Showing posts with label anthropology. Show all posts
Showing posts with label anthropology. Show all posts

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

Friday, December 2, 2011

Blacks with Bullets Embedded in Bone






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.

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,

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.


Here is the figure:


He cites Eric Monkkonen’s Murder in New York City, which says,

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.


Pinker’s characterization of homicide data is another example of his distortions on matters pertaining to race and violence. See my previous post 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.


In fact, Roth further qualified the data for Philadelphia:


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.


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.

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.

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.

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.”

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.

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.

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, even in childhood,. (Recall that the media accused research oncologist Kathy Albain of “racial medical profiling” 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 National Health and Nutrition Examination Survey-III, 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.

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.

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.

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.

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.


Here is Jeffrey Adler’s homicide graph for Chicago when African Americans were a tiny minority of the population.


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.




ResearchBlogging.org






Adler, Jeffrey S. 2006. First in Violence, Deepest in Dirt: Homicide in Chicago, 1875-1920. Cambridge, Mass.: Harvard University Press.

De La Cova C (2010). Cultural patterns of trauma among 19th-century-born males in cadaver collections. American Anthropologist, 112 (4), 589-606 PMID: 21132946

Gurr, T. (1981). Historical Trends in Violent Crime: A Critical Review of the Evidence Crime and Justice, 3 DOI: 10.1086/449082

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? The Journal of clinical endocrinology and metabolism, 88 (2), 642-9 PMID: 12574194

Jimenez M, Dietrich T, Shih MC, Li Y, & Joshipura KJ (2009). Racial/ethnic variations in associations between socioeconomic factors and tooth loss. Community dentistry and oral epidemiology, 37 (3), 267-75 PMID: 19302573

Lane, Roger. 1979. Violent Death in the City: Suicide, Accident, and Murder in Nineteenth-Century Philadelphia. Cambridge, Mass.: Harvard University Press.

Monkkonen, Eric H. 2001. Murder in New York City. Berkeley: University of California Press.

Pinker, Steven. 2011. The Better Angels of Our Nature: Why Violence Has Declined. New York, New York: Viking Penguin.

Roth, Randolph. 2009. American Homicide. Cambridge, Mass.: Harvard University Press.