Sunday, December 30, 2012

Scientists Rediscover the Violence Gene, MAOA-2R



“It’s estimated that a third of all men carry what’s been called the warrior gene.”

— Dr. Phil

“There were three genes, as you mentioned. Call them violence genes. Call them bad-behavior genes. But what they found was that if people had these genes, they’re much more likely to be violent. There were certain triggers, as well: stress, family problems, low popularity, failing in school. To take it a step further, Karen, they sort of predict that about one percent of the population has these genes.”

— Dr. Sanjay Gupta, CNN

Both of these men are wrong, and both are referring to the same gene, monoamine oxidase A (MAOA). Roughly a third of white men inherit the 3-repeat allele of MAOA (MAOA-3R), which has received considerable research attention for influencing aggression. However, every other group, particularly African Americans, reach much higher allele frequencies, making MAOA-3R the most common version of the gene. Gupta was referring to a study of three potential violence-causing genes. One was the heterozygous pairing of ANKK1’s Taq1A allele (once thought to belong to DRD2), found in 37% of the subjects. Another was DAT1’s 10-repeat allele, found in 95% of the subjects. However, the strongest association with violence occurred in the third gene, MAOA, specifically the 2-repeat allele (MAOA-2R) found in that one percent that Gupta mentioned. I previously documented how this especially violent version of “the warrior gene” can be found much more commonly in African-American men than white or Asian men. Recently, an unusual study filled in some knowledge gaps about this highly understudied allele, specifically its effect on African-American men.

One unusual aspect of this study, Beaver et al, is that it essentially reexamined the exact same data as Guo et al, the study Gupta mentioned. The latter actually coincided with another study, also led by Guang Guo, on MAOA-2R in 2008 that determined that the allele doubles the rate of serious and violent delinquency. The impact most affected those aged twelve to fifteen, more than tripling the violent delinquency score based on eight questions. All three papers obtained their data from the National Longitudinal Study of Adolescent Health that totaled about 20,000 participants. However, only a seventh of that sample provided DNA, and Beaver et al focused on as few as eight black men for some of its findings.


That number might induce a healthy skepticism, but one should recall that this is not some newly discovered point mutation obtained in a “fishing expedition” bound for the annals of false positives. This gene produces an extremely important neurotransmitter enzyme that became the target of the first antidepressants in the 1950s. In the 1970s, studies linked its metabolites to aggression. In the late 80s, Hans Brunner discovered and became the eponym for a syndrome of violence resultant from complete deactivation of MAOA. His initial study included only five instances out of a family history of fourteen possible cases. Follow-up research increased the total subjects to nine from this single family. However, other researchers were able to induce Brunner syndrome in mice and eventually to discover such knockout-allele mice in a spontaneous form. Of course, a 2002 study instigated a tremendous amount of research on the gene-environment interaction, in which MAOA-3R coupled with the experience of child abuse triggers aggressive tendencies. The number of the “repeats” in the allele refers to the length of the more studied of the two promoters of the gene, and so those repeats can represent, to some extent, discrete levels of the enzyme’s dosage. In fact, the Guo et al 2008 study in the European Journal of Human Genetics included an in-vitro functional analysis of MAOA in human brain-tumor cells. MAOA-2R was less active than MAOA-3R, which was less active than MAOA-4R, the most common version in white people. MAOA-4R was more than three times as active as MAOA-2R.

I shall now briefly detail the sample characteristics that each of the three studies examined in order to ascertain how common MAOA-2R is in white and African-American men. Beaver et al claimed that the overall sample consisted of 2574 individuals, though Guo et al claimed a sample of 2524, including 1200 men. If Beaver et al was in error, then they have consistently repeated the error in other papers. In American Sociological Review, Guo et al only included 1111 men who met that study’s requirements, but both 2008 papers show that only eleven men had the 2R allele, and this study actually provided a racial breakdown of the sample: 60% white, 17% African American, 15% Hispanic American, and 8% Asian. The full genotyped Add Health male population is 57% white, which is 680 men. Beaver et al has listed 174 African-American men. Thus, nine black men by interviewer-assessed race (5.2%) or ten by self-reported race (5.5%) had the 2R allele. Beaver et al revealed that only 0.1% of white males had the 2R allele, which would equal just one man out of 680. That probably leaves none for Asians and Hispanics.

These numbers roughly correspond to other studies but suggest that I might have been too generous to African-American men in suggesting that they are only ten times more likely to have this especially dangerous version of MAOA. Reti et al previously genotyped a sample of 618 men and women who were 59% white and 38% African American. That study did not use a purely random sample. Seventy-five percent of that group received psychiatric evaluation within the Hopkins Epidemiology of Personality Disorders Study. That sample included 224 men and 391 women (with apparently three individuals missing possibly from rounding). Assuming both the black people and white people are 64% female, only three alleles out of 595 would have been 2-repeat alleles for white people. Eighteen of 377 would have been 2R for black people. Only about one white man out of possibly 133 would have been likely to have it, if even that, compared to four out of 85 black men. Likewise, Caspi et al in 2002 found one man with the 2R allele out of 499 white males. The trend seems to be that only a token white man in each study has this rare allele. Therefore, to say that the prevalence in whites is higher than Asians is sketchy. Since the new Beaver et al study uses a more random sample than Reti et al, and its white-male 2R prevalence is in closer agreement with Caspi et al than Reti et al, I suspect that this allele is closer to 50 times more common in black men than white men rather than 10 times, as I previously wrote.

Most research on MAOA compares MAOA-3R to MAOA-4R in white males with token instances of MAOA-2R thrown in with MAOA-3R under the label “MAOA-L.” So, these studies are made more shocking by the lumping of “the warrior gene,” MAOA-3R, together with the high-activity allele, MAOA-4R, as the non-violent versions of the gene. The astounding results speak for themselves. Beaver et al found that the ten black men who possessed MAOA-2R had triple the risk of incarceration and almost quadruple their risk of arrest, (accounting for 8.6% of the arrested and 9.5% of the incarcerated). A sample of only eight black men with MAOA-2R out of 130 black men had a statistically significant increased risk of self-reported violence. Scientists have tried to ameliorate the politically unpalatable nature of violence-gene research by emphasizing the environmental trigger for aggression with MAOA-3R, but the findings of Beaver et al and Guo et al did not depend on any environmental trigger. Beaver et al asserted that “the low base-rate of 2-repeat allele carriers prevented an exploration of gene-environment interaction…” However, Guo et al went right ahead and also tested for an interaction between MAOA-2R and being held back a grade in school and three questions regarding feelings of school attachment. The gene’s interaction increased violent delinquency 21 times as much as grade retention alone and seven times as much as school attachment alone.

Given that the men with MAOA-2R in the National Longitudinal Study of Adolescent Health are ten African Americans and one white, I doubt the effectiveness of the regression analysis adjustment for race and ethnicity claimed by Guo et al. Put another way, 91% of the exposed cohort come from a racial group that is 13% of all Americans. Their studies should have laid bare this fact. Beaver et al limited their analysis to the black men, but even that raises concerns of population stratification because African Americans are a mixed population, averaging 22% European ancestry. Africa, itself, has produced no MAOA research, (but it did copy a sensational National Geographic documentary on MAOA). If MAOA-2R is so closely associated with African ancestry, then it could serve as a proxy for having more African alleles. Of course, this logic never stopped any of the other research on African Americans, and the implication that multiple other African violence alleles confound this association does not fit the mold of politically correct impugnment usually directed at MAOA research.



Part of my fascination with the sparse research on MAOA-2R comes from my belief that scientists have inadvertently underplayed the true power of this gene. Comparing the two most common versions of MAOA requires less effort and funding, and emphasizing an environmental trigger, like child abuse, varnishes genetics research with a politically correct gloss. However, the trigger for MAOA-3R quickly multiplied to include testosterone levels, maternal smoking, IQ, education, and socio-economic status. Some of those “environmental” factors actually have a dominant hereditary influence. Now, studies have triggered aggression in MAOA-3R men with much more immediate experimental adversities in the form of game unfairness. Furthermore, people like Dr. Phil assume that a gene-environment interaction is synonymous with a “genetic predisposition,” but the “non-active” allele actually appears to play a protective role that negates an environmental trigger’s impact. For instance, low IQ does not increase violent tendencies in men with MAOA-4R, but it does in men with MAOA-3R.

Incidentally, Steven Pinker’s latest book addressed the Flynn Effect. “If smarter people and smarter societies are less likely to be violent, then perhaps the recent rise in intelligence can help explain the recent decline of violence.” However, a hypothesis of much longer-term IQ decline has recently ridden a wave of genetic-load angst, so allow me to point out the tension between these competing paradigms as a challenge to Pinker’s broader thesis. The complex associations between intelligence, executive function, and aggression might have also drawn in olfaction research. Both judgment and the ability to discern smells localize to the frontal lobes, and research has linked poor olfactory acuity to aggression. As with MAOA allele frequencies, racial disparities exist for odor identification.

Since Brunner syndrome and MAOA-2R seem to have a “main effect” without an environmental trigger, I see the MAOA-3R gene-environment interaction as a penumbra of the possible enzymatic effects. In an entire population, the prevalence of violence must have a specific total MAOA component that would consist of all of the MAOA variants (including potential epigenetic effects, SNPs, and both VNTR promoters, only one of which is the subject of most “warrior gene” research) and each variant’s potential when unlocked by all possible environmental triggers. Even with enormous samples, whole-genome studies are capable of studying a tiny fraction of this genetic potential. Similarly, quantitative genetics research, like twins studies, underestimates heritability when some large genetic effects are unlocked by environmental stimuli, as opposed to a merely additive nature-nurture relationship. Terrie Moffitt and Avshalom Caspi, who spearheaded early gene-environment research, wrote an extended analysis of this approach with Michael Rutter. “For understanding the influence of such conditional-effect genes, large samples may be less necessary than strategic [gene-environment interaction] research.”

Rather than use the penumbra of gene-environment interactions to appreciate the extensiveness of a gene’s effect, scientists like Moffitt, Caspi, and Rutter seek to dispel genetic “determinism.” Citing a two-hour student protest of a scientific conference on the genetics of violence, they explained, “Ethicists attribute the root of the public’s concern about genes to a pervasive belief in the power of genetic determinism: ‘ … genetic determinism implies that knowing a person’s genetic makeup is tantamount to knowing his or her future.’” If the public detests genetic determinism due to its unyielding quality, then surely such people would rather seek methods to circumnavigate genetic fate than to simply disacknowledge the power of heredity. However, Moffitt et al wish for the opposite: “Concrete data needed to counter genetic determinism are provided by new [gene-environment interaction] findings…. Such understanding should make eugenics and other misuses of genetic information much more difficult.” This discussion calls for a debate over both the feasibility and the ethics of changes to environmental triggers, like poverty, versus those of the ill-defined “misuses” of genetic knowledge. Presumably hypothetical therapeutic drugs and diagnostic tests for violent tendencies would not necessarily misuse the research, and the solutions to poverty and educational failure are not just around the corner.


Obviously, many scientists and activists who oppose genetic determinism believe in a greater role for nurture or even blank-slate nurture determinism, but they wish to leverage the masses, who ascribe behavior to supernatural “free will.” To qualify as deterministic, must genetic aggressivity present itself constantly? Though MAOA has no activity in Brunner syndrome, the subjects need not reside in cages, gnawing on the bars. Most men with the MAOA knockout allele are afflicted with conduct disorder and “conflict with the law” during their lifetime. A provocation of some sort might set off aggression, but minor provocations exist in the lives of all people, so Brunner syndrome should still qualify as deterministic. Whether the existence of such determinism is “nice” or not has no bearing on its existence, so do not mistake denial for virtue.

Wickedpedia

I might have missed the recent Beaver et al study, if others had not pointed it out to me. Unlike most MAOA research, it did not surface in the PubMed database. I think that is true of all studies from the Journal of Personality and Individual Differences of the London School of Differential Psychology. Some of the journal’s board members, including recently deceased Arthur Jensen, received the label “scientific racist” from certain activists. So, Kevin Beaver refused to submit to an interview for this blog, but he saw fit to publish in a journal that recently reviewed research on penis length and circumference differences among “Negroids,” “Caucasoids,” and “Mongoloids.” A year ago, I was able to send him a list of questions, in which I confronted him for conflating MAOA-2R and MAOA-3R as “MAOA-L.” He told me that a study on MAOA-2R was “in the pipeline.” However, I would like to think that I inspired the study, and I find it jarring that four years could pass without any research on MAOA-2R and violence.

Is anyone following this research as well as I am? Many professions fight “turf wars.” This occurs among medical professionals and physician specialties. Study of MAOA and violence likens less to competition over a lucrative procedure and more to a game of “hot potato.” Violence, itself, does not have a dedicated category in the Diagnostic and Statistical Manual of Mental Disorders. Though psychiatrists have contributed some research, it seems that psychologists and criminologists like Beaver have taken the lead usually with low-cost data mining from databases like the National Longitudinal Study of Adolescent Health.

Meanwhile, public attention to the gene increasingly falls to self-appointed experts and “ethicists,” who cannot even report some very basic facts about the gene correctly. Pseudointellectuals are claiming that “most if not all of this literature [on MAOA] is wrong, and [sic] will soon be forgotten” and that a “single molecule” like serotonin or dopamine cannot explain “complex behavior.” When Scientologists mouth these stupid ideas, most people roll their eyes, but now the same ideas are coming from “science reporters” and Harvard professors. Therefore, I decided to take the drastic measure of addressing what I think might be the source of the problem by editing Wikipedia. Before I started editing the Wikipedia pages for Brunner syndrome and MAOA, activists had peppered them with qualifications that the evidence was “flawed” or “controversial” or that the emerging field of epigenetics made the gene’s effects “hard to predict.” Apparently, methyl moieties escape the rule that a single type of molecule cannot determine a complex behavior. Never mind studies that show the epigenetics of MAOA in men is minimal, low in variance, and high in hereditary influence. Of course, it is never enough to simply edit a fix into a Wikipedia page. First, one makes the edit. Then, one reapplies the edit repeatedly after activists try to undo one’s work. Finally, one replies to the activist on one’s personal “talk” page when the activist threatens to undo one’s work again unless one attaches to an email the study that proves the activist’s sacred belief is based on a copy-and-paste error. A stronger commitment predicates some Wikipedia myths than that of many a marriage.

Some are rightfully criticizing this research and candidate-gene behavioral genetics, in general, because small sample sizes can cause false positives by measure of statistical significance. However, since no other approach is capable of studying VNTRs like MAOA, the only current solution would be to fund the research more rather than to advocate censorship of the research that is being done. Rarely do I hear similar criticism of functional magnetic resonance imaging (fMRI) research, which tends to have small samples due to the expense of the imaging but makes up for it with pretty color explosions on brain maps. When I worked with fMRI, I thought that the arbitrary threshold settings that defined the “areas of increased activity” added an extra layer of bias. Perhaps the Harvard establishment has singled out behavioral genetics for rebuke in order to centralize the potential for offensive findings and to avoid “misuse.”

Congratulations! You Have Cancer!

The study of MAOA has received a beautiful gift—the gift of cancer. One might recall the fad cureall and supplier of immortality known as antioxidants. Antioxidants are supposed to save cells by counteracting free radicals. However, too much of a good thing like cell survival is cancer. MAOA deserves to be called the “warrior gene” because it makes oxidases that slay cancer cells. Malorni et al first discovered this in 1998 when the MAOA-inhibiting drug, clorgyline, saved melanoma cells, in vitro. Ten years later, Alpini et al concluded that epigenetic effects on the MAOA VNTR could explain its lower enzyme levels in cholangiocarcinoma, cancer of the liver bile ducts. Now, Huang et al has determined that higher MAOA expression decreased the risk of metastasis and improved prognosis and survival in patients with cholangiocarcinoma. Though the decline in MAOA expression seemed mostly limited to the areas of malignancy, I have found some online family-member portrayals of men with the disease becoming “distant,” “difficult,” “angry,” “grumpy,” “horrible,” and “mean,” in some cases prior to diagnosis.


This calls for drugs that increase MAOA levels, and maybe the resulting therapies could metastasize to psychiatric uses. A few contestants already have records of accomplishment. Doctors sometimes use risperidone, an older-generation antipsychotic, to treat impulsive aggression. In fact, Tuinier et al detailed a case report of a Brunner syndrome patient who successfully responded for a time to risperidone. Nevertheless, the drug has serious adverse reactions, causing many patients to gain weight, and a small percentage develop permanent tardive dyskinesia, involuntary movements often of the lips. Tetrabenazine and ketanserin reduced aggression in MAOA-knockout mice. Tetrabenazine is used to treat chorea, the involuntary movements of Huntington’s disease. The FDA granted it official orphan-drug status in 2008, but it is incredibly expensive for Americans to use. Ketanserin has applications for high blood pressure, but it is unavailable in the US.

Maybe this cancer research could save MAOA from its “controversial” reputation. Harvard professors might hesitate to dismiss a violence gene that became a cancer gene. After all, lives are at stake.



ResearchBlogging.org






Alpini G, Invernizzi P, Gaudio E, Venter J, Kopriva S, Bernuzzi F, Onori P, Franchitto A, Coufal M, Frampton G, Alvaro D, Lee SP, Marzioni M, Benedetti A, & DeMorrow S (2008). Serotonin metabolism is dysregulated in cholangiocarcinoma, which has implications for tumor growth. Cancer research, 68 (22), 9184-93 PMID: 19010890

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

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

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

Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, Taylor A, & Poulton R (2002). Role of genotype in the cycle of violence in maltreated children. Science (New York, N.Y.), 297 (5582), 851-4 PMID: 12161658

Crabtree, G. (2013). Our fragile intellect. Part II Trends in Genetics, 29 (1), 3-5 DOI: 10.1016/j.tig.2012.10.003

Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA (2012). Moderating role of the MAOA genotype in antisocial behaviour. The British journal of psychiatry : the journal of mental science, 200 (2), 116-23 PMID: 22297589

Gallardo-Pujol D, Andrés-Pueyo A, & Maydeu-Olivares A (2012). MAOA genotype, social exclusion and aggression: an experimental test of a gene-environment interaction. Genes, brain, and behavior PMID: 23067570

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

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

Huang L, Frampton G, Rao A, Zhang KS, Chen W, Lai JM, Yin XY, Walker K, Culbreath B, Leyva-Illades D, Quinn M, McMillin M, Bradley M, Liang LJ, & DeMorrow S (2012). Monoamine oxidase A expression is suppressed in human cholangiocarcinoma via coordinated epigenetic and IL-6-driven events. Laboratory investigation; a journal of technical methods and pathology, 92 (10), 1451-60 PMID: 22906985

Jones, R., Brown, C., & Ship, J. (1995). Odor identification in young and elderly African-Americans and Caucasians Special Care in Dentistry, 15 (4), 138-143 DOI: 10.1111/j.1754-4505.1995.tb00501.x

Mahmut, M., & Stevenson, R. (2012). Olfactory Abilities and Psychopathy: Higher Psychopathy Scores Are Associated with Poorer Odor Discrimination and Identification Chemosensory Perception, 5 (3-4), 300-307 DOI: 10.1007/s12078-012-9135-7

Malorni W, Giammarioli AM, Matarrese P, Pietrangeli P, Agostinelli E, Ciaccio A, Grassilli E, & Mondovi B (1998). Protection against apoptosis by monoamine oxidase A inhibitors. FEBS letters, 426 (1), 155-9 PMID: 9598998

McDermott R, Tingley D, Cowden J, Frazzetto G, & Johnson DD (2009). Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation. Proceedings of the National Academy of Sciences of the United States of America, 106 (7), 2118-23 PMID: 19168625

Moffitt, T., Caspi, A., & Rutter, M. (2006). Measured Gene-Environment Interactions in Psychopathology. Concepts, Research Strategies, and Implications for Research, Intervention, and Public Understanding of Genetics Perspectives on Psychological Science, 1 (1), 5-27 DOI: 10.1111/j.1745-6916.2006.00002.x

Murphy SM, Puwanant A, Griggs RC, & Consortium for Clinical Investigations of Neurological Channelopathies (CINCH) and Inherited Neuropathies Consortium (INC) Consortia of the Rare Disease Clinical Research Network (2012). Unintended effects of orphan product designation for rare neurological diseases. Annals of neurology, 72 (4), 481-90 PMID: 23109143

Pietrangeli, P. (2004). Amine Oxidases and Tumors NeuroToxicology, 25 (1-2), 317-324 DOI: 10.1016/S0161-813X(03)00109-8

Reti IM, Xu JZ, Yanofski J, McKibben J, Uhart M, Cheng YJ, Zandi P, Bienvenu OJ, Samuels J, Willour V, Kasch-Semenza L, Costa P, Bandeen-Roche K, Eaton WW, & Nestadt G (2011). Monoamine oxidase A regulates antisocial personality in whites with no history of physical abuse. Comprehensive psychiatry, 52 (2), 188-94 PMID: 21295226

Roush, W. (1995). Conflict marks crime conference Science, 269 (5232), 1808-1809 DOI: 10.1126/science.7569909

Scott, A., Bortolato, M., Chen, K., & Shih, J. (2008). Novel monoamine oxidase A knock out mice with human-like spontaneous mutation NeuroReport, 19 (7), 739-743 DOI: 10.1097/WNR.0b013e3282fd6e88

Shih JC, Ridd MJ, Chen K, Meehan WP, Kung MP, Seif I, & De Maeyer E (1999). Ketanserin and tetrabenazine abolish aggression in mice lacking monoamine oxidase A. Brain research, 835 (2), 104-12 PMID: 10415365

Sjöberg, R., Ducci, F., Barr, C., Newman, T., Dell'Osso, L., Virkkunen, M., & Goldman, D. (2007). A Non-Additive Interaction of a Functional MAO-A VNTR and Testosterone Predicts Antisocial Behavior Neuropsychopharmacology, 33 (2), 425-430 DOI: 10.1038/sj.npp.1301417

Tuinier S, Verhoeven WMA, Scherders MJWT, Fekkes D, & Pepplinkhuizen L (1995). Neuropsychiatric and biological characteristics of X-linked MAOA deficiency syndrome: A single-intervention case study. New Trends in Experimental and Clinical Psychiatry, 11 (4), 99-107

Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, Moffitt TE, & Mill J (2010). A longitudinal study of epigenetic variation in twins. Epigenetics : official journal of the DNA Methylation Society, 5 (6), 516-26 PMID: 20505345

18 comments:

Anonymous said...

And Greg Cochran had this to say about Epigentics

Anonymous said...

"If MAOA-2R is so closely associated with African ancestry"

I don't think it is. I think it's been bred out in other populations and this breeding out is the underlying cause of hence Pinker's violence graphs.

African slaves were taken from populations who were still in the Pre-Pinker stage of endemic tribal warfare where genes like MAOA are adaptive i.e. the fiercest men (if they survive) have the most kids.

.
"The trend seems to be that only a token white man in each study has this rare allele."

If it has been bred out you'll find it in higher quantities among blue-collar men (as a certain level of violence isn't that big a problem) and especially among cops and soldiers. I'd say cops who volunteer for the worst gangbanger districts are likely to have it in very high proportions imo.

nb If it has been bred out over centuries then logically it would survive best in families where it's paired with genes which give high levels of self control as well - hence the cop thing and cop families.

.
"Scientists have tried to ameliorate the politically unpalatable nature of violence-gene research by emphasizing the environmental trigger for aggression with MAOA-3R"

In that regard it's its own environment really because the presence of large amounts of it in a population - in its uncontrolled form - guarantees high levels of beatings and rape from adults.

Devin Rogers said...

Too many blogs and bullshit about nothing. The proof (truth) is in the pudding. When we educated the primal inferior human, we were warned. A small frontal lobe structure is proven in the African human. If you teach a dog to talk, he may bite you in words. Unfortunately even Einstein warned about capitalization of other sub cultures. He said "leave them alone". Now we are faced with an embarrassment and we have to pretend they are equal.

Anonymous said...

I forgot to add to my earlier post judging purely by the behavioral hints given in the reporting of this gene i don't think MAOA is a violence gene exactly i think it's a lethality gene.

In very violent gangbanger type environments you can get at one extreme people who get involved in violent altercations 2-3 times a day but those altercations involve escalation: words, pushing, fists etc, and are almost never lethal except by accident. At the other extreme you get individuals who might only get involved in a violent altercation once every six months but they *always* end in at least hospitalization.

So two separate components with proneness to violence being one and lethality being the second, leading to four combinations:

1) non-violent and non-lethal
2) non-violent and lethal
3) violent and non-lethal
4) violent and lethal

So imagine a population that over centuries is breeding out violence genes a la Pinker's graphs. The selection is strongest on the group who are both violent and lethal, less strong on those who are violent but non-lethal and weak on those who are non-violent even if they are also theoretically lethal).

So populations who go through the pacifying process will go through distinct stages e.g.

1)
- many fewer violent and lethal
- fewer but still substantial numbers of violent but non-lethal
- substantial numbers of non-violent but lethal

2)
- very few violent and lethal
- few violent but non-lethal
- fewer but still substantial numbers of non-violent but lethal

3)
- very few violent and lethal
- very few violent but non-lethal
- very few non-violent but lethal

Those populations which haven't gone through this process - or to the same extent - will still contain lots of individuals who have the impulsive form of lethality - which (imo) is the cause of the much higher black homicide rate.

Europeans still have quite a large amount of propensity to violence genes but mostly concentrated in the bluecollar population and also (imo) quite high levels of the lethal gene *but* mostly combined in the non-violent (i.e. self-controlled) form because that's the only way it could survive the breeding out process.

Hence why if you pick a multipally self-selected group like: military
to cop to volunteer in the worst districts, you should find very high concentrations of this gene imo - i wouldn't be surprised at anything up to 20-40%.

Anonymous said...

Ugh, forgot a critical point,

The lethal "type" - which i think may be connected to MAOA - don't escalate from words to pushing to fists etc. They go from neutral to lethal instantly and in one step.

That's the big difference.

Dexter Whimsley said...

Violence Genes are ludicrous. They are racially bias and arbitrarily ascribed. Why is it that most of the violence on the entire Planet is perpetrated by White men?? Yet this study shows it is more prevalent in African Males. racist studies produce racist results.

Anonymous said...

The comment above mine has shined so much light on these studies. Why should we be studying genetics at all if it only tells us racist facts? These "hate facts" have no place in our body of knowledge.

Felix Lanzalaco said...

I respect your rigor in sifting through the scientific errors and dealing with the dismissive political bias which must be frustrating in the extreme. We also face this same problem in gender – cognition differences research, and the area was closed down only to be re-opened when it was found we need gender specific profile for early detection in most neurological conditions. Also latterly similar problems occur in an area called neuro-poitics.

However can the author of this blog apply the same self rigor to his aims and plans for this line of inquiry ? i.e. What is the point ? We cant have a situation where the public latches onto this type of information because humans have a history of mis-using this type of information and demonizing entire groups with no exceptions allowed. Reversion to tribalism in an increasingly small world is not a wise option. What we do is proceed with enforcing the criminal justice situation for violent crimes. Over the long term Jails do curtail the numbers of any given dysfunctional population. It may be a slow process, but its far better than any alternatives.. unless you have some ideas that are reasonable. All I hear is a lot of complaining and no solution.

Why is that…are your solutions unpalatable? Maybe these dismissive scientists are more afraid of your approach…have you considered there might be some intelligence to their dismissal. i.e. They feel responsible to not allow fuel for mob racial mentality.. or do you think they are liberal sheep.. in the mindless sense ? They would still ask you the same question as me…whats your solution? If you dont offer any reasonable solution, then this blog is interesting, but ultimately it will go nowhere.

nooffensebut said...

I agree that we should resist “mob mentality.” Although the paradigm of “white male patriarchy” might actually reduce tribalism, just as people like Steven Pinker have argued that Western empires contained less violence than the state of affairs that replaced them. As white majorities recede in places like the United States, ethnic rivalries and tensions might develop greater complexity and intensity.

It is not clear why you think I lack palatable solutions, since you are commenting on a post with extensive discussion of drug therapies for low MAOA levels. Even if no gold-standard treatment comes to fruition, a single-gene explanation for a significant component to society’s violence leaves open an option of pre-implantation genetic diagnosis with embryo selection or CRISPR genetic engineering. Such an approach might be less expensive and more humane for a select population of willing female carriers of MAOA-2R, whom could be discovered with free diagnostic testing for women of African descent, than the alternative that you suggest, continuing to rely on the criminal justice system after violence is already committed, or the typical liberal approach, lip service for poverty reduction. Just improving the diagnosis of violence predisposition could lead to better uses of preventive interventions to help young men who are at-risk. In fact, I would argue that liberal resistance to this science is an unintentional form of racial genocide against African Americans.

Since I speak of allele frequencies, I obviously do not engage in “demonizing entire groups with no exceptions allowed.” However, my writing on this subject might be relevant to “stereotypes” or common fears that some people have of men of African descent. I did not invent these perceptions and do not deserve substantial blame for their existence. However, I think the greatest beauty of science is its ability to project the light of reason upon mysterious or taboo phenomena.

Lanzalaco said...

"nooffensebut said..."It is not clear why you think I lack palatable solutions, since you are commenting on a post with extensive discussion of drug therapies for low MAOA levels"

these drugs you mentioned cant be used for behaviour modification as the side effects are too diverse and extreme, putting them in the use for physical illness as a lesser of evils category. I mean we think SSRI and Ritalin etc are bad.. These are way beyond that scale because once you have an excess of amines there are just way too many interactions to deal with. It easier to treat for overactive MAOA as that’s controlling the tap upstream before the system gets a “hot shower”. If it does turn out there is a single gene fix, and we can be sure about that, then that is something to look at and save a bit of suffering as the gene is not adaptive anymore.. The world is too small and socialized now.

get the impression here this website has aspects of white supremacy? I mean you replied here with “white male patriarchy” at the start and end with marking out black men and women for modern eugenics. A country that votes for a black president, and increasing representation of black people in politics and celebrity status is never going to allow this ? so again I don’t get the point of all this work as that line of thinking cant come to any fruition..i.e. You can only make a case for 2R eugenics in general.

nooffensebut said...

I think you are incorrectly assuming that visitors to my blog are illiterate because you equate my suggestion that “willing female carriers” might choose to exercise their reproductive rights to prevent transmission of this or, presumably, other disease-causing genes to their children with “marking out black men and women for modern eugenics.” Eugenics was a practice of forcibly sterilizing people just for scoring a little below average on IQ tests. It is not racist for doctors or epidemiologists to consider a racial group as a possible risk factor, as with sickle cell anemia or cystic fibrosis. This is a rare gene in people without African ancestry. I categorically reject white supremacy, and I have a history of making white supremacists very angry at me. Being politically incorrect in defense of science is a matter of necessity, and I’ll say again that using political correctness to suppress science that will help African Americans more than other people is a form of racial genocide against African Americans.

Of course, clinicians must consider therapeutic ratio when prescribing treatments, but the presence of adverse reactions does not necessarily preclude drug approval. Anti-psychotics have horrible adverse reactions, some of which cause permanent disability, but they are still a gold-standard treatment for schizophrenia. Subsequent generations of drugs can reduce adverse reactions. Similar improvement has been observed for electroconvulsive therapy. Meanwhile, there has been a trend in our society of increasing numbers of perfectly healthy people making a hobby of taking herbal medicines that might do little but expose them to lead and arsenic, and some doctors promote that, as well. Besides, I mostly have been just defending the research and calling for more research.

Lanzalaco said...

right ok.. so sure the science can be stupified by political correctness, as long as we are sensitive if the reasons are sound. e.g. Genes and IQ.. we need some of this for different leverage to understand how the brain works, and same for sex differences.

So back to 2R has anybody studied if there is a positive side to it ? i.e. maybe there maybe many prominent scientists/creatives.. the more maverick freewheeler hot-headed types or successful sportsmen. Remember Jim Fallon the neuroscientist who found he had psychopathic brain structure.

nooffensebut said...

That’s a good question. There isn’t really an answer, which gets to the crux of the issue and why I write about it. Most of the research on MAOA has been on the interaction between MAOA-3R and child abuse as an influence on antisocial tendencies. Why? Is it the most powerful interaction effect of MAOA? No, the interaction with IQ was stronger, according to Ferguson et al, and no one has tried to replicate that. Is MAOA-3R the allele with the strongest effect? No, MAOA-2R appears to be worse, but it’s only been studied in one sample. Scientists have not studied MAOA-2R much partly because it is uncommon, and therefore, hard to study, but it’s actually quite common in African Americans. Of course, I think political correctness and fear of controversy explain this lack of emphasis. The scientists whom I call GWAS Jihadists engage in circular logic regarding this subject. They dismiss candidate-gene research for being plagued by false positives. The obvious solution is replication of positive findings, especially when a GWAS with a SNP array cannot study a repeat polymorphism like the MAOA VNTR. However, that would suggest greater funding and journal space for candidate-gene research, which the GWAS Jihadists oppose. Some GWAS Jihadists seem especially angry at MAOA research because it has had successful replications, and, therefore, it undermines their radical position. On blogs, I have been criticized for being “obsessed” with this “pet issue.” The fact that I am so closely associated with this gene is a testament to the irrational lack of interest on the part of others. Many people online are obsessed with the subject of race and IQ, which is controversial but usually not an issue of life-and-death importance, as MAOA is.

There are studies that suggest MAOA-3R might have benefits. It might make women happy or decrease antisocial behavior in women. There is a theoretical basis for thinking that MAOA-3R and MAOA-2R would result in less depression, but the research for MAOA-3R does not back up that theory. Of course, the totality of research on MAOA suggests that it effects many diseases and behaviors. This is a fact which GWAS Jihadists jump on as proof that all MAOA research is a false positive because one gene couldn’t possibly affect so many phenotypes. I would like to show one of these morons the list of adverse reactions listed on the label of an antipsychotic drug to see if they conclude that antipsychotics don’t do anything.

I have mixed feelings about Dr. Fallon. Compared to other public speakers on this subject, he is way above average, and I’m glad that he can make money and bring positive attention to the subject. He even gave a speech, which is online, in which he said there was an effort going on to study MAOA in Africa. I don’t believe that, but it takes courage to bring up the subject to a live audience. It sounds like one of the GWAS Jihadists got to him because he stopped talking about MAOA research and seemed to distance himself from it in one interview. He is obviously no expert on MAOA genetics, and he sort of sensationalized the subject by harping on how he has the warrior gene. He only has MAOA-3R, which is the most common version of the gene.

Anonymous said...

I saw another study that said the warrior gene was more prevalent in Asian men.

Lanzalaco said...

that would be east pacific warrior tribes you probably read about.

on the authors comments, we should be looking for a set of direct positive behaviour associations for MAOA-2R, because that would be the falsification for the hypothesis its a negative trait.

Also there has to be a biological mechanism if it is completely negative. i.e why would it impact IQ ? an idea that springs to mind is the neuro-modulation systems are so over-active they are interfering with regular LTP encoding or the perceptual attention control mostly mediated by unmodulated ionotropic cortical neurons.

nooffensebut said...

“I saw another study that said the warrior gene was more prevalent in Asian men.”

What you saw was a copy-and-paste error, which has been incorporated into a politically correct conspiracy to bury this science. See my blog post and video about it.

“why would it impact IQ ?”

The evidence that MAOA affects IQ is weak. MAOA-3R interacts with IQ to cause antisocial behavior. In Brunner syndrome, the rare complete dysfunction of MAOA, the average IQ has been found to be 85 for one family. It has also been mistaken for severe autism. One study found that MAOA-3R interacted with COMT to increase IQ in boys with ADHD.

Lanzalaco said...

ive also seen a link with MAOA and autism mechanisms a while back but i dont have the paper here. i.e. The cortical columns become more densely packed with neurons so its a perceptual booster in some context. As if the MAOA is able to ramp up the cortical activity.. Not sure what the mechanism would be. Dopamine does not innervate all the cortex.. Serotonin does, but its more bottom up and sparse so I dont think it could cause that. Extra norepinephrine NE could maybe increase the activity of all the astrocytes top down which can act like gain modulators to cortical columns.

http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=7643199

also NE limits the damage when cortical neurons become too active, so maybe this can allow the cortical collumns to be hyperactive and grow strong without the usual disorders. i.e. The warrior gene could also act like a steroid for sharpening up sensory perception.

http://www.jneurosci.org/content/29/1/263.full

nooffensebut said...

Cohen et al, 2010, found more aggression in autistic children with MAOA-3R. Your points sound plausible and would be a good avenue for further research. It actually appears that MAOA research is slowing a bit, but the attention that Nicholas Wade's new book brought to MAOA-2R suggests that the public might be increasing their interest in the subject.