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.

[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.

[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.

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74 replies

  1. If in any science I tried to reach conclusions from sample sizes of 5 and 6 (black “violent” males with the alleged gene in this article) I would, correctly, be ignored and ridiculed. Now that no scientist believes the falsified Black IQ data, time to look for another hypothesis with specious data to show intrinsic inferiority for Blacks.. A disgrace.

    JG

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  2. I’d like to thank the author for this well-written and seemingly well-researched article. Obviously a great deal of time was spent in preparing it, and research concerning the roles of the various factors involved in antisocial behavior along with evaluations of their respective importance is of great concern to most of us.

    Like

  3. Re epigenetics changing geneticists’ view, I’m not sure this is true. People like John Harshman, Joe Felsenstein, Larry Moran, Jerry Coyne, Richard Dawkins, Steven Pinker, all very eminent in one way or another, are thoroughly convinced this is all nonsense perpetrated by self-serving propagandists. The logic of the selfish gene is that essentially all genes are selected one way or another and genomes are optimized in some sense or another. The explosive assault on that article by David Dobbs, “Die, Selfish Gene, Die!” makes it pretty clear I think that nothing, not even neutral evolution, is going to change people’s minds about that. Not so long ago Carl Zimmer blessed the BBC with an article explaining the science of the adaptivity of human blood types without considering the possibility none of the alleles were selected, were neutral and random.

    I think it’s true that this kind of genetics and the sociobiology/evolutionary psychology that uses it are basically the new scientific racism. But when looking at controversies I can only conclude: However nuanced or complex their individual research may be, when it comes the intersection of genetic science and popular understanding, the majority reject the various proposed modifications of genetic determinism, all of them, from neutral evolution on to epigenetics, as trivial or even wrong, and misleading to the public as signficantly changing the popular picture of the gene. Whether the new scientific racism is a bug or a feature is not an interesting question either way.

    But maybe, despite my interest and efforts to keep informed, our host can tell about other scientists and authority figures who do reject this kind of genetic determinism? After all, it’s not like I’ve conducted a scientific poll.

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  4. Hi Steven,

    People like John Harshman, Joe Felsenstein, Larry Moran, Jerry Coyne, Richard Dawkins, Steven Pinker, all very eminent in one way or another, are thoroughly convinced [epigenetics] is all nonsense perpetrated by self-serving propagandists.

    Well, not really. It’s more that they think it is a real and interesting part of the story, but over-blown in its implications. Coyne has written about this a number of times, for example this one.

    The logic of the selfish gene is that essentially all genes are selected one way or another …

    Not really, most advocates of “selfish genes” are ok with genetic drift being a significant part of the story.

    The explosive assault on that article by David Dobbs, “Die, Selfish Gene, Die!” makes it pretty clear …

    Plenty of biologists thought that a bad article, e.g. Coyne again here.

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  5. Just to suggest some balance. There were some real heavyweights who were critical of Dobb’s article, but it was far from universal.

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  6. Steven, I don’t know about Felsenstein, but Pinker and Dawkins are simply demonstrably ignorant on the matter, and their comments should not be taken seriously at all. There is a lot of very good research been done on epigenetic inheritance, including my former students and postdocs in my lab, and the phenomenon is here to stay. The interesting discussions pertain to its various forms, how widespread it is, and what sort of long-term effect it can have on evolution.

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  7. 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 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 amygdale. Cerasa eta 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.

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  8. I’m not qualified to comment on the quality of the research cited by the author, but do you find the conclusions in the last two sentences objectionable and, if so, how? I hope the author will address your concerns.

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  9. Other people don’t think it’s overblown. P.Z. Myers, for example, has “gone after” both Dawkins and Coyne that I know of.

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  10. Very good stuff. Not only refutes the old one gene = one protein, etc., but also brings into question the old one neurotransmitter = one behavior cluster idea, which is getting just about as hoary. And, beyond that, brings epigenetic research fully into the picture.

    Especially in the case of issues like addiction, compulsive disorders, etc., I am so tired of the one neutrotransmitter = one behavior cluster idea still being used as a fallback. “Depressed? You just need serotonin! OK, maybe with a dash of norepinephrine.”

    All of this ignores that there are as many as 100 or so different neutransmitters, whose brain/nervous system influence affects each other, and that almost all of them have multiple different receptor sites.

    We may, I say MAY, be in the Early Bronze Age in neuroscience. Or, we may just be in the Neolithic instead of the Paleolithic.

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  11. Coel, when I reread the article, the final paragraph concluded with an extremely negative judgment. I don’t think in practice Coyne uses the concept of genetic drift any more than Carl Zimmer did in analyzing human blood groups.

    Thomas Jones, the only popular defender I know of was PZ Meyers. He was merely lukewarm and in an internet kerfuffle that’s damning with faint praise. Maybe not fair, but that’s how it is. Also, not to insult PZ but he isn’t nearly as prominent as Dawkins or Pinker or even Coyne.

    SciSal, how could I disagree about Pinker and Dawkins’ demonstrable ignorance? Save that no demonstrations have had any visible effect. Both are huge names in science popularization, reaching mass media. Coyne for one disagrees about Pinker’s ignorance, promoting Pinker’s attack on group selection as definitive. And of course, if the take down on criticism of Dawkins wasn’t universal, it sure seemed to be. I mean, if biologists were really taking genetic drift as a Darwinian mechanism seriously, evolutionary psychologists would be identifying variations in human nature from one deme to another, wouldn’t they? How many books demonstrating the way genes affect human nature are there yearly?

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  12. What, eugenics again? Will this bunk never go away? A bad science derived from a bad philosophy (propounded by the enormously boring and wrong Herbert Spencer) leading to bad politics (yes, have to play the N card here – e.g., in Germany during the ’30s and ’40s) but also in Britain as a ‘scientific’ explanation of class and in the US as a ‘scientific’ explanation of crime and, of course, “race.”
    There is no such thing as “race,” only gene pools.
    Of course our genes may promote tendencies, but to what? The introduction of chemicals and nutrients into our physiology, certainly; but to social environments? Baloney.
    What constitutes “antisocial behavior?” If I’m running around with a street gang, I may be very violent, but my behavior is highly socialized. The only ‘antisocial’ behavior that is truly antisocial is becoming a hermit. (“Criminal behavior” is not a scientific category, it is a set of legal classifications. A woman not wearing a veil on her head is defined as criminal behavior in several Islamic states – what gene could ever cause a woman not to wear a veil?)
    There is no way to correlate statistically the relationship between genes, behavior, and environment, no matter how large the samples because the variables in each are far too complex to establish an adequate control group. Consider this ‘butterfly effect:’ A young person with a ‘warrior gene’ goes out looking for a fight (why? well, did the gene tell him to do that?), when suddenly a butterfly lands on his/her arm. The young person stops and studies the butterfly; suddenly the triviality of the expected fight occurs to him/her, he/she chooses to meditate on the frailty of life instead. (what does the ‘warrior gene’ have to say about this?) The young person grows up to become a scientist. This sort of occurrence happens all the time, this is well documented in personal biographies and case studies. How do you isolate your studied groups away from possible encounters with butterflies long enough to establish your correlatives? And how long is long enough? (There is an answer to that one – not only a lifetime, but the lifetimes of several succeeding generations.)
    It is easy to predict – sociologically, without any need of genetics – that those growing up in socially harsh environments will need to learn survival patterns not expected from those who grow up in social environments that are not harsh – whatever the color of their skin.
    “Biosocial criminology” is not a science at all; it is a maneuver to win grant money from conservative interest groups. ‘If only we can provide an ‘scientific’ explanation for why there are more black people than white in the American prison system, maybe those dam’ libruls will shut up!’ No, maybe not.
    Or let me put it another way: Eugenics and its derivatives, like ‘biosocial criminology,’ can only become convincing once all social factors have been eliminated. How? Through the establishment of a perfect communist state where no one could ever suffer from poverty or otherwise harsh social environments. Now that would be an interesting experiment, but unfortunately, to be successful, it would have to be undertaken globally – literally world-wide.
    Nope, don’t see that happening.
    All these arguments have been made; but apparently the worshipers of the Cult of the Holy Eugene won’t give it up. The hope that we can manufacture progressive human evolution (and eradicate the nastiness from messy social experience) operates in some brains like an endorphin trigger – clearly causing antisocial behaviors, such as racial profiling. It’s an addiction, and may need some 12 Step program therapy.
    Oh, well; the actual genetics research – just as such – shows some promise; but not anything that would justify ‘biosocial criminology’ or its variants.

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  13. Maybe not so much?
    “Jerry Coyne is mildly incensed — once again, there’s a lot of
    recent hype about epigenetics, and he doesn’t believe it’s at all revolutionary. Well, I’ve written about epigenetics before, I think it’s an extremely important subject central to our understanding of development, and…I agree with him completely.” PZ Myers, http://scienceblogs.com/pharyngula/2011/08/21/the-epigenetics-miracle/

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  14. Thank you for the links; Coyne’s especially clarified the confusion between the two “epigenetics,” as well as reminding me of the differences between a gene’s internal environment and any external environment that a species may be adapting to.

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  15. Steven, you can read other assessments of Dobbs’s article, including Dobbs’s own take on the controversy here: http://aeon.co/magazine/nature-and-cosmos/an-expert-roundtable-on-the-selfish-gene-and-evolution/

    I also follow a blog of the neuroscientist Bill Skaggs. He writes very clearly and succinctly about this matter.

    Here: http://weskaggs.net/?p=461

    And here: http://weskaggs.net/?p=507

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  16. There are several commenters mentioning epigenetics, genetic drift, group selection, Dobbs’s pseudo-Lamarkism, et cetera. These are all different things, and we should be clear which we’re talking about.

    While PZ Myers has “gone after” Dawkins on various “issues”, I don’t think he has majorly disagreed with Dawkins or Coyne on biology. E.g. ejwinner’s link: “I agree with [Coyne] completely” on epigentics.

    Also, no-one disputes that epigenetics is real and interesting. The issue is whether it is a radical departure from Darwinism. To quote PZ: “What epigenetic modification does is broaden the range of phenotypes produced by a given genotype”, which is still conventional neo-Darwinism, and “it’s all about the process of gene expression, not about radically changing our concepts of evolution”.

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  17. Actually, Dawkins for one disputes whether it is interesting at all. In a footnote to one of his recent books he dismissed the entire field as a fad. And he does confuse it with neo-Lamarckism, which is actually an entirely different thing. (Though, to be fair, some researchers on epigenetic inheritance, like Eva Jablonka, are guilty of purposefully propagating that same confusion.)

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  18. EDITOR’S NOTE: As predictable, this is a controversial topic, likely to provoke emotional responses. A few of the comments I let through were actually barely acceptable, from the point of view of respectful and constructive discourse. Others were not and I blocked them. Unfortunately, not all commenters play by the rules, signing up to the site using fake email addresses, which means that my usual response to blocked comments does not reach them: if one of your comments is blocked you will receive an email from me alerting you to the fact; the email will include the full text of the offending comment, so that you may edit and resubmit it if you wish. Happy conversation!

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  19. Hi Massimo,

    It’d be interesting to have that actual quote from Dawkins. In a recent essay Coyne said:

    “… certain discoveries in [epigenetics] are interesting, and have certainly expanded our notion about how genes work, [but] there is not the slightest evidence that the findings of epigenetics will dispel the main ideas of neo-Darwinism, which include the ideas of evolutionary change via natural selection and genetic drift …”.

    Dawkins commented, “Bravo Jerry! Spot on, in every particular”, which presumably includes the particular that there is indeed some interest in epigenetics.

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  20. Coel, I’ll look for the quote, but I think you are being too charitable to Dawkins.

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  21. Maybe I am, but I think that’s the better direction in which to err; too much internet discourse involves erring in the other direction.

    (I’ve never seen a substantial comment by RD on epigenetics, so don’t really know much about his views on it.)

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  22. Nice and constructive policy, Massimo! (Not ironical). I am looking forward my first officially frown-upon comment, and will strive to make it acceptable. Any debate is best at the edge!

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  23. Right on, EJWinner. There is more evidence that a first encounter with the criminal justice system (an experience most Black kids and a few white kids endure before they are 15) causes incarceration than genetic makeup. I don’t have the reference, but a little noticed study some years back interviewed Black male college graduates and a matched sample of incarcerated Black men, and found that the incarcerated group had encountered the criminal justice system before age 15 and the other group hadn’t — although what they had done as kids was remarkably similar. As I said before, if the sample sizes and data cited were submitted for publication in, say, a genetics journal no one would even bother to explain why it was so bad.

    JG

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  24. I’m sorry for the lengthy reply, but I do feel strongly about the dangers of confusing social issues and scientific issues, in any form of research.
    To better understand why I went off as I did in arguing against the eugenics undertones of biosocial criminology, let’s consider the following two sentence pairs from Dr. Oubré’s article:

    “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.”

    “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].”

    The problem is that these two remarks belong to completely different language regimes. The first sentence of the first remark includes language from neurobiology and genetics; the second sentence comes out of psychiatry. So far, we have value-neutral language that has been validated through clinical research. This is standard scientific language describing a phenomenon of interest.
    The first sentence of the second remark comes out of the a collective of sociological and legal definitions, developed over years by psychiatrists, psychologists, social workers, sociologists, and politicians – Wait, politicians? How did they get in there? Well, because they’re the ones who, as elected legislators, enact laws determining what constitutes ‘criminal behavior,’ as well as the laws that fund mental health support organizations, and agencies for psychiatric (or related) monitoring of convicted transgressors of various laws. Because politicians are part of the process of developing this language, of course it cannot possibly be value-neutral! Their entire careers depend upon their ability to persuade their constituency that they represent that constituency’s values in determining the law. Of course they are going to want psychiatrists, psychologists, social workers, sociologists to provide behavioral definitions compatible with the values they claim to represent. And they get that from psychiatrists, et. al., not simply because the psychiatrists, et. al., have their own careers to worry about, but because they honestly think they can effect the law in a humane and progressive way by doing so. And let’s not be cynical about the politician either – he/ she may also sincerely share the values of the constituency she/he represents.
    The word in this sentence announcing the involvement of politics is “undesirable.” This cannot indicate anything other than a value judgement within a particular community. Gambling is considered a socially normative behavior in many cultures. While it may lead to obsessive behavior, this is hardly equatable with acts of violence. But it is sternly frowned upon in cultures with strong histories of conservative religious values.
    The second sentence of the second remark just gets us into more problems. It is recognizably the language of journalism, as it is used to report science to the public. As such it promises way too much, while eliding an enormous amount of knowledge concerning the history, economics, and politics of New Zealand. Genetics will “explain” a “divide in achievement and social outcomes”? History is irrelevant? Economics irrelevant? I don’t think so.
    Finally this sentence – and much of the article, curiously – makes the mistake of delineating one ethnic group that is presumed genetically homogenous, the Maori, apart from another ethnic group “white.” Are we to presume that the “white” ethnic group is also and equally homogenous? Are we to make no genetic distinctions between Italians and Swedes? Because we know such distinctions exist. People of eastern European descent are routinely classified “white” although they share many traits with west Asians, thanks to a long history of conquest and trade, resulting in intermarriage and tribal resettlement.
    Oh, Dr. Oubré does remark history, just before the sentences I’ve criticized: “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.” This sentence has questionable relevance; it seems to imply that the Maori have been violent long before the coming of “white” settlers. Unfortunately, warfare has been a central part of ALL traditional cultures, including those of Europe. This cannot implicate particularly violent tendencies embedded in the genetic development of any ethnic group, except to suggest that something in the genetic make up of ALL human beings tends toward responses leading to organized violence. That question has been raised, and is still (as far as I know) awaiting adequate answer; but it is a much more interesting question than the ones being asked by some of the researchers referenced in this article.

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  25. Excellent article. You have covered almost all areas (genes, epigenetics, and environment, etc.). But, seemingly Guo and Beaver did differently, and I have a problem with their procedure.

    Alondra Oubré: “In 2008, University of North Carolina sociologist Guang Guo and his colleagues found that antisocial behaviors in male youth were associated with three genes …searching for a still illusive genetic basis of criminal predispositions. … More recently, Beaver’s team has focused only on the 2R variant rather than the low-expression variants combined … to be involved in extreme violence — shooting and stabbing … Beaver’s sample of 133 African American men from the Add Health database included 6% …”

    Seemingly, they both are using a ‘single variable’ model, the ‘variable/data’ correlation. All single variable models presume that that single model is the total ‘cause’ for the data. It could be a fine tool for in-depth measurement of an already established model. But, I think that this issue is far away from being ‘established’.

    For the fact (data) of ‘shooting and stabbing’, a model can be constructed easily, with at least three parts (variables).

    Part one, gun or knife is readily available (GKA) for this data-‘point’. By all means, the GKA is not a comment situation. Thus, this situation is ‘acquired’ which can be the results of {gene effect (GE), association-gangs (AG), etc.}.

    Part two, the threshold of temper tantrum (TTT) is low. This can be the result of {GE, up-bringing (UB), AG, drug usage (DU), etc.}

    Part three, the cost for the action (CFA) is low. This can be the result of {the punishment is low (PL), something to lose (SL), etc.}. SL is definitely a result of a social factor and could be the determining factor as the ‘trigger’ for this data-point.

    There could be a lot more parts in this ‘shooting and stabbing’ data point. But, it at least consists of these three parts, and we can write a simple ‘function’ for this data point.

    F (shooting and stabbing) = F (part one, part two, part three)
    = F {Gene effect (GE), association-gang (AG), up-bringing (UB), drug usage (DU), punishment low (PL), something lose (SL)}

    For this multivariable function, one variable could over power the other variables. Just review a hypothetical case.

    One white man’s violent gene is 10 times more powerful than one black man’s but his SL is 100 times of that black man. So,
    F (shooting and stabbing, white man) = 0
    F (shooting and stabbing), black man) = 1

    If Guo and Beaver did not consider this kind of multivariable model, their works are not very useful.

    Coel: “The issue is whether it [epigenetics] is a radical departure from Darwinism.

    I think so, 100%.

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  26. ” But the fact that I didn’t go out of my way to stress it doesn’t even begin to mean that it is incompatible with the central thesis of The Selfish Gene. I can think of no reason why Dobbs should suggest such a thing, other than a journalistic desire to fabricate controversy where none exists. Which pretty much sums up his whole article.

    __________________________________

    Afterthought. After this was written, Steven Pinker sent an email commenting on Jerry Coyne’s article on the same theme. Steve said

    “Brilliant! This seems to be a congenital problem with science journalists — they think that it’s a profound and revolutionary discovery that genes are regulated, not stopping to think that the alternative would consist of every cell in the body synthesizing all 21,000 proteins around the clock. Part of the blame goes to molecular biologists, who hijacked the term “gene” for protein-coding sequences, confusing everyone.”

    I think this quote demonstrates nicely how important it is to the most prominent selfish gene advocates to accuse critics of dishonesty for personal gain. Bill Skaggs didn’t, which is much more polite.It is also much more prudent, since none of the parties is telepathic. Personally I am strongly impressed (in a bad way) by assertion that a science journalist like Dobbs could somehow benefit from being attacked by prominent scientists. That strikes me as blatant BS. That kind of bad faith argument makes me suspicious of the people who make it. But maybe that’s just me?

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  27. Extreme war is clearly driven by extreme history, not an extreme race somewhere. History clearly shows that, given peculiar psycho-historical cultural circumstances, extreme bellicosity will know no bounds. To believe genes give a plus seems superfluous.

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  28. I know this has sparked a fair number of responses quickly, so this may seem belated. But I can’t agree that the people who attacked Dobbs and other journalists and other scientists are deliberately falsifying their claims for personal benefit are just distressed over bragging.

    Also, I gave an example of another prominent popularizer, the very eminent Carl Zimmer, who never even suggested that genetic drift might have played a role in the evolution of human blood types. I don’t think most selfish gene advocates use the concepts of neutral evolution and genetic drift in their popularization, but merely give it lip service, lest they sound too extreme.

    Here’s the quote from Dawkins: “Bravo Jerry! Spot on, in every particular.

    I now groan audibly when a journalist (usually from continental Europe where they spend too much time learning philosophy rather than science) asks me the now inevitable ‘what about epigenetics?’ question. It is a real disease among science journalists, this unseemly eagerness to find something that enables them to say “Darwin was wrong” (New Scientist under Roger Highfield is a lamentable example). I am heartily sick of the ‘epigenetics’ bandwagon and almost look forward to the next one, whatever it turns out to be.

    Richard”

    No, I don’t think this justly expresses a properly proportional interest in epigenetics.

    Dawkins’ selfish gene isn’t Darwin, who lived before modern genetics. It’s not even the Modern Synthesis, which also came before Dawkins.. I do think that selfish gene popularization implicitly assumes genetic determinism. When the people sympathetic to that viewpoint see new discoveries interpreted as undermining genetic determinism, they react negatively. I think that the science is against them, which is why they tend to conflate their determinist version of gene selection with Darwin instead of Dawkins, or even identify gene selection with the DNA theory of heredity (I think Coyne is particularly bad for this,) then launch ad hominem attacks.

    Personally I think the gene (however defined) is indisputably the unit of heredity, but the primary unit of selection is the organism. I don’t think the gene is a replicator, which sounds to me like saying that a CF or DVD is the replicator instead of the computer that burn a copy. But maybe that’s just me?

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  29. Er, nice try, Coel. You didn’t check Freethought Blogs, where PZ had a more in-depth piece later. So, to you and Steven?

    I quote:

    I think they all miss the mark, and represent an attempt to shoehorn everything into an established, successful research program, without acknowledging any of the inadequacies of genetic reductionism.

    The “they” includes Dawkins and Coyne by name.

    http://freethoughtblogs.com/pharyngula/2013/12/07/the-reification-of-the-gene/

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  30. If anyone is interested, here is my professional take on epigenetic inheritance: http://philpapers.org/rec/RICWRD

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  31. Here’s more from PZ Myers’ comment: “I like to argue that what multigenerational epigenetic effects do is blur out or modulate the effects of genetic change over time, and it might mask out or highlight allelic variation, but ultimately, it’s all about the underlying genetic differences.”

    I’m sorry but to me masking or highlighting allelic variations means changing the power of gene selection, which does I think mean undermining the selfish gene version of evolution. And it also means that the effects of the same genes are variant, which isn’t as determinist as some would like genes to be. So, no, I don’t think PZ really agrees, however politic it might be for him to say so.

    PZ does say, and I agree, that “ultimately” hereditary differences are genetic. But I don’t know of anyone, not even scientific creationists, who disbelieve in DNA as storehouse of information. I think it’s disingenuous to imply that gene selection is the same thing as genetics.

    By the way, so far as the clarity of the differences in internal and external environments go, for me the selfish gene metaphor is uncomfortably close to claiming the environment of a library book is the other books on the shelf, but not the library.

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  32. Hi Socratic,
    Yeah, I read that article by PZ when it came out, and actually it isn’t really incompatible with anything Coyne or Dawkins were saying. Perhaps it was emphasising different things.

    That’s one of the problems, all of this genetic-expression and evolution stuff is so complicated that all articles about it are simplified and focus on only some aspects. It is therefore always possible for someone else to come and along and say, but hey, you’ve ignored such and such, and more emphasis should have been put on other complications, which are highly interesting, et cetera.

    By the way, I thought PZ’s “they” referred to comments he’d received on his previous piece, but I guess it can be interpreted either way.

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  33. According to Mr. Unsilenced Science, who does not have a website linked on his/her Twitter account, here’s who the author is:

    Damn Wikipedia troll! Screwed up author & anthropology PhD Alondra Oubré attempt to trash #MAOA research! Who’s next?

    Nice ….

    That said, per his blog, which he links?

    It seems we have a full-blown racialist, here. Massimo, I suggest you take a look at some of the more interesting posts at: http://theunsilencedscience.blogspot.com/

    And, that’s reinforced by his listing The Bell Curve as among his favorite books on his profile:

    https://www.blogger.com/profile/02461190919466049463

    I suggest anybody with brains not further feed the troll.

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  34. If you believe so fully in racialism, which it seems is what your “unsilenced science” is, and, per your Blogger profile, you work in the field of medicine, and you’re also on Research Blogging? Identify yourself, eh?

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  35. @Coel … that’s an “interesting” interpretation on the “they,” given that Dawkins and Coyne are mentioned two sentences earlier, in the same graf.

    I guess I’ll have to quote the whole first paragraph:

    Razib Khan poked me on twitter yesterday on the topic of David Dobbs’ controversial article, which I’ve already discussed (I liked it). I’m in the minority here; Jerry Coyne has two rebuttals, and Richard Dawkins himself has replied. There has also been a lot of pushback in the comments here. I think they all miss the mark, and represent an attempt to shoehorn everything into an established, successful research program, without acknowledging any of the inadequacies of genetic reductionism.

    Seems pretty clear to me that Coyne and Dawkins are part of the “They.” Did so when I first read it.

    I think that “they” can only be read otherwise if one is looking for proof that Myers has no real disagreement with Coyne and Dawkins on this issue,

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  36. I just wanted to thank you for your later post on this thread with the link to Myers’ “The reification of the gene.” This was actually much more what I was looking for when I first searched the discussions you referenced.

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  37. If he is wrong then address his facts. You are the one trolling here.

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  38. Hi Socratic,

    On the minor point, “they all miss the mark” can be taken as about “comments”, i.e.:

    There has also been a lot of pushback in the comments here. I think they all miss the mark …

    But, yes, it could also be taken your way. Anyhow, that is not important. The personalities don’t matter as much as the science. Too many people (including PZ, and indeed Dobbs) are too interested in emphasising differences with others, rather than getting at the truth of the matter.

    I’ve read PZ’s article (both when written and just now). Ditto for Coyne’s and Dawkins’s articles on Dobbs. Which aspects of the science in PZ’s article do you think that Coyne and others would not agree with, or would find inconsistent with what they wrote?

    Sure, there are differences of emphasis in the articles, and differences of which issues they talk about, but I’m struggling to see any actual fundamental differences in the biology.

    As I said, the biology of that stuff is so complicated that *all* accounts are simplified and deal with only some aspects of the topic. Thus, a reader can always come along and say: “you got it wrong, you’re oblivious to such-and-such complications, silly you”. To which a good reply can be “no I’m not, I just didn’t write about them”.

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  39. Reblogged this on Liam Uber's Blog and commented:
    Remember! We live in an ultra super-complex world. These little bits of information may or may not represent a clue to the real picture.

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  40. The nesting of posts is very confusing for me. If reposting a portion of another comment is a Bad Thing, I’m sorry, but I’m not sure I’m addressing everyone otherwise.

    PZ Myers also wrote: “I like to argue that what multigenerational epigenetic effects do is blur out or modulate the effects of genetic change over time, and it might mask out or highlight allelic variation, but ultimately, it’s all about the underlying genetic differences.”

    What I think is going on with the desperate need for ad hominem attacks is a discomfort with any work that claims to undermine the selfish gene view, which in popularizations is gene selection with genetic determinism assumed as default, beyond which the selfish gene popularizations rarely go. I don’t think anybody in recent years has ever argued that changes in the genetic information are not needed for permanent changes in the population’s phenotype. I think what people have at various times argued that changes in genes do not necessarily change a population’s phenotype; that you cannot use only gene sequences to explain development in an organism; that since genes do not determine the phenotype in the way selfish gene depicts, the intensity of gene selection is highly variable, which limits the power of selection to optimize the genome, which means organism may not be optimal; that natural selection of phenotypes can take place without significant selection of genes inasmuch as genes are not so deterministic that natural selection can actually see the genes to select them.

    If some people agree that none of these propositions means repudiating Darwin any more than the Modern Synthesis does, they are correct. But all these propositions do I think directly correct the popularized version of selfish gene/gene selection and the accompanying default of genetic determinism and panadaptationism.

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  41. First, certainly on Dobbs, tho perhaps not quite as much on PZ, I disagree that their primary angle is “emphasising differences with others, rather than getting at the truth of the matter.” Between that and saying “the biology of that stuff is so complicated,” that itself seems to be an attempt to avoid getting at the truth of the matter, or to avoid facing the fact that there are serious issues at play.

    I think PZ’s already made itself clear that he … well, he disagrees with Coyne et al being greedy reductionists. It’s a methodological agreement, and a serious one. I think that’s part of where Massimo comes from too.

    And, the issue of greedy reductionism is an issue, and an important one, in all sciences. And beyond sciences. It is, of course, what’s behind scientism.

    And, one could make the “ohh, it’s the Internet and everybody’s oversimplifying” about everthing this side of the full online corpus of Nature’s or Science’s websites, if one wanted to. The PZ link I presented was pretty long. The collective length of the subpieces on the Aeon link was pretty long.

    Speaking of, and greedy reductionism, Sapolsky’s piece there was spot-on. Dobbs still didn’t look at environmental issues enough.

    Anyway, this will likely be my last comment on this subthread. I think you’re coming at this from different presuppositional angles, etc., therefore wanting to interpret Dobbs, and supporters of the broader issues behind this, differently. I’ve said what I needed to, in a bit more depth in each response.

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  42. I want to add one more thing to @Coel. Since I mentioned on my previous comment that greedy reductionism ultimately leads to scientism, and now seeing that you have a “defending scientism” tab on your blog, I know we’re going to disagree on this issue, I know why, and I’m going to stop arguing more. Either on this thread, or on others in the future that veer in the direction of greedy reductionism or other scientism-related directions.

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  43. Steven,

    I’d been wondering whether to reply, since your comments tend to mash together a range of issues in a way that makes any succinct reply difficult. But:

    What I think is going on with the desperate need for ad hominem attacks is a discomfort with any work that claims to undermine the selfish gene view …

    For someone who writes the phrase “desperate need for ad hominem attacks”, you seem, in many of your comments, rather keen on being somewhat disparaging about some of the people you are talking about.

    which in popularizations is gene selection with genetic determinism assumed as default,

    Your use of the phrase “genetic determinism” has the whiff of a strawman about it. What do you mean by it? From wiki: “Genetic determinism is the belief that genes, along with environmental conditions, determine morphological and behavioral phenotypes.” Is that in line with your use of it?

    I think what people have at various times argued that changes in genes do not necessarily change a population’s phenotype;

    Well obviously. No-one would disagree.

    … that you cannot use only gene sequences to explain development in an organism;

    Well obviously. No-one would disagree.

    that since genes do not determine the phenotype in the way selfish gene depicts, …

    My straw-man-alert detector has just gone off again. What do you think that the selfish-gene model says about this?

    the intensity of gene selection is highly variable, …

    Well obviously. No-one would disagree.

    which limits the power of selection to optimize the genome, …

    Who said it would “optimize” the genome? This sounds like a dubious concept anyhow. Optimize for what? The good of the animal? The good of the gene? Most people accept the presence of lots of “junk” (which is still the case, despite ENCODE etc).

    … which means organism may not be optimal; …

    Who said the organism would be optimal? And optimal according to what metric? And if you’re getting at selfish genery, why would you expect the *organism* to be “optimal”?

    that natural selection of phenotypes can take place without significant selection of genes inasmuch as genes are not so deterministic that natural selection can actually see the genes to select them.

    Again, if you’re using “genetic determinism” in the above quoted sense, so that genes+environment produce a phenotype, then natural selection can indeed “see” the genes.

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  44. I did address his facts. I said he’s a racialist for how and why he’s wrong, and pointed to his blog for specific evidence of that.

    Given your link to the Morgan/Wright piece on your Twitter feed ( http://t.co/2fneBEXJjO ) I can understand why you might not like my original response. That’s your problem, not mine.

    As is the racialist background of Wright: http://news.google.com/newspapers?nid=1298&dat=19961114&id=yekyAAAAIBAJ&sjid=zwcGAAAAIBAJ&pg=5977,2486077

    If you give a favorable hat tip, at least, toward some type of racialism, or racialism-lite, yourself? Which, since I also looked at who you Tweeted that link to, seems to be the case?

    DO NOT call me a troll for pointing that out.

    And, I won’t “feed” you any more, either.

    Why don’t all you seeming racialists at least do the rest of us a favor of saying in your first post exactly where you’re coming from, rather than making others take a few minutes of Googling when we’re going to find that out, from that Googling, anyway?

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  45. Hi Socratic,

    I think PZ’s already made itself clear that he … well, he disagrees with Coyne et al being greedy reductionists.

    Well does he? That’s just “commentary”, but it is not pointing to an actual issue of biology on which PZ’s and Coyne’s articles differ.

    I’ll quote a commentator from the PZ thread: “I read PZ’s original take and this latest and agreed with it. Then I went and read Coyne’s take and agreed with that too. Then I went back and read Dobbs’s piece and found it mostly without merit. I think that’s the real problem. Dobbs bends over backwards to be contrarian and hypes ideas that are neither new nor earth-shattering.”

    And then: “To get to the point, a gene-centric view and appreciating the complexity of gene expression and phenotype are not mutually exclusive.”

    And, the issue of greedy reductionism is an issue …

    So now elucidate an example of where Coyne is wrong. Not by vague claims that he is a “greedy reductionist”, but by actually quoting something that he has said about biology and then arguing that it is wrong.

    Like the above commenter, I read both Coyne’s and PZ’s articles and can agree with all of the biology in both of them.

    I’m not an expert in biology, so may be misunderstanding or overlooking things, but if so please point it out, in terms of actual discussion of the biology. Simply labelling something “greedy reductionism” is not a demonstration of error.

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  46. I’m sorry, I give up on tracing the nesting.

    Coel, I always feel I should at least answer direct questions. But I’ve given several quotes with Coyne, Pinker and Dawkins’ direct personal assaults. If you can only respond that “you seem, in many of your comments, rather keen on being somewhat disparaging about some of the people you are talking about,” I can only think that you are not going to heed any facts, answers or take any questions seriously.

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  47. Steven,

    If you can only respond that “you seem, in many of your comments, rather keen on being somewhat disparaging about some of the people you are talking about,” I can only think that …

    Well that’s how it seems to me. You are repeatedly accusing people essentially of intellectual dishonesty, in defending what you see as outdated views by “reacting badly” and “bad faith arguments” and saying that “the desperate need for ad hominem attacks is a discomfort with any work that …”. What you’re saying about them is thus essentially a disparaging attack on them.

    It also seems to me (see previous reply, though again I admit that I’m not an expert on biology so could be wrong) that your criticisms are a somewhat confused mash of misunderstandings of various concepts.

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  48. Okay, people, at this point just a little reminder to play nice and constructive, or the Editor’s Filter will have to see some action…

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