian MAOA-2R allele frequency: 1.0%<br>
- Depression, bipolar disorder, and suicide outcomes<br>
- Negative finding (p=0.46)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=1.26, 95% confidence interval 0.60-2.66; and in women, odds ratio=0.96, 95% confidence interval 0.62-1.49<br>
- Fan <i>et al</i> bipolar disorder meta-analysis equivalent: in men, odds ratio=1.14, 95% confidence interval 0.60-2.14; and in women, odds ratio=1.08, 95% confidence interval 0.75-1.58
<br><br>
Furlong <i>et al</i>. (8-20-1999). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfV1RTTkQ2RmhEVTA/edit">Analysis of the monoamine oxidase A (MAOA) gene in bipolar affective disorder by association studies, meta-analyses, and sequencing of the promoter.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 88(4): 398-406.
<br>
- Bipolar disorder and depression outcomes<br>
- Also includes a bipolar meta-analysis, using Craddock <i>et al</i>, Kawada <i>et al</i>, Nothen <i>et al</i>, Lim <i>et al</i>, Muramatsu <i>et al</i>, and Parsian and Todd<br>
- Negative findings for MAOA-CA (for depression: chi-squared=3.349, 3 df, p=0.34; for bipolar disorder: chi-squared=0.317, 3df, p=0.96), MAOA-Fnu (for depression: chi-squared=0.821, 1 df, p=0.37; for bipolar disorder: chi-squared=0.004, 1 df, p=0.95), and MAOA-3R (for depression: chi-squared=0.958, 2 df, p=0.62; for bipolar disorder: chi-squared=0.082, 2 df, p=0.96)<br>
- Positive meta-analysis for MAOA-CA in whites (odds ratio 1.55, 95% confidence interval 1.06-2.28, p < 0.02) and Japanese (odds ratio 2.65, 95% confidence interval 1.29-5.45)<br>
- Positive meta-analysis for MAOA-Fnu only in white women (odds ratio 0.70, confidence interval 0.49-0.99)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=0.72, 95% confidence interval 0.34-1.52; and in women, odds ratio=1.31, 95% confidence interval 0.85-2.02<br>
- Fan <i>et al</i> bipolar disorder meta-analysis equivalent: in men, odds ratio=0.72, 95% confidence interval 0.35-1.50; and in women, odds ratio=1.05, 95% confidence interval 0.65-1.69
<br><br>
Ho <i>et al</i>. (2-7-2000). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfcXVxRGVSdnBpaGc/edit">Genetic associations with clinical characteristics in bipolar affective disorder and recurrent unipolar depressive disorder.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 96(1): 36-42.
<br>
- Subjects selected for depression and bipolar disorder without controls<br>
- Suicide outcome<br>
- Positive for women (p=0.035)
<br><br>
Schulze <i>et al</i>. (12-2000). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTFd3Z3A3UzM2UDQ/edit">Association between a functional polymorphism in the monoamine oxidase A gene promoter and major depressive disorder.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 96(6): 801-803.
<br>
- Main effect of MAOA-3.5R, MAOA-4R, or MAOA-5R in women (p=0.029)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=1.28, 95% confidence interval 0.45-3.61; and in women, odds ratio=1.37, 95% confidence interval 0.87-2.14
<br><br>
Ono <i>et al</i>. (4-8-2002). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdG1YWkRqVUlDWVU/edit">No evidence of an association between a functional monoamine oxidase A gene polymorphism and completed suicides.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 114(3): 340-342.
<br>
- Asian MAOA-2R allele frequency: 0.47%<br>
- Negative finding (p=0.34)
<br><br>
Gutierrez <i>et al</i>. (12-2004). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNnoxVVZacDh4cms/edit">Association analysis between a functional polymorphism in the monoamine oxidase A gene promoter and severe mood disorders.</a> Psychiatric Genetics 14(4): 203-208.
<br>
- Depression, bipolar disorder, suicide, psychosis, seasonal symptoms, Hamilton index, comorbidity, recurrence, episode number, episode length, psychiatric admissions, and family history of mental disorder outcomes<br>
- Positive MAOA-3.5R/4R/5R link in bipolar women to longer psychiatric admission (F=4.604, p=0.037)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=0.97, 95% confidence interval 0.51-1.84; and in women, odds ratio=1.01, 95% confidence interval 0.67-1.52<br>
- Fan <i>et al</i> bipolar disorder meta-analysis equivalent: in men, odds ratio=1.35, 95% confidence interval 0.57-3.21; and in women, odds ratio=1.02, 95% confidence interval 0.59-1.76
<br><br>
Yu <i>et al</i>. (9-2005). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfdGZNcGtoNDMxMVk/edit">Association study of a monoamine oxidase A gene promoter polymorphism with major depressive disorder and antidepressant response.</a> Neuropsychopharmacology 30(9): 1719-1723.
<br>
- Sample sizes of control subjects by gender listed incorrectly<br>
- Asian MAOA-2R allele frequency: 0.92%<br>
- Major depressive disorder and Hamilton Depression Rating Scale outcomes<br>
- Main effect of MAOA-4R for depression women (chi-squared=6.93, df=1, p=0.009), for men (chi-squared=6.27, df=1, p=0.015), and for both (chi-squared=12.48, p < 0.001)<br>
- Main effect of MAOA-3R to improve the effect of 4-weeks of fluoxetine on Hamilton Depression Rating Scale in women (p=0.024)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=2.07, 95% confidence interval 1.17-3.67; and in women, odds ratio=1.64, 95% confidence interval 1.13-2.37
<br><br>
Lin <i>et al</i>. (5-24-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfSTZsSHZHMjdJcWs/edit">Association analysis of monoamine oxidase A gene and bipolar affective disorder in Han Chinese.</a> Behavioral and Brain Functions 4(21): 1-6.
<br>
- Unknown allele frequencies of MAOA-4R and MAOA-5R lumped together as the “long allele”<br>
- MAOA-3R with MAOA-CA significantly not associated with bipolar disorder in women (odds ratio=1.22, 95% confidence interval: 0.41-3.67, p=0.72). For men, association is listed as significant with p=0.01 but 95% confidence interval of odds ratio includes null value (odds ratio=12.64, 95% confidence interval: 0.69-232.88)<br>
- Fan <i>et al</i> bipolar meta-analysis equivalent: in men, odds ratio=0.61, 95% confidence interval 0.28-1.32; and in women, odds ratio=1.29, 95% confidence interval 0.71-2.33
<br><br>
Huang <i>et al</i>. (9-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfYmgwNUNjUXJaczA/edit">Neither single-marker nor haplotype analyses support an association between monoamine oxidase A gene and bipolar disorder.</a> European Archives of Psychiatry and Clinical Neuroscience 258(6): 350-356.
<br>
- Asian MAOA-2R allele frequency: 0.73%<br>
- Negative finding (p=0.525)
<br><br>
Huang <i>et al</i>. (2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfOXpOdElkRkNVOEE/edit">Association of monoamine oxidase A (MAOA) polymorphisms and clinical subgroups of major depressive disorders in the Han Chinese population.</a> World Journal of Biological Psychiatry 10(4 Part 2): 544-551.
<br>
- Outcomes were major depressive disorder, Hamilton depression rating scale (severe is > 24), and family history of first-degree relatives with depression or bipolar disorder<br>
- Asian MAOA-2R allele frequency: 0.95%<br>
- Only positive in women for linking MAOA-3R to severe depression (p=0.041) and for linking MAOA-EcoRV to depression (p=0.049), to depression with family history (p=0.047), and to severe depression (p=0.017)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=1.23, 95% confidence interval 0.76-1.99; and in women, odds ratio=0.91, 95% confidence interval 0.64-1.28
<br><br>
Fan <i>et al</i>. (2-2010). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfVHRoUHlsTzd0OWs/edit">Meta-analysis of the association between the monoamine oxidase-A gene and mood disorders.</a> Psychiatric Genetics 20(1): 1-7.
<br>
- Used Craddock <i>et al</i>, Lim <i>et al</i>, Muramatsu <i>et al</i>, Parsian and Todd, Sasaki <i>et al</i>, Furlong <i>et al</i>, Kunugi <i>et al</i>, Schulze <i>et al</i>, Preisig <i>et al</i>, Lin <i>et al</i> (2000), Syagailo <i>et al</i>, Tadic <i>et al</i>, Gutierrez <i>et al</i>, Yu <i>et al</i>, Huang <i>et al</i> (2007), Lin <i>et al</i> (2008), and Huang <i>et al</i> (2008)<br>
- Only positive for major depressive disorder in Asians (odds ratio=1.23, 95% confidence interval 1.02-1.47, p=0.03) and Asian men (odds ratio=1.47, 95% confidence interval 1.06-2.05, p=0.02) with MAOA-3.5R, MAOA-4R, or MAOA-5R<br>
- Only positive for bipolar disorder in whites with MAOA T941G SNP (odds ratio=1.28, 95% confidence interval 1.01-1.62, p=0.04) and MAOA-CA a6 (odds ratio=1.35, 95% confidence interval 1.11-1.64, p=0.002) alleles and in white women with MAOA T941G (odds ratio=1.36, 95% confidence interval 1.03-1.81) and MAOA-CA a5 (odds ratio=1.44, 95% confidence interval 1.04-1.99, p=0.03) and a6 (odds ratio=1.41, 95% confidence interval 1.12-1.78, p=0.004) alleles
<br><br>
Hung <i>et al</i>. (2-2012). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfUFdzZW1BaEFwTzQ/edit">Monoamine oxidase A gene polymorphism and suicide: An association study and meta-analysis.</a> Journal of Affective Disorders 136(3): 643-649.
<br>
- Also includes negative suicide meta-analysis, using Ho <i>et al</i>, Ono <i>et al</i>, Huang <i>et al</i>, Courtet <i>et al</i>, Steiger <i>et al</i>, Lung <i>et al</i>, and Hung <i>et al</i>, for males (odds ratio=0.85, 95% confidence interval 0.67-1.10, p=0.22) and females (odds ratio=1.13, 95% confidence interval 0.94-1.36, p=0.21)<br>
- Asian MAOA-2R allele frequency: 0.50%<br>
- Negative finding (p=0.34)
<br><br>
Nikulina <i>et al</i>. (2-15-2012). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfbzNyU1lGRlVSckU/edit">Child abuse and neglect, MAOA, and mental health outcomes: a prospective examination.</a> Biological Psychiatry 71(4): 350-357
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfX1JUZnY1UUlkbEE/edit">Supplement</a><br>
- Same sample as Widom and Brzustowicz with additional racial data<br>
- Does not control for gender<br>
- Physical abuse, sexual abuse, and neglect before age 12 as environmental factors<br>
- Depression, dysthymia, and alcohol abuse outcomes<br>
- MAOA-4R interacted with physical abuse or with having experienced multiple forms of abuse (physical abuse, sexual abuse, or neglect) to affect dysthymia symptoms in women only<br>
- MAOA-3R and MAOA-4R interacted with race and sexual abuse to affect depression, dysthymia, and alcohol abuse (beta=-0.19, P < 0.05 for depression, beta=-0.22, P < 0.05 for dysthymia, beta=-0.27, P < 0.01 for alcohol abuse). MAOA-3R decreased symptoms in sexually abused whites. MAOA-4R decreased symptoms in sexually abused non-whites. (Gender is not controlled, and racial groups differ in gender proportions with each allele. See Widom and Bruzstowicz, 2006)
<br><br>
Chen <i>et al</i>. (1-10-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMlFIRWhzRXNfblU/edit">The MAOA gene predicts happiness in women.</a> Progressive in Neuro-Psychopharmacology & Biological Psychiatry 40: 122-125.
<br><br>
Melas <i>et al</i>. (3-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfc2lDS3hXVmFQMFE/edit">Genetic and epigenetic associations of MAOA and NR3C1 with depression and childhood adversities.</a> International Journal of Neuropsychopharmacology: epub ahead of print.
<br>
- Supplements: <a href="https://docs.google.com/file/d/0B4NGOBcoYImfRXRycHFUdkpYaHc/edit">1</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfd19SbnFwOC1lalU/edit">2</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMTNSVHRlQjlaQmM/edit">3</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfN3NDMG1Semg1UVU/edit">4</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMmtpYjhKWEtsOUU/edit">5</a>, <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMHl0WkR5R3F6OHM/edit">6</a><br>
- Subjects were Swedish citizens but race is unidentified and not controlled. Of the 11% who are non-Swedish, most have “Nordic origin that is primarily Finnish.” (Source cited does not give this information.)<br>
- Large sample with no MAOA-2R<br>
- Prior to age 18, early parental death, parental divorce, financial problems, and other familial constraints as environmental factors<br>
- Major Depression Inventory, mixed anxiety depression, dysthymia, and MAOA and NR3C1 methylation outcomes<br>
- Main effect of MAOA-3R on depression in women (odds ratio=1.7, 95% confidence interval 1.2-2.4)<br>
- Positive MAOA-3R x environment interaction for depression in women (Wald=16.4, df=5, p=0.006), in men (Wald=13.4, df=5, p=0.02), and both (Wald=26.8, df=5, p < 0.001)<br>
- Positive association of epigenetic hypomethylation of MAOA with depression in women (p=0.001)<br>
- Positive interaction of MAOA-3R x early parental death effect on NR3C1 hypermethylation (F=23.484, p < 0.001)
<br><br>
Ma <i>et al</i>. (7-2013). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfYV8wcXI5dElIQm8/">Association between MAOA-u VNTR polymorphism and its interaction with stressful life events and major depressive disorder in adolescents.</a> Zhongguo Dang Dai Er Ke Za Zhi 15(7): 563-568.
<br><br>
<b>MAO Inhibitors</b>
<br><br>
Robinson <i>et al</i>. (10-5-1983). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfWU9RR2dwbWRsVTQ/view">Plasma levels of catecholamines and dihydroxyphenylglycol during antidepressant drug treatment.</a> Journal of Clinical Psychopharmacology 3(5): 282-287.
<br><br>
Whitaker-Azmitia <i>et al</i>. (10-1994). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfNkE5OUdXT0E1LUk/">Effects of gestational exposure to monoamine oxidase inhibitors in rats: preliminary behavioral and neurochemical studies.</a> Neuropsychopharmacology 11(2): 125-132.
<br><br>
Witkin <i>et al</i>. (4-4-2013). <a href="">Further evaluation of the neuropharmacological determinants of the antidepressant-like effects of curcumin.</a> CNS Neurological Disorders – Drug Targets: epub ahead of print.
<br><br>
<b>MAOA & Panic Disorder</b>
<br><br>
<br><br>
<b>MAOA & Schizophrenia</b>
<br><br>
Coron <i>et al</i>. (6-1-1996). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfaXdwbVVlenZQSGs/edit">Association study between schizophrenia and monoamine oxidase A and B DNA polymorphisms.</a> Psychiatry Research 62(3): 221-226.
<br>
- Negative finding for MAOA EcoRV polymorphism
<br><br>
Syagailo <i>et al</i>. (3-8-2001). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMXNHWXhmX3lUVms/edit">Association analysis of the functional monoamine oxidase A gene promoter polymorphism in psychiatric disorders.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 105(2): 168-171.
<br>
- Negative finding for depression (p=0.731), bipolar disorder (p=0.863), and schizophrenia (p=0.574)<br>
- Fan <i>et al</i> depression meta-analysis equivalent: in men, odds ratio=0.68, 95% confidence interval 0.32-1.47; and in women, odds ratio=1.40, 95% confidence interval 0.79-2.49<br>
- Fan <i>et al</i> bipolar disorder meta-analysis equivalent: in men, odds ratio=0.90, 95% confidence interval 0.43-1.87; and in women, odds ratio=1.03, 95% confidence interval 0.63-1.66
<br><br>
Norton <i>et al</i>. (7-8-2002). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfY3hOVWJJRHlzbnc/edit">Schizophrenia and functional polymorphisms in the MAOA and COMT genes: No evidence for association or epistasis.</a> American Journal of Medical Genetics (Neuropsychiatric Genetics) 114(5): 491-496.
<br>
- Negative finding for MAOA 941T>G SNP (p=0.55), MAOA-3R & MAOA-5R (p=0.68), and COMT epistasis (p=0.43)
<br><br>
Grant <i>et al</i>. (1-24-2013). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfRGpPcm0ySFJfWTQ/edit">Dopaminergic foundations of schizotypy as measured by the German version of the Oxford-Liverpool Inventory of Feelings and Experiences (O-LIFE)—a suitable endophenotype of schizophrenia.</a> Frontiers in Human Neuroscience 7(1): epub ahead of print.
<br>
- Higher cognitive disorganization (p=0.046) and introvertive anhedonia (p=0.016) in men with MAOA-3R<br>
- Nonsignificant epistasis with COMT for unusual experiences
<br><br>
<b>MAOA, Substance Use, & Addiction</b>
<br><br>
Vanyukov <i>et al</i>. (4-24-1995). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfdzVqSHlDUXp6YUU/">Preliminary evidence for an association of a dinucleotide repeat polymorphism at the MAOA gene with early onset alcoholism/substance abuse.</a> American Journal of Medical Genetics 60(2): 122-126.
<br><br>
Hsu <i>et al</i>. (9-1-1996). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMjhWdnZNbmtxclU/edit">Association of monoamine oxidase A alleles with alcoholism among male Chinese in Taiwan.</a> American Journal of Psychiatry 153(9): 1209-1211.
<br><br>
Fowler <i>et al</i>. (11-26-1996). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfTzJIZUt3ZVpUczA/edit">Brain monoamine oxidase A inhibition in cigarette smokers.</a> PNAS 93(24): 14065-14069.
<br>
- Smoking lowers brain MAOA enzyme levels 28%, half of the effect of brief tranylcypromine treatment<br>
- PET imaging
<br><br>
Gade <i>et al</i>. (1-1998). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfd2dpVlF5N2JINzg/edit">Correlation of length of VNTR alleles at the X-linked MAOA gene and phenotypic effect in Tourette syndrome and drug abuse.</a> Molecular Psychiatry 3(1): 50-60.
<br><br>
Rossing. (5-1998). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfU2g3cS1hemc3Q2s/edit">Genetic influences on smoking: Candidate genes.</a> Environmental Health Perspectives 106(5): 231-238.
<br><br>
Berlin <i>et al</i>. (10-15-2009). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfblIwcmFOUWdXOGs/edit">Reduced monoamine oxidase A activity in pregnant smokers and in their newborns.</a> Biological Psychiatry 66(8): 728-733.
<br>
- MAOA activity of births from smoking pregnant women measured by umbilical artery metabolites correlate with newborn facial twitching and grimaces
<br><br>
<b>MAOA, BMI, & Diabetes</b>
<br><br>
Camarena <i>et al</i>. (2004). <a href="https://drive.google.com/file/d/0B4NGOBcoYImfWWItclk5Zl9YX3c/">Family-based association study between the monoamine oxidase A gene and obesity: Implications for psychopharmacogenetic studies.</a> Neuropsychobiology 49(3): 126-129.
<br><br>
Need <i>et al</i>. (5-2006). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfakJhX3cxdHU2OVE/edit">Obesity is associated with genetic variants that alter dopamine availability.</a> Annals of Human Genetics 70(3): 293-303.
<br><br>
Fuemmeler <i>et al</i>. (2-2008). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfNGFscXJvdXYxWmM/edit">Genes implicated in serotonergic and dopaminergic functioning predict BMI categories.</a> Obesity 16(2): 348-355.
<br>
- National Longitudinal Study of Adolescent Health<br>
- Male odds ratio 1.85, 95% confidence interval 1.18-2.94, p=0.04
<br><br>
Elgzyri <i>et al</i>. (7-2012). <a href="https://docs.google.com/file/d/0B4NGOBcoYImfMUVlVTFSZVRGaHc/edit">First-degree relatives of type 2 diabetic patients have reduced expression of genes involved in fatty acid metabolism in skeletal muscle.</a> Journal of Clinical Endocrinology and Metabolism 97(7): E1332.
<br>
- <a href="https://docs.google.com/file/d/0B4NGOBcoYImfWG1tZ21jc2ZCY3M/edit">Supplement</a>
<br><br>
<b>MAOA Cancer Research</b>
<br><br>
<br><br>
<b>MAOA in Popular Non-Fiction</b>
<br><br>
Walsh, Anthony. <a href="https://docs.google.com/file/d/0B4NGOBcoYImfb1Rha0ZhXzIwRG8/edit"><i>Race and Crime: A Biosocial Analysis</i></a>. Nova Science Publishers, Inc., 1-1-2004.
<br><br>
“<a href="http://www.youtube.com/watch?v=35cOqZI067E">Born to Rage?</a>” National Geographic Explorer. National Geographic Channel. 12-14-2010.
<br><br>
“<a href="http://www.youtube.com/watch?v=_mbe3SSIj-4">Born to Rage?</a>” Dr. Phil. 4-4-2011.
<br>
- Falsely claimed “It’s estimated that a third of all men carry what’s been called the warrior gene.”<br>
- Falsely claimed “… in the old days MAO inhibitors were used as antidepressants.” They are still used.<br>
- Claimed that “… the genes give you the loaded pistol, and the environment is what pulls the trigger. You need to have both of those things to have the gun shoot.” This neglects the main effects of MAOA-2R and Brunner syndrome.<br>
- Falsely claimed “It is more rare in women, of course.”
<br><br>
Pinker, Steven. <i>The Better Angels of Our Nature: Why Violence Has Declined</i>. New York: Viking Adult, 10-4-2011.
<br>
- Falsely claimed that “the racial disparity in American homicide has not always been with us.”<br>
- Falsely claimed that “an association between the gene and aggression has not been found in non-European populations…” based on Widom and Brzustowicz.<br>
- Falsely claimed that 70 percent of the Maori carry the low-activity version of MAOA<br>
- Repeated the copy-and-paste error from Lea and Chambers, saying “the low-activity version of the gene is even more common in Chinese men (77 percent of whom carry it)…”
<br><br>
“How Evil are You?” Curiosity. Discovery Channel. 10-30-2011.
<br><br>
“<a href="http://www.youtube.com/watch?v=g6UtV0d9DcE">The Warrior Gene?</a>” Carte Blanche. M-Net. 10-7-2012.
<br><br>
Raine, Adrian. <i>The Anatomy of Violence: The Biological Roots of Crime</i>. Pantheon: New York, 4-30-2013.
<br>
- Falsely claimed that “[a]bout 30 percent of us have a variation in the MAOA gene that gives rise to relatively low levels of this enzyme…”<br>
- Repeated the copy-and-paste error from Lea and Chambers, saying “[w]hile the base rate of the low-MAOA gene is about 34 percent in Caucasian males and 56 percent in the Maori, it is 77 percent in Chinese males.”<br>
- Claimed that “It should be noted that the MAOA-antisocial relationship has not been found in all cultures. Shih and colleagues did not observe such a relationship with either antisocial personality disorder or antisocial alcoholism in participants from Taiwan…. Neither antisocial personality disorder nor antisocial alcoholism is associated with the MAO-A gene in Han Chinese males…. Furthermore, the interaction between abuse and low MAOA has not been found in African-Americans in one report: see Widom, C. S. & Brzustowicz, L. M. (2006).” Widom & Brzustowicz did not control for gender. Weder <i>et al</i> found the interaction in African Americans.
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com0tag:blogger.com,1999:blog-5002675950760488813.post-20263924463981257172012-12-30T02:11:00.000-08:002013-01-01T07:18:32.334-08:00Scientists Rediscover the Violence Gene, MAOA-2R<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<iframe width="415" height="259" src="http://www.youtube.com/embed/_mbe3SSIj-4" frameborder="0" allowfullscreen></iframe>
<br>
<blockquote>“It’s estimated that a third of all men carry what’s been called the warrior gene.”
<br><br>
— Dr. Phil
<br><br>
“There were three genes, as you mentioned. Call them violence genes. Call them bad-behavior genes. But what they found was that if people had these genes, they’re much more likely to be violent. There were certain triggers, as well: stress, family problems, low popularity, failing in school. To take it a step further, Karen, they sort of predict that about one percent of the population has these genes.”
<br><br>
— Dr. Sanjay Gupta, CNN</blockquote>
<br>
Both of these men are wrong, and both are referring to the same gene, monoamine oxidase A (MAOA). Roughly a third of white men inherit the 3-repeat allele of MAOA (MAOA-3R), which has received considerable research attention for influencing aggression. However, every other group, particularly African Americans, reach much higher allele frequencies, making MAOA-3R the most common version of the gene. Gupta was referring to a study of three potential violence-causing genes. One was the heterozygous pairing of ANKK1’s Taq1A allele (once thought to belong to DRD2), found in 37% of the subjects. Another was DAT1’s 10-repeat allele, found in 95% of the subjects. However, the strongest association with violence occurred in the third gene, MAOA, specifically the 2-repeat allele (MAOA-2R) found in that one percent that Gupta mentioned. I previously <a href="http://theunsilencedscience.blogspot.com/2011/03/racial-controversy-of-violent-gene.html">documented</a> how this especially violent version of “the warrior gene” can be found much more commonly in African-American men than white or Asian men. Recently, an unusual study filled in some knowledge gaps about this highly understudied allele, specifically its effect on African-American men.
<br><br>
One unusual aspect of this study, <a href="http://www.soc.iastate.edu/staff/delisi/MAOA%202013.pdf">Beaver <i>et al</i></a>, is that it essentially reexamined the exact same data as <a href="http://andosciasociology.net/resources/Genetics+and+Sociology.pdf">Guo <i>et al</i></a>, the study Gupta mentioned. The latter actually coincided with <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2922855/">another study</a>, also led by Guang Guo, on MAOA-2R in 2008 that determined that the allele doubles the rate of serious and violent delinquency. The impact most affected those aged twelve to fifteen, more than tripling the violent delinquency score based on eight questions. All three papers obtained their data from the National Longitudinal Study of Adolescent Health that totaled about 20,000 participants. However, only a seventh of that sample provided DNA, and Beaver et al focused on as few as eight black men for some of its findings.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-2_01sei4C8s/UN__TKEtC4I/AAAAAAAAAzs/unQckth1yvI/s1600/maoa%2B2R%2Bguo%2Beuro%2Bj%2Bhum%2Bgenetics%2B5-2008%2Bfig%2B2.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="252" width="400" src="http://3.bp.blogspot.com/-2_01sei4C8s/UN__TKEtC4I/AAAAAAAAAzs/unQckth1yvI/s400/maoa%2B2R%2Bguo%2Beuro%2Bj%2Bhum%2Bgenetics%2B5-2008%2Bfig%2B2.jpg" /></a></div>
<br>
That number might induce a healthy skepticism, but one should recall that this is not some newly discovered point mutation obtained in a “fishing expedition” bound for the annals of false positives. This gene produces an extremely important neurotransmitter enzyme that became the target of the first antidepressants in the 1950s. In the 1970s, studies linked its metabolites to aggression. In the late 80s, Hans Brunner discovered and became the eponym for a syndrome of violence resultant from complete deactivation of MAOA. His <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1682278/pdf/ajhg00064-0013.pdf">initial study</a> included only five instances out of a family history of fourteen possible cases. Follow-up research increased the total subjects to nine from this single family. However, other researchers were able to induce Brunner syndrome <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmc2844866/">in mice</a> and eventually to discover such knockout-allele mice in a <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435113/">spontaneous form</a>. Of course, a 2002 <a href="http://www.crassh.cam.ac.uk/uploads/documents/Caspi1.pdf">study</a> instigated a tremendous amount of research on the gene-environment interaction, in which MAOA-3R coupled with the experience of child abuse triggers aggressive tendencies. The number of the “repeats” in the allele refers to the length of the more studied of the two promoters of the gene, and so those repeats can represent, to some extent, discrete levels of the enzyme’s dosage. In fact, the Guo <i>et al</i> 2008 study in the European Journal of Human Genetics included an <i>in-vitro</i> functional analysis of MAOA in human brain-tumor cells. MAOA-2R was less active than MAOA-3R, which was less active than MAOA-4R, the most common version in white people. MAOA-4R was more than three times as active as MAOA-2R.
<br><br>
I shall now briefly detail the sample characteristics that each of the three studies examined in order to ascertain how common MAOA-2R is in white and African-American men. Beaver <i>et al</i> claimed that the overall sample consisted of 2574 individuals, though Guo <i>et al</i> claimed a sample of 2524, including 1200 men. If Beaver <i>et al</i> was in error, then they have consistently repeated the error in other papers. In American Sociological Review, Guo <i>et al</i> only included 1111 men who met that study’s requirements, but both 2008 papers show that only eleven men had the 2R allele, and this study actually provided a racial breakdown of the sample: 60% white, 17% African American, 15% Hispanic American, and 8% Asian. The full genotyped Add Health male population is 57% white, which is 680 men. Beaver <i>et al</i> has listed 174 African-American men. Thus, nine black men by interviewer-assessed race (5.2%) or ten by self-reported race (5.5%) had the 2R allele. Beaver <i>et al</i> revealed that only 0.1% of white males had the 2R allele, which would equal just one man out of 680. That probably leaves none for Asians and Hispanics.
<br><br>
These numbers roughly correspond to other studies but suggest that I might have been too generous to African-American men in suggesting that they are only ten times more likely to have this especially dangerous version of MAOA. <a href="http://static.aws.pdf-archive.com/2011/05/10/monoamine-oxidase-a-regulates/monoamine-oxidase-a-regulates.pdf">Reti <i>et al</i></a> previously genotyped a sample of 618 men and women who were 59% white and 38% African American. That study did not use a purely random sample. Seventy-five percent of that group received psychiatric evaluation within the Hopkins Epidemiology of Personality Disorders Study. That sample included 224 men and 391 women (with apparently three individuals missing possibly from rounding). Assuming both the black people and white people are 64% female, only three alleles out of 595 would have been 2-repeat alleles for white people. Eighteen of 377 would have been 2R for black people. Only about one white man out of possibly 133 would have been likely to have it, if even that, compared to four out of 85 black men. Likewise, Caspi <i>et al</i> in 2002 found one man with the 2R allele out of 499 white males. The trend seems to be that only a token white man in each study has this rare allele. Therefore, to say that the prevalence in whites is higher than Asians is sketchy. Since the new Beaver <i>et al</i> study uses a more random sample than Reti <i>et al</i>, and its white-male 2R prevalence is in closer agreement with Caspi <i>et al</i> than Reti <i>et al</i>, I suspect that this allele is closer to 50 times more common in black men than white men rather than 10 times, as I previously wrote.
<br><br>
Most research on MAOA compares MAOA-3R to MAOA-4R in white males with token instances of MAOA-2R thrown in with MAOA-3R under the label “MAOA-L.” So, these studies are made more shocking by the lumping of “the warrior gene,” MAOA-3R, together with the high-activity allele, MAOA-4R, as the non-violent versions of the gene. The astounding results speak for themselves. Beaver <i>et al</i> found that the ten black men who possessed MAOA-2R had triple the risk of incarceration and almost quadruple their risk of arrest, (accounting for 8.6% of the arrested and 9.5% of the incarcerated). A sample of only eight black men with MAOA-2R out of 130 black men had a statistically significant increased risk of self-reported violence. Scientists have tried to ameliorate the politically unpalatable nature of violence-gene research by emphasizing the environmental trigger for aggression with MAOA-3R, but the findings of Beaver <i>et al</i> and Guo <i>et al</i> did not depend on any environmental trigger. Beaver <i>et al</i> asserted that “the low base-rate of 2-repeat allele carriers prevented an exploration of gene-environment interaction…” However, Guo <i>et al</i> went right ahead and also tested for an interaction between MAOA-2R and being held back a grade in school and three questions regarding feelings of school attachment. The gene’s interaction increased violent delinquency 21 times as much as grade retention alone and seven times as much as school attachment alone.
<br><br>
Given that the men with MAOA-2R in the National Longitudinal Study of Adolescent Health are ten African Americans and one white, I doubt the effectiveness of the regression analysis adjustment for race and ethnicity claimed by Guo <i>et al</i>. Put another way, 91% of the exposed cohort come from a racial group that is 13% of all Americans. Their studies should have laid bare this fact. Beaver <i>et al</i> limited their analysis to the black men, but even that raises concerns of population stratification because African Americans are a mixed population, averaging 22% European ancestry. Africa, itself, has produced no MAOA research, (but it did <a href="http://www.youtube.com/watch?v=g6UtV0d9DcE">copy</a> a sensational National Geographic <a href="http://www.youtube.com/watch?v=35cOqZI067E">documentary</a> on MAOA). If MAOA-2R is so closely associated with African ancestry, then it could serve as a proxy for having more African alleles. Of course, this logic never stopped any of the other research on African Americans, and the implication that multiple other African violence alleles confound this association does not fit the mold of politically correct impugnment usually directed at MAOA research.
<br><br>
<iframe width="393" height="259" src="http://www.youtube.com/embed/g6UtV0d9DcE " frameborder="0" allowfullscreen></iframe>
<br><br>
Part of my fascination with the sparse research on MAOA-2R comes from my belief that scientists have inadvertently underplayed the true power of this gene. Comparing the two most common versions of MAOA requires less effort and funding, and emphasizing an environmental trigger, like child abuse, varnishes genetics research with a politically correct gloss. However, the trigger for MAOA-3R quickly <a href="http://bjp.rcpsych.org/content/200/2/116.short">multiplied</a> to include <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmc2665792/">testosterone levels</a>, maternal smoking, IQ, education, and socio-economic status. Some of those “environmental” factors actually have a <a href="http://theunsilencedscience.blogspot.com/2010/01/epistemology-endocrinology.html">dominant hereditary influence</a>. Now, studies have triggered aggression in MAOA-3R men with much more immediate experimental adversities in the form of <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1601-183X.2012.00868.x/abstract">game</a> <a href="http://www.pnas.org/content/106/7/2118.full.pdf+html">unfairness</a>. Furthermore, people like Dr. Phil assume that a gene-environment interaction is synonymous with a “genetic predisposition,” but the “non-active” allele actually appears to play a protective role that negates an environmental trigger’s impact. For instance, low IQ does not increase violent tendencies in men with MAOA-4R, but it does in men with MAOA-3R.
<br><br>
Incidentally, Steven Pinker’s latest book addressed the Flynn Effect. “If smarter people and smarter societies are less likely to be violent, then perhaps the recent rise in intelligence can help explain the recent decline of violence.” However, a <a href="http://www.cell.com/trends/genetics/abstract/S0168-9525%2812%2900159-X">hypothesis</a> of much longer-term IQ decline has recently ridden a wave of genetic-load angst, so allow me to point out the tension between these competing paradigms as a challenge to Pinker’s broader thesis. The complex associations between intelligence, executive function, and aggression might have also drawn in olfaction research. Both judgment and the ability to discern smells localize to the frontal lobes, and <a href="http://link.springer.com/article/10.1007%2Fs12078-012-9135-7">research</a> has linked poor olfactory acuity to aggression. As with MAOA allele frequencies, racial disparities <a href="http://deepblue.lib.umich.edu/bitstream/2027.42/72304/1/j.1754-4505.1995.tb00501.x.pdf">exist</a> for odor identification.
<br><br>
Since Brunner syndrome and MAOA-2R seem to have a “main effect” without an environmental trigger, I see the MAOA-3R gene-environment interaction as a penumbra of the possible enzymatic effects. In an entire population, the prevalence of violence must have a specific total MAOA component that would consist of all of the MAOA variants (including potential epigenetic effects, SNPs, and both VNTR promoters, only one of which is the subject of most “warrior gene” research) and each variant’s potential when unlocked by all possible environmental triggers. Even with enormous samples, whole-genome studies are capable of studying a tiny fraction of this genetic potential. Similarly, quantitative genetics research, like twins studies, underestimates heritability when some large genetic effects are unlocked by environmental stimuli, as opposed to a merely additive nature-nurture relationship. Terrie Moffitt and Avshalom Caspi, who spearheaded early gene-environment research, wrote an extended <a href="http://www.psy.miami.edu/faculty/dmessinger/c_c/rsrcs/rdgs/temperament/moffit.caspi.rutter2006.pdf">analysis</a> of this approach with Michael Rutter. “For understanding the influence of such conditional-effect genes, large samples may be less necessary than strategic [gene-environment interaction] research.”
<br><br>
Rather than use the penumbra of gene-environment interactions to appreciate the extensiveness of a gene’s effect, scientists like Moffitt, Caspi, and Rutter seek to dispel genetic “determinism.” Citing a two-hour student <a href="http://www.ncbi.nlm.nih.gov/pubmed/7569909">protest</a> of a scientific conference on the genetics of violence, they explained, “Ethicists attribute the root of the public’s concern about genes to a pervasive belief in the power of genetic determinism: ‘ … genetic determinism implies that knowing a person’s genetic makeup is tantamount to knowing his or her future.’” If the public detests genetic determinism due to its unyielding quality, then surely such people would rather seek methods to circumnavigate genetic fate than to simply disacknowledge the power of heredity. However, Moffitt <i>et al</i> wish for the opposite: “Concrete data needed to counter genetic determinism are provided by new [gene-environment interaction] findings…. Such understanding should make eugenics and other misuses of genetic information much more difficult.” This discussion calls for a debate over both the feasibility and the ethics of changes to environmental triggers, like poverty, versus those of the ill-defined “misuses” of genetic knowledge. Presumably hypothetical therapeutic drugs and diagnostic tests for violent tendencies would not necessarily misuse the research, and the solutions to poverty and educational failure are not just around the corner.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-tpXfFjcp18M/UN__u9BUW8I/AAAAAAAAAz4/0mHZQtQADpw/s1600/genetics%2Bconference%2Bprotest.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="400" width="285" src="http://1.bp.blogspot.com/-tpXfFjcp18M/UN__u9BUW8I/AAAAAAAAAz4/0mHZQtQADpw/s400/genetics%2Bconference%2Bprotest.png" /></a></div>
<br>
Obviously, many scientists and activists who oppose genetic determinism believe in a greater role for nurture or even blank-slate nurture determinism, but they wish to leverage the masses, who ascribe behavior to supernatural “free will.” To qualify as deterministic, must genetic aggressivity present itself constantly? Though MAOA has no activity in Brunner syndrome, the subjects need not reside in cages, gnawing on the bars. Most men with the MAOA knockout allele are <a href="http://3.bp.blogspot.com/-XbqD-TGIsNQ/TXD69_mNB6I/AAAAAAAAAHA/rJVYujEL8Io/s1600/table1.jpg">afflicted</a> with conduct disorder and “conflict with the law” during their lifetime. A provocation of some sort might set off aggression, but minor provocations exist in the lives of all people, so Brunner syndrome should still qualify as deterministic. Whether the existence of such determinism is “nice” or not has no bearing on its existence, so do not mistake denial for virtue.
<br><br>
<b><center>Wickedpedia</center></b>
<br>
I might have missed the recent Beaver et al study, if others had not pointed it out to me. Unlike most MAOA research, it did not surface in the PubMed database. I think that is true of all studies from the Journal of Personality and Individual Differences of the London School of Differential Psychology. Some of the journal’s <a href="http://www.journals.elsevier.com/personality-and-individual-differences/editorial-board/">board members</a>, including recently deceased <a href="http://theunsilencedscience.blogspot.com/2012/11/arthur-jensen-jp-rushton.html">Arthur Jensen</a>, received the label “scientific racist” from certain <a href="http://www.splcenter.org/get-informed/intelligence-files/groups/pioneer-fund">activists</a>. So, Kevin Beaver refused to submit to an interview for this blog, but he saw fit to publish in a journal that recently reviewed research on penis length and circumference differences among “Negroids,” “Caucasoids,” and “Mongoloids.” A year ago, I was able to send him a <a href="http://theunsilencedscience.blogspot.com/2011/09/pulling-empty-chair-on-dr-kevin-beaver.html">list of questions</a>, in which I confronted him for conflating MAOA-2R and MAOA-3R as “MAOA-L.” He told me that a study on MAOA-2R was “in the pipeline.” However, I would like to think that I inspired the study, and I find it jarring that four years could pass without any research on MAOA-2R and violence.
<br><br>
Is anyone following this research as well as I am? Many professions fight “turf wars.” This occurs among medical professionals and physician specialties. Study of MAOA and violence likens less to competition over a lucrative procedure and more to a game of “hot potato.” Violence, itself, does not have a dedicated category in the Diagnostic and Statistical Manual of Mental Disorders. Though psychiatrists have contributed some research, it seems that psychologists and criminologists like Beaver have taken the lead usually with low-cost data mining from databases like the National Longitudinal Study of Adolescent Health.
<br><br>
Meanwhile, public attention to the gene increasingly falls to self-appointed <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">experts</a> and “ethicists,” who cannot even report some very basic facts about the gene correctly. <a href="http://www.genomesunzipped.org/2011/11/size-matters-and-other-lessons-from-medical-genetics.php">Pseudointellectuals</a> are claiming that “most if not all of this literature [on MAOA] is wrong, and [<i>sic</i>] will soon be forgotten” and that a “<a href="http://alandove.com/content/2012/11/single-molecule-determines-complex-behavior-say-scientists/">single molecule</a>” like serotonin or dopamine cannot explain “<a href="http://theunsilencedscience.blogspot.com/2011/08/picture-is-worth-thousand-blogs.html">complex behavior</a>.” When Scientologists mouth these stupid ideas, most people roll their eyes, but now the same ideas are coming from “science reporters” and Harvard professors. Therefore, I decided to take the drastic measure of addressing what I think might be the source of the problem by editing Wikipedia. Before I started editing the Wikipedia pages for Brunner syndrome and MAOA, activists had peppered them with qualifications that the evidence was “flawed” or “controversial” or that the emerging field of epigenetics made the gene’s effects “hard to predict.” Apparently, methyl moieties escape the rule that a single type of molecule cannot determine a complex behavior. Never mind <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322496/">studies</a> that show the epigenetics of MAOA in men is minimal, low in variance, and high in hereditary influence. Of course, it is never enough to simply edit a fix into a Wikipedia page. First, one makes the edit. Then, one reapplies the edit repeatedly after activists try to undo one’s work. Finally, one replies to the activist on one’s personal “<a href="http://en.wikipedia.org/wiki/User_talk:Unsilencedscience">talk</a>” page when the activist threatens to undo one’s work again unless one attaches to an email the study that proves the activist’s sacred belief is based on a copy-and-paste error. A stronger commitment predicates some Wikipedia myths than that of many a marriage.
<br><br>
Some are rightfully criticizing this research and candidate-gene behavioral genetics, in general, because small sample sizes can cause false positives by measure of statistical significance. However, since no other approach is capable of studying VNTRs like MAOA, the only current solution would be to fund the research more rather than to <a href="http://theunsilencedscience.blogspot.com/2012/07/just-say-no-limit-trayvon.html">advocate censorship</a> of the research that is being done. Rarely do I hear similar criticism of functional magnetic resonance imaging (fMRI) research, which tends to have small samples due to the expense of the imaging but makes up for it with pretty color explosions on brain maps. When I worked with fMRI, I thought that the arbitrary threshold settings that defined the “areas of increased activity” added an extra layer of bias. Perhaps the Harvard establishment has singled out behavioral genetics for rebuke in order to centralize the potential for offensive findings and to avoid “misuse.”
<br><br>
<b><center>Congratulations! You Have Cancer!</center></b>
<br>
The study of MAOA has received a beautiful gift—the gift of cancer. One might recall the fad cureall and supplier of immortality known as antioxidants. Antioxidants are supposed to save cells by counteracting free radicals. However, too much of a good thing like cell survival is cancer. MAOA deserves to be called the “warrior gene” because it makes <a href="http://www.sciencedirect.com/science/article/pii/S0161813X03001098">oxidases</a> that slay cancer cells. <a href="http://www.ncbi.nlm.nih.gov/pubmed/9598998">Malorni <i>et al</i></a> first discovered this in 1998 when the MAOA-inhibiting drug, clorgyline, saved melanoma cells, <i>in vitro</i>. Ten years later, <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593938/">Alpini <i>et al</i></a> concluded that epigenetic effects on the MAOA VNTR could explain its lower enzyme levels in cholangiocarcinoma, cancer of the liver bile ducts. Now, <a href="http://www.nature.com/labinvest/journal/v92/n10/full/labinvest2012110a.html">Huang <i>et al</i></a> has determined that higher MAOA expression decreased the risk of metastasis and improved prognosis and survival in patients with cholangiocarcinoma. Though the decline in MAOA expression seemed mostly limited to the areas of malignancy, I have found some online <a href="http://www.cholangiocarcinoma.org/punbb/viewtopic.php?id=1325">family-member portrayals</a> of men with the disease becoming “distant,” “difficult,” “angry,” “grumpy,” “horrible,” and “mean,” in some cases prior to diagnosis.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-PjuD97NnT9I/UOAAEmLN0aI/AAAAAAAAA0E/BGOQMltcC8U/s1600/maoa%2Benzyme%2Bepigenetics%2Bcholangiocarcinoma%2Bhuang%2Blaboratory%2Binvestigation%2B8-20-2012%2Bfig%2B1.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="314" width="393" src="http://2.bp.blogspot.com/-PjuD97NnT9I/UOAAEmLN0aI/AAAAAAAAA0E/BGOQMltcC8U/s400/maoa%2Benzyme%2Bepigenetics%2Bcholangiocarcinoma%2Bhuang%2Blaboratory%2Binvestigation%2B8-20-2012%2Bfig%2B1.png" /></a></div>
<br>
This calls for drugs that increase MAOA levels, and maybe the resulting therapies could metastasize to psychiatric uses. A few contestants already have records of accomplishment. Doctors sometimes use risperidone, an older-generation antipsychotic, to treat impulsive aggression. In fact, Tuinier <i>et al</i> detailed a case report of a Brunner syndrome patient who successfully responded for a time to risperidone. Nevertheless, the drug has serious adverse reactions, causing many patients to gain weight, and a small percentage develop permanent tardive dyskinesia, involuntary movements often of the lips. <a href="http://www.sciencedirect.com/science/article/pii/S000689939901478X">Tetrabenazine and ketanserin</a> reduced aggression in MAOA-knockout mice. Tetrabenazine is used to treat chorea, the involuntary movements of Huntington’s disease. The FDA <a href="http://onlinelibrary.wiley.com/doi/10.1002/ana.23672/abstract">granted</a> it official orphan-drug status in 2008, but it is incredibly expensive for Americans to use. Ketanserin has applications for high blood pressure, but it is unavailable in the US.
<br><br>
Maybe this cancer research could save MAOA from its “controversial” reputation. Harvard professors might hesitate to dismiss a violence gene that became a cancer gene. After all, lives are at stake.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Cancer+research&rft_id=info%3Apmid%2F19010890&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Serotonin+metabolism+is+dysregulated+in+cholangiocarcinoma%2C+which+has+implications+for+tumor+growth.&rft.issn=0008-5472&rft.date=2008&rft.volume=68&rft.issue=22&rft.spage=9184&rft.epage=93&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2593938%2F&rft.au=Alpini+G&rft.au=Invernizzi+P&rft.au=Gaudio+E&rft.au=Venter+J&rft.au=Kopriva+S&rft.au=Bernuzzi+F&rft.au=Onori+P&rft.au=Franchitto+A&rft.au=Coufal+M&rft.au=Frampton+G&rft.au=Alvaro+D&rft.au=Lee+SP&rft.au=Marzioni+M&rft.au=Benedetti+A&rft.au=DeMorrow+S&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Alpini G, Invernizzi P, Gaudio E, Venter J, Kopriva S, Bernuzzi F, Onori P, Franchitto A, Coufal M, Frampton G, Alvaro D, Lee SP, Marzioni M, Benedetti A, & DeMorrow S (2008). Serotonin metabolism is dysregulated in cholangiocarcinoma, which has implications for tumor growth. <span style="font-style: italic;">Cancer research, 68</span> (22), 9184-93 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19010890">19010890</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Personality+and+Individual+Differences&rft_id=info%3Adoi%2F10.1016%2Fj.paid.2012.08.014&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Exploring+the+association+between+the+2-repeat+allele+of+the+MAOA+gene+promoter+polymorphism+and+psychopathic+personality+traits%2C+arrests%2C+incarceration%2C+and+lifetime+antisocial+behavior&rft.issn=01918869&rft.date=2013&rft.volume=54&rft.issue=2&rft.spage=164&rft.epage=168&rft.artnum=http%3A%2F%2Fwww.soc.iastate.edu%2Fstaff%2Fdelisi%2FMAOA%25202013.pdf&rft.au=Beaver%2C+K.&rft.au=Wright%2C+J.&rft.au=Boutwell%2C+B.&rft.au=Barnes%2C+J.&rft.au=DeLisi%2C+M.&rft.au=Vaughn%2C+M.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Beaver, K., Wright, J., Boutwell, B., Barnes, J., DeLisi, M., & Vaughn, M. (2013). Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior <span style="font-style: italic;">Personality and Individual Differences, 54</span> (2), 164-168 DOI: <a rev="review" href="http://dx.doi.org/10.1016/j.paid.2012.08.014">10.1016/j.paid.2012.08.014</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+human+genetics&rft_id=info%3Apmid%2F8503438&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=X-linked+borderline+mental+retardation+with+prominent+behavioral+disturbance%3A+phenotype%2C+genetic+localization%2C+and+evidence+for+disturbed+monoamine+metabolism.&rft.issn=0002-9297&rft.date=1993&rft.volume=52&rft.issue=6&rft.spage=1032&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1682278%2Fpdf%2Fajhg00064-0013.pdf&rft.au=Brunner+HG&rft.au=Nelen+MR&rft.au=van+Zandvoort+P&rft.au=Abeling+NG&rft.au=van+Gennip+AH&rft.au=Wolters+EC&rft.au=Kuiper+MA&rft.au=Ropers+HH&rft.au=van+Oost+BA&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Brunner HG, Nelen MR, van Zandvoort P, Abeling NG, van Gennip AH, Wolters EC, Kuiper MA, Ropers HH, & van Oost BA (1993). X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. <span style="font-style: italic;">American journal of human genetics, 52</span> (6), 1032-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/8503438">8503438</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft_id=info%3Apmid%2F7792602&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Aggressive+behavior+and+altered+amounts+of+brain+serotonin+and+norepinephrine+in+mice+lacking+MAOA.&rft.issn=0036-8075&rft.date=1995&rft.volume=268&rft.issue=5218&rft.spage=1763&rft.epage=6&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2Fpmc2844866%2F&rft.au=Cases+O&rft.au=Seif+I&rft.au=Grimsby+J&rft.au=Gaspar+P&rft.au=Chen+K&rft.au=Pournin+S&rft.au=M%C3%BCller+U&rft.au=Aguet+M&rft.au=Babinet+C&rft.au=Shih+JC&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, & Shih JC (1995). Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. <span style="font-style: italic;">Science (New York, N.Y.), 268</span> (5218), 1763-6 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/7792602">7792602</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft_id=info%3Apmid%2F12161658&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Role+of+genotype+in+the+cycle+of+violence+in+maltreated+children.&rft.issn=0036-8075&rft.date=2002&rft.volume=297&rft.issue=5582&rft.spage=851&rft.epage=4&rft.artnum=http%3A%2F%2Fwww.crassh.cam.ac.uk%2Fuploads%2Fdocuments%2FCaspi1.pdf&rft.au=Caspi+A&rft.au=McClay+J&rft.au=Moffitt+TE&rft.au=Mill+J&rft.au=Martin+J&rft.au=Craig+IW&rft.au=Taylor+A&rft.au=Poulton+R&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, Taylor A, & Poulton R (2002). Role of genotype in the cycle of violence in maltreated children. <span style="font-style: italic;">Science (New York, N.Y.), 297</span> (5582), 851-4 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/12161658">12161658</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Trends+in+Genetics&rft_id=info%3Adoi%2F10.1016%2Fj.tig.2012.10.003&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Our+fragile+intellect.+Part+II&rft.issn=01689525&rft.date=2013&rft.volume=29&rft.issue=1&rft.spage=3&rft.epage=5&rft.artnum=http%3A%2F%2Fwww.cell.com%2Ftrends%2Fgenetics%2Fabstract%2FS0168-9525%252812%252900159-X&rft.au=Crabtree%2C+G.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Crabtree, G. (2013). Our fragile intellect. Part II <span style="font-style: italic;">Trends in Genetics, 29</span> (1), 3-5 DOI: <a rev="review" href="http://dx.doi.org/10.1016/j.tig.2012.10.003">10.1016/j.tig.2012.10.003</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft_id=info%3Apmid%2F22297589&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Moderating+role+of+the+MAOA+genotype+in+antisocial+behaviour.&rft.issn=0007-1250&rft.date=2012&rft.volume=200&rft.issue=2&rft.spage=116&rft.epage=23&rft.artnum=http%3A%2F%2Fbjp.rcpsych.org%2Fcontent%2F200%2F2%2F116.short&rft.au=Fergusson+DM&rft.au=Boden+JM&rft.au=Horwood+LJ&rft.au=Miller+A&rft.au=Kennedy+MA&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA (2012). Moderating role of the MAOA genotype in antisocial behaviour. <span style="font-style: italic;">The British journal of psychiatry : the journal of mental science, 200</span> (2), 116-23 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22297589">22297589</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Genes%2C+brain%2C+and+behavior&rft_id=info%3Apmid%2F23067570&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+genotype%2C+social+exclusion+and+aggression%3A+an+experimental+test+of+a+gene-environment+interaction.&rft.issn=1601-1848&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.1111%2Fj.1601-183X.2012.00868.x%2Fabstract&rft.au=Gallardo-Pujol+D&rft.au=Andr%C3%A9s-Pueyo+A&rft.au=Maydeu-Olivares+A&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Gallardo-Pujol D, Andrés-Pueyo A, & Maydeu-Olivares A (2012). MAOA genotype, social exclusion and aggression: an experimental test of a gene-environment interaction. <span style="font-style: italic;">Genes, brain, and behavior</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23067570">23067570</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Sociological+Review&rft_id=info%3Adoi%2F10.1177%2F000312240807300402&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+Integration+of+Genetic+Propensities+into+Social-Control+Models+of+Delinquency+and+Violence+among+Male+Youths&rft.issn=0003-1224&rft.date=2008&rft.volume=73&rft.issue=4&rft.spage=543&rft.epage=568&rft.artnum=http%3A%2F%2Fandosciasociology.net%2Fresources%2FGenetics%2Band%2BSociology.pdf&rft.au=Guo%2C+G.&rft.au=Roettger%2C+M.&rft.au=Cai%2C+T.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Guo, G., Roettger, M., & Cai, T. (2008). The Integration of Genetic Propensities into Social-Control Models of Delinquency and Violence among Male Youths <span style="font-style: italic;">American Sociological Review, 73</span> (4), 543-568 DOI: <a rev="review" href="http://dx.doi.org/10.1177/000312240807300402">10.1177/000312240807300402</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=European+Journal+of+Human+Genetics&rft_id=info%3Adoi%2F10.1038%2Fsj.ejhg.5201999&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+VNTR+2+repeat+in+MAOA+and+delinquent+behavior+in+adolescence+and+young+adulthood%3A+associations+and+MAOA+promoter+activity&rft.issn=1018-4813&rft.date=2008&rft.volume=16&rft.issue=5&rft.spage=626&rft.epage=634&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2922855%2F&rft.au=Guo%2C+G.&rft.au=Ou%2C+X.&rft.au=Roettger%2C+M.&rft.au=Shih%2C+J.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Guo, G., Ou, X., Roettger, M., & Shih, J. (2008). The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity <span style="font-style: italic;">European Journal of Human Genetics, 16</span> (5), 626-634 DOI: <a rev="review" href="http://dx.doi.org/10.1038/sj.ejhg.5201999">10.1038/sj.ejhg.5201999</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft_id=info%3Apmid%2F22906985&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidase+A+expression+is+suppressed+in+human+cholangiocarcinoma+via+coordinated+epigenetic+and+IL-6-driven+events.&rft.issn=0023-6837&rft.date=2012&rft.volume=92&rft.issue=10&rft.spage=1451&rft.epage=60&rft.artnum=+http%3A%2F%2Fwww.nature.com%2Flabinvest%2Fjournal%2Fv92%2Fn10%2Ffull%2Flabinvest2012110a.html&rft.au=Huang+L&rft.au=Frampton+G&rft.au=Rao+A&rft.au=Zhang+KS&rft.au=Chen+W&rft.au=Lai+JM&rft.au=Yin+XY&rft.au=Walker+K&rft.au=Culbreath+B&rft.au=Leyva-Illades+D&rft.au=Quinn+M&rft.au=McMillin+M&rft.au=Bradley+M&rft.au=Liang+LJ&rft.au=DeMorrow+S&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Huang L, Frampton G, Rao A, Zhang KS, Chen W, Lai JM, Yin XY, Walker K, Culbreath B, Leyva-Illades D, Quinn M, McMillin M, Bradley M, Liang LJ, & DeMorrow S (2012). Monoamine oxidase A expression is suppressed in human cholangiocarcinoma via coordinated epigenetic and IL-6-driven events. <span style="font-style: italic;">Laboratory investigation; a journal of technical methods and pathology, 92</span> (10), 1451-60 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22906985">22906985</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Special+Care+in+Dentistry&rft_id=info%3Adoi%2F10.1111%2Fj.1754-4505.1995.tb00501.x&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Odor+identification+in+young+and+elderly+African-Americans+and+Caucasians&rft.issn=0275-1879&rft.date=1995&rft.volume=15&rft.issue=4&rft.spage=138&rft.epage=143&rft.artnum=http%3A%2F%2Fdeepblue.lib.umich.edu%2Fbitstream%2F2027.42%2F72304%2F1%2Fj.1754-4505.1995.tb00501.x.pdf&rft.au=Jones%2C+R.&rft.au=Brown%2C+C.&rft.au=Ship%2C+J.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Jones, R., Brown, C., & Ship, J. (1995). Odor identification in young and elderly African-Americans and Caucasians <span style="font-style: italic;">Special Care in Dentistry, 15</span> (4), 138-143 DOI: <a rev="review" href="http://dx.doi.org/10.1111/j.1754-4505.1995.tb00501.x">10.1111/j.1754-4505.1995.tb00501.x</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Chemosensory+Perception&rft_id=info%3Adoi%2F10.1007%2Fs12078-012-9135-7&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Olfactory+Abilities+and+Psychopathy%3A+Higher+Psychopathy+Scores+Are+Associated+with+Poorer+Odor+Discrimination+and+Identification&rft.issn=1936-5802&rft.date=2012&rft.volume=5&rft.issue=3-4&rft.spage=300&rft.epage=307&rft.artnum=http%3A%2F%2Flink.springer.com%2Farticle%2F10.1007%252Fs12078-012-9135-7&rft.au=Mahmut%2C+M.&rft.au=Stevenson%2C+R.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Mahmut, M., & Stevenson, R. (2012). Olfactory Abilities and Psychopathy: Higher Psychopathy Scores Are Associated with Poorer Odor Discrimination and Identification <span style="font-style: italic;">Chemosensory Perception, 5</span> (3-4), 300-307 DOI: <a rev="review" href="http://dx.doi.org/10.1007/s12078-012-9135-7">10.1007/s12078-012-9135-7</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=FEBS+letters&rft_id=info%3Apmid%2F9598998&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Protection+against+apoptosis+by+monoamine+oxidase+A+inhibitors.&rft.issn=0014-5793&rft.date=1998&rft.volume=426&rft.issue=1&rft.spage=155&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpubmed%2F9598998&rft.au=Malorni+W&rft.au=Giammarioli+AM&rft.au=Matarrese+P&rft.au=Pietrangeli+P&rft.au=Agostinelli+E&rft.au=Ciaccio+A&rft.au=Grassilli+E&rft.au=Mondovi+B&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Malorni W, Giammarioli AM, Matarrese P, Pietrangeli P, Agostinelli E, Ciaccio A, Grassilli E, & Mondovi B (1998). Protection against apoptosis by monoamine oxidase A inhibitors. <span style="font-style: italic;">FEBS letters, 426</span> (1), 155-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/9598998">9598998</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft_id=info%3Apmid%2F19168625&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidase+A+gene+%28MAOA%29+predicts+behavioral+aggression+following+provocation.&rft.issn=0027-8424&rft.date=2009&rft.volume=106&rft.issue=7&rft.spage=2118&rft.epage=23&rft.artnum=http%3A%2F%2Fwww.pnas.org%2Fcontent%2F106%2F7%2F2118.full.pdf%2Bhtml&rft.au=McDermott+R&rft.au=Tingley+D&rft.au=Cowden+J&rft.au=Frazzetto+G&rft.au=Johnson+DD&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">McDermott R, Tingley D, Cowden J, Frazzetto G, & Johnson DD (2009). Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation. <span style="font-style: italic;">Proceedings of the National Academy of Sciences of the United States of America, 106</span> (7), 2118-23 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19168625">19168625</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Perspectives+on+Psychological+Science&rft_id=info%3Adoi%2F10.1111%2Fj.1745-6916.2006.00002.x&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Measured+Gene-Environment+Interactions+in+Psychopathology.+Concepts%2C+Research+Strategies%2C+and+Implications+for+Research%2C+Intervention%2C+and+Public+Understanding+of+Genetics&rft.issn=1745-6916&rft.date=2006&rft.volume=1&rft.issue=1&rft.spage=5&rft.epage=27&rft.artnum=http%3A%2F%2Fwww.psy.miami.edu%2Ffaculty%2Fdmessinger%2Fc_c%2Frsrcs%2Frdgs%2Ftemperament%2Fmoffit.caspi.rutter2006.pdf&rft.au=Moffitt%2C+T.&rft.au=Caspi%2C+A.&rft.au=Rutter%2C+M.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Moffitt, T., Caspi, A., & Rutter, M. (2006). Measured Gene-Environment Interactions in Psychopathology. Concepts, Research Strategies, and Implications for Research, Intervention, and Public Understanding of Genetics <span style="font-style: italic;">Perspectives on Psychological Science, 1</span> (1), 5-27 DOI: <a rev="review" href="http://dx.doi.org/10.1111/j.1745-6916.2006.00002.x">10.1111/j.1745-6916.2006.00002.x</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Annals+of+neurology&rft_id=info%3Apmid%2F23109143&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Unintended+effects+of+orphan+product+designation+for+rare+neurological+diseases.&rft.issn=0364-5134&rft.date=2012&rft.volume=72&rft.issue=4&rft.spage=481&rft.epage=90&rft.artnum=http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.1002%2Fana.23672%2Fabstract&rft.au=Murphy+SM&rft.au=Puwanant+A&rft.au=Griggs+RC&rft.au=Consortium+for+Clinical+Investigations+of+Neurological+Channelopathies+%28CINCH%29+and+Inherited+Neuropathies+Consortium+%28INC%29+Consortia+of+the+Rare+Disease+Clinical+Research+Network&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Murphy SM, Puwanant A, Griggs RC, & Consortium for Clinical Investigations of Neurological Channelopathies (CINCH) and Inherited Neuropathies Consortium (INC) Consortia of the Rare Disease Clinical Research Network (2012). Unintended effects of orphan product designation for rare neurological diseases. <span style="font-style: italic;">Annals of neurology, 72</span> (4), 481-90 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/23109143">23109143</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=NeuroToxicology&rft_id=info%3Adoi%2F10.1016%2FS0161-813X%2803%2900109-8&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Amine+Oxidases+and+Tumors&rft.issn=0161813X&rft.date=2004&rft.volume=25&rft.issue=1-2&rft.spage=317&rft.epage=324&rft.artnum=http%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fpii%2FS0161813X03001098&rft.au=Pietrangeli%2C+P.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Pietrangeli, P. (2004). Amine Oxidases and Tumors <span style="font-style: italic;">NeuroToxicology, 25</span> (1-2), 317-324 DOI: <a rev="review" href="http://dx.doi.org/10.1016/S0161-813X(03)00109-8">10.1016/S0161-813X(03)00109-8</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Comprehensive+psychiatry&rft_id=info%3Apmid%2F21295226&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidase+A+regulates+antisocial+personality+in+whites+with+no+history+of+physical+abuse.&rft.issn=0010-440X&rft.date=2011&rft.volume=52&rft.issue=2&rft.spage=188&rft.epage=94&rft.artnum=http%3A%2F%2Fstatic.aws.pdf-archive.com%2F2011%2F05%2F10%2Fmonoamine-oxidase-a-regulates%2Fmonoamine-oxidase-a-regulates.pdf&rft.au=Reti+IM&rft.au=Xu+JZ&rft.au=Yanofski+J&rft.au=McKibben+J&rft.au=Uhart+M&rft.au=Cheng+YJ&rft.au=Zandi+P&rft.au=Bienvenu+OJ&rft.au=Samuels+J&rft.au=Willour+V&rft.au=Kasch-Semenza+L&rft.au=Costa+P&rft.au=Bandeen-Roche+K&rft.au=Eaton+WW&rft.au=Nestadt+G&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Reti IM, Xu JZ, Yanofski J, McKibben J, Uhart M, Cheng YJ, Zandi P, Bienvenu OJ, Samuels J, Willour V, Kasch-Semenza L, Costa P, Bandeen-Roche K, Eaton WW, & Nestadt G (2011). Monoamine oxidase A regulates antisocial personality in whites with no history of physical abuse. <span style="font-style: italic;">Comprehensive psychiatry, 52</span> (2), 188-94 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21295226">21295226</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science&rft_id=info%3Adoi%2F10.1126%2Fscience.7569909&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Conflict+marks+crime+conference&rft.issn=0036-8075&rft.date=1995&rft.volume=269&rft.issue=5232&rft.spage=1808&rft.epage=1809&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpubmed%2F7569909&rft.au=Roush%2C+W.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Roush, W. (1995). Conflict marks crime conference <span style="font-style: italic;">Science, 269</span> (5232), 1808-1809 DOI: <a rev="review" href="http://dx.doi.org/10.1126/science.7569909">10.1126/science.7569909</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=NeuroReport&rft_id=info%3Adoi%2F10.1097%2FWNR.0b013e3282fd6e88&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Novel+monoamine+oxidase+A+knock+out+mice+with+human-like+spontaneous+mutation&rft.issn=0959-4965&rft.date=2008&rft.volume=19&rft.issue=7&rft.spage=739&rft.epage=743&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3435113%2F&rft.au=Scott%2C+A.&rft.au=Bortolato%2C+M.&rft.au=Chen%2C+K.&rft.au=Shih%2C+J.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Scott, A., Bortolato, M., Chen, K., & Shih, J. (2008). Novel monoamine oxidase A knock out mice with human-like spontaneous mutation <span style="font-style: italic;">NeuroReport, 19</span> (7), 739-743 DOI: <a rev="review" href="http://dx.doi.org/10.1097/WNR.0b013e3282fd6e88">10.1097/WNR.0b013e3282fd6e88</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Brain+research&rft_id=info%3Apmid%2F10415365&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Ketanserin+and+tetrabenazine+abolish+aggression+in+mice+lacking+monoamine+oxidase+A.&rft.issn=0006-8993&rft.date=1999&rft.volume=835&rft.issue=2&rft.spage=104&rft.epage=12&rft.artnum=http%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fpii%2FS000689939901478X&rft.au=Shih+JC&rft.au=Ridd+MJ&rft.au=Chen+K&rft.au=Meehan+WP&rft.au=Kung+MP&rft.au=Seif+I&rft.au=De+Maeyer+E&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Shih JC, Ridd MJ, Chen K, Meehan WP, Kung MP, Seif I, & De Maeyer E (1999). Ketanserin and tetrabenazine abolish aggression in mice lacking monoamine oxidase A. <span style="font-style: italic;">Brain research, 835</span> (2), 104-12 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/10415365">10415365</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Neuropsychopharmacology&rft_id=info%3Adoi%2F10.1038%2Fsj.npp.1301417&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+Non-Additive+Interaction+of+a+Functional+MAO-A+VNTR+and+Testosterone+Predicts+Antisocial+Behavior&rft.issn=0893-133X&rft.date=2007&rft.volume=33&rft.issue=2&rft.spage=425&rft.epage=430&rft.artnum=http%3A%2F%2Fwww.nature.com%2Fdoifinder%2F10.1038%2Fsj.npp.1301417&rft.au=Sj%C3%B6berg%2C+R.&rft.au=Ducci%2C+F.&rft.au=Barr%2C+C.&rft.au=Newman%2C+T.&rft.au=Dell%27Osso%2C+L.&rft.au=Virkkunen%2C+M.&rft.au=Goldman%2C+D.&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Sjöberg, R., Ducci, F., Barr, C., Newman, T., Dell'Osso, L., Virkkunen, M., & Goldman, D. (2007). A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior <span style="font-style: italic;">Neuropsychopharmacology, 33</span> (2), 425-430 DOI: <a rev="review" href="http://dx.doi.org/10.1038/sj.npp.1301417">10.1038/sj.npp.1301417</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=New+Trends+in+Experimental+and+Clinical+Psychiatry&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Neuropsychiatric+and+biological+characteristics+of+X-linked+MAOA+deficiency+syndrome%3A+A+single-intervention+case+study.&rft.issn=&rft.date=1995&rft.volume=11&rft.issue=4&rft.spage=99&rft.epage=107&rft.artnum=&rft.au=Tuinier+S&rft.au=Verhoeven+WMA&rft.au=Scherders+MJWT&rft.au=Fekkes+D&rft.au=Pepplinkhuizen+L&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Tuinier S, Verhoeven WMA, Scherders MJWT, Fekkes D, & Pepplinkhuizen L (1995). Neuropsychiatric and biological characteristics of X-linked MAOA deficiency syndrome: A single-intervention case study. <span style="font-style: italic;">New Trends in Experimental and Clinical Psychiatry, 11</span> (4), 99-107</span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Epigenetics+%3A+official+journal+of+the+DNA+Methylation+Society&rft_id=info%3Apmid%2F20505345&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+longitudinal+study+of+epigenetic+variation+in+twins.&rft.issn=1559-2294&rft.date=2010&rft.volume=5&rft.issue=6&rft.spage=516&rft.epage=26&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3322496%2F&rft.au=Wong+CC&rft.au=Caspi+A&rft.au=Williams+B&rft.au=Craig+IW&rft.au=Houts+R&rft.au=Ambler+A&rft.au=Moffitt+TE&rft.au=Mill+J&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CChemistry%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, Moffitt TE, & Mill J (2010). A longitudinal study of epigenetic variation in twins. <span style="font-style: italic;">Epigenetics : official journal of the DNA Methylation Society, 5</span> (6), 516-26 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20505345">20505345</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com25tag:blogger.com,1999:blog-5002675950760488813.post-20386392329741618532012-12-06T19:23:00.000-08:002012-12-08T23:22:27.141-08:00Inscrutable Voters<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
Debates about religion fascinate me, and I confess that I have always felt more inclined to the skeptical side. However, I have to respect the sheer cynical self-centeredness of Pascal’s wager. Fortunately, a new and equally pragmatic contention has arisen before my death: Republicans must convert to atheism to win the Asian vote! At least, that is my summation of the reaction to an exit poll from the recent presidential election that revealed strong support for President Obama among Asian Americans. <a href="http://isteve.blogspot.com/2012/11/did-gops-asian-vote-really-drop-9-points.html">Steve Sailer</a> questioned the validity of this exit poll, but if there is one salient lesson from this election, it would have to be that polls are always right. The concern seems to center on the belief that Republicans swung too far towards the religious right by choosing a Mormon Massachusetts governor. LDS is a strict, conservative denomination, but I implore for imperturbation for two reasons: one, Mormons are a collection of happy-go-lucky genealogy and board-game enthusiasts, and, two, Mormonism might follow the trajectory that I predict for Scientology. When Scientology becomes the largest religion, a sealed envelope will provide L Ron Hubbard’s final testament: “Gotcha! Hope you enjoyed it.” In any case, the facts on the ground hardly matter when the libertarian elite must spin a loss to thwart populists with pitchforks. Who knows? Maybe in fifty years, the Asian vote will grow significant enough to turn this strategy into a comeback.
<br><br>
My first encounter with this strategy was on the <a href="http://blogs.discovermagazine.com/gnxp/2012/11/religion-determines-politics-for-asian-americans">site</a> of temperamental science blogger Razib Khan. He did not so much lay out a plan as call everyone retarded for not seeing how obvious it is that Asians moved left as a direct consequence of losing their religion. “It’s not even in the class of a non-obvious prediction. Rather, the description screams at you.” To bolster his argument, he began swearing.
<br><br>
Soon thereafter, author Charles Murray <a href="http://www.aei-ideas.org/2012/11/why-arent-asians-republicans/">joined in</a>. “Republicans are seen by Asians—as they are by Latinos, blacks, and some large proportion of whites—as the party of Bible-thumping, anti-gay, anti-abortion creationists.” By creationism, he means the absurd, literal interpretation of the Book of Genesis, not the process by which liberals and libertarians create new rights out of nothingness. Murray might have a point. Why could not Governor Romney have paused his gay-bashing for a proper discussion of the issue of, say, taxation policy? Come to think of it, some of my best friends are Asians, and they see the Republican Party as the party of fat-cat, universal-healthcare-bashing global-warming deniers.
<br><br>
So, Murray and I seem to be on the same wavelength, but then I came across a curious statement. “Politically, a college education is a wash—in the General Social Survey, almost identical proportions of college graduates identify themselves as liberals and conservatives.” Razib contends that religious beliefs recently precipitated an attitudinal shift, and Murray describes this Asian political persuasion, while postulating that education played no role. Since Murray co-wrote The Bell Curve, perhaps he has noticed the radical improvement of <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">SAT</a> and <a href="http://theunsilencedscience.blogspot.com/2012/09/the-sat-zombie-apocalypse.html">ACT</a> scores among Asians that could easily rival other cultural shifts, and since he works for a conservative think tank, perhaps he understands that university culture tends to espouse a certain ideology of its own. Though Asians are so much the Other that social scientists still label them “other race,” as the General Social Survey (GSS) does, Asians nevertheless adapt well. Confucius said, “Speak with sincerity and honesty, be humble and respectful, and you will get along even if you live among the barbarians.” Chinese people are the Asian prototype of nice folks who blend with the scenery. They adopt Islamic last names in Muslim nations and Christian first names in the lands of the West. Some Asians fled Communism, as Murray noted, but the Chinese diaspora was considered a bastion of Marxist agitation just a generation ago in pre-independence Singapore. How hard is it to imagine that some Asians adapt to the university ideology? In addition, I have noted <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">previously</a> that high intellect is more associated with liberal values and that the SAT is an IQ test, though not by design.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-muDcrLqa-Pc/UMFUHzJhT9I/AAAAAAAAAto/zLB586_Skj0/s1600/GSS%2Bconservativism%2Beducation.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-muDcrLqa-Pc/UMFUHzJhT9I/AAAAAAAAAto/zLB586_Skj0/s400/GSS%2Bconservativism%2Beducation.png" /></a></div>
<br>
Murray is mostly correct about political ideology and education. This scale of conservativism is from one to seven with four being “moderate” and one being “extremely liberal.” Only those with graduate degrees are much more liberal than people with other education levels. However, for education to be “a wash” for Republicans, should not party identification receive the attention?
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-YrHB_-PyOXI/UMFU0FnBEyI/AAAAAAAAAt0/GFSS1DgiGGo/s1600/GSS%2Beducation%2Bparty.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://1.bp.blogspot.com/-YrHB_-PyOXI/UMFU0FnBEyI/AAAAAAAAAt0/GFSS1DgiGGo/s400/GSS%2Beducation%2Bparty.png" /></a></div>
<br>
Education is not “a wash,” but it appears to be the opposite of my expectations. The scale extends from zero to six with three being “independent” and zero being “strong Democrat.” Republicans sensibly educate themselves to the level of a bachelor’s degree, before seeking out the upper-middle class and a house in the suburbs. Benighted high school dropouts are more conservative than they are Republican probably because the uglier aspects of conservativism that Murray so detests define their values. Indeed, high school dropouts are the least likely to agree that humans evolved from prior species.
<br><br>
Now to the premise, have Asians changed their political views? Since the GSS had not been using Asian as a race in its primary race survey question, I have graphed each Asian ethnic category. For conservativism, the main trend appears to be a reduction of statistical noise as the sample size increased. Filipino-Americans had the largest sample, followed by Chinese-Americans. Japanese-Americans, with the least, had about half as many respondents as the Filipinos and Chinese. Therefore, perhaps the uptick of Chinese-American Republicanism since 2008 is a real shift to the right. The conservativism trend for this group does echo party affiliation.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-2XlXkaid2as/UMFVD41o71I/AAAAAAAAAuA/E2qk98DEiSw/s1600/GSS%2Bconservativism%2BAsian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://3.bp.blogspot.com/-2XlXkaid2as/UMFVD41o71I/AAAAAAAAAuA/E2qk98DEiSw/s400/GSS%2Bconservativism%2BAsian.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-9mz-W5r4ElA/UMFVPr3C7EI/AAAAAAAAAuM/pitI26iWmP4/s1600/GSS%2Bparty%2BAsian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-9mz-W5r4ElA/UMFVPr3C7EI/AAAAAAAAAuM/pitI26iWmP4/s400/GSS%2Bparty%2BAsian.png" /></a></div>
<br>
The evidence for an Asian political shift in the GSS is either not there or perhaps starting towards the political right, at least for the Chinese. The survey’s most recent results were 2010, but if Khan is right about religious beliefs playing the dominant role of influencing votes or if my hypothesis was right that the academic or intellectual progress was having an effect, I would have expected many years demonstrating a political shift, barring inadequacies of the survey. Surely, the study acknowledges that Asians have advanced in their educational accomplishments.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-e_WnZvKrkCg/UMFVehBkSdI/AAAAAAAAAuY/eBYpguI0vMk/s1600/GSS%2Beducation%2BAsian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-e_WnZvKrkCg/UMFVehBkSdI/AAAAAAAAAuY/eBYpguI0vMk/s400/GSS%2Beducation%2BAsian.png" /></a></div>
<br>
Yes, it does. The GSS also contains Wordsum, a ten-word vocabulary test that has some correlation with intelligence. Given the very clear evidence of improvement for Asian Americans on both the SAT and the ACT, as well as the improved education levels, one would expect a positive trend for Wordsum, too.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-TWvYDGsLlMg/UMFVtOl8gFI/AAAAAAAAAuk/3Ni5zrVNwjg/s1600/GSS%2Bwordsum%2BAsian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-TWvYDGsLlMg/UMFVtOl8gFI/AAAAAAAAAuk/3Ni5zrVNwjg/s400/GSS%2Bwordsum%2BAsian.png" /></a></div>
<br>
Unfortunately, these scores show no such evidence. Any number of explanations could address the discrepancy, while allowing for one’s personal biases to enter the equation. Those with contempt for Asians could find fault with the college entrance exams or explain away SAT scores as soulless cramming endeavors. Asian defenders can point out that the GSS has a small Asian sample size of about a thousand cumulatively over 38 years rather than the SAT’s tens of thousands each year, that a short vocabulary test does not represent general intelligence as well, or that a high proportion of Asians are not native-English speakers. The scores appear unbelievably low for Asians. For instance, in 2010 the average Indian American had a lower Wordsum score than the average African American. Indian Americans have the highest household annual income of any Asian-American ethnic group at over <a href="http://www.census.gov/newsroom/releases/archives/facts_for_features_special_editions/cb12-ff09.html">$90,000</a>, which is more than <a href="http://www.census.gov/compendia/statab/2012/tables/12s0695.pdf">twice</a> that of the average African-American family.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-UbXjZ8JxGXo/UMFV5eznAyI/AAAAAAAAAuw/oSyV3eYZt3o/s1600/GSS%2Bwordsum%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-UbXjZ8JxGXo/UMFV5eznAyI/AAAAAAAAAuw/oSyV3eYZt3o/s400/GSS%2Bwordsum%2Brace.png" /></a></div>
<br>
An ongoing debate in America concerns whether Hispanic people are a race or are mostly members of the white race, having Hispanic ethnicity. Since they are the largest minority, they might account for the bulk of those in the graph delineated as “other race,” whose scores seem flat and at about the level of African Americans. Ron Unz recently <a href="http://theunsilencedscience.blogspot.com/2012/08/the-hispanic-asian-flynn-effect.html?showComment=1352694503137">asserted</a> that the GSS shows dramatic score improvement for Mexican Americans. Apparently, the blog, <a href="http://inductivist.blogspot.ca/2008/02/flynn-effect-among-mexican-americans.html">Inductivist</a>, first noticed this.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-nnMQXlU3ygI/UMFWEHdfHbI/AAAAAAAAAu8/xdN4D5hmREY/s1600/GSS%2Bwordsum%2BHispanic%2BNA.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://3.bp.blogspot.com/-nnMQXlU3ygI/UMFWEHdfHbI/AAAAAAAAAu8/xdN4D5hmREY/s400/GSS%2Bwordsum%2BHispanic%2BNA.png" /></a></div>
<br>
Here we see Ron Unz’s “super-Flynn effect,” through which “ the Mexican-American Wordsum-IQ increased from 84.4 in the 1980s to 95.1 in the 2000s, while the rise for American whites was from 99.2 to 101.3.” Wait! I see that just prior to the super-Flynn effect an even larger super-dimming effect from 1976 to 1982 deflated Mexican-American scores in many fewer years. Likewise, Puerto Ricans’ Wordsum average fell from over five to under three in only two years! Come to think of it, Japanese Wordsum average rose six points from 1990 to 1991, (which I attribute to the release of the Violator album by Depeche Mode). The GSS sample is 4.1% Mexican-American. Mexican Americans are <a href="http://www.infoplease.com/spot/hhmcensus1.html">10.5%</a> of the US population. So, one can imagine that earlier decades of survey samples had small numbers for this group, which would explain the noise in the graph. This teaches the valuable lesson that graphs reveal truths better than carefully selected numbers.
<br><br>
If the Asian sample is not large or representative enough to properly detect shifts of voting behavior, improved intellect, or even a ballpark range of Asian intellectual abilities, I can muster little confidence in any information that I can glean for this group. However, I decided to create more detailed graphs of each Asian ethnic group for political views, Wordsum scores, and educational attainment to look for patterns. Most had none.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-Krr1-1jf0Qw/UMFWP77jy1I/AAAAAAAAAvI/Zax-WQ08HCw/s1600/GSS%2Beducation%2Bparty%2BChinese.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-Krr1-1jf0Qw/UMFWP77jy1I/AAAAAAAAAvI/Zax-WQ08HCw/s400/GSS%2Beducation%2Bparty%2BChinese.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-fL7RG512sGA/UMFWXPIN7WI/AAAAAAAAAvU/iKSrpZny-j8/s1600/GSS%2Bwordsum%2Bparty%2BChinese.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://1.bp.blogspot.com/-fL7RG512sGA/UMFWXPIN7WI/AAAAAAAAAvU/iKSrpZny-j8/s400/GSS%2Bwordsum%2Bparty%2BChinese.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-gPaZp7RLXwg/UMFWh7GCRbI/AAAAAAAAAvg/_kdpQ9Os73g/s1600/GSS%2Bwordsum%2Bideology%2BChinese.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://1.bp.blogspot.com/-gPaZp7RLXwg/UMFWh7GCRbI/AAAAAAAAAvg/_kdpQ9Os73g/s400/GSS%2Bwordsum%2Bideology%2BChinese.png" /></a></div>
<br>
Despite the apparent recent trend toward conservative politics, Chinese people do not appear to have clear links between politics, education, and scores. On the political-ideology graph, notice the unwillingness of Chinese people to be extremely anything.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-LBRzien2_RU/UMFWsQIDABI/AAAAAAAAAvs/EcwiZVS6FCI/s1600/GSS%2Beducation%2Bparty%2BIndian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-LBRzien2_RU/UMFWsQIDABI/AAAAAAAAAvs/EcwiZVS6FCI/s400/GSS%2Beducation%2Bparty%2BIndian.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-hvLlUJGE6AU/UMFW2ijJKwI/AAAAAAAAAv4/u-sCSYzukCQ/s1600/GSS%2Bwordsum%2Bparty%2BIndian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://3.bp.blogspot.com/-hvLlUJGE6AU/UMFW2ijJKwI/AAAAAAAAAv4/u-sCSYzukCQ/s400/GSS%2Bwordsum%2Bparty%2BIndian.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-YeN-xTfs2Gk/UMFXEXUYjWI/AAAAAAAAAwE/DradykVGWL4/s1600/GSS%2Bwordsum%2Bideology%2BIndian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="288" width="393" src="http://1.bp.blogspot.com/-YeN-xTfs2Gk/UMFXEXUYjWI/AAAAAAAAAwE/DradykVGWL4/s400/GSS%2Bwordsum%2Bideology%2BIndian.png" /></a></div>
<br>
For Indian Americans, I do see a consistent pattern that the most educated and intelligent have recently started becoming more conservative and Republican. Consistency between graphs does not discount issues with sample size, but the recent years for Indian Americans with graduate degrees look smoother, which could reflect an increasing sample thanks to the H1B visa program. Contrast that with the noise in a graph for Japanese people.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-ZXqsKi8KUtQ/UMFXU_U11gI/AAAAAAAAAwQ/9t8DUcxvN5w/s1600/GSS%2Beducation%2Bparty%2BJapanese.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-ZXqsKi8KUtQ/UMFXU_U11gI/AAAAAAAAAwQ/9t8DUcxvN5w/s400/GSS%2Beducation%2Bparty%2BJapanese.png" /></a></div>
<br><br>
<b><center>Coulter’s Fallacy</center></b>
<br><br>
Using Wordsum, the GSS can check the purported relationship between liberal political views and intelligence. For political ideology, the relationship presents itself. However, party affiliation appears different.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-2mIGuKDOk8Q/UMFXj6CkcJI/AAAAAAAAAwc/uzMnMqngICM/s1600/GSS%2Bwordsum%2Bideology.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://3.bp.blogspot.com/-2mIGuKDOk8Q/UMFXj6CkcJI/AAAAAAAAAwc/uzMnMqngICM/s400/GSS%2Bwordsum%2Bideology.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-121ttsXD2mA/UMFXtsodDKI/AAAAAAAAAwo/D7KHmASXBT0/s1600/GSS%2Bwordsum%2Bparty.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="289" width="393" src="http://3.bp.blogspot.com/-121ttsXD2mA/UMFXtsodDKI/AAAAAAAAAwo/D7KHmASXBT0/s400/GSS%2Bwordsum%2Bparty.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-7ZHLY9ygEKI/UMFX4phMlgI/AAAAAAAAAw0/4sny_nOgF4s/s1600/GSS%2Bwordsum%2Bparty%2Bstrong.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-7ZHLY9ygEKI/UMFX4phMlgI/AAAAAAAAAw0/4sny_nOgF4s/s400/GSS%2Bwordsum%2Bparty%2Bstrong.png" /></a></div>
<br>
These graphs do not control for any confounding variables, and race is an obvious potential confounder. However, the associations also appear when the graphs are limited to white people, except for strong party identification in recent years.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-Vcqz_uWne8Y/UMFYFYtjBTI/AAAAAAAAAxA/EzSwEPfL1UU/s1600/GSS%2Bwordsum%2Bideology%2Bwhite.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-Vcqz_uWne8Y/UMFYFYtjBTI/AAAAAAAAAxA/EzSwEPfL1UU/s400/GSS%2Bwordsum%2Bideology%2Bwhite.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-b_2AyWRF3WM/UMFYRnL4cjI/AAAAAAAAAxM/kUev3xEfzCw/s1600/GSS%2Bwordsum%2Bparty%2Bwhite.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="288" width="393" src="http://2.bp.blogspot.com/-b_2AyWRF3WM/UMFYRnL4cjI/AAAAAAAAAxM/kUev3xEfzCw/s400/GSS%2Bwordsum%2Bparty%2Bwhite.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-RXWddwWKdGQ/UMFYa_0RXiI/AAAAAAAAAxY/TrAstcNvK50/s1600/GSS%2Bwordsum%2Bparty%2Bstrong%2Bwhite.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-RXWddwWKdGQ/UMFYa_0RXiI/AAAAAAAAAxY/TrAstcNvK50/s400/GSS%2Bwordsum%2Bparty%2Bstrong%2Bwhite.png" /></a></div>
<br>
Republicans tend to be smarter than Democrats, but liberals tend to be smarter than conservatives. Republican strategists should take note of the obvious strategy to appeal to the stupid vote. Maybe they already have. On the contrary, the party has been focusing on reaching out to minority voters, and the following graphs give some indication of the results:
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-K0HByOs_0vE/UMFYoodM5gI/AAAAAAAAAxk/QC6m6Qohs0s/s1600/GSS%2Bparty%2Brace%2Bstrong.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-K0HByOs_0vE/UMFYoodM5gI/AAAAAAAAAxk/QC6m6Qohs0s/s400/GSS%2Bparty%2Brace%2Bstrong.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-_seLFCTjRjQ/UMFY0A-eYxI/AAAAAAAAAxw/ewjSXXH6jXE/s1600/GSS%2Bideology%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-_seLFCTjRjQ/UMFY0A-eYxI/AAAAAAAAAxw/ewjSXXH6jXE/s400/GSS%2Bideology%2Brace.png" /></a></div>
<br>
The graphs are distorted by the designation of “other race” as being worth three points, whereas African Americans are worth two points. (At least it is not three-fifths.)
<br><br>
Minorities should be joining the GOP by the boatload, considering effusive praise like this from author Ann Coulter:
<blockquote>That’s why our blacks are so much better than their blacks. To become a black Republican, you don’t just roll into it. You’re not going with the flow. You have fought against probably your family members, probably your neighbors. You have thought everything out, and that’s why we have very impressive blacks in our party.</blockquote>
According to the GSS, their blacks are actually better than her blacks. Perhaps that is changing for those who are the strongest Republicans, but the sample size for that group is likely to be very, very small.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-yKVGjeeiktQ/UMFZJYK2NrI/AAAAAAAAAx8/FKNJSuwKQVc/s1600/GSS%2Bwordsum%2Bideology%2Bblack.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://3.bp.blogspot.com/-yKVGjeeiktQ/UMFZJYK2NrI/AAAAAAAAAx8/FKNJSuwKQVc/s400/GSS%2Bwordsum%2Bideology%2Bblack.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-9cF1IckKE2U/UMFZUOEJ4TI/AAAAAAAAAyI/Ay1qXpa3vnw/s1600/GSS%2Bwordsum%2Bparty%2Bblack.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="288" width="393" src="http://1.bp.blogspot.com/-9cF1IckKE2U/UMFZUOEJ4TI/AAAAAAAAAyI/Ay1qXpa3vnw/s400/GSS%2Bwordsum%2Bparty%2Bblack.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-aV_ahx-TiJg/UMFZeZEPLjI/AAAAAAAAAyU/bNJL9zWjLYg/s1600/GSS%2Bwordsum%2Bparty%2Bstrong%2Bblack.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-aV_ahx-TiJg/UMFZeZEPLjI/AAAAAAAAAyU/bNJL9zWjLYg/s400/GSS%2Bwordsum%2Bparty%2Bstrong%2Bblack.png" /></a></div>
<br>
What Republicans really hunger for is the Hispanic vote, so I present this very important graph about Mexican Americans:
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-JCupTyLBTIA/UMFZrUZxLpI/AAAAAAAAAyg/5QjHNcqsbWg/s1600/GSS%2Bwordsum%2Bparty%2BMexican.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://2.bp.blogspot.com/-JCupTyLBTIA/UMFZrUZxLpI/AAAAAAAAAyg/5QjHNcqsbWg/s400/GSS%2Bwordsum%2Bparty%2BMexican.png" /></a></div>
<br>
At first, a pattern might not jump out, but if one stares long enough, everything makes sense. Then, if one closes one’s eyes, a photo negative of the graph will appear.
<br><br>
Republicans commit a basic error when envisioning Hispanic Americans or African Americans as “natural conservatives” in that they conflate conservativism and Republicanism. Minorities tend to identify with conservativism much more than the Republican Party.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-EL8C2RsdL6k/UMFZ4tpLv5I/AAAAAAAAAys/MFwD0fHhj3c/s1600/GSS%2Bparty%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://1.bp.blogspot.com/-EL8C2RsdL6k/UMFZ4tpLv5I/AAAAAAAAAys/MFwD0fHhj3c/s400/GSS%2Bparty%2Brace.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-crtowBnnoPc/UMFaB7c1HYI/AAAAAAAAAy4/z5nZtYgZzcw/s1600/GSS%2Bconservativism%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="290" width="393" src="http://4.bp.blogspot.com/-crtowBnnoPc/UMFaB7c1HYI/AAAAAAAAAy4/z5nZtYgZzcw/s400/GSS%2Bconservativism%2Brace.png" /></a></div>
<br>
For some, the vagueness or emptiness of the term conservative might allow for posturing about values or lifestyle. Still others actually embody the vulgar close-minded thinking and parochialism that puts off Murray. It helps to consider how some socially conservative beliefs are natural reactions to some unhealthy societal changes, and values that sustain a family contrast with the blandness of haggling over the budgetary pie for already well-off interests. Confucianism serves as a fine example of an Asian social philosophy that contrasts with the libertarian, Randian individualism. Murray is right to defend science and reason, but the best strategy to win the votes of Asians and others is an intelligent populism.
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com2tag:blogger.com,1999:blog-5002675950760488813.post-33150280500201353982012-11-01T11:19:00.001-07:002012-11-01T11:19:44.955-07:00Arthur Jensen & JP Rushton<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
As many regular readers probably know, two controversial psychometricians, Arthur Jensen and Jean Philippe Rushton, recently died. I had collected nearly every document that the two had published with the intention of widely sharing. Unfortunately, a catastrophic hard drive failure erased most of it. For now, here are books by them and a televised debate featuring Rushton.<br><br>
<a href="https://docs.google.com/open?id=0B4NGOBcoYImfVmRWTWJIRzlsems">Arthur Jensen - The g Factor</a><br><br>
<a href="https://docs.google.com/open?id=0B4NGOBcoYImfZzc4Q2F3V0U4UmM">JP Rushton - Race, Evolution, & Behavior (Unabridged)</a>
<br><br><br>
<iframe width="415" height="259" src="http://www.youtube.com/embed/i9FGHtfnYWY" frameborder="0" allowfullscreen></iframe>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com9tag:blogger.com,1999:blog-5002675950760488813.post-26294539991298336442012-09-29T03:29:00.001-07:002012-09-29T04:09:50.460-07:00The SAT Zombie Apocalypse<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-4FN9vpf3FJg/UGa-8bRbzWI/AAAAAAAAAnQ/fqzr3xqFRsg/s1600/zombiesahead.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="226" width="400" src="http://1.bp.blogspot.com/-4FN9vpf3FJg/UGa-8bRbzWI/AAAAAAAAAnQ/fqzr3xqFRsg/s400/zombiesahead.jpg" /></a></div>
<br>
It’s the most wonderful time of the year: Halloween in an election year! ‘Tis the season for a bevy of fright flicks designed to put your girlfriend in your arms and a bad taste in your mouth. Granted, high-art horror, like Antichrist, Pan’s Labyrinth, and The Passion of the Christ, usually do not enter this season’s strategic lineup, but it is good to know that today’s zombies have taken up running because, really, who wants to see a bunch of fat zombies?
<br><br>
This year is special because a multitude of new Americans might very well bring to fruition one-party democracy, much like 20th-century Mexico. Pundits are lauding the Hispanic-American population boom, as if it were an accomplishment akin to putting a flag on the moon or Iwo Jima. Meanwhile, a few bitter white men are expected to vote for the Republican presidential candidate because they have no pity for the new majority.
<br><br>
Halloween season also brings scary stories about falling SAT scores. At Breitbart.com, Ben Shapiro <a href="http://www.breitbart.com/Big-Government/2012/09/24/American-students-hit-record-low-SATs">lamented</a> that “2012’s high school seniors have the worst SAT reading scores since 1972; they scored 486 on reading, out of a possible 800.” The Washington Post <a href="http://www.washingtonpost.com/local/education/sat-reading-scores-hit-a-four-decade-low/2012/09/24/7ec9cb1e-0643-11e2-afff-d6c7f20a83bf_story_1.html">reported</a> that the scores “reached a four-decade low.” The good news and the bad news are that the elite media are reporting falsehoods, again. Shapiro can take a deep breath because his copy-and-paste error (his <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">Pinker error</a>?) dropped ten points from the actual reading score. However, being too lazy to investigate the scores prior to 1972, the earliest year shown in the annual SAT report, gives the false impression that verbal scores were ever worse than now. In fact, reading scores before Woodstock stood far above the present.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-GTSvBrfyum4/UGa9xRSuhFI/AAAAAAAAAnE/AfISAacwXfs/s1600/sat%2Ball%2Brecentered.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://4.bp.blogspot.com/-GTSvBrfyum4/UGa9xRSuhFI/AAAAAAAAAnE/AfISAacwXfs/s400/sat%2Ball%2Brecentered.png" /></a></div>
<br>
A single year is unlikely to provide a momentous pivot in any of the multiple-decade trends, many of which, it seems, only my readers are aware. It is worth mentioning that the male mathematics advantage slightly grew despite the fact that the upper score limit held down an increased proportion of men relative to women.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-jjdjjl8DytI/UGa_XED7ItI/AAAAAAAAAnc/DNiqh0dJIe8/s1600/sat%2Bmf%2Brecentered.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://4.bp.blogspot.com/-jjdjjl8DytI/UGa_XED7ItI/AAAAAAAAAnc/DNiqh0dJIe8/s400/sat%2Bmf%2Brecentered.png" /></a></div>
<center> <a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmfmdist-1.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmfmdist-1.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<br>
Here are some updated graphs:
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-DpGIrHWYJUQ/UGa_m1fdCbI/AAAAAAAAAno/WQ5m061PP3Q/s1600/sat%2Brace%2Bparticipation.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-DpGIrHWYJUQ/UGa_m1fdCbI/AAAAAAAAAno/WQ5m061PP3Q/s400/sat%2Brace%2Bparticipation.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-65Y_sTtprfs/UGa_9pqywzI/AAAAAAAAAn0/4Rr5IkT6gdo/s1600/sat%2Brace%2Braw%2Bverbal.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-65Y_sTtprfs/UGa_9pqywzI/AAAAAAAAAn0/4Rr5IkT6gdo/s400/sat%2Brace%2Braw%2Bverbal.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-86BfoNJxlio/UGbAGlQWPrI/AAAAAAAAAoA/-aDVHtON6gU/s1600/sat%2Brace%2Braw%2Bmath.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-86BfoNJxlio/UGbAGlQWPrI/AAAAAAAAAoA/-aDVHtON6gU/s400/sat%2Brace%2Braw%2Bmath.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-S2Ead9xztNM/UGbAP9d2pxI/AAAAAAAAAoM/R3Aj2Ox2MIo/s1600/sat%2Bblack.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://2.bp.blogspot.com/-S2Ead9xztNM/UGbAP9d2pxI/AAAAAAAAAoM/R3Aj2Ox2MIo/s400/sat%2Bblack.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-bXSbBrLqZH8/UGbAZwepXXI/AAAAAAAAAoY/F4BV_EnvKX8/s1600/sat%2Bhispanic.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://1.bp.blogspot.com/-bXSbBrLqZH8/UGbAZwepXXI/AAAAAAAAAoY/F4BV_EnvKX8/s400/sat%2Bhispanic.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-G5lCNjci9_Q/UGbAih2EkII/AAAAAAAAAok/IJ1AiN_q3fQ/s1600/sat%2Bnative.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://3.bp.blogspot.com/-G5lCNjci9_Q/UGbAih2EkII/AAAAAAAAAok/IJ1AiN_q3fQ/s400/sat%2Bnative.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/--L8HbjveuE4/UGbAq7p2Z0I/AAAAAAAAAow/Kt1VugvND5I/s1600/sat%2Basian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://2.bp.blogspot.com/--L8HbjveuE4/UGbAq7p2Z0I/AAAAAAAAAow/Kt1VugvND5I/s400/sat%2Basian.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-kYQP4ff7atU/UGbAzFED4dI/AAAAAAAAAo8/7m-RBgDxP0g/s1600/sat%2Bgrades%2Bverbal.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="393" src="http://4.bp.blogspot.com/-kYQP4ff7atU/UGbAzFED4dI/AAAAAAAAAo8/7m-RBgDxP0g/s400/sat%2Bgrades%2Bverbal.png" /></a></div>
<br>
SAT examinees mirror the demographic changes in America, but racial score gaps (not counting Asians) declare their constancy. With its gargantuan participation levels of highly engaged students, the SAT offers relatively noise-free output and immunity to the growing <a href="http://www.sas.upenn.edu/~duckwort/images/Role%20of%20test%20motivation%20in%20intelligence%20testing.full.pdf">criticism</a> of differential motivation confounding IQ tests that lack incentives. Still, Alexander Abad-Santos, at the Atlantic’s blog, <a href="http://www.theatlanticwire.com/national/2012/09/sat-reading-scores-are-lowest-theyve-been-40-years/57208/">promised</a> that the “sweeping assumption that minority test-takers are naturally worse than their non-minority counterparts at the ‘reading’ section doesn’t tell the entire story.” He read this assumption into words that the Post apparently removed from their article that “the declining national reading averages may in part reflect the ever widening pool of students who take the SAT…. Nearly half were minorities….” Abad-Santos seems unmoved by the new numbers. Perhaps the data require a fresh style of presentation—something that fits the spirit of the season. I think back to how the Centers for Disease Control produced an <a href="http://theunsilencedscience.blogspot.com/2011/08/politically-incorrect-guide-to-weight.html">animated graph</a> that defined the obesity epidemic as we know it. America has diversified but not with uniformity. Maybe this calls for a map that illustrates the score changes like an infectious outbreak—or a zombie apocalypse!
<br><br>
Forget the numbers. This night of the testing dread is in full color. White (and light pink) represent superior scores. Red is mid-range. Yellow and the more yellow shades of orange mark the worst states (and Washington, DC, the gold star).
<br><br>
<center><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satcrmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satcrmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satwmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satwmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://4.bp.blogspot.com/-FS6IHT5xhsQ/UGbBGZpGnuI/AAAAAAAAApI/8-tP8ARkpI8/s1600/sat%2Bmap%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="75" src="http://4.bp.blogspot.com/-FS6IHT5xhsQ/UGbBGZpGnuI/AAAAAAAAApI/8-tP8ARkpI8/s400/sat%2Bmap%2Blegend.png" /></a></div>
<br>
Now, compare those results with this map of the percentage of white and Asian SAT takers out of those who identified their race.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://3.bp.blogspot.com/-UStMdyxPfJM/UGbBoqGUG4I/AAAAAAAAApU/N5CkbQdi2rA/s1600/sat%2Bmap%2Baw%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="76" src="http://3.bp.blogspot.com/-UStMdyxPfJM/UGbBoqGUG4I/AAAAAAAAApU/N5CkbQdi2rA/s320/sat%2Bmap%2Baw%2Blegend.png" /></a></div>
<br>
State SAT scores do reflect demographic change, but also test participation. Maine is among the whitest states, but its SAT scores fell when it greatly increased the proportion of students who take the test. Delaware did the same. I have expressed some doubts about the effects on scores of participation rates for various groups, but racial and gender groups cannot achieve total participation in a test, like states can. That phenomenon pushes students to take part regardless of their ability or desire to attend college. Midwestern states seem to fare best, but those states emphasize the ACT rather than the SAT. In a state like Illinois, which currently has 100% ACT participation and 5% SAT participation among high-school graduates, a student who takes both tests probably outperforms most of his or her classmates. That student may want to take the SAT to apply to a more prestigious university outside the region.
<br><br>
According to the Washington Post, “questions about whether the SAT is biased in favor of middle-class and wealthy students have led many colleges and universities to use other gauges or to accept an alternative exam, the ACT, which edged out the SAT in 2012 for the first time…” With regard to racial groups, ACT scores act just like those of the SAT.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-4shn9p19EDQ/UGbQtgu7RWI/AAAAAAAAAsU/Eds1puUwtNg/s1600/act%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://2.bp.blogspot.com/-4shn9p19EDQ/UGbQtgu7RWI/AAAAAAAAAsU/Eds1puUwtNg/s400/act%2Brace.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-tmvba08XErw/UGbECDhimYI/AAAAAAAAAps/BFL-DhQU6Iw/s1600/act%2Brace%2Be.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-tmvba08XErw/UGbECDhimYI/AAAAAAAAAps/BFL-DhQU6Iw/s400/act%2Brace%2Be.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-DNSAhvRvIck/UGbEMsKoi2I/AAAAAAAAAp4/Ls_jieY83H8/s1600/act%2Brace%2Br.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-DNSAhvRvIck/UGbEMsKoi2I/AAAAAAAAAp4/Ls_jieY83H8/s400/act%2Brace%2Br.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-FxjnUmPRLPs/UGbET571DHI/AAAAAAAAAqE/dAIZ7mHLydU/s1600/act%2Brace%2Bw.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-FxjnUmPRLPs/UGbET571DHI/AAAAAAAAAqE/dAIZ7mHLydU/s400/act%2Brace%2Bw.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-jHt9KZaNXew/UGbEb5kUOEI/AAAAAAAAAqQ/WwmShGyUo7g/s1600/act%2Brace%2Bm.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://4.bp.blogspot.com/-jHt9KZaNXew/UGbEb5kUOEI/AAAAAAAAAqQ/WwmShGyUo7g/s400/act%2Brace%2Bm.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-BExZD_2e0q8/UGbEjx3HvFI/AAAAAAAAAqc/xH54Fo5mLes/s1600/act%2Brace%2Bs.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-BExZD_2e0q8/UGbEjx3HvFI/AAAAAAAAAqc/xH54Fo5mLes/s400/act%2Brace%2Bs.png" /></a></div>
<br>
The ACT even had the same surge of people who would not respond to the racial identity question, except ACT non-responders peaked in 2007 instead of 2003.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-2QmvxJAShC8/UGbEwbNj7FI/AAAAAAAAAqo/iylfcH267U0/s1600/act%2Brace%2Bparticipation.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-2QmvxJAShC8/UGbEwbNj7FI/AAAAAAAAAqo/iylfcH267U0/s400/act%2Brace%2Bparticipation.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-RrlBkuNAIvY/UGbE31H3bZI/AAAAAAAAAq0/snWKtGRyqss/s1600/act%2Brace%2Bparticipation%2Bpercent.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://3.bp.blogspot.com/-RrlBkuNAIvY/UGbE31H3bZI/AAAAAAAAAq0/snWKtGRyqss/s400/act%2Brace%2Bparticipation%2Bpercent.png" /></a></div>
<br>
Over the years, African Americans, Hispanic Americans, and Native Americans have fallen further behind whites on the ACT.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-mXjyJy_ruas/UGbFDFWcSyI/AAAAAAAAArA/eaLZylsoYQs/s1600/act%2Brace%2Bgaps.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="258" width="393" src="http://1.bp.blogspot.com/-mXjyJy_ruas/UGbFDFWcSyI/AAAAAAAAArA/eaLZylsoYQs/s400/act%2Brace%2Bgaps.png" /></a></div>
<br>
The map of ACT scores does show a developing North-South divide somewhat like the demographic map. However, it mostly looks red because the District of Columbia used to be such an outlier. Likewise, certain New England states with low ACT participation served as outliers at the other end.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=actmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/actmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://1.bp.blogspot.com/-VRE1_0s2aqM/UGbF5CycLLI/AAAAAAAAArY/mdqDDQuSt5Q/s1600/act%2Bmap%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="80" src="http://1.bp.blogspot.com/-VRE1_0s2aqM/UGbF5CycLLI/AAAAAAAAArY/mdqDDQuSt5Q/s320/act%2Bmap%2Blegend.png" /></a></div>
<br>
To better account for state test preferences, I created a composite SAT-ACT map. I designed a crude linear formula based on a conversion table to convert ACT scores to SAT equivalents. Then I weighted each of the two tests according to the relative participation for each state. In accordance with the conversion table, I did not consider writing scores.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sat-actmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-actmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
Even though I kept the same color scheme as the other SAT maps, the white and pink disappeared because the map reduces the influence of overachievers who take both tests when their state has a clear preference. A worsening North-South divide clearly presents itself.
<br><br>
I consider this the best and most reliable map, but participation issues limit even it. I controlled for the relative participation between the tests, but not for the overall participation rates. The states that moved to total or near total participation on one of the tests were Colorado, Delaware, Illinois, Kentucky, Louisiana, Maine, Michigan, Mississippi, North Dakota, Tennessee, Utah, and Wyoming. Only Delaware and Maine have chosen to go with the SAT. By contrast, Arizona sticks out for its extremely low participation on <i>both</i> tests. Clearly, Arizona has an unfair score advantage, and Iowa and California also do not have especially high testing rates, either. I decided to program a map that punishes the scores of states in which the combined participation percentages of both tests is less than 100% by a factor proportional to its deficit below 100%. The punishment is somewhat arbitrary and probably quite excessive, but at least it shows that the American Southwest has inflated scores. I consider this neither to be a “score” map nor truly “controlled,” so I reset the color ranges.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sat-actconmap.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-actconmap.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://2.bp.blogspot.com/-lsBMg8di8Rc/UGbGwocjvII/AAAAAAAAArk/ZK-mU0SKUKM/s1600/sat-act%2Bmap%2Bcon%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="72" src="http://2.bp.blogspot.com/-lsBMg8di8Rc/UGbGwocjvII/AAAAAAAAArk/ZK-mU0SKUKM/s320/sat-act%2Bmap%2Bcon%2Blegend.png" /></a></div>
<br>
For clarity, here is a map just of the addition of the participation percentages for both tests without regard to scores. States like Florida are seeing high rates of participation on both tests because they have not settled upon a single standard.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sat-actparticipation.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sat-actparticipation.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
<div class="separator" style="clear: both; text-align: left;">
<a href="http://1.bp.blogspot.com/-xV6yKg6A5YM/UGbHDHnIxpI/AAAAAAAAArw/2Do4Kx5B1PA/s1600/sat-act%2Bparticipation%2Blegend.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="320" width="82" src="http://1.bp.blogspot.com/-xV6yKg6A5YM/UGbHDHnIxpI/AAAAAAAAArw/2Do4Kx5B1PA/s320/sat-act%2Bparticipation%2Blegend.png" /></a></div>
<br>
State participation changes confound state scores in multiple ways, but a movement towards full participation on the ACT could settle this issue. States increasingly seem to favor the ACT over the SAT, which I suspect is partly due to the false impression that ACT scores are less racist. Demographic changes correspond to falling test scores, and one can see it, at least in terms of a North-South divide, on these maps. America is bearing a zombie apocalypse, which is sweeping the nation and coming for our brains.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft_id=info%3Apmid%2F21518867&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Role+of+test+motivation+in+intelligence+testing.&rft.issn=0027-8424&rft.date=2011&rft.volume=108&rft.issue=19&rft.spage=7716&rft.epage=20&rft.artnum=http%3A%2F%2Fwww.sas.upenn.edu%2F%7Educkwort%2Fimages%2FRole%2520of%2520test%2520motivation%2520in%2520intelligence%2520testing.full.pdf&rft.au=Duckworth+AL&rft.au=Quinn+PD&rft.au=Lynam+DR&rft.au=Loeber+R&rft.au=Stouthamer-Loeber+M&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Duckworth AL, Quinn PD, Lynam DR, Loeber R, & Stouthamer-Loeber M (2011). Role of test motivation in intelligence testing. <span style="font-style: italic;">Proceedings of the National Academy of Sciences of the United States of America, 108</span> (19), 7716-20 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21518867">21518867</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com13tag:blogger.com,1999:blog-5002675950760488813.post-32904758339062057452012-09-10T03:54:00.000-07:002012-09-10T03:54:37.062-07:00Genes Dealt Made Asians Svelte<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
Another <a href="http://www.enquete-debat.fr/archives/la-television-norvegienne-ose-aborder-la-difficile-question-de-linegalite-43900">documentary</a> has surfaced that leans on the apprehension or anticipation that genetics will confirm the intellectual advantages of certain racial groups over others. Realistically, I doubt Nature or The New York Times will break such a story. The media generally does not even address racial differences in the warrior gene. Why should anyone expect a mainstream science reporter to painstakingly calculate the cumulative effect of who-knows-how-many single nucleotide polymorphisms (SNPs) potentially to prove right Southern bigots? Nevertheless, curiosity abhors a pat tune, and I think questions of race naturally meld into one of the most basic existential questions: What does it mean to be human? In general, examinations of the genetics of obesity and intelligence would complement each other not only because both traits have complex genetic architectures, but also because obesity is a less controversial subject for many than intelligence, especially when these subjects intersect with race. So, an approach that gains acceptance for less contested phenotypes will streamline an IQ juggernaut. Since stepping on a scale is far simpler than measuring intelligence, temperament, personality, or behavior, that genome-wide association studies (GWAS) for body-mass index (BMI) are further along does not surprise.
<br><br>
So far, GWAS have <a href="http://ukpmc.ac.uk/articles/PMC3014648/pdf/nihms237282.pdf">identified</a> 32 genetic loci for obesity. Different studies have used different SNPs to represent these loci. In order to compare diverse ethnic populations at these loci, I entered each SNP into the HapMap online database. Then, I selected the SNP from each locus for which HapMap provides the most information. HapMap has very thorough data for Northern Europeans, the Yoruba of Africa, Chinese people, and Japanese people. By multiplying the respective effect sizes of each SNP by each group’s allele frequency and adding the results for each group, I could graph a genetic index of obesity for each of those four groups. I also added the data from those four groups to data from less represented ethnic groups to create the following broader racial or ethnic designations. “Black” refers to the Yoruba, the Luhya, the Maasai, and African Americans. “Whites” are Northern Europeans and Italians. “East Asians” are Chinese and Japanese people, and the group “Asians” also adds people from India. The resulting graph suggests that Asians have a lower genetic risk for obesity.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-XqsxvFZajcw/UE2ne3NG1YI/AAAAAAAAAjU/v6DC7laHxzA/s1600/graph%2Bobesity%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="368" width="393" src="http://1.bp.blogspot.com/-XqsxvFZajcw/UE2ne3NG1YI/AAAAAAAAAjU/v6DC7laHxzA/s400/graph%2Bobesity%2Brace.png" /></a></div>
<br>
For a more detailed picture of the full range of ethnic groups, I removed 7 of the 32 loci that had more limited data. This graph still seems to show less obesity propensity for Asians. In fact, graphs like this can serve as counterpoints to the social deconstruction of race, since ethnic groups within a continental racial group do tend to cluster together in allele frequencies. This fits with recent population genetics studies. For instance, a <a href="http://www.genetics.org/gca?submit=Get+All+Checked+Abstracts&gca=genetics%3Bgenetics.112.144071v1">new study</a> of natural selection in African populations found that “positive selection does not appear to have substantially shaped present-day allele frequency differences among the African populations in our dataset…. Our results agree with Coop <i>et al</i> (2009) and Pickrell <i>et al</i> (2009), who found that selective sweep signals tend to cluster by broad geographic and continental regions…”
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-ij5TUZLwg4A/UE2ohrkrLZI/AAAAAAAAAjg/ixF4dhFABw4/s1600/graph%2Bobesity%2Bethnicity.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="240" width="393" src="http://1.bp.blogspot.com/-ij5TUZLwg4A/UE2ohrkrLZI/AAAAAAAAAjg/ixF4dhFABw4/s400/graph%2Bobesity%2Bethnicity.png" /></a></div>
<br>
Perhaps the similarity of genetic risk for white and black people should not surprise. <a href="http://www.foodpolitics.com/wp-content/uploads/ObesityRates_JAMA_12.pdf">Currently</a>, in the United States, adult black women have nearly twice the prevalence of obesity as adult white women, but for the men no statistically significant difference exists. Therefore, I suspect that the unfortunate obesity epidemic among African-American women is a cultural phenomenon, rather than genetic destiny.
<br><br>
A relevant criticism of my genetic racial comparisons is that the GWAS that identified these genes were conducted in Europeans. Moreover, Chinese people have allele frequencies of zero for 5 of the loci, and Japanese people have allele frequencies of zero for those 5 and one more. If those loci would not be identified in Chinese or Japanese obesity GWAS, one could certainly imagine that those GWAS could identify obesity-causing alleles which whites or Africans lack. Therefore, I recreated the first graph minus those 6 loci to attempt a more fair comparison.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-prpOAgJgT1E/UE2oxRvSgvI/AAAAAAAAAjs/Z4U0KRqTVvA/s1600/graph%2Bobesity%2Bmod.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="368" width="393" src="http://3.bp.blogspot.com/-prpOAgJgT1E/UE2oxRvSgvI/AAAAAAAAAjs/Z4U0KRqTVvA/s400/graph%2Bobesity%2Bmod.png" /></a></div>
<br>
The racial genetic risk gap is lessened but is still very much present.
<br><br>
A different set of five loci (four for the detailed ethnicity breakdown graph) affect extreme obesity risk, with extreme obesity defined as an adult BMI of greater than or equal to 40 or a childhood BMI greater than or equal to 99 percent of the age and gender cohort. In the case of extreme obesity, Asians appear to be at greater risk than whites. Japanese people, in particular, apparently possess a sumo-sized extreme obesity risk, despite having low overall genetic obesity risk.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-Rgvw62WezI4/UE2o9mld_XI/AAAAAAAAAj4/34cV8TZecDs/s1600/graph%2Bextreme%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="368" width="393" src="http://3.bp.blogspot.com/-Rgvw62WezI4/UE2o9mld_XI/AAAAAAAAAj4/34cV8TZecDs/s400/graph%2Bextreme%2Brace.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-mgNHLL1G2qo/UE2pIip6S4I/AAAAAAAAAkE/EHY9qHHFmS8/s1600/graph%2Bextreme%2Bethnicity.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="240" width="393" src="http://4.bp.blogspot.com/-mgNHLL1G2qo/UE2pIip6S4I/AAAAAAAAAkE/EHY9qHHFmS8/s400/graph%2Bextreme%2Bethnicity.png" /></a></div>
<br>
Three SNPs affect body fat composition, as measured by bioimpedance analysis and dual energy X-ray absorptiometry. One of the alleles is a member of the 32 obesity loci. Another was found to affect body fat percentage in Europeans but not Indians. The third, IRS1, has an allele that raises body fat but paradoxically lowers type 2 diabetes risk in men, seemingly by shifting fat storage to the layer just beneath the skin where it is less harmful. Asians are much less likely to have that allele, which could help explain why <a href="http://www.nature.com/oby/journal/vaop/ncurrent/full/oby2012152a.html">studies</a> are finding that nonoverweight Chinese people have high rates of metabolic abnormalities more commonly associated with obesity. Specifically, one-third of nonoverweight Chinese people have at least one metabolic risk factor.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-E1f9iYgSd0Y/UE2pUXbeCTI/AAAAAAAAAkQ/slnaA4mgieI/s1600/graph%2Bfat%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="366" width="393" src="http://3.bp.blogspot.com/-E1f9iYgSd0Y/UE2pUXbeCTI/AAAAAAAAAkQ/slnaA4mgieI/s400/graph%2Bfat%2Brace.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-zymuweCsX0c/UE2pesge1GI/AAAAAAAAAkc/KRtiDy8sRtQ/s1600/graph%2Bfat%2Bethnicity.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="239" width="393" src="http://4.bp.blogspot.com/-zymuweCsX0c/UE2pesge1GI/AAAAAAAAAkc/KRtiDy8sRtQ/s400/graph%2Bfat%2Bethnicity.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-L-Re5sxsfu8/UE2pqBotuPI/AAAAAAAAAko/MEnQL9RTJag/s1600/graph%2Birs1.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="366" width="393" src="http://1.bp.blogspot.com/-L-Re5sxsfu8/UE2pqBotuPI/AAAAAAAAAko/MEnQL9RTJag/s400/graph%2Birs1.png" /></a></div>
<br>
GWAS have <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3000924/">found</a> fourteen SNPs so far for waist-to-hip ratio after controlling for BMI, age, and sex. The detailed ethnicity breakdown bar graph includes eleven of them. These graphs do not show strong racial or ethnic differences, but perhaps these alleles further contribute to unhealthy fat distribution in Asians.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-SBbsXgq3hXs/UE2p2dyF-WI/AAAAAAAAAk0/rBB3IAkqCaY/s1600/graph%2Bwth%2Brace.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="368" width="393" src="http://2.bp.blogspot.com/-SBbsXgq3hXs/UE2p2dyF-WI/AAAAAAAAAk0/rBB3IAkqCaY/s400/graph%2Bwth%2Brace.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-dgiK9q36kyc/UE2qBdov3pI/AAAAAAAAAlA/XxBzJauRP50/s1600/graph%2Bwth%2Bethnicity.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="240" width="393" src="http://4.bp.blogspot.com/-dgiK9q36kyc/UE2qBdov3pI/AAAAAAAAAlA/XxBzJauRP50/s400/graph%2Bwth%2Bethnicity.png" /></a></div>
<br>
The overriding concern that troubles this form of analysis is that the totality of the molecular genetics of any of these phenotypes is still so poorly detailed that the known loci account for almost none of the genetic heritability determined by twins studies and the like. The obesity GWAS used a quarter of a million subjects to lay out just 2 to 4 percent of the estimated heritability. The GWAS for waist-to-hip ratio used 190,000 subjects to account for 2 to 5 percent of the estimated heritability. The three body-fat SNPs using 76,000 subjects explain a mere 0.25% of body fat composition heritability. Despite such low levels of explained variance, this genetic data accurately samples the whole of which it is part. <a href="http://archpedi.jamanetwork.com/article.aspx?articleid=1171937">Belsky <i>et al</i></a> recently demonstrated this to be the case, using the same method of calculating an obesity genetic risk score applied to individuals rather than groups. In fact, the effect size of the genetic risk index correlated only slightly less than familial risk based on each individual’s parents’ BMI, and their genetic risk index did not even include 3 of the 32 loci. Also, as the graphs below reveal, the genetic risk was not merely a subset of the parental risk. The two risk scores (listed as high or low for being one standard deviation above or below the mean, respectively) could not completely match the predictive quality of a risk based on the two in combination.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-Q4X97XUiyzs/UE2qNTHLFPI/AAAAAAAAAlM/TdfNU2Or1RQ/s1600/obesity%2Bbelsky%2Bgrs%2Bbmi.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="285" width="390" src="http://4.bp.blogspot.com/-Q4X97XUiyzs/UE2qNTHLFPI/AAAAAAAAAlM/TdfNU2Or1RQ/s400/obesity%2Bbelsky%2Bgrs%2Bbmi.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-KMcNwZ8CTBs/UE2qanQh_II/AAAAAAAAAlY/b8BrqOHcwB0/s1600/obesity%2Bbelsky%2Bgrs%2Bbar.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="285" width="390" src="http://3.bp.blogspot.com/-KMcNwZ8CTBs/UE2qanQh_II/AAAAAAAAAlY/b8BrqOHcwB0/s400/obesity%2Bbelsky%2Bgrs%2Bbar.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-zj7cBhjn2AI/UE2ql7q_BHI/AAAAAAAAAlk/uJd9PIhepfQ/s1600/obesity%2Bbelsky%2Bgrs%2Bfamilial.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="400" width="297" src="http://2.bp.blogspot.com/-zj7cBhjn2AI/UE2ql7q_BHI/AAAAAAAAAlk/uJd9PIhepfQ/s400/obesity%2Bbelsky%2Bgrs%2Bfamilial.png" /></a></div>
<br>
Presumably individual and population differences in important characteristics have some comprehensible root cause or causes. Regardless of the precise contributions to polygenic trait evolution from natural selection, the Founder effect, deleterious mutations, and so on, the order of allele identification is sufficiently independent of these forces, and the effect sizes are sufficiently distributed so as to make, I predict, nearly any genetic index a representative sample. If I am wrong, then at least I have started a scalable database as additional loci trickle in.
<br><br>
<center><b>The Latest Intelligence on Intelligence</b></center>
<br><br>
The concern about applicability to non-Europeans has greater salience, considering recent findings about rare SNPs. These GWAS only consider the independent effects of common SNPs, not the effects of rare SNPs or the “non-additive” genetic effects of the interactions between genes (called epistasis). A pair of studies recently addressed rare SNPs in the journal Science. <a href="http://wuos.org/content/337/6090/64.abstract">One</a> determined that 86% of the 500,000 SNPs found with “deep sequencing” of the protein-coding exomes were “rare,” meaning that their less common allele frequency was less than 0.5%. Rare SNPs were mostly race-specific and mostly recent deleterious mutations. Among the 1,351 European Americans (EA), 65% of all of the SNPs were race-specific. Among the 1,088 African Americans (AA), the percentage was 72%. One Native American (NA) was also examined. Below is a diagram depicting the population overlap of these SNPs and a bar graph detailing the proportion that was race-specific by allele frequency.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-TftYwDomx8I/UE2sARtPDSI/AAAAAAAAAlw/CvE5XaPQwPk/s1600/tennessen%2Boverlap.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="323" width="393" src="http://4.bp.blogspot.com/-TftYwDomx8I/UE2sARtPDSI/AAAAAAAAAlw/CvE5XaPQwPk/s400/tennessen%2Boverlap.jpg" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-CnzA-YD4V_M/UE2sLOsHjvI/AAAAAAAAAl8/YmvdADENmsg/s1600/tennessen%2Bbar.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="375" width="393" src="http://3.bp.blogspot.com/-CnzA-YD4V_M/UE2sLOsHjvI/AAAAAAAAAl8/YmvdADENmsg/s400/tennessen%2Bbar.jpg" /></a></div>
<br>
Research into the genetics of intelligence might also face this dilemma. A <a href="http://westhunt.wordpress.com/2012/07/14/too-darn-hot/">new hypothesis</a> from Gregory Cochran suggests that deleterious mutations determine a postulated genetic component of racial IQ gaps, with the driving force being temperature’s acceleration of the mutation rate or differences in paternal age. The authors of these studies try to explain the differences with population-size dynamics. Population growth amplifies the number of the mutations or “derived alleles” present per individual. Natural selection lowers the proportion of mutations that are “functional” or “non-synonymous,” meaning that such mutations change the protein for which the DNA codes and are usually deleterious. Recent population bottlenecks, like the exodus from Africa of Eurasians, both amplify derived alleles and only allow a shorter period of natural selection for those alleles.
<br><br>
It turns out that deleterious mutations are more likely to be rare SNPs in African Americans than in European Americans.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-q5Z1jl4Ok0s/UE2si3hE4JI/AAAAAAAAAmI/IDBh0A0ZLhY/s1600/proportion%2Bdeleterious.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="326" width="393" src="http://3.bp.blogspot.com/-q5Z1jl4Ok0s/UE2si3hE4JI/AAAAAAAAAmI/IDBh0A0ZLhY/s400/proportion%2Bdeleterious.jpg" /></a></div>
<br>
Consequently, a study with a smaller sample, such as <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923434/">Lohmueller <i>et al</i></a>, will tend to find a higher proportion of deleterious-to-synonymous mutations in Europeans than Africans. For just this reason, a genetic index comparison of common SNPS for intelligence along the lines of what I have done for obesity might underestimate the genetic component of the IQ gap between black people and white people, until later research with higher sample sizes take into account rare alleles.
<br><br>
On the other hand, the African exodus bottleneck seems to have increased homozygosity (matching pairs) of deleterious mutations in Europeans. Although Africans seem to have more deleterious mutations per person overall, perhaps their genetic diversity and the possible recessive quality of these mutations help balance out that effect. The graph below shows the number of homozygous pairs that are synonymous (S), non-synonymous (NS), possibly damaging (PO), and probably damaging (PR).
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-hP6IeXaWBZ4/UE2su2gPpmI/AAAAAAAAAmU/GfBuEaCl3dQ/s1600/homozygosity.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="400" width="193" src="http://2.bp.blogspot.com/-hP6IeXaWBZ4/UE2su2gPpmI/AAAAAAAAAmU/GfBuEaCl3dQ/s400/homozygosity.jpg" /></a></div>
<br>
Moreover, <a href="http://www.sciencemag.org/content/335/6070/823.short">MacArthur <i>et al</i></a> found much higher numbers of deleterious mutations in Asians and Africans than Europeans, but detailed follow-up determined many of these to be false positives. Thus, whites and Asians each had an equal number of true loss-of-function variants per person (104). Africans still had more (122), but each group had a roughly equal number of homozygous pairs.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-PFs55zrR-Fc/UE2s4V3rMoI/AAAAAAAAAmg/AsrdI_yfFD0/s1600/false%2Bpositive.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="346" width="393" src="http://4.bp.blogspot.com/-PFs55zrR-Fc/UE2s4V3rMoI/AAAAAAAAAmg/AsrdI_yfFD0/s400/false%2Bpositive.jpg" /></a></div>
<br>
Another <a href="http://www.pnas.org/content/109/4/1193.full">study</a> that postulated a significant epistatic component to heredity used an equation based on twins studies to estimate how much of the variability of different phenotypes owes to the additive effects of SNPs (and, therefore, resulting from the sort of alleles that I am tracking). The equation result was closer to zero as the influence of those effects rose. BMI between the ages of 30 and 39 was about as close to zero (-4) as “performance IQ” (5), fitness (4), and exercise participation (5), and quite closer than general IQ (-10). BMI between the ages of 20 and 29 (18) was not as close but was still the same distance from zero as verbal IQ (-18). For comparison, birth weight was -73, and having fainting spells not in response to blood was -63. Since GWAS for IQ have already found that common SNPs account for about half of its variability, which is the bulk of its heritable component, and since those equation results showed comparable results for BMI and IQ, my approach might work fairly well for both obesity and intelligence. Nevertheless, I cannot yet reconcile that with the research on exome rare SNPs.
<br><br>
Steve Hsu, who recently became the Michigan State University vice president for research and graduate studies, is working on an IQ GWAS and has offered some amazing revelations in a <a href="http://infoproc.blogspot.com/2012/06/plenty-of-room-at-top.html">recent presentation</a>. He appears to endorse deleterious mutations as the major genetic contribution to individual IQ differences, and he estimates that having 39 such mutations lowers IQ 15 points (one standard deviation), about 10,000 IQ SNPs exist, and removal of such mutations could raise IQ perhaps as much as 30 standard deviations. If today’s geniuses have IQs above about 145, one can hardly imagine the potential of a person whose IQ is over 500. Of course, no IQ test today could verify such a level, but after humanity creates those dorks, maybe they could invent one. Hsu <a href="http://infoproc.blogspot.com/2012/07/whole-genome-sequence-from-10-to-20.html#disqus_thread">points</a> to embryo selection as a realistic means of consumer-driven eugenics. He seems to think that Asian societies might be amenable to this approach, but he hopes that “progressive governments will make this procedure free for everyone.” Perhaps his work with the Beijing Genomics Institute will help identify IQ SNPs specific to Asians.
<br><br>
Society is used to a somewhat sporadic quality to genius because extraordinary intelligence often benefits from favorable epistasis, but embryo selection would raise the “additive” IQ potential, so the children and grandchildren of these people would invariably be super-geniuses, as well. I could conjecture about the implications of this form of eugenics. The potential to spread genius far and wide could negate a key reactionary theme, while bolstering a liberal intellectual elite. “Elite” might become a tenuous term, as genius might no longer incur reward and professional status, that is, if embryo selection becomes ubiquitous. Such circumstances multiply leftist agitants. That this might occur concomitant with global warming and automation’s realization of Marx’s “labor-saving devices” prophecy could precipitate a re-birth of Communism. At least initially, willingness to abort many healthy embryos will be a major determinant of participation, making for a far-left leading edge.
<br><br>
Then again, when living embodiments of eugenics ideology make quaint the quasi-religious adjective, “gifted,” an entire right-wing historical narrative will march to the fore. Intelligence will become a choice of responsible parents, and liberals will grow frustrated in their attempts to invite evolution-disbelieving African Americans.
<br><br>
For some, other races will always be “the other,” regardless of IQ, and universal genius promotion might sooner reach out to the family-pet community. Don’t laugh! If humans can reach a new brilliance beyond superlatives, who could say how far into the animal kingdom human intellect could penetrate? If scientists can resurrect Neandertals or Denisovans, those creatures might even share some of the target IQ variants with modern humans. All this existential tumult will owe to a movement that began with elites’ innumerable abortions. Personhood will never be the same.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Archives+of+pediatrics+%26+adolescent+medicine&rft_id=info%3Apmid%2F22665028&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Polygenic+risk%2C+rapid+childhood+growth%2C+and+the+development+of+obesity%3A+evidence+from+a+4-decade+longitudinal+study.&rft.issn=1072-4710&rft.date=2012&rft.volume=166&rft.issue=6&rft.spage=515&rft.epage=21&rft.artnum=http%3A%2F%2Farchpedi.jamanetwork.com%2Farticle.aspx%3Farticleid%3D1171937&rft.au=Belsky+DW&rft.au=Moffitt+TE&rft.au=Houts+R&rft.au=Bennett+GG&rft.au=Biddle+AK&rft.au=Blumenthal+JA&rft.au=Evans+JP&rft.au=Harrington+H&rft.au=Sugden+K&rft.au=Williams+B&rft.au=Poulton+R&rft.au=Caspi+A&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Belsky DW, Moffitt TE, Houts R, Bennett GG, Biddle AK, Blumenthal JA, Evans JP, Harrington H, Sugden K, Williams B, Poulton R, & Caspi A (2012). Polygenic risk, rapid childhood growth, and the development of obesity: evidence from a 4-decade longitudinal study. <span style="font-style: italic;">Archives of pediatrics & adolescent medicine, 166</span> (6), 515-21 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22665028">22665028</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=JAMA+%3A+the+journal+of+the+American+Medical+Association&rft_id=info%3Apmid%2F22253363&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Prevalence+of+obesity+and+trends+in+the+distribution+of+body+mass+index+among+US+adults%2C+1999-2010.&rft.issn=0098-7484&rft.date=2012&rft.volume=307&rft.issue=5&rft.spage=491&rft.epage=7&rft.artnum=http%3A%2F%2Fwww.foodpolitics.com%2Fwp-content%2Fuploads%2FObesityRates_JAMA_12.pdf&rft.au=Flegal+KM&rft.au=Carroll+MD&rft.au=Kit+BK&rft.au=Ogden+CL&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2Cgenetics">Flegal KM, Carroll MD, Kit BK, & Ogden CL (2012). Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. <span style="font-style: italic;">JAMA : the journal of the American Medical Association, 307</span> (5), 491-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22253363">22253363</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Obesity+%28Silver+Spring%2C+Md.%29&rft_id=info%3Apmid%2F22714089&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Discordant+Risk%3A+Overweight+and+cardiometabolic+risk+in+Chinese+adults+Gordon-Larsen%3A+Overweight+and+Cardiometabolic+Risk+in+China.&rft.issn=1930-7381&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.nature.com%2Foby%2Fjournal%2Fvaop%2Fncurrent%2Ffull%2Foby2012152a.html&rft.au=Gordon-Larsen+P&rft.au=Adair+LS&rft.au=Meigs+JB&rft.au=Mayer-Davis+E&rft.au=Herring+A&rft.au=Yan+S&rft.au=Zhang+B&rft.au=Shufa+D&rft.au=Popkin+BM&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Gordon-Larsen P, Adair LS, Meigs JB, Mayer-Davis E, Herring A, Yan S, Zhang B, Shufa D, & Popkin BM (2012). Discordant Risk: Overweight and cardiometabolic risk in Chinese adults Gordon-Larsen: Overweight and Cardiometabolic Risk in China. <span style="font-style: italic;">Obesity (Silver Spring, Md.)</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22714089">22714089</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Genetics&rft_id=info%3Adoi%2F10.1534%2Fgenetics.112.144071&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Limited+Evidence+for+Classic+Selective+Sweeps+in+African+Populations&rft.issn=&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.genetics.org%2Fgca%3Fsubmit%3DGet%2BAll%2BChecked%2BAbstracts%26gca%3Dgenetics%253Bgenetics.112.144071v1&rft.au=Granka%2C+JM&rft.au=Henn%2C+BM&rft.au=Gignoux%2C+CR&rft.au=Kidd%2C+JM&rft.au=Bustamante%2C+CD&rft.au=Feldman%2C+MW&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Granka, JM, Henn, BM, Gignoux, CR, Kidd, JM, Bustamante, CD, & Feldman, MW (2012). Limited Evidence for Classic Selective Sweeps in African Populations <span style="font-style: italic;">Genetics</span> DOI: <a rev="review" href="http://dx.doi.org/10.1534/genetics.112.144071">10.1534/genetics.112.144071</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature+genetics&rft_id=info%3Apmid%2F20935629&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Meta-analysis+identifies+13+new+loci+associated+with+waist-hip+ratio+and+reveals+sexual+dimorphism+in+the+genetic+basis+of+fat+distribution.&rft.issn=1061-4036&rft.date=2010&rft.volume=42&rft.issue=11&rft.spage=949&rft.epage=60&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3000924%2F&rft.au=Heid+IM&rft.au=Jackson+AU&rft.au=Randall+JC&rft.au=Winkler+TW&rft.au=Qi+L&rft.au=Steinthorsdottir+V&rft.au=Thorleifsson+G&rft.au=Zillikens+MC&rft.au=Speliotes+EK&rft.au=M%C3%A4gi+R&rft.au=Workalemahu+T&rft.au=White+CC&rft.au=Bouatia-Naji+N&rft.au=Harris+TB&rft.au=Berndt+SI&rft.au=Ingelsson+E&rft.au=Willer+CJ&rft.au=Weedon+MN&rft.au=Luan+J&rft.au=Vedantam+S&rft.au=Esko+T&rft.au=Kilpel%C3%A4inen+TO&rft.au=Kutalik+Z&rft.au=Li+S&rft.au=Monda+KL&rft.au=Dixon+AL&rft.au=Holmes+CC&rft.au=Kaplan+LM&rft.au=Liang+L&rft.au=Min+JL&rft.au=Moffatt+MF&rft.au=Molony+C&rft.au=Nicholson+G&rft.au=Schadt+EE&rft.au=Zondervan+KT&rft.au=Feitosa+MF&rft.au=Ferreira+T&rft.au=Lango+Allen+H&rft.au=Weyant+RJ&rft.au=Wheeler+E&rft.au=Wood+AR&rft.au=MAGIC&rft.au=Estrada+K&rft.au=Goddard+ME&rft.au=Lettre+G&rft.au=Mangino+M&rft.au=Nyholt+DR&rft.au=Purcell+S&rft.au=Smith+AV&rft.au=Visscher+PM&rft.au=Yang+J&rft.au=McCarroll+SA&rft.au=Nemesh+J&rft.au=Voight+BF&rft.au=Absher+D&rft.au=Amin+N&rft.au=Aspelund+T&rft.au=Coin+L&rft.au=Glazer+NL&rft.au=Hayward+C&rft.au=Heard-Costa+NL&rft.au=Hottenga+JJ&rft.au=Johansson+A&rft.au=Johnson+T&rft.au=Kaakinen+M&rft.au=Kapur+K&rft.au=Ketkar+S&rft.au=Knowles+JW&rft.au=Kraft+P&rft.au=Kraja+AT&rft.au=Lamina+C&rft.au=Leitzmann+MF&rft.au=McKnight+B&rft.au=Morris+AP&rft.au=Ong+KK&rft.au=Perry+JR&rft.au=Peters+MJ&rft.au=Polasek+O&rft.au=Prokopenko+I&rft.au=Rayner+NW&rft.au=Ripatti+S&rft.au=Rivadeneira+F&rft.au=Robertson+NR&rft.au=Sanna+S&rft.au=Sovio+U&rft.au=Surakka+I&rft.au=Teumer+A&rft.au=van+Wingerden+S&rft.au=Vitart+V&rft.au=Zhao+JH&rft.au=Cavalcanti-Proen%C3%A7a+C&rft.au=Chines+PS&rft.au=Fisher+E&rft.au=Kulzer+JR&rft.au=Lecoeur+C&rft.au=Narisu+N&rft.au=Sandholt+C&rft.au=Scott+LJ&rft.au=Silander+K&rft.au=Stark+K&rft.au=Tammesoo+ML&rft.au=Teslovich+TM&rft.au=Timpson+NJ&rft.au=Watanabe+RM&rft.au=Welch+R&rft.au=Chasman+DI&rft.au=Cooper+MN&rft.au=Jansson+JO&rft.au=Kettunen+J&rft.au=Lawrence+RW&rft.au=Pellikka+N&rft.au=Perola+M&rft.au=Vandenput+L&rft.au=Alavere+H&rft.au=Almgren+P&rft.au=Atwood+LD&rft.au=Bennett+AJ&rft.au=Biffar+R&rft.au=Bonnycastle+LL&rft.au=Bornstein+SR&rft.au=Buchanan+TA&rft.au=Campbell+H&rft.au=Day+IN&rft.au=Dei+M&rft.au=D%C3%B6rr+M&rft.au=Elliott+P&rft.au=Erdos+MR&rft.au=Eriksson+JG&rft.au=Freimer+NB&rft.au=Fu+M&rft.au=Gaget+S&rft.au=Geus+EJ&rft.au=Gjesing+AP&rft.au=Grallert+H&rft.au=Gr%C3%A4ssler+J&rft.au=Groves+CJ&rft.au=Guiducci+C&rft.au=Hartikainen+AL&rft.au=Hassanali+N&rft.au=Havulinna+AS&rft.au=Herzig+KH&rft.au=Hicks+AA&rft.au=Hui+J&rft.au=Igl+W&rft.au=Jousilahti+P&rft.au=Jula+A&rft.au=Kajantie+E&rft.au=Kinnunen+L&rft.au=Kolcic+I&rft.au=Koskinen+S&rft.au=Kovacs+P&rft.au=Kroemer+HK&rft.au=Krzelj+V&rft.au=Kuusisto+J&rft.au=Kvaloy+K&rft.au=Laitinen+J&rft.au=Lantieri+O&rft.au=Lathrop+GM&rft.au=Lokki+ML&rft.au=Luben+RN&rft.au=Ludwig+B&rft.au=McArdle+WL&rft.au=McCarthy+A&rft.au=Morken+MA&rft.au=Nelis+M&rft.au=Neville+MJ&rft.au=Par%C3%A9+G&rft.au=Parker+AN&rft.au=Peden+JF&rft.au=Pichler+I&rft.au=Pietil%C3%A4inen+KH&rft.au=Platou+CG&rft.au=Pouta+A&rft.au=Ridderstr%C3%A5le+M&rft.au=Samani+NJ&rft.au=Saramies+J&rft.au=Sinisalo+J&rft.au=Smit+JH&rft.au=Strawbridge+RJ&rft.au=Stringham+HM&rft.au=Swift+AJ&rft.au=Teder-Laving+M&rft.au=Thomson+B&rft.au=Usala+G&rft.au=van+Meurs+JB&rft.au=van+Ommen+GJ&rft.au=Vatin+V&rft.au=Volpato+CB&rft.au=Wallaschofski+H&rft.au=Walters+GB&rft.au=Widen+E&rft.au=Wild+SH&rft.au=Willemsen+G&rft.au=Witte+DR&rft.au=Zgaga+L&rft.au=Zitting+P&rft.au=Beilby+JP&rft.au=James+AL&rft.au=K%C3%A4h%C3%B6nen+M&rft.au=Lehtim%C3%A4ki+T&rft.au=Nieminen+MS&rft.au=Ohlsson+C&rft.au=Palmer+LJ&rft.au=Raitakari+O&rft.au=Ridker+PM&rft.au=Stumvoll+M&rft.au=T%C3%B6njes+A&rft.au=Viikari+J&rft.au=Balkau+B&rft.au=Ben-Shlomo+Y&rft.au=Bergman+RN&rft.au=Boeing+H&rft.au=Smith+GD&rft.au=Ebrahim+S&rft.au=Froguel+P&rft.au=Hansen+T&rft.au=Hengstenberg+C&rft.au=Hveem+K&rft.au=Isomaa+B&rft.au=J%C3%B8rgensen+T&rft.au=Karpe+F&rft.au=Khaw+KT&rft.au=Laakso+M&rft.au=Lawlor+DA&rft.au=Marre+M&rft.au=Meitinger+T&rft.au=Metspalu+A&rft.au=Midthjell+K&rft.au=Pedersen+O&rft.au=Salomaa+V&rft.au=Schwarz+PE&rft.au=Tuomi+T&rft.au=Tuomilehto+J&rft.au=Valle+TT&rft.au=Wareham+NJ&rft.au=Arnold+AM&rft.au=Beckmann+JS&rft.au=Bergmann+S&rft.au=Boerwinkle+E&rft.au=Boomsma+DI&rft.au=Caulfield+MJ&rft.au=Collins+FS&rft.au=Eiriksdottir+G&rft.au=Gudnason+V&rft.au=Gyllensten+U&rft.au=Hamsten+A&rft.au=Hattersley+AT&rft.au=Hofman+A&rft.au=Hu+FB&rft.au=Illig+T&rft.au=Iribarren+C&rft.au=Jarvelin+MR&rft.au=Kao+WH&rft.au=Kaprio+J&rft.au=Launer+LJ&rft.au=Munroe+PB&rft.au=Oostra+B&rft.au=Penninx+BW&rft.au=Pramstaller+PP&rft.au=Psaty+BM&rft.au=Quertermous+T&rft.au=Rissanen+A&rft.au=Rudan+I&rft.au=Shuldiner+AR&rft.au=Soranzo+N&rft.au=Spector+TD&rft.au=Syvanen+AC&rft.au=Uda+M&rft.au=Uitterlinden+A&rft.au=V%C3%B6lzke+H&rft.au=Vollenweider+P&rft.au=Wilson+JF&rft.au=Witteman+JC&rft.au=Wright+AF&rft.au=Abecasis+GR&rft.au=Boehnke+M&rft.au=Borecki+IB&rft.au=Deloukas+P&rft.au=Frayling+TM&rft.au=Groop+LC&rft.au=Haritunians+T&rft.au=Hunter+DJ&rft.au=Kaplan+RC&rft.au=North+KE&rft.au=O%27Connell+JR&rft.au=Peltonen+L&rft.au=Schlessinger+D&rft.au=Strachan+DP&rft.au=Hirschhorn+JN&rft.au=Assimes+TL&rft.au=Wichmann+HE&rft.au=Thorsteinsdottir+U&rft.au=van+Duijn+CM&rft.au=Stefansson+K&rft.au=Cupples+LA&rft.au=Loos+RJ&rft.au=Barroso+I&rft.au=McCarthy+MI&rft.au=Fox+CS&rft.au=Mohlke+KL&rft.au=Lindgren+CM&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Heid IM, Jackson AU, Randall JC, Winkler TW, Qi L, Steinthorsdottir V, Thorleifsson G, Zillikens MC, Speliotes EK, Mägi R, Workalemahu T, White CC, Bouatia-Naji N, Harris TB, Berndt SI, Ingelsson E, Willer CJ, Weedon MN, Luan J, Vedantam S, Esko T, Kilpeläinen TO, Kutalik Z, Li S, Monda KL, Dixon AL, Holmes CC, Kaplan LM, Liang L, Min JL, Moffatt MF, Molony C, Nicholson G, Schadt EE, Zondervan KT, Feitosa MF, Ferreira T, Lango Allen H, Weyant RJ, Wheeler E, Wood AR, MAGIC, Estrada K, Goddard ME, Lettre G, Mangino M, Nyholt DR, Purcell S, Smith AV, Visscher PM, Yang J, McCarroll SA, Nemesh J, Voight BF, Absher D, Amin N, Aspelund T, Coin L, Glazer NL, Hayward C, Heard-Costa NL, Hottenga JJ, Johansson A, Johnson T, Kaakinen M, Kapur K, Ketkar S, Knowles JW, Kraft P, Kraja AT, Lamina C, Leitzmann MF, McKnight B, Morris AP, Ong KK, Perry JR, Peters MJ, Polasek O, Prokopenko I, Rayner NW, Ripatti S, Rivadeneira F, Robertson NR, Sanna S, Sovio U, Surakka I, Teumer A, van Wingerden S, Vitart V, Zhao JH, Cavalcanti-Proença C, Chines PS, Fisher E, Kulzer JR, Lecoeur C, Narisu N, Sandholt C, Scott LJ, Silander K, Stark K, Tammesoo ML, Teslovich TM, Timpson NJ, Watanabe RM, Welch R, Chasman DI, Cooper MN, Jansson JO, Kettunen J, Lawrence RW, Pellikka N, Perola M, Vandenput L, Alavere H, Almgren P, Atwood LD, Bennett AJ, Biffar R, Bonnycastle LL, Bornstein SR, Buchanan TA, Campbell H, Day IN, Dei M, Dörr M, Elliott P, Erdos MR, Eriksson JG, Freimer NB, Fu M, Gaget S, Geus EJ, Gjesing AP, Grallert H, Grässler J, Groves CJ, Guiducci C, Hartikainen AL, Hassanali N, Havulinna AS, Herzig KH, Hicks AA, Hui J, Igl W, Jousilahti P, Jula A, Kajantie E, Kinnunen L, Kolcic I, Koskinen S, Kovacs P, Kroemer HK, Krzelj V, Kuusisto J, Kvaloy K, Laitinen J, Lantieri O, Lathrop GM, Lokki ML, Luben RN, Ludwig B, McArdle WL, McCarthy A, Morken MA, Nelis M, Neville MJ, Paré G, Parker AN, Peden JF, Pichler I, Pietiläinen KH, Platou CG, Pouta A, Ridderstråle M, Samani NJ, Saramies J, Sinisalo J, Smit JH, Strawbridge RJ, Stringham HM, Swift AJ, Teder-Laving M, Thomson B, Usala G, van Meurs JB, van Ommen GJ, Vatin V, Volpato CB, Wallaschofski H, Walters GB, Widen E, Wild SH, Willemsen G, Witte DR, Zgaga L, Zitting P, Beilby JP, James AL, Kähönen M, Lehtimäki T, Nieminen MS, Ohlsson C, Palmer LJ, Raitakari O, Ridker PM, Stumvoll M, Tönjes A, Viikari J, Balkau B, Ben-Shlomo Y, Bergman RN, Boeing H, Smith GD, Ebrahim S, Froguel P, Hansen T, Hengstenberg C, Hveem K, Isomaa B, Jørgensen T, Karpe F, Khaw KT, Laakso M, Lawlor DA, Marre M, Meitinger T, Metspalu A, Midthjell K, Pedersen O, Salomaa V, Schwarz PE, Tuomi T, Tuomilehto J, Valle TT, Wareham NJ, Arnold AM, Beckmann JS, Bergmann S, Boerwinkle E, Boomsma DI, Caulfield MJ, Collins FS, Eiriksdottir G, Gudnason V, Gyllensten U, Hamsten A, Hattersley AT, Hofman A, Hu FB, Illig T, Iribarren C, Jarvelin MR, Kao WH, Kaprio J, Launer LJ, Munroe PB, Oostra B, Penninx BW, Pramstaller PP, Psaty BM, Quertermous T, Rissanen A, Rudan I, Shuldiner AR, Soranzo N, Spector TD, Syvanen AC, Uda M, Uitterlinden A, Völzke H, Vollenweider P, Wilson JF, Witteman JC, Wright AF, Abecasis GR, Boehnke M, Borecki IB, Deloukas P, Frayling TM, Groop LC, Haritunians T, Hunter DJ, Kaplan RC, North KE, O'Connell JR, Peltonen L, Schlessinger D, Strachan DP, Hirschhorn JN, Assimes TL, Wichmann HE, Thorsteinsdottir U, van Duijn CM, Stefansson K, Cupples LA, Loos RJ, Barroso I, McCarthy MI, Fox CS, Mohlke KL, & Lindgren CM (2010). Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution. <span style="font-style: italic;">Nature genetics, 42</span> (11), 949-60 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20935629">20935629</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Obesity+research&rft_id=info%3Apmid%2F15800289&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Heritability+of+body+composition+measured+by+DXA+in+the+diabetes+heart+study.&rft.issn=1071-7323&rft.date=2005&rft.volume=13&rft.issue=2&rft.spage=312&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.nature.com.liboff.ohsu.edu%2Foby%2Fjournal%2Fv13%2Fn2%2Fpdf%2Foby200542a.pdf&rft.au=Hsu+FC&rft.au=Lenchik+L&rft.au=Nicklas+BJ&rft.au=Lohman+K&rft.au=Register+TC&rft.au=Mychaleckyj+J&rft.au=Langefeld+CD&rft.au=Freedman+BI&rft.au=Bowden+DW&rft.au=Carr+JJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Hsu FC, Lenchik L, Nicklas BJ, Lohman K, Register TC, Mychaleckyj J, Langefeld CD, Freedman BI, Bowden DW, & Carr JJ (2005). Heritability of body composition measured by DXA in the diabetes heart study. <span style="font-style: italic;">Obesity research, 13</span> (2), 312-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/15800289">15800289</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature+genetics&rft_id=info%3Apmid%2F21706003&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genetic+variation+near+IRS1+associates+with+reduced+adiposity+and+an+impaired+metabolic+profile.&rft.issn=1061-4036&rft.date=2011&rft.volume=43&rft.issue=8&rft.spage=753&rft.epage=60&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3262230%2Fpdf%2Fnihms-329020.pdf&rft.au=Kilpel%C3%A4inen+TO&rft.au=Zillikens+MC&rft.au=Stan%C4%8D%C3%A1kova+A&rft.au=Finucane+FM&rft.au=Ried+JS&rft.au=Langenberg+C&rft.au=Zhang+W&rft.au=Beckmann+JS&rft.au=Luan+J&rft.au=Vandenput+L&rft.au=Styrkarsdottir+U&rft.au=Zhou+Y&rft.au=Smith+AV&rft.au=Zhao+JH&rft.au=Amin+N&rft.au=Vedantam+S&rft.au=Shin+SY&rft.au=Haritunians+T&rft.au=Fu+M&rft.au=Feitosa+MF&rft.au=Kumari+M&rft.au=Halldorsson+BV&rft.au=Tikkanen+E&rft.au=Mangino+M&rft.au=Hayward+C&rft.au=Song+C&rft.au=Arnold+AM&rft.au=Aulchenko+YS&rft.au=Oostra+BA&rft.au=Campbell+H&rft.au=Cupples+LA&rft.au=Davis+KE&rft.au=D%C3%B6ring+A&rft.au=Eiriksdottir+G&rft.au=Estrada+K&rft.au=Fern%C3%A1ndez-Real+JM&rft.au=Garcia+M&rft.au=Gieger+C&rft.au=Glazer+NL&rft.au=Guiducci+C&rft.au=Hofman+A&rft.au=Humphries+SE&rft.au=Isomaa+B&rft.au=Jacobs+LC&rft.au=Jula+A&rft.au=Karasik+D&rft.au=Karlsson+MK&rft.au=Khaw+KT&rft.au=Kim+LJ&rft.au=Kivim%C3%A4ki+M&rft.au=Klopp+N&rft.au=K%C3%BChnel+B&rft.au=Kuusisto+J&rft.au=Liu+Y&rft.au=Ljunggren+O&rft.au=Lorentzon+M&rft.au=Luben+RN&rft.au=McKnight+B&rft.au=Mellstr%C3%B6m+D&rft.au=Mitchell+BD&rft.au=Mooser+V&rft.au=Moreno+JM&rft.au=M%C3%A4nnist%C3%B6+S&rft.au=O%27Connell+JR&rft.au=Pascoe+L&rft.au=Peltonen+L&rft.au=Peral+B&rft.au=Perola+M&rft.au=Psaty+BM&rft.au=Salomaa+V&rft.au=Savage+DB&rft.au=Semple+RK&rft.au=Skaric-Juric+T&rft.au=Sigurdsson+G&rft.au=Song+KS&rft.au=Spector+TD&rft.au=Syv%C3%A4nen+AC&rft.au=Talmud+PJ&rft.au=Thorleifsson+G&rft.au=Thorsteinsdottir+U&rft.au=Uitterlinden+AG&rft.au=van+Duijn+CM&rft.au=Vidal-Puig+A&rft.au=Wild+SH&rft.au=Wright+AF&rft.au=Clegg+DJ&rft.au=Schadt+E&rft.au=Wilson+JF&rft.au=Rudan+I&rft.au=Ripatti+S&rft.au=Borecki+IB&rft.au=Shuldiner+AR&rft.au=Ingelsson+E&rft.au=Jansson+JO&rft.au=Kaplan+RC&rft.au=Gudnason+V&rft.au=Harris+TB&rft.au=Groop+L&rft.au=Kiel+DP&rft.au=Rivadeneira+F&rft.au=Walker+M&rft.au=Barroso+I&rft.au=Vollenweider+P&rft.au=Waeber+G&rft.au=Chambers+JC&rft.au=Kooner+JS&rft.au=Soranzo+N&rft.au=Hirschhorn+JN&rft.au=Stefansson+K&rft.au=Wichmann+HE&rft.au=Ohlsson+C&rft.au=O%27Rahilly+S&rft.au=Wareham+NJ&rft.au=Speliotes+EK&rft.au=Fox+CS&rft.au=Laakso+M&rft.au=Loos+RJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Kilpeläinen TO, Zillikens MC, Stančákova A, Finucane FM, Ried JS, Langenberg C, Zhang W, Beckmann JS, Luan J, Vandenput L, Styrkarsdottir U, Zhou Y, Smith AV, Zhao JH, Amin N, Vedantam S, Shin SY, Haritunians T, Fu M, Feitosa MF, Kumari M, Halldorsson BV, Tikkanen E, Mangino M, Hayward C, Song C, Arnold AM, Aulchenko YS, Oostra BA, Campbell H, Cupples LA, Davis KE, Döring A, Eiriksdottir G, Estrada K, Fernández-Real JM, Garcia M, Gieger C, Glazer NL, Guiducci C, Hofman A, Humphries SE, Isomaa B, Jacobs LC, Jula A, Karasik D, Karlsson MK, Khaw KT, Kim LJ, Kivimäki M, Klopp N, Kühnel B, Kuusisto J, Liu Y, Ljunggren O, Lorentzon M, Luben RN, McKnight B, Mellström D, Mitchell BD, Mooser V, Moreno JM, Männistö S, O'Connell JR, Pascoe L, Peltonen L, Peral B, Perola M, Psaty BM, Salomaa V, Savage DB, Semple RK, Skaric-Juric T, Sigurdsson G, Song KS, Spector TD, Syvänen AC, Talmud PJ, Thorleifsson G, Thorsteinsdottir U, Uitterlinden AG, van Duijn CM, Vidal-Puig A, Wild SH, Wright AF, Clegg DJ, Schadt E, Wilson JF, Rudan I, Ripatti S, Borecki IB, Shuldiner AR, Ingelsson E, Jansson JO, Kaplan RC, Gudnason V, Harris TB, Groop L, Kiel DP, Rivadeneira F, Walker M, Barroso I, Vollenweider P, Waeber G, Chambers JC, Kooner JS, Soranzo N, Hirschhorn JN, Stefansson K, Wichmann HE, Ohlsson C, O'Rahilly S, Wareham NJ, Speliotes EK, Fox CS, Laakso M, & Loos RJ (2011). Genetic variation near IRS1 associates with reduced adiposity and an impaired metabolic profile. <span style="font-style: italic;">Nature genetics, 43</span> (8), 753-60 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21706003">21706003</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature&rft_id=info%3Apmid%2F18288194&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Proportionally+more+deleterious+genetic+variation+in+European+than+in+African+populations.&rft.issn=0028-0836&rft.date=2008&rft.volume=451&rft.issue=7181&rft.spage=994&rft.epage=7&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2923434%2F&rft.au=Lohmueller+KE&rft.au=Indap+AR&rft.au=Schmidt+S&rft.au=Boyko+AR&rft.au=Hernandez+RD&rft.au=Hubisz+MJ&rft.au=Sninsky+JJ&rft.au=White+TJ&rft.au=Sunyaev+SR&rft.au=Nielsen+R&rft.au=Clark+AG&rft.au=Bustamante+CD&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Lohmueller KE, Indap AR, Schmidt S, Boyko AR, Hernandez RD, Hubisz MJ, Sninsky JJ, White TJ, Sunyaev SR, Nielsen R, Clark AG, & Bustamante CD (2008). Proportionally more deleterious genetic variation in European than in African populations. <span style="font-style: italic;">Nature, 451</span> (7181), 994-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/18288194">18288194</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft_id=info%3Apmid%2F22344438&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+systematic+survey+of+loss-of-function+variants+in+human+protein-coding+genes.&rft.issn=0036-8075&rft.date=2012&rft.volume=335&rft.issue=6070&rft.spage=823&rft.epage=8&rft.artnum=http%3A%2F%2Fwww.sciencemag.org%2Fcontent%2F335%2F6070%2F823.short&rft.au=MacArthur+DG&rft.au=Balasubramanian+S&rft.au=Frankish+A&rft.au=Huang+N&rft.au=Morris+J&rft.au=Walter+K&rft.au=Jostins+L&rft.au=Habegger+L&rft.au=Pickrell+JK&rft.au=Montgomery+SB&rft.au=Albers+CA&rft.au=Zhang+ZD&rft.au=Conrad+DF&rft.au=Lunter+G&rft.au=Zheng+H&rft.au=Ayub+Q&rft.au=DePristo+MA&rft.au=Banks+E&rft.au=Hu+M&rft.au=Handsaker+RE&rft.au=Rosenfeld+JA&rft.au=Fromer+M&rft.au=Jin+M&rft.au=Mu+XJ&rft.au=Khurana+E&rft.au=Ye+K&rft.au=Kay+M&rft.au=Saunders+GI&rft.au=Suner+MM&rft.au=Hunt+T&rft.au=Barnes+IH&rft.au=Amid+C&rft.au=Carvalho-Silva+DR&rft.au=Bignell+AH&rft.au=Snow+C&rft.au=Yngvadottir+B&rft.au=Bumpstead+S&rft.au=Cooper+DN&rft.au=Xue+Y&rft.au=Romero+IG&rft.au=1000+Genomes+Project+Consortium&rft.au=Wang+J&rft.au=Li+Y&rft.au=Gibbs+RA&rft.au=McCarroll+SA&rft.au=Dermitzakis+ET&rft.au=Pritchard+JK&rft.au=Barrett+JC&rft.au=Harrow+J&rft.au=Hurles+ME&rft.au=Gerstein+MB&rft.au=Tyler-Smith+C&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">MacArthur DG, Balasubramanian S, Frankish A, Huang N, Morris J, Walter K, Jostins L, Habegger L, Pickrell JK, Montgomery SB, Albers CA, Zhang ZD, Conrad DF, Lunter G, Zheng H, Ayub Q, DePristo MA, Banks E, Hu M, Handsaker RE, Rosenfeld JA, Fromer M, Jin M, Mu XJ, Khurana E, Ye K, Kay M, Saunders GI, Suner MM, Hunt T, Barnes IH, Amid C, Carvalho-Silva DR, Bignell AH, Snow C, Yngvadottir B, Bumpstead S, Cooper DN, Xue Y, Romero IG, 1000 Genomes Project Consortium, Wang J, Li Y, Gibbs RA, McCarroll SA, Dermitzakis ET, Pritchard JK, Barrett JC, Harrow J, Hurles ME, Gerstein MB, & Tyler-Smith C (2012). A systematic survey of loss-of-function variants in human protein-coding genes. <span style="font-style: italic;">Science (New York, N.Y.), 335</span> (6070), 823-8 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22344438">22344438</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature+genetics&rft_id=info%3Apmid%2F19151714&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genome-wide+association+study+for+early-onset+and+morbid+adult+obesity+identifies+three+new+risk+loci+in+European+populations.&rft.issn=1061-4036&rft.date=2009&rft.volume=41&rft.issue=2&rft.spage=157&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.nature.com%2Fng%2Fjournal%2Fv41%2Fn2%2Fabs%2Fng.301.html&rft.au=Meyre+D&rft.au=Delplanque+J&rft.au=Ch%C3%A8vre+JC&rft.au=Lecoeur+C&rft.au=Lobbens+S&rft.au=Gallina+S&rft.au=Durand+E&rft.au=Vatin+V&rft.au=Degraeve+F&rft.au=Proen%C3%A7a+C&rft.au=Gaget+S&rft.au=K%C3%B6rner+A&rft.au=Kovacs+P&rft.au=Kiess+W&rft.au=Tichet+J&rft.au=Marre+M&rft.au=Hartikainen+AL&rft.au=Horber+F&rft.au=Potoczna+N&rft.au=Hercberg+S&rft.au=Levy-Marchal+C&rft.au=Pattou+F&rft.au=Heude+B&rft.au=Tauber+M&rft.au=McCarthy+MI&rft.au=Blakemore+AI&rft.au=Montpetit+A&rft.au=Polychronakos+C&rft.au=Weill+J&rft.au=Coin+LJ&rft.au=Asher+J&rft.au=Elliott+P&rft.au=J%C3%A4rvelin+MR&rft.au=Visvikis-Siest+S&rft.au=Balkau+B&rft.au=Sladek+R&rft.au=Balding+D&rft.au=Walley+A&rft.au=Dina+C&rft.au=Froguel+P&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Meyre D, Delplanque J, Chèvre JC, Lecoeur C, Lobbens S, Gallina S, Durand E, Vatin V, Degraeve F, Proença C, Gaget S, Körner A, Kovacs P, Kiess W, Tichet J, Marre M, Hartikainen AL, Horber F, Potoczna N, Hercberg S, Levy-Marchal C, Pattou F, Heude B, Tauber M, McCarthy MI, Blakemore AI, Montpetit A, Polychronakos C, Weill J, Coin LJ, Asher J, Elliott P, Järvelin MR, Visvikis-Siest S, Balkau B, Sladek R, Balding D, Walley A, Dina C, & Froguel P (2009). Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European populations. <span style="font-style: italic;">Nature genetics, 41</span> (2), 157-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19151714">19151714</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PLoS+genetics&rft_id=info%3Apmid%2F20421936&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Two+new+Loci+for+body-weight+regulation+identified+in+a+joint+analysis+of+genome-wide+association+studies+for+early-onset+extreme+obesity+in+French+and+german+study+groups.&rft.issn=1553-7390&rft.date=2010&rft.volume=6&rft.issue=4&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.plosgenetics.org%2Farticle%2Finfo%253Adoi%252F10.1371%252Fjournal.pgen.1000916&rft.au=Scherag+A&rft.au=Dina+C&rft.au=Hinney+A&rft.au=Vatin+V&rft.au=Scherag+S&rft.au=Vogel+CI&rft.au=M%C3%BCller+TD&rft.au=Grallert+H&rft.au=Wichmann+HE&rft.au=Balkau+B&rft.au=Heude+B&rft.au=Jarvelin+MR&rft.au=Hartikainen+AL&rft.au=Levy-Marchal+C&rft.au=Weill+J&rft.au=Delplanque+J&rft.au=K%C3%B6rner+A&rft.au=Kiess+W&rft.au=Kovacs+P&rft.au=Rayner+NW&rft.au=Prokopenko+I&rft.au=McCarthy+MI&rft.au=Sch%C3%A4fer+H&rft.au=Jarick+I&rft.au=Boeing+H&rft.au=Fisher+E&rft.au=Reinehr+T&rft.au=Heinrich+J&rft.au=Rzehak+P&rft.au=Berdel+D&rft.au=Borte+M&rft.au=Biebermann+H&rft.au=Krude+H&rft.au=Rosskopf+D&rft.au=Rimmbach+C&rft.au=Rief+W&rft.au=Fromme+T&rft.au=Klingenspor+M&rft.au=Sch%C3%BCrmann+A&rft.au=Schulz+N&rft.au=N%C3%B6then+MM&rft.au=M%C3%BChleisen+TW&rft.au=Erbel+R&rft.au=J%C3%B6ckel+KH&rft.au=Moebus+S&rft.au=Boes+T&rft.au=Illig+T&rft.au=Froguel+P&rft.au=Hebebrand+J&rft.au=Meyre+D&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Scherag A, Dina C, Hinney A, Vatin V, Scherag S, Vogel CI, Müller TD, Grallert H, Wichmann HE, Balkau B, Heude B, Jarvelin MR, Hartikainen AL, Levy-Marchal C, Weill J, Delplanque J, Körner A, Kiess W, Kovacs P, Rayner NW, Prokopenko I, McCarthy MI, Schäfer H, Jarick I, Boeing H, Fisher E, Reinehr T, Heinrich J, Rzehak P, Berdel D, Borte M, Biebermann H, Krude H, Rosskopf D, Rimmbach C, Rief W, Fromme T, Klingenspor M, Schürmann A, Schulz N, Nöthen MM, Mühleisen TW, Erbel R, Jöckel KH, Moebus S, Boes T, Illig T, Froguel P, Hebebrand J, & Meyre D (2010). Two new Loci for body-weight regulation identified in a joint analysis of genome-wide association studies for early-onset extreme obesity in French and german study groups. <span style="font-style: italic;">PLoS genetics, 6</span> (4) PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20421936">20421936</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature+genetics&rft_id=info%3Apmid%2F20935630&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Association+analyses+of+249%2C796+individuals+reveal+18+new+loci+associated+with+body+mass+index.&rft.issn=1061-4036&rft.date=2010&rft.volume=42&rft.issue=11&rft.spage=937&rft.epage=48&rft.artnum=http%3A%2F%2Fukpmc.ac.uk%2Farticles%2FPMC3014648%2Fpdf%2Fnihms237282.pdf&rft.au=Speliotes+EK&rft.au=Willer+CJ&rft.au=Berndt+SI&rft.au=Monda+KL&rft.au=Thorleifsson+G&rft.au=Jackson+AU&rft.au=Lango+Allen+H&rft.au=Lindgren+CM&rft.au=Luan+J&rft.au=M%C3%A4gi+R&rft.au=Randall+JC&rft.au=Vedantam+S&rft.au=Winkler+TW&rft.au=Qi+L&rft.au=Workalemahu+T&rft.au=Heid+IM&rft.au=Steinthorsdottir+V&rft.au=Stringham+HM&rft.au=Weedon+MN&rft.au=Wheeler+E&rft.au=Wood+AR&rft.au=Ferreira+T&rft.au=Weyant+RJ&rft.au=Segr%C3%A8+AV&rft.au=Estrada+K&rft.au=Liang+L&rft.au=Nemesh+J&rft.au=Park+JH&rft.au=Gustafsson+S&rft.au=Kilpel%C3%A4inen+TO&rft.au=Yang+J&rft.au=Bouatia-Naji+N&rft.au=Esko+T&rft.au=Feitosa+MF&rft.au=Kutalik+Z&rft.au=Mangino+M&rft.au=Raychaudhuri+S&rft.au=Scherag+A&rft.au=Smith+AV&rft.au=Welch+R&rft.au=Zhao+JH&rft.au=Aben+KK&rft.au=Absher+DM&rft.au=Amin+N&rft.au=Dixon+AL&rft.au=Fisher+E&rft.au=Glazer+NL&rft.au=Goddard+ME&rft.au=Heard-Costa+NL&rft.au=Hoesel+V&rft.au=Hottenga+JJ&rft.au=Johansson+A&rft.au=Johnson+T&rft.au=Ketkar+S&rft.au=Lamina+C&rft.au=Li+S&rft.au=Moffatt+MF&rft.au=Myers+RH&rft.au=Narisu+N&rft.au=Perry+JR&rft.au=Peters+MJ&rft.au=Preuss+M&rft.au=Ripatti+S&rft.au=Rivadeneira+F&rft.au=Sandholt+C&rft.au=Scott+LJ&rft.au=Timpson+NJ&rft.au=Tyrer+JP&rft.au=van+Wingerden+S&rft.au=Watanabe+RM&rft.au=White+CC&rft.au=Wiklund+F&rft.au=Barlassina+C&rft.au=Chasman+DI&rft.au=Cooper+MN&rft.au=Jansson+JO&rft.au=Lawrence+RW&rft.au=Pellikka+N&rft.au=Prokopenko+I&rft.au=Shi+J&rft.au=Thiering+E&rft.au=Alavere+H&rft.au=Alibrandi+MT&rft.au=Almgren+P&rft.au=Arnold+AM&rft.au=Aspelund+T&rft.au=Atwood+LD&rft.au=Balkau+B&rft.au=Balmforth+AJ&rft.au=Bennett+AJ&rft.au=Ben-Shlomo+Y&rft.au=Bergman+RN&rft.au=Bergmann+S&rft.au=Biebermann+H&rft.au=Blakemore+AI&rft.au=Boes+T&rft.au=Bonnycastle+LL&rft.au=Bornstein+SR&rft.au=Brown+MJ&rft.au=Buchanan+TA&rft.au=Busonero+F&rft.au=Campbell+H&rft.au=Cappuccio+FP&rft.au=Cavalcanti-Proen%C3%A7a+C&rft.au=Chen+YD&rft.au=Chen+CM&rft.au=Chines+PS&rft.au=Clarke+R&rft.au=Coin+L&rft.au=Connell+J&rft.au=Day+IN&rft.au=den+Heijer+M&rft.au=Duan+J&rft.au=Ebrahim+S&rft.au=Elliott+P&rft.au=Elosua+R&rft.au=Eiriksdottir+G&rft.au=Erdos+MR&rft.au=Eriksson+JG&rft.au=Facheris+MF&rft.au=Felix+SB&rft.au=Fischer-Posovszky+P&rft.au=Folsom+AR&rft.au=Friedrich+N&rft.au=Freimer+NB&rft.au=Fu+M&rft.au=Gaget+S&rft.au=Gejman+PV&rft.au=Geus+EJ&rft.au=Gieger+C&rft.au=Gjesing+AP&rft.au=Goel+A&rft.au=Goyette+P&rft.au=Grallert+H&rft.au=Gr%C3%A4ssler+J&rft.au=Greenawalt+DM&rft.au=Groves+CJ&rft.au=Gudnason+V&rft.au=Guiducci+C&rft.au=Hartikainen+AL&rft.au=Hassanali+N&rft.au=Hall+AS&rft.au=Havulinna+AS&rft.au=Hayward+C&rft.au=Heath+AC&rft.au=Hengstenberg+C&rft.au=Hicks+AA&rft.au=Hinney+A&rft.au=Hofman+A&rft.au=Homuth+G&rft.au=Hui+J&rft.au=Igl+W&rft.au=Iribarren+C&rft.au=Isomaa+B&rft.au=Jacobs+KB&rft.au=Jarick+I&rft.au=Jewell+E&rft.au=John+U&rft.au=J%C3%B8rgensen+T&rft.au=Jousilahti+P&rft.au=Jula+A&rft.au=Kaakinen+M&rft.au=Kajantie+E&rft.au=Kaplan+LM&rft.au=Kathiresan+S&rft.au=Kettunen+J&rft.au=Kinnunen+L&rft.au=Knowles+JW&rft.au=Kolcic+I&rft.au=K%C3%B6nig+IR&rft.au=Koskinen+S&rft.au=Kovacs+P&rft.au=Kuusisto+J&rft.au=Kraft+P&rft.au=Kval%C3%B8y+K&rft.au=Laitinen+J&rft.au=Lantieri+O&rft.au=Lanzani+C&rft.au=Launer+LJ&rft.au=Lecoeur+C&rft.au=Lehtim%C3%A4ki+T&rft.au=Lettre+G&rft.au=Liu+J&rft.au=Lokki+ML&rft.au=Lorentzon+M&rft.au=Luben+RN&rft.au=Ludwig+B&rft.au=MAGIC&rft.au=Manunta+P&rft.au=Marek+D&rft.au=Marre+M&rft.au=Martin+NG&rft.au=McArdle+WL&rft.au=McCarthy+A&rft.au=McKnight+B&rft.au=Meitinger+T&rft.au=Melander+O&rft.au=Meyre+D&rft.au=Midthjell+K&rft.au=Montgomery+GW&rft.au=Morken+MA&rft.au=Morris+AP&rft.au=Mulic+R&rft.au=Ngwa+JS&rft.au=Nelis+M&rft.au=Neville+MJ&rft.au=Nyholt+DR&rft.au=O%27Donnell+CJ&rft.au=O%27Rahilly+S&rft.au=Ong+KK&rft.au=Oostra+B&rft.au=Par%C3%A9+G&rft.au=Parker+AN&rft.au=Perola+M&rft.au=Pichler+I&rft.au=Pietil%C3%A4inen+KH&rft.au=Platou+CG&rft.au=Polasek+O&rft.au=Pouta+A&rft.au=Rafelt+S&rft.au=Raitakari+O&rft.au=Rayner+NW&rft.au=Ridderstr%C3%A5le+M&rft.au=Rief+W&rft.au=Ruokonen+A&rft.au=Robertson+NR&rft.au=Rzehak+P&rft.au=Salomaa+V&rft.au=Sanders+AR&rft.au=Sandhu+MS&rft.au=Sanna+S&rft.au=Saramies+J&rft.au=Savolainen+MJ&rft.au=Scherag+S&rft.au=Schipf+S&rft.au=Schreiber+S&rft.au=Schunkert+H&rft.au=Silander+K&rft.au=Sinisalo+J&rft.au=Siscovick+DS&rft.au=Smit+JH&rft.au=Soranzo+N&rft.au=Sovio+U&rft.au=Stephens+J&rft.au=Surakka+I&rft.au=Swift+AJ&rft.au=Tammesoo+ML&rft.au=Tardif+JC&rft.au=Teder-Laving+M&rft.au=Teslovich+TM&rft.au=Thompson+JR&rft.au=Thomson+B&rft.au=T%C3%B6njes+A&rft.au=Tuomi+T&rft.au=van+Meurs+JB&rft.au=van+Ommen+GJ&rft.au=Vatin+V&rft.au=Viikari+J&rft.au=Visvikis-Siest+S&rft.au=Vitart+V&rft.au=Vogel+CI&rft.au=Voight+BF&rft.au=Waite+LL&rft.au=Wallaschofski+H&rft.au=Walters+GB&rft.au=Widen+E&rft.au=Wiegand+S&rft.au=Wild+SH&rft.au=Willemsen+G&rft.au=Witte+DR&rft.au=Witteman+JC&rft.au=Xu+J&rft.au=Zhang+Q&rft.au=Zgaga+L&rft.au=Ziegler+A&rft.au=Zitting+P&rft.au=Beilby+JP&rft.au=Farooqi+IS&rft.au=Hebebrand+J&rft.au=Huikuri+HV&rft.au=James+AL&rft.au=K%C3%A4h%C3%B6nen+M&rft.au=Levinson+DF&rft.au=Macciardi+F&rft.au=Nieminen+MS&rft.au=Ohlsson+C&rft.au=Palmer+LJ&rft.au=Ridker+PM&rft.au=Stumvoll+M&rft.au=Beckmann+JS&rft.au=Boeing+H&rft.au=Boerwinkle+E&rft.au=Boomsma+DI&rft.au=Caulfield+MJ&rft.au=Chanock+SJ&rft.au=Collins+FS&rft.au=Cupples+LA&rft.au=Smith+GD&rft.au=Erdmann+J&rft.au=Froguel+P&rft.au=Gr%C3%B6nberg+H&rft.au=Gyllensten+U&rft.au=Hall+P&rft.au=Hansen+T&rft.au=Harris+TB&rft.au=Hattersley+AT&rft.au=Hayes+RB&rft.au=Heinrich+J&rft.au=Hu+FB&rft.au=Hveem+K&rft.au=Illig+T&rft.au=Jarvelin+MR&rft.au=Kaprio+J&rft.au=Karpe+F&rft.au=Khaw+KT&rft.au=Kiemeney+LA&rft.au=Krude+H&rft.au=Laakso+M&rft.au=Lawlor+DA&rft.au=Metspalu+A&rft.au=Munroe+PB&rft.au=Ouwehand+WH&rft.au=Pedersen+O&rft.au=Penninx+BW&rft.au=Peters+A&rft.au=Pramstaller+PP&rft.au=Quertermous+T&rft.au=Reinehr+T&rft.au=Rissanen+A&rft.au=Rudan+I&rft.au=Samani+NJ&rft.au=Schwarz+PE&rft.au=Shuldiner+AR&rft.au=Spector+TD&rft.au=Tuomilehto+J&rft.au=Uda+M&rft.au=Uitterlinden+A&rft.au=Valle+TT&rft.au=Wabitsch+M&rft.au=Waeber+G&rft.au=Wareham+NJ&rft.au=Watkins+H&rft.au=Procardis+Consortium&rft.au=Wilson+JF&rft.au=Wright+AF&rft.au=Zillikens+MC&rft.au=Chatterjee+N&rft.au=McCarroll+SA&rft.au=Purcell+S&rft.au=Schadt+EE&rft.au=Visscher+PM&rft.au=Assimes+TL&rft.au=Borecki+IB&rft.au=Deloukas+P&rft.au=Fox+CS&rft.au=Groop+LC&rft.au=Haritunians+T&rft.au=Hunter+DJ&rft.au=Kaplan+RC&rft.au=Mohlke+KL&rft.au=O%27Connell+JR&rft.au=Peltonen+L&rft.au=Schlessinger+D&rft.au=Strachan+DP&rft.au=van+Duijn+CM&rft.au=Wichmann+HE&rft.au=Frayling+TM&rft.au=Thorsteinsdottir+U&rft.au=Abecasis+GR&rft.au=Barroso+I&rft.au=Boehnke+M&rft.au=Stefansson+K&rft.au=North+KE&rft.au=McCarthy+MI&rft.au=Hirschhorn+JN&rft.au=Ingelsson+E&rft.au=Loos+RJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Speliotes EK, Willer CJ, Berndt SI, Monda KL, Thorleifsson G, Jackson AU, Lango Allen H, Lindgren CM, Luan J, Mägi R, Randall JC, Vedantam S, Winkler TW, Qi L, Workalemahu T, Heid IM, Steinthorsdottir V, Stringham HM, Weedon MN, Wheeler E, Wood AR, Ferreira T, Weyant RJ, Segrè AV, Estrada K, Liang L, Nemesh J, Park JH, Gustafsson S, Kilpeläinen TO, Yang J, Bouatia-Naji N, Esko T, Feitosa MF, Kutalik Z, Mangino M, Raychaudhuri S, Scherag A, Smith AV, Welch R, Zhao JH, Aben KK, Absher DM, Amin N, Dixon AL, Fisher E, Glazer NL, Goddard ME, Heard-Costa NL, Hoesel V, Hottenga JJ, Johansson A, Johnson T, Ketkar S, Lamina C, Li S, Moffatt MF, Myers RH, Narisu N, Perry JR, Peters MJ, Preuss M, Ripatti S, Rivadeneira F, Sandholt C, Scott LJ, Timpson NJ, Tyrer JP, van Wingerden S, Watanabe RM, White CC, Wiklund F, Barlassina C, Chasman DI, Cooper MN, Jansson JO, Lawrence RW, Pellikka N, Prokopenko I, Shi J, Thiering E, Alavere H, Alibrandi MT, Almgren P, Arnold AM, Aspelund T, Atwood LD, Balkau B, Balmforth AJ, Bennett AJ, Ben-Shlomo Y, Bergman RN, Bergmann S, Biebermann H, Blakemore AI, Boes T, Bonnycastle LL, Bornstein SR, Brown MJ, Buchanan TA, Busonero F, Campbell H, Cappuccio FP, Cavalcanti-Proença C, Chen YD, Chen CM, Chines PS, Clarke R, Coin L, Connell J, Day IN, den Heijer M, Duan J, Ebrahim S, Elliott P, Elosua R, Eiriksdottir G, Erdos MR, Eriksson JG, Facheris MF, Felix SB, Fischer-Posovszky P, Folsom AR, Friedrich N, Freimer NB, Fu M, Gaget S, Gejman PV, Geus EJ, Gieger C, Gjesing AP, Goel A, Goyette P, Grallert H, Grässler J, Greenawalt DM, Groves CJ, Gudnason V, Guiducci C, Hartikainen AL, Hassanali N, Hall AS, Havulinna AS, Hayward C, Heath AC, Hengstenberg C, Hicks AA, Hinney A, Hofman A, Homuth G, Hui J, Igl W, Iribarren C, Isomaa B, Jacobs KB, Jarick I, Jewell E, John U, Jørgensen T, Jousilahti P, Jula A, Kaakinen M, Kajantie E, Kaplan LM, Kathiresan S, Kettunen J, Kinnunen L, Knowles JW, Kolcic I, König IR, Koskinen S, Kovacs P, Kuusisto J, Kraft P, Kvaløy K, Laitinen J, Lantieri O, Lanzani C, Launer LJ, Lecoeur C, Lehtimäki T, Lettre G, Liu J, Lokki ML, Lorentzon M, Luben RN, Ludwig B, MAGIC, Manunta P, Marek D, Marre M, Martin NG, McArdle WL, McCarthy A, McKnight B, Meitinger T, Melander O, Meyre D, Midthjell K, Montgomery GW, Morken MA, Morris AP, Mulic R, Ngwa JS, Nelis M, Neville MJ, Nyholt DR, O'Donnell CJ, O'Rahilly S, Ong KK, Oostra B, Paré G, Parker AN, Perola M, Pichler I, Pietiläinen KH, Platou CG, Polasek O, Pouta A, Rafelt S, Raitakari O, Rayner NW, Ridderstråle M, Rief W, Ruokonen A, Robertson NR, Rzehak P, Salomaa V, Sanders AR, Sandhu MS, Sanna S, Saramies J, Savolainen MJ, Scherag S, Schipf S, Schreiber S, Schunkert H, Silander K, Sinisalo J, Siscovick DS, Smit JH, Soranzo N, Sovio U, Stephens J, Surakka I, Swift AJ, Tammesoo ML, Tardif JC, Teder-Laving M, Teslovich TM, Thompson JR, Thomson B, Tönjes A, Tuomi T, van Meurs JB, van Ommen GJ, Vatin V, Viikari J, Visvikis-Siest S, Vitart V, Vogel CI, Voight BF, Waite LL, Wallaschofski H, Walters GB, Widen E, Wiegand S, Wild SH, Willemsen G, Witte DR, Witteman JC, Xu J, Zhang Q, Zgaga L, Ziegler A, Zitting P, Beilby JP, Farooqi IS, Hebebrand J, Huikuri HV, James AL, Kähönen M, Levinson DF, Macciardi F, Nieminen MS, Ohlsson C, Palmer LJ, Ridker PM, Stumvoll M, Beckmann JS, Boeing H, Boerwinkle E, Boomsma DI, Caulfield MJ, Chanock SJ, Collins FS, Cupples LA, Smith GD, Erdmann J, Froguel P, Grönberg H, Gyllensten U, Hall P, Hansen T, Harris TB, Hattersley AT, Hayes RB, Heinrich J, Hu FB, Hveem K, Illig T, Jarvelin MR, Kaprio J, Karpe F, Khaw KT, Kiemeney LA, Krude H, Laakso M, Lawlor DA, Metspalu A, Munroe PB, Ouwehand WH, Pedersen O, Penninx BW, Peters A, Pramstaller PP, Quertermous T, Reinehr T, Rissanen A, Rudan I, Samani NJ, Schwarz PE, Shuldiner AR, Spector TD, Tuomilehto J, Uda M, Uitterlinden A, Valle TT, Wabitsch M, Waeber G, Wareham NJ, Watkins H, Procardis Consortium, Wilson JF, Wright AF, Zillikens MC, Chatterjee N, McCarroll SA, Purcell S, Schadt EE, Visscher PM, Assimes TL, Borecki IB, Deloukas P, Fox CS, Groop LC, Haritunians T, Hunter DJ, Kaplan RC, Mohlke KL, O'Connell JR, Peltonen L, Schlessinger D, Strachan DP, van Duijn CM, Wichmann HE, Frayling TM, Thorsteinsdottir U, Abecasis GR, Barroso I, Boehnke M, Stefansson K, North KE, McCarthy MI, Hirschhorn JN, Ingelsson E, & Loos RJ (2010). Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index. <span style="font-style: italic;">Nature genetics, 42</span> (11), 937-48 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20935630">20935630</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft_id=info%3Apmid%2F22604720&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Evolution+and+functional+impact+of+rare+coding+variation+from+deep+sequencing+of+human+exomes.&rft.issn=0036-8075&rft.date=2012&rft.volume=337&rft.issue=6090&rft.spage=64&rft.epage=9&rft.artnum=http%3A%2F%2Fwuos.org%2Fcontent%2F337%2F6090%2F64.abstract&rft.au=Tennessen+JA&rft.au=Bigham+AW&rft.au=O%27Connor+TD&rft.au=Fu+W&rft.au=Kenny+EE&rft.au=Gravel+S&rft.au=McGee+S&rft.au=Do+R&rft.au=Liu+X&rft.au=Jun+G&rft.au=Kang+HM&rft.au=Jordan+D&rft.au=Leal+SM&rft.au=Gabriel+S&rft.au=Rieder+MJ&rft.au=Abecasis+G&rft.au=Altshuler+D&rft.au=Nickerson+DA&rft.au=Boerwinkle+E&rft.au=Sunyaev+S&rft.au=Bustamante+CD&rft.au=Bamshad+MJ&rft.au=Akey+JM&rft.au=Broad+GO&rft.au=Seattle+GO&rft.au=NHLBI+Exome+Sequencing+Project&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Tennessen JA, Bigham AW, O'Connor TD, Fu W, Kenny EE, Gravel S, McGee S, Do R, Liu X, Jun G, Kang HM, Jordan D, Leal SM, Gabriel S, Rieder MJ, Abecasis G, Altshuler D, Nickerson DA, Boerwinkle E, Sunyaev S, Bustamante CD, Bamshad MJ, Akey JM, Broad GO, Seattle GO, & NHLBI Exome Sequencing Project (2012). Evolution and functional impact of rare coding variation from deep sequencing of human exomes. <span style="font-style: italic;">Science (New York, N.Y.), 337</span> (6090), 64-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22604720">22604720</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft_id=info%3Apmid%2F22223662&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+mystery+of+missing+heritability%3A+Genetic+interactions+create+phantom+heritability.&rft.issn=0027-8424&rft.date=2012&rft.volume=109&rft.issue=4&rft.spage=1193&rft.epage=8&rft.artnum=http%3A%2F%2Fwww.pnas.org%2Fcontent%2F109%2F4%2F1193.full&rft.au=Zuk+O&rft.au=Hechter+E&rft.au=Sunyaev+SR&rft.au=Lander+ES&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Zuk O, Hechter E, Sunyaev SR, & Lander ES (2012). The mystery of missing heritability: Genetic interactions create phantom heritability. <span style="font-style: italic;">Proceedings of the National Academy of Sciences of the United States of America, 109</span> (4), 1193-8 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22223662">22223662</a></span>
nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com9tag:blogger.com,1999:blog-5002675950760488813.post-68219718270273802542012-08-05T10:28:00.000-07:002012-08-07T22:21:30.221-07:00The Hispanic Asian Flynn Effect<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-utcnzosPSYQ/UB57sHI4isI/AAAAAAAAAhI/XhQrdv3iLdk/s1600/unz.jpg" imageanchor="1" style="clear:right; float:right; margin-left:1em; margin-bottom:1em"><img border="0" height="200" width="159" src="http://1.bp.blogspot.com/-utcnzosPSYQ/UB57sHI4isI/AAAAAAAAAhI/XhQrdv3iLdk/s200/unz.jpg" /></a></div>
Recently, activist and entrepreneur Ron Unz used results from a short English vocabulary test, called Wordsum, <a href="http://www.theamericanconservative.com/articles/race-iq-and-wealth/">to argue</a> that Mexican Americans have risen in intelligence, shrinking their intellectual disadvantage relative to white Americans by two-thirds. David Sanders (an alias) <a href="http://www.vdare.com/articles/has-ron-unz-refuted-hard-hereditarianism">countered</a> this claim, using one of my previous posts on racial group differences in SAT performance.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-C9hgzQQxcsU/UB6TlaqYWUI/AAAAAAAAAho/_faVtosqavk/s1600/sat%2Bhispanic.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://2.bp.blogspot.com/-C9hgzQQxcsU/UB6TlaqYWUI/AAAAAAAAAho/_faVtosqavk/s400/sat%2Bhispanic.png" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-mBy-9dQQZkU/UB6Ttvbu0OI/AAAAAAAAAh0/3OdNJu04kaw/s1600/sat%2Bmexican.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://1.bp.blogspot.com/-mBy-9dQQZkU/UB6Ttvbu0OI/AAAAAAAAAh0/3OdNJu04kaw/s400/sat%2Bmexican.png" /></a></div>
<br>
<a href="http://www.theamericanconservative.com/unz-on-raceiq-incorporating-the-racialist-perspective/?utm_source=rss&utm_medium=rss&utm_campaign=unz-on-raceiq-incorporating-the-racialist-perspective">Here</a> is how Unz responded:
<blockquote>Although several different arguments were made, the strongest and most detailed focused on an examination of the ethnic distribution of American SAT scores between 1980 and 2010 [<i>sic</i>], performed by another highly quantitive racialist blogger. The article pointed out that there was virtually no net change in the substantial Hispanic/white performance gap on the SAT during those four decades. Since the SAT is a far better proxy for IQ than my Wordsum values, and the number of participants across those years number in the millions, any possibility of a large rise in Hispanic IQ would seem completely disproven. My claims had focused on American-born Mexican-Americans rather than Hispanics in general, but since the former group represented a large and rapidly growing portion of the latter, my argument would seem to have suffered a very serious blow.
<br><br>However, this is incorrect…. With some effort, I managed to obtain the ethnic distribution of SAT test-takers back to 1975 and then compared these results with the ethnic distribution of 18-year-olds during those years, found in the Census-CPS [Current Population Survey] data.
<br><br>Just as I had suspected, the changes were dramatic. In 1975, 22% of whites took the SAT, and this had risen to 33% by 2011, a substantial rise of 50%. However, during these same decades, the percentage of Hispanic test-takers had grown from 6% to 32%, an enormous rise of over 400%. Thus, in 1975 white 18-year-olds were nearly four times more likely to take the SAT, but by 2011 the ratios were almost exactly the same…. Since the white/Hispanic gap remained unchanged during this tremendous broadening of the Hispanic testing pool rather than greatly widening, the only possible explanation would seem to be a huge rise in average Hispanic academic performance, just as was reflected in the Wordsum-IQ scores….
<br><br>Thus, upon closer examination the SAT evidence cited for the alleged lack of Hispanic gains actually becomes very powerful evidence for strong Hispanic gains.</blockquote>
After going through <a href="http://www.census.gov/hhes/school/data/cps/index.html">reports from CPS</a>, I have been unable to replicate these numbers precisely. Most of the reports that I found give combined totals of 18- and 19-year-olds, so I divided those in half, which I consider a fair estimation. I also cannot locate a report for 2011. Assuming CPS has released it somewhere, the notion that the participation gap dropped from nine percentage points to one in a single year defies credulity.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-IUElrOKhkDw/UB56VojyTDI/AAAAAAAAAgM/vJU5EG--rYg/s1600/sat%2Bparticipation.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://1.bp.blogspot.com/-IUElrOKhkDw/UB56VojyTDI/AAAAAAAAAgM/vJU5EG--rYg/s400/sat%2Bparticipation.png" /></a></div>
<br>
For white students, my results are similar to those of Unz. Their participation rose from 21% to 34%, an increase of 61%. If one looks at the full range, rather than just the bookend years, the rise is 19% to 34%, 79% higher. I found that Hispanics rose from 7% to 25%, which is a 257% increase. That is still a huge jump, even if it is not 433%. The rates of change of participation in the graph look similar, but Hispanic students start much lower.
<br><br>
However, discussion of the exact calculations is moot because both sets are based on a falsehood. Take a close look at the graph. Notice anything strange? In 1987, non-Mexican Hispanic students suddenly resolved to take the SAT in much greater numbers. Before one goes searching for a mind-blowing ‘80s Spanish public service announcement, I must reveal (<a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">again</a>) that the College Board added a third category of Hispanic in 1987, in addition to Mexican and Puerto Rican, and this new category was “other Hispanic.” A group of people who had previously been something other than Hispanic consequently metamorphosed into Hispanic people with sombreros, I think. Other Hispanic students (or, as I prefer, “Hispanica Miscellanea”) rival Mexican-American students in number. The dramatic quality of the rise in Hispanic participation merely represents an artifact of definitional change. Calculations with a starting year of 1987 give a white student range of 23% to 34% (a 48% increase), an African-American student range of 12% to 29% (a 71% increase), and a Hispanic student range of 14% to 25% (a 79% increase).
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-ZmoS8fussNU/UB6YSOTBuPI/AAAAAAAAAiU/8VOTXmReRa0/s1600/sat%2Bhispanic%2Bparticipation.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://2.bp.blogspot.com/-ZmoS8fussNU/UB6YSOTBuPI/AAAAAAAAAiU/8VOTXmReRa0/s400/sat%2Bhispanic%2Bparticipation.png" /></a></div>
<br>
Unz was making the point that SAT data support a secular rise in Hispanic cognitive ability, according to the fundamental law of participation level-actual ability direct correlation. This law allows us to assume that Hispanics are becoming smarter if they can take the test in greater numbers while only slightly worsening their score performance relative to white students. My only problem with the law is that the SAT dataset is riddled with countervailing examples, as I <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">previously discussed</a>.
<br><br>
One counterexample is particularly illustrative. In 1998, CPS discovered the existence of a group of people called the Asian Americans. This extraordinary new tribe possesses a pleasing aesthetic, but they can only eat with primitive sticks. After a detailed analysis of Asian SAT performance and participation, I can confidently state the broad conclusion that Asians are different.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-jbmXYeK3MoY/UB56mHIqnaI/AAAAAAAAAgY/SJJ021eXp9A/s1600/sat%2Bparticipation%2Bw%2Basian.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://3.bp.blogspot.com/-jbmXYeK3MoY/UB56mHIqnaI/AAAAAAAAAgY/SJJ021eXp9A/s400/sat%2Bparticipation%2Bw%2Basian.png" /></a></div>
<br>
As the above graph proves, Asian Americans so enthusiastically partake in the SAT that they achieve participation proportions greater than <i>all of them</i>. It seems that some proportion of Asian SAT takers are foreign students unrecognized by the US Census. I wonder if the Hispanic-American community also includes a group of census-undercounted individuals who nonetheless live here. Asian students are the one racial group whose SAT performance is taking off, and they have achieved this while increasing their test participation 105%, and I <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">already</a> dispelled attempts to use foreign-student involvement to explain away Asian score advancement. For emphasis, I shall present this graph of the Asian-Hispanic score gap in standard deviations, superimposed over the Asian-white score gap, with the colors of the latter set to grey.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-VW_R80yO2I0/UCH3D2ChY2I/AAAAAAAAAi0/zBhi6SIBtGk/s1600/sat%2Basian%2Bhispanic.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://4.bp.blogspot.com/-VW_R80yO2I0/UCH3D2ChY2I/AAAAAAAAAi0/zBhi6SIBtGk/s400/sat%2Basian%2Bhispanic.png" /></a></div>
<br>
In fairness, my essay raised the possibility to white aptitude decline relative to other groups and included in the reasoning a possible decline of white participation. If those who do not identify their race are largely white, as I hypothesized, then white students have decreased their participation from 43% in 2003 to 37% in 2010. However, that would also mean that white students had increased their participation since 1987 by 87%, at their peak, which is a greater increase than that of Hispanics, and the possible rise and fall left no footprint in the graph of the Hispanic-white gap.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-Dx5IvQJnNH0/UB57ExgvTFI/AAAAAAAAAgw/pcpdS02FHBw/s1600/sat%2Bparticipation%2Bw%2Bnr.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://3.bp.blogspot.com/-Dx5IvQJnNH0/UB57ExgvTFI/AAAAAAAAAgw/pcpdS02FHBw/s400/sat%2Bparticipation%2Bw%2Bnr.png" /></a></div>
<br>
Despite the racial disquiet that the SAT invokes, the test might actually be hiding the full extent of the racial gaps. First of all, the College Board altered its scoring algorithm in 1996 with the <a href="http://theunsilencedscience.blogspot.com/2011/09/sat-in-red-white-and-brown.html">explicit</a> purpose of narrowing racial gaps. Second, unlike the score range of many IQ tests, the SAT score range is, itself, sufficiently narrow so as to construct a secure floor for the bell curve’s far left and a ceiling that holds down the absolute best. I have perhaps overemphasized in the past the fact that African-American students have a larger gap with white students on the SAT mathematics subtest than on the writing and reading subtests. I cannot rule out that the subtest differences result purely from the massive number of African Americans who occupy the floor of the reading and writing subtests, as I <a href="http://theunsilencedscience.blogspot.com/2012/04/sat-bell-curve.html">previously graphed</a>. Likewise, I can now reveal additional years of the white and Asian mathematics subtest bell curves that demonstrate substantial increases in perfection or near perfection of what was already outstanding Asian mathematics success.
<br><br>
<center><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawmdist81-92.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawmdist81-92.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>Therein lies the crux of the issue. If all Unz wanted to prove was that the “Strong IQ Hypothesis” fails to account for the malleability of cognitive results, he could have cited the Asian advancement on the SAT. By bothering to analyze SAT results over time and by describing the progress of Asians, I have already implicitly acknowledged that some things do change and environment matters, at least under some circumstances. Usually, efforts to deny the existence of, minimize the importance of, or supply loose elasticity to IQ share the same impetus as the linguistic pursuit of calling “race” a “social construct.” The canards aspire to overrule by abstraction or technicality evidence for sociological generalizations labelled “stereotypes” or to beg the question regarding biological causality without dirtying one's hands with biological evidence. Recognizing an Asian academic model only reinforces a stereotype, to which even many Asians strain to take offense. That the SAT does not yet demonstrate an unmet potential in Hispanic Americans provides no paradox of proven unmet potential. To even engage the issue is to take for granted a stereotype. All good people are asleep and dreaming.nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com6tag:blogger.com,1999:blog-5002675950760488813.post-31695392968880322082012-07-05T05:22:00.000-07:002012-07-05T06:10:38.409-07:00Just Say No Limit: Trayvon, Dextromethorphan, Marijuana, and MAOA<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
When I <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">recently posted</a> a photograph of Trayvon Martin, the African-American victim of a shooting during a confrontation with a neighborhood-watch volunteer, making an obscene gesture, many of my readers missed the inside joke. The national media packaged the earliest reports on this case to maximize sympathy for the 17-year-old Martin. We knew him by his cute, smiling visage from a few professional pictures taken when he was not older than thirteen. These appeared alongside a 2005 mug shot of the shooter. When a more recent photograph of Martin extending one middle finger at a camera came to light, a <a href="http://dailycaller.com/2012/03/29/second-trayvon-martin-twitter-feed-identified/">conspiracy theory</a> emerged to defend his honor. Some insisted that the hand must have been photoshopped because another photograph exists utterly lacking said digit.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=Trayvon-images-comparison.gif" target="_blank"><img src="http://i1087.photobucket.com/albums/j471/nooffensebut/Trayvon-images-comparison.gif" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
Alas, Martin’s YouTube page, which had not been accessed since before Martin’s death when I arrived at it, utilized the controversial photograph that I would post, containing, not one, but (count them!) two middle fingers! Similar photographs subsequently made the rounds, and it became clear that the new-media-savvy Mr. Martin had something of a trademark pose. Not only was Martin’s innocent image taking flak, but I felt my own moral sensibilities slipping away under the onslaught of a greater quantity of this vulgar sign than I had previously imagined.
<br><br>
At least Americans understood the senselessness of the shooting, given that Martin was merely taking a stroll to a corner convenience store to buy a package of Skittles and a can of iced tea. Well, the police report noted an “Arizona tea can,” but a photograph of the can clearly reveals it to be Arizona Watermelon Fruit Juice Cocktail. So what? Actually, this beverage and Skittles are ingredients of a recreational drug called “watermelon lean,” the knowledge of which I must credit to the blog <a href="http://theconservativetreehouse.com/2012/05/24/update-26-part-2-trayvon-martin-shooting-a-year-of-drug-use-culminates-in-predictable-violence/">The Conservative Treehouse</a>. Martin actually acknowledged his use of lean on Facebook. The psychoactive ingredient of lean is the over-the-counter cough medicine, dextromethorphan, which happens to carry the street name, “Skittles.” At high doses, dextromethorphan acts as an addictive drug with the same dissociative symptoms as phencyclidine (PCP or “angel dust”). Case reports of psychotic symptoms, including paranoia and <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1556-4029.2012.02133.x/abstract">aggression</a>, have followed dextromethorphan toxicity since the 1960s. Perhaps, then, it is small wonder that the young lady whom Martin’s family falsely described as his “girlfriend” shared that, in the cell phone conversation leading up to the shooting, Martin had told her that the shooter, George Zimmerman, was “looking crazy.” Even if the prosecution’s narrative is accurate, (cliché or not) another being out to get one cannot preclude one’s paranoia.
<br><br>
<center>
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=arizona-watermelon.jpg" target="_blank"><img src="http://i1087.photobucket.com/albums/j471/nooffensebut/arizona-watermelon.jpg" border="0" alt="Photobucket"></a>
<br/><br/>
</center>
Much like Martin, dextromethorphan benefits from an innocent public image far removed from angel dust comparisons. However, the <a href="http://www.cjem-online.ca/v13/n1/p53">case reports</a> have described “cough-syrup psychosis” as lasting several days even after disuse, and some factors, to which Martin was subject, can accentuate the effective dosage and half life of Skittles.
<br><br>
One such factor, arguably, is marijuana. Marijuana hashish is 2.5% cannabidiol, the second most common cannabinoid in marijuana after THC, which is the primary cause of marijuana’s psychological effects. Cannabidiol inhibits a liver enzyme called CYP2D6, which is the major enzyme of dextromethorphan metabolism. While a recent <a href="http://dmd.aspetjournals.org/content/39/11/2049.short">study</a> called this inhibition “potent,” the blood levels of cannabidiol from smoking a single marijuana joint would be too low to significantly impact dextromethorphan metabolism. THC also inhibits CYP2D6 but with about three times less potency than cannabidiol. However, marijuana could interact with dextromethorphan by another pathway involving the enzyme produced by “the warrior gene.”
<br><br>
Because the liver enzyme CYP2D6 is inhibited or enhanced in its activity by a number of drugs, there are a number of potential drug interactions for dextromethorphan. However, only one class of drug received a specific drug interaction warning in a best-selling medical school pharmacology textbook, Katzung’s Basic and Clinical Pharmacology, as well as on UpToDate, a subscription-based Internet site heavily used by internal medicine physicians. This class of drug is called monoamine oxidase inhibitors (MAOIs), which were the first anti-depressants and are now much less commonly used since selective serotonin reuptake inhibitors (SSRIs) are available with far less severe side effects. Regular readers of my blog know that one of my obsessions is the study of the genetics of violence. The best understood gene that affects violent behavior is monoamine oxidase A (MAOA), which produces an enzyme of the same name. This enzyme is one of the two enzymes that MAOIs inhibit. The MAOA enzyme breaks down mostly the neurotransmitters serotonin and norepinephrine. Doctors believe that MAOIs work because having too few of such neurotransmitters in the synapses between neurons can result in depression. Many doctors and scientists also believe that having too many such neurotransmitters in synapses can result in antisocial personality disorder, conduct disorder, delinquency, and aggression. Of course, neurochemistry is more complicated than I am describing, but I think this is a fair summation of many decades of medical expertise on the treatment of depression. When dextromethorphan and MAOIs interact, serotonin levels can acutely rise and cause a potentially deadly reaction called serotonin syndrome. According to the Katzung text, the predictability of the interaction lacks sufficient data to qualify as “established.” Trayvon Martin was not taking MAOIs, but if he had reduced MAOA function for other reasons, it could have boosted his levels of serotonin and norepinephrine and given him a greater tendency towards aggression and delinquency.
<br><br>
THC inhibits the enzyme MAOA at roughly the same potency as it inhibits CYP2D6, according to a <a href="http://psych.lf1.cuni.cz/zf/publikace/d1020.pdf">study</a> of brain MAOA from pigs. That study also questioned whether common marijuana usage would have any meaningful effect on behavior or emotion with such a low level of potency, but it noted that brain levels of THC are higher than blood levels, and THC accumulates in neurons. Martin’s blood THC level was 1.5 ng/mL, far below the average peak concentration of 162 ng/mL caused by smoking a single marijuana cigarette. Peak concentration tends to occur about eight minutes after someone begins smoking, whereas Martin’s level matches a person who smoked one joint 3-6 hours prior. A professor of forensic science named Larry Kobilinsky <a href="http://www.cbsnews.com/8301-504083_162-57437018-504083/trayvon-martin-shooting-new-evidence-shows-wounds-on-zimmermans-head-thc-found-in-martins-body/">claimed</a> that the marijuana use could have been days earlier, but that conclusion does not match the results of a <a href="http://jat.oxfordjournals.org/content/16/5/276.abstract">study</a> from the National Institute on Drug Abuse, at least if the marijuana is limited to a single cigarette. Plus, Martin’s cousin, Stephen Martin, appears to have <a href="https://twitter.com/RIP_TRAY9/statuses/181251936119570434">posted</a> on Twitter that Trayvon Martin was “high” within twenty-four hours of the shooting.
<br><br>
Smoking tobacco seems to inhibit monoamine oxidase much more than smoking an occasional joint. Smokers typically have <a href="http://journals.cambridge.org/action/displayAbstract;jsessionid=C2B8DEBCE8F9D34E97BA5211D87A88BC.journals?fromPage=online&aid=73851">20-30% lower</a> MAOA enzyme activity and 30-40% lower activity of the other monoamine oxidase enzyme, MAOB, which accounts for about 30% of monoamine oxidase enzymes in the brain. <a href="http://www.pnas.org/content/93/24/14065.long">Fowler et al</a> determined that cigarette smoking lowers brain MAOA half as much as taking the MAOI tranylcypromine.
<br><br>
Martin might have been a smoker. He seemed to obtain cigarillos from three young men, according to some interpretations of the 7/11 surveillance videos, and a lighter was among his belongings at the scene of the shooting. Also, his lungs had mild anthracosis, which is a black discoloration that can result from smoking. Even if Martin only smoked marijuana, if he used cigarillos as marijuana blunts, then he was smoking the tobacco that constitutes the blunts with his marijuana, likely without filters.
<br><br>
Genetic differences can influence dextromethorphan response. Wide variation exists in the gene for CYP2D6, such that poor metabolizers experience blood concentration levels <a href="http://journals.lww.com/psychopharmacology/Abstract/1998/08000/Psychotropic_Effects_of_Dextromethorphan_Are.14.aspx">five times</a> greater than extensive metabolizers. Martin’s African-American heritage <a href="http://www2.webmatic.it/workO/s/113/pr-473-file_it-Pharmacogenetics%20and%20Genomics%2017.pdf">does not affect</a> his likelihood of having a version of the CYP2D6 gene that would cause him to slowly metabolize dextromethorphan, but this is not the case for the gene that determines MAOA levels.
<br><br>
Black people have <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=491991">62% lower</a> monoamine oxidase activity than white people, as measured by MAOB activity in the platelets of blood. Black men are <a href="http://theunsilencedscience.blogspot.com/2010/01/deus-ex-machina-genetics.html">about twice</a> as likely as white people to have the “warrior gene,” which is basically just the 3-repeat allele of the MAOA gene promoter (rather than the 4-repeat allele, which most white people have). <a href="http://theunsilencedscience.blogspot.com/2011/03/racial-controversy-of-violent-gene.html">Five percent</a> of African-American men (or about 10 times the prevalence of white men) have the understudied 2-repeat allele of MAOA, which appears to double the rate of aggression compared to men with the more common versions of the gene. However, the label of “warrior gene” for the less dangerous 3-repeat version is still highly appropriate. In fact, I would argue that the association of aggression with the interaction between the 3-repeat allele and childhood maltreatment is the strongest single-gene finding in all of behavioral genetics. I could list the breadth of corroborating lines of evidence: behavioral associations exist for the gene’s promoter, its enzyme product, the metabolites of the enzyme’s reaction, gene activity demonstrated in functional MRI, the degree of epigenetic methylation, epistatic interactions between the gene’s promoter and other genes, an interaction between this promoter and a second promoter of the MAOA gene, interactions between the MAOA gene promoter and sex hormones, and completely inactivating “knock-out” alleles in humans and animal models.
<br><br>
As the designs of the studies on this gene have improved, the robustness of their conclusions strengthened. Last year, I posed some <a href="http://theunsilencedscience.blogspot.com/2011/09/pulling-empty-chair-on-dr-kevin-beaver.html">pointed questions</a> to one researcher about how more thorough consideration of confounding variables could produce more startling results, and a team of New Zealand researchers have recently published a <a href="http://bjp.rcpsych.org/content/200/2/116.short">study</a> demonstrating exactly what I predicted. They sought to determine whether any of a list of possible risk factors could, in the presence of the 3-repeat allele but not the 4-repeat allele, increase the likelihood of violent behavior. Their study did not report all of the factors that failed this test, but five such measures did trigger the genetic predisposition: childhood maltreatment, the mother smoking during pregnancy, ten years of an interviewer’s assessment of poor material living standards, dropping out of school by age 18, and a low average of two IQ scores at ages 8 and 9 from the revised Wechsler Intelligence Scale for Children. In each case, the 4-repeat allele protected against adopting violent tendencies, and all five factors melded into a combined risk index that greatly accentuated the genetic differences at the highest index levels. I found it particularly interesting that, after ten years of studies replicating the original childhood-maltreatment-gene interaction, this study determined that the IQ-gene interaction influenced violence with a greater degree of certainty than the gene’s interaction with physical or sexual child abuse.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-jfDyh1zM2fk/T_WF7m7oNsI/AAAAAAAAAfw/QddSOLbgEUc/s1600/MAOA%2BViolence.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="355" width="400" src="http://2.bp.blogspot.com/-jfDyh1zM2fk/T_WF7m7oNsI/AAAAAAAAAfw/QddSOLbgEUc/s400/MAOA%2BViolence.jpg" /></a></div>
<br>
<center><b>GWAS Jihadists</b></center>
<br><br>
Opposition to the science of the MAOA gene has dwindled to an embattled coterie of shrieking moralists and charlatan scientists. When Harvard psychologist Steven Pinker published The Better Angels of Our Nature, Pulitzer Prize-winning columnist Nicholas Kristof <a href="http://www.nytimes.com/2011/11/24/opinion/kristof-are-we-getting-nicer.html">bet</a> that Pinker would join the ranks of Pulitzer winners. However, I used this little blog to <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">point out</a> that Pinker had passed on in the book a falsehood based on a copy-and-paste error, among other mistakes, to malign MAOA research. In the weeks prior to the Pulitzer committee’s decision, my Pinker post experienced a surge of readers. Ultimately, Pinker’s book would not win even an official nomination. None of this prevented yet another cheap “ethics” journal from publishing a <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1467-8519.2012.01970.x/abstract">screed</a> by a “philosopher and biologist,” who repeated the error once more. Meanwhile, researchers who focus on genome-wide association studies (GWAS) have led a failed campaign to silence all candidate-gene research. According to <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3222234/">Duncan and Keller</a>, “the possibility that most or <b>even all</b> positive [candidate gene-by-environment interaction] findings in psychiatry discovered to date represent type I errors cannot be discounted [emphasis added].” In other words, every single association between a single gene allele in a certain environmental milieu affecting a behavior, including a decade of studies on the 3-repeat MAOA promoter, might be merely one of a series of falsely positive flukes. Well, if the studies are all wrong, then why publish them? According to <a href="http://w.leadingteams.org/~cfc/Chabris2012a-FalsePositivesGenesIQ.pdf">Chabris et al</a>:
<blockquote>At the time most of the results we have attempted to replicate were obtained, candidate gene studies of complex traits were commonplace in medical genetics research. Such studies are now rarely published in leading journals…. In our view, excitement over the value of behavioral and molecular genetic studies in the social sciences should be tempered—as it has been in the medical sciences—by an appreciation that for complex phenotypes, individual common genetic variants of the sort assayed by SNP [single-nucleotide polymorphism] microarrays are likely to have very small effects.</blockquote>
So, psychiatric and psychological journals should follow the lead of respectable medical journals and stop publishing studies on individual genes and instead wait for GWAS to fill the void. That might take a while because SNP microarrays only study common SNPs and a select number of copy-number variations and have no capacity to study a third form of genetic variation, called variable number tandem repeats (VNTR), which includes the MAOA promoter.
<br><br>
Psychiatry is an applied science. The gold standards for treating psychiatric illnesses include powerful drugs that target neurotransmitters. Doctors cannot afford to ignore gene variants that also interact with neurotransmitters, any more than they can ignore drug-drug interactions, therapeutic or recreational. Violent behavior is a diagnostic criterion of many mental illnesses. Indeed, I would advocate giving impulsive aggression a diagnostic label of its own (one that doctors and researchers would actually use, unlike “intermittent explosive disorder”).
<br><br>
In the Trayvon Martin shooting case, the defense might need to establish that Martin had a violent predisposition to strengthen a self-defense claim. Drug use and any indication of his cognitive abilities are relevant, and it would be useful to conduct genetic tests for the MAOA promoter and CYP2D6. If that is impermissible, then Martin’s African-American racial identity becomes more relevant with its associated allele frequencies. In some trials, MAOA gene tests have already served as exculpatory evidence in the mold of the insanity defense. The right to fight back against an individual who is warrior-gene positive makes just as much sense.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=CJEM&rft_id=info%3Apmid%2F21324299&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Cough+syrup+psychosis.&rft.issn=1481-8035&rft.date=2011&rft.volume=13&rft.issue=1&rft.spage=53&rft.epage=6&rft.artnum=http%3A%2F%2Fwww.cjem-online.ca%2Fv13%2Fn1%2Fp53&rft.au=Amaladoss+A&rft.au=O%27Brien+S&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Amaladoss A, & O'Brien S (2011). Cough syrup psychosis. <span style="font-style: italic;">CJEM, 13</span> (1), 53-6 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21324299">21324299</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+International+Journal+of+Neuropsychopharmacology&rft_id=info%3Adoi%2F10.1017%2FS1461145701002188&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidases+and+tobacco+smoking&rft.issn=&rft.date=2001&rft.volume=4&rft.issue=01&rft.spage=33&rft.epage=42&rft.artnum=http%3A%2F%2Fjournals.cambridge.org%2Faction%2FdisplayAbstract%3Bjsessionid%3DC2B8DEBCE8F9D34E97++BA5211D87A88BC.journals%3FfromPage%3Donline%26aid%3D73851&rft.au=Ivan+Berlin&rft.au=Robert+Anthenelli&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Ivan Berlin, & Robert Anthenelli (2001). Monoamine oxidases and tobacco smoking <span style="font-style: italic;">The International Journal of Neuropsychopharmacology, 4</span> (01), 33-42 DOI: <a rev="review" href="http://dx.doi.org/10.1017/S1461145701002188">10.1017/S1461145701002188</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+Science&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Most+Reported+Genetic+Associations+with+General+Intelligence+are+Probably+False+Positives&rft.issn=&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fw.leadingteams.org%2F%7Ecfc%2FChabris2012a-FalsePositivesGenesIQ.pdf&rft.au=Christopher+Chabris&rft.au=Benjamin+Hebert&rft.au=Daniel+Benjamin&rft.au=Jonathan+Beauchamp&rft.au=David+Cesarini&rft.au=Matthijs+van+der+Loos&rft.au=Magnus+Johannesson&rft.au=Patrik+Magnusson&rft.au=Paul+Lichtenstein&rft.au=Craig+Atwood&rft.au=Jeremy+Freese&rft.au=Taissa+Hauser&rft.au=Robert+Hauser&rft.au=Nicholas+Christakis&rft.au=David+Laibson&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Christopher Chabris, Benjamin Hebert, Daniel Benjamin, Jonathan Beauchamp, David Cesarini, Matthijs van der Loos, Magnus Johannesson, Patrik Magnusson, Paul Lichtenstein, Craig Atwood, Jeremy Freese, Taissa Hauser, Robert Hauser, Nicholas Christakis, & David Laibson (2012). Most Reported Genetic Associations with General Intelligence are Probably False Positives <span style="font-style: italic;">Psychological Science</span></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+American+journal+of+psychiatry&rft_id=info%3Apmid%2F21890791&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+critical+review+of+the+first+10+years+of+candidate+gene-by-environment+interaction+research+in+psychiatry.&rft.issn=0002-953X&rft.date=2011&rft.volume=168&rft.issue=10&rft.spage=1041&rft.epage=9&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3222234%2F&rft.au=Duncan+LE&rft.au=Keller+MC&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Duncan LE, & Keller MC (2011). A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry. <span style="font-style: italic;">The American journal of psychiatry, 168</span> (10), 1041-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21890791">21890791</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft_id=info%3Apmid%2F22297589&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Moderating+role+of+the+MAOA+genotype+in+antisocial+behaviour.&rft.issn=0007-1250&rft.date=2012&rft.volume=200&rft.issue=2&rft.spage=116&rft.epage=23&rft.artnum=http%3A%2F%2Fbjp.rcpsych.org%2Fcontent%2F200%2F2%2F116.short&rft.au=Fergusson+DM&rft.au=Boden+JM&rft.au=Horwood+LJ&rft.au=Miller+A&rft.au=Kennedy+MA&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA (2012). Moderating role of the MAOA genotype in antisocial behaviour. <span style="font-style: italic;">The British journal of psychiatry : the journal of mental science, 200</span> (2), 116-23 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22297589">22297589</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft_id=info%3Apmid%2F20401651&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Inhibition+of+monoamine+oxidase+activity+by+cannabinoids.&rft.issn=0028-1298&rft.date=2010&rft.volume=381&rft.issue=6&rft.spage=563&rft.epage=72&rft.artnum=http%3A%2F%2Fpsych.lf1.cuni.cz%2Fzf%2Fpublikace%2Fd1020.pdf&rft.au=Fisar+Z&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Fisar Z (2010). Inhibition of monoamine oxidase activity by cannabinoids. <span style="font-style: italic;">Naunyn-Schmiedeberg's archives of pharmacology, 381</span> (6), 563-72 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20401651">20401651</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Nature&rft_id=info%3Apmid%2F8602220&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Inhibition+of+monoamine+oxidase+B+in+the+brains+of+smokers.&rft.issn=0028-0836&rft.date=1996&rft.volume=379&rft.issue=6567&rft.spage=733&rft.epage=6&rft.artnum=http%3A%2F%2Fwww.pnas.org%2Fcontent%2F93%2F24%2F14065.long&rft.au=Fowler+JS&rft.au=Volkow+ND&rft.au=Wang+GJ&rft.au=Pappas+N&rft.au=Logan+J&rft.au=MacGregor+R&rft.au=Alexoff+D&rft.au=Shea+C&rft.au=Schlyer+D&rft.au=Wolf+AP&rft.au=Warner+D&rft.au=Zezulkova+I&rft.au=Cilento+R&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Fowler JS, Volkow ND, Wang GJ, Pappas N, Logan J, MacGregor R, Alexoff D, Shea C, Schlyer D, Wolf AP, Warner D, Zezulkova I, & Cilento R (1996). Inhibition of monoamine oxidase B in the brains of smokers. <span style="font-style: italic;">Nature, 379</span> (6567), 733-6 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/8602220">8602220</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Archives+of+General+Psychiatry&rft_id=info%3Adoi%2F10.1001%2Farchpsyc.1978.01770340048004&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Activities+of+Types+A+and+B+MAO+and+Catechol-O-methyltransferase+in+Blood+Cells+and+Skin+Fibroblasts+of+Normal+and+Chronic+Schizophrenic+Subjects&rft.issn=&rft.date=1978&rft.volume=35&rft.issue=10&rft.spage=1198&rft.epage=1205&rft.artnum=http%3A%2F%2Farchpsyc.jamanetwork.com%2Farticle.aspx%3Farticleid%3D491991&rft.au=Regina+Groshong&rft.au=Ross+Baldessarini&rft.au=Ann+Gibson&rft.au=Joseph+Lipinski&rft.au=Doris+Axelrod&rft.au=Alfred+Pope&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Regina Groshong, Ross Baldessarini, Ann Gibson, Joseph Lipinski, Doris Axelrod, & Alfred Pope (1978). Activities of Types A and B MAO and Catechol-O-methyltransferase in Blood Cells and Skin Fibroblasts of Normal and Chronic Schizophrenic Subjects <span style="font-style: italic;">Archives of General Psychiatry, 35</span> (10), 1198-1205 DOI: <a rev="review" href="http://dx.doi.org/10.1001/archpsyc.1978.01770340048004">10.1001/archpsyc.1978.01770340048004</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+analytical+toxicology&rft_id=info%3Apmid%2F1338215&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Blood+cannabinoids.+I.+Absorption+of+THC+and+formation+of+11-OH-THC+and+THCCOOH+during+and+after+smoking+marijuana.&rft.issn=0146-4760&rft.date=1992&rft.volume=16&rft.issue=5&rft.spage=276&rft.epage=82&rft.artnum=http%3A%2F%2Fjat.oxfordjournals.org%2Fcontent%2F16%2F5%2F276.abstract&rft.au=Huestis+MA&rft.au=Henningfield+JE&rft.au=Cone+EJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Huestis MA, Henningfield JE, & Cone EJ (1992). Blood cannabinoids. I. Absorption of THC and formation of 11-OH-THC and THCCOOH during and after smoking marijuana. <span style="font-style: italic;">Journal of analytical toxicology, 16</span> (5), 276-82 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/1338215">1338215</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+forensic+sciences&rft_id=info%3Apmid%2F22537430&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Dextromethorphan+Abuse+Leading+to+Assault%2C+Suicide%2C+or+Homicide.&rft.issn=0022-1198&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.1111%2Fj.1556-4029.2012.02133.x%2Fabstract&rft.au=Logan+BK&rft.au=Yeakel+JK&rft.au=Goldfogel+G&rft.au=Frost+MP&rft.au=Sandstrom+G&rft.au=Wickham+DJ&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Logan BK, Yeakel JK, Goldfogel G, Frost MP, Sandstrom G, & Wickham DJ (2012). Dextromethorphan Abuse Leading to Assault, Suicide, or Homicide. <span style="font-style: italic;">Journal of forensic sciences</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22537430">22537430</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Bioethics&rft_id=info%3Apmid%2F22494506&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=THE+%27WARRIOR+GENE%27+AND+THE+M%C3%83ORI+PEOPLE%3A+THE+RESPONSIBILITY+OF+THE+GENETICISTS.&rft.issn=0269-9702&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.1111%2Fj.1467-8519.2012.01970.x%2Fabstract&rft.au=Perbal+L&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Perbal L (2012). THE 'WARRIOR GENE' AND THE MÃORI PEOPLE: THE RESPONSIBILITY OF THE GENETICISTS. <span style="font-style: italic;">Bioethics</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22494506">22494506</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Pharmacogenetics+and+genomics&rft_id=info%3Apmid%2F17301689&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=CYP2D6+worldwide+genetic+variation+shows+high+frequency+of+altered+activity+variants+and+no+continental+structure.&rft.issn=1744-6872&rft.date=2007&rft.volume=17&rft.issue=2&rft.spage=93&rft.epage=101&rft.artnum=http%3A%2F%2Fwww2.webmatic.it%2FworkO%2Fs%2F113%2Fpr-473-file_it-Pharmacogenetics%2520and%2520Genomics%252017.pdf&rft.au=Sistonen+J&rft.au=Sajantila+A&rft.au=Lao+O&rft.au=Corander+J&rft.au=Barbujani+G&rft.au=Fuselli+S&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Sistonen J, Sajantila A, Lao O, Corander J, Barbujani G, & Fuselli S (2007). CYP2D6 worldwide genetic variation shows high frequency of altered activity variants and no continental structure. <span style="font-style: italic;">Pharmacogenetics and genomics, 17</span> (2), 93-101 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/17301689">17301689</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Drug+Metabolism+%26+Disposition&rft_id=info%3Adoi%2F10.1124%2Fdmd.111.041384&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Cannabidiol%2C+a+Major+Phytocannabinoid%2C+As+a+Potent+Atypical+Inhibitor+for+CYP2D6&rft.issn=&rft.date=2011&rft.volume=39&rft.issue=11&rft.spage=2049&rft.epage=2056&rft.artnum=http%3A%2F%2Fdmd.aspetjournals.org%2Fcontent%2F39%2F11%2F2049.short&rft.au=Satoshi+Yamaori&rft.au=Yasuka+Okamoto&rft.au=Ikuo+Yamamoto&rft.au=Kazuhito+Watanabe&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Satoshi Yamaori, Yasuka Okamoto, Ikuo Yamamoto, & Kazuhito Watanabe (2011). Cannabidiol, a Major Phytocannabinoid, As a Potent Atypical Inhibitor for CYP2D6 <span style="font-style: italic;">Drug Metabolism & Disposition, 39</span> (11), 2049-2056 DOI: <a rev="review" href="http://dx.doi.org/10.1124/dmd.111.041384">10.1124/dmd.111.041384</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+clinical+psychopharmacology&rft_id=info%3Apmid%2F9690700&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Psychotropic+effects+of+dextromethorphan+are+altered+by+the+CYP2D6+polymorphism%3A+a+pilot+study.&rft.issn=0271-0749&rft.date=1998&rft.volume=18&rft.issue=4&rft.spage=332&rft.epage=7&rft.artnum=http%3A%2F%2Fjournals.lww.com%2Fpsychopharmacology%2FAbstract%2F1998%2F08000%2FPsychotropic_Effects_of_Dextromethorphan_Are.14.aspx&rft.au=Zawertailo+LA&rft.au=Kaplan+HL&rft.au=Busto+UE&rft.au=Tyndale+RF&rft.au=Sellers+EM&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Psychiatry">Zawertailo LA, Kaplan HL, Busto UE, Tyndale RF, & Sellers EM (1998). Psychotropic effects of dextromethorphan are altered by the CYP2D6 polymorphism: a pilot study. <span style="font-style: italic;">Journal of clinical psychopharmacology, 18</span> (4), 332-7 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/9690700">9690700</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com6tag:blogger.com,1999:blog-5002675950760488813.post-1607972759335950252012-05-31T01:06:00.000-07:002012-05-31T01:12:13.706-07:00“Beware of Exercise” is a Sexy Headline<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
A new <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0037887">study</a> purports to muddle the health benefits of exercise. I sense that the fat acceptance movement will delight in the findings, but they should pause to consider the details of the study. The New York Times reacted to the study by asking “<a href="http://well.blogs.nytimes.com/2012/05/30/can-exercise-be-bad-for-you/?hp">Can Exercise be Bad for You?</a>” (That headline was later replaced.) I would counter that exercise is good, but the body is unforgiving.
<br><br>
The study reviewed the findings of six other studies, one of which consisted of considerably younger adult subjects. Two other included studies consisted of groups with average body-mass indices in the obese range, whereas all other studies had average body-mass indices in the overweight range.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-nbK9uJbwr5s/T8cf6RPH9yI/AAAAAAAAAfU/xN5zssQVfSI/s1600/BMI.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="132" width="400" src="http://2.bp.blogspot.com/-nbK9uJbwr5s/T8cf6RPH9yI/AAAAAAAAAfU/xN5zssQVfSI/s400/BMI.jpg" /></a></div>
<br>
The paper made its primary conclusion that about 7% of the subjects suffered a worsening of two out of four heart disease risk factors, consisting of fasting insulin, HDL or “good” cholesterol, triglycerides, and systolic blood pressure. However, the included study with younger participants consistently had relatively low rates of adverse reactions. The studies with obese-range body-mass indices suffered adverse reactions more frequently. Eating behavior received no direct examination.
<br><br>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-5npjr6ETAwc/T8cgEuVrfCI/AAAAAAAAAfg/hpe6NN2V4To/s1600/Adverse%2BReactions.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="244" width="400" src="http://3.bp.blogspot.com/-5npjr6ETAwc/T8cgEuVrfCI/AAAAAAAAAfg/hpe6NN2V4To/s400/Adverse%2BReactions.jpg" /></a></div>
<br>
Rather than denigrate the role of exercise in countering the obesity epidemic, as the media response has done, I would conclude that an exercise regimen should begin earlier in life. Rather than bolster the fat acceptance movement, this study should warn against ever becoming obese.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PLOS+One&rft_id=info%3A%2F10.1371%2Fjournal.pone.0037887&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Adverse+Metabolic+Response+to+Regular+Exercise%3A+Is+It+a+Rare+or+Common+Occurrence%3F&rft.issn=&rft.date=2012&rft.volume=7&rft.issue=5&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.plosone.org%2Farticle%2Finfo%253Adoi%252F10.1371%252Fjournal.pone.0037887&rft.au=Claude+Bouchard&rft.au=Steven+Blair&rft.au=Timothy+Church&rft.au=Conrad+Earnest&rft.au=James+Hagberg&rft.au=Keijo+H%C3%A4kkinen&rft.au=Nathan+Jenkins&rft.au=Laura+Karavirta&rft.au=William+Kraus&rft.au=Arthur+Leon&rft.au=DC+Rao&rft.au=Mark+Sarzynski&rft.au=James+Skinner&rft.au=Cris+Slentz&rft.au=Tuomo+Rankinen&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics">Claude Bouchard, Steven Blair, Timothy Church, Conrad Earnest, James Hagberg, Keijo Häkkinen, Nathan Jenkins, Laura Karavirta, William Kraus, Arthur Leon, DC Rao, Mark Sarzynski, James Skinner, Cris Slentz, & Tuomo Rankinen (2012). Adverse Metabolic Response to Regular Exercise: Is It a Rare or Common Occurrence? <span style="font-style: italic;">PLOS One, 7</span> (5) : <a rev="review" href="10.1371/journal.pone.0037887">10.1371/journal.pone.0037887</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com1tag:blogger.com,1999:blog-5002675950760488813.post-33203318331205325952012-04-25T01:34:00.000-07:002013-06-08T06:33:02.664-07:00The SAT Bell Curve<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
In The Mismeasure of Man, Stephen Jay Gould wrote an extended criticism of the quantification of general intelligence with factor analysis. I half expected public rebukes of Gaussian normal curves following the publication of The Bell Curve by Richard Herrnstein and Charles Murray. When the IQ distributions of whites and African Americans appear on the same graph in proportion to each group’s population, it can evoke a sense that one bell curve is physically dominating or even raping the other.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-PtP-9Hzfe9s/T5eRcTfFFMI/AAAAAAAAAaI/02XRuV-KVZE/s1600/bell%2Bcurve%2Bn.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="224" width="400" src="http://4.bp.blogspot.com/-PtP-9Hzfe9s/T5eRcTfFFMI/AAAAAAAAAaI/02XRuV-KVZE/s400/bell%2Bcurve%2Bn.jpg" /></a></div>
What the graph actually illustrates is that about as many dim white people live among us as dim black people because the graphs overlap at the left tail. This point can escape attention when this data, which Herrnstein and Murray borrowed from the National Longitudinal Survey of Youth, appears under the assumption of equal group size.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-C9-3fvlG5_Q/T5eRnflxkOI/AAAAAAAAAaU/pVKqnvo2tFM/s1600/bell%2Bcurve.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="232" width="400" src="http://4.bp.blogspot.com/-C9-3fvlG5_Q/T5eRnflxkOI/AAAAAAAAAaU/pVKqnvo2tFM/s400/bell%2Bcurve.jpg" /></a></div>
I decided to attempt to replicate these graphs with SAT data. Like it or not, the SAT is a sort of intelligence test, more so than the ACT exam that college applicants in the American heartland so commonly take. I shall quote extensively from a <a href=http://personal.lse.ac.uk/Kanazawa/pdfs/I2006.pdf>paper</a> by Satoshi Kanazawa because he fairly succinctly summarized the case for the SAT as an intelligence test.<br>
<blockquote>The SAT has a significant advantage as a proxy IQ test over other standardized academic tests, such as the American College Testing (ACT), an alternative university admissions test, or the National Assessment of Educational Progress (NAEP), administered to representative samples of fourth and eighth graders in public schools every year. While the SAT measures the students' critical reasoning ability, both the ACT and the NAEP measure their learned knowledge of academic subjects. This distinction between the SAT and the ACT is well recognized by both testing services…. A principal component analysis of SAT and ACT scores shows that the former load on two factors (verbal and quantitative) while the latter load on four additional factors (information, English, natural sciences, and social studies). Frey and Detterman (2004) show that the correlation between SAT scores and g is .857 (corrected for nonlinearity) when the measure of g is the Armed Services Vocational Aptitude Battery, and it is .72 (corrected for restricted range) when the measure of g is Raven's Advanced Progressive Matrices.</blockquote>
<br>
This is not to deny the complicating nuances of the research. After all, a genome-wide association <a href="http://www.nature.com/mp/journal/v16/n10/full/mp201185a.html">study</a> of intelligence determined that the examined single nucleotide polymorphisms of our DNA influenced the fluid intelligence, which was partially derived from Raven’s Matrices, more than crystallized-type intelligence, which tests of acquired knowledge (like vocabulary) can measure. However, the mysterious <a href="http://www.stat.columbia.edu/~gelman/stuff_for_blog/hiscock.pdf">Flynn effect</a> of rising intelligence in the industrialized world has more rapidly elevated Raven’s Matrices scores than other intelligence tests.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://2.bp.blogspot.com/-vSytDzyX1Ys/T5eRxC94JkI/AAAAAAAAAag/s8HU-OHu27Y/s1600/flynn%2Beffect.jpg" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="273" width="400" src="http://2.bp.blogspot.com/-vSytDzyX1Ys/T5eRxC94JkI/AAAAAAAAAag/s8HU-OHu27Y/s400/flynn%2Beffect.jpg" /></a></div>
SAT data can construct score distribution graphs for racial groups but only for four years in the 1980’s. In the case of black and white students, the years in question still likely reflect the present situation because the rapid decline in the black-white score gap occurred just prior to these years, and these score differences have, more or less, persisted since then.
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwvdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwvdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwmdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwmdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwwdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwwdist.gif" border="0" alt="Photobucket"></a>
Though the verbal and writing subtests might not elicit a Pavlovian reaction to bell curves, this seems to result from the test range chopping the black students’ curves into wedges. If the true IQ distribution of African Americans follows a bell-shaped Gaussian curve, then an artificial minimum SAT score could be misrepresenting the full ability spectrum of black students.<br><br>
In 1996, SAT score distributions “recentered” to reflect a new 1990 reference group that replaced the old 1941 reference group. Prior to the recentering, the greater decline of average verbal scores relative to mathematics subtest scores had concerned the College Board. Recentering also lowered the mathematics standard deviation to make black, Hispanic, and female students “appear less below average.” The following graph shows that recentering increased verbal scores even more for the black students in the 1990 reference group, giving them a bell-shaped distribution.
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbref.jpg" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbref.jpg" border="0" alt="Photobucket"></a>
This does not convince me that the same occurred for actual post-recentering black SAT scores because the black-white gap remained virtually unchanged.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://4.bp.blogspot.com/-c5iJYDF4wXk/T5eTOLuW8AI/AAAAAAAAAbc/tva9PPBhPGA/s1600/sat%2Bbw%2Braw.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://4.bp.blogspot.com/-c5iJYDF4wXk/T5eTOLuW8AI/AAAAAAAAAbc/tva9PPBhPGA/s400/sat%2Bbw%2Braw.png" /></a></div>
Certainly, the SAT verbal and math subtest distribution for the general population shifted higher, as shown below:
<a href="http://s1087.photobucket.com/user/nooffensebut/media/satvdist-1.gif.html" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satvdist-1.gif" border="0" alt=" photo satvdist-1.gif"/></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satwdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satwdist.gif" border="0" alt="Photobucket"></a>
Notice that the percentages with the highest scores continued to increase even after the recentering, especially on the mathematics subtest.<br><br>
Shifting all groups higher could hurt the black average verbal and writing SAT scores by revealing a full bell curve and thereby allowing the artificial floor to fall out from under the worst students, unless black performance improved simultaneously, causing the two phenomena to mask each other. However, if African Americans suddenly attained an extended bell-shaped distribution, I would expect an increase in their score variance on the verbal subtest, which would be reflected in an increased standard deviation. On the contrary, black students have long held the lowest standard deviations, and the graph of this quantity has been equally flat for math and verbal subtests.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-QJopWrue_8c/T5eUI8x2WeI/AAAAAAAAAcM/tDPjnMLANRY/s1600/sat%2Bv%2Bsd.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://3.bp.blogspot.com/-QJopWrue_8c/T5eUI8x2WeI/AAAAAAAAAcM/tDPjnMLANRY/s400/sat%2Bv%2Bsd.png" /></a></div><div class="separator" style="clear: both; text-align: center;">
<a href="http://3.bp.blogspot.com/-L43jHnshdYc/T5eUcr_7TfI/AAAAAAAAAck/2amQ6p8QhNM/s1600/sat%2Bm%2Bsd.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://3.bp.blogspot.com/-L43jHnshdYc/T5eUcr_7TfI/AAAAAAAAAck/2amQ6p8QhNM/s400/sat%2Bm%2Bsd.png" /></a></div>
The following graphs show the black and white score distributions without the population sizes being held equal. At the time, African Americans were the largest minority, and similar graphs for Hispanics and Asians make the respective groups’ curves almost imperceptible puddles, so I shall forgo posting them.
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwvndist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwvndist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwmndist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwmndist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satbwwndist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satbwwndist.gif" border="0" alt="Photobucket"></a>
As the standard deviations graph above already revealed, Asians comprise the most heterogeneous group, and I find their distribution to be the most fascinating.
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawvdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawvdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawmdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawmdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satawwdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satawwdist.gif" border="0" alt="Photobucket"></a>
The most obvious characteristic of the verbal and writing graphs are the bimodal distributions, which one would expect in a group for whom English frequently is the second language. This matches the writing subtest distribution for Hispanics below, but the Asian verbal subtest graph has one other aspect lacking in the Hispanic counterpart. Despite the large number of poor performers on the left side, the most elite performers of the Asian graph appear to present in roughly equal proportion to those of the white graph. In fact, a slightly higher proportion of Asians achieved the highest two verbal score ranges compared to the white group for each of the four years, and these were years prior to most of the Asian score improvement that I <a href="http://theunsilencedscience.blogspot.com/2012/04/racial-amplitudes-of-scholastic.html">previously discussed</a>.<br><br>
On the mathematics subtest graph, the Asian distribution extends noticeably more into the higher ranges than the white distribution. Thus, a much greater proportion of Asians achieve the highest range of math performance, a point that I shall also extend to men.
<div class="separator" style="clear: both; text-align: center;">
<a href="http://1.bp.blogspot.com/-HMj23gI5bdE/T5eVryL44JI/AAAAAAAAAd4/sMEPKgE_X2A/s1600/sat%2Baw%2Braw.png" imageanchor="1" style="margin-left:1em; margin-right:1em"><img border="0" height="241" width="400" src="http://1.bp.blogspot.com/-HMj23gI5bdE/T5eVryL44JI/AAAAAAAAAd4/sMEPKgE_X2A/s400/sat%2Baw%2Braw.png" /></div></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sathwvdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sathwvdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sathwmdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sathwmdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=sathwwdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/sathwwdist.gif" border="0" alt="Photobucket"></a>
A 2006 no-confidence vote compelled Larry Summers to resign from his position as president of Harvard because he gave a speech in which he said the following:<br>
<blockquote> There are three broad hypotheses … with respect to the presence of women in high-end scientific professions…. The second is what I would call different availability of aptitude at the high end…. It does appear that on many, many different human attributes—height, weight, propensity for criminality, overall IQ, mathematical ability, scientific ability—there is relatively clear evidence that whatever the difference in means—which can be debated—there is a difference in the standard deviation, and variability of a male and a female population…. Even small differences in the standard deviation will translate into very large differences in the available pool substantially out.</blockquote>
<br>
The standard deviations graph above validates Summers’ observation about differing aptitude variability between the sexes, and this is especially the case on the mathematics subtest. The following graphs illustrate just how much the standard deviation difference in math (plus a difference in mean) translates into substantially more male students in the highest aptitude levels.
<a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmfvdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmfvdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmfmdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmfmdist.gif" border="0" alt="Photobucket"></a><a href="http://s1087.photobucket.com/albums/j471/nooffensebut/?action=view&current=satmfwdist.gif" target="_blank"><img style="width:400px;" src="http://i1087.photobucket.com/albums/j471/nooffensebut/satmfwdist.gif" border="0" alt="Photobucket"></a>
Dr. Summers, on behalf of Harvard University, I would like to offer you your job back.
<br><br><br><br>
<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span>
<br><br><br><br><br><br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Molecular+psychiatry&rft_id=info%3Apmid%2F21826061&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genome-wide+association+studies+establish+that+human+intelligence+is+highly+heritable+and+polygenic.&rft.issn=1359-4184&rft.date=2011&rft.volume=16&rft.issue=10&rft.spage=996&rft.epage=1005&rft.artnum=http%3A%2F%2Fwww.nature.com%2Fmp%2Fjournal%2Fv16%2Fn10%2Ffull%2Fmp201185a.html&rft.au=Davies+G&rft.au=Tenesa+A&rft.au=Payton+A&rft.au=Yang+J&rft.au=Harris+SE&rft.au=Liewald+D&rft.au=Ke+X&rft.au=Le+Hellard+S&rft.au=Christoforou+A&rft.au=Luciano+M&rft.au=McGhee+K&rft.au=Lopez+L&rft.au=Gow+AJ&rft.au=Corley+J&rft.au=Redmond+P&rft.au=Fox+HC&rft.au=Haggarty+P&rft.au=Whalley+LJ&rft.au=McNeill+G&rft.au=Goddard+ME&rft.au=Espeseth+T&rft.au=Lundervold+AJ&rft.au=Reinvang+I&rft.au=Pickles+A&rft.au=Steen+VM&rft.au=Ollier+W&rft.au=Porteous+DJ&rft.au=Horan+M&rft.au=Starr+JM&rft.au=Pendleton+N&rft.au=Visscher+PM&rft.au=Deary+IJ&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Davies G, Tenesa A, Payton A, Yang J, Harris SE, Liewald D, Ke X, Le Hellard S, Christoforou A, Luciano M, McGhee K, Lopez L, Gow AJ, Corley J, Redmond P, Fox HC, Haggarty P, Whalley LJ, McNeill G, Goddard ME, Espeseth T, Lundervold AJ, Reinvang I, Pickles A, Steen VM, Ollier W, Porteous DJ, Horan M, Starr JM, Pendleton N, Visscher PM, & Deary IJ (2011). Genome-wide association studies establish that human intelligence is highly heritable and polygenic. <span style="font-style: italic;">Molecular psychiatry, 16</span> (10), 996-1005 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21826061">21826061</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Journal+of+Clinical+and+Experimental+Neuropsychology&rft_id=info%3Adoi%2F10.1080%2F13803390600813841&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+Flynn+effect+and+its+relevance+to+neuropsychology&rft.issn=1380-3395&rft.date=2007&rft.volume=29&rft.issue=5&rft.spage=514&rft.epage=529&rft.artnum=http%3A%2F%2Fwww.stat.columbia.edu%2F%7Egelman%2Fstuff_for_blog%2Fhiscock.pdf&rft.au=Hiscock%2C+M.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Hiscock, M. (2007). The Flynn effect and its relevance to neuropsychology <span style="font-style: italic;">Journal of Clinical and Experimental Neuropsychology, 29</span> (5), 514-529 DOI: <a rev="review" href="http://dx.doi.org/10.1080/13803390600813841">10.1080/13803390600813841</a></span>
<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Intelligence&rft_id=info%3Adoi%2F10.1016%2Fj.intell.2006.04.003&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=IQ+and+the+wealth+of+states&rft.issn=01602896&rft.date=2006&rft.volume=34&rft.issue=6&rft.spage=593&rft.epage=600&rft.artnum=http%3A%2F%2Fpersonal.lse.ac.uk%2FKanazawa%2Fpdfs%2FI2006.pdf&rft.au=Kanazawa%2C+S.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Kanazawa, S. (2006). IQ and the wealth of states <span style="font-style: italic;">Intelligence, 34</span> (6), 593-600 DOI: <a rev="review" href="http://dx.doi.org/10.1016/j.intell.2006.04.003">10.1016/j.intell.2006.04.003</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com18tag:blogger.com,1999:blog-5002675950760488813.post-37354737702881878622012-04-11T21:31:00.001-07:002012-04-14T19:50:49.886-07:00Racial Amplitudes of Scholastic AptitudeIQ tests have an image problem. Sure, they remind some of defunct movements like state-sponsored eugenics, overturned legal and judicial regimes that allowed racial segregation, or suspicious research-funding organizations, like the Pioneer Fund. However, in the minds of most people, IQ tests denote a tribulation with greater immediacy: taking a test. The unpleasantness of test taking also pertains to the validity of test results. One class of criticisms of the tests concerns the potential for test anxiety to overwhelm an examinee, and since everyone has an equal ability to underperform by choice, a lack of motivation during challenging mental tasks also has the potential to confound. The latter concern underlines why the high-stakes SAT exam is so central to studying broad cross-sections of the American public.<br /><br />I have just compiled what I consider the most comprehensive data set of national SAT scores anywhere on the Internet. I am now able to further expound on points that I <a href="http://theunsilencedscience.blogspot.com/2011/08/meet-towelie-iq-test-of-future.html">made</a> <a href="http://theunsilencedscience.blogspot.com/2011/09/sats-cohens-d-topography-of-iq.html">in</a> <a href="http://theunsilencedscience.blogspot.com/2011/09/sat-in-red-white-and-brown.html">previous</a> <a href="http://theunsilencedscience.blogspot.com/2011/10/girls-versus-boys-final-battle.html">posts</a> and share some equally startling new findings. The first reports on racial SAT score gaps occurred in 1976, but many years did not include corresponding standard deviations, which are necessary for calculating Cohen’s d. Cohen’s d is an expression of score gaps in the units of standard deviations. The SAT has undergone so many adjustments over the years that merely graphing raw scores without this statistical device would fail to edify. However, for completeness I shall post the raw score graphs here.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-jWGF6qT4SqM/T4VtAOD18aI/AAAAAAAAARU/OxYc1U7Np3U/s1600/sat%2Brace%2Braw%2Bverbal.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-jWGF6qT4SqM/T4VtAOD18aI/AAAAAAAAARU/OxYc1U7Np3U/s400/sat%2Brace%2Braw%2Bverbal.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730105951440466338" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-CKSGB3MTfhw/T4VszQ6IJNI/AAAAAAAAARI/X8RrlhthRWY/s1600/sat%2Brace%2Braw%2Bmath.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-CKSGB3MTfhw/T4VszQ6IJNI/AAAAAAAAARI/X8RrlhthRWY/s400/sat%2Brace%2Braw%2Bmath.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730105728866723026" /></a><br />The verbal subtest became the critical reading subtest, following the addition of the writing subtest in 2006. In the early 80’s, the SAT briefly included a writing subtest on a radically different scale, and Cohen’s d can allow comparisons of writing subtest scores between that and the modern version.<br /><br />Two equations by <a href="http://pss.sagepub.com/content/15/6/373.short">Frey and Detterman</a> allow the transformation of SAT scores into IQ score estimates. One of the equations serves those who took the test prior to the 1996 “recentering” of score allocation. The second equation for more recent scores resulted from a study sample with higher scores, so it is better suited for the higher score range. However, Mensans should be disappointed with both equations, since, as the following graphs of the full SAT range for both equations show, neither calculation can predict IQ scores greater than 130. Very intelligent people with high SAT scores will find <a href="http://www.iqcomparisonsite.com/oldSATIQ.aspx">conversion tables</a> more useful.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-L7HGpKUnLlo/T4VvP_AauxI/AAAAAAAAARg/Vjqe6MEAJmk/s1600/sat%2Biq%2B1%2Brange.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-L7HGpKUnLlo/T4VvP_AauxI/AAAAAAAAARg/Vjqe6MEAJmk/s400/sat%2Biq%2B1%2Brange.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730108421300730642" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-4urBboY_6no/T4VvZ3f1niI/AAAAAAAAARs/wO7tjRRlpGI/s1600/sat%2Biq%2B2%2Brange.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-4urBboY_6no/T4VvZ3f1niI/AAAAAAAAARs/wO7tjRRlpGI/s400/sat%2Biq%2B2%2Brange.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730108591083724322" /></a><br />The equations do allow comparisons between groups, but the disparate interpretations of the average SAT score range between the two mathematical expressions overshadow the yearly trends, as shown in the following graph.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-RiIKxmyEXx8/T4VwLJ9CIqI/AAAAAAAAAR4/nTu6TcDSP0c/s1600/sat%2Brace%2Biq.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-RiIKxmyEXx8/T4VwLJ9CIqI/AAAAAAAAAR4/nTu6TcDSP0c/s400/sat%2Brace%2Biq.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730109437851607714" /></a><br />Frey and Detterman have <a href="http://pss.sagepub.com/content/16/9/747.extract">acknowledged</a> that their second equation grossly underestimates IQ for the average student who takes the SAT.<br /><br />As I previously wrote based on a more limited collection of data, the SAT gap between white and black students is large but used to be much larger and now seems to be slightly growing, again. The following graph is a 36-year illustration of this Cohen’s d gap. Years marked by dotted lines required estimates of the two groups’ respective standard deviations. These numbers are usually fairly constant, so I estimated them to be equal to those of 1981 for the years from 1976 to 1980. Likewise, I set the other estimated standard deviations to be halfway between those of the years that bookend each of those two periods.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-WXKDJeIoQe4/T4Vw1Vy5gmI/AAAAAAAAASE/jrLcuXvmYOA/s1600/sat%2Bblack%2Bzoom.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-WXKDJeIoQe4/T4Vw1Vy5gmI/AAAAAAAAASE/jrLcuXvmYOA/s400/sat%2Bblack%2Bzoom.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730110162584830562" /></a><br />The inflection point between the years of rapid progress for black students and the present stagnation seems to be around 1990. <a href="http://isteve.blogspot.com/2011/09/unsilenced-silence-blog-has-good-graph.html">Steve Sailer</a> pointed to the crack epidemic, as well as increased black participation in SAT testing over the years and disparate rates of test preparation course usage. Actually, black, Hispanic, Asian, and Native-American students are all <a href="http://sf.oxfordjournals.org/content/89/2/435.short">more likely</a> to employ test preparation courses than white students. Alternatively, one could posit that black students just happened to reach their intellectual potential at that time, causing genetic influences to overtake societal inequities, and one could explore the converse assumption that educational or economic racial progress suddenly reversed despite the magnificent bubble economy of the 90’s.<br /><br />I would like to conjecture my own hypothesis. Baby-boomers often advance cultural biases centered on the music of their youth, which marked the beginning of civilization, of course. I do not believe that the production of music ended after The Beatles disbanded. In fact, whether music is an agent of change or a mere mirror, I consider the artistic landscape of the early 90’s to be highly relevant to this analysis. This was when buttrock hair bands scratched their heads as they stood in shock before the spectacle of dress-clad, (male) grunge rockers, who obsessively screeched anti-rape songs. Even the rip-roaring comedy of South Park stopped to declare <a href="http://www.youtube.com/watch?v=w-g1gRzoq98&feature=results_video&playnext=1&list=PL6EB8C8F171153A08">“Disintegration is the best album, ever,”</a> referring to probably the most lugubrious (and greatest) contribution to the goth genre.<br /><br />As white culture took a sudden turn towards introspection and sensitivity, black culture veered elsewhere. Not one for subtlety, in 1992 rapper <a href="http://www.youtube.com/watch?v=r_zSt-qQfn4">Ice Cube</a> depicted himself literally kidnapping the feel-good, mainstream rapper MC Hammer and forcing him into a Kahlid “Kill the White Babies” Muhammad re-education camp. Via such proud celebration of a violent stereotype, rap music <a href="http://www.icce.rug.nl/~soundscapes/VOLUME02/Trends_and_shifts_in_music_sales.shtml">surged</a> from 4.2% of music sales in 1988 to 10.1% in 1997. Though the tumult surrounding the crack epidemic might have helped inspire gangsta rap, thug posturing remained frozen in time long after the decline of crack and materialized in a succession of martyrs, the most recent being the troubled, young Trayvon Martin. While I might suffer accusations of selecting a facile scapegoat, historians should acknowledge the lasting impact of what seems too obvious to contemporaries.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-76ENjTWA2r0/T4VxJ14hysI/AAAAAAAAASQ/LHjdti1a29E/s1600/trayvon.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 320px;" src="http://4.bp.blogspot.com/-76ENjTWA2r0/T4VxJ14hysI/AAAAAAAAASQ/LHjdti1a29E/s400/trayvon.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5730110514795760322" /></a><center><b>Standing on the Shoulders of Giants</b></center><br />Black-white SAT score gaps dwarf those between male and female students. However, the case for macho anti-intellectualism as a chief detriment to black SAT scores coincides with a remarkable decline of those scores for black men relative to black women, as shown in these gender Cohen’s d gaps:<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-cWZNYD5GhEs/T4VynQrNaCI/AAAAAAAAAS0/mVdtc71KmHQ/s1600/sat%2Bgender%2Brace%2Bverbal.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-cWZNYD5GhEs/T4VynQrNaCI/AAAAAAAAAS0/mVdtc71KmHQ/s400/sat%2Bgender%2Brace%2Bverbal.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730112119715489826" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-e1-HVcyXAdQ/T4VygjGc7-I/AAAAAAAAASo/1285Ph-7R74/s1600/sat%2Bgender%2Brace%2Bmath.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-e1-HVcyXAdQ/T4VygjGc7-I/AAAAAAAAASo/1285Ph-7R74/s400/sat%2Bgender%2Brace%2Bmath.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730112004402507746" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-ndsLen94sHg/T4VyZxLQPQI/AAAAAAAAASc/uF3u4aQaw9A/s1600/sat%2Bgender%2Brace%2Bwriting.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-ndsLen94sHg/T4VyZxLQPQI/AAAAAAAAASc/uF3u4aQaw9A/s400/sat%2Bgender%2Brace%2Bwriting.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730111887921659138" /></a><br />By contrast, the gaps between white men and white women have not changed so greatly over those three decades. Overall, women have had some improvement, at least on the mathematics subtest, despite increasing their participation faster than men did.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/--rwtO7Es-nc/T4VzpDAIHqI/AAAAAAAAATM/iVu54CZiL58/s1600/sat%2Bgender.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/--rwtO7Es-nc/T4VzpDAIHqI/AAAAAAAAATM/iVu54CZiL58/s400/sat%2Bgender.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730113249916493474" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-uwYlgxmKOjU/T4VzjmWUQ9I/AAAAAAAAATA/QA1AW_VRLTU/s1600/sat%2Bgender%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-uwYlgxmKOjU/T4VzjmWUQ9I/AAAAAAAAATA/QA1AW_VRLTU/s400/sat%2Bgender%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730113156325589970" /></a><br />I have selected a narrow y-axis range to focus on the yearly trends in the previous graphs, but comparisons of different gaps benefit from having the axis range in common. All of the following graphs show the extent of white advantage over minorities, even though that is a mostly negative gap for high-achieving Asians.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/--nG9NAUOohE/T4V0ZPJLN4I/AAAAAAAAAT8/CiP1A0drKDE/s1600/sat%2Bblack.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/--nG9NAUOohE/T4V0ZPJLN4I/AAAAAAAAAT8/CiP1A0drKDE/s400/sat%2Bblack.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730114077809391490" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-mUYQsoNtAo4/T4V0RyVXvJI/AAAAAAAAATw/bJvMbAYpZME/s1600/sat%2Bhispanic.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-mUYQsoNtAo4/T4V0RyVXvJI/AAAAAAAAATw/bJvMbAYpZME/s400/sat%2Bhispanic.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730113949816831122" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-MIien3FjRHQ/T4V0MAeVt1I/AAAAAAAAATk/gwCYnZa6X10/s1600/sat%2Bnative.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-MIien3FjRHQ/T4V0MAeVt1I/AAAAAAAAATk/gwCYnZa6X10/s400/sat%2Bnative.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730113850533328722" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-E2LjiI65isU/T4V0GBeY1aI/AAAAAAAAATY/C2-9Xp8oOXo/s1600/sat%2Bother.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-E2LjiI65isU/T4V0GBeY1aI/AAAAAAAAATY/C2-9Xp8oOXo/s400/sat%2Bother.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730113747722753442" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-5k-hLPQbtTA/T4V0e034mbI/AAAAAAAAAUI/MOya83ZSdL8/s1600/sat%2Basian.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-5k-hLPQbtTA/T4V0e034mbI/AAAAAAAAAUI/MOya83ZSdL8/s400/sat%2Basian.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730114173836761522" /></a><br />These score gaps could be interpreted as white admixture tests. White students have SAT score advantages over all non-Asian minorities. The gaps shrink in order from African Americans to Hispanic Americans to Native Americans to “other” race students. This order seems to correspond to white admixture (African Americans: <a href="http://genomebiology.com/content/pdf/gb-2009-10-12-r141.pdf">22%</a>, Hispanic Americans: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867092/pdf/AJHGv80p1024.pdf">48%</a>, Native American: <a href="http://onlinelibrary.wiley.com/doi/10.1002/ajpa.21506/abstract">50-60%</a>). Granted, those admixture estimates are debatable, and I am reluctant to draw strident conclusions related to the small, fluctuating number of students who call themselves Native-American on the SAT, let alone “others.”<br /><br />I compiled this data set from multiple sources. (The online sources are <a href="http://nces.ed.gov/programs/digest/d10/tables/dt10_152.asp">here</a>, <a href="http://nces.ed.gov/programs/digest/d01/dt134.asp">here</a>, <a href="http://www.arthurhu.com/97/01/satrace/satrace.htm">here</a>, <a href="http://www.nsf.gov/statistics/wmpdse94/tf/tfch3.htm">here</a>, <a href="http://www.ets.org/Media/Research/pdf/RR-91-13-Pennock-Roman.pdf">here</a>, <a href="http://statweb.calpoly.edu/rsmidt/APStat/ripple.pdf">here</a>, <a href="http://library.nku.edu/govcrs/IP0249S.pdf">here</a>, <a href="http://professionals.collegeboard.com/profdownload/pdf/200211_20702.pdf">here</a>, and <a href="http://professionals.collegeboard.com/data-reports-research/sat/archived">here</a>.) I confess some anomalies for the Hispanic data, which is a composite of data from Mexican Americans, Puerto Ricans, and those labeled “other Hispanics.” Unfortunately, my sources for Puerto Ricans slightly contradicted each other for the years 1981, 1982, 1984, and 1985, requiring a value judgment of trustworthiness. The College Board, which oversees the SAT, did not even create the “other Hispanic” category until 1987. Even so, the composite Hispanic data does not strike me as particularly noisy. Interestingly, the separate gaps for each of the three Hispanic groups seem to be converging after many years of Puerto Rican relative deficiency.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-dBU1KYGQrm4/T4V2EUX89UI/AAAAAAAAAUg/t6SlJ63O4SA/s1600/sat%2Bhispanic%2Bsubgroups%2Bverbal.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-dBU1KYGQrm4/T4V2EUX89UI/AAAAAAAAAUg/t6SlJ63O4SA/s400/sat%2Bhispanic%2Bsubgroups%2Bverbal.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730115917459551554" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-JHzE3_qDEwg/T4V1-e1WM_I/AAAAAAAAAUU/jXzEKnX4igw/s1600/sat%2Bhispanic%2Bsubgroups%2Bmath.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-JHzE3_qDEwg/T4V1-e1WM_I/AAAAAAAAAUU/jXzEKnX4igw/s400/sat%2Bhispanic%2Bsubgroups%2Bmath.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730115817187980274" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-6Elk4o_h5fc/T4V2J3Ah8rI/AAAAAAAAAUs/Apas71o-lHI/s1600/sat%2Bhispanic%2Bsubgroups%2Bwriting.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-6Elk4o_h5fc/T4V2J3Ah8rI/AAAAAAAAAUs/Apas71o-lHI/s400/sat%2Bhispanic%2Bsubgroups%2Bwriting.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730116012655899314" /></a><br /><center><h3>Yellow Peril</h3></center><br />This complete collection of national SAT data reveals an even more dramatic degree of progress for Asians than I previously realized, particularly on the writing subtest. Asians have always had a mathematics advantage over whites, just as the black-white gap has always been larger for the mathematics subtest than the verbal subtest. After so many years of complaints of cultural bias on standardized tests, one would expect a complimentary appraisal of Asians’ near closing of the verbal score gap with whites. Instead, Sailer and many commenters seemed to reach for arguments to explain away Asian success: test prep courses game the SAT, Asian foreign students have started swamping the Asian Americans, or smarter Asians recently started immigrating. Whether test preparation constitutes “gaming” or learning I shall leave open to debate, but I feel confident that I can lay to rest the other disputes.<br /><br />First, I shall graph the SAT participation levels of Asians, Hispanics, those who marked “other” for race, English-as-a-second-language (ESL) students, foreign students, US residents, and multilingual students. Residents are either US permanent residents or refugees to America. Foreign students are simply all students with foreign citizenship and who do not fit into the resident category. Students in my “multilingual” category grew up with English and another language.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-wTrxajjTkGk/T4V3egeuEHI/AAAAAAAAAU4/Q3rM8Wfe34s/s1600/sat%2Besl%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-wTrxajjTkGk/T4V3egeuEHI/AAAAAAAAAU4/Q3rM8Wfe34s/s400/sat%2Besl%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730117466897387634" /></a><br />Asians and Hispanics greatly outnumber foreign students and residents but not multilingual students or ESL students. One <a href="http://www.jstor.org/discover/10.2307/27541876">study</a> reported that 44% of Asians who took the test in 1991 were foreign students. Now, I shall graph the gaps between Americans and foreign students, with that graph overlaying for comparison the Asian-white gaps graph with its colors set to gray. I defined Americans as a composite of US citizens, permanent residents, and refugees.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-6ekmX2VIkbs/T4V36ynHt3I/AAAAAAAAAVE/-zy1JrZ_WhA/s1600/sat%2Bforeigner.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-6ekmX2VIkbs/T4V36ynHt3I/AAAAAAAAAVE/-zy1JrZ_WhA/s400/sat%2Bforeigner.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730117952800798578" /></a><br />The gaps for foreign students almost completely overlap the Asian-white gaps. Foreign students might slightly outperform Asian-Americans on the mathematics subtest but not so much that the smaller number of foreign students could significantly raise the scores of Asians. In fact, the foreign student-Asian mathematics gap disappears when the comparison group is changed from Americans to white students.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-NUhUfqhlyf8/T4V4TR6PlUI/AAAAAAAAAVQ/oI1wF1q5Yfk/s1600/sat%2Bforeigner%2Bwhite.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-NUhUfqhlyf8/T4V4TR6PlUI/AAAAAAAAAVQ/oI1wF1q5Yfk/s400/sat%2Bforeigner%2Bwhite.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730118373519365442" /></a><br />Resident students and ESL students can offer clues about Asian immigrants, even though they lack racial breakdowns. As one of the previous graphs illustrated, the number of Hispanics who take the SAT does not greatly outnumber the number of Asians who take the test despite the fact that Hispanic Americans are about three-and-a-half times more numerous than Asian Americans, according to the <a href="http://2010.census.gov/news/releases/operations/cb11-cn125.html">latest Census figures</a>. Plus, the contours of the gaps graphs for ESL students and resident students more closely tracks the Asian-white score gaps graph than a Hispanic-white gaps graph, which I shall include below with a more restricted axis range.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-4FvBKWZxD18/T4V46Ae-8wI/AAAAAAAAAV0/0tuMGEGuf00/s1600/sat%2Besl.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-4FvBKWZxD18/T4V46Ae-8wI/AAAAAAAAAV0/0tuMGEGuf00/s400/sat%2Besl.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730119038856524546" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-vhI_KbzPAnw/T4V40rB29_I/AAAAAAAAAVo/vNtAdS8weoc/s1600/sat%2Bresident.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-vhI_KbzPAnw/T4V40rB29_I/AAAAAAAAAVo/vNtAdS8weoc/s400/sat%2Bresident.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730118947197876210" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-UWu8UB5NXA4/T4V4tSkxEhI/AAAAAAAAAVc/MKtyk1xNhB4/s1600/sat%2Bhispanic%2Bzoom.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-UWu8UB5NXA4/T4V4tSkxEhI/AAAAAAAAAVc/MKtyk1xNhB4/s400/sat%2Bhispanic%2Bzoom.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730118820374319634" /></a><br />Though the inclusion of Hispanics in the ESL and resident student data probably contributes to some of the relative score weakness in comparison to white students, I think these graphs effectively falsify the notion that recent immigration explains away Asian progress.<br /><br />Multilingual students further complicate this discussion. I shall post the ESL graph again next to a gaps graph for multilingual students.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-9bYjTZ8qKqA/T4WE2thzWBI/AAAAAAAAAWM/3IYN15uAfvk/s1600/sat%2Besl.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-9bYjTZ8qKqA/T4WE2thzWBI/AAAAAAAAAWM/3IYN15uAfvk/s400/sat%2Besl.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730132176367998994" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-9TqappxCSYI/T4WEwJ_DE7I/AAAAAAAAAWA/xlolcCXqJc8/s1600/sat%2Bmultilingual.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-9TqappxCSYI/T4WEwJ_DE7I/AAAAAAAAAWA/xlolcCXqJc8/s400/sat%2Bmultilingual.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730132063747773362" /></a><br />If one ignored race and immigration status, one would only expect the multilingual students to have a greater advantage over ESL students because their only difference is the criterion of growing up with English. They have had a shrinking verbal score advantage, but the graphs seem to suggest that raising one’s children to be multilingual by adding English lowers math skills. More likely, ESL students have a greater probability of being math-oriented Asians. On the other hand, perhaps ESL students are more likely to be more capable recent immigrants, or multilingual students might have a greater likelihood of being 2nd- or 3rd-generation immigrants who experience a racialized IQ regression to the mean. I would argue against that because Asians outscore both ESL and multilingual students. Therefore, greater association with the United States and its language is not necessarily a hindrance.<br /><br /><center><h3>White Decline?</h3></center><br /><br />Getting stumped on the first SAT question might not bode well, especially if that question is, “What is your race?” At the turn of the millennium, the SAT experienced a surge of underachievers who failed to respond to the race question. The surge seemed to precede major growth of black, Hispanic, and Asian SAT participation. Whereas the no-response surge seemed to coincide with a “bite” out of the white participation rate, the gradual growth of minority participation went uninterrupted through a no-response peak that towered over each group.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-fS19CbwaKSc/T4WFjqUL1BI/AAAAAAAAAWY/sDZ2BSqGJVI/s1600/sat%2Brace%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-fS19CbwaKSc/T4WFjqUL1BI/AAAAAAAAAWY/sDZ2BSqGJVI/s400/sat%2Brace%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730132948599690258" /></a><br />As the no-response peak passed, the SAT score gap between white students and non-responders shot up almost vertically.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-ZOZXe0VKNjI/T4WF1NPVGmI/AAAAAAAAAWk/6nQBqiUZY-M/s1600/sat%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-ZOZXe0VKNjI/T4WF1NPVGmI/AAAAAAAAAWk/6nQBqiUZY-M/s400/sat%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730133250032343650" /></a><br />Based on this data, I conclude that non-responders are an overwhelmingly white group of poor performers. Without detailed knowledge of SAT procedure, I cannot comment authoritatively on where the surge came from or why it went away. Was there a period of test administration that required students to fill out this data after they finished, if they had time or the inclination? A greater tendency to not respond must be associated with poorer testing ability because the declining remnants of the force behind the surge are now selecting for increasingly worse test takers. At first, I suspected that non-responders were conservative proponents of race-blindness or opponents of racial preferences. <a href="http://secure.asanet.org/images/journals/docs/pdf/spq/Mar10SPQFeature.pdf">Three</a> <a href="http://scottbarrykaufman.com/wp-content/uploads/2012/02/Psychological-Science-2012-Hodson-0956797611421206.pdf">recent</a> <a href="http://www.pagetwister.com/docs/Low-Effort%20Thought%20Promotes%20Politial%20Conservatism.pdf">studies</a> have associated conservative tendencies with worse intellectual ability. However, race non-response exactly corresponds with surges for non-response to the language, citizenship, and reported average grade questions.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-ovKXBnwMrR4/T4WGavVE_QI/AAAAAAAAAWw/ASjpvNJ8iHY/s1600/sat%2Bnr%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-ovKXBnwMrR4/T4WGavVE_QI/AAAAAAAAAWw/ASjpvNJ8iHY/s400/sat%2Bnr%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730133894838418690" /></a><br />If my assumption that white students comprise the vast majority of non-responders is correct, then white students have significantly declined in their SAT participation just as minority participation is ramping up.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-7JTXezH1Bss/T4WG25Pni1I/AAAAAAAAAW8/FikwPx_Y114/s1600/sat%2Brace%2Bnr%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-7JTXezH1Bss/T4WG25Pni1I/AAAAAAAAAW8/FikwPx_Y114/s400/sat%2Brace%2Bnr%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730134378536209234" /></a><br />I decided to repeat my analysis, combining the white-student and non-responder data. This time, the trends calculated with whites by themselves are gray for comparison with the overlaid combined-group graphs.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-GmkjggFmvnM/T4WHxX4kCnI/AAAAAAAAAXs/YE-OzMDqXbA/s1600/sat%2Bblack%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-GmkjggFmvnM/T4WHxX4kCnI/AAAAAAAAAXs/YE-OzMDqXbA/s400/sat%2Bblack%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135383193422450" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-3pUShuZKO-E/T4WHpdJO_-I/AAAAAAAAAXg/ToMJ_YETxug/s1600/sat%2Bhispanic%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-3pUShuZKO-E/T4WHpdJO_-I/AAAAAAAAAXg/ToMJ_YETxug/s400/sat%2Bhispanic%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135247166570466" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-62mAPoYQcoE/T4WHjqQx4fI/AAAAAAAAAXU/CR7CGVzTpns/s1600/sat%2Bnative%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-62mAPoYQcoE/T4WHjqQx4fI/AAAAAAAAAXU/CR7CGVzTpns/s400/sat%2Bnative%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135147608662514" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-Z4R93NIn-dk/T4WHcJm9N1I/AAAAAAAAAXI/7Npb9v9mV2w/s1600/sat%2Basian%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-Z4R93NIn-dk/T4WHcJm9N1I/AAAAAAAAAXI/7Npb9v9mV2w/s400/sat%2Basian%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135018584225618" /></a><br />While the changes might appear minor, the case for an increasing black-white SAT score gap has vanished, which becomes more evident in the following graph with a restricted y-axis range.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-jjeZfSICb38/T4WIDqtH3hI/AAAAAAAAAX4/IJuXNxWHnz4/s1600/sat%2Bblack%2Bnr%2Bzoom.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-jjeZfSICb38/T4WIDqtH3hI/AAAAAAAAAX4/IJuXNxWHnz4/s400/sat%2Bblack%2Bnr%2Bzoom.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135697483357714" /></a><br />Similarly, any growth in the Hispanic-white gap barely escapes the yearly noise.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-LVydZogBr3Q/T4WIPbL2PxI/AAAAAAAAAYE/2Heqs350K7E/s1600/sat%2Bhispanic%2Bnr%2Bzoom.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-LVydZogBr3Q/T4WIPbL2PxI/AAAAAAAAAYE/2Heqs350K7E/s400/sat%2Bhispanic%2Bnr%2Bzoom.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730135899475689234" /></a><br />A long-held assumption of SAT results analysis holds that participation varies inversely with average performance. Usually, participation increases as more students who would not have been college material in a previous era pursue higher education and lower average SAT scores in the process. If we promote that assumption to a law of nature, then white students could be in serious relative decline, considering the Asian advancement, the non-respondent white score bubble, and declining white SAT participation when non-respondents are added to the white totals. Perhaps whites can take comfort in the fact that both Asians and, to some extent, women have broken this law by simultaneously increasing their scores and participation. Moreover, the assumption appears to be based upon a major SAT score decline from the late 60’s to early 70’s. Here are the raw scores and recentered scores graphs:<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-K00kVliPDbI/T4X9RmH4vrI/AAAAAAAAAZ8/-UYt7J4oyio/s1600/sat%2Ball%2Braw.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-K00kVliPDbI/T4X9RmH4vrI/AAAAAAAAAZ8/-UYt7J4oyio/s400/sat%2Ball%2Braw.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730264579632053938" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-sTqRBZ-SJQw/T4WIj75vgXI/AAAAAAAAAYQ/RuDUThKy0cI/s1600/sat%2Ball%2Brecentered.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-sTqRBZ-SJQw/T4WIj75vgXI/AAAAAAAAAYQ/RuDUThKy0cI/s400/sat%2Ball%2Brecentered.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730136251855503730" /></a><br />The enormous participation growth since the early 90’s has not further sunk SAT scores. Maybe the late 60’s decline resulted from listening to The Beatles. Maybe it was from listening to The Beatles high. Even the considerably left-wing psychologist Steven Pinker linked the 1960’s counterculture to a “decivilizing mindset.” The Woodstock Generation might have struck the logical balance between SAT preparation and making the most out of the last moments before the nuclear annihilation they were expecting. For its part, the College Board convened an advisory panel, which <a href="http://shawleyville.com/Critique%20of%20Sandia%20Report-1.pdf">reported</a> in 1977 that two-thirds to three-fourths of the 1960’s decline was due to demographic changes, such as more minority participation, but this proportion fell to 30% or less for the 1970’s decline.<br /><br />With regard to the presumptive white participation decline, the popping of an education bubble could be bearing an increasing proportion of smart, young white people skipping the college experience, even during this dismal economy. It could but probably is not. Superior high school class rank and self-reported average grade is now more associated with greater SAT participation, albeit amidst some grade inflation, judging by the raw SAT scores corresponding to each average grade since 1996.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-rRldKJRIY8U/T4WJzD1QRLI/AAAAAAAAAZw/JCOlwukJDGs/s1600/sat%2Brank%2Bparticipation%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://4.bp.blogspot.com/-rRldKJRIY8U/T4WJzD1QRLI/AAAAAAAAAZw/JCOlwukJDGs/s400/sat%2Brank%2Bparticipation%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730137611193828530" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-50tET20Fyq8/T4WJuaLI1sI/AAAAAAAAAZk/H9OrdLQo2is/s1600/sat%2Brank%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-50tET20Fyq8/T4WJuaLI1sI/AAAAAAAAAZk/H9OrdLQo2is/s400/sat%2Brank%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730137531291850434" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-YoqV-ZXpdDA/T4WJiX2WNvI/AAAAAAAAAZY/ArhTnOC_s6o/s1600/sat%2Bgrades%2Bparticipation%2Bnr.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-YoqV-ZXpdDA/T4WJiX2WNvI/AAAAAAAAAZY/ArhTnOC_s6o/s400/sat%2Bgrades%2Bparticipation%2Bnr.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730137324509345522" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-o6F26I5YRSA/T4WJctjHYKI/AAAAAAAAAZM/gP44pgwXEYU/s1600/sat%2Bgrades%2Bparticipation.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://1.bp.blogspot.com/-o6F26I5YRSA/T4WJctjHYKI/AAAAAAAAAZM/gP44pgwXEYU/s400/sat%2Bgrades%2Bparticipation.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730137227255046306" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-MS_21r_lfO4/T4WJSAuOxfI/AAAAAAAAAZA/Hlpf8tJIyAo/s1600/sat%2Bgrades%2Bverbal.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-MS_21r_lfO4/T4WJSAuOxfI/AAAAAAAAAZA/Hlpf8tJIyAo/s400/sat%2Bgrades%2Bverbal.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730137043423380978" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-ZACY6ete7Ho/T4WJL2CEoGI/AAAAAAAAAY0/eDgAyVMleR8/s1600/sat%2Bgrades%2Bmath.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://3.bp.blogspot.com/-ZACY6ete7Ho/T4WJL2CEoGI/AAAAAAAAAY0/eDgAyVMleR8/s400/sat%2Bgrades%2Bmath.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730136937474596962" /></a><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-3gZ8X4kItgU/T4WJGMKqIvI/AAAAAAAAAYo/8gGkCn_uuyU/s1600/sat%2Bgrades%2Bwriting.png"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 241px;" src="http://2.bp.blogspot.com/-3gZ8X4kItgU/T4WJGMKqIvI/AAAAAAAAAYo/8gGkCn_uuyU/s400/sat%2Bgrades%2Bwriting.png" border="0" alt=""id="BLOGGER_PHOTO_ID_5730136840336974578" /></a><br />Since white students are still such a high proportion of SAT examinees, their apparent stagnation rather than improvement during a period of probable declining white participation and increased participation of highly ranked students warrants concern.<br /><br />In total, SAT trends offer a complex interpretation of societal changes plus new perplexities ripe for further study. My first suggestion to my fellow white people is to finally accept Asian Americans as a veritable model.<br /><br /><br /><br /><span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span><br /><br /><br /><br /><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Social+Forces&rft_id=info%3Adoi%2F10.1353%2Fsof.2010.0105&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Shadow+Education%2C+American+Style%3A+Test+Preparation%2C+the+SAT+and+College+Enrollment&rft.issn=0037-7732&rft.date=2010&rft.volume=89&rft.issue=2&rft.spage=435&rft.epage=461&rft.artnum=http%3A%2F%2Fsf.oxfordjournals.org%2Fcgi%2Fdoi%2F10.1353%2Fsof.2010.0105&rft.au=Buchmann%2C+C.&rft.au=Condron%2C+D.&rft.au=Roscigno%2C+V.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Buchmann, C., Condron, D., & Roscigno, V. (2010). Shadow Education, American Style: Test Preparation, the SAT and College Enrollment <span style="font-style: italic;">Social Forces, 89</span> (2), 435-461 DOI: <a rev="review" href="http://dx.doi.org/10.1353/sof.2010.0105">10.1353/sof.2010.0105</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Personality+%26+Social+Psychology+Bulletin&rft_id=info%3Apmid%2F22427384&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Low-Effort+Thought+Promotes+Political+Conservatism.&rft.issn=0146-1672&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.pagetwister.com%2Fdocs%2FLow-Effort%2520Thought%2520Promotes%2520Politial%2520Conservatism.pdf&rft.au=Eidelman+S&rft.au=Crandall+CS&rft.au=Goodman+JA&rft.au=Blanchar+JC&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Eidelman S, Crandall CS, Goodman JA, & Blanchar JC (2012). Low-Effort Thought Promotes Political Conservatism. <span style="font-style: italic;">Personality & Social Psychology Bulletin</span> PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22427384">22427384</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+Science&rft_id=info%3Adoi%2F10.1111%2Fj.1467-9280.2005.01607.x&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Regression+Basics%3A+Rejoinder+to+Bridgeman&rft.issn=0956-7976&rft.date=2005&rft.volume=16&rft.issue=9&rft.spage=747&rft.epage=747&rft.artnum=http%3A%2F%2Fpss.sagepub.com%2Fcontent%2F16%2F9%2F747.extract&rft.au=Frey%2C+M.&rft.au=Detterman%2C+D.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Frey, M., & Detterman, D. (2005). Regression Basics: Rejoinder to Bridgeman <span style="font-style: italic;">Psychological Science, 16</span> (9), 747-747 DOI: <a rev="review" href="http://dx.doi.org/10.1111/j.1467-9280.2005.01607.x">10.1111/j.1467-9280.2005.01607.x</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+Science&rft_id=info%3Adoi%2F10.1111%2Fj.0956-7976.2004.00687.x&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Scholastic+Assessment+or+g%3F%3A+The+Relationship+Between+the+Scholastic+Assessment+Test+and+General+Cognitive+Ability+++++++&rft.issn=09567976&rft.date=2004&rft.volume=15&rft.issue=6&rft.spage=373&rft.epage=378&rft.artnum=http%3A%2F%2Fpss.sagepub.com%2Fcontent%2F15%2F6%2F373.short&rft.au=Frey%2C+M.&rft.au=Detterman%2C+D.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Frey, M., & Detterman, D. (2004). Scholastic Assessment or g?: The Relationship Between the Scholastic Assessment Test and General Cognitive Ability <span style="font-style: italic;">Psychological Science, 15</span> (6), 373-378 DOI: <a rev="review" href="http://dx.doi.org/10.1111/j.0956-7976.2004.00687.x">10.1111/j.0956-7976.2004.00687.x</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychological+Science&rft_id=info%3Apmid%2F22222219&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Bright+minds+and+dark+attitudes%3A+lower+cognitive+ability+predicts+greater+prejudice+through+right-wing+ideology+and+low+intergroup+contact.&rft.issn=0956-7976&rft.date=2012&rft.volume=23&rft.issue=2&rft.spage=187&rft.epage=95&rft.artnum=http%3A%2F%2Fscottbarrykaufman.com%2Fwp-content%2Fuploads%2F2012%2F02%2FPsychological-Science-2012-Hodson-0956797611421206.pdf&rft.au=Hodson+G&rft.au=Busseri+MA&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Hodson G, & Busseri MA (2012). Bright minds and dark attitudes: lower cognitive ability predicts greater prejudice through right-wing ideology and low intergroup contact. <span style="font-style: italic;">Psychological Science, 23</span> (2), 187-95 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22222219">22222219</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Journal+of+Physical+Anthropology&rft_id=info%3Apmid%2F21913174&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+impact+of+founder+effects%2C+gene+flow%2C+and+European+admixture+on+native+American+genetic+diversity.&rft.issn=0002-9483&rft.date=2011&rft.volume=146&rft.issue=4&rft.spage=530&rft.epage=8&rft.artnum=http%3A%2F%2Fonlinelibrary.wiley.com%2Fdoi%2F10.1002%2Fajpa.21506%2Fabstract&rft.au=Hunley+K&rft.au=Healy+M&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Hunley K, & Healy M (2011). The impact of founder effects, gene flow, and European admixture on native American genetic diversity. <span style="font-style: italic;">American Journal of Physical Anthropology, 146</span> (4), 530-8 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21913174">21913174</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Social+Psychology+Quarterly&rft_id=info%3Adoi%2F10.1177%2F0190272510361602&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Why+Liberals+and+Atheists+Are+More+Intelligent&rft.issn=0190-2725&rft.date=2010&rft.volume=73&rft.issue=1&rft.spage=33&rft.epage=57&rft.artnum=http%3A%2F%2Fsecure.asanet.org%2Fimages%2Fjournals%2Fdocs%2Fpdf%2Fspq%2FMar10SPQFeature.pdf&rft.au=Kanazawa%2C+S.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Kanazawa, S. (2010). Why Liberals and Atheists Are More Intelligent <span style="font-style: italic;">Social Psychology Quarterly, 73</span> (1), 33-57 DOI: <a rev="review" href="http://dx.doi.org/10.1177/0190272510361602">10.1177/0190272510361602</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Journal+of+Human+Genetics&rft_id=info%3Apmid%2F17503322&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=A+Genomewide+Admixture+Map+for+Latino+Populations.&rft.issn=0002-9297&rft.date=2007&rft.volume=80&rft.issue=6&rft.spage=1024&rft.epage=36&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1867092%2Fpdf%2FAJHGv80p1024.pdf&rft.au=Price+AL&rft.au=Patterson+N&rft.au=Yu+F&rft.au=Cox+DR&rft.au=Waliszewska+A&rft.au=McDonald+GJ&rft.au=Tandon+A&rft.au=Schirmer+C&rft.au=Neubauer+J&rft.au=Bedoya+G&rft.au=Duque+C&rft.au=Villegas+A&rft.au=Bortolini+MC&rft.au=Salzano+FM&rft.au=Gallo+C&rft.au=Mazzotti+G&rft.au=Tello-Ruiz+M&rft.au=Riba+L&rft.au=Aguilar-Salinas+CA&rft.au=Canizales-Quinteros+S&rft.au=Menjivar+M&rft.au=Klitz+W&rft.au=Henderson+B&rft.au=Haiman+CA&rft.au=Winkler+C&rft.au=Tusie-Luna+T&rft.au=Ruiz-Linares+A&rft.au=Reich+D&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Price AL, Patterson N, Yu F, Cox DR, Waliszewska A, McDonald GJ, Tandon A, Schirmer C, Neubauer J, Bedoya G, Duque C, Villegas A, Bortolini MC, Salzano FM, Gallo C, Mazzotti G, Tello-Ruiz M, Riba L, Aguilar-Salinas CA, Canizales-Quinteros S, Menjivar M, Klitz W, Henderson B, Haiman CA, Winkler C, Tusie-Luna T, Ruiz-Linares A, & Reich D (2007). A Genomewide Admixture Map for Latino Populations. <span style="font-style: italic;">American Journal of Human Genetics, 80</span> (6), 1024-36 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/17503322">17503322</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+Educational+Research&rft_id=info%3Adoi%2F10.1080%2F00220671.1993.9941211&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Perspectives+on+Education+in+America%3A+College+and+University+Data&rft.issn=0022-0671&rft.date=1993&rft.volume=86&rft.issue=5&rft.spage=273&rft.epage=288&rft.artnum=http%3A%2F%2Fwww.jstor.org%2Fdiscover%2F10.2307%2F27541876&rft.au=Sandia+National+Laboratories&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Sandia National Laboratories (1993). Perspectives on Education in America: College and University Data <span style="font-style: italic;">The Journal of Educational Research, 86</span> (5), 273-288 DOI: <a rev="review" href="http://dx.doi.org/10.1080/00220671.1993.9941211">10.1080/00220671.1993.9941211</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+Educational+Research&rft_id=info%3Adoi%2F10.1080%2F00220671.1994.9941235&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=The+Sandia+Report+and+U.S.+Achievement%3A+An+Assessment&rft.issn=0022-0671&rft.date=1994&rft.volume=87&rft.issue=3&rft.spage=133&rft.epage=146&rft.artnum=http%3A%2F%2Fwww.tandfonline.com%2Fdoi%2Fabs%2F10.1080%2F00220671.1994.9941235&rft.au=Stedman%2C+L.&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CNeuroscience%2CGenetics%2C+Psychiatry">Stedman, L. (1994). The Sandia Report and U.S. Achievement: An Assessment <span style="font-style: italic;">The Journal of Educational Research, 87</span> (3), 133-146 DOI: <a rev="review" href="http://dx.doi.org/10.1080/00220671.1994.9941235">10.1080/00220671.1994.9941235</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Genome+Biology&rft_id=info%3Apmid%2F20025784&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Characterizing+the+admixed+African+ancestry+of+African+Americans.&rft.issn=1465-6906&rft.date=2009&rft.volume=10&rft.issue=12&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fgenomebiology.com%2Fcontent%2Fpdf%2Fgb-2009-10-12-r141.pdf&rft.au=Zakharia+F&rft.au=Basu+A&rft.au=Absher+D&rft.au=Assimes+TL&rft.au=Go+AS&rft.au=Hlatky+MA&rft.au=Iribarren+C&rft.au=Knowles+JW&rft.au=Li+J&rft.au=Narasimhan+B&rft.au=Sidney+S&rft.au=Southwick+A&rft.au=Myers+RM&rft.au=Quertermous+T&rft.au=Risch+N&rft.au=Tang+H&rfe_dat=bpr3.included=1;bpr3.tags=Medicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CGenetics%2C+Psychiatry">Zakharia F, Basu A, Absher D, Assimes TL, Go AS, Hlatky MA, Iribarren C, Knowles JW, Li J, Narasimhan B, Sidney S, Southwick A, Myers RM, Quertermous T, Risch N, & Tang H (2009). Characterizing the admixed African ancestry of African Americans. <span style="font-style: italic;">Genome Biology, 10</span> (12) PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20025784">20025784</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com38tag:blogger.com,1999:blog-5002675950760488813.post-86515795311541530642011-12-02T15:10:00.000-08:002011-12-02T21:06:17.776-08:00Blacks with Bullets Embedded in Bone<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-P1FHLpYFA14/TtlcbPyxR2I/AAAAAAAAAQM/6QHLNPEgiKk/s1600/once%2Bupon%2Ba%2Btime.jpg"><img style="float:left; margin:0 10px 10px 0;cursor:pointer; cursor:hand;width: 200px; height: 166px;" src="http://1.bp.blogspot.com/-P1FHLpYFA14/TtlcbPyxR2I/AAAAAAAAAQM/6QHLNPEgiKk/s200/once%2Bupon%2Ba%2Btime.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5681674028070291298" /></a><br /><br /><br /><br /><br />nce upon a time, a people now known as African Americans left plantations of slavery to live in relative peace among white people. Unfortunately, the mean, villainous whites schemed systems of organized crime that allowed them to enrich themselves into tranquil opulence, while they excluded the African Americans from their illegal get-rich connivances. Amidst their impoverishment, the African Americans experienced a psychological transformation that forced many of them to become violent criminals. The End.<br /><br />This story emerges from the works cited by Steven Pinker in his bestselling, and possibly Pulitzer Prize-winning book, The Better Angels of Our Nature. Pinker writes,<br /><br /><blockquote>Figure 3-14 shows the rates for two cities in which black-on-black and white-on-white homicides can be distinguished. The graph reveals that the racial disparity in American homicide has not always been with us.</blockquote><br /><br />Here is the figure:<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://4.bp.blogspot.com/-TLPHKKAusVc/Ttlc6DL0GdI/AAAAAAAAAQY/Gwd4jPEA_bk/s1600/steven%2Bpinker%2B-%2Bny%2Bphiladelphia%2Brace%2Bhomicide.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 249px;" src="http://4.bp.blogspot.com/-TLPHKKAusVc/Ttlc6DL0GdI/AAAAAAAAAQY/Gwd4jPEA_bk/s400/steven%2Bpinker%2B-%2Bny%2Bphiladelphia%2Brace%2Bhomicide.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5681674557261617618" /></a><br />He cites Eric Monkkonen’s Murder in New York City, which says,<br /><br /><blockquote>Essentially, crime was more profitable for whites, whereas even in crime, discrimination blocked the more lucrative opportunities for African Americans and encouraged more violent, destructive offenses.</blockquote><br /><br />Pinker’s characterization of homicide data is another example of his distortions on matters pertaining to race and violence. See my <a href="http://theunsilencedscience.blogspot.com/2011/10/kill-popular-science.html">previous post</a> on how Pinker flubbed his summary of the decades of research on the best understood violence gene, including his citation of a copy-and-paste error. Much of his data for New York City in the above graph, including all years of equal homicide rates, comes from American History by Randolph Roth, who plotted a similar graph shown below and made clear that the data plotted actually do not represent known intraracial homicide assailants, but just homicide victims. <br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://2.bp.blogspot.com/-0JrGJCahwlQ/Ttle42XH9iI/AAAAAAAAAQk/h8vuWt5pEbw/s1600/randolph%2Broth%2B-%2Bny%2Bphiladelphia%2Brace%2Bhomicide.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 366px; height: 290px;" src="http://2.bp.blogspot.com/-0JrGJCahwlQ/Ttle42XH9iI/AAAAAAAAAQk/h8vuWt5pEbw/s400/randolph%2Broth%2B-%2Bny%2Bphiladelphia%2Brace%2Bhomicide.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5681676735662781986" /></a><br />In fact, Roth further qualified the data for Philadelphia:<br /><br /><br /><blockquote>It may prove that blacks accounted for a greater proportion of homicide perpetrators than victims in Philadelphia, but determining that will require more data, including a tally of blacks and whites killed in riots. Blacks committed homicide there at over twice the rate whites did, 1839-1846, according to indictment records (6.5 per 100,000 adults per year versus 2.7), because they were more likely to commit both intraracial and interracial homicide. It may be that Philadelphia’s antiblack riots, the disfranchisement of blacks in Pennsylvania, and increased competition with whites for unskilled jobs were beginning to take their toll.</blockquote><br /><br />Roger Lane also questioned Philadelphia’s homicide victimhood data because coroners’ records “proved unreliable.” Coroners frequently failed to indicate that a death was a homicide. Ted Robert Gurr thought this problem might exist in other American cities of that era, but no one had bothered to check as Lane had done in Philadelphia.<br /><br />Roth did provide actual estimates of New York City homicides, which doubled the very small racial gap in victimization. For Philadelphia, Pinker was not clear whether and for what years he made use of Roth’s data. Roth estimated that, from 1839 to 1846, Philadelphia’s African-American rate of homicide victimization was 28 percent higher than that of whites.<br /><br />Monkkonen provided some context for the period of purported New York City homicide racial equality. First, he advised caution about the quality of the data. “Even though we can outline this demographic history of black New Yorkers, we cannot yet establish precise population measures… Thus, any construction of rates with at-risk denominators must be understood as estimates.” How unfortunate that this important historic moment of violence equality was so poorly documented.<br /><br />Generalizing New York City to the rest of America has other complicating factors. Monkkonen offered estimates that suggest that racial homicide equality resulted from enormous white ethnic inequality. “My best estimate for the decade centered on 1860,” he wrote, “sets the Irish homicide rate at 37.5 per 100,000 adult males, the German rate at 15.7, and the black rate at 32.” About half of New York City’s population was immigrant in 1860. It is ironic that Pinker is allowing the violent tendencies of New York Irish-American immigrants to characterize the behavior of American whites in general because English Americans took to calling them “white Negroes.”<br /><br />Lastly, the age demographics of these groups differed. In 1850, Irish immigrant males in New York City were 19 percent more likely to be in the potentially more violent age range of 16 to 45 than African-American men, and, despite being half as homicidal, German immigrant men were 73 percent more likely than African-American men to be in that age range. Monkkonen does not entirely attribute the eventual growth of a large racial homicide gap to poverty because New York City experienced a massive growth of young black men, such that in 1940 only 19 percent of African-American New York City men in this age range were born there.<br /><br />Another recently published study, which Pinker did not consider, about this period described a qualitative distinction of racial patterns of violence. Last year, Carlina de la Cova published the first large-scale analysis of its kind, reviewing 651 male cadavers “of low socioeconomic status born between 1825 and 1877” from Cleveland, St. Louis, and Washington DC. Though these remains are apparently not of homicide victims, they do offer evidence of racial differences in violence from that era, but only among the poor, as none owned property, and most were transient. Thus, the study should bias towards exaggerating white delinquency with a sample more unrepresentative of whites than African Americans.<br /><br />Although fully 92 percent of all cadavers had skeletal fractures, in every category of fracture, whites had more. The smallest differences were for injuries that were most plausibly from serious fights. 50 percent of whites had cranial fractures, compared to 48 percent of African Americans. 44.8 percent of whites had nasal fractures, compared to 42.3 percent of African Americans. Differences for vertebrae fracture rates were much greater, at 72.7 percent for whites and 35.8 percent for African Americans. De la Cova considered osteoporosis as a possible explanation. She noted that African Americans have less osteoporosis, greater bone mass, denser cortical bone, and lower bone resorption. Indeed, black people have greater bone mineral density from infancy, and hormonal levels contribute to such racial differences, <a href="http://jcem.endojournals.org/content/88/2/642.full">even in childhood,</a>. (Recall that the media accused research oncologist Kathy Albain of <a href="http://theunsilencedscience.blogspot.com/2010/01/epistemology-endocrinology.html">“racial medical profiling”</a> for discovering that racial disparities in cancer mortality remain only in cancers related to sex hormones after accounting for zip code.) Of course, skin color affects the pathways of the hormone vitamin D. De la Cova checked for an influence of osteoporosis and age of death, but that negative result does not negate the fact that black people have stronger bones even in comparisons of whites and blacks without osteoporosis. This seems to extend to tooth loss, which de la Cova also utilized in her attempt to support differing rates of fighting. Even in the present-era <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758161/">National Health and Nutrition Examination Survey-III</a>, in which whites were better educated, white people still had a higher rate of tooth loss than African Americans and Mexican Americans. In fact, having less education was significantly associated with tooth loss in white people, but not African Americans and Mexican Americans.<br /><br />Even so, de la Cova points to historical accounts of popular and “ritualized” pugilism among poor white men to settle disputes and protect their “honor,” which logically might play less of a role in the violent behavior of a systematically oppressed minority.<br /><br />On the other hand, black men comprised all eight of the gunshot wounds, most having a bullet embedded in a bone. Though this was a small number of the cadavers, historical accounts and African-American newspaper advertisements also reflected a gun-oriented African-American culture. Perhaps their early association with guns made fistfights an untenable means of resolving conflicts.<br /><br />The US Census Bureau did not start tracking crime until 1880, and despite being a minority, African Americans were receiving 54 percent of unlawfully concealed weapons charges and 75 percent of exhibiting a deadly weapon charges and were committing 83 percent of shootings, 85 percent of stabbings, 48 percent of manslaughter homicides, and 43 percent of murders.<br /><br />Perhaps the best argument for an era of relative homicide equality would be the well-documented, enormous widening of the racial homicide gap in the years that followed. Gurr provided an illustrative graph of this for Washington DC.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-lWVCcrMRkTQ/TtlfUo87atI/AAAAAAAAAQ8/IEqyUWo6HcM/s1600/homicide%2Bdc.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 296px;" src="http://1.bp.blogspot.com/-lWVCcrMRkTQ/TtlfUo87atI/AAAAAAAAAQ8/IEqyUWo6HcM/s400/homicide%2Bdc.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5681677213099584210" /></a><br />Here is Jeffrey Adler’s homicide graph for Chicago when African Americans were a tiny minority of the population.<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-tL5l08B388k/TtlfHIIjMII/AAAAAAAAAQw/AraeWla5ZUM/s1600/homicide%2Bchicago.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 256px;" src="http://3.bp.blogspot.com/-tL5l08B388k/TtlfHIIjMII/AAAAAAAAAQw/AraeWla5ZUM/s400/homicide%2Bchicago.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5681676980951658626" /></a><br />Societal changes can influence patterns of violence, and these years certainly qualified as profoundly transformative for African Americans. However, given that African Americans have higher allele frequencies than whites of all or (debatably) nearly all identified violence genes, anyone who advertises a distant past of black peaceableness deserves an inspection of their data. I suggest this should even be so for a beloved Harvard celebrity professor.<br /><br /><br /><br /><br /><span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span><br /><br /><br /><br /><br /><br /><br />Adler, Jeffrey S. 2006. First in Violence, Deepest in Dirt: Homicide in Chicago, 1875-1920. Cambridge, Mass.: Harvard University Press.<br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Anthropologist&rft_id=info%3Apmid%2F21132946&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Cultural+patterns+of+trauma+among+19th-century-born+males+in+cadaver+collections.&rft.issn=0002-7294&rft.date=2010&rft.volume=112&rft.issue=4&rft.spage=589&rft.epage=606&rft.artnum=&rft.au=De+La+Cova+C&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CEcology+%2F+Conservation%2CGenetics%2C+Psychiatry">De La Cova C (2010). Cultural patterns of trauma among 19th-century-born males in cadaver collections. <span style="font-style: italic;">American Anthropologist, 112</span> (4), 589-606 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21132946">21132946</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Crime+and+Justice&rft_id=info%3Adoi%2F10.1086%2F449082&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Historical+Trends+in+Violent+Crime%3A+A+Critical+Review+of+the+Evidence&rft.issn=0192-3234&rft.date=1981&rft.volume=3&rft.issue=&rft.spage=295&rft.epage=&rft.artnum=http%3A%2F%2Fucp.uchicago.edu%2Fcgi-bin%2Fresolve%3Fid%3Ddoi%3A10.1086%2F449082&rft.au=Gurr%2C+T.&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CEcology+%2F+Conservation%2CGenetics%2C+Medicine%2C+Psychiatry">Gurr, T. (1981). Historical Trends in Violent Crime: A Critical Review of the Evidence <span style="font-style: italic;">Crime and Justice, 3</span> DOI: <a rev="review" href="http://dx.doi.org/10.1086/449082">10.1086/449082</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft_id=info%3Apmid%2F12574194&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Difference+in+bone+mass+between+black+and+white+American+children%3A+attributable+to+body+build%2C+sex+hormone+levels%2C+or+bone+turnover%3F&rft.issn=0021-972X&rft.date=2003&rft.volume=88&rft.issue=2&rft.spage=642&rft.epage=9&rft.artnum=http%3A%2F%2Fjcem.endojournals.org%2Fcontent%2F88%2F2%2F642.full&rft.au=Hui+SL&rft.au=Dimeglio+LA&rft.au=Longcope+C&rft.au=Peacock+M&rft.au=McClintock+R&rft.au=Perkins+AJ&rft.au=Johnston+CC+Jr&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CEcology+%2F+Conservation%2CGenetics%2C+Medicine%2C+Psychiatry">Hui SL, Dimeglio LA, Longcope C, Peacock M, McClintock R, Perkins AJ, & Johnston CC Jr (2003). Difference in bone mass between black and white American children: attributable to body build, sex hormone levels, or bone turnover? <span style="font-style: italic;">The Journal of clinical endocrinology and metabolism, 88</span> (2), 642-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/12574194">12574194</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Community+dentistry+and+oral+epidemiology&rft_id=info%3Apmid%2F19302573&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Racial%2Fethnic+variations+in+associations+between+socioeconomic+factors+and+tooth+loss.&rft.issn=0301-5661&rft.date=2009&rft.volume=37&rft.issue=3&rft.spage=267&rft.epage=75&rft.artnum=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2758161%2F&rft.au=Jimenez+M&rft.au=Dietrich+T&rft.au=Shih+MC&rft.au=Li+Y&rft.au=Joshipura+KJ&rfe_dat=bpr3.included=1;bpr3.tags=Anthropology%2CBiology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CEcology+%2F+Conservation%2CGenetics%2C+Medicine%2C+Psychiatry">Jimenez M, Dietrich T, Shih MC, Li Y, & Joshipura KJ (2009). Racial/ethnic variations in associations between socioeconomic factors and tooth loss. <span style="font-style: italic;">Community dentistry and oral epidemiology, 37</span> (3), 267-75 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/19302573">19302573</a></span><br /><br />Lane, Roger. 1979. Violent Death in the City: Suicide, Accident, and Murder in Nineteenth-Century Philadelphia. Cambridge, Mass.: Harvard University Press.<br /><br />Monkkonen, Eric H. 2001. Murder in New York City. Berkeley: University of California Press.<br /><br />Pinker, Steven. 2011. The Better Angels of Our Nature: Why Violence Has Declined. New York, New York: Viking Penguin.<br /><br />Roth, Randolph. 2009. American Homicide. Cambridge, Mass.: Harvard University Press.nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com3tag:blogger.com,1999:blog-5002675950760488813.post-75415028938237407272011-10-24T16:02:00.000-07:002011-10-24T17:42:00.797-07:00The Education BubbleOccupy Wall Street protests are drawing more attention to the Education Bubble. Since I coined the phrase, “Education Bubble,” I thought that I should repost my YouTube video about it. I originally posted this on May 4th, 2006, two years before Charles Murray published Real Education and three years before articles about the bubble began appearing in mainstream publications like The Chronicle of Higher Education and The Economist. Wikipedia claims that Bill Bennett originated the concept, but his <a href="http://www.nytimes.com/1987/02/18/opinion/our-greedy-colleges.html?pagewanted=all&src=pm">editorial</a> in 1987 did not use the phrase, and, of course, could not relate it to the series of economic bubbles that have occurred since.<br /><br /><iframe width="415" height="259" src="http://www.youtube.com/embed/4SwrjYvPOnQ" frameborder="0" allowfullscreen></iframe><br /><br />The idea has really caught fire recently. PayPal founder Peter Thiel created a grant to encourage young people to skip college and start a business. He joined Murray in an Intelligence Squared <a href="http://intelligencesquaredus.org/index.php/media/">debate</a> on the subject. On Friday, comedian Bill Maher endorsed the existence of an education bubble on his HBO <a href="http://www.youtube.com/watch?v=t50P1__1l9o">program</a>, which elicited the typical, kneejerk reaction from liberal columnist Thomas Friedman to pump more money into educating more students. Friedman wants another GI Bill, but we did have a Post-9/11 GI Bill.<br /><br />In order for credentials to have solid value, they must be a precious resource (to the extent that educational benefit bolsters zero-sum competitiveness), represent value added, and represent a quality of enduring merit. Because one often associates education with intelligence, and IQ tends to hold a stable value throughout an individual’s adulthood, one way to strengthen education’s value would be to make it more closely approximate IQ through stiffer admission policies or more challenging coursework. This also begs the question of whether allowing IQ testing in hiring would not be more efficient and, thereby, allow education to fill a different niche. Columnists like Friedman like to emphasize the role of education in teaching skills, but many skills do not necessarily endure as IQ and perhaps perseverance can. After the dot-com bubble burst and many engineers and computer scientists lost jobs, I recall James Fallows suggesting that graduates be able to purchase skills insurance so that their heavy investment does not crash when their particular set of specialized skills becomes obsolete. Maher quotes <a href="http://www.fareedzakaria.com/home/Articles/Entries/2011/10/6_The_Hard_Truth_About_Going_%E2%80%98Soft%E2%80%99.html">Fareed Zakaria</a> in repeating the clichéd complaint about America’s paucity of engineers, but why should young people invest in advanced high-technology skills when someone as experienced and intelligent as Warren Buffett does not even feel confident in betting some money in high-technology companies. Even if the modern “information age” economy demands a more educated populace, there is no other age in which everyday folks had more access to cheap or free knowledge without needing to earn college credits in the process. Books are now available via illegal downloads as music has been for years, and bookstores are closing down permanently. Higher education is too expensive to constantly retrain workers, but tests could inexpensively verify knowledge or abilities.<br /><br />What I find most ironic about the Education Bubble is that a liberal like Maher would endorse it without seeing that nearly any implication of it endorses politically incorrect concepts like IQ and the limitations of the well-meaning societal intervention that higher education is. All of this discussion is a high-wire act over the issue of race. It might not be “nice” to talk about race honestly, but racial disparities in IQ, <a href="http://theunsilencedscience.blogspot.com/2011/09/sat-in-red-white-and-brown.html">SAT scores</a>, and college majors are constants with profound economic impacts. Any reform will stir racial controversies with new disparities. Businesses cannot use straight IQ tests for reasons of race, alone. Can we afford our racial consensus?nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com1tag:blogger.com,1999:blog-5002675950760488813.post-51906510960744049542011-10-13T05:04:00.000-07:002011-10-21T21:57:37.821-07:00Kill Popular Science<a href="http://www.reddit.com/r/blogger/submit" onclick="window.location = 'http://www.reddit.com/r/blogger/submit?url=' + encodeURIComponent(window.location); return false"> <img src="http://www.reddit.com/static/spreddit6.gif" alt="submit to reddit" border="0" /> </a><br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://3.bp.blogspot.com/-MoH-EJuB3K4/Tpbagfi9LVI/AAAAAAAAAP0/xVp1WM_QoGI/s1600/Steven%2BPinker.JPG"><img style="float:right; margin:0 0 10px 10px;cursor:pointer; cursor:hand;width: 200px; height: 150px;" src="http://3.bp.blogspot.com/-MoH-EJuB3K4/Tpbagfi9LVI/AAAAAAAAAP0/xVp1WM_QoGI/s200/Steven%2BPinker.JPG" border="0" alt=""id="BLOGGER_PHOTO_ID_5662953833223761234" /></a>Steven Pinker’s new book, “The Better Angels of Our Nature,” is out, and the reception reminds me of an album release from a trendy band during the 1990’s. I must beg my readers’ forgiveness for writing this very preliminary review for a book that I have not finished because the subject matter is so important. Most reviews and buzz for this book center on Pinker’s observations about the decline of violence and the advance of enlightened views. Pinker has been <a href="http://www.youtube.com/watch?v=ramBFRt1Uzk">speaking</a> about this phenomenon for years, and many facets of it are apparent in my own lifetime, such as the utter metamorphosis of public consensus regarding homosexuality. The book has a number of fascinating graphs that speak to the changes, and I have little reason to critique his central thesis, other than to say that I am not sure the trend entirely represents genuine progress. For example, I suspect that he could have placed a graph of the decline of fat jokes alongside his graphs of the decline of racial prejudices. While society has improved control over physical aggression, the obesity epidemic proves that indiscipline still finds expression. In fact, when one considers the growing acceptance of “alternative”—excuse me, “integrative” medicine, one can see how the triumph of enlightened tolerance can coincide with a lax shrug off of reason and scientific rigor.<br /><br />Though I perused the tome in the modern cursory version of the word’s contradictory meanings, I gave special attention to the latter chapters, particularly chapters 8 and 9 on the nature of violence, itself, which has been one of my obsessions. That discussion concerns the overriding paradox of this work. How could this man, who wrote The Blank Slate to passionately declare that we are not and that behavior is part heredity, reconcile with a belief that societal evolution pushed radical behavioral modification? I regret to say that this was a serious weakness of an otherwise well-reasoned exposition.<br /><br />First let me stress that I do not see Pinker’s observations as fundamentally opposed to the revolution taking place in biosocial criminology and genetic psychiatry. On the contrary, making aggression anomalous likely accentuates the role of genetics and biology in what deserves to be considered a veritable behavioral disease. What science really calls into question is whether historic trends justify extrapolation, and from what I can tell, Pinker has dodged such speculation. To illustrate his handling, the book contains extensive discussion of how the secular rise in IQ, known as the Flynn effect, could be reducing violence, but I found no mention of the evidence for subsequent plateauing. Then again, my hope is that the research on the genetics of violence, which I attempt to elucidate, could help channel efforts to find new ways, including pharmacological developments, to sustain aggression’s decline.<br /><br />Judging by Pinker’s treatment of the subject, my message is not getting out. He dismissed research on monoamine oxidase A (MAOA) using a study with which my regular readers are all too familiar.<br /><br /><blockquote>[A]n association between the gene and aggression has not been found in non-European populations, perhaps because they have evolved other ways of regulating their catecholamine levels. (Genes often act in networks regulated by feedback loops, so in populations in which a particular gene is less effective, other genes may step up their activity to compensate.) For now, the Warrior Gene theory is staggering around with possibly fatal wounds.</blockquote><br /><br />Nice try. Pinker is referencing the <a href="http://www.ncbi.nlm.nih.gov/pubmed/16814261">Widom and Brzustowicz paper</a> that combined men and women to compare “whites” to “non-whites.” Gender was not controlled, and that white sample was 33% female. Non-whites were 38% female, but women were far more represented among non-white subjects with the low-activity, 3-repeat allele. For the subjects with the 3-repeat allele, which is the allele considered most impacted by the environmental trigger, whites were 24% female, and non-whites were 43% female. Antisocial behavior in women, but not men, is <a href="http://theunsilencedscience.blogspot.com/2011/09/attack-of-warrior-gene-babies.html">mediated</a> by the epigenetic <a href="http://onlinelibrary.wiley.com/doi/10.1002/ajmg.b.30778/full">methylation</a> of MAOA as well as a newly discovered <a href="http://www.sciencedirect.com/science/article/pii/S0301051111001116">second promoter</a> that actually has more effect in women than the alleles mentioned. Also, of course, MAOA is located on the X chromosome. Women have two copies, which helps explain why even the radical Brunner-syndrome mutation that completely disables the gene does not seem to affect the behavior of women. It can be nice to have a spare.<br /><br />Pinker seems to have received his introduction to this subject through the New Zealand Maori <a href="http://theunsilencedscience.blogspot.com/2010/01/no-amore-for-maoa-from-maori.html">controversy</a>, in which Rod Lea had to make amends for allegedly saying that the Maori are prone to criminality. Thus, Pinker is completely unaware that studies have found that MAOA influences aggression in non-whites. <a href="http://www.sciencedirect.com/science/article/pii/S0006322308011050">Weder et al</a> found that the gene-environment association of MAOA and aggression held for a 58-subject sample of African-American and biracial children. Kevin Beaver’s research also helps support this association. His 2009 <a href="http://sipura.pp.fi/Artikkelit/Beaver.pdf">study</a> on MAOA’s effect on gang membership and weapon use included African Americans. His 2010 <a href="http://www.sciencedirect.com/science/article/pii/S0165178109000547">study</a> on African-American men and violence used a genetic index that included MAOA and four other genes that affect catecholamine levels.<br /><br />At least claiming that MAOA does not affect non-white people fits a politically correct agenda of raising the self-esteem of minorities who feel the burden of a violent stereotype. What would you think of Steven Pinker if he spread a complete falsehood that could label a group of people genetically violent without any scientific basis whatsoever?<br /><br /><blockquote>[T]he low-activity version of the gene is even more common in Chinese men (77 percent of whom carry it), and the Chinese are neither descended from warriors in their recent history nor particularly prone to social pathology in modern societies.</blockquote><br /><br />I <a href="http://theunsilencedscience.blogspot.com/2011/09/attack-of-warrior-gene-babies.html">previously</a> debunked this, but I guess I must do so, again. A study by <a href="http://www.sciencedirect.com/science/article/pii/S0278584601002883">Lu et al</a> found that 42 Taiwanese men, or 55% of their 77-subject control sample, had the 3-repeat allele of MAOA. <a href="http://journal.nzma.org.nz/journal/120-1250/2441/">Lea and Chambers</a> copied the information incorrectly. Then, an <a href="http://review.mai.ac.nz/index.php/MR/article/viewFile/265/285">editorial</a> against MAOA research by a doctoral student repeated the falsehood. Now, Pinker has immortalized this slander against Chinese people in a bestselling book. The actual allele frequency given by Lu et al matches the allele frequency found for Asians in subsequent research, which is not higher than that of other groups besides white people. Pinker, like so many others, conflated the 3-repeat allele with the 2-repeat allele as the “low-activity allele,” even though the 2-repeat allele doubles the association with violence without needing an environmental trigger. The 2-repeat allele accounts for <a href="http://theunsilencedscience.blogspot.com/2011/03/racial-controversy-of-violent-gene.html">4.7%</a> of African-American MAOA genes and 0.00067% of Asian MAOA genes (assuming that the only Chinese control subject with the allele did not have mixed ancestry). Not only does this bogus insult create a new stereotype for Chinese people, but the numbers error reinforces an <a href="http://theunsilencedscience.blogspot.com/2011/09/sat-in-red-white-and-brown.html">old generalization</a>, as all four guilty parties were white boys. (Chinese people, when you buy my neighborhood, recall that I personally sent Pinker a corrigendum request.)<br /><br /><a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/-Oie0RFnQPRg/TpbZigYiP-I/AAAAAAAAAPc/rjYCcImAIrY/s1600/MathFail.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 393px; height: 293px;" src="http://1.bp.blogspot.com/-Oie0RFnQPRg/TpbZigYiP-I/AAAAAAAAAPc/rjYCcImAIrY/s400/MathFail.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5662952768296599522" /></a><br />Herein lies the problem with popular science. Steven Pinker is a Harvard professor who previously chastised Malcolm Gladwell for misspelling “igon value.” Pinker’s new book encompasses a prodigious collection of disparate lines of evidence. Even so, he dismissed a vital segment of potentially life-saving research using biased sources that were motivated at least in one case by racial politics. When Dr. Phil stumbled through his television show <a href="http://theunsilencedscience.blogspot.com/2011/08/why-youtube-sucks.html">episode</a> on the warrior gene, he made mistakes and showed his ignorance, but he did not bring an entire field of study into disrepute. However, when Malcolm Gladwell or Stephen Jay Gould call IQ testing an “ice flow” or decry its “reification,” it has consequences for science. Gladwell and Pinker inhabit a pantheon of respected liberal thinkers whose influence reverberates throughout academia. Their stature alone can transform an ignorant statement into an authoritative observation. Their superficial summations can leave a lasting imprint on another’s life’s work, as they bring along a vast audience of comparative ignoramuses to boo rogue points of view (not unlike a daytime talk show).<br /><br /><br /><br /><span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border:0;"/></a></span><br /><br /><br /><br /><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychiatry&rft_id=info%3Apmid%2F16814261&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+and+the+%22cycle+of+violence%3A%22+childhood+abuse+and+neglect%2C+MAOA+genotype%2C+and+risk+for+violent+and+antisocial+behavior.&rft.issn=0006-3223&rft.date=2006&rft.volume=60&rft.issue=7&rft.spage=684&rft.epage=9&rft.artnum=&rft.au=Widom+CS&rft.au=Brzustowicz+LM&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Medicine%2C+Psychiatry">Widom CS, & Brzustowicz LM (2006). MAOA and the "cycle of violence:" childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. <span style="font-style: italic;">Biological psychiatry, 60</span> (7), 684-9 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/16814261">16814261</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychiatry&rft_id=info%3Apmid%2F18996506&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+genotype%2C+maltreatment%2C+and+aggressive+behavior%3A+the+changing+impact+of+genotype+at+varying+levels+of+trauma.&rft.issn=0006-3223&rft.date=2009&rft.volume=65&rft.issue=5&rft.spage=417&rft.epage=24&rft.artnum=&rft.au=Weder+N&rft.au=Yang+BZ&rft.au=Douglas-Palumberi+H&rft.au=Massey+J&rft.au=Krystal+JH&rft.au=Gelernter+J&rft.au=Kaufman+J&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Medicine%2C+Psychiatry">Weder N, Yang BZ, Douglas-Palumberi H, Massey J, Krystal JH, Gelernter J, & Kaufman J (2009). MAOA genotype, maltreatment, and aggressive behavior: the changing impact of genotype at varying levels of trauma. <span style="font-style: italic;">Biological psychiatry, 65</span> (5), 417-24 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/18996506">18996506</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Comprehensive+psychiatry&rft_id=info%3Apmid%2F20152292&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidase+A+genotype+is+associated+with+gang+membership+and+weapon+use.&rft.issn=0010-440X&rft.date=2010&rft.volume=51&rft.issue=2&rft.spage=130&rft.epage=4&rft.artnum=&rft.au=Beaver+KM&rft.au=DeLisi+M&rft.au=Vaughn+MG&rft.au=Barnes+JC&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Medicine%2C+Psychiatry">Beaver KM, DeLisi M, Vaughn MG, & Barnes JC (2010). Monoamine oxidase A genotype is associated with gang membership and weapon use. <span style="font-style: italic;">Comprehensive psychiatry, 51</span> (2), 130-4 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/20152292">20152292</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Psychiatry+Research&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Genetic+risk%2C+parent%E2%80%93child+relations%2C+and+antisocial+phenotypes+in+a+sample+of+African-American+males&rft.issn=&rft.date=2010&rft.volume=175&rft.issue=1-2&rft.spage=160&rft.epage=164&rft.artnum=http%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fpii%2FS0165178109000547&rft.au=Kevin+Beaver&rft.au=Ashley+Sak&rft.au=Jamie+Vaske&rft.au=Jessica+Nilsson&rfe_dat=bpr3.included=1;bpr3.tags=Biology%2CMedicine%2CPsychology%2CSocial+Science%2CResearch+%2F+Scholarship%2COther%2CHealth%2CNeuroscience%2CGenetics%2C+Medicine%2C+Psychiatry">Kevin Beaver, Ashley Sak, Jamie Vaske, & Jessica Nilsson (2010). Genetic risk, parent–child relations, and antisocial phenotypes in a sample of African-American males <span style="font-style: italic;">Psychiatry Research, 175</span> (1-2), 160-164</span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Progress+in+neuro-psychopharmacology+%26+biological+psychiatry&rft_id=info%3Apmid%2F11999895&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=No+association+of+the+MAOA+gene+with+alcoholism+among+Han+Chinese+males+in+Taiwan.&rft.issn=0278-5846&rft.date=2002&rft.volume=26&rft.issue=3&rft.spage=457&rft.epage=61&rft.artnum=&rft.au=Lu+RB&rft.au=Lee+JF&rft.au=Ko+HC&rft.au=Lin+WW&rft.au=Chen+K&rft.au=Shih+JC&rfe_dat=bpr3.included=1;bpr3.tags=Other%2CGenetics%2C+Medicine%2C+Psychiatry">Lu RB, Lee JF, Ko HC, Lin WW, Chen K, & Shih JC (2002). No association of the MAOA gene with alcoholism among Han Chinese males in Taiwan. <span style="font-style: italic;">Progress in neuro-psychopharmacology & biological psychiatry, 26</span> (3), 457-61 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/11999895">11999895</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+New+Zealand+medical+journal&rft_id=info%3Apmid%2F17339897&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Monoamine+oxidase%2C+addiction%2C+and+the+%22warrior%22+gene+hypothesis.&rft.issn=0028-8446&rft.date=2007&rft.volume=120&rft.issue=1250&rft.spage=&rft.epage=&rft.artnum=&rft.au=Lea+R&rft.au=Chambers+G&rfe_dat=bpr3.included=1;bpr3.tags=Other%2CGenetics%2C+Medicine%2C+Psychiatry">Lea R, & Chambers G (2007). Monoamine oxidase, addiction, and the "warrior" gene hypothesis. <span style="font-style: italic;">The New Zealand medical journal, 120</span> (1250) PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/17339897">17339897</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=MAI+Review&rft_id=info%3A%2F&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Darwinism+and+the+nature+of+M%C4%81ori&rft.issn=1177-5904&rft.date=2009&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Freview.mai.ac.nz%2Findex.php%2FMR%2Farticle%2FviewFile%2F265%2F285&rft.au=Patrick-Michael+Whittle&rfe_dat=bpr3.included=1;bpr3.tags=Other%2CGenetics%2C+Medicine%2C+Psychiatry">Patrick-Michael Whittle (2009). Darwinism and the nature of Māori <span style="font-style: italic;">MAI Review</span></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+journal+of+medical+genetics.+Part+B%2C+Neuropsychiatric+genetics+%3A+the+official+publication+of+the+International+Society+of+Psychiatric+Genetics&rft_id=info%3Apmid%2F18454435&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=MAOA+methylation+is+associated+with+nicotine+and+alcohol+dependence+in+women.&rft.issn=1552-4841&rft.date=2008&rft.volume=147B&rft.issue=5&rft.spage=565&rft.epage=70&rft.artnum=&rft.au=Philibert+RA&rft.au=Gunter+TD&rft.au=Beach+SR&rft.au=Brody+GH&rft.au=Madan+A&rfe_dat=bpr3.included=1;bpr3.tags=Other%2CGenetics%2C+Medicine%2C+Psychiatry">Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A (2008). MAOA methylation is associated with nicotine and alcohol dependence in women. <span style="font-style: italic;">American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B</span> (5), 565-70 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/18454435">18454435</a></span><br /><br /><span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=Biological+psychology&rft_id=info%3Apmid%2F21554924&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Gene+environment+interactions+with+a+novel+variable+Monoamine+Oxidase+A+transcriptional+enhancer+are+associated+with+antisocial+personality+disorder.&rft.issn=0301-0511&rft.date=2011&rft.volume=87&rft.issue=3&rft.spage=366&rft.epage=71&rft.artnum=&rft.au=Philibert+RA&rft.au=Wernett+P&rft.au=Plume+J&rft.au=Packer+H&rft.au=Brody+GH&rft.au=Beach+SR&rfe_dat=bpr3.included=1;bpr3.tags=Other%2CGenetics%2C+Medicine%2C+Psychiatry">Philibert RA, Wernett P, Plume J, Packer H, Brody GH, & Beach SR (2011). Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder. <span style="font-style: italic;">Biological psychology, 87</span> (3), 366-71 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/21554924">21554924</a></span>nooffensebuthttp://www.blogger.com/profile/02461190919466049463noreply@blogger.com17