CHAPTER SEVEN

America’s Biggest Lie

Race and Intelligence

RACE AND INTELLIGENCE WAS A QUESTION I DID NOT EXPECT to take on as a major part of my scholarly work. As a graduate student at Michigan, I became aware of the history of biological determinism and its relationship to race and IQ claims. However, despite a substantial history of social activism, I was not deeply engaged in the intellectual fallacies at the core of race and intelligence claims. It turns out that my work in the evolutionary genetics of aging prepared me to take on the problem of biological determinism, race, and intelligence. Intelligence, however defined, is a complex trait, just like aging. Complex traits are always determined by the interaction of genes, environment, and chance. Thus, the quantitative genetic tools I used to understand how life history evolved in fruit flies could just as easily be deployed to understand how intelligence could have evolved in mammals (including people). Quantitative traits differ from those of classical Mendelian genetics in that they must be measured. For example, life span, cognitive performance, height, weight, blood pressure, endurance, running speed, immune function, and physical strength are examples of things that are measured. Simple traits such as eye color or whether one can move one’s fingers independently are determined qualitatively and controlled by variation at one or a few genes.

Quantitative genetics concerns itself with the sources of variance in a given trait. For example, if you measure the height of thirty-five one-year-old female children in your neighborhood, you can calculate their average height, as well as the variance (or statistical spread) of the group’s height. Your intuition should tell you that the genetic makeup of the individuals whose height you measured contributed to the variance. The variance in traits resulting from genetic influences is symbolized as V_g. Many psychometricians (those who measure intelligence), biological determinists, and eugenicists would have you believe that genes tell the whole story. They do not. The environment individuals experience also contributes to variance in traits. The variance in traits that results from environmental influences is symbolized as V_e. A group of kids from a wealthy neighborhood who had experienced excellent nutrition, had not been exposed to high levels of environmental toxins, and had been given regular physical checkups would approach the average value in height expected for their age group and would have some small measurable variance in height. However, if added to this group were children from an impoverished neighborhood who had experienced poor nutrition, had routinely been exposed to toxic materials, and had been given few visits to doctors, then the group’s mean height would be well below the expected value for their age group, and the variance in the group’s height would increase.

If genes and environment were the only two factors contributing to the complex traits, things would be a whole lot easier to understand. However, specific genes may react to the environment in different ways (called gene-by-environment interaction, V_g×e). Furthermore, specific genes may be distributed in a nonrandom way with respect to a given environmental factor. This is captured by a statistic known as the covariance, symbolized as Cov(G,E). Finally, our ability to accurately measure the trait in question may also come into play, so we need a term that captures this (symbolized as V_error). For a simple trait such as weight or height, the error term is probably very small. However, more complex traits, such as those associated with behavior, could contain a very high amount of error. The interaction of all the factors involved in producing a complex trait can be measured, and comparing the amount of interaction produced by genetic factors to the interaction produced by all the others allows one to determine the heritability of the trait. Heritability is how much the offspring resemble their parents. It plays a crucial role in the power of natural selection to modify a trait. Understanding heritability has always been an important aspect of debates concerning intelligence. It is at the root of the nature/nurture controversy.

MY WAR WITH RACIAL PSYCHOMETRY BEGAN WITH A PHONE call. Benjamin Bowser (California State University, Hayward, and associate editor of SAGE Race Relations Abstracts) asked me to write a piece addressing resurgent biological determinism and pseudoscience. It was to focus on Afrocentric pseudoscience and biological determinism. In the essay I addressed one of the core fallacies of so-called Afrocentric science. This was the theory that a deficiency of melanin caused the psychological problems of white people. This idea was championed by the psychiatrist Frances Cress Welsing, who characterized the “quality of whiteness” as a disease associated with the inability to produce color.¹ The problem with the melanin theory is that it conflates different melanin molecules (and portions of these molecules) as if they carry out the same functions. Melanin pigments are widely distributed throughout the animal kingdom, found in hair, skin, the irises of the eye, and the substantia nigra and locus coeruleus of the brain.² Black and brown melanins (eumelanins) arise from the amino acids L-tyrosine and L-dopa, while yellow and red melanins (phaeomelanins) arise from eumelanins containing sulphydryl compounds. Sulphydryl compounds are any carbon-containing compounds linked to a -SH (thiol) group. They are powerful antioxidants. Black melanin synthesized by the brain is called neuromelanin. Eumelanin and phaeomelanin synthesis occurs in specialized organelles of the melanocytes called melanosomes and become insoluble granules. Neuromelanins, on the other hand, are found in the cytoplasm of catecholamine-producing neurons. The value of eumelanin and phaeomelanin lies in their capacity to absorb ultraviolet light; neuromelanin is not found in light-sensing tissue. Its value is as a neurotransmitter, due to the capacity of a different portion of the molecule to transfer electrons. It is also obvious that the patterns of gene expression in neurons and in skin cells differ dramatically.³ Therefore, there is simply no way to evaluate how differences in skin pigmentation would account for differences in complex behavior.

IN 1993 I WAS BEGINNING TO MORE FULLY UNDERSTAND HOW white supremacy operated in the context of the scientific enterprise. Specifically, I now realized the importance of the ideological justification required to convince millions of Americans to hold back other Americans because of their racial identity. A key element of this program was the idea that the flaws of the racialized people themselves, rather than the structural racism in society, prevented their success. This classic tactic of blaming the victim is deeply woven into the psyches of white Americans by the legacy of slavery and Jim Crow.⁴ The 1990s saw a resurgence of this kind of thinking, particularly directed at affirmative action programs.⁵ Two prominent American academicians, psychometrician Richard Herrnstein and political scientist Charles R. Murray, provided a powerful tool buttressing anti–affirmative action arguments: The Bell Curve, published on September 1, 1994.⁶ The book was not peer reviewed. Prior to publication the manuscript had been read by some of the authors’ fellow travelers, but it had not been subjected to any objective scholarly examination. The book’s message, reduced to its simplest elements, was that intelligence (IQ) was a generally agreed upon concept that could be objectively measured by a variety of standardized tests. Such tests taken together measured the concept called generalized intelligence, “g,” which was defined as a multidimensional measure of an individual’s capacity to solve novel problems and of the amount of their stored knowledge. Thus, the authors of The Bell Curve would have claimed that the “g” of Nobel laureates such as William Shockley or of UC Berkeley professors such as Arthur Jensen was very high, while that of the person collecting garbage or stocking grocery shelves would be much, much lower. Thus, they proposed that America was a meritocracy in which an individual’s social status was primarily determined by his or her general intelligence. Herrnstein’s model of IQ and social status had been well-known for at least two decades. It was published by the Atlantic Monthly in 1971 in an essay titled “IQ.”⁷

One of the book’s most controversial claims was that racial groups differ in their average intelligence. In Chapter 13, “Ethnic Differences in Cognitive Ability,” the authors presented a graph showing the Black and white distribution of IQ based on data from the Armed Forces Qualifying Test (AFQT, the army’s version of the Scholastic Aptitude Test) administered in 1980 from the National Longitudinal Survey of Youth (NLSY) (Figure 7.1). This figure compared the distribution of IQ-test scores for an equal population size and showed that the mean Black IQ was approximately 84 and that of whites approximately 104. The difference between the mean scores was 1.2 standard deviations (SD). Using any standard statistical test for the difference between averages (or means), one would conclude that these distributions are highly statistically different from each other.

The authors examined these differences in Chapter 13. They began with a reformulation of the core racial principles of psychometry:

Despite the forbidding air that envelops the topic, ethnic differences in cognitive ability are neither surprising nor in doubt. Large human populations differ in many ways, both cultural and biological. It is not surprising that they might differ at least slightly in their cognitive characteristics. (269; emphasis in the original)

Figure 7.1. Black and white IQ distribution in the National Longitudinal Survey of Youth. From Herrnstein and Murray’s The Bell Curve. This figure shows the Black and white IQ distributions derived from the Armed Forces Qualifying Test for populations of equal size.
Source: Black and white IQ distribution in the NLSY, r/Hategraphs, www.reddit.com/r/hategraphs/comments/8w8tog/black_and_white_iq_distribution_in_the_nlsy/, accessed December 28, 2020; original source: Herrnstein R and Murray CR, The Bell Curve: Intelligence and Class Structure in American Social Life (New York: Free Press, 1994), 279.

They then claimed that this point is confirmed by data on cognitive ability from around the world. They stated that the data showed that East Asians (e.g., Chinese, Japanese) had higher cognitive scores than white Americans, and that both groups were at least 1 standard deviation higher in intelligence scores than Blacks. They further claimed that the universality of the contrasts between nonverbal and verbal skills between European whites and East Asians as well as the fact that tests that most closely measure “g” differ consistently between whites and Blacks was highly suggestive of the genetic roots of these differences.

When I first read this chapter it became clear to me that a major flaw in their reasoning resulted from the way they were defining populations. The chapter included a box explaining that they were identifying the groups in their analysis essentially by self-identification (271). However, if the goal was to seriously examine both the phenotype of cognitive ability and its potential genetic roots, then self-identification was entirely inadequate. In this regard Herrnstein and Murray went no further than such predecessors as Francis Galton, Arthur de Gobineau, or Charles Davenport.⁸ For Galton, Gobineau, and Davenport, the social definitions were equivalent to biological races. The flaw in this way of thinking is that humans do not have biological races. In 1995, when I wrote “Race and IQ Revisited: Figures Never Lie, but Often Liars Figure” (an article on The Bell Curve), I was just beginning to understand that fact, but more importantly, I was new at explaining this idea to nonscientists.⁹

How you define “ethnic” or “racial” groups has important impacts on whether you find differences between them. Herrnstein and Murray were careful to define East Asians to mean Japanese, Chinese, and perhaps also Koreans (272; emphasis added). This is quite strange, in that even before whole genome sequencing began in earnest for human populations, it was generally thought that the inhabitants of the Japanese islands resulted from a dual colonization by persons from the Chinese mainland to the southwest and by persons from the Korean peninsula to the northwest.¹⁰ Today we know that the Japanese and Korean populations are extremely close to each other genetically.¹¹ In addition to failing to explicitly include the Koreans in the East Asian group, Herrnstein and Murray also neglected to include the Bhutanese, Tibetans, Ainu, Uralic Siberians, and Mongolians. Again, according to the science of the time, calculated genetic distances placed these populations within the phylogenetic grouping of the Chinese and Japanese.¹²

It is possible to suggest some reasons why Herrnstein and Murray’s analysis neglected these populations. First, it is probable that very few studies of IQ (general intelligence) tests have been conducted in these groups. The East Asian IQ scores reported in The Bell Curve relied primarily on the work of the psychometrician Richard Lynn (who routinely published in The Mankind Quarterly, a journal dedicated to “race” science). Interestingly, in 2007 Lynn published a report of IQ scores resulting from two samples of Mongolian children living in China.¹³ He found that their average IQ scores on two tests, Raven’s Progressive Matrices (RPM) and the Wechsler Preschool and Primary Scale of Intelligence (WPPSI), were 99.1 and 94.9, respectively, compared to 101.6 and 99.1, respectively, obtained from a sample of Han Chinese children in the same school. He argued that these scores were consistent with the genetic distance between Han/Japanese/Koreans and Mongolians, who were midway genetically between Han/Japanese/Koreans and the Inuit people (with recorded average IQs of about 91).

Second, in addition to the simple absence of test scores from genetically related East Asians, is the possibility that the IQ scores of these groups might not fit the model of genetic determination of IQ differences between populations. Neither then nor now do data exist to determine whether this is true. What we do know is that IQ testing has oversampled some populations and undersampled others across the globe. This is also true of whole genome sequencing. The result of this imbalance is a series of hypothetical claims concerning genetic distance and the IQ phenotype.

And finally, as I explained in “Race and IQ Revisited: Figures Never Lie, but Often Liars Figure,” it was certainly true that genes contributed to the cognitive function of individuals but were probably not responsible for the measured IQ differences between racialized people in American society. Let me be clear: IQ tests do measure various aspects of cognitive performance. I have explained this in several articles.¹⁴ The million-dollar question is whether they measure something that can or should determine one’s position in society. Putting that question aside for the moment, the question of what intelligence actually amounts to is by no means settled. However, the function of the human brain is complex, as is evidenced by the fact that at least 82 percent of the twenty thousand genes in the human exome are expressed in brain tissue. This is nearly double the 46 percent of genes that are normally expressed in other tissue types.¹⁵ The complexity of this organ means that it is subject to a variety of environmental factors that strongly influence how it works. We came to understand that in the mid-1990s, when there were a plethora of studies on the impact of environmental deprivation in creating behavioral deficits in mice.¹⁶ There were correlative studies on how poor environment affected learning and intelligence in humans. One of the best-known environmental effects is the impact lead has on neural development of learning in all primates (including humans).¹⁷ Today we understand so much more about how cognitive function is impaired by poor environment—including the impact of social factors such as racism. One of the most surprising revelations about the way racism harms people is that it has effects similar to those of any traumatic event, except that the trauma of living under racism never ends (until you die from it). In the last two decades it has been shown that traumatic events alter cellular function by inducing epigenetic changes (that is, non-nucleotide-based changes) to the genome.¹⁸ These modifications occur over the lifetime of an individual. Epigenetic changes affect the way genes are expressed and are known to play a substantial role in a variety of complex diseases, including cancer, heart disease, cerebrovascular disease, peripheral artery disease, inflammatory bowel disease, liver disease, and a variety of mental illnesses. A recent study of over 250 African American women found a highly significant association between perceived racial discrimination and the methylation levels in their genomes.¹⁹ DNA methylation is a mechanism of epigenetic change that affects the expression of genes. It is also considered a biomarker of cellular age, meaning the more methylation, the greater the age-related cellular damage in an individual. Thus, as I argued in “Race and IQ Revisited” and other articles I wrote in this period, the underperformance of African Americans on various tests of cognitive function was not the result of inherent genetic differences between them and other racialized groups in America; it was due to the toxic cultural, physical, and social environments they have endured and are still enduring. Herrnstein and Murray present a figure showing the magnitude of Black-white mean differences in IQ scores across the twentieth century (277); it is exactly what one would expect in a society with persistent racial subordination. Such epigenetic trauma also explains why the IQ-test differential narrows but does not completely go away as the socioeconomic status of racially subordinated individuals goes up. Indeed, in some ways the racism experienced by African Americans in high-status social positions is even more vicious then garden-variety racism. For example, Michelle Obama was undoubtedly the only first lady to be compared to an “ape” wearing heels.²⁰

In addition to their problematic genetics, Herrnstein and Murray’s statistical techniques were flawed, and even if one accepted their results, the inferences to be drawn from them are weak. And finally, they relied on questionable sources to support their claims about the centrality of IQ to American social life. Even worse for them was the nature of their arguments for the relative contributions of genetic and environmental determinations of intelligence and their relationship to “race.” Throughout their book they attempted to associate IQ with social outcomes, and they notably did not cite studies that countered their central thesis. For example, an earlier study of IQ and intergenerational wealth showed that IQ scores did not correlate with years of schooling and economic success in white males. Furthermore, that study demonstrated that IQ did not correlate with income and inherited social status. Individuals of average IQ scores and identical years of schooling had the same probability of ending up in the top quintile of income as those in the general population.²¹

HERRNSTEIN AND MURRAY CLAIMED TO BE “AGNOSTIC” CONCERNING whether racial differences in IQ-test scores were primarily caused by genetic or environmental differences. However, in their discussion of their agnosticism, they relied heavily on the thinking of Canadian psychologist J. Philippe Rushton. Rushton felt that racial differences in intelligence were primarily caused by genetic differences, which were best explained by the evolution of life history features between human races.²² Despite Rushton’s argument, evidence supporting a differential genetic foundation for racialized intelligence has never been found. However, a new variant of this idea has recently surfaced to explain the supposed greater intelligence of Europeans over non-Europeans. This variant relies on the principle of phenotypic plasticity—that is, the idea that environment (particularly during development) influences the expression of genes in such a way that different physical traits are formed from the same genetic foundation. For example, the temperature at which fruit fly larvae develop dramatically affects adult body size. Flies that develop at a lower temperature attain a larger adult body size.²³ The development of the human brain is also powerfully influenced by environment. The list of things that negatively affect brain development is extensive, including malnutrition, environmental toxins (such as lead), and emotional abuse.²⁴ On the other hand, extensive mental and physical activity positively affects brain development.²⁵ In a recent book examining the differences in psychological profiles between populations primarily derived from Europe (Westerners) and those in the rest of the world, Harvard scholar Joseph Henrich argues that phenotypic plasticity related to a cultural decision in western Europe played a role in the eventual greater intelligence of these populations compared to others. This is a component of what he describes as WEIRD (Western, educated, industrialized, rich, democratic) psychology.²⁶ His argument is that the Protestant insistence that individuals needed to read and interpret the scriptures themselves drove an increase in literacy in the Western Protestant societies. The increase in reading, he argued, resulted in neurobiological changes in European Protestant brains: verbal memory expanded, face-processing shifted, and the corpus callosum thickened over the centuries. The corpus callosum is a wide nerve tract that runs beneath the cerebral cortex and facilitates communication between the right and left hemispheres of the brain. His evidence for proposing that there was an increase in reading is data showing the increase in literacy rates for various European countries from 1550 to 1900.²⁷

There are some real problems with this reasoning, however. First, there is no direct measurement of the widths of the corpora callosa of Protestants in 1500 to be compared to those in 1800. Second, the definition of literacy is never explained in the text. Was a literate person in 1500 or 1800 someone who could read the name of a building or someone who could read a passage from the Bible? The evidence for increased European literacy across this period is derived from the number of printed books over the time period. Prior to the invention of the Gutenberg printing press (in 1450), there were few books in Europe. In 1500, there were only 4,999,161 printed books.²⁸ The population of western Europe in 1500 was about thirty-five million. So there would have been 0.14 books per person. However, the authors of the study on book printing recognized that books were luxury items and thus, as such, were probably only owned by the wealthier segments of the population. Thus, it is highly likely that the vast majority of Protestant European children did not have access to a book on a regular basis (if they did, it was probably the Bible). For an increase to occur in the thickness of an individual’s corpus callosum, he or she would need regular access to books and reading during his or her developmental years. This was highly unlikely in 1500, and even by 1800 books would still not have been widely available (about 2.8 books per person).

Thus, the notion that European economic success was driven by phenotypic plasticity resulting in greater “intelligence” associated with reading is difficult to support for all social classes. It is far more likely that this mechanism made a difference only for wealthy families, and thus those responsible for the growth of European capitalism were derived from such families. Indeed, this was a primary point made by the father of eugenics, Francis Galton, in his 1869 book Hereditary Genius.²⁹ Galton noted that the great accomplishments in English society were limited to a few families, a fact that he erroneously attributed to their genetic superiority. A simpler explanation is that having wealth creates the prerequisites for passing that wealth on to one’s offspring, including the capacity to provide them with excellent developmental environments. In addition, the European ruling class obtained its wealth through brutal exploitation of labor and a lack of attention to the squalid living conditions of their own working classes. Their lack of concern for the suffering of others was seen even more clearly in the transatlantic slave trade and colonialism in Africa, the Americas, and Asia.

THE ACADEMIC POPULARITY OF “RACE AND IQ REVISITED: FIGURES Never Lie, but Often Liars Figure” and another article I wrote on The Bell Curve, “The Pseudoscience of Psychometry and The Bell Curve,” was part of the reason I was invited to speak on a panel addressing race and intelligence at the John Jay College of Criminal Justice in New York, held on March 22, 1997.³⁰ I accepted the invitation because I knew J. Philippe Rushton would be there. The panel was organized in such a way that each panel member was given an opportunity to make a presentation and then to address questions from the audience. I will admit to having been very nervous going into this panel (and it shows on the video).³¹ Over the course of my career I had engaged the ideological basis of scientific racism but had rarely had the opportunity to face its authors head-to-head. I imagine that before his bout with Max Schmeling, Joe Louis must have felt very much like I did. However, I knew I had three advantages going into the confrontation. First, Rushton’s worldview concerning the intellectual inferiority of persons of African descent would make him too confident of his ability to carry any exchange between us. Second, I had read Rushton’s book Race, Evolution, and Behavior: A Life History Perspective from cover to cover. From that read it was clear to me that he did not understand life history evolution at all. Finally, I was absolutely sure that if he had read any of my papers, it was probably only the ones addressing race and intelligence, so he would have no comprehension of my evolutionary science credentials.

Because I had read Race, Evolution, and Behavior, I already had a list of his various mistakes and fallacies well cataloged in preparation for the panel. The most significant of these misconceptions were (1) his characterization of human biological variation into the old five-races typologically and (2) the fact that he had applied Robert MacArthur and E. O. Wilson’s theory of r-selection and K-selection backward. The category of r-selection refers to species that invest more of their energy into rapid reproduction and less into the maintenance of somatic tissue. The K-selected species, on the other hand, are more slow growing, with less reproductive than somatic investment. To understand the comparison, think weeds (r-selected species) compared to trees (K-selected species). Rushton thought Black people are weeds and white/yellow people are trees. The problem was that MacArthur and Wilson thought r-selection would dominate the temperate zones (where whites and yellows evolved) and K-selection would dominate the tropics (where Blacks evolved).

The panel began with Todd Disotell, an evolutionary anthropologist from New York University. Todd’s talk pulled the rug out from under Rushton’s core argument about the racial determination of life history features. He was followed by Rushton, me, and finally the political scientist Walter Stafford from New York University. Rushton made every mistake in his presentation that I thought he would. My presentation was organized to debunk each one of his core ideas. The knockout came when I pointed out that he had applied classical r- and K-theory backward. By that theory, Eurasians should have had small brains, large gonads, and big families, not vice versa. The panel can be thought of as the Graves versus Rushton debate because most of the interaction during the question-and-answer period was the two of us going at each other’s positions. I am ashamed of myself for losing my temper during the panel (again, you will note this if you watch the YouTube video). While I do believe my anger was righteous and justified, someone who hadn’t made his or her mind up concerning the facts might have been swayed in Rushton’s direction by my lack of emotional control.

Eventually I presented my critique of Rushton in a book chapter and a paper outlining the error in his thinking.³² Shortly after my critique of Rushton’s methods in the book chapter, I was threatened with a lawsuit by the Pioneer Fund. The Pioneer Fund was founded by the Nazi sympathizer Wickliffe Draper in 1937. Rushton was its chairman from 2002 to 2012 (the year he died). It is devoted to the study of heredity and human differences and is listed as a white supremacist hate group by the Southern Poverty Law Center. The fund threatened to sue me for libel for suggesting that Rushton was a racist.

In my book chapter I demonstrated that Rushton had manipulated data from an original publication without explaining the nature of the manipulation or why it was done in his text. The manipulation altered the data in a way that supported his hypothesis. If one removed the data manipulation, the support was not as clear. The simple fact is that, in support of a hypothesis or not, it is academic misconduct to manipulate data from an original source without explaining how the data were transformed.

After receiving the letter from the Pioneer Fund, I approached my dean and university counsel to ask whether the university would defend me from the charge of libel. Their answer was no. In hindsight this should not have been surprising, as HWIs in the main are spineless when it comes to taking principled stands against racism (e.g., look at how long Confederate monuments have stood at HWIs across the country and the number of buildings still named for eugenicists and white supremacists on these campuses). In the end, I had to alter the wording on my web page to say something to the effect that Rushton’s work is consistent with the views of racists and I had to remove the characterization of Rushton as a “racist” from the book chapter (though I kept intact the critique of his unscrupulous data manipulation). Despite these attacks, it is notable that after my confrontation with Rushton and the published critiques of his mistakes, he moved away from the r- and K-selection justification for racial differences in intelligence and personality.

This is important. He and his supporters still maintained that there is a biological/genetic basis to racial differences, but they could no longer claim the scientific high ground of an evolutionary rationale for it based in natural selection. Of course, populations could differ in important gene frequencies related to cognitive performance simply by chance (genetic drift). However, this rationale cannot account for the “racial” differences in intelligence that the psychometricians seek. They would have to explain how, by chance alone, Eurasians always managed to win in the genetic lottery for these genes. God would have been playing with loaded dice when the genes for intelligence were being handed out.

Without an evolutionary support, their ideas stood on shaky ground in the realm of modern biological science. In the twentieth century, creationist ideas about the biological variation within our species died out. Thus, to explain the distribution of any biological trait, one has to relate it to the evolutionary mechanisms of natural selection and genetic drift. Classic studies of these mechanisms explained the distribution of antimalarial adaptations such as sickle cell anemia. The sickled hemoglobin variant was found in high frequency in malarial zones because of an advantage conferred by being heterozygous (having two different alleles of a gene inherited from one’s mother and father). Individuals with two copies of the sickle cell variant suffer from sickle cell disease, whereas individuals with two copies of the standard variant die at high rates from malaria. On the other hand, individuals who have one copy of the sickle cell gene and one copy of the standard gene do not suffer from sickle cell disease and have superior survivorship against malaria. Thus, the gene is found in elevated frequencies in populations living in malaria zones, from western Africa through the Mediterranean and into Indochina. No such case can be made in large populations for any gene purportedly related to greater intelligence.

After my battles with scientists like Herrnstein, Murray, and Rushton, the ideology that insists that natural selection must have played a role in favoring greater Eurasian intelligence was wounded, but it was not yet dead. I would go on to face racist pseudoscience over and over in my career, and I would always rise to fight against it. One of my most important victories came with the publication of my first book, The Emperor’s New Clothes.