The Extreme Warrior gene: a reality check

Monoamine_oxidase_A_2BXSby 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].

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].

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].

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].

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].

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].

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.

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[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.

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[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.

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[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.

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[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.

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[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.

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74 thoughts on “The Extreme Warrior gene: a reality check

  1. Coming in late on this one, though it is related to my own field (neuroscience) and work experience. I agree with and would with strongly second the author’s cautionary conclusions regarding this gene (or any gene) and behavior.

    I would disagree with (or wish to correct) one statement by the author.

    “The field of epigenetics is largely theoretical, at least insofar as humans are concerned.”

    While it is certainly not well fleshed out in its details (because it is so new), epigenetics as a field is not “largely theoretical”. It is well established that cell identity is dependent on epigenetic mechanisms, otherwise each type of cell would require its own DNA code. Humans would not be an exception.

    It is only the possibility of inherited epigenetic marks which is largely theoretical. Given that we still don’t know how epigenetic marks are cleared during reproduction, it is very hard to claim that epigenetic marks can, much less are, passed on. It could very well be that it is the conditions which the mother experiences during gestation of the fetus that leads to specific epigenetic labeling and so not truly “passed on” by a parent.

    As far as discussion on this topic is going, while I certainly would not think epigenetics trumps genetics in terms of evolutionary mechanisms, it is surprising if Dawkins really dismisses this critical field as it underpins our understanding of cell identity… and so personal identity. Epigenetics is what allows for the great diversity of multi-cellular organisms, and (likely) the plasticity of our highly adaptable nervous systems.


  2. There are a few issues here. Firstly, a majority of studies find that individuals carrying the low-MAOA-activity genotypes are (roughly) a modest 1.1-fold more likely to be aggressive. This is a “marginal effect”, in that it averages over the levels of adversity in the particular sample studied. Most of these studies are limited to ethnically homogenous samples, and the
    meta-analysis of Ficks and Waldman (2014) suggests that ethnic makeup of the sample is not a significant modifier of effect size. Skeptics of this finding have to find a mechanism by which the investigator’s rating of the aggressiveness of an individual can be biased by that individual’s genotype. The only plausible cause of confounding of this type is that genotype is associated with membership of a particular social group.

    One recent study
    Kuepper et al (2013) is quite nice. It is carried out in 239 university students of “Caucasian ethnicity”, who performed a competitive reaction-time test that is designed to be irritating, and measures aggression by the individual to an unknown (actually computer) opponent (volume of noise to be played in the loser’s ears). There are 56 low-activity individuals, 69 mixed (female, MAOA is on the X chromosome), and 114 high-activity individuals. The low group (male or female) responded 30% more aggressively. So numbers in each genotype group in both observational and experimental studies are quite adequate (a total of 13600 individuals in the Ficks and Waldman meta-analysis).

    The second point is that the differences in genotype frequencies between different ethnic groups are also robust. Therefore, in the absence of interactions (different genetic backgrounds on which this particular polymorphism acts, and gene by environment interactions), we would predict a 1.02-fold difference in rates of aggression between a population with 60% as opposed to 40% frequency of the low-allele (3-repeat). Obviously, this is not a particularly easy to detect, or particularly important cause of inter-group differences
    Pop1: P(3R)=0.4, male risk of aggression 3R=11%, 4R=10%: Pop1 rate=10.4%;
    Pop2: P(3R)=0.6, Pop2 rate=10.6%).

    This may be amplified slightly by the adversity-genotype interaction if there are significant between population differences in adversity. In terms of population attributable risk (what difference would we see if a wonder drug changed all “3R”‘s to “4R”): population rates only drop from 10.4% to 10%, or 10.6% to 10%.

    So does this alter my understanding of human nature – that some people have shorter fuses than others, and may have to work harder to contain this tendency…


  3. 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.



  4. brandholm: “it is surprising if Dawkins really dismisses this critical field as it underpins our understanding of cell identity…”


    brandholm: “… it is very hard to claim that epigenetic marks can, much less are, passed on. … while I certainly would not think epigenetics trumps genetics in terms of evolutionary mechanisms, …”

    With the current definition and thus the evidences in accordance to that definition, I think that you are right. But, I would like to take this opportunity to put my bet on epigenetics (with a broader definition) which is the ‘major’ pathway for ‘evolution’, that is, much more important than the Darwinism (a blind way of evolution). In this broader definition, epigenetics is a pathway for evolution ‘intelligently’ by the species intelligence. I simply cannot stand the ‘blind’ evolution. Of course, this is not a place to make any more detailed description on this for now.

    But, note, this species intelligent evolution is not the religious ‘intelligent design’.


  5. Hi Dwayne,

    It is well established that cell identity is dependent on epigenetic mechanisms, otherwise each type of cell would require its own DNA code.

    For clarity, there is a nomenclature issue that needs highlighting. Some use the word “gene” to refer only to the DNA sequences that are transcribed into proteins. Under this definition, one does indeed need non-genetic factors (= epigenetics) to do a vast amount of regulating of what genes do.

    In the other definition, “gene” also includes all the regulatory DNA that controls these “epigenetic” factors. E.g. wiki says: “A modern working definition of a gene is “a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions, and or other functional sequence regions”.”

    In this definition “genes” are any length of DNA that have any affect on the resulting phenotype. And under this definition much of “epigenetics” is “genetics”, (albeit a more complicated version of genetics than simple gene => protein, but then no-one has ever regarded that simple statment alone as adequate).

    … it is surprising if Dawkins really dismisses this critical field as it underpins our understanding of cell identity

    What Dawkins would say (from the viewpoint of the second definition) is that the need for regulatory genes turning other genes off and on has always been obvious. Thus, adopting the narrower definition of gene, and thus claiming that gene-centred viewpoints are hopelessly inadequate, is a complete strawman, because the gene-centered viewpoint has always been based on the second definition of gene, which has always included regulatory function. (E.g. Dobbs’s article is constructing a whole edifice of straw along these lines, and then claiming that Dawkins is an old fuddy-duddy for refusing to see anything beyond the straw edifice.)


  6. Hi Coel, I guess I’d quibble a bit with “genes” being defined so broadly that epigenetics becomes genetics.

    Especially for clarity in discussing mechanisms effecting cell identity or function, it is important to distinguish between permanent changes in the sequence of the gene itself, versus temporary changes in expression of a gene.

    For example I work with induced pluripotent stem cells, and there is always a concern for whether changes have occurred to genes themselves (basically creating mutations during a conversion process) or if errant epigenetic marks are present (whether added or previous marks insufficiently removed). These are two very different problems. It would be odd, or at least insufficiently vague to refer to both as “genetic”.

    I think such a move is also deceiving, by suggesting that epigenetics is all about genes regulating other genes. Those marks can be effected by their environment (purely chemical-induced), this is especially important in long term cell culture.


  7. brandholm –

    First let me say I only have a superficial knowledge of the subject at best.

    “Given that we still don’t know how epigenetic marks are cleared during reproduction, it is very hard to claim that epigenetic marks can, much less are, passed on. It could very well be that it is the conditions which the mother experiences during gestation of the fetus that leads to specific epigenetic labeling and so not truly “passed on” by a parent.”

    Just to be clear, do you mean epigenetic marks are not passed on through DNA, by changes to the genetic code itself, but that they are clearly passed on form one generation to the next in a way we do not fully understand?


  8. Statistical significance is not definitive in and of itself. Chance means that there will be statistically significant clusters that nonetheless are random. They are indeed still unlikely, therefore “outliers on a distribution,” which I think gives a better sense of what “signficant” means in statistics. Statistical significance does not mean significance in ordinary language, what we might call genuine significance.

    The MOA gene variants were first distinguished as low activity variant and high activity variant. It was suggested that the statistically significant correlation between male Maori crime rates and the low activity variant was genuinely significant. There were apparently no hypotheses about why or how the gene and aggression did not significantly correlate in females.

    When it was discovered that one of the low activity variants was prominent in ethnic groups that were not members of discriminated minorities, the story changed focus to distinguish low activity variants from each other. Then it was decided that the statistically significant correlation between low activity variant MOA-2R and the was the one that was genuinely significant, setting aside any question as to why or how one low activity variant is significantly correlated with aggression etc. in Maori men but not in Chinese/Taiwanese men.

    Further it has been found that the greatest statistical significance was for correlation between low activity MOA and punitive discipline in youth with aggression etc. It is uncertain low activity in neurotransmitter degradation would contribute to the development. It is not even certain that the low activity MOA-2R gene isn’t simply activated more often so that the degradation is more or less the same, in a process analogous to polycythemia and other physiological changes compensating for hypoxia.

    Lastly, variations in the deleterious effects from the MOA-2R variant are hypothesized to be due to plasticity genes. I gather this is to explain (or some might say, explain away?) a kind of mismatch in the presence of the gene and the quantitatively variable results. That is, why some with the gene are violent criminals and others not. After all, 5.5% of the African-American population are estimated to carry the gene.

    I think we have here an example of science chasing spurious correlations. Each time further research loses the correlation, the hypothesis of genetic causality of crime is refined, or redefined, to preserve it. I think you can see the process at work in the history retailed in the OP. When the Ficks and Walman metastudy found a “marginal” increase in aggressivity, they were saying that it was not even certain there was a statistical significance! The alleged phenomenon, as expected in spurious correlations, is disappearing.

    Further, there are wide variations in the standard for criminal behavior. Gambling addiction counted in one study. Even the more careful studies which specified behaviors such as shooting or stabbing seem to be unclear as to how they distinguished the aggressors in fights. The worst thing of all is that crime statistics are suspect for massive systematic errors due to racial discrimination. It is a reasonable alternate hypothesis that gangs flourish where the police treat the population as enemies. I think you can reasonably say that quite a few CEOs engage in antisocial behavior, but their genomes aren’t analyzed for correlations.

    You don’t just falsify hypotheses (contra Popper) but choose the best. I think the whole process has started with a Mars effect like Michel Gauquelin found for astrology. This chance correlation has been pursued with all the elaborate methods available, in the same way parapsychology pursues esp. But statistical significance only serves as a control when the statistics are properly used, which means truly asking is the phenomenon is real. When it keeps moving somewhere else, as in this case, we can be pretty sure it’s not.

    As to how such intelligent and hard-working people could get themselves lost like this? I think it’s because they think a gene, the product of natural selection, simply must do something, and that the organism and its behavior (in this case, Maoris and African-Americans,) are due to the action of the genes. Everything is genetic, even plasticity. There’s no epigenetics, it’s all just genetics.

    Personally if I try to picture this on a molecular level I can’t see how membranes or ribosomes that may have predated DNA chromosomes in evolution can tell how orders from genes are any different from other biomolecular influcences. I tend to think of regulatory genes as more like flocking rules for the way cells flock together. The simple rules generate information so to speak that were not present, as they would be in a blueprint or computer program.

    Of course it’s only my confusion that led me to think the insistence on genes as the unit of selection could possibly imply the view that denying the powers of genes is equivalent to denying natural selection. I hope this is more constructive.


  9. davidlduffy,

    From your last link:

    “This indicates that the low-functional alleles of the MAOA-uVNTR are not associated with increased aggressive behavior per se, but rather with an increased aggressive reactivity to provocation”

    And your comment:

    “So does this alter my understanding of human nature – that some people have shorter fuses than others, and may have to work harder to contain this tendency…”

    I’m wondering if you think it makes sense genetically that a rise in aggressive tendencies in a part of a population could follow from a rise in provocative tendencies in some other part of the population?


  10. Hi Marclevesque,

    “Just to be clear, do you mean epigenetic marks are not passed on through DNA, by changes to the genetic code itself,”

    Yes, the concept of epigenetics is that the phenotype of a cell is determined by regulated gene expression, independent of any changes to the genetic code. If you think about it, that is really what has to happen. You have basically one genetic code which is found in almost all of your cells. So the difference in each cell type must come from something other than “just” the genes within it,

    Epigenetic regulation of gene expression takes many forms. It can be repressive microRNAs which block translation of mRNA into proteins. Or it can be modifications (methylation, hydroxymethylation, etc) to the DNA itself which effects binding of transcription machinery and so blocks production of mRNA from DNA. Or it can be “marks” on the “tails” of histones (histones are proteins around which DNA is wrapped) which likewise influence transcription machinery, both positively and negatively.

    So a “parent” cell can divide to produce “daughter” cells which have the exact same DNA, but based on epigenetic marks (and other mechanisms) will express genes in a different manner and so be a totally different cell type. Such changes can ultimately influence the entire organism. Of course they could just alter cell functions, without even changing cell identity. Neuronal plasticity is almost certainly driven by epigenetics, yet neurons stay neurons.

    A nice introductory book on epigenetics for nonscientists is “The Epigenetics Revolution”, by Nessa Carey.

    “that they are clearly passed on form one generation to the next in a way we do not fully understand?”

    This is where it gets trickier. From one cell to the next generation of cells, yes it is clear that this happens and all of the mechanisms are not fully understood at this time. Even all of the potential marks are not fully understood. For example DNA methylation was considered a very important epigenetic mark. Recently it was discovered that DNA can also be hydroxymethylated, yet prior tests devised for methylation could not discriminate between the two. Oops.

    And histone modifications? That is one massive can of worms.

    Moving beyond cells, passing epigenetic marks from a parent organism to the next generation of offspring through the reproductive cells has not (to my knowledge) been proven at all. Almost all epigenetic marks are cleared during reproduction, in a mechanism that is not known (once we figure it out, cell reprogramming will become a lot easier). The reason for this cleansing of marks is so that the cells in the embryo will have the potential to form any other cell type.

    I should mention I am being simplistic in my descriptions, the marks are not simply removed (no marks) but reset to create a sort of blank phenotype. But you can think of it as clearing any prior cell type demarcations.

    It is certainly possible that some marks are not reset or cleared and so get passed on to bias gene expression and so cell function (even if not cell identity) in the child. But like I said, this has not been proven. So far the strongest suggestion has been that environmental factors effecting the mother during gestation have led to epigenetic effects in their offspring. But that does not mean the mother shared such epigenetic changes (which she passed on) at all.

    It is of course a fascinating idea and worthy of much greater research.


  11. Perhaps something more up to date would be of interest? From io9 (you can’t get much more popular than that!):

    “These commonalities came to the attention of Lewis Petrinovich, a professor of psychology who studies the roles of emotion, reason and biology in making ethical decisions. “To a Darwinist,” he says, “the suggestion that behavior is universal sparks interest because it might signal unexplored aspects of an evolved human nature.” Petrinovich published the findings of his research in a book, The Cannibal Within. His key conclusion: The patterns of decision-making in cases of survival cannibalism reflect behavioral tendencies that have evolved to perpetuate one’s genes into future generations.

    This is also known as “reproductive success.”

    Further details at

    Of course Petrinovich speaks of genes and the difficulties of explaining altruism. And again no alternative hypotheses are considered. In social life, reciprocating services with a delay for reward feels pretty much like altruism. Even if you managed to convince yourself that genes can program such unconscious “thinking” the selected habit of reciprocation would bleed into altruism. After all, how does ordinary altruism lower reproductive fitness so that natural selection would favor reciprocation and disfavor altruism? If you follow the link Petrinovich imagines something called “reciprocal altruism,” which is supposed to be how services can be reciprocated between non-kin. Petrinovich forgets to demonstrate that the services received later received by the altruist from non-kin are somehow consistently great enough that selection would favor these genes for their contribution to the genetic success of the altruist’s lineage. Instead, Petrinovich suddenly talks of the “evolutionarily based social glue that solidifies cooperative tendencies…” Petrinovich also forgets to demonstrate that this group selection increases the genes “for” altruism throughout the human population. As Coynes tells us, see Pinker on group selection for the takedown!

    Possibly the funniest aspect of the whole thing is how they don’t notice that letting your children starve to death before you do (or not committing suicide to provide food with your body,) does not contribute to reproductive success for the genes. I suppose they thought the fact that children have only half the genes meant they were also half competitors to your genes?

    How foolish of me to think a head full of selfish gene thinking perpetrates stuff like this!


  12. Brandholm –

    Fascinating stuff, very interesting, thanks for your reply. Lots of new information for me, like I’d never even considered the transmission of epigenetic marks from one cell to the next generation of cells.

    “passing epigenetic marks from a parent organism to the next generation of offspring through the reproductive cells has not (to my knowledge) been proven at all”

    I’m realizing to what extent a lot of talk about epigenetics can be pretty imprecise when using words like a generation, intergenerational, or transgenerational. So, if I’ve got this right:

    Environmental influence on mother > Epigenetic modification to mother’s DNA > Modification to mother’s DNA expression > Modification to mother’s in utero/fetus’ environment > Environmental influence on fetus > Epigenetic modification to its DNA > Modification to infant’s DNA expression

    And that’s not a clear case of the mother’s epigenetic mark being inherited by her child, and though there is influence or transmission of something across generations, it’s nothing like epigenetic inheritance observed in plants.

    “It is certainly possible that some marks are not reset or cleared and so get passed on to bias gene expression and so cell function (even if not cell identity) in the child. But like I said, this has not been proven”

    From wikipedia: “Robin Holliday defined epigenetics as “the study of the mechanisms of temporal and spatial control of gene activity during the development of complex organisms.”[18] Thus epigenetic can be used to describe anything other than DNA sequence that influences the development of an organism.The more recent usage of the word in science has a stricter definition. It is, as defined by Arthur Riggs and colleagues, “the study of mitotically and/or meiotically heritable changes in gene function that cannot be explained by changes in DNA sequence.[19]”

    Just considering those two definitions, it’s not surprising there is a lot of confusion surrounding epigenetics. Though I feel I can parse those definitions better now and navigate the literature more safely. : )

    “It is of course a fascinating idea and worthy of much greater research.”

    Yes, absolutely.


  13. Hi Marclevesque,

    “So, if I’ve got this right:

    Environmental influence on mother > Epigenetic modification to mother’s DNA > Modification to mother’s DNA expression > Modification to mother’s in utero/fetus’ environment > Environmental influence on fetus > Epigenetic modification to its DNA > Modification to infant’s DNA expression”

    It could be that or just part of it, for example…

    Environmental influence on in utero/fetus’ environment > Environmental influence on fetus > Epigenetic modification to its DNA > Modification to infant’s DNA expression

    Nutrients or toxic substances can enter the womb and effect the fetus directly without having to effect the mother’s gene expression levels (to such an effect it would then effect the fetus).

    BTW it would be more accurate to talk about “gene expression” rather than “DNA expression”.

    “Though I feel I can parse those definitions better now and navigate the literature more safely. : )”

    Glad I could be of help. And I really would recommend that book by Nessa Carey if you are interested in the subject. It gets you relatively close to the current state of the field, with some really interesting examples of epigenetics at work.


  14. Thank you for making some of the points I was trying to make in language more to the point than that available to me, and more appropriate in the context.


  15. I rather feared “marginal effect” would be confusing, in that it referred to averaging over one margin of a cross-classified table (a la “main effect”). The random-effects model P-value for the overall effect of MAOA was 1.37×10-6, difficult to explain as due to just to “moving somewhere else”.

    With respect to Genotype x Treatment interaction, the meta-analysis of
    Byrd and Manuck (2014) found
    that the low-activity MAOA genotype heightened risk for antisocial behavior among males exposed to maltreatment specifically (p = .00000082) combining across 13 different studies, a result they found robust to several sensitivity analyses. There was no such effect seen in 11 female cohorts.

    So my original point stands, that the associations have been found within particular ethnic groups on multiple occasions, and it only when this is combined with the equally strongly supported fact that genotype frequencies differ between ethnic groups that we arrive at the hypothesis that you find so odious. This has nothing to do with any particular models of evolution, they are straightforward observations.

    However, there are good examples of interactions between ethnic background and what might seem to be straightforward associations. My favourite example is Apolipoprotein E (APOE) and Alzheimer’s Disease (AD). The APOE*4 allele is very robustly associated with increased risk of AD in European and Asian populations. Since the APOE*4 allele is the ancestral allele, it is much more common in African populations. However in African and to a lesser extent African-American populations (bearing in mind there is significant European admixture in the AA population), the APOE*4 allele does not predict AD. I suspect that there are environmental differences or differences in genetic background on which APOE variation is acting that explain this observation. One could further speculate that the more recently derived APOE*3 and APOE*2 alleles have been selected for after the loss of either these protective genetic or environmental factors by the move out of Africa. As I noted previously, Ficks and Waldeman tested to see if study participant ethnicity was an explanation for the considerable between-study heterogeneity they observed, and found it not statistically significant.


  16. @marclevesque:

    The variance components approach has been extended to include a variety of interactions and correlations. An obvious point is that one’s parents share genes with you, and if these genes alter parental behaviour and treatment of you, then we get gene-environment covariation. The reciprocal Interactions between siblings are also commonly modelled – the classic example of this is where identical twins become less similar by “rubbing” against each other – one becomes more extroverted and the other more introverted as a result.

    I don’t think there is data or statistical power to test complex population level models a la Maynard Smith (frequency-dependent selection and interaction etc). MAOA is supposed to exhibit some signals of selection in humans but not other species in a couple of older studies, but doesn’t seem to pop out
    in the more recent genome-wide selection scans. The actual VNTR is only in humans and macaques.


  17. I do not understand the first paragraph. I do not even know how common it is to average over one margin of cross-classified table, as opposed to many or none. Nonetheless, sad as it may be, p-values alone are not definitive proof of significance as meant in everyday language. In this instance, systematic errors in crime statistics may be the cause of a real correlation, if there is one. I’m not very familiar with meta-studies, but isn’t it widely acknowledge that improperly accounting for systematic errors will derange any results? I went back to the OP today to double check the usage of “marginal” there, yet I do not seem to be able to find any reference to Ficks and Walman.

    The second paragraph is also hard to understand. I’m not sure it’s relevant. The reference to “Genotype x Treatment interaction” suggests that some of the sampling was in a therapeutic setting, A kind of agreed upon confabulation that seems to occur in many forms of psychotherapy raises yet more possibility of systematic errors of a different sort.

    The third paragraph mentions Anonymous’ original point. I don’t know what the original point was, not knowing where Anonymous made it. It mentions “associations” that were found within particular ethnic groups but I can’t be sure what that refers to. In context with the previous paragraph, it may mean between MAOA-2R and punitive discipline and aggressive behavior differing in ethnic groups? At any rate, the further statistically significant correlation with different genotype frequencies in various ethnic groups may be a straightforward observation.I still do not think that strengthening the correlation by adding another variable should be interpreted as showing the original correlation is strengthened. When you check for a statistically significant correlation and don’t find it but notice that a slightly modified version of the one you looked for is…That’s awfully close to drawing the bullseye after you shot the arrow. Further the hypothesis that MAOA-2R must be the causal correlate really seems to rest on nothing more than the assumption that since it’s not junk DNA but a gene, the target of natural selection, it must do something!

    The last paragraph is mostly irrelevant. But the last sentence suddenly changes tack: “As I noted previously, Ficks and Waldeman tested to see if study participant ethnicity was an explanation for the considerable between-study heterogeneity they observed, and found it not statistically significant.”
    I think the between-study heterogeneity is likely due to the nonexistence of the alleged phenomenon.
    But, although I found the original reference somewhat opaque, if the Ficks & Waldeman meta-study did not find a statistically significant correlation between ethnicity and the widely variant results, isn’t that a curious result? If MAOA-2R is genuinely causal and it is much more prominent comparatively in African-Americans, then shouldn’t there be an ethnic correlation?

    This is a good point to remind everyone that the high incidence of low activity MAOA in Chinese and Taiwanese with no noticeably distinct levels of aggression show there is no correlation. It would also be good to point out that the absence of studies of the supposed correlation between MAOA-2R (and African-Americans) and aggression should also hold in Africa, but there is no data. I suspect that if such studies are finally conducted the spuriousness of the correlation will be hard to deny.


  18. Carl Zimmer pursued another question of the adaptive value of genes chosen by natural selection, in this article: He explained that while all red blood cells have molecules called H antigens, a single ABO gene manufactures an enzyme that can add another antigen as well. A few key mutations distinguish the allele that form type A blood or type B blood. (If a personal has both alleles they have type AB.) But more mutations prevents the enzyme from being manufactured leaving RBCs with only H antigens, called type O. Genetic studies of other primates reveal that sometimes type A was excluded, other times type B, and sometimes type A mutated into type B. Type O can be formed by “hundreds” of mutations.

    Zimmer’s preliminary conclusion? “Being type A is not a legacy of my proto-farmer ancestors, in other words. It’s a legacy of my monkey-like ancestors. Surely, if my blood type has endured for millions of years, it must be providing me with some obvious biological benefit. Otherwise, why do my blood cells bother building such complicated molecular structures?” Thank goodness that gene selection doesn’t lead you to believe that all genes must be adaptive!

    Zimmer, knowing that blood types must be adaptive, then announces a great puzzle in the existence of the Bombay phenotype, people whose RBCs not only have no A or B antigens, but no H antigens as well. Thus they are neither A, B, AB nor O. No blood type in effect. (Yes if they receive any other kind of blood they can suffer transfusion shock.) The rest is speculations about possible advantages in disease resistance, even to diseases that do not appear to be directly related to blood.

    As in the OP, these speculations have I think seized upon statistically significant correlations that are nonetheless still random variations. Even more to the point, there is no effort to measure the power of the selection effect (which is basically the danger to reproduction posed by the disease promoted as a selector) or to compare to the effectiveness of blood type in resisting said selection. Statistically significant correlations between any of a multitude of diseases and blood types don’t tell us about that. If you went through the records comparing all diseases and blood types, chance dictates you will get larger correlations with higher p-values that meet the conventional standard.

    As in the OP, there is an ignored discovery that suggests the effect is nonexistent. In this case, I think the Bombay phenotype shows pretty conclusively in the same way the discovery of low MAOA-R3 in Chinese and Taiwanese did, the effect being studied is nonexistent.

    As in the OP, the neglect of other possibilities paints a false reasonableness onto the arguments. In this case, the possibility that the wide variation in blood groups a fine real world example of genetic drift. (Genetic drift is often confused with one form of it, a founder effect.)

    As in the OP, there is also a whole phenomenon as unexamined as MAOA-R2 in African males. In this case, the Rh factor. This is particularly interesting as it can be argued there is an identifiable selection pressure. An Rh negative mother can be sensitized to the Rh factor by the first Rh positive infant, leading to miscarriage of subsequent Rh positive infants, killed by the mother’s antibodies. (Some decades ago, there were Rho-Gam shots to prevent the mother’s reaction forming.) Why that isn’t relevant to natural selection for blood types is anybody’s guess?


  19. 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.)

    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.

    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.


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