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

Parents’ Income Poorly Predicts SAT Score

Abstract
Parents’ annual income lacks statistical significance as a predictor of state SAT scores when additional variables are well controlled. Spearman rank correlation coefficients reveal parents’ income to be a weaker predictor of average SAT scores for each income bracket within each state than parents’ education level as a predictor of average SAT scores for each education level within each state. Multiple linear regression of state SAT scores with covariates for sample size, state participation, year, and each possible combination of ordinal variables for parents’ income, parents’ education, and race shows income to lack statistical significance in 49% of the iterations with greater frequency of insignificance among iterations with higher explained variance. Cohen’s d comparisons of the yearly individual SAT advantage of having educated parents show a fairly consistently increasing positive relationship over time, whereas similar analysis of the yearly individual SAT advantage of having high-income parents shows variability somewhat coinciding with the business cycle.

Read the whole study at Open Differential Psychology.

See below for important excerpts and extra super-awesome graphs.

“Sackett et al (2009) recounted a series of accusations that the SAT merely measures family wealth. The College Board’s announcement of 2016 SAT reforms has stirred anew claims that 'the only persistent statistical result from the SAT is the correlation between high income and high test scores' (Botstein, 2014). Thus, income as an important predictor of SAT scores somewhat fits a view critical of the SAT, which is that financial resources and class privilege unduly enable higher SAT achievement. If the education component of socioeconomic status dominates over the income component, then the relationship between socioeconomic status and scores might instead more accurately reflect a family’s values towards education and a hereditary influence shared between test performance and educability.”

“This study seeks to thoroughly parse the effects of multiple covariates, including family income, parents’ highest education level, and potential confounding variables specific to state or multiple-year comparisons. To do this, full advantage will be taken from all sixteen years of state data.”

Income p-values without race as a covariate (p-values are shown on an inverse logarithmic scale)

Income p-values with race as a covariate (p-values are shown on an inverse logarithmic scale)

“The racial variable was the most consistently significant variable of these three ordinal variables for composite scores and subtests, which speaks to its independence from socioeconomic status. Race also explained much of the SAT advantage that appeared to be attributable to parents’ income prior to the addition of the racial variable in iterations with low income thresholds simultaneous with the education cutoff being graduate degree.”

Critical-reading and mathematics standardized coefficients compared to adjusted R² values, organized by education first, race within each educational category, and income within each racial category

“Parents’ income has a significant association with SAT scores, but parents’ education is consistently stronger, and regression with effective controls for race, education, and other factors, usually suppresses the income variable to insignificance. The income variable achieved significance when the education threshold was high school diploma most likely because so few parents were dropouts that education was no longer effectively controlled, and parents’ income became a proxy variable for parents’ education…. Part of this dominance could result from heritability in test performance corresponding to parents’ educational attainment, given the high heritability estimates from twins studies for high-stakes standardized exams in the UK and the Netherlands (Bartels et al, 2002; Shakeshaft et al, 2013).”

“Figure 1 seems to contradict Dixon- Román et al in finding that the racial variable had its greatest influence at the highest education level and at high income levels.”

“Asian Americans have historically high average mathematics subtest scores but lower verbal/critical-reading average scores than the white majority…. Despite their likely small average verbal disadvantage and small population in many states, this study’s consistent regression results for Asian race match verifiable individual SAT-score phenomena. A study with fewer observations, a much smaller represented sample, or fewer or poorly chosen covariates might not have achieved that level of definition, but, fundamentally, states do not take the SAT; people do.”

Cohen’s d SAT advantage of having parents’ annual income above $60,000

“Family educational advantage seems to evince virtually undeviating growth as a predictor of SAT scores, but financial advantage seems to grow as the economy worsens. Rather than postulate that times of economic difficulty almost immediately make wealthy people smarter, one should focus on the exclusivity of the income category…. The declining relative income advantage on the mathematics subtest compared to the critical-reading subtest also could be related to structural changes to the economy since the decline of the high-technology boom of the 1990’s, which also fits this interpretation of persistence within families.”

For those readers who do not have a heart condition, I recommend the spirited and colorful statistics debate in the open peer-review forum. One may also find there data supplements of state data that required many months of typing out the data from 816 state reports into a database, which makes a fun toy.










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