The Hispanic Asian Flynn Effect

Recently, activist and entrepreneur Ron Unz used results from a short English vocabulary test, called Wordsum, to argue that Mexican Americans have risen in intelligence, shrinking their intellectual disadvantage relative to white Americans by two-thirds. David Sanders (an alias) countered this claim, using one of my previous posts on racial group differences in SAT performance.

Here is how Unz responded:

Although several different arguments were made, the strongest and most detailed focused on an examination of the ethnic distribution of American SAT scores between 1980 and 2010 [sic], performed by another highly quantitive racialist blogger. The article pointed out that there was virtually no net change in the substantial Hispanic/white performance gap on the SAT during those four decades. Since the SAT is a far better proxy for IQ than my Wordsum values, and the number of participants across those years number in the millions, any possibility of a large rise in Hispanic IQ would seem completely disproven. My claims had focused on American-born Mexican-Americans rather than Hispanics in general, but since the former group represented a large and rapidly growing portion of the latter, my argument would seem to have suffered a very serious blow.

However, this is incorrect…. With some effort, I managed to obtain the ethnic distribution of SAT test-takers back to 1975 and then compared these results with the ethnic distribution of 18-year-olds during those years, found in the Census-CPS [Current Population Survey] data.

Just as I had suspected, the changes were dramatic. In 1975, 22% of whites took the SAT, and this had risen to 33% by 2011, a substantial rise of 50%. However, during these same decades, the percentage of Hispanic test-takers had grown from 6% to 32%, an enormous rise of over 400%. Thus, in 1975 white 18-year-olds were nearly four times more likely to take the SAT, but by 2011 the ratios were almost exactly the same…. Since the white/Hispanic gap remained unchanged during this tremendous broadening of the Hispanic testing pool rather than greatly widening, the only possible explanation would seem to be a huge rise in average Hispanic academic performance, just as was reflected in the Wordsum-IQ scores….

Thus, upon closer examination the SAT evidence cited for the alleged lack of Hispanic gains actually becomes very powerful evidence for strong Hispanic gains.

After going through reports from CPS, I have been unable to replicate these numbers precisely. Most of the reports that I found give combined totals of 18- and 19-year-olds, so I divided those in half, which I consider a fair estimation. I also cannot locate a report for 2011. Assuming CPS has released it somewhere, the notion that the participation gap dropped from nine percentage points to one in a single year defies credulity.

For white students, my results are similar to those of Unz. Their participation rose from 21% to 34%, an increase of 61%. If one looks at the full range, rather than just the bookend years, the rise is 19% to 34%, 79% higher. I found that Hispanics rose from 7% to 25%, which is a 257% increase. That is still a huge jump, even if it is not 433%. The rates of change of participation in the graph look similar, but Hispanic students start much lower.

However, discussion of the exact calculations is moot because both sets are based on a falsehood. Take a close look at the graph. Notice anything strange? In 1987, non-Mexican Hispanic students suddenly resolved to take the SAT in much greater numbers. Before one goes searching for a mind-blowing ‘80s Spanish public service announcement, I must reveal (again) that the College Board added a third category of Hispanic in 1987, in addition to Mexican and Puerto Rican, and this new category was “other Hispanic.” A group of people who had previously been something other than Hispanic consequently metamorphosed into Hispanic people with sombreros, I think. Other Hispanic students (or, as I prefer, “Hispanica Miscellanea”) rival Mexican-American students in number. The dramatic quality of the rise in Hispanic participation merely represents an artifact of definitional change. Calculations with a starting year of 1987 give a white student range of 23% to 34% (a 48% increase), an African-American student range of 12% to 29% (a 71% increase), and a Hispanic student range of 14% to 25% (a 79% increase).

Unz was making the point that SAT data support a secular rise in Hispanic cognitive ability, according to the fundamental law of participation level-actual ability direct correlation. This law allows us to assume that Hispanics are becoming smarter if they can take the test in greater numbers while only slightly worsening their score performance relative to white students. My only problem with the law is that the SAT dataset is riddled with countervailing examples, as I previously discussed.

One counterexample is particularly illustrative. In 1998, CPS discovered the existence of a group of people called the Asian Americans. This extraordinary new tribe possesses a pleasing aesthetic, but they can only eat with primitive sticks. After a detailed analysis of Asian SAT performance and participation, I can confidently state the broad conclusion that Asians are different.

As the above graph proves, Asian Americans so enthusiastically partake in the SAT that they achieve participation proportions greater than all of them. It seems that some proportion of Asian SAT takers are foreign students unrecognized by the US Census. I wonder if the Hispanic-American community also includes a group of census-undercounted individuals who nonetheless live here. Asian students are the one racial group whose SAT performance is taking off, and they have achieved this while increasing their test participation 105%, and I already dispelled attempts to use foreign-student involvement to explain away Asian score advancement. For emphasis, I shall present this graph of the Asian-Hispanic score gap in standard deviations, superimposed over the Asian-white score gap, with the colors of the latter set to grey.

In fairness, my essay raised the possibility to white aptitude decline relative to other groups and included in the reasoning a possible decline of white participation. If those who do not identify their race are largely white, as I hypothesized, then white students have decreased their participation from 43% in 2003 to 37% in 2010. However, that would also mean that white students had increased their participation since 1987 by 87%, at their peak, which is a greater increase than that of Hispanics, and the possible rise and fall left no footprint in the graph of the Hispanic-white gap.

Despite the racial disquiet that the SAT invokes, the test might actually be hiding the full extent of the racial gaps. First of all, the College Board altered its scoring algorithm in 1996 with the explicit purpose of narrowing racial gaps. Second, unlike the score range of many IQ tests, the SAT score range is, itself, sufficiently narrow so as to construct a secure floor for the bell curve’s far left and a ceiling that holds down the absolute best. I have perhaps overemphasized in the past the fact that African-American students have a larger gap with white students on the SAT mathematics subtest than on the writing and reading subtests. I cannot rule out that the subtest differences result purely from the massive number of African Americans who occupy the floor of the reading and writing subtests, as I previously graphed. Likewise, I can now reveal additional years of the white and Asian mathematics subtest bell curves that demonstrate substantial increases in perfection or near perfection of what was already outstanding Asian mathematics success.



Therein lies the crux of the issue. If all Unz wanted to prove was that the “Strong IQ Hypothesis” fails to account for the malleability of cognitive results, he could have cited the Asian advancement on the SAT. By bothering to analyze SAT results over time and by describing the progress of Asians, I have already implicitly acknowledged that some things do change and environment matters, at least under some circumstances. Usually, efforts to deny the existence of, minimize the importance of, or supply loose elasticity to IQ share the same impetus as the linguistic pursuit of calling “race” a “social construct.” The canards aspire to overrule by abstraction or technicality evidence for sociological generalizations labelled “stereotypes” or to beg the question regarding biological causality without dirtying one's hands with biological evidence. Recognizing an Asian academic model only reinforces a stereotype, to which even many Asians strain to take offense. That the SAT does not yet demonstrate an unmet potential in Hispanic Americans provides no paradox of proven unmet potential. To even engage the issue is to take for granted a stereotype. All good people are asleep and dreaming.

Just Say No Limit: Trayvon, Dextromethorphan, Marijuana, and MAOA

When I recently posted a photograph of Trayvon Martin, the African-American victim of a shooting during a confrontation with a neighborhood-watch volunteer, making an obscene gesture, many of my readers missed the inside joke. The national media packaged the earliest reports on this case to maximize sympathy for the 17-year-old Martin. We knew him by his cute, smiling visage from a few professional pictures taken when he was not older than thirteen. These appeared alongside a 2005 mug shot of the shooter. When a more recent photograph of Martin extending one middle finger at a camera came to light, a conspiracy theory emerged to defend his honor. Some insisted that the hand must have been photoshopped because another photograph exists utterly lacking said digit.



Alas, Martin’s YouTube page, which had not been accessed since before Martin’s death when I arrived at it, utilized the controversial photograph that I would post, containing, not one, but (count them!) two middle fingers! Similar photographs subsequently made the rounds, and it became clear that the new-media-savvy Mr. Martin had something of a trademark pose. Not only was Martin’s innocent image taking flak, but I felt my own moral sensibilities slipping away under the onslaught of a greater quantity of this vulgar sign than I had previously imagined.

At least Americans understood the senselessness of the shooting, given that Martin was merely taking a stroll to a corner convenience store to buy a package of Skittles and a can of iced tea. Well, the police report noted an “Arizona tea can,” but a photograph of the can clearly reveals it to be Arizona Watermelon Fruit Juice Cocktail. So what? Actually, this beverage and Skittles are ingredients of a recreational drug called “watermelon lean,” the knowledge of which I must credit to the blog The Conservative Treehouse. Martin actually acknowledged his use of lean on Facebook. The psychoactive ingredient of lean is the over-the-counter cough medicine, dextromethorphan, which happens to carry the street name, “Skittles.” At high doses, dextromethorphan acts as an addictive drug with the same dissociative symptoms as phencyclidine (PCP or “angel dust”). Case reports of psychotic symptoms, including paranoia and aggression, have followed dextromethorphan toxicity since the 1960s. Perhaps, then, it is small wonder that the young lady whom Martin’s family falsely described as his “girlfriend” shared that, in the cell phone conversation leading up to the shooting, Martin had told her that the shooter, George Zimmerman, was “looking crazy.” Even if the prosecution’s narrative is accurate, (cliché or not) another being out to get one cannot preclude one’s paranoia.



Much like Martin, dextromethorphan benefits from an innocent public image far removed from angel dust comparisons. However, the case reports have described “cough-syrup psychosis” as lasting several days even after disuse, and some factors, to which Martin was subject, can accentuate the effective dosage and half life of Skittles.

One such factor, arguably, is marijuana. Marijuana hashish is 2.5% cannabidiol, the second most common cannabinoid in marijuana after THC, which is the primary cause of marijuana’s psychological effects. Cannabidiol inhibits a liver enzyme called CYP2D6, which is the major enzyme of dextromethorphan metabolism. While a recent study called this inhibition “potent,” the blood levels of cannabidiol from smoking a single marijuana joint would be too low to significantly impact dextromethorphan metabolism. THC also inhibits CYP2D6 but with about three times less potency than cannabidiol. However, marijuana could interact with dextromethorphan by another pathway involving the enzyme produced by “the warrior gene.”

Because the liver enzyme CYP2D6 is inhibited or enhanced in its activity by a number of drugs, there are a number of potential drug interactions for dextromethorphan. However, only one class of drug received a specific drug interaction warning in a best-selling medical school pharmacology textbook, Katzung’s Basic and Clinical Pharmacology, as well as on UpToDate, a subscription-based Internet site heavily used by internal medicine physicians. This class of drug is called monoamine oxidase inhibitors (MAOIs), which were the first anti-depressants and are now much less commonly used since selective serotonin reuptake inhibitors (SSRIs) are available with far less severe side effects. Regular readers of my blog know that one of my obsessions is the study of the genetics of violence. The best understood gene that affects violent behavior is monoamine oxidase A (MAOA), which produces an enzyme of the same name. This enzyme is one of the two enzymes that MAOIs inhibit. The MAOA enzyme breaks down mostly the neurotransmitters serotonin and norepinephrine. Doctors believe that MAOIs work because having too few of such neurotransmitters in the synapses between neurons can result in depression. Many doctors and scientists also believe that having too many such neurotransmitters in synapses can result in antisocial personality disorder, conduct disorder, delinquency, and aggression. Of course, neurochemistry is more complicated than I am describing, but I think this is a fair summation of many decades of medical expertise on the treatment of depression. When dextromethorphan and MAOIs interact, serotonin levels can acutely rise and cause a potentially deadly reaction called serotonin syndrome. According to the Katzung text, the predictability of the interaction lacks sufficient data to qualify as “established.” Trayvon Martin was not taking MAOIs, but if he had reduced MAOA function for other reasons, it could have boosted his levels of serotonin and norepinephrine and given him a greater tendency towards aggression and delinquency.

THC inhibits the enzyme MAOA at roughly the same potency as it inhibits CYP2D6, according to a study of brain MAOA from pigs. That study also questioned whether common marijuana usage would have any meaningful effect on behavior or emotion with such a low level of potency, but it noted that brain levels of THC are higher than blood levels, and THC accumulates in neurons. Martin’s blood THC level was 1.5 ng/mL, far below the average peak concentration of 162 ng/mL caused by smoking a single marijuana cigarette. Peak concentration tends to occur about eight minutes after someone begins smoking, whereas Martin’s level matches a person who smoked one joint 3-6 hours prior. A professor of forensic science named Larry Kobilinsky claimed that the marijuana use could have been days earlier, but that conclusion does not match the results of a study from the National Institute on Drug Abuse, at least if the marijuana is limited to a single cigarette. Plus, Martin’s cousin, Stephen Martin, appears to have posted on Twitter that Trayvon Martin was “high” within twenty-four hours of the shooting.

Smoking tobacco seems to inhibit monoamine oxidase much more than smoking an occasional joint. Smokers typically have 20-30% lower MAOA enzyme activity and 30-40% lower activity of the other monoamine oxidase enzyme, MAOB, which accounts for about 30% of monoamine oxidase enzymes in the brain. Fowler et al determined that cigarette smoking lowers brain MAOA half as much as taking the MAOI tranylcypromine.

Martin might have been a smoker. He seemed to obtain cigarillos from three young men, according to some interpretations of the 7/11 surveillance videos, and a lighter was among his belongings at the scene of the shooting. Also, his lungs had mild anthracosis, which is a black discoloration that can result from smoking. Even if Martin only smoked marijuana, if he used cigarillos as marijuana blunts, then he was smoking the tobacco that constitutes the blunts with his marijuana, likely without filters.

Genetic differences can influence dextromethorphan response. Wide variation exists in the gene for CYP2D6, such that poor metabolizers experience blood concentration levels five times greater than extensive metabolizers. Martin’s African-American heritage does not affect his likelihood of having a version of the CYP2D6 gene that would cause him to slowly metabolize dextromethorphan, but this is not the case for the gene that determines MAOA levels.

Black people have 62% lower monoamine oxidase activity than white people, as measured by MAOB activity in the platelets of blood. Black men are about twice as likely as white people to have the “warrior gene,” which is basically just the 3-repeat allele of the MAOA gene promoter (rather than the 4-repeat allele, which most white people have). Five percent of African-American men (or about 10 times the prevalence of white men) have the understudied 2-repeat allele of MAOA, which appears to double the rate of aggression compared to men with the more common versions of the gene. However, the label of “warrior gene” for the less dangerous 3-repeat version is still highly appropriate. In fact, I would argue that the association of aggression with the interaction between the 3-repeat allele and childhood maltreatment is the strongest single-gene finding in all of behavioral genetics. I could list the breadth of corroborating lines of evidence: behavioral associations exist for the gene’s promoter, its enzyme product, the metabolites of the enzyme’s reaction, gene activity demonstrated in functional MRI, the degree of epigenetic methylation, epistatic interactions between the gene’s promoter and other genes, an interaction between this promoter and a second promoter of the MAOA gene, interactions between the MAOA gene promoter and sex hormones, and completely inactivating “knock-out” alleles in humans and animal models.

As the designs of the studies on this gene have improved, the robustness of their conclusions strengthened. Last year, I posed some pointed questions to one researcher about how more thorough consideration of confounding variables could produce more startling results, and a team of New Zealand researchers have recently published a study demonstrating exactly what I predicted. They sought to determine whether any of a list of possible risk factors could, in the presence of the 3-repeat allele but not the 4-repeat allele, increase the likelihood of violent behavior. Their study did not report all of the factors that failed this test, but five such measures did trigger the genetic predisposition: childhood maltreatment, the mother smoking during pregnancy, ten years of an interviewer’s assessment of poor material living standards, dropping out of school by age 18, and a low average of two IQ scores at ages 8 and 9 from the revised Wechsler Intelligence Scale for Children. In each case, the 4-repeat allele protected against adopting violent tendencies, and all five factors melded into a combined risk index that greatly accentuated the genetic differences at the highest index levels. I found it particularly interesting that, after ten years of studies replicating the original childhood-maltreatment-gene interaction, this study determined that the IQ-gene interaction influenced violence with a greater degree of certainty than the gene’s interaction with physical or sexual child abuse.

GWAS Jihadists

Opposition to the science of the MAOA gene has dwindled to an embattled coterie of shrieking moralists and charlatan scientists. When Harvard psychologist Steven Pinker published The Better Angels of Our Nature, Pulitzer Prize-winning columnist Nicholas Kristof bet that Pinker would join the ranks of Pulitzer winners. However, I used this little blog to point out that Pinker had passed on in the book a falsehood based on a copy-and-paste error, among other mistakes, to malign MAOA research. In the weeks prior to the Pulitzer committee’s decision, my Pinker post experienced a surge of readers. Ultimately, Pinker’s book would not win even an official nomination. None of this prevented yet another cheap “ethics” journal from publishing a screed by a “philosopher and biologist,” who repeated the error once more. Meanwhile, researchers who focus on genome-wide association studies (GWAS) have led a failed campaign to silence all candidate-gene research. According to Duncan and Keller, “the possibility that most or even all positive [candidate gene-by-environment interaction] findings in psychiatry discovered to date represent type I errors cannot be discounted [emphasis added].” In other words, every single association between a single gene allele in a certain environmental milieu affecting a behavior, including a decade of studies on the 3-repeat MAOA promoter, might be merely one of a series of falsely positive flukes. Well, if the studies are all wrong, then why publish them? According to Chabris et al:

At the time most of the results we have attempted to replicate were obtained, candidate gene studies of complex traits were commonplace in medical genetics research. Such studies are now rarely published in leading journals…. In our view, excitement over the value of behavioral and molecular genetic studies in the social sciences should be tempered—as it has been in the medical sciences—by an appreciation that for complex phenotypes, individual common genetic variants of the sort assayed by SNP [single-nucleotide polymorphism] microarrays are likely to have very small effects.

So, psychiatric and psychological journals should follow the lead of respectable medical journals and stop publishing studies on individual genes and instead wait for GWAS to fill the void. That might take a while because SNP microarrays only study common SNPs and a select number of copy-number variations and have no capacity to study a third form of genetic variation, called variable number tandem repeats (VNTR), which includes the MAOA promoter.

Psychiatry is an applied science. The gold standards for treating psychiatric illnesses include powerful drugs that target neurotransmitters. Doctors cannot afford to ignore gene variants that also interact with neurotransmitters, any more than they can ignore drug-drug interactions, therapeutic or recreational. Violent behavior is a diagnostic criterion of many mental illnesses. Indeed, I would advocate giving impulsive aggression a diagnostic label of its own (one that doctors and researchers would actually use, unlike “intermittent explosive disorder”).

In the Trayvon Martin shooting case, the defense might need to establish that Martin had a violent predisposition to strengthen a self-defense claim. Drug use and any indication of his cognitive abilities are relevant, and it would be useful to conduct genetic tests for the MAOA promoter and CYP2D6. If that is impermissible, then Martin’s African-American racial identity becomes more relevant with its associated allele frequencies. In some trials, MAOA gene tests have already served as exculpatory evidence in the mold of the insanity defense. The right to fight back against an individual who is warrior-gene positive makes just as much sense.









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