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.

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


HBDAnon said...

Massimo is an utterly dishonest fool. Further down the comments one of his not so intelligent commenters "SocraticGadfly" leaves this obvious trolling comment ( where he disproves science by pointing out the authors are "racialists" and then slanders the background of John Paul Wright with a newspaper column.

If he or Massimo had half a brain they would have realized right away how implausible it is that someone making comments of that sort could become a professor in PC academia. A quick google search would reveal that the John Paul Wright in question has never attended George Mason (

Of course multiple people can have the same name. Who would've thought!

So for Massimo publishing worthless trolling and slander is ok but a comment pointing out the dishonestly is disapproved of. Meanwhile Massimo leaves SocraticGadfly's comment up uncorrected. Complete charlatan.

nooffensebut said...

For reference, here is the full original text.

The Extreme Warrior gene: a reality check

on July 31, 2014

by Alondra Oubré

MAOA — Genetic culprit for violence?

Theories about inborn race-based aggression, violence, and criminality are back in the news [1]. In the ongoing search for genes underlying social behavior, none has sparked more curiosity, if not controversy, than the gene that codes for monoamine oxidase A — MAOA [2, 3, 4]. Nicknamed the “warrior gene,” a variant of the MAOA drew international attention nearly a decade ago when geneticist Rod Lea reported that it was more common in Maori — the indigenous Polynesians of New Zealand — than in whites [2]. According to one journalist, Lea suggested this gene might be the source of poor health and increased rates of violent crime in Maori [5]. The media frenzy over “bad genes causing bad behavior” didn’t stop there. A rare, seemingly even more detrimental version — the “extreme warrior gene” — has since stirred debate because it occurs more frequently in African Americans than in whites [6, 7].

MAOA — an enzyme that degrades neurotransmitters such as serotonin and dopamine in the brain — is coded for by the MAOA gene [8, 9, 10]. Neurotransmitters play a pivotal role in mood, arousal, and emotions, even affecting impulse control. Since the 1990s scientists have identified several versions of the MAOA, which are usually categorized as low-activity or high-activity variants. MAOA genes are classified based on how many times a short sequence — a functional strip of DNA — repeats itself within a variable region of the gene [8]. The most common variant, MAOA-4R, has four repeats and is associated with high-activity breakdown of neurotransmitters [8]. Alternate forms of the MAOA, including the 2-repeat (2R) and 3-repeat (3R) versions, contain fewer repeat sequences.

The 2R and 3R variants are often lumped together in studies of the low-activity MAOA gene. (Although the 5R version has a large number of repeats, it too is less active than the 4R version.) The two classes of MAOA versions correlate with different behavioral tendencies. Low-activity variants are thought to lead to reduced levels of MAOA in the brain, possibly shifting mood by changing serotonin levels [8].

Over the past 12 years research on MAOA genes has examined how low-activity gene variants interact with environmental factors to influence violence and other antisocial behaviors [11]. In 2002, Avshalom Caspi, then at King’s College in London, and his colleagues published their landmark study [12]. Caspi’s team reported that adults with the low-expression MAOA who were mistreated as children were more prone to developing antisocial problems later in life. But maltreated children with the high-activity variant were less likely to engage in delinquent or criminal activities. It seems low-activity MAOA variants make people more responsive to abuse [12]. 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. Historically, warfare was a central part of traditional Maori culture because, after all, these South Pacific islanders had to compete vigorously for limited natural resources. Today, some Maori are integrated into New Zealand society. Yet, overall they still lag behind other ethnic groups in their country in income, education, and health, and crime rates are higher. For many experts, this ethnic gap is the result of numerous environmental causes, including poverty [13]. In 2006, Lea reported that MAOA-3R — one of the low-activity risky variants — was more common in Maori males than in white males [2]. According to Lea, the 3R version was associated with a lineup of undesirable personality traits: risk-taking, violence, aggression, gambling, addiction and criminal behavior. Suddenly, it seemed genetics could possibly explain the Maori/white ethnic divide in achievement and social outcomes [2].

nooffensebut said...

(Continued – 2 of 8)
MAOA-3R — the “original warrior gene” — was the first gene linked with antisocial characteristics. But Maori were not the only ethnic group with a high frequency of this variant. 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 [2]. Misinterpreted by the media, the 3R variant quickly became a lead character in a pop science narrative intended to explain why certain racial groups appear to have increased tendencies toward violence. When a disproportionately high number of males of an ethnic group carries a less common gene linked with aggressive behaviors, the discussion about that gene immediately takes on racial overtones [3, 14]. (Interestingly, the press ignored studies indicating that the 3R variant occurred in 61% of Taiwanese males [15] and 56% of Chinese males [16]).

Research on the MAOA gene

Over the last few years, multiple studies have replicated the original findings of Caspi’s team. The evidence as a whole continues to show that the interaction between low-activity MAOA variants and early exposure to abuse increases the risk for antisocial behavior in men throughout their lifetime [11, 17]. Offending, conduct problems, and hostility have been observed in males carrying low-expression versions of the MAOA gene [6, 7, 18].

Kevin Beaver of Florida State University is a researcher in biosocial criminology — a field that explores the role of both genes and environment in criminal and other antisocial behaviors. One of Beaver’s studies has linked low-activity MAOA variants with increased likelihood of males joining a gang and using a weapon in a fight [18]. Most of the early investigations comparing low- and high-expression MAOA genes probed only the moderately risky 3R version. A few looked at a combination of 3R and 2R. However, the effects of these two variants on social behaviors were not teased apart in most of the initial studies [6, 7, 8].

In 2008, University of North Carolina sociologist Guang Guo and his colleagues found that antisocial behaviors in male youth were associated with three genes — low-activity MAOA variants and two dopamine-related genes [19]. But it was 2R — the “extreme warrior gene” — that captivated researchers searching for a still illusive genetic basis of criminal predispositions. Guo’s team analyzed data on male youth from Add Health — a national sample of adolescents in grades 7-12. Their findings showed that the rare variant, 2R, was correlated with higher levels of self-reported serious and violent delinquency. The association was also observed in females, but it was too weak to merit further study [19].

More recently, Beaver’s team has focused only on the 2R variant rather than the low-expression variants combined [6, 7]. He and his colleagues have discovered that African American males carrying 2R were more likely to be involved in extreme violence — shooting and stabbing — than African American men with other MAOA variants [6]. The relationship between the rare MAOA version and antisocial behaviors has raised eyebrows because, quite simply, this gene is not distributed equally across ethnic groups. In the Add Health database, 5.5% of African American men, 0.9% of Caucasian men, and 0.00067% of Asian men have 2R. (No information is currently available on the frequency of 2R in males of African black descent outside the United States.) Since the rare MAOA variant is virtually non-existent in whites, all of the males in Beaver’s study were black Americans [6].

nooffensebut said...

(Continued – 3 of 8)

Beaver’s sample of 133 African American men from the Add Health database included 6% that carried 2R. Overall, 5.6% of the men in the sample reported shooting or stabbing someone at some point in their lifetime. The association between 2R and committing a shooting or stabbing crime was statistically significant. Based on Beaver’s evidence, 2R appears to increase the risk of shooting or stabbing a victim during adolescence or adulthood [6]. For some commentators in the public arena, MAOA-2R has become a symbol of a new era in behavioral genetics research — an era that has reintroduced race into the nature versus nurture debate over the source of ethnic behavioral differences [1].

In a recent interview I asked Kevin Beaver if he had found any correlation between males in his study who carried 2R and socioeconomic status — SES. After all, a sample of African American young men is likely to disproportionately come from lower SES backgrounds. Beaver noted that the Add Health survey had deliberately over-sampled African Americans from the middle and upper middle classes to compensate for this imbalance. “No one knows how the over-sampling — the relatively larger number of middle to upper income participants — translates into the frequencies of MAOA-2R in the sample,” Beaver said. “The small number of 2R subjects, however, makes it difficult to examine the link between SES and the 2R variant” [20].

Beaver’s studies have shown that the 2R variant has a robust association with violent behaviors, arrest, and incarceration [6, 7]. His research is applauded by supporters of behavioral genetics, but it has also drawn criticism. It focuses on an antisocial-linked gene that reportedly occurs more frequently in African American men than in males of other ethnic groups. 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].

Part of the skepticism surrounding Beaver’s studies may lie in popular misinterpretations of his research. As Beaver explains, “It is probably correct to assume that social behaviors are due to gene-environment interaction. But statistical models are quantifying variance — that is, they are looking at differences between persons. Why an individual turns out a certain way might be due to gene-environment interaction. But person-to-person differences do not always result from gene-environment interaction. The reason that people vary in criminal propensities could be due to only genetics, only environments, or either of these free from gene-environment interaction.”

Beaver’s findings may shed light on whether a single gene might underlie individual differences in criminal tendencies. So far, his investigations have targeted only African American males because too few whites carry the rare MAOA variant to include them. 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 [6]. Beaver claims that 2R alone may be strong enough to account for a significant amount of violent behavior in African American men. But he doesn’t think this rare gene version explains all of the variation between men who have and don’t have severe antisocial traits. As he puts it, “Even if MAOA-2R is causally linked with antisocial behaviors, it is not common enough in African Americans to solely account for crime rates in blacks” [20].

nooffensebut said...

(Continued 4 of 8)

Like many other genetic studies in criminology, Beaver’s research on MAOA-2R explores the heritability of specific antisocial behaviors — in this case, shooting and stabbing. Heritability — not to be confused with heredity — refers to the proportion of variance in a trait within a population due to genetic variation [22]. A heritability estimate does not pertain to the amount of genetic influence on a particular trait in a particular person. Each estimate is valid only for a single population at a specific point in time. Heritability estimates can change, depending upon the strength or weakness of environmental factors, which along with various genes, shape social behaviors [22].

Although genes affect individual differences in behavior, the effect of each individual gene is usually small. The genetic underpinnings of a specific social behavior typically involve multiple genes that have a cumulative influence [8]. It is not clear if MAOA-2R is an exception. The more common low-activity variant, 3R, interacts with adverse social effects such as childhood maltreatment [11, 12]. But other possible environmental factors, which conceivably could interact with the 2R, may not have been explored in-depth as yet. One such environmental influence that has recently received attention is parents and caregivers’ punitive discipline — spanking and yelling — of a young child [23]. Punitive practices are not necessarily abuse. But in families that traditionally use harsh discipline with their children, corporeal punishment or even loud verbal chastising can at times turn into maltreatment.

Daniel Choe, a developmental psychologist, and his colleagues at the University of Pittsburgh investigated the effects of punitive discipline on antisocial behavior in young white and African American men [23]. The researchers examined 189 young, low-income white and African American males with both low- and high-expression MAOA genes. As the researchers predicted, punitive discipline was associated with increased antisocial behavior only in men with the low-activity 3R variant. This pattern held for both white and black males. There was no relationship between harsh punishment and antisocial behavior in men carrying 4R, the high-activity version of MAOA [23].

Importantly, the effects on behavior depended on the age at which the children were punished [23]. Kids who had been disciplined at 1.5, 2, and 5 years were more likely to develop antisocial behaviors when they were older — between 15 and 20 years old. Specific antisocial behaviors, including violent attitudes and juvenile arrests, were more likely to occur at a specific age and to be linked with the age when the boys were abused [23].

Choe’s study is the first to demonstrate that ethnic minority children— African Americans, not just Caucasians — with a low-expression MAOA gene variant who face harsh discipline have an increased risk for antisocial behavior [23]. Choe’s team published the effects of just the 3R variant, excluding five African American participants in their study carrying the 2R version. Curious about possibly different effects of 2R, they then reanalyzed the data to include the five black males with 2R. The findings remained the same. Combining the boys with 2R — the highest risk variant — and those with the less severe risky 3R did not change the differences the researchers found between the 3R and 4R variants. The five males with 2R comprised a very small sample, but the fact that both low-activity MAOA variants, 2R and 3R, interacted with an environmental factor — punitive discipline — at specific ages, or developmental milestones, is noteworthy. It suggests the effects of MAOA-2R on antisocial behaviors are partly mediated by non-genetic factors [24].

nooffensebut said...

(Continued – 5 of 8)

Choe stresses that genetic influences on social behaviors such as juvenile delinquency cannot be fully understood outside the context of social circumstances. He is referring not only to parenting styles, but also to the in utero environment of the unborn fetus. As he explains, compared to the white youth in his study, the African Americans were more likely to grow up in poorer, urban, dangerous neighborhoods. A high percentage of these youth are being raised by single mothers, and they grow up without the attention found in most middle-class homes. Choe acknowledges the role of genes in behavior, but he clearly thinks that environmental factors contribute substantially to ethnic differences in antisocial behaviors. As he points out, the white kids in the sample were also poor, but they lived in low-income suburban communities, not in densely concentrated inner cities. The suburbs pose less of a risk than urban communities for group delinquent behavior [24].

Most experts agree that social behaviors stem from complex interactions between genes and environment [11]. Does MAOA-R2 go against the grain? Is it unaffected or only minimally affected by social experience and other elements of the environment? According to Beaver, MAOA-2R might act independently of environmental influence, but its effects might be masked by MAOA-3R. If the 2R version raises the risk of criminal behavior regardless of environmental influence, then perhaps it is indeed the source of a strong genetic propensity toward violence. If so, then violent tendencies associated with 2R — the “extreme warrior gene” — are not likely to be easily curtailed.

Yet many scientists think that behavioral traits are determined not only by the interplay between genes and environment. Antisocial behaviors also may be molded by the interaction of multiple genes — not simply a single gene [10, 19, 25]. When asked if he plans to examine the effects of 2R combined with genes other than MAOA, Beaver said he does not. As he explains, “the frequency of the 2R variant is too low to analyze. In the future we’ll need extremely large samples to have enough males with 2R to study.”

Epigenetics and MAOA in the brain

Epigenetics is revolutionizing how scientists think about genetics. Epigenetics refers to external changes to DNA that turn genes “on” or “off” without altering the DNA sequence [26]. Gene expression — the manifestation of genetic potential — is modified in epigenetic processes, even though the gene itself stays intact. The field of epigenetics is largely theoretical, at least insofar as humans are concerned. But growing evidence suggests that epigenetic changes can, in some cases, be passed on from parents to children. They are handed down not as inherited traits, but as non-hereditary modifications transmitted to offspring along with genes from their parents [26].

Various environmental factors are thought to influence epigenetic processes. Could epigenetics modify behavioral traits by acting on MAOA gene activity? Scientists are just beginning to understand the effects of MAOA variants on the brain. The low-expression MAOA-3R variant has been linked with a heightened response from the amygdala, a structure in the brain that regulates emotion [27]. 3R is also associated with decreased activity in prefrontal regions of the brain that protect against anxiety [27].

Elena Shumay of the Brookhaven National Laboratory and her team conducted a study to determine how MAOA variants affect brain levels of the MAOA enzyme in healthy men [28]. Using PET imaging scans, these researchers found no correlation between MAOA brain levels and MAOA gene variants. Shumay and her colleagues reasoned that MAOA levels must be regulated by the same region of the MAOA gene where the 2R, 3R, 4R, or other repeat sequence are located. The evidence supported their prediction: it appears that MAOA expression associated with MAOA brain levels is under the control of epigenetic mechanisms [28].

nooffensebut said...

(Continued – 6 of 8)

In other words, epigenetics may influence whether a tendency toward higher or lower MAOA genetic activity actually manifests itself. The amount of genetic activity, in turn, determines whether there is a larger or smaller quantity of the MAOA enzyme in the brain, which is needed to break down certain neurotransmitters [28]. The findings of Shumay’s team are preliminary, however. Their data do not prove that antisocial behaviors are not influenced by the low-activity 2R and 3R variants of the MAOA [8]. Nonetheless, their results suggest that MAOA brain levels, which affect mood, are at least partially regulated by non-genetic factors — i.e., epigenetically.

Genes, environment and plasticity

There are limits to studying the role of a single gene in antisocial behavior outside of its environmental context. Even when a gene correlates closely with violence or criminal acts, it does not mean that the gene itself codes for aggressive tendencies. According to Kevin Beaver and University of California at Davis’ Jay Belsky, plasticity genes seem to affect how much or how little male youth are influenced by their parents. Beaver and Belsky claim these genes appear to increase susceptibility to environmental effects, “for better and for worse” [29]. Supportive and unsupportive parents are more likely to have a positive or negative impact, respectively, on their children if their kids carry plasticity genes [29].

Yet plasticity genes appear to have a cumulative effect. Determining the influence of each separate gene on a behavior can be difficult. The combined genetic effects may vary, depending upon the individual. For a gene to have a plasticity effect on a behavior, it has to interact with an environmental factor [29, 30]. Are we then back to the notion that gene-environment interactions ultimately determine social behaviors?

MAOA is one of several candidate genes for plasticity that appear to mediate a person’s susceptibility to his or her environment [8]. Complex interactions between genes — and between genes and environmental factors — may explain why males with multiple plasticity genes are at heightened risk for developing aggressive behaviors if, at a young age, they have traumatic experiences with their caregivers. MAOA variants are not necessarily directly associated with brain changes that could lead to violence. But two or three plasticity genes working in tandem might increase a young male’s risk of sensitivity to early terrifying encounters with parental figures [29]. As Choe’s findings demonstrate, the timing of stressful life events may influence whether or not a genetic proclivity for antisocial behavior manifests itself [23].

MAOA research — The future

In matters as sensitive as race, genes, and behaviors — especially antisocial behaviors reported in African American males — the conventional wisdom is to balance the search for behavior-linked genes with a probe of environmental influences. Many experts doubt that violent behaviors are conditioned exclusively by genetics without any influence from social circumstances [11, 31]. Unless scientists have ruled out all the subtle and nuanced (or even plainly obvious) adverse social and ecological factors that can affect gene expression, they might miss profound interactions between MAOA-2R and the environment. As Choe and his colleagues point out, “multiple genes of small effects are likely to interact with multiple environments to lead to many outcomes” [23].

nooffensebut said...

(Continued – 7 of 8)

The recent work of both Kevin Beaver and Daniel Choe highlights just how complicated research on behavior-linked genes — particularly MAOA-2R — can be. The findings of a study may depend partly on whether scientists are looking for genetic effects, environmental effects, various combinations of gene-environment interactions, or genetic variance (heritability) between individuals — not to mention epigenetic complications. If researchers are focusing only on a genetic influence on adversity, they might miss environmental contributions. Conversely, by honing in on a single gene, investigators might discover a genetic trait that helps to differentiate males who do and don’t develop antisocial behaviors. With improved understanding of how violence-linked genes are expressed, it may someday be feasible to develop safe, noninvasive, and ethical psychosocial interventions to reduce offending and potential crime in males carrying high-risk genes linked with antisocial proclivities.

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. While experts continue to unravel complex interactions between genes, epigenetics, and environment, it may be best for scientists and society alike to take a prudent position on this issue. We forsake our scientific heritage if, at this point in time, we leap to conclusions about what MAOA-2R means — or doesn’t mean — for antisocial tendencies in males of any ethnic or racial group.


My thanks to Kevin Beaver and Daniel Choe for their input while writing this article.

Alondra Oubré is a science and medical writer who works primarily for the medical device, pharmaceutical and biotechnology industries. She holds a doctorate in medical anthropology, and is the author of various publications on human biodiversity, the ethnic achievement divide, health disparities, and plant drug research. She has published a two-volume collection entitled Race, Genes and Ability: Rethinking Ethnic Differences.

[1] Wade N. A Troublesome Inheritance: Genes, Race and Human History. New York: Penguin Press. 2014.

[2] Lea R, Chambers G. Monoamine oxidase, addiction, and the “warrior” gene hypothesis. N Z Med J. 2007. 120 (1250) PMID: 17339897.

[3] Merriman T, Cameron V. Risk-taking: behind the warrior gene story. N Z Med J. 2007 Mar 2;120(1250):U2440.

[4] Perbal L. The ‘warrior gene’ and the Mãori people: the responsibility of the geneticists. Bioethics. 2013 Sep;27(7):382-7. doi:10.1111/j.1467-8519.2012.01970.x.

[5] Stokes J. Scientist defends ‘warrior’ gene. The New Zealand Herald. Mar 5, 2007.

[6] Beaver K, Barnes J, Boutwell B. The 2-repeat allele of the MAOA gene confers an increased risk for shooting and stabbing behaviors. Psychiatr Q. 2013a. Dec 11.

[7] Beaver K, Wright, J, Boutwell B, Barnes J, DeLisi M, Vaughn M. 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. 2013b. 54(2):164-168.

[8] Buckholtz JW, Meyer-Lindenberg A. MAOA and the neurogenetic architecture of human aggression. Trends Neurosci. 2008 Mar;31(3):120-9. doi: 10.1016/j.tins.2007.12.006.

[9] Dorfman H, Meyer-Lindenberg A, Buckholtz JW. Neurobiological mechanisms for impulsive-aggression: The role of MAOA. Curr Top Behav Neurosci. 2014 Jan 28.

[10] Pavlov KA, Chistiakov DA, Chekhonin VP. Genetic determinants of aggression and impulsivity in humans. J Appl Genet. 2012 Feb;53(1):61-82. doi:10.1007/s13353-011-0069-6.

[11] Byrd AL, Manuck SB. MAOA, childhood maltreatment, and antisocial behavior: meta-analysis of a gene-environment interaction. Biol Psychiatry. 2014 Jan 1;75(1):9-17. doi:10.1016/j.biopsych.2013.05.004.

[12] Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, Taylor A, Poulton R. Role of genotype in the cycle of violence in maltreated children. Science. 2002. Aug 2;297(5582):851-4.

nooffensebut said...

(Continued – 8 of 8)

[13] O’Sullivan J, Dana T. Redefining Maori economic development. International Journal of Social Economics. 2008. 35(5):364-379.

[14] Crampton P, Parkin C. Warrior genes and risk-taking science. N Z Med J. 2007. Mar 2;120(1250):U2439.

[15] Lu RB, Lee JF, Ko HC, Lin WW, Chen K, & Shih JC. No association of the MAOA gene with alcoholism among Han Chinese males in Taiwan. Progress in Neuro-psychopharmacology & Biological Psychiatry. 2002. 26 (3), 457-61 PMID: 11999895

[16] Lung FW, Tzeng DS, Huang MF, Lee MB. Association of the MAOA promoter uVNTR polymorphism with suicide attempts in patients with major depressive disorder. BMC Med Genet. 2011. 24;12:74. doi:10.1186/1471-2350-12-74.

[17] Fergusson DM, Boden JM, Horwood LJ, Miller AL, Kennedy MA. MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study. Br J Psychiatry. 2011. 198(6):457-63. doi:10.1192/bjp.bp.110.086991.

[18] Beaver K, DeLisi M, Vaughn M, Barnes JC. Monoamine oxidase A genotype is associated with gang membership and weapon use. Compr Psychiatry. 2010. 51(2):130-4. doi:10.1016/j.comppsych.2009.03.010.

[19] Guo G, Ou X, Roettger M, Shih J. The VNTR 2-repeat in MAOA and delinquent behavior in adolescence and young adulthood: Associations and MAOA promoter activity. European Journal of Human Genetics. 2008. 16(5):626-634

[20] Beaver K. Personal communication. May 2014.

[21] Allen A. Charging Into the Minefield of Genes and Racial Difference. Nicholas Wade’s ‘A Troublesome Inheritance.’ Book Review. New York Times. May 15, 2014.

[22] Visscher PM, Hill WG, Wray NR. Heritability in the genomics era–concepts and misconceptions. Nat Rev Genet. 2008 Apr;9(4):255-66. doi:10.1038/nrg2322.

[23] Choe D, Shaw D, Hyde L, Forbes E. Interactions between monoamine oxidase A and punitive discipline in African American and Caucasian men’s antisocial behavior. Clinical Psychological Science. 2014. March 14. doi:10.1177/2167702613518046

[24] Choe D. Personal communication. May 2014.

[25] Simons RL, Beach SR, Barr AB. Differential susceptibility to context: A promising model of the interplay of genes and the social environment. Adv Group Process. 2012;29. doi:10.1108/S0882-6145(2012)0000029008.

[26] Rothstein MA, Cai Y, Marchant GE. The ghost in our genes: legal and ethical implications of epigenetics. Health Matrix Clevel. 2009 Winter;19(1):1-62.

[27] Zhong S, Israel S, Hong X, Ebstein R, Chew S. Monoamine oxidase A gene (MAOA) associated with attitude towards longshot risks. PLoS ONE. 2009. 4(12):e8516 doi:10.1371/journal.pone.0008516

[28] Shumay E, Logan J, Volkow ND, Fowler JS. Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men. Epigenetics. 2012 Oct;7(10):1151-60. doi:10.4161/epi.21976.

[29] Belsky J, Beaver KM. Cumulative-genetic plasticity, parenting and adolescent self-regulation. J Child Psychol Psychiatry. 2011 May;52(5):619-26. doi:10.1111/j.1469-7610.2010.02327.x.

[30] Belsky J, Jonassaint C, Pluess M, Stanton M, Brummett B, Williams R. Vulnerability genes or plasticity genes? Mol Psychiatry. 2009 Aug;14(8):746-54. doi:10.1038/mp.2009.44.

[31] Weder N, Yang BZ, Douglas-Palumberi H, Massey J, Krystal JH, Gelernter J, Kaufman J. MAOA genotype, maltreatment, and aggressive behavior: the changing impact of genotype at varying levels of trauma. Biol Psychiatry. 2009 Mar 1;65(5):417-24. doi:10.1016/j.biopsych.2008.09.013.

nooffensebut said...

For reference, here is her first response to my critique.

Alondra Oubre (@AlondraOubre)
August 4, 2014 • 12:15 am

I should clarify that this article was written as a brief commentary for lay audiences, primarily to illustrate contrasting approaches to studying behavior linked genes/alleles. MAOA gene variants seem to make interesting conversation pieces.

One issue which intrigues me — and which perhaps can expand our still “Bronze Age” grasp of “nature vs. nurture and behavior” — is the role of plasticity genes. I am curious about both established and putative associations between plasticity genes and epigenetic mechanisms in the CNS, and their range of effects on gene expression.

How modifiable are plasticity genes by other forces — environmental, perhaps epigenetic, and possibly gene-gene interactions?

Do plasticity genes likely evolve at the same rate as, say, disease-related alleles?

Can plasticity genes give us a window on the bioevolutionary underpinnings of human behavioral phenotypes — yep, across populations?

Or, instead, are plasticity genes more likely to shed light only on ontogenetic adaptations (and perhaps short-term intergenerational transmission of stress-mitigating traits via genes, gene-environment interactions, and/or epigenetics)?

I welcome any insights from informed experts.

By the way, I did not use Wikipedia for this article.


nooffensebut said...

For reference, here is her second response.

Alondra Oubre (@AlondraOubre)
August 6, 2014 • 5:25 pm

To Unsilenced Science

I finally have had time to read your post and to recheck my references.

First, I see that you are right about the MAOA-2R frequencies I listed as having come from Wikipedia. I unknowingly did use numbers that were excerpted from Wikipedia. I added numbers that I had collected before I started writing this paper. The numbers were included in notes that were only partially referenced. I originally wrote this article as a lightweight commentary, without references, intended to be submitted to a popular, non-technical publication. It was meant to offer a brief, deliberately superficial, sampling of some of the research and approaches and data related to MAOA gene variants. References were not appropriate for this online magazine, so I did not include them. I was told my article was too technical for the general readership of this magazine. When Scientia Salon expressed a possible interest in my article, I went back to my files, including a few reprints as well as text pages of notes, and added references compiled from various sources I had used. The frequencies I used were taken from raw notes, not a web page or any source identifying Wikipedia. At any rate, not only should the citation be corrected (and perhaps changed to multiple sources), but also the frequencies may need to be altered.

You call me a scholar and/or academic, but that is far from reality, despite some labels that appear online about me. Quite simply, I am neither in terms of the type of work I do nor the types of products I create. I have a graduate degree in anthropology, but I do not consider myself an anthropologist — certainly not a practicing anthropologist and at this point in my life, not even an armchair anthropologist. I have seen Alondra Oubré described as an evolutionary biologist, geneticist, or ethnopharmacologist in various print and online sources. None of these titles is accurate in regard to my vocation. With all due respect to the world’s fine scholars and academics, I clearly do not fit the criteria for either category, nor have I ever wanted to. Even when I was engaged in activities where I loosely could be called an anthropologist or medical anthropologist, my armchair work was, at best, marginally anthropological.

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, as though my life revolves around unearthing a wide range of articles on the subject, as though I am supposed to spend the little free time I have doing this. MAOA-2R and related topics are a secondary, perhaps tertiary, interest of mine that I occasionally explore when time permits, which it does rarely. My rather superficial, or generalist, level of analysis was appropriate for the article I wrote targeting general readers (and even then, it was reportedly too detailed).

Apparently you have followed the MAOA-2R story (and yes, from my non-scholarly purview I see it as a story) for quite awhile. You just might possess more intellectual knowledge about published research in this field than any other single person on the planet. You seem to be very passionate about the topic. But why do you assume that I am passionate about it too? Why must I be invested in research on this subject just because you seem to think I am or should be? Why should I spend my time combing through numerous articles I haven’t heard of simply because you insist I should do this, or must have already done this, but then suppressed it? (In the past when I wrote about nature-nurture and race, and had the time to do a reasonable but certainly not exhaustive amount of research, I eagerly embraced research reports with opposing conclusions. I enjoyed that process. I never shunned relevant research studies, nor would I now if I had the time to read them and write about them.)

nooffensebut said...

(Continued – 2 of 3)

Also, I never changed any data in Wikipedia. If I had, I would have added citations and would have listed those citations in my article. I have no motive to change any data, and if I did, I would willingly admit it. More fundamentally, why do you assume that I am biased toward lower frequencies of MAOA-2R, or would want to distort evidence to make the frequency of this variant in African Americans appear lower?

Your presumption about my views toward Wade is way off. I have not read his latest book, so I had no intention of rendering a book review. I cited him because I was aware of his mention of MAOA-2R, just as I cited a reviewer who critiqued Wade. Both authors became, in a loose sense, proxies for people who are perceived to take diametrically opposed positions on the subject. I was not thinking of any particular person when I wrote the original, unreferenced article. These two authors became suitable to cite — without a value judgment on my part — when I had to add references to the paper. (By the way, recent mention of Beaver’s work in the popular press has put MAOA-2R in the news, especially over the past 2 or 3 years. That was the original idea behind “back in the news” — an idea I had last year, but no time to write about.)

Why do you assume I am opposed to Wade’s notion that MAOA-2R might contribute to the disproportionately high rates of violent crime in African Americans? After all, Wade’s commentary, which to his credit was cautious, was based largely on Kevin Beaver’s studies. In case you didn’t noticed, Beaver’s research plays a prominent role in my article. Indeed, my article does not negate the value of research on MAOA-2R. Quite the opposite, in fact.

You imply that I am anti-science, and against Wade’s consideration of a role of MAOA-2R in the ethnic gap in social outcomes. That is patently false. For decades I have been a strong proponent of exploring — and comparing — genetic associations with social behaviors across populations (or to put it crudely, examining the role of race based genetics in social behaviors). My personal views (which, incidentally, are continually changing, as I become aware of new research findings) — are irrelevant. I am intrigued equally with evidence that seemingly supports my perspective as I am with data that seemingly negates my view. Furthermore, some of my current ideas about nature versus nurture and ethnic behavioral differences have shifted from my views of even a few years ago.

While I do not have presumptions of what the data on, for example MAOA-2R, eventually might reveal, I remain supportive of scientifically rigorous studies to determine the effects of this particular gene variant (and alleles of other genes) on behavior. Simultaneously, I am intrigued with scientific evidence on the effects of varying environmental (and potentially epigenetic and various other genetic) factors that affect gene expression of behavior-linked alleles, possibly including MAOA-2R. Insofar as my limited time permits, I am interested in learning about different interpretations of what the data might mean.

You repeatedly make multiple, uninformed assumptions about my worldview, my belief system, and my categorizations of people that are not grounded in reality. I cannot speak to your characterization of anthropologists, as a whole, but your characterization of me is, well, definitely not who I am. I find the science behind nature versus nurture fascinating, but it is not my life’s mission. The scientists and scholars with whom I have had exchanges over the years represent a wide range of perspectives. My own views have always been hybrid, and even then, perhaps somewhat unconventional hybridizations. I have no impulse to suppress either scientific evidence or claims about such evidence. I always have been open to debating variable vantage points based on established and emerging evidence. Of course, engaging in these types of debates requires time.

nooffensebut said...

(Continued – 3 of 3)

You act as though the MAOA gene should be my life’s ultimate purpose. Please re-read your post. Do I have a choice in the matter? Am I allowed to choose the subjects that interest me in life and pursue them? Am I permitted to form my own worldview about issues? Am I entitled to even have a life?

Last time I checked, I had a right to form my own views about nature versus nature, even if those views do not conform to preconceived notions of what I am expected to believe, or supposedly ought to believe.

If you repost this post to another site, please extend the courtesy to repost it in its entirety.

nooffensebut said...

Thank you for admitting your source and calling with me for correction. If I wanted to write a “lightweight commentary,” I think that I would not make racial differences in the warrior gene my first choice. Of course, you have every right to express yourself as you wish. I would certainly prefer that those who choose to write about monoamine oxidase A have a firmer grasp of the broad conclusions of the scientific literature, especially if those writers seek to write for a lay audience as “popular science.” To list every commentary that dismissively addressed the gene or otherwise misrepresented the science would require a lengthy scroll. They have ranged from brief, vague mooting in the New York Times to prolonged student “civil” disobedience. Like climatology, the science of this gene has an artificial controversy in the popular press with recurring themes, upon most of which your piece touched. Perhaps you and similar writers truly meant no harm and thought you were merely expounding upon an existing consensus that you did not realize was pseudoscientific. Your reference to the Rod Lea/Maori commotion shows your familiarity with that side of the “issue.” Unlike climatology, which has a well-financed opposition but also has a vocal and sometimes contemptuous cadre of professional defenders, only I appear to be defending the warrior gene in the public realm from my little blog. Rather than receive any kind of financing, I receive a lot of name-calling. Look no further than the many vacuous comments underneath your piece for verification that your readers saw your work as a righteous attack on MAOA science and saw me as racist for my dissent. The irony is that African Americans probably stand the most to gain from medical/scientific follow-through on this lead. I have reason to believe that I influenced Wade to discuss MAOA-2R in his book and Beaver to extend his research to this specific allele. Therefore, I would not prefer to sit idly by while the literati viciously attack them for broaching the subject, whether or not I am the planet’s leading expert. I grant that the tone of your article was expressing more of a cautionary note compared to flagrant attempts at “debunking” MAOA science. However, I oppose both because this is a life-and-death issue that needs more attention, defending, and funding.

(Note: Massimo Pigliucci closed all commenting on Oubré’s article before I could post this and did not alter the incorrect data in the article, which Oubré now admits is from Wikipedia.)

Microraptor said...

The Wikipedia criticism site Wikipediocracy has been collecting examples of hoaxes that originate in Wikipedia articles and end up being repeated elsewhere. You might be interested to know that I've mentioned this example involving MAO-A there:

nooffensebut said...

Good job! Thanks!

Anonymous said...

"[Wade] called a book by JP Rushton racist in an interview"

He kind of had this coming then.

ScttBn said...

According to an ARIN lookup, the IP address from which the Wikipedia changes came is registered to the University of Mary Washington in Virginia:

Unknown said...

I worry that you initial comments and the title of this article are gross violations of
Hanlon's Razor:'s_razor

Unknown said...

Forgot to mention this, but I honestly feel that as she has apologised for this screw up, you should apologize for your attitude.

nooffensebut said...

Her apology was of the non-apologetic variety. Her article continues to receive undue positive attention while still lacking a proper correction. You might notice that the label "extreme warrior gene" that she coined became a major theme of an unintelligent major-network prime-time television drama. My ideas (and humorous insults) don't receive that level of attention, but, more importantly, actual research on this "extreme" genetic allele has ceased apparently, which is probably a worse tragedy for the African-American community than any number of unjustified police shootings. The few others who have even bothered to write about it have all received accusations of racism. These kinds of blithe errors tend to echo, and I intend to attack all in the chain. Nobody even knows who I am, and all the real attention goes to the subject. I receive no benefit other than a chance to serve the truth as a lowly "blogger."