Sunday, August 24, 2014

Correcting the Critics of Nicholas Wade & MAOA

Critics of Nicholas Wade’s latest book, A Troublesome Inheritance, have tried their best to pull discussion away from science and into the fluffy philosophy of racial semantics. They figure that if discussion never escapes the bog of racial constructivism, then no need exists for consideration of anything specific that would threaten or offend the modern paradigm. Wade deserves credit for effectively anticipating the critics’ points and blame for entertaining the critics’ points. However, Wade interrupted anthropological meanderings about the lack of perfect racial boundaries by introducing the subject of the warrior gene, monoamine oxidase A (MAOA). This is a specific gene with allele frequencies in a specific promoter sequence that differ tremendously by race.

Science reporter Fiona MacRae conveyed her alarm with the headline, “Author: Africans prone to violence.” The body of her article offered no attempt to dispatch with the inconvenient gene, but I have collected all such attempts to put on display right here.

An unremarkable dismissal presumably became a centerpiece due to its placement in the pages of Wade’s employer, The New York Times. Science writer David Dobbs provided glib assurance.
He tells, for instance, of specific gene variants that reputedly create less trust and more violence in African-Americans and, he says, explain their resistance to modern economic institutions and practices. Alas, the scientific literature he draws on is so uneven and disputed that many geneticists dismiss it outright.
One recurring motif of MAOA skeptics is stealing tactics from global-warming skeptics. After all, Dobbs is only a journalist. One must not expect him to conduct a thorough survey or even read a meta-analysis of 31 published studies on the gene. One should simply trust that the “many geneticists” he had in mind have some grasp of the evidence.

Many—143 to be exact—population geneticists published a five-sentence letter in The New York Times Book Review. The brief letter explicitly thanked Dobbs and falsely accused Wade of claiming that natural selection “led to worldwide differences in IQ test results.” Columbia University biologist Molly Przeworski was one of the five geneticists who authored the letter. She told a Canadian radio program, “We just don’t have any of the types of genetic variants that are associated with societal or social or behavioral changes that he’s speculating about.” So, not only do population geneticists object to Wade’s book and dismiss outright the scientific literature for MAOA, but they also categorically rule out having any knowledge of any behavioral genes. (I presume that she did not mean that no human has genes that influence behavior.) Ironically, Przeworski also wrote a study with two other signatories to the letter, Yoav Gilad and Karl Skorecki, that contributed to the outright dismissed MAOA scientific literature. Wade cited their study to suggest that natural selection had acted upon this gene. However, that is not a study of a behavioral phenotype. In fact, I did not recognize any names on the letter as having contributed to behavioral research on MAOA. Certainly none of the authors of the two studies on the MAOA-2R allele that Wade singled out (and pointed out was about fifty times more common in African-American men) signed the letter. Contrary to popular perceptions, geneticists are not the leading experts on behavioral genetics. I have been tabulating the academic backgrounds of authors of MAOA research studies. Out of 76 studies, 67 percent had psychiatrist authors. Only 43 percent of studies had a geneticist author. 20 percent had neuroscientist authors, and 18 percent had psychologist authors. One author, criminologist Kevin Beaver, writes on the subject of biosocial criminology. No one writes about “biosocial psychiatry” because the transition from Freudian psychotherapy to the management of psychotropic drugs has been nearly uniform. Psychiatrists understand that some behaviors reveal mental illnesses, and targeting the relevant neurotransmitters, as the MAOA enzyme does, can save lives. Indeed, criticism of MAOA research does extend to criticism of the relationship between neurotransmitters and behavior, which some scientists openly mock.

Another letter signatory, University of Pennsylvania geneticist Sarah Tishkoff, seemed to be working from the same script as Przeworski when she told science reporter Ewen Callaway, “We don’t have any strong candidates for playing a role in behaviour.” I wonder what standard of evidence Tishkoff awaits. Besides the aforementioned 31-study meta-analysis by Ficks and Waldman, a 27-study meta-analysis by Byrd and Manuck confirmed that MAOA has a powerful effect on antisocial behavior when coupled with childhood maltreatment. Both meta-analyses determined that the research did not show evidence of publication bias. This forest plot from the study just screams the words “uneven” and “disputed,” does it not?

University of North Carolina biologist Joseph Graves, Jr. signed the letter and reviewed Wade’s book, saying “Similar just-so-stories appear throughout the text including his discussion of the MAO-A gene and aggression.” A “just-so story” is supposed to be unverifiable and unfalsifiable. Research on MAOA has verified its effect on behavior. If the evidence had failed to show an effect on behavior, it would have falsified the hypothesized role of MAOA. MAOA research has many facets, such as the purported stronger effect of MAOA-2R on violence than MAOA-4R or even MAOA-3R. Some facets are supported by evidence but not adequately replicated in multiple samples. The unwillingness of scientists to further replicate the effect of MAOA-2R since its discovery in 2008 or the interaction effect of MAOA-3R with low IQ in no way makes those findings legitimately unfalsifiable. Labeling scientific claims as “just-so stories” is a convenient way to dismiss scientific evidence without offering alternative hypotheses or evidence and has been used to describe the theory of evolution and global warming.

Harvard geneticist Daniel MacArthur diligently covered all of his bases. He signed the letter and put out clear statements both for (“[T]he evidence for an association between the [MAOA] VNTR variant and antisocial behavior is substantially more consistent than most of these associations. This may well be one of the rare cases of genuine associations.”) and against (“By historical analogy, most if not all of this [MAOA] literature is wrong and will soon be forgotten.”) the conclusions of MAOA research. Speaking of history, I wonder how perceptions of a connection between genetics research and reactionary ideas would impact genetics research funding.

Though University of North Carolina anthropologist Jonathan Marks could not sign the geneticists’ letter, he did show them that flippant dismissal of MAOA science need not be so lacking in flowery finesse.
Rather, he takes an enormous leap and speculates retrogressively that groups of people may simply differ in genes that affect personality and behavior. In his earlier book Before the Dawn (2007), Wade opined freely about the possible existence of ping-pong genes among the Chinese. Now he speculates about genetic propensities for violence among Africans, obedience in Chinese and capitalism in Jews. Mercifully, he stops short of inventing genes for basketball, laundry and stand-up comedy.
I am sure that he meant no implied insult of Chinese people’s ping-pong skills. Unlike ping-pong, violence is universal not only to humans but also to the entire animal kingdom and portions of the plant kingdom. Though none of these people mentioned it, scientists discovered Brunner syndrome, which is marked by aggressive behavior apparently resulting from a completely nonfunctional MAOA gene, over twenty years ago. This lack of a functional MAOA gene also is present in some unusually aggressive mice. Scientists who attempted to interact with these MAOA-knockout mice found themselves in a real-life reenactment of Tom and Jerry.

Science writer Meredith Knight similarly described the twenty years of replicating the influence of MAOA on aggressiveness as a new, fragile overreach.
The scientific community largely agrees that Wade oversteps when making any claims about race, genetics and behavior, largely because evidence linking genetics and human behavior is so new and somewhat fragile. Even linking genes to major mental health disorders, like schizophrenia, is contentious. Relating genes to a more qualitative characteristic, like aggressiveness or social obedience seems rather an overreach.
Lest one think only liberal academics and reporters volunteer such brief, zero-substance slights of MAOA science, Charles Murray claimed MAOA was a case in point of “tentative and often disputed” findings. Like the others, Murray’s brevity probably resulted from a lack of expertise that unfortunately did not accompany a more modest assertion. During Murray’s first public mention of Wade’s book (at the 45-minute mark), Harvard Professor of National Security and Military Affairs Stephen Peter Rosen brought up MAOA to Murray, confusing its gene-environment interaction with “epigenetics.” The environmental variable is measured in the environment, but that does not mean its mechanism of effect is nurture or epigenetics (which can also be influenced by genetics) rather than genetics.

Reporter Robert VerBruggen questioned whether Wade’s treatment of MAOA and other research relating to race was “suitable for a book aimed at the general public.” Apparently attacking MAOA science is suitable for the popular press, so why would defending it not be? I do not think most violent racists think about MAOA allele frequencies. Just as climate-change science belongs in many public policy discussions, well-reasoned and respectful discussion of MAOA can appropriately inform some social-justice debates and courtroom deliberations.

As Willamette University biologist Christopher Irwin Smith and author Alondra Oubré demonstrated, brief dismissals of MAOA research can make sense for a deluded scientist or writer because writing a lengthier composition will fill the Internet with more falsehoods and risk overspill. University of Maryland sociologist Philip Cohen wrote a somewhat lengthy critique, and it contains a number of mistakes, but perhaps these were honest mistakes.
Wade devotes considerable attention to MAO-A, the gene that encodes the enzyme monoamine oxidase A, which is related to aggression. He singles out studies showing that a rare version of the gene is associated with violence in U.S. male adolescents. Out of 1,200 young men surveyed in the National Longitudinal Study of Adolescent Health, eleven particularly violent young men carried the 2R version of MAO-A, subsequently known as the “warrior gene.” Nine of those eleven were African American, comprising 5 percent of the black male adolescents in the study…. Now Wade is off and running. He has a gene variant that is more common (though still rare) among black men and is associated with elevated rates of violence.
First, these basic facts need clarification. The National Longitudinal Study of Adolescent Health deliberately oversampled African Americans with college-educated parents. Mixed racial ancestry is common among African Americans, so allele frequencies that are higher among African Americans than whites are probably even higher still among West Africans. The National Longitudinal Study of Adolescent Health contained nine African-American men with MAOA-2R based on interviewer-assessed race and ten based on self-reported race, constituting 5.2 percent or 5.5 percent of the African-American men, respectively. The term “warrior gene” dates back to a 2004 Science article by Ann Gibbons and explicitly refers to MAOA-3R, the most common allele of this VNTR promoter as providing a predisposition to violence, compared to MAOA-4R, which is the allele most common in white people. So, the relationship between MAOA and violence is already well-established in a large collection of research for a version that is not rare in any group.
This may be true. But it certainly overstates the strength of the case. Consider that, in the Adolescent Health data, black male adolescents were more than twice as likely as whites to report having committed an act of violence. If you found any gene that happened to be correlated with violence, chances are good it would also be correlated with race. Confirmation with more powerful genetic testing methods may strengthen this case in the future, but Wade’s inflated interpretation is not justified by the existing evidence.
This suggests that Cohen did not understand an extremely important fact about Beaver et al. That study compared African-American men with MAOA-2R to African-American men without MAOA-2R. Sociological inequities for African Americans could not confound a study that only included African Americans. The amount of African ancestry could confound, but that could result from genetic associations rather than class associations, since the percentage of African ancestry and class are probably not perfectly correlated.
Sometimes in genetics there is some gene or coding that produces some measureable effect, and that’s how most people seem to think about genetics most of the time – there is “a gene for” something. In the days before today’s genome-wide association (GWA) studies, before scientists had the means to investigate hundreds of thousands of genetic markers at a time, they often looked for effects of such “candidate” genes. This approach was valuable, especially when the role of specific genes was known (as in the case of the BRCA1 gene, associated with higher risk of breast cancer). However, with most diseases, and even more so with behavior, which is presumed to be more complicated than single-gene mechanisms, candidate gene studies were (are) often fishing expeditions, with a high risk of false-positive results, amplified by selective publication of positive findings. It is quite possible that’s at least part of what happened with MAO-A and aggression.
Genome-wide association studies on the genetics of violence and related mental illnesses have only used single-nucleotide polymorphism arrays, so far. Scientists can only study repeat polymorphisms like this promoter for MAOA with candidate-gene studies until whole-genome research technology becomes more advanced and widely available. However, the discovery of Brunner syndrome does not deserve to be called a “fishing expedition.” The rare missense mutation is virtually deterministic in its influence on behavior. Diseases like Norrie disease take out both MAOA and MAOB function and result in a severe set of morbidities. The standard GWAS attack on candidate-gene research that you are repeating is flawed even for single-nucleotide polymorphisms but certainly lacks relevance for MAOA research. Meta-analyses for MAOA replicated the original findings, and the Byrd and Manuck meta-analysis found the effect was “no less likely to replicate in studies with sample sizes larger (or smaller)” than the original finding “or in studies published later.”
Most studies about MAOA have been gene-environment interaction studies, where some version of MAOA has a statistical association with a behavior only in the presence of a particular social factor, such as a history of child abuse.
No, they have not. Studies on the “main effect” of MAOA (the effect of MAOA on antisocial behavior without an interacting variable) began years earlier than the gene-environment interaction studies. The Ficks and Waldman meta-analysis of the main effect included 31 studies. The Byrd and Manuck meta-analysis of the gene-environment interaction only included 20 studies for the analysis of men.
First, that 2R version of MAO-A is very rare, and the two studies Wade cites about it … both used the same sample from Add Health – 11 boys with the variant. Two studies doesn’t mean two independent results. You could never get a drug approved based on that (I hope). Second, as far as I can tell there was no strong reason a priori to suspect that this 2R variant would be especially associated with violence. So that’s a caution. I have to say, as I did in the review, that it may be correct. But the evidence is not there (and you shouldn’t say “not there yet,” either). Those two studies are the entire evidentiary basis for Wade saying that genes that shape social behavior vary by race (“one behavioral gene … known to vary between races”.) I didn’t find any other studies that show MAO-A 2R varies by race (though maybe there are some).
No, research established the effect of MAOA in alleles that are not rare. When the Food and Drug Administration approves a drug, doctors receive wide leeway to prescribe it off-label and at dosages they deem appropriate. So, why should MAOA-2R not constitute a higher dosage of “warrior gene”? The strong a priori reason to suspect that MAOA-2R is especially associated with violence is that the study by Guo et al that Cohen reviewed also included an in vitro analysis of gene expression, which showed much lower expression for MAOA-2R. Brunner syndrome shows the effect of having an MAOA gene with zero gene expression. There are two additional studies on MAOA-2R and aggression in the Add Health sample. (I also would like to see more research on this in other samples.) However, the list of studies that establish differing allele frequencies for MAOA-2R, MAOA-3R, and MAOA-4R by race is long, and I have been attempting to tabulate them in a convenient table.

In fairness, even Wade’s treatment of MAOA research was good but not perfect. He repeatedly referred to MAOA-2R as “two promoters.” It is actually two repeats of a DNA sequence within a single promoter. The distinction is important because MAOA actually does have multiple other promoters, including one other found to affect antisocial behavior in women more than this one, and this relates to Wade’s attempt to downplay the importance of MAOA.
Second, a large number of genes are evidently involved in controlling aggression, so even if African Americans are more likely to carry the violence-linked allele of MAO-A promoters than are Caucasians, Caucasians may carry the aggressive allele of other genes yet to be identified. Indeed a variant of a gene called HTR2B, an allele that predisposes carriers to impulsive and violent crimes when under the influence of alcohol, has been found in Finns. It is therefore impossible, by looking at single genes, to say on genetic grounds that one race is genetically more prone to violence than any other.
Determining the relative importance of MAOA compared to all other violence genes poses a significant challenge, but scientists have not even determined the importance of MAOA to overall aggression heritability, yet. Perhaps the controversy surrounding MAOA research or Wade’s book could convince the National Institutes of Health to fund a very large, international study to attempt to replicate and fully quantify the effects of every MAOA allele for every single-nucleotide polymorphism and promoter, every gene-environment interaction, every gene-drug interaction, every gene-hormone interaction, every gene-gene interaction, and every epigenetic effect together in the same study. Clues do exist that this single gene deserves all of the attention that I have been giving it. The fact that MAOA research has discovered so many of these interaction effects could be evidence of the gene’s high importance. The other 2008 Guo et al study of MAOA-2R that Cohen did not review determined that the allele affected violent behavior more than two other candidate genes known for their effect on the neurotransmitter dopamine and that it had a large gene-environment interaction effect, as well. Brunner syndrome, itself, provides another clue. If MAOA is unimportant compared to unidentified functional alleles of other genes, why have scientists not discovered those through rare knockout polymorphisms?

Wade is pointing out such a knockout polymorphism syndrome for HTR2B. Like Brunner syndrome, only a small number of known cases exist, and that study claimed it was “apparently exclusive to Finns,” 1.2 percent of whom have it. Seven cases of the HTR2B knockout allele did not induce violent behavior, whereas Brunner syndrome research uncovered only four cases of MAOA knockout allele without accompanying antisocial behavior in men. HTR2B is on chromosome 2, and MAOA is on the X chromosome. So, men with an MAOA knockout allele have no MAOA enzyme. Men with the HTR2B knockout allele still have some HTR2B function except the one homozygote, and 1.2 percent is not the true allele frequency; 0.68 percent is. The hemizygosity of X-chromosome genes could increase their importance for behavior and help explain why men tend to commit more violent crime than women. Alcohol use precipitated 94 percent of violent crimes among these men with the HTR2B knockout allele. Follow-up research looked for personality effects of other alleles of the gene and came to contradicting conclusions.

Whatever evidentiary gaps exist should be taken to signify the need for more research, not an excuse for ignorant dismissals of the decades of existing research. I have good reason to interpret many of the listed errors and misjudgments as dishonest, politically motivated opposition to science. Oubré tried to pass off her work as a serious “reality check” for MAOA research. Her essay was full of careless errors, including completely wrong numbers taken from Wikipedia vandalism and attributed to the National Longitudinal Study of Adolescent Health. When I corrected the errors, her reply was complete denial (“I did not use Wikipedia for this article. Cheers.”), followed by admission with hysterical defensiveness against my unrealistic demand for correctness (“You imply that I should have a wider grasp of the literature on the MAOA gene, as though I am obligated to make this my raison d’etre…. Am I entitled to even have a life?”). When I suggested that the essay was a criticism of Wade’s book because she cited his book in a critical way, she responded that she had not even read it. Her editor’s response to me was initial denial, continued refusal to make a correction, and the statement, “I see not taking others seriously is your modus operandi.” Well, it is not simply a matter of an inability to take Alondra Oubré seriously. I am actually wondering whether anyone should take seriously anthropologists, sociologists, biologists, or population geneticists.

Beaver KM, Barnes JC, & Boutwell BB (2013). The 2-Repeat Allele of the MAOA Gene Confers an Increased Risk for Shooting and Stabbing Behaviors. The Psychiatric quarterly PMID: 24326626

Beaver, K., Wright, J., Boutwell, B., Barnes, J., DeLisi, M., & Vaughn, M. (2013). Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior Personality and Individual Differences, 54 (2), 164-168 DOI: 10.1016/j.paid.2012.08.014

Bevilacqua L, Doly S, Kaprio J, Yuan Q, Tikkanen R, Paunio T, Zhou Z, Wedenoja J, Maroteaux L, Diaz S, Belmer A, Hodgkinson CA, Dell'osso L, Suvisaari J, Coccaro E, Rose RJ, Peltonen L, Virkkunen M, & Goldman D (2010). A population-specific HTR2B stop codon predisposes to severe impulsivity. Nature, 468 (7327), 1061-6 PMID: 21179162

Brunner HG, Nelen MR, van Zandvoort P, Abeling NG, van Gennip AH, Wolters EC, Kuiper MA, Ropers HH, & van Oost BA (1993). X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. American journal of human genetics, 52 (6), 1032-9 PMID: 8503438

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

Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Müller U, Aguet M, Babinet C, & Shih JC (1995). Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Science (New York, N.Y.), 268 (5218), 1763-6 PMID: 7792602

Donnai D, Mountford RC, & Read AP (1988). Norrie disease resulting from a gene deletion: clinical features and DNA studies. Journal of medical genetics, 25 (2), 73-8 PMID: 3162283

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

Gibbons, A. (2004). AMERICAN ASSOCIATION OF PHYSICAL ANTHROPOLOGISTS MEETING: Tracking the Evolutionary History of a "Warrior" Gene Science, 304 (5672), 818-818 DOI: 10.1126/science.304.5672.818a

Guo, G., Roettger, M., & Cai, T. (2008). The Integration of Genetic Propensities into Social-Control Models of Delinquency and Violence among Male Youths American Sociological Review, 73 (4), 543-568 DOI: 10.1177/000312240807300402

Guo, G., Ou, X., Roettger, M., & Shih, J. (2008). The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity European Journal of Human Genetics, 16 (5), 626-634 DOI: 10.1038/sj.ejhg.5201999

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

Tsuchimine S, Taniguchi T, Sugawara N, Kaneda A, & Yasui-Furukori N (2013). No Association between a polymorphism in the serotonin receptor 2B (HTR2B) gene and personality traits in healthy Japanese subjects. Neuropsychobiology, 68 (1), 59-62 PMID: 23774082

Tuinier S, Verhoeven WMA, Scherders MJWT, Fekkes D, & Pepplinkhuizen L (1995). Neuropsychiatric and biological characteristics of X-linked MAO-A deficiency syndrome. A single case intervention study. New Trends in Experimental and Clinical Psychiatry, 95, 99-107

Zhu B, Chen C, Moyzis R, Dong Q, Chen C, He Q, Li J, Lei X, & Lin C (2012). Association between the HTR2B gene and the personality trait of fun seeking Personality and Individual Differences, 53 (8), 1029-1033 DOI: 10.1016/j.paid.2012.07.026

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,, 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 Is she Oubré? Is he Pigliucci? Who knows? Maybe he is Eric Holder. Nobody who knows is saying.

Massimo Pigliucci

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.

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