The Stupid Stupidity Surrounding the Warrior Gene, MAOA, is Stupid

Byrd AL, & Manuck SB (2013). MAOA, Childhood Maltreatment, and Antisocial Behavior: Meta-analysis of a Gene-Environment Interaction. Biological psychiatry PMID: 23786983

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.











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.

Kill Popular Science

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 speaking 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.

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.

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.

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.

[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.

Nice try. Pinker is referencing the Widom and Brzustowicz paper 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 mediated by the epigenetic methylation of MAOA as well as a newly discovered second promoter 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.

Pinker seems to have received his introduction to this subject through the New Zealand Maori controversy, 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. Weder et al 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 study on MAOA’s effect on gang membership and weapon use included African Americans. His 2010 study on African-American men and violence used a genetic index that included MAOA and four other genes that affect catecholamine levels.

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?

[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.

I previously debunked this, but I guess I must do so, again. A study by Lu et al found that 42 Taiwanese men, or 55% of their 77-subject control sample, had the 3-repeat allele of MAOA. Lea and Chambers copied the information incorrectly. Then, an editorial 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 4.7% 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 old generalization, as all four guilty parties were white boys. (Chinese people, when you buy my neighborhood, recall that I personally sent Pinker a corrigendum request.)


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 episode 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).









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

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. Biological psychiatry, 65 (5), 417-24 PMID: 18996506

Beaver KM, DeLisi M, Vaughn MG, & Barnes JC (2010). Monoamine oxidase A genotype is associated with gang membership and weapon use. Comprehensive psychiatry, 51 (2), 130-4 PMID: 20152292

Kevin Beaver, Ashley Sak, Jamie Vaske, & Jessica Nilsson (2010). Genetic risk, parent–child relations, and antisocial phenotypes in a sample of African-American males Psychiatry Research, 175 (1-2), 160-164

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. Progress in neuro-psychopharmacology & biological psychiatry, 26 (3), 457-61 PMID: 11999895

Lea R, & Chambers G (2007). Monoamine oxidase, addiction, and the "warrior" gene hypothesis. The New Zealand medical journal, 120 (1250) PMID: 17339897

Patrick-Michael Whittle (2009). Darwinism and the nature of Māori MAI Review

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

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. Biological psychology, 87 (3), 366-71 PMID: 21554924