Friday, June 4, 2010

Neandertal Miscegenation

I like to imagine science as the mind’s eye for the human collective. We became more fully conscious when we realized that Earth is not the center of the universe, that species evolved from shared ancestors, and that human activities alter the atmosphere and climate. Each epiphany, in its own way, disturbed our kind’s self-image. Add to that list the recent discovery that non-African humans are the product of human and Neandertal admixture. In one respect, this underlines what Luigi Luca Cavalli-Sforza called the most important difference in the human gene pool, the genetic Yarlung Zangbo Canyon between Africans and non-Africans. Then again, to discover in their family tree a race once universally considered an inferior species must be lowering the serum testosterone levels of my fellow supra-Saharans. If he were still alive, the politically correct paleontologist, Stephen Jay Gould, would have cause to reconsider the merits of genocide, for he wrote in his 1980 book, The Mismeasure of Man:

"The world might have been ordered differently. Suppose, for example, that one or several species of our ancestral genus Australopithecus had survived—a perfectly reasonable scenario in theory, since new species arise by splitting off from old ones (with ancestors usually surviving, at least for a time), not by the wholesale transformation of ancestors to descendants. We—that is, Homo sapiens—would have faced all the moral dilemmas involved in treating a human species of distinctly inferior mental capacity. What would we have done with them—slavery? extirpation? coexistence? menial labor? reservations? zoos?"

Well, at least we get a choice, right? To be fair, Australopithecus inhabited an entirely different genus. A common definition of species for organisms that reproduce sexually is the group of organisms that would be capable of producing fertile offspring with another member of the group. By that definition, Neandertals are not a separate species. If one categorizes them as a race, they would be a more distant race than any currently in existence, but that distance lends itself to some startling statements, such as a new application of Lewontin’s fallacy, as told by University of Wisconsin—Madison professor John Hawks:

"If you compare humans with other humans today, we differ by about one base pair out of a thousand. So, we’re between ten and twenty times more similar to each other, compared to what we are with chimpanzees. So, if you think about this in terms of years, we think that we divided from chimpanzees—our population split from them something like five-million years ago. Well, that means that humans, on average—two human genes split from each other, in ancestry, something like 500,000 years ago. If you look at us and Neandertals, they’re different from us by just a shade more than we’re different from each other, so that if you compare their genes and our genes, it looks like about maybe 800,000 years is the average. However, that’s recent enough that there are some human genes for which two human copies taken at random are more different from each other than one of them is from the Neandertal."

Hawks is referring to an estimate of the average divergence of autosomal DNA sequences between Neandertals and modern humans of 825,000 years. One should not confuse this with the timing of the populations diverging between 270,000 and 440,000 years ago. The overall genomes of modern humans and Neandertals are 99.84% identical, and only 78 protein-altering DNA changes separate Neandertals from the whole of modern humanity. In the study’s supplement, divergence is calculated not only for Neandertals, but also for a French person, a Han Chinese person, a Papua New Guinean, a Yoruban from West Africa, and a San person from Southern Africa. Here are the autosomal DNA divergence values calculated from a standard ratio of Neandertal-to-human distance over half of the chimpanzee-to-human distance:

French: 8.00
Han: 8.45
Papuan: 9.32
Yoruban: 9.43
San: 10.32
Neandertal: 12.67

This data would seem to suggest a genetic distance spectrum from Europeans to Neandertals with Africans closest to the Neandertals. That is an erroneous conclusion. This data made use of a reference human genome consisting of the DNA of an African-American who is genetically 50% white and 50% African. The numbers are composite autosomal divergences. For the European regions of autosomal DNA, shown below, the values are similar. However, the Neandertal divergence is slightly less, in accordance with the conclusion that Neandertals and non-Africans share 13 regions of DNA or an average of 2% of DNA from mixing.

French: 7.03
Han: 7.69
Papuan: 8.61
Yoruban: 9.27
San: 10.08
Neandertal: 12

The data for the African regions of autosomal DNA, below, look far more confusing. The Yoruban individual was actually not significantly closer to the African regions of DNA than the European regions, and the San person was even slightly (not significantly) closer to the European regions. Africa is the most genetically diverse region of the world. Perhaps its wealth of genetic diversity provided for such a manifestation of Lewontin’s fallacy.

French: 9.28
Han: 9.59
Papuan: 10.14
Yoruban: 9.17
San: 10.19
Neandertal: 13

Part of what makes this revelation so fascinating is its challenge to politically correct notions of race and the out-of-Africa anthropological model. Indeed, Green et al cite an estimate by Wall et al that non-Africans have 14% archaic ancestry. The implication is that the remainder of this archaic ancestry came from some other ancient primate population.

Equally intriguing is how Green et al inadvertently pits a traditional anthropocentrism against taboo, but perhaps commonly held, views of racial supremacy. Now, one should not consider the evidence of intimate relations between Neandertals and the ancestors of non-Africans a comeuppance. Obviously, "neanderthal" became an epithet on par with "cretin" or "jerk." On Razib Khan’s blog, one of the many co-authors of Green et al saw fit to defend Neandertals. "… I see no reason to think that they were not as smart as us."

Suppose the Neandertals were in some meaningful sense an inferior race. At least in a Darwinian sense, leaving a mere 1-to-4% of their genome is an underwhelming legacy. (Actually, Hawks says that each non-African has a different makeup of Neandertal DNA, and Green et al found that when the reference genome European regions were closest to Neandertal DNA, they diverged from the genome of Craig Venter, who is of European descent. Therefore, it is unclear to me exactly what percentage of Neandertal DNA collectively exists today in humans. Plus, Hawks thinks that it is still possible that Africans also have some Neandertal DNA that the study could not detect. That would result in a higher calculation of Neandertal ancestry for both Africans and non-Africans.) Even such a small percentage is a sufficient legacy to discredit the neurotic meme of racial supremacists/nationalists/separatists that impurity is abominable. Many possibilities could explain why so little Neandertal DNA remains in humanity, including natural selection. This leads to one useful argument against the supremacist meme: a Mendelian model.

White supremacists obsess over the dominance of certain phenotypes. Therefore, imagine that a population of brown-eyed individuals completely pair off with a population of blue-eyed individuals, and assume brown eyes are a phenotype with Mendelian complete dominance. There. In a single generation, all blue-eyed people vanish. But don’t cry, because they all passed their DNA onto a generation of brown-eyed heterozygotes. Statistically, about a quarter of the third generation will have blue eyes. Since blue eyes are so superior to brown, the forth generation will consist entirely of the blue-eyed.

Natural selection depends upon context or environment, which leads to a second argument, that of the inevitability of change. Skin color is a perfect example of environmental adaptation. The genes that influence human skin tone appear to be relatively few, and skin-expressed genes comprised the most common genetic differences between modern humans and Neandertals. If white people lost the ability to attain sufficient dietary folic acid, those who live in sunny climates would probably gradually evolve darker, melanin-pigmented skin. Even an otherwise inferior race of Neandertals could have had adaptations to the colder environs that they inhabited. Mixing and millennia may have allowed the non-Africans to absorb such advantages without ultimately losing advantageous African phenotypes.

One counterargument to consider is that holding off on mixing or preserving a differentiating subspecies could allow for further differentiation of some possible value. The process of natural selection is not teleological. Rather, evolution proceeds in whichever direction is immediately advantageous. Genetic separation helps to create a diversity of abilities and biological strategies. Moreover, often evolving in a distant environment leads to adaptations with nearly universal applicability. Just ask the brown tree snake, which immigrated to and now overruns the island of Guam, causing millions of dollars in damages each year. Invasive species cause damages in the United States worth $120 billion annually.

Animal predators as invasive species can devastate an ecosystem. However, a study by Sax and Gaines found that plant invasions of island ecosystems have actually doubled the amount of species diversity. Likewise, when two human populations come in contact, a gradient of mixing can result that creates a more complex form of diversity. Of course, it is hard to argue that leaving tiny segments of their DNA in the human genome was an adequate hedge against extinction for Neandertals. In fact, Harvard geneticist George Church hopes to bring them back from the dead. Nevertheless, the process of evolution did somehow work against these beings. The ethics and logistics of humanity guiding its own evolution receives surprisingly little analysis either from the scientists who might develop new means or from racialists who might possess the will.

With as much impact as humans have on the environment, of course they can shape the forces of evolution, but evolution will never stop. Even with the sprawling health care industry presumably treating hyperlipidemia and hypertension, humans are evolving to have lower cholesterol and systolic blood pressure, according to a recent study by Byars et al. The fact that humans are also evolving to be shorter and fatter may beg the label "dysgenics." However, such oversimplification flies in the face of a study by evolutionary psychologist Satoshi Kanazawa. He found that very liberal individuals have a nearly 12-IQ-point advantage and that atheists have a 6-IQ-point advantage. Monogamous men, but not women, have an IQ advantage, and that says it all. IQ allows one to overcome instinct. Liberal inclinations and abandonment of traditional beliefs can often come with personal costs. Liberals might sacrifice to help unrelated poor people. Atheists might miss opportunities for fellowship. Rather than higher IQ proving the evolutionary superiority of liberals and atheists, these associations may suggest that some height of IQ reduces biological fitness. However expedient blaming the welfare state for the apparent plateau of the Flynn effect in industrialized societies may seem, the context in which high IQ is actually genetically beneficial may be more limited than one might intuit.

The true meaning of the new understanding of Neandertals is that race is simultaneously more real and less important than the previous paradigm led some to believe. Racial purity is neither necessary nor sufficient to preserve the qualities by which some judge races, civilizations, and individuals. Those qualities would include intelligence, peaceableness, functional family values, productivity, and so forth. Nevertheless, race-realism has an important place in modern intellectual thought not only because race is real, but also because leftists have used racial disparities to discount these qualities and to discount the role of genetics in the formation of those qualities. Still, preserving human exceptionalism from fading into the background of natural selection is a cause more extreme and more just than the fancy to preserve any race.

Friday, January 8, 2010

Epistemology & Endocrinology

     How does one really know anything? As I have been researching genetic racial differences, I have frequently reencountered the dilemmas of scientific knowledge, such as the meanings of certainty and consensus. The skeptic Marcello Truzzi has been credited with originating the phrase "extraordinary claims require extraordinary proof." He actually defined extraordinary claims as being "revolutionary in their implications for established scientific generalizations already accumulated and verified." In that sense, skeptical claims also bear a burden of proof.
     Currently, the so-called Climategate scandal is receiving substantial attention from race realist bloggers. Skepticism can serve science well, but this particular movement has a clear political and financial constituency, and the climate science debate in the decades ahead could reach such an obvious conclusion that a veil of shame might extend to movements associated with global warming skepticism. Race realism science should stand on its own without its reception depending on unrelated causes. After all, race realism owes most of its taboo nature to World War II and Hitler rather than empirical disfavor.
     Therefore, I would like to briefly offer my own assessment of climate science before I detail the science of racial endocrinology, which could ultimately serve as the focal point of scientific understanding of racial differences. Though I must confess to the limitations of my knowledge of global warming research, I am cynical about global warming skeptics latching onto phenomena like El Niño or sun activity to repeatedly prophesy that the end is not nigh, as if they are Jehovah's Witnesses in reverse. In fact, I distinctly recall (though I cannot find a transcript) that Rush Limbaugh on his old television show interpreted the albedo effect of cooling caused by Mount Pinatubo's eruption as "Mother Nature" reversing global warming. How ironic that a conservative would employ the Gaia hypothesis to suggest that a living Earth would take it upon herself to negate human environmental impact. Even as skeptics attribute warming to a myriad of causes other than human activity, they refuse to accept that a temperature trend could have noise. Instead, they consider the record temperatures of 1998 as marking the year of complete reversal of global warming, which is not apparent from this graph:

     Even if all of that data is scientific fraud, no one seems to be disputing the rise of greenhouse gases or the greenhouse effect, itself. Therefore, even if anthropogenic global warming has not happened thus far, the greenhouse effect would presumably eventually overtake other influences on the climate.

     The fickleness of American public opinion on the matter seems to be contingent on gradients, much like support for the wars in Iraq and Afghanistan. How do things seem to be going? How soon and how bad will things get? What can be accomplished and at what cost? I, myself, felt relief when Archer et al placed radical positive feedback on global temperature escalations from a potential oceanic methane "belch" on the time scale of "millennia or longer." Then, Jain and Juanes detailed a mechanism by which methane could rise from the ocean much faster than previously thought. Methane is a more potent greenhouse gas than carbon dioxide.
     The Climategate scandal demonstrates politically correct liberals, who happen to be climate scientists, behaving like politically correct liberals. I consider it a greater scandal that the right wing has allowed the left wing to steal the cause of ecology. Even the Nazis had a green wing.

Polyglutamine Expansion Size Matters

     One link between race realism and environmentalism has been the alternative moniker "human biodiversity." As imperfect or imprecise as race realism may seem, I consider it superior to this pretentious ingratiation. It reminds me of atheists who demand that they be called "brights." Besides, every Seinfeld fan knows that one may not choose one's own nickname. As far as liberals are concerned, anyone who thinks independently about diversity is just a fascist white supremacist, anyway. Even worse, "human biodiversity" sounds prescriptive. I think it is fine if race realism informs one's views of interracial mixing—or global warming, for that matter. However, race realism science neither cares whom one marries nor what one drives. It just is.
     Author Steve Sailer explored the topic of interracial marriage in his 1997 National Review essay "Is Love Colorblind?" In particular, he offered his thoughts about the startling gender disparities of interracial marriage, pointing out that "on average, black men tend to appear slightly more and Asian men slightly less masculine than white men, while Asian women are typically seen as slightly more and black women as slightly less feminine than white women." Readers welcomed his insights by calling him "racist," "white supremacist," and a "typical white male" for peddling "age-old racial stereotypes," "prejudice," and "ignorance." If the media had reported the latest science on racial differences, Mr. Sailer would not have needed to postulate so modestly, and his oppugners could have skipped a self-induced hypertensive episode.
     Masculinity, of course, owes much to male hormones collectively called androgens. The level of expression of those androgens depends not only on the concentration of those hormones in the blood but also on the nature of the androgen receptor. At one end of the androgen receptor gene, which is alternatively labeled AR or NR3C4, there are varying amounts of the trinucleotide repeats CAG and GGC. The 1994 in vitro study by Chamberlain et al found that fewer CAG repeats caused increased transactivation of the receptor (meaning that the receptor became more activated to increase gene expression). Choong et al uncovered an association between fewer CAG repeats and higher amounts of receptors. In 1995, Irvine et al identified a 2.1-fold increased prostate cancer risk from having both fewer than 22 CAG repeats and not having the protective 16-repeat GGC allele. They surmised that the increased transactivation increased prostate cell proliferation, which "is known to promote tumorigenesis." They also produced the two tables below, showing African Americans to be the possessors of the alleles with the highest transactivation.

     Thus, African Americans average 18.5 CAG repeats, whites average 21, and Asians average 21.9. These results parallel both the prevalence of prostate cancer by population and Rushton's Rule, in which whites tend to be between the extremes of blacks and Asians. Sartor et al and Sasaki et al replicated these results. Edwards et al found such racial differences and also determined that the high rate of homozygosity in African Americans likely resulted from selection pressure.
     Genetic racial differences in the androgen receptor can give rise to disease susceptibility and trait disparities in the absence of racial differences in hormone levels. Research seems divided on the effects of CAG and GGC repeats on the actual baseline testosterone levels. Likewise, not all studies have found significantly higher baseline testosterone levels in African Americans, but Roney et al elicited transient salivary testosterone spikes that those other studies overlooked by developing an ingenious laboratory technique: expose men to young, attractive, and flirtatious women. Although the men scored the average of these women’s beauty a 5.83 on a scale from one to seven, the study failed to publish photographs. Nevertheless, men with fewer CAG repeats produced stronger testosterone responses to these ladies.
     This study also found that higher baseline cortisol suppressed testosterone increases with a beta coefficient equal to that of having more CAG repeats. Cortisol suppresses testosterone production, per Sapolsky and Dong et al.

Just How Nice is Sugar & Spice?

     Cortisol research has actually become a Holy Grail for politically correct liberals and people who make "alternative" or "integrative" medicine their hobby. The "central dogma," as one study put it, of cortisol research has been that stress is bad, and cortisol is a bad stress hormone. However, some research suggests that low cortisol or flattening of the daily circadian cycle of cortisol levels may be worse than high cortisol levels. DeSantis et al and Ukkola et al have found that African Americans have lower cortisol than whites. Liberals want to link this stress hormone to racism, which they presume is detrimental to the African-American psyche and physical well-being. Some research suggests that glucocorticoid hormones like cortisol affect memory processing and, therefore, cognition. Liberals also hope that cortisol stress response to discrimination will explain the higher rate of preterm births among African Americans. Two studies gave equivocal but arguably supportive results for this hypothesis. However, Lu and Chen failed to link preterm birth to stressful events other than "traumatic" events like becoming homeless or physical fights. Cohen et al also failed to link a higher level of evening cortisol to reported discrimination. DeSantis et al made much of the new evidence linking poor health outcomes to lower cortisol and the African Americans' considerably lower morning cortisol levels shown on the graph below. However, they also acknowledged the twin study by Bartels et al, showing a 60% heritability to morning cortisol levels. Hence, they turned their focus to a modestly higher evening cortisol level in African Americans, since this is apparently not heritable.

     This flip-flopping on the cortisol "central dogma" reminds me of the black-white suicide paradox. As an undergraduate, I came across some speculation as to why the universal oppressors, white males, have much higher suicide rates than the universal victims, black men. As author David Lester wrote, "The low rates of suicide in Africans in general, and African Americans in particular, may represent an African worldview which accepts suicide only in the very last resort in the face of extreme stress, an attitude consistent with the Afrocentric optimal psychology proposed by Myers and others." White men commit suicide more because they are prisoners to their own privileged status, which they must escape through suicide or bungee jumping. By the time I matriculated into medical school, the African-American male suicide rate was accelerating. The professors cited those startling statistics as further evidence of the oppression of the black man, while neglecting to mention that white men still had a higher suicide rate.

     Beginning with the 2004 Wust et al study on the effects of glucocorticoid receptor alleles on cortisol levels, progress in understanding cortisol heritability at the molecular level is slowly coming to fruition. Now, a new study by Way and Taylor has found that the short allele of 5-HTTLPR causes increased cortisol responses to a perceived social threat provided by the Trier Social Stress Test. As I previously mentioned, about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans possess this short allele. Also, a new study by Armbruster et al found that the 7R allele of DRD4 causes lower cortisol responses and that this allele interacted with the long allele of 5-HTTLPR to lower cortisol response to social stress. Beaver et al determined that African-Americans have significantly more 7R alleles than whites. The possibility that low cortisol levels in African Americans could be partly genetic has important implications for research on the genetics of violence. As I previously pointed out, the violence gene MAOA has a glucocorticoid and androgen response element, through which cortisol can up-regulate and testosterone can down-regulate MAOA enzyme levels. Sjoberg et al proved that higher testosterone levels increased aggressive tendencies in males with the 3R allele that is the most common MAOA allele in black people but did not increase aggression in males with the 4R allele that is the most common MAOA allele in whites.
     To summarize, African Americans have fewer CAG repeats in the androgen receptor gene, which somehow increases testosterone spikes. Higher testosterone decreases MAOA enzyme levels in those with the 3-repeat allele. Plus, androgen receptor alleles with fewer CAG repeats beget more androgen receptor activity. These receptors translocate to the cell nucleus and down-regulate the MAOA gene. African Americans likely have a significant genetic component to their lower baseline cortisol levels and lower cortisol spikes in response to threats. This further allows higher testosterone levels and decreases MAOA levels directly. Lower MAOA enzyme levels increase aggressive behavior, as my previous blog posts explain. These racial hormonal differences help to answer the black-Asian MAOA paradox: somehow Asians are much less inclined towards delinquent violence despite possessing about the same proportion of the 3R allele of MAOA. Greater prevalence of the 2R allele in black people cannot entirely explain the difference.
     The puzzle pieces are fitting together. One might predict based on this synthesis that fewer CAG repeats would correlate with aggression. Indeed, in 2008 Rajender et al determined that male control subjects average 21.19 repeats, rapists average 18.44 repeats, murderers average 17.59 repeats, and men who murder after they finish raping average 17.31 repeats. The shortest repeat lengths are associated with a higher degree of violence, earlier criminal records, verbal aggression, assertive personalities, extraversion, neuroticism, and self-transcendence (mystical tendencies), according to Cheng et al, Jonsson et al, and Westberg et al. Fewer GGC repeats are associated with aggression, impulsivity, promiscuity, and early menarche, according to Comings et al. A new study by Manuck et al localized the neural effects of shorter CAG repeat polymorphisms to the ventral amygdala, and previous research by Buckholtz et al found that the 3-repeat allele of MAOA is associated with increased amygdala activation.

Estrogen Poisoning

     Endocrinology studies a fascinating and complex web of hormonal interactions. Testosterone and cortisol decrease sex hormone-binding globulin (SHBG). SHBG, in turn, binds testosterone, which stimulates the hypothalamus to produce gonadotropin-releasing hormone, which acts on the pituitary gland to release follicle-stimulating hormone and luteinizing hormone. These hormones cause testicular aromatase to convert testosterone to estradiol. Studies show that young black men have higher SHBG than young white men. Specifically, I am referring to Abdelrahaman et al, Winters et al, Ross et al, Wright et al, and Gapstur et al (revealed only in a personal communication to Abdelrahaman et al). Black men have higher estradiol levels than white men, according to Morrison et al, Wright et al, and Rohrmann et al. The higher estradiol levels in black men have implications for bone mass, cardiovascular health, and, yes, violent behavior. Since estradiol decreases MAOA enzyme levels, one would expect higher estradiol levels to increase aggressive tendencies.
     By studying the plasma content of 214 twin pairs, Meikle et al calculated a 38% heritability for estradiol and a 62% heritability for SHBG. When Ahn et al published "the first comprehensive characterization of genetic variation in the sex steroid pathway" this past summer, I became somewhat disappointed that it could not definitively explain racial hormone disparities. Their supplement offered a list of 874 single nucleotide polymorphisms (SNPs) from 37 genes with p-values and beta coefficients for their effects on SHBG, testosterone, estradiol, and androstanediol-glucuronide (which converts testosterone to the more potent androgen dihydrotestosterone). To get a rough idea of how this data might relate to racial differences in hormones, I created graphs with p-values as the independent variable (making the graph most trustworthy towards the left side) and with the accumulative sums of beta coefficients multiplied by the allele prevalences for each population the dependent variable. In other words, the amount the graph rises with increasing uncertainty depends on both how common the more active alleles are in that group and how much effect that allele has on the hormone (or SHBG) concentration in blood. I calculated prevalences for whites, blacks, Chinese people, and Japanese people by combining all relevant populations in the HapMap database. Since the study population consisted entirely of white men, I expected a bias towards higher levels in whites, for whom these SNPs were selected and the beta coefficients were determined. In fact, each graph produced exactly that result with the exception of estradiol, shown below. The line for black people jumps above that of whites due to the adenine (A) allele of rs2687105 in the gene CYP3A4. The significance of this is questionable, as I have found no studies of breast or prostate cancer that found any correlation for this SNP. CYP3A4 produces an enzyme that mostly metabolizes testosterone but can also metabolize estrogen. Other variants of this gene may play a role in racial disparities in prostate and breast cancer.

Sweet and Noble It is to Die for One’s Meme

     Surely, everyone can comprehend that they will not wake up tomorrow and read the morning paper headline, "Cancer Cured!" The fight against cancer is incremental with multiple simultaneous strategies. One strategy would be to individually customize pharmacology based on decoded DNA. Every day you take the pill that is perfect just for you. Unfortunately, this approach is in its infancy. A superior approach to just waiting for this science to mature would be ethnopharmacology, in which drug approval is categorized for specific populations based on probability of benefit for individuals. Since different populations tend to have different medically-relevant allele frequencies, doctors could prescribe drugs based on the probability that the patient is like others in his or her ethnic group.
     The US Food and Drug Administration has already done this for BiDil, which was just a combination of existing approved generic drugs. It might not surprise that a drug created for improved compliance would help African Americans more given the new study by Roth et al, showing that African Americans had worse medical literacy (29% had adequate short test of functional health literacy in adults [S-TOFHLA] scores versus 58% of whites) and more medication-related problems, despite taking fewer medications. After poor sales, NitroMed stopped marketing BiDil and sold it to JHB Pharmaceuticals.

     In July, the Journal of the National Cancer Institute published a nearly 20,000-subject study, which sought to determine whether race affects cancer mortality independent of socioeconomic status. The "provocative aspect" of the study's conclusion was that the only cancers that have higher mortality for black people are the "sex-specific cancers (breast, ovarian, and prostate)." Apparently not knowing where they were supposed to stop, the authors continued that "one explanation for our findings might be that there are hormonal factors . . . that differ by race." Kathy Albain led the study. An accompanying editorial by Otis Brawley of the American Cancer Society decried "racial medical profiling," reminding the reader that race "is not a scientific categorization and is a construct rejected by anthropologists." Then, Catherine Elton wrote a tract in Time magazine that would have seemed like a slander that Dr. Albain is racist had it not included the disclaimer "no one is accusing authors like Albain of racism." Elton is a recipient of an exclusively female fellowship "to focus exclusively on human rights journalism and social justice issues."
     Progress in racial endocrinology may require braving (and possibly proving) a muck of the most offensive and sexualized stereotypes in order to better treat some of the most common and deadly cancers, (not to mention the disease of violence). I am hopeful in that I expect that we shall accomplish this before the methane belch ends our pitiful existence.

No Amore for MAOA from Maori

      It would be easier for me to keep up with the latest celebrity deaths if there were not such accelerating developments in genetics of violence research.
      Here in the US, most liberals seem to have made up their minds that they are the true defenders of science against the evil forces of the religious right. However, in some parts of the world, liberals have clued into the fact that science threatens some of their own presumptions. With regard to the genetics of violence, New Zealand liberals are standing up for the Maori, New Zealand’s most violent ethnic group, against a specter of a scientific right. It seems to have begun with a 2006 interview with Dr. Rod Lea about the fact that about two-thirds of Maori have the moderately violence-associated 3-repeat allele of MAOA.
      “Obviously, this means they are going to be more aggressive and violent and more likely to get involved in risk-taking behaviour like gambling,” he reportedly said. “It is controversial because it has implications suggesting links with criminality among Maori people. I think there is a link. It definitely predisposes people to be more likely to be criminals and engage in that type of behaviour as they grow older.”
      Seven months later, The New Zealand Medical Journal featured two essays that presented no new evidence. Rather, the first by Merriman and Cameron merely criticized the assumption that a genetic association found in whites can be applied to other racial groups. The second was co-written by Dr. Lea, himself. This essay attacked the anonymous journalist who conducted the 2006 interview for distortion, “misquotes,” “misunderstandings,” “misconception,” and “negative media hype.” This essay declared that their “research agenda” “does not involve investigation of aggressive traits in Maori or any other population.” Furthermore, “the extrapolation and negative twisting of this notion by journalists or politicians to try to explain non-medical antisocial issues like criminality need to be recognised as having no scientific support whatsoever and should be ignored.”
      That anyone could fail to see violent criminality as a medical issue should give emergency room doctors pause. Genetic or not, understanding this issue has life-and-death consequences. The most extreme manifestation of MAOA dysfunction, Brunner syndrome, revealed the value of dexamethasone treatment in raising MAOA levels in female carriers. Research in mice showed the potential of the experimental drugs Fenclonine, ketanserin, and tetrabenazine to lower neurotransmitter levels to normal levels. At the very least, at-risk youth could alter their diets because they may have excess tyramine from chocolate, red wine, or cheese, and restricting the amino acids phenylalanine and tryptophan could lower neurotransmitter levels without drugs.
      The point made by Merriman and Cameron was a reference to a study by Widom and Brzustowicz, which was recently echoed in an essay by G Raumati Hook, who compared Preimplantation Genetic Diagnosis to Nazi eugenics. I previously pointed out how the Widom and Brzustowicz paper hid their data on African Americans because it probably showed that the extremely violence-inductive MAOA 2-repeat allele is not so rare in African Americans. Another conclusion of Widom and Brzustowicz was that maltreated white males demonstrate greater lifetime aggression if they have the 3-repeat allele rather than the 4-repeat allele, but that this is not the case for non-whites. Here again, they drew a deceptive conclusion by hiding their data. They found that white females with 3R alleles did not have higher lifetime aggression, only higher juvenile aggression. This parallels other research such as Sjöberg et al (2007) that suggest the MAOA 3-repeat allele does not increase female aggression. When Widom and Brzustowicz reported on the effect of MAOA in “non-whites,” they only gave data on men and women in combination. Their entire sample was only 39% non-white, and their non-white sample of 3-repeat allele subjects was 57% male, compared to 76% of white 3-repeat allele individuals. (2-repeat allele subjects were excluded from analysis.) It is also questionable what conclusions can be determined from the presumably diverse group of only 35 non-white men with the 3-repeat allele. Perhaps the results would have been different if the six non-white men with the 2-repeat allele were included. Nevertheless, the conclusion that a gene would behave differently in different races is a remarkable break from the traditional politically-correct assumption that race is a mere social construct. However, their conclusion about MAOA in non-whites was contradicted by studies by Weder et al and Beaver et al.

      It would be difficult to overstate how intense the research focus on MAOA has become. I took the time to create a table that summarizes just the evidence comparing the 3-repeat allele to the 4-repeat allele in their effect on aggressive behavior. Even many of the scientists who study it seem to be missing the big picture, so I color-coded each study. Red studies either showed that the 4-repeat allele was more associated with aggression or that the difference was not statistically significant. Blue studies showed a significant association between the 3-repeat allele and aggression either with or without childhood maltreatment as a precipitating factor, at least in men. Purple studies had debatable results.
      Some points can be drawn from this table. One is that MAOA has bucked the trend of early studies’ positive findings giving way to negating studies, which has been common among gene associations that did not bear out. Another is that aggression is just one manifestation of antisocial behavior, which could explain why many such studies found no association. Yet another is how the pace of research has increased over the years.

      The table also illustrates the importance of the gene-environment combined effect on aggression, in which childhood maltreatment is also factored. Here is the same table with just those studies investigating this effect. It was originally discovered by Caspi et al, who spent decades interviewing and observing their subjects to discover maltreatment. The other studies that came out so quickly afterwards did not have time to investigate so thoroughly, and their outcomes when they successfully replicated Caspi et al tended to be less robust.

      Here is the table with only studies of adult males. Those studies that are still red are either just not quite statistically significant or have explanatory qualifiers. Thus, there really should be no question that MAOA is a violence gene even with the relatively modest difference between the 3-repeat allele and the 4-repeat allele.

      Now, MAOA is probably not the only gene that affects violent behavior, even if it is the most important gene for this. Reif et al found that the short allele of 5-HTTLPR enhanced the aggression effect of the 3-repeat allele of MAOA. Reif et al did not find a “main effect” of 5-HTTLPR alone on aggression, but a few other studies have. In the case of MAOA, the 3-repeat allele is much more common in Africans and Asians than in whites, but for 5-HTTLPR, the short allele is found in about 70-80% of East Asians, 40-50% of Europeans, and just 10-30% of Africans and African Americans. This should serve as a warning to watch out for any gangs of violent Asians on their way home from the library. In truth, Retz determined that the short allele only increased violence 5%. Plus, Patkar et al failed to find an effect of the short allele on aggression in African Americans, suggesting that the gene could have different effects in different races. (See above, regarding the novel consensus that race is not a social construct.)
      Genetics research is rapidly moving humanity towards an understanding of violence that is complex and, for some, deeply offensive. Sadly, as violent crime claims 17,000 lives per year in the US alone, some progressives are aligning themselves against progress.

Deus ex Machina Genetics

Since I began speaking out about the genetics of violence, the entire field of genetics has reached a tipping point of high stakes and high drama. The stakes are that this field, which I would characterize as being presided over to some extent by ivory tower liberals, may be on the verge of proving once and for all that black people have a greater genetic predisposition to violence, or the field may wipe away this evidence along with a couple of decades of knowledge from gene association studies.

Prior to this scientific cataclysm, I received some interesting feedback from a presentation on the genetics of black violence that I created. When the blog Half Sigma reported on the recent study that associated gang violence with the 3-repeat allele in the promoter of the violence gene MAOA, the readers immediately wanted to know about racial prevalences of the alleles. Henry Harpending, the famous researcher who has studied recent human evolution and who co-wrote a new book with Gregory Cochran, pointed to the Sabol et al study, which determined that two-thirds of white people have the 4-repeat allele that is not associated with violent behavior and that 60% of African-Americans and Asian-Americans have the more violence-associated 3-repeat allele.

As one of the few studies of MAOA that lays out such racial prevalences, this study is quite an enigma to me. One might expect a study of nearly 1,500 subjects to more accurately reflect reality than smaller studies, but the study apparently discovered no subjects with the 2-repeat allele, which has a markedly greater association with violence than the 3-repeat allele that has received so much attention. Other studies, like one of 1,100 American males by Guo et al, found that 1% of American males possess this allele. MAOA is on the X chromosome, of which females have two, giving the Sabol et al study well over 2,000 chromosomes to examine. Therefore, I would have expected about 20 or so chromosomes to have the 2-repeat allele, instead of none.

I point all this out because Harpending, for one, relied on Sabol et al to describe the allele frequency of the MAOA promoter in black people. Other studies have replicated the allele frequency of Sabol et al for white males, always with about 1% having the 2-repeat allele. However, two smaller studies offered evidence of a significant proportion of black people having the 2-repeat allele. After I showed the Half Sigma readers my video, someone who goes by the pseudonym, Nanonymous, drew my attention to an important hidden fact about one of the two smaller studies. It was the study by Widom and Brzustowicz, detailing prevalences of rare MAOA alleles, including the 2-repeat allele. The study considered one of its major findings to be a lack of an association between violence and the 3-repeat allele just in non-whites, but it only had 98 non-white male subjects. Then, it claimed to re-analyze the data just for black subjects with “no change in the results.” We do not receive any hints as to how many of the 98 non-whites are black. However, as Nanonymous pointed out, some of the subjects in this 2006 study also took part in a 1989 study by Widom. That study did not look at genetics, but it did reveal that its 1,575 subjects were 67% white and 31% black, leaving just 2% for other groups. For the 2006 study, just over 600 agreed to undergo DNA analysis out of the original 1989 cohort plus 1,196 additional subjects. They were 60.9% non-Hispanic white and 39.1% “non-white.” Having successfully covered up the proportion who are black, Widom and Brzustowicz felt comfortable revealing that 6% of the non-white men had the ultra-violent 2-repeat allele, and none had the other rare alleles. In 2006, Rosenberg et al found that 5 of 37 (13.5%) African-Americans had rare MAOA alleles, which was corroborated by a greater frequency of associated rare haplotypes of the MAOA gene, itself. In general, Africans would be expected to have more rare alleles because non-Africans descend from only a subset of the African population.

Then, the earth shook. Risch et al published a meta-analysis on the association between depression risk and the interaction of stressful life events and a serotonin transporter gene. They went beyond disproving this association to indicting the whole enterprise of candidate gene association studies. Then, they suggested that delinquency “may not even be under strong genetic influence” and specifically attacked the use of MAOA gene testing in forensics, referring to it as one of the “nonreplicated genetic associations.” The influential genetics blog, Gene Expression, picked up the story, with the writer known as P-ter declaring that the majority of gene association studies, including that of MAOA, are likely wrong. He later posted that correct associations found in genome-wide association studies tend to require thousands or tens of thousands of subjects, making studies with just hundreds of subjects essentially worthless. P-ter singled out for criticism Avshalom Caspi, the researcher who first published an association study for the serotonin transporter gene and depression and who first published an association study comparing the MAOA 3- and 4-repeat alleles’ influence on violent delinquency. “[E]verything he’s published is probably wrong,” P-ter sneered.

I was the first to comment, and I conveyed my shock. “So, I guess you don’t believe in Brunner syndrome, either,” I said. Brunner syndrome was first identified in 1993 as a point mutation that caused complete MAOA deficiency, and it is associated with aggressive outbursts, arson, attempted rape, and exhibitionism. P-ter tried to deny that the existence of Brunner syndrome is sufficient to lend credence to the influence of the promoter alleles. I reminded him that the MAOA Caspi et al study was not a study of the 2-repeat allele (since only one subject had it), and this allele has consistently shown a greater association with violence than the 3-repeat allele. Therefore, MAOA expression has a continuum from Brunner syndrome, to the 2-repeat allele, to the 3-repeat allele, and, finally, to the 4-repeat allele. However, P-ter may be right that the many other phenotypes studied in association with the MAOA promoter may be disproved.

I did my own review of the scientific literature that specifically sought to replicate the Caspi et al study of the 3- and 4-repeat alleles of MAOA in white males. Twelve total studies sought to replicate the study in one manner or another. Only three of these had unequivocally non-significant results. Confirmatory studies raised questions about the methods of those studies, such as the narrow definition of the environmental exposures. A study by Sjoberg et al found an association between the 3-repeat allele of MAOA and aggression when testosterone levels are high. Thus, even though this study did not try to replicate Caspi et al, it gives additional indirect support by using an aggravating environmental exposure (testosterone), which can be objectively measured. All told, the studies that looked at the interaction between the 3- versus 4-repeat allele genotype and maltreatment had a combined sample size of over four-thousand white male subjects. Granted, a serious meta-analysis would exclude some studies. Kim-Cohen et al attempted a meta-analysis, but it included its own cohort, and rather than look at an outcome of aggression in that cohort, it noted an association with composite mental health problems, and ADHD, in particular.

During the discussion on the Gene Expression blog, the Australian researcher, Daniel MacArthur, first hedged, “As for MAOA: I wouldn’t bet my house on this not turning up in [a] well-powered GWAS [genome-wide association study] for violent behaviour (as P-ter predicts), but I’d say the odds of this happening are much better than 50%.” He later conceded “that the evidence for an association between the VNTR [variable number of tandem repeats] variant and antisocial behaviour is substantially more consistent than most of these associations. This may well be one of the rare cases of genuine associations.…” I am pleased if a rank amateur, like myself, can help to convince a group of researchers not to glibly dismiss the past seven years of research on a gene for violent delinquency just due to an embarrassing failed association in the study of depression. I noticed that the original study on Brunner syndrome found that dexamethasone treatment increased MAOA expression of female carriers of the mutation. I really believe that this line of research will save lives. I was also happy to see contributions to the discussion from writers that I admire like Steve Sailer and Gregory Cochran.

This may indeed be a watershed moment that will lead to far more skepticism of future candidate gene association studies. Hopefully, replication studies will become more standardized. I look forward to reading any potential large genome-wide association studies for violent delinquency. P-ter envisioned that such studies would uncover multitudes of genes with each having very small effects. However, I agree with Cochran that violent behavior can be biologically advantageous. Plus, I have long been intrigued by the possibility of “master genes” or other ways of coordinating evolutionary change, so that life can adapt to changing environments.

I also think that it is important to be mindful of the politicization of science. Much of the articulation in the popular press of the notion that race is a social construct that I have come across was actually in the defense of the Human Genome Diversity Project. This project has sought to decode the genomes of all the diverse branches of our human race. However, some activists tried to shut it down out of a fear that biological weapons against specific peoples would result. Therefore, the defense that there, in fact, is no one gene for being black was put forth. Furthermore, as MAOA demonstrates, genetic racial differences are almost always just disparities of allele frequencies. Even so, those differences are enough to cause hysteria. Consider this statement at the end of Ellis and Nyborg’s study of racial differences in testosterone levels: “scientists should be on guard against even the hint of any misuse of research findings in this area.” I suppose it is a sort of misuse of science for one to childishly berate a group of people and identify with a “superior” group to compensate for one’s own inadequacies. The irony is that this statement was followed by an acknowledgement for the help given by J. Philippe Rushton, a scientist well-known for his courageous disregard for suppressive sensitivities concerning everything from brain size to penis length.

Other examples of science politicization abound. Last year, the blogger known as "gc" was concerned that the Obama administration might censor human biodiversity science. Harpending responded that he received an invitation from the National Human Genome Research Institute to attend a workshop about the ethics of researching and publishing evidence of natural selection in humans. Another example is how Bruce Lahn seemed to be under pressure when he decided to forswear IQ-related genetics research. Now I am wondering if the actions taken in the Widom and Brzustowicz study and the gratuitous linking to the MAOA-aggression association by Risch et al were further examples.

The Gene Expression blog has been an invaluable ally of human biodiversity research. The writers are highly intelligent freethinkers. The fact that some of them have some liberal-leaning views and were early supporters of Howard Dean is no more an incongruity with their race realism than is the Christian faith of Steve Sailer and Charles Murray. It would only help this line of research to make it a little more acceptable in polite (that is, liberal) company. On the other hand, I am noticing eroding anonymity for certain writers, which could be a problem for them because liberal academia, I believe, is their home. (Full disclosure: nooffensebut is not my real name.)

If, somehow, MAOA promoter alleles should ever be proven meaningless, as P-ter suggested they would be, I shall follow the scientific ideal described by Richard Dawkins in The Root of All Evil. I shall rejoice at having been proven wrong, such that scientific truth is advanced. Thankfully, we all believe in science.

Why I am a Supremacist

During medical school, The Spirit Catches You and You Fall Down by Anne Fadiman was required reading. This is the story of a little Hmong girl with epilepsy. Her refugee parents preferred traditional folk remedies to Western medicine. Consequently, the child developed mental retardation. At one point, the state took custody of the child because her parents kept rejecting medical advice. Throughout the book, Fadiman laid out how the arrogance of the doctors created barriers between the medical community and the Hmong community. She also extolled cultural relativism and faith healing and endorses patient referrals to shaman priests. The book was right to advocate for a diplomatic approach to practicing medicine through cultural sensitivity and employment of the Kleinman questions. However, I am thankful that the medical establishment has discarded her oppressive cultural permissiveness. Recently, several high-profile, tragic stories have drawn attention to the ironically-named practice of “faith healing.” In one case of particularly outrageous horror, 16-year-old Neil Beagley died painfully from bladder constriction. Catheterization, a procedure so simple that many people perform it on themselves multiple times each day, would have saved his life. His parents were charged with negligent homicide.

Just as one does not choose one’s race or one’s parents, one does not choose to be brought up in a religion or culture that disallows modern medicine. Therefore, if a physician believes that the welfare of a child under his or her care absolutely depends upon an intervention which the parents oppose for religious reasons, that physician is ethically bound to treat. 90% of court decisions favor physicians in such disputes, and Prince vs. Massachusetts found that parents may not “make martyrs of their children.”

Therefore, I would like to dissent from a seemingly disingenuous defensive posture that some white nationalists and other race realists take by declaring myself a supremacist. I am at least a supremacist of Western allopathic medicine. Furthermore, some of my values have absolute applicability. Granted, I use “absolute” in a relative sense. I am not seeking to refute the whole post-modernist movement, as Edward O. Wilson once tried. Nevertheless, within the limited confines of modern human civilization, I dedicate myself to the Enlightenment, including science, medicine, and the appropriate employment of technology. Not only am I a supremacist, but I am also a conniving, swindling supremacist, in that I want Western medicine to suck the very the life from every folk, Chinese, or “complimentary” medicinal treatment. If acupuncture is any better than placebo shams, I want a big pharmaceutical company to find out why, put it in a pill form, and get filthy rich in the process.

Self-described race realist, Jared Taylor, with all due respect, seems to be playing a game. His American Renaissance Web site updates daily with media headlines and accompanying, often clever and sardonic subheadings that unclothe racial angles. Rather than expound on white culture and heritage, Taylor is confronting black people and immigrants. I vaguely remember a few cheap shots, and I think some failures in the white community could deserve similar ridicule, but basically I agree. I think white Americans have legitimate grievances with our black community, such as their rate of violent crime, and we are right to defend standards like the SAT against them. I do not currently feel aggrieved towards, say, Nepalese people. In other words, whites are right, except when we are not. We stand for some things that are greater than ourselves. Still, Taylor wishes to back away from moral judgments and to affirm unconditional love for whites, as his people and his family.

Reading these reports might give white people a sense of pride. However, it is also possible that non-white people might acquaint themselves with this information and agree. Some of them might be inspired to bring change to their own ethnic community. Others might develop a fondness for white people and wish to assimilate into a white society more so. Many persuasive arguments remonstrate against immigration law relaxation, for instance, and for those reasons, I oppose it, as well. Yet, saving one’s worst rancor for those non-whites who most admire whites seems maladroit to me.

For all the accomplishments of white people, non-white people also develop ideas and tools, and it has been our Western tradition to engage in trade and even some cultural exchange. Japan understood the value of such exchange, and they adopted American Total Quality Management, to the long-term detriment of the US auto industry. Francis Galton understood the value of trade. He felt that Chinese people made better trade partners than Africans, so he wanted to Sinicize Africa. China has successfully adopted Western science, and I just discovered that Richard Lynn has a new book, which predicts Chinese ascendence on the order of the Roman Empire due to their adoption of something like Western eugenics. Jared Taylor has paralleled his own fight against immigration to the Dalai Lama’s protestations against Chinese settlement in Tibet. Considering China’s enormous investments in Tibet, I think a race realist should admire this spread of Western standards of living.

I reject the generic humanities professor’s stock straw man for racial realism. I am not an incurious, belligerent curmudgeon who must define “Us” by defining the “Other.” I am aware of Robert Putnam’s inadvertent discovery that diversity is not necessarily a strength, but I also understand a basic truism that diversity is not always the same. The experience of diversity from working with fellow physicians feels different from experiencing diversity by living near the Rio Grande. (In fact, Putnam’s figures show high levels of trust in diverse Silicon Valley.) For those who disagree with me, I suggest a “big tent” approach. Race realism is also about science, understanding the human condition, and finding cures by acknowledging biological differences. Jared Taylor should continue to forgo sowing discord with those race realists who lack the agenda of sowing discord.

The Post-Racial Era is Over

The headline from LiveScience reads, “Boys with ‘warrior gene’ more likely to join gangs.” The byline reads, “By LiveScience Staff.” This is an era in which the death of a popular president is met with the reminder that he supported “states’ rights,” which was supposed to be racist code to win white votes. Therefore, surely the mainstream media must have had some unease to pass along research on the genetics of the “gangsta.” Despite the Borat-reminiscent choice of subject, the actual study did not broach genetic racial differences. The study reported that males with 2, 3, or 5 repeats of the promoter to the MAOA gene were twice as likely to join gangs and violently use weapons and four times as likely to both join gangs and violently use weapons. Another statistically significant finding was that white males were a third as likely to join gangs as non-white males. That MSNBC would pick up the story about race, violence, and genetics only a week after YouTube banned me for reporting on similar studies is rapid progress, indeed.

Change is here.

Last year, Jared Taylor and John Zmirak had an interesting exchange about race and IQ. Put me in Taylor’s camp, insofar as discussion of IQ is self-defense against blacks’ smashing of American education and standardized testing with disparate impact. However, the IQ emphasis is a throwback to the era of political correctness. This was a time of obfuscation about social science and statistics. The evidence was unsatisfying, and the debates were ugly. Despite some studies uncovering apparent IQ genes like DTNBP1, CHRM2, SNAP25, and COMT, the search for a genetic map of IQ has eluded scientists. A recent review article determined that the effect of any one such gene accounts for less than 1% of IQ variance, and not a single genetic locus is “unequivocally associated” with IQ. Moreover, as Taylor admits, “comparisons are odious.” Comparing IQ scores is particularly unseemly, as the very concept inspires ambivalence. Obsessing over IQ creates the impression that race realists consider the human brain to be little more than an IQ-producing machine. An inability to grasp the multifaceted nature of the personality suggests a lack of dimensionality in one’s own. It is not anti-intellectual to stay the boldest assertions about the genetics of race and IQ until the evidence exceeds mere statistical associations between behaviors and test scores.

So, it is time for race realists to get real. The time for arguing about the biology of intelligence has not yet come. Now is the time to educate people about the steady flow of data showing how recent evolution and the Founder effect have resulted in manifold genetic differences and genetic disparities between racial and ethnic groups. Usually the evidence will be nuanced with different prevalences of specific alleles in specific populations, as is the case with MAOA. However, a patience for working through the daunting complexity will have a lasting impact. The totality of the evidence will take heat off of groups that are traditional scapegoats due to their strengths and successes, such as Asians and whites. Likewise, it will end the patronizing implicit suggestion that sub-Saharan Africans are uniquely lacking in free will, such that oppression is to blame for their every problem. Obviously, the evidence will face resistance. As Jonathan Haidt predicted, “the ‘Bell Curve’ wars of the 1990s, over race differences in intelligence, will seem genteel and short-lived compared to the coming arguments over ethnic differences in moralized traits.”

On the other hand, notice how lacking in dissension the media’s reporting on the “warrior gene” has been. Violence is about as manifest as a phenotype can get. Violent delinquency possesses no equivalent of the Flynn effect. In terms of ethics, racial differences in genetic violence beg the question, “Who is oppressing whom?” I remember how a news anchor empathized with African-Americans who rioted in Los Angeles in 1992. When Indonesians rioted against Chinese people in 1998, no Western media outlet, to my knowledge, bestowed the Indonesians with righteous excuses. Mao Tse-tung said, “political power grows out of the barrel of a gun.” In our media-driven society, the interpretation of violence has a far greater effect than the violence, itself.

The single greatest obstacle to the new racial realism may be overcoming the sense that it is a hopeless conclusion. Considering the latest progress in genetic engineering, as well as the possibility of other treatment modalities and early screening, a moral argument against spreading this knowledge is far more subjugating. What if race realism could cure inequality?