The Alondra Oubré Academic Fraud Exposed

Alondra Oubré Wikipedia Scholar

As further proof that a specific violence gene common to Africans threatens the worldview of fundamentalist anthropologists, Wikipedia scholar Alondra Oubré became the latest anthropologist to post an error-riddled Internet screed against the warrior gene, monoamine oxidase A (MAOA). Oubré is the author of Instinct and Revelation: Reflections on the Origins of Numinous Perception and Race, Genes and Ability: Rethinking Ethnic Differences. She is also an expert at copying errors from Wikipedia into her writing. Her *Wikipedia* page lists her as a “newsmaker,” “prominent African American,” and an “African American achiever.” As an anti-science anthropologist, she joined her colleagues in writing another editorial against Nicholas Wade’s recent book, A Troublesome Inheritance, as well as the study of MAOA, a gene verified as causing violence in multiple meta-analyses. Unlike previous attacks on this science, no possibility exists that this is anything other than academic fraud. Oubré took false information from Wikipedia, for which I provide here the proof, and she deliberately lied about her source. I repeatedly requested an official correction from her editor, author and City University of New York professor Massimo Pigliucci, who refused to do so. What follows is a point-by-point refutation of Oubré’s work.

Wow! What a poorly researched Internet post! I hope you don’t mind if I post the factual corrections here for you.

“The most common variant, MAOA-4R, has four repeats and is associated with high-activity breakdown of neurotransmitters.”

I guess it would be true that MAOA-4R is the most common variant if everyone in the world was white.

“Up to this point, all of the studies on the MAOA gene had been conducted in Caucasians. That changed when researchers started investigating this gene in the Maori of New Zealand.”

No, here is a list of studies that looked at non-whites prior to that study: Sabol et al, Kunugi et al, Balciuniene et al, Gilad et al, Ono et al, Williams et al, Koen et al, Huang et al, Yu et al, Young et al, Widom & Brzustowicz, and Rosenberg et al.

“For many experts, this ethnic gap is the result of numerous environmental causes, including poverty.”

I think you should revise this sentence.

“It turned out that while 3R was found in 56% of Maori males, it occurred in 58% of African American males and 34% of European males.”

Notice how the African-American number is slightly lower than the source? Someone in Wikipedia has been tweaking the numbers at will. I don’t recommend that you rely so heavily on Wikipedia as your source for just this sort of reason. I also don’t recommend that you rely on that “study” by Lea and Chambers, which was the source of the “idiot test” copy-and-paste error that slandered Chinese men as having an MAOA-3R allele frequency of 77%.

“Interestingly, the press ignored studies indicating that the 3R variant occurred in 61% of Taiwanese males [15] and 56% of Chinese males [16].”

You switched your sources. Both samples were Taiwanese. You rounded 54.5% to 56%. That’s kind of sloppy.

“In the Add Health database, 5.5% of African American men, 0.9% of Caucasian men, and 0.00067% of Asian men have 2R.”

So, you took these numbers from Add Health, did you? No, you didn’t. I know because I calculated the number for Asian men and posted it on my blog and Wikipedia. Once again, the Wikipedia troll screwed up your numbers for white men by a factor of 9. The Asian allele frequency was based on eight studies. I only found one Asian with MAOA-2R in those studies, but I have since looked at other studies and revised the number upwards. I have been maintaining a table with my tabulated allele frequencies (without excluding any sample).

“This has led some popular writers to speculate that MAOA-2R might account for — or at least play a significant role in — the relatively higher rates of violent crime in African Americans. Not everyone agrees [21].”

If one writes, “Not everyone agrees,” it is good form to make sure that the source cited expresses some disagreement with what one wrote before “Not everyone agrees.”

“The rates of 2R are more than five times higher in African American males than in American white males, at least in the Add Health sample.”

Yeah, I guess 55 is more than 5. Damn that Wikipedia troll! Choe et al, which you cited, found it in 6% of black men and 0% of white men, so maybe it’s infinity times more common. Seriously, considering how rare it is in whites and Asians, why should we believe that those rare exceptions are actually genetically 100% white or Asian?

“Although genes affect individual differences in behavior, the effect of each individual gene is usually small.”

I think you meant to say “allele.” If the effects of individual genes are usually small, then missense mutations that completely shut off the gene and eliminate the protein should have little effect. Of course, you failed to mention the missense mutation specific to MAOA, which causes Brunner syndrome. The effect of Brunner syndrome on behavior is not small.

“The more common low-activity variant, 3R, interacts with adverse social effects such as childhood maltreatment. But other possible environmental factors, which conceivably could interact with the 2R, may not have been explored in-depth as yet.”

I think Fergusson et al did the most in-depth analysis of various environmental factors. Interestingly, the interaction effect of IQ on violence was more powerful than the interaction effect of childhood maltreatment. I’m afraid that you’ll have to look up for yourself whether African Americans differ from whites and Asians in average IQ because that is outside my area of expertise.

“Using PET imaging scans, these researchers found no correlation between MAOA brain levels and MAOA gene variants.”

However, Alia-Klein et al did find MAOA promoter effects on anger in an fMRI study. That study and Buckholtz et al found MAOA gene effects on the amygdala. Cerasa et al found that the gene influenced orbitofrontal cortical thickness with MRI. Buckholtz et al and Cerasa et al had much larger samples than the 34 men in Shumay et al. Shouldn’t you have mentioned those findings?

“Nonetheless, their results suggest that MAOA brain levels, which affect mood, are at least partially regulated by non-genetic factors — i.e., epigenetically.”

Of course, genes do influence epigenetics. In fact, the “environmental” interaction factors, like childhood maltreatment, might also have a component of heritability. Wong et al found that, compared to women, epigenetics of MAOA in men is minimal, low in variance, and high in hereditary influence. Pinsonneault et al was unable to detect any MAOA methylation in men. Philibert et al found less MAOA methylation in men and that MAOA methylation had no effect on antisocial personality disorder in men or women. That seems like a relevant finding.

“The jury is still out on whether 2R, the rare MAOA gene, acts independently of the environment (and independently of other genes) to shape antisocial personality traits.”

First of all, is MAOA-2R rare in Africans? A common definition of a rare allele is having an allele frequency less than 5%. It might not be rare in African-American men. We can extrapolate to the higher allele frequency in a population of Africans who are not racially mixed. All of the evidence we have on MAOA-2R, so far, suggests that it has a powerful effect independently of environment. The assumption is that this distinguishes MAOA-2R from MAOA-3R, which supposedly only has a gene-environment interaction effect. A recent meta-analysis of 31 studies actually disproved this and found that MAOA-3R has a slight effect on antisocial behavior independent of interaction factors.

Pigliucci allowed me to post this comment only so that others could harass me with baseless ad hominem, but he censored all of my other responses.

Exposing falsehoods about the warrior gene is nothing new for me, but this is different. It might be hard to believe that a respected scientist like Steven Pinker or an experienced writer like John Horgan would fall for the idiot test or that Scientific American, The Chronicle of Higher Education, and various journals and book publishers would reprint it. While one might not expect such incompetence from these sources, no evidence proves malfeasance. Also, Oubré’s mischaracterization of the science of MAOA epigenetics and brain imaging (also see Lei et al) is likely but not positively deceptive. In other words, she probably came across the evidence against her thesis and chose to keep it to herself, but one cannot absolutely demonstrate this as such. However, she unmistakingly lied when she attributed Wikipedia data to the Add Health subsample of the famous, widely used National Longitudinal Study of Adolescent Health database.

Interestingly, the idiot test almost constitutes a photographic negative of this fraud. The original copy-and-paste error by Rod Lea and Geoffrey Chambers first appeared in a scientific journal—perhaps not a highly respected journal, but a journal nonetheless—and subsequently spread to the public through mass media. This time, misinformation sprouted from the lowly, anonymously edited Wikipedia and traveled up the media food chain to scientific blogs. The Wikipedia page for MAOA originally contained correct information that I and other responsible agents copied correctly from peer-reviewed studies. Then, someone identified only by their Internet Protocol address, 76.78.226.57, began altering the data. One can observe from this person’s contributions page, that he or she has a history of altering numbers in Wikipedia that relate to immigration and ethnicity helter-skelter without providing new sources. On March 22nd, the offender made three unsourced edits to the same group of numbers on the MAOA page. At 2:25, the change was as follows:

Two minutes later, another change occurred:

At 23:55, the offender changed the same numbers, again:

This allowed for an error of an order of magnitude in Oubré’s numbers. So, who is 76.78.226.57? Is she Oubré? Is he Pigliucci? Who knows? Maybe he is Eric Holder. Nobody who knows is saying.

Massimo Pigliucci “Editor-in-Chief”

To prevent confusion among the lay public, I politely asked Scientia Salon editor-in-chief Pigliucci for an official correction in this e-mail:

You posted my corrections for "The Extreme Warrior gene: a reality check" as a comment. However, the errors were quite serious, such as claiming that data from Wikipedia (which was false information) actually came from the National Longitudinal Study of Adolescent Health. Such errors should not only be addressed by an outsider's comment. As the editor-in-chief of Scientia Salon, you should see that someone actually investigates my claims and posts a complete correction, if true. Alternatively, you could direct me to the appropriate authority within your site who handles corrections.

Pigliucci could not bother himself with more than a curt reply.

your comment has been published, so I’m not sure what additional action you expect from me, or why.

I tried repeatedly.

Yes or no, did Alondra Oubré falsely claim on your site that information she took from Wikipedia had actually come from the Add Health subsample of the National Longitudinal Study of Adolescent Health? If yes, was the information from Wikipedia all accurate? If she falsely attributed false information from Wikipedia, why do you refuse to post an official correction at the end of her piece, as any reputable source of information would? I noted numerous other errors, but this one in particular seems especially egregious because it reveals a lack of integrity and provides a conduit for anyone to make up information on Wikipedia and disseminate it through disreputable blogs.

No reply came.

As shown by her citations, Oubré obviously intended her perversion of MAOA science as a rebuttal to Wade. Less than three weeks prior, Pigliucci spent forty-two minutes in a podcast expatiating the standard semantic criticism that has amounted to basically the entirety of the fundamentalist anthropologist attack on Wade’s book. They call Wade a racist, and, in modern civilization, racists might be preferred to pedophiles but are considered far worse than necrophiliacs, cannibals, terrorists, zombies, Democrats, rapists, and even boy-band alumnae. Wade spent a good portion of his book criticizing white supremacy and called a book by JP Rushton racist in an interview. If idiotic anthropologists label every prestigious intellectual with whom they disagree a white supremacist, then the desire to be white supremacist among average white folks will grow like the tuition rates that young people pay to hear idiotic anthropologists bloviate. The colloquial definition of racism is the belief that average ability and tendency differences (stereotypes) exist between peoples grouped by place of origin. Heritability mathematics has nothing to do with it. Therefore, all anti-racists are racists. Actually, I would like to see the forces of good defeat white supremacy, which is why I know that the perceptual and strategic superiority lies with the recognition that the face of neo-Nazi white supremacy is the one covered in tattoos.










Alia-Klein N, Goldstein RZ, Tomasi D, Woicik PA, Moeller SJ, Williams B, Craig IW, Telang F, Biegon A, Wang GJ, Fowler JS, & Volkow ND (2009). Neural mechanisms of anger regulation as a function of genetic risk for violence. Emotion (Washington, D.C.), 9 (3), 385-96 PMID: 19485616

Balciuniene J, Syvänen AC, McLeod HL, Pettersson U, & Jazin EE (2001). The geographic distribution of monoamine oxidase haplotypes supports a bottleneck during the dispersion of modern humans from Africa. Journal of molecular evolution, 52 (2), 157-63 PMID: 11231895

Buckholtz JW, Callicott JH, Kolachana B, Hariri AR, Goldberg TE, Genderson M, Egan MF, Mattay VS, Weinberger DR, & Meyer-Lindenberg A (2008). Genetic variation in MAOA modulates ventromedial prefrontal circuitry mediating individual differences in human personality. Molecular psychiatry, 13 (3), 313-24 PMID: 17519928

Cerasa A, Cherubini A, Quattrone A, Gioia MC, Magariello A, Muglia M, Manna I, Assogna F, Caltagirone C, & Spalletta G (2010). Morphological correlates of MAO A VNTR polymorphism: new evidence from cortical thickness measurement. Behavioural brain research, 211 (1), 118-24 PMID: 20303364

Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. Behavior genetics PMID: 24902785

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

Gilad Y, Rosenberg S, Przeworski M, Lancet D, & Skorecki K (2002). Evidence for positive selection and population structure at the human MAO-A gene. Proceedings of the National Academy of Sciences of the United States of America, 99 (2), 862-7 PMID: 11805333

Huang YY, Cate SP, Battistuzzi C, Oquendo MA, Brent D, & Mann JJ (2004). An association between a functional polymorphism in the monoamine oxidase a gene promoter, impulsive traits and early abuse experiences. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 29 (8), 1498-505 PMID: 15150530

Koen L, Kinnear C, Corfield V, Emsley R, Jordaan E, Keyter N, Moolman-Smook J, Stein D, & Niehaus D (2004). Violence in male patients with schizophrenia: risk markers in a South African population Australian and New Zealand Journal of Psychiatry, 38 (4), 254-259 DOI: 10.1111/j.1440-1614.2004.01338.x

Kunugi H, Ishida S, Kato T, Tatsumi M, Sakai T, Hattori M, Hirose T, & Nanko S (1999). A functional polymorphism in the promoter region of monoamine oxidase-A gene and mood disorders. Molecular psychiatry, 4 (4), 393-5 PMID: 10483059

Lei H, Zhang X, Di X, Rao H, Ming Q, Zhang J, Guo X, Jiang Y, Gao Y, Yi J, Zhu X, & Yao S (2014). A Functional Polymorphism of the MAOA Gene Modulates Spontaneous Brain Activity in Pons. BioMed research international, 2014 PMID: 24971323

Ono H, Shirakawa O, Nishiguchi N, Nishimura A, Nushida H, Ueno Y, & Maeda K (2002). No evidence of an association between a functional monoamine oxidase a gene polymorphism and completed suicides. American journal of medical genetics, 114 (3), 340-2 PMID: 11920860

Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A (2008). MAOA methylation is associated with nicotine and alcohol dependence in women. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B (5), 565-70 PMID: 18454435

Pinsonneault JK, Papp AC, & Sadée W (2006). Allelic mRNA expression of X-linked monoamine oxidase a (MAOA) in human brain: dissection of epigenetic and genetic factors. Human molecular genetics, 15 (17), 2636-49 PMID: 16893905

Rosenberg S, Templeton AR, Feigin PD, Lancet D, Beckmann JS, Selig S, Hamer DH, & Skorecki K (2006). The association of DNA sequence variation at the MAOA genetic locus with quantitative behavioural traits in normal males. Human genetics, 120 (4), 447-59 PMID: 16896926

Sabol S, Hu S, & Hamer D (2014). A functional polymorphism in the monoamine oxidase A gene promoter Human Genetics, 103 (3), 273-279 DOI: 10.1007/s004390050816

Widom CS, & Brzustowicz LM (2006). MAOA and the "cycle of violence:" childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological psychiatry, 60 (7), 684-9 PMID: 16814261

Williams RB, Marchuk DA, Gadde KM, Barefoot JC, Grichnik K, Helms MJ, Kuhn CM, Lewis JG, Schanberg SM, Stafford-Smith M, Suarez EC, Clary GL, Svenson IK, & Siegler IC (2003). Serotonin-related gene polymorphisms and central nervous system serotonin function. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 28 (3), 533-41 PMID: 12629534

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

Young SE, Smolen A, Hewitt JK, Haberstick BC, Stallings MC, Corley RP, & Crowley TJ (2006). Interaction between MAO-A genotype and maltreatment in the risk for conduct disorder: failure to confirm in adolescent patients. The American journal of psychiatry, 163 (6), 1019-25 PMID: 16741202

Yu YW, Tsai SJ, Hong CJ, Chen TJ, Chen MC, & Yang CW (2005). Association study of a monoamine oxidase a gene promoter polymorphism with major depressive disorder and antidepressant response. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 30 (9), 1719-23 PMID: 15956990

Christopher Irwin Smith is an Idiot

Poopy-Faced Idiot
Deep inside an underground compound within the evil lair of the American Anthropological Association, Lord Skeletor summoned a scientist to spread falsehoods about the science of monoamine oxidase A, the warrior gene. That scientist was Christopher Irwin Smith, Associate Professor of Biology at Willamette University. Dr. Smith set about penning a diatribe full of errors and misleading innuendo. “I shall post this on the Internet and not allow better-informed people to comment on it,” he muttered before mustering an evil cackle that echoed through his dark private chamber.

Our investigators have uncovered the following especially telling response comment:

Dr. Smith,

Your impressive background prevents me from having any sympathy for you regarding the multiple egregious errors in this post. Probably the worst aspect of it is the timing because the last two years have produced two important meta-analyses confirming MAOA as an aggression and antisocial behavior gene. I’m guessing you have no awareness of either one.

“…Nielsen and Williamson’s studies were able to identify many regions in the genome that appear to have experienced recent natural selection, but MAO-A is not one of them.”

You neglected to mention that their study examined single-nucleotide polymorphisms, not repeat polymorphisms, like either of the functional MAOA-uVNTR promoters. The same is true for Voight et al.

“it is likely that these genetic variants are not –on their own– associated with violent or impulsive behavior… Simply carrying the ‘low expression’ allele in the MAO-A promoter does not have any effect at all on impulsivity or aggression.”

I doubt that you would have written this if you had been aware of the new meta-analysis by Ficks and Waldman, which came to the opposite conclusion.

“Instead, genetic variation in the MAO-A promoter seems to make some children less able to recover from abuse and childhood trauma, and therefore more likely to act out later in life (Caspi et al. 2002; Widom & Brzustowicz 2006).”

You are misrepresenting the findings of Caspi et al. It is MAOA-4R, not MAOA-3R that has the effect, which is a protective effect. According to Caspi et al, abuse could not affect those with MAOA-4R at all. Other studies have found the same protective effect against high testosterone levels and low IQ. Byrd and Manuck recently provided a meta-analysis verifying the abuse-MAOA interaction effect.

“Indeed, genetic variants associated with lower resilience to trauma are most common in Asian populations, not African ones (Sabol et al. 1998).”

Are you seriously saying that 61.0% is significantly higher than 59.1%? I think you must have been thinking about the copy-and-paste error by Lea and Chambers that claimed that 77% of Chinese men have MAOA-3R. I have labeled that the “idiot test” because it has caught many highly credentialed idiots who were trying to do the same thing that you are trying to do now: brush off decades of good research on MAOA. Ficks and Waldman only found a modest main effect of MAOA-3R, so you would need to argue not only that the gene is as common in Asians but also that the interacting factors (child abuse, high testosterone, an IQ less than 85) are as common in Asians, as well. Then, there is the issue of MAOA-2R….

“Note that Sabol study did not consider differences between populations in the frequencies of the ‘2-repeat’ alleles that Wade references…”

Did not consider? Gee, that is an interesting way of putting it. Of course, they tried to determine the allele frequency of each kind of allele in that VNTR, and they reported absolutely no instances of MAOA-2R in any group out of a total sample of over 2,000 X-chromosomes. MAOA-2R had not been discovered until the next year by Kunugi et al. Ever since, we have known that MAOA-2R is rare in whites but not that rare. Something is seriously wrong with the Sabol et al allele frequencies.

“To my knowledge, the frequency of the 2-repeat allele across populations has not been extensively measured; studies that have looked at its incidence appear to have focused on specific cohorts in the US as part of epidemiological studies.”

Is this your way of trying to cast doubt upon the allele frequencies reported in the literature for MAOA-2R in African-American men? Establishing an allele frequency does not require a 31-study meta-analysis. We have consistent findings from multiple studies that MAOA-2R is many times more common in African-American men than either white or Asian men. Would you like to read each study?

The Warrior Gene, Back from the Grave

Recently I read a phenomenal book called A Troublesome Inheritance by Nicholas Wade. It has science and sociological “speculation,” but most of the speculation actually just cited the speculation of other writers. I would say the scholarship was relatively good compared to other works of popular science. I assumed that critical appraisal would universally approve, but I would like to report that this was not entirely true. The book was actually panned by a group of people called “anthropologists,” who are almost like real scientists with their own journals and everything. Anthropologists only had one criticism: they wished Wade had scratched every use of the word “race” and written in “population,” which is ironic because a recent survey of anthropologists determined that “racist” was their second most commonly used word after “the.” It is troubling that while anthropologists have taken their courageous stand against racism, they are as of yet blind to the scourge of populationism. I think it was Confucius who said, “We have come so far but have so much farther to go.” I think “further” would have been more grammatically correct, but distance is a metaphor, and “farther” resembles a parallel construction.

Nicholas Wade took up my cause of drawing attention to an allele of monoamine oxidase A, "the warrior gene," that is rare in non-Africans and thought to predispose one to violence. However, an anthropologist named Jennifer Raff succeeded in invading the field of genetics, and she countered our claim by posting a study by Vassos et al.

"MAO-A’s effects (as well as those of any other candidate gene known at this point) appear to be very, very minor (if they even exist at all)…"

Good gravy! You mean to tell me that all that research that I have been following all these years has been debunked by a single study?! Well, I decided that before I take the drastic step of erasing half of my blog, I should actually read the study. Then, I read the other study that was on basically the same subject and published at almost the same time but that came to the opposite conclusion. Then, I magnanimously offered up my very own blog as a moderated forum for a discussion with the correspondence authors of each study. They did not respond to my request, so I shall do what I usually do and post the empty-chair interview questions.

Questions posed to Dr. Evangelos Vassos:

1. Your study mentions “increased aggressive behavior in … MAOA knockout mice.” Why does your study make no mention of the equivalent MAOA knockout condition, Brunner syndrome, in humans?
2. Your study concludes that “it is unlikely that few candidate genes explain a complex behavior like aggression” and “aggression and even violence are complex behaviors.” Does the existence of Brunner syndrome contradict your conclusions?
3. For MAOA in females, your study included Guo et al, “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity.” Unlike other studies on MAOA, that study obviously defined MAOA-2R as a distinct allele rather than another “low-activity allele” paired with MAOA-3R. How did your study account for this difference? Why did your study not note that Guo et al found a main effect of MAOA-2R, for which no attempt at replication with a different sample has been attempted?
4. Have you heard of the meta-analysis by Ficks and Waldman, “Candidate genes for aggression and antisocial behavior: A meta-analysis of association studies of the 5HTTLPR and MAOA-uVNTR”? Would you care to comment on how that study’s meta-analysis for MAOA differs from your meta-analysis?
5. Unlike Ficks and Waldman, your meta-analysis elected to include studies that used clinical psychiatric patients with mental illnesses and substance abuse problems. In fact, I count that 12 of the 17 studies on MAOA in males used such clinical patients. What is your rationale for this approach?
6. Supplementary Table 1 shows sample sizes for Gerra et al and Koller et al that suggest that your study did not consider the effects of MAOA on the aggression or hostility of each study’s control sample. It appears that you excluded the control samples and only considered the effects on the alcoholic or heroin-dependent subjects. Why is that?
7. Your meta-analysis found studies partly by scanning “reference lists of all included studies,” but these reference lists included multiple studies that Ficks and Waldman included but not your meta-analysis, specifically Manuck et al, Jacob et al, Beitchman et al, and Kim-Cohen et al. Manuck et al was listed in 4 of the 17 studies for MAOA in males. Ficks and Waldman were able to include 31 MAOA studies despite excluding studies of other psychiatric disorders, and neither meta-analysis included Williams et al (2003), Rosenberg et al (2006), Nilsson et al (2007), or Kuepper et al (2013). Why were these studies not included?
8. Like other negative studies of MAOA, your meta-analysis criticizes the entire project of candidate-gene behavioral genetics, saying “Our study provides evidence that the candidate gene approach has not succeeded in identifying genes associated with these outcomes. This is consistent with recent observations in the field that candidate gene studies of human characteristics and complex diseases at large have failed to produce consistent and clinically useful findings.” Ficks and Waldman included more studies for MAOA and found a modest positive effect, consistent with other lines of evidence (MAOA knockout mice, Brunner syndrome, gene-environment interaction, brain imaging, etc.). Should their meta-analysis have made just as strong of a judgment in favor of the usefulness of a candidate-gene approach to studying behavioral genetics? Why do only negative studies reflect upon this issue?
9. Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science?

Questions posed to Courtney Ficks:

1. For MAOA, your study included Guo et al, “The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity.” Unlike other studies on MAOA, that study obviously defined MAOA-2R as a distinct allele rather than another “low-activity allele” paired with MAOA-3R. How did your study account for this difference? Why did your study not note that Guo et al found a main effect of MAOA-2R, for which no attempt at replication with a different sample has been attempted?
2. Have you heard of the meta-analysis by Vassos, Collier, and Fazel, “Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression”? Would you care to comment on how that study’s meta-analysis for MAOA differs from your meta-analysis?
3. It appears that their study was published by a journal with a higher impact factor than yours (15 versus 3 in 2012), but they elected to include studies that used clinical psychiatric patients with mental illnesses and substance abuse problems and included fewer studies on MAOA. Why is your study in a journal with a lower impact factor? Is it possible that the outcome of their study was ideologically favored over that of your study?
4. Did you consider including the studies by Williams et al (2003), Rosenberg et al (2006), Nilsson et al (2007), or Kuepper et al (2013)? If so, why were these studies not included?
5. Like other negative studies of MAOA, Vassos et al criticized the entire project of candidate-gene behavioral genetics, saying “Our study provides evidence that the candidate gene approach has not succeeded in identifying genes associated with these outcomes. This is consistent with recent observations in the field that candidate gene studies of human characteristics and complex diseases at large have failed to produce consistent and clinically useful findings.” Your study found a modest positive effect, consistent with other lines of evidence (MAOA knockout mice, Brunner syndrome, gene-environment interaction, brain imaging, etc.). Why didn’t your study conclude with just as strong of a judgment in favor of the usefulness of a candidate-gene approach to studying behavioral genetics? Why do only negative studies reflect upon this issue?
6. Your study claimed that “there is growing evidence that we must be wary of” gene-environment interaction findings. However, Byrd and Manuck published a meta-analysis last year that seemed to show a robust gene-environment interaction for MAOA and childhood maltreatment. Some GxE interaction studies for MAOA have had positive results for fairly common environmental factors, like an IQ less than 85, high cerebral spinal fluid free testosterone, and poverty. Is it possible that the totality of suspected environmental factors are so common that your finding of a modest main effect was actually picking up these effects, even though you didn’t try to isolate them? Should those factors be control variables in this type of research?
7. Would you be willing to have your responses appear unedited on my personal blog, The Unsilenced Science?

I completely empathize with the decisions of Ficks and Vassos to ignore the interview requests. Ficks probably did not want to answer a question that would insult a prestigious journal, like Molecular Psychiatry. Dr. Vassos probably didn’t feel like answering because he must know that his study is complete garbage, and he doesn’t want to talk about it.










Ficks CA, & Waldman ID (2014). Candidate Genes for Aggression and Antisocial Behavior: A Meta-analysis of Association Studies of the 5HTTLPR and MAOA-uVNTR. Behavior genetics PMID: 24902785

Vassos E, Collier DA, & Fazel S (2014). Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression. Molecular psychiatry, 19 (4), 471-7 PMID: 23546171