Showing posts with label heredity. Show all posts
Showing posts with label heredity. Show all posts

Saturday, October 18, 2014

Merit’s Liquidity

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?

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 study.

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 previous writings and flesh out some trends the media missed.

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.
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.


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.

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.


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.
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.

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 high test performers from higher economic strata. In The Bell Curve, Richard Herrnstein and Charles Murray claimed that the twenty-first century would continue “the emergence of a cognitive elite.”
The isolation of the brightest from the rest of society is already extreme; the forces driving it are growing stronger rather than weaker.
Of course, the economy of the 1990’s, when they wrote that, usually appeared to be growing stronger rather than weaker.

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 The Bell Curve 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.

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.


Merit’s Mobility

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.


Last year, 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.”

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.


Native-American scores remain just slightly above those of Hispanic Americans after a significant drop in Native-American ACT scores from 2010 to 2013.


Overall, Asian scores have continued their amazing progress. The Asian SAT mathematics subtest advantage over whites rose to 64 points.


Asians are not closer to surpassing whites on the critical-reading subtest only because white scores rose by the same amount this year.


In contrast to all other groups, Asian SAT writing subtest scores rose in seven of the past nine years.


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.


It would be tempting to surmise that foreign students are causing the continued progress of Asians on the SAT, but, as I previously discussed, 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.


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 recently defended The Bell Curve 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?

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 previously described methodology for adjusting scores according to state SAT and ACT participation rates.

For comparison, here is the map of the percentage of white and Asian SAT-taking students over the years:

 photo sat aw map.gif


















Student diversity increased especially among coastal states. I previously claimed, “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.

 photo sat-act part cont.gif


















One can more easily notice the change by just looking at the oldest and newest maps without animation.


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.

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.



ResearchBlogging.org






nooffensebut (2014). Parents’ Income is a Poor Predictor of SAT Score Open Differential Psychology, 1-19

Sunday, August 3, 2014

The Alondra Oubré Academic Fraud Exposed


Alondra Oubré
Wikipedia Scholar


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 error-riddled Internet screed against the warrior gene, monoamine oxidase A (MAOA). Oubré is the author of Instinct and Revelation: Reflections on the Origins of Numinous Perception and Race, Genes and Ability: Rethinking Ethnic Differences. 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, A Troublesome Inheritance, 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.

Wow! What a poorly researched Internet post! I hope you don’t mind if I post the factual corrections here for you.

“The most common variant, MAOA-4R, has four repeats and is associated with high-activity breakdown of neurotransmitters.”

I guess it would be true that MAOA-4R is the most common variant if everyone in the world was white.

“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.”

No, here is a list of studies that looked at non-whites prior to that study: Sabol et al, Kunugi et al, Balciuniene et al, Gilad et al, Ono et al, Williams et al, Koen et al, Huang et al, Yu et al, Young et al, Widom & Brzustowicz, and Rosenberg et al.

“For many experts, this ethnic gap is the result of numerous environmental causes, including poverty.”

I think you should revise this sentence.

“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.”

Notice how the African-American number is slightly lower than the source? Someone in Wikipedia 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 “idiot test” copy-and-paste error that slandered Chinese men as having an MAOA-3R allele frequency of 77%.

“Interestingly, the press ignored studies indicating that the 3R variant occurred in 61% of Taiwanese males [15] and 56% of Chinese males [16].”

You switched your sources. Both samples were Taiwanese. You rounded 54.5% to 56%. That’s kind of sloppy.

“In the Add Health database, 5.5% of African American men, 0.9% of Caucasian men, and 0.00067% of Asian men have 2R.”

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 my blog and Wikipedia. Once again, the Wikipedia troll 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 table with my tabulated allele frequencies (without excluding any sample).

“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].”

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.”

“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.”

Yeah, I guess 55 is more than 5. Damn that Wikipedia troll! Choe et al, 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?

“Although genes affect individual differences in behavior, the effect of each individual gene is usually small.”

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.

“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.”

I think Fergusson et al 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.

“Using PET imaging scans, these researchers found no correlation between MAOA brain levels and MAOA gene variants.”

However, Alia-Klein et al did find MAOA promoter effects on anger in an fMRI study. That study and Buckholtz et al found MAOA gene effects on the amygdala. Cerasa et al found that the gene influenced orbitofrontal cortical thickness with MRI. Buckholtz et al and Cerasa et al had much larger samples than the 34 men in Shumay et al. Shouldn’t you have mentioned those findings?

“Nonetheless, their results suggest that MAOA brain levels, which affect mood, are at least partially regulated by non-genetic factors — i.e., epigenetically.”

Of course, genes do influence epigenetics. In fact, the “environmental” interaction factors, like childhood maltreatment, might also have a component of heritability. Wong et al found that, compared to women, epigenetics of MAOA in men is minimal, low in variance, and high in hereditary influence. Pinsonneault et al was unable to detect any MAOA methylation in men. Philibert et al 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.

“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.”

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 recent meta-analysis of 31 studies actually disproved this and found that MAOA-3R has a slight effect on antisocial behavior independent of interaction factors.

Pigliucci allowed me to post this comment only so that others could harass me with baseless ad hominem, but he censored all of my other responses.

Exposing falsehoods about the warrior gene is nothing new for me, but this is different. It might be hard to believe that a respected scientist like Steven Pinker or an experienced writer like John Horgan would fall for the idiot test or that Scientific American, The Chronicle of Higher Education, 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 et al) 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.

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 contributions page, that he or she has a history of altering numbers in Wikipedia that relate to immigration and ethnicity 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 change was as follows:


Two minutes later, another change occurred:


At 23:55, the offender changed the same numbers, again:


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.

Massimo Pigliucci
“Editor-in-Chief”


To prevent confusion among the lay public, I politely asked Scientia Salon editor-in-chief Pigliucci for an official correction in this e-mail:

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.

Pigliucci could not bother himself with more than a curt reply.

your comment has been published, so I’m not sure what additional action you expect from me, or why.

I tried repeatedly.

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.

No reply came.

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 podcast 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 racist, 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.



ResearchBlogging.org






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. Emotion (Washington, D.C.), 9 (3), 385-96 PMID: 19485616

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. Journal of molecular evolution, 52 (2), 157-63 PMID: 11231895

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. Molecular psychiatry, 13 (3), 313-24 PMID: 17519928

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. Behavioural brain research, 211 (1), 118-24 PMID: 20303364

Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. Behavior genetics PMID: 24902785

Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA (2012). Moderating role of the MAOA genotype in antisocial behaviour. The British journal of psychiatry : the journal of mental science, 200 (2), 116-23 PMID: 22297589

Gilad Y, Rosenberg S, Przeworski M, Lancet D, & Skorecki K (2002). Evidence for positive selection and population structure at the human MAO-A gene. Proceedings of the National Academy of Sciences of the United States of America, 99 (2), 862-7 PMID: 11805333

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. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 29 (8), 1498-505 PMID: 15150530

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 Australian and New Zealand Journal of Psychiatry, 38 (4), 254-259 DOI: 10.1111/j.1440-1614.2004.01338.x

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. Molecular psychiatry, 4 (4), 393-5 PMID: 10483059

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. BioMed research international, 2014 PMID: 24971323

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. American journal of medical genetics, 114 (3), 340-2 PMID: 11920860

Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A (2008). MAOA methylation is associated with nicotine and alcohol dependence in women. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B (5), 565-70 PMID: 18454435

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. Human molecular genetics, 15 (17), 2636-49 PMID: 16893905

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. Human genetics, 120 (4), 447-59 PMID: 16896926

Sabol S, Hu S, & Hamer D (2014). A functional polymorphism in the monoamine oxidase A gene promoter Human Genetics, 103 (3), 273-279 DOI: 10.1007/s004390050816

Widom CS, & Brzustowicz LM (2006). MAOA and the "cycle of violence:" childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological psychiatry, 60 (7), 684-9 PMID: 16814261

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. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 28 (3), 533-41 PMID: 12629534

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. Epigenetics : official journal of the DNA Methylation Society, 5 (6), 516-26 PMID: 20505345

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. The American journal of psychiatry, 163 (6), 1019-25 PMID: 16741202

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. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 30 (9), 1719-23 PMID: 15956990

Tuesday, July 8, 2014

The Warrior Gene, Back from the Grave



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 other works of popular science. 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 only had one criticism: 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.

Nicholas Wade took up my cause 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 Jennifer Raff succeeded in invading the field of genetics, and she countered our claim by posting a study by Vassos et al.
"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)…"
Good gravy! You mean to tell me that all that research 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 what I usually do and post the empty-chair interview questions.

Questions posed to Dr. Evangelos Vassos:
  1. 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?
  2. 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?
  3. 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?
  4. 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?
  5. 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?
  6. 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?
  7. 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?
  8. 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?
  9. Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science?

Questions posed to Courtney Ficks:
  1. 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?
  2. 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?
  3. 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?
  4. 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?
  5. 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?
  6. 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?
  7. Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science?

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.



ResearchBlogging.org






Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. Behavior genetics PMID: 24902785

Vassos E, Collier DA, & Fazel S (2014). Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression. Molecular psychiatry, 19 (4), 471-7 PMID: 23546171

Friday, July 4, 2014

Parents’ Income Poorly Predicts SAT Score


Abstract
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.

Read the whole study at Open Differential Psychology.

See below for important excerpts and extra super-awesome graphs.

“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.”

“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.”


Income p-values without race as a covariate (p-values are shown on an inverse logarithmic scale)


Income p-values with race as a covariate (p-values are shown on an inverse logarithmic scale)

“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.”


Critical-reading and mathematics standardized coefficients compared to adjusted R2 values, organized by education first, race within each educational category, and income within each racial category

“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).”

“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.”

“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.”


Cohen’s d SAT advantage of having parents’ annual income above $60,000

“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.”

For those readers who do not have a heart condition, I recommend the spirited and colorful statistics debate in the open peer-review forum. 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.



ResearchBlogging.org






nooffensebut (2014). Parents’ Income is a Poor Predictor of SAT Score Open Differential Psychology, 1-19

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/

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.

Bartels M, Rietveld MJ, Van Baal GC, & Boomsma DI (2002). Heritability of educational achievement in 12-year-olds and the overlap with cognitive ability. Twin research : the official journal of the International Society for Twin Studies, 5 (6), 544-53 PMID: 12573186

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/.

Buchmann, C., Condron, D., & Roscigno, V. (2010). Shadow Education, American Style: Test Preparation, the SAT and College Enrollment Social Forces, 89 (2), 435-461 DOI: 10.1353/sof.2010.0105

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. Teachers College Record, 115 (4), 1-33

Duckworth AL, Quinn PD, Lynam DR, Loeber R, & Stouthamer-Loeber M (2011). Role of test motivation in intelligence testing. Proceedings of the National Academy of Sciences of the United States of America, 108 (19), 7716-20 PMID: 21518867

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 Science, 289 (5478), 457-460 DOI: 10.1126/science.289.5478.457

Everson, H.T., and Millsap, R.E. (2004). Beyond individual differences: Exploring school effects on SAT scores. (RR-2004-3). New York: College Board.

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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? Psychological bulletin, 135 (1), 1-22 PMID: 19210051

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. Psychological science, 23 (9), 1000-7 PMID: 22858524

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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. PloS one, 8 (12) PMID: 24349000

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