Political Correctness/Totalitarian Humanism

The Straw Man of ‘Race’

Article by Jon Entine. Hat tip to MRDA.


Summary:Genetic scientists who know better continue to utter such falsehoods as “there are no scientific differences between humans,” or “race has no biological reality.” The unrelenting attack on the straw man of race is an attempt to subordinate science to politics.

Branding evolution as racism is an old Creationist trick dating back to Charles Darwin’s time. It was Bishop of Oxford Samuel Wilberforce’s tactic in his infamous face off with British naturalist and evolution defender Thomas Huxley only months after the publication of On the Origins of Species. Wilberforce portrayed Darwin, variously, as snake-oil salesman, heretic, or fool for suggesting that humans “descended” from apes. Unintimidated by the bilious bishop, Huxley offered a wide-ranging rebuttal of Wilberforce’s invocation of a higher order:

… A man has no reason to be ashamed of having an ape for his grandfather. If there were an ancestor of whom I would feel shame in recalling, it would be a man, a man of restless and versatile intellect, who, not content with an equivocal success in his own sphere of activity, plunges into scientific questions with which he has not real acquaintance, only to obscure them by an aimless rhetoric, and distract the attention of his hearers from the real point at issue by eloquent digressions, and skilled appeals to religious prejudice.

Today, the science of genetics faces a far more sophisticated Creationist inspired attack, though this time the right is finding unnatural allies among the political left. In the United Sates earlier this year, the Louisiana House Education Subcommittee approved a resolution asserting, “Charles Darwin, the father of evolution, promoted the justification of racism” by ignoring “the commonalities of people groups.” Although the final measure approved by the full House took out direct references to Darwin, the intent remained. The twist to this assault on evolution is that proponents of the Human Genome Project, not the far right, inspired it.

The Louisiana folly (and similar legislative campaigns underway in at least a half dozen other states) can be traced to statements made last February by Francis Collins of the National Human Genome Research Project and Craig Venter of Celera Genomics. When these two distinguished scientists unveiled their crude early maps of the human genome last February, they went out of their way to emphasize the oft-stated belief that, in the words of Venter, “race has no genetic or scientific basis.”

Venter’s unambiguous declaration created hardly a ripple in social science circles, which have long embraced this position. “Differentiating species into biologically defined ‘races’ has proven meaningless and unscientific as a way of explaining variation,” the American Anthropological Association has proclaimed in one of numerous widely publicized encyclicals on race.

One can hardly blame scientifically challenged journalists who report such statements as fact, like one who wrote, “there are no scientific differences between humans – ‘race has no biological reality’, it is only a ‘social construction’ that perpetuates racism.” More disturbing, however, is when science writers for publications like the New York Times encourage this simplistic analysis. “As it turns out,” wrote Natalie Angier in “Do Races Differ? Not Really, DNA Shows,” “scientists say, the human species is so evolutionarily young, and its migratory patterns so wide, restless and rococo, that it has simply not had a chance to divide itself into separate biological groups or ‘races’ in any but the most superficial ways.”

Now, if such conclusions were taken at face value, legislatures would be remiss if they did not condemn the teaching of human evolution. Darwin unequivocally discussed the “endless” and “numerous” differences between human populations even as he stressed our unifying humanity. “[T]he various races, when carefully compared and measured, differ much from each other,” he wrote in The Descent of Man, “as in the texture of hair, the relative proportions of all parts of the body, the capacity of the lungs, the form and capacity of the skull, and even the convolutions of the brain.”

If there are no patterned biological races differences between populations as Venter and Collins appear to have asserted, then Darwin’s theory is subversive, scientifically as well as religiously. Yet, these two scientists are ardent evolutionists. The paradox revolves around the disingenuousness of scientists. Unfortunately, those with large research budgets often dissimulate when the incendiary issue of human biodiversity, popular known as “race”, is broached. Yet, the human genome project is based on isolating patterns of gene-based differences. And on a practical level, “racial” differences are in evidence everywhere, from body types to disease proclivities, that more or less fit traditional notions of race.


So, what’s behind this scientific tartuffery? And how do we sort out sometimes-slippery facts about “race” from folkloric nonsense? A number of commentators, such as Steve Sailer, founder of the Human Biodiversity Society, have deconstructed the popular myths that underlie the cant that human differences are only “skin deep.” Here are my five myths of race.

1. Humans are 99.9 percent the same. Therefore, race is “biologically meaningless.”

This statement finds its origins in the research of Harvard University geneticist Richard Lewontin during the 1960s. “Human racial classification is of no social value and is positively destructive of social and human relations,” Lewontin concluded in The Genetic Basis of Evolutionary Change in 1974. “Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its continuance.”

Coming from a geneticist, Lewontin’s views had enormous influence and he was making a valid argument at the time. As Laval University anthropologist Peter Frost points out, Lewontin was referring to classic genetic markers such as blood types, serum proteins, and enzymes, which do show much more variability within races than between them. But his comments are widely misinterpreted even today to extend beyond that limited conclusion. Further research has shown this pattern of variability cannot reliably be extrapolated to all traits with higher adaptive value.

The 99.9 percent figure is based on DNA sequences that do not differ much between people or even between most mammals. As Jared Diamond, UCLA physiologist has noted, if an alien were to arrive on our planet and analyze our DNA, humans would appear as a third race of chimpanzees, who share 98.4 percent of our DNA. Just 50 out of the 32,00 genes that humans and chimps are thought to possess, or approximately 0.15 percent, may account for all of the cognitive differences between man and ape.

The impact of minute genetic differences is magnified in more sophisticated species. From a genetic perspective, humans and chimpanzees are almost identical because their genes code for similar phenotypes, such as bone structure, which are remarkably similar in many animals. For that matter, dogs share about 95 percent of our genome and mice 90 percent, which is why these species make good laboratory animals. Looked at another way, while the human genome contains some 32,000 genes, that’s not much more than the nematode worm (18,000), which is naked to the human eye. Humans only have 25 percent more genes than the mustard weed (26,000). The real story of the annotation of the human genome is that human beings do not have much more genomic information than plants and worms.

A large-scale study of the variability in the human genome by Genaissance Pharmaceuticals, a biotechnology company in Connecticut, has convincingly shown the fallaciousness of arguments tied to the 99.9 percent figure. The research shows that while humans have only 32,000 genes, there are between 400,000 and 500,000 gene versions. More specifically, they found that different versions of a gene are more common in a group of people from one geographical region, compared with people from another.

The implications are far reaching. By grouping individuals by the presence and variety of gene types, physicians may someday be able to offer treatments based on race or ethnic groups that will have been predetermined to work on a genetic level. Kenneth Kidd, a population geneticist at Yale University who is not connected to the study, said it confirmed the conclusions of those who have maintained that there is in fact considerable variability in the human population. He also chided the government and some genetic researchers for having stripped ethnic identities from the panel of people whose genomes have been searched for gene sequences. The study prompted Francis Collins, director of the National Human Genome Research Institute, to backtrack from earlier assertions that the small percentage of gross gene differences was meaningful or shed light on the debate over “racial” differences. “We have been talking a lot about how similar all our genomes are, that we’re 99.9 percent the same,” he said. “That might tend to create an impression that it’s a very static situation. But that 0.1 percent is still an awful lot of nucleotides.”

In other words, local populations are genetically far more different than the factoid that humans are 99.9 percent the same implies. The critical factor is not which genes are passed along but how they are patterned and what traits they influence.

2. The genetic variation among European, African and Asian populations is minuscule compared to differences between individuals within those populations.

This factoid, which is a variation on the first myth, has been elevated to the level of revealed truth. According to Lewontin, “based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals.”

What does that mean? Not much by today’s nuanced understanding of genetics, it turns out. Consider the cichlid fish found in Africa’s Lake Nyas. The chiclid, which has differentiated from one species to hundreds over a mere 11,500 years, “differ among themselves as much as do tigers and cows,” noted Diamond. “Some graze on algae, others catch other fish, and still others variously crush snails, feed on plankton, catch insects, nibble the scales off other fish, or specialize in grabbing fish embryos from brooding mother fish.” The kicker: these variations are the result of infinitesimal genetic differences–about 0.4 percent of their DNA studied.

As retired University of California molecular biologist Vincent Sarich has noted, there are no clear differences at the level of genes between a wild wolf, a Labrador, a pit pull and a cocker spaniel, but there are certainly differences in gene frequencies and therefore biologically based functional differences between these within-species breeds.

There are other more fundamental problems resulting from misinterpretations of Lewontin’s original studies about gene variability. Numerous scientists since have generalized from his conclusions to the entire human genome, yet no such study has been done, by Lewontin or anyone else. Today, it is believed that such an inference is dicey at best. The trouble with genetic markers is that they display “junk” variability that sends a signal that variability within populations exceeds variability between populations. Most mammalian genes, as much as 70 percent, are “junk” that have accumulated over the course of evolution with almost no remaining function; whether they are similar or different is meaningless. The “junk” DNA that has not been weeded out by natural selection accounts for a larger proportion of within-population variability. Genetic makers may therefore be sending an exaggerated and maybe false signal.

The entire issue of gene variability is widely misunderstood. “In almost any single African population or tribe, there is more genetic variation than in all the rest of the world put together,” Kenneth Kidd told me in an interview in 1999. “Africans have the broadest spectrum of variability, with rarer versions at either end [of the bell curve distribution]. If everyone in the world was wiped out except Africans, almost all human genetic variability would be preserved.”

Many journalists and even some scientists have taken Kidd’s findings to mean that genetic variability equates with phenotypic variability. Since Africans have about 10–15 percent more genetic differences than people from anywhere else in the world, the argument goes, Africans and their Diaspora descendents should show more variability across a range of phenotypic characteristics including body type, behavior, and intelligence. This “fact” is often invoked to explain why athletes of African ancestry dominate elite running: it’s a product of variability, not inherent population differences.

This is a spurious interpretation of Kidd’s data. Chimpanzees display more genetic diversity than do humans. That’s because genetic variability is a marker of evolutionary time, not phenotypic variability. Each time an organism, human or otherwise, propagates, genetic “mistakes” occur as genes are mixed. The slightly increased variability in Africans reflects the accumulation of junk DNA as mutations have occurred over time. Such data “prove” little more than the fact that Africa is the likely home of modern humans–and it may not even signify that.

University of Utah anthropologist and geneticist Henry Harpending and John Relethford, a biological anthropologist from the State University of New York at Oneonta, have found that this genetic variation results from the fact that there were more people in Africa than everywhere else combined during most of the period of human evolution. In other words, greater African genetic variability may be the result of nothing more than fast population growth.

When I asked Kidd directly whether his findings of genetic variability, which showed that blacks meant that Africans were most likely to show the most phenotypic variability in humans–the tallest and shortest, the fastest and slowest, the most intelligent and most retarded–he laughed at first. “Wouldn’t that be mud in the eye for the bigots,” he said, not eager to puncture the politically correct balloon. Finally, he turned more serious. “Genes are the blueprint and the blueprint is identifiable in local populations. No matter what the environmental influences, you can’t deviate too far from it.”

Part of the confusion stems from the fact that some scientists, and certainly the general public, have embraced the popular shorthand that discrete genes have specific effects. This is sometimes expressed as there is a “gene for illness X.” Lewontin himself expresses scorn for what he calls the “religion” of molecular biology and their “prophets”, geneticists, who make grandiose statements about what genes prove or disprove. Genes only specify the sequence of amino acids that are linked together in the manufacture of a molecule called a polypeptide, which must then fold up to make a protein, a process that may be different in different organisms and depends in part on the presence of yet other proteins. “[A] gene is divided up into several stretches of DNA, each of which specifies only part of the complete sequence in a polypeptide,” Lewontin has written. “Each of these partial sequences can then combine with parts specified by other genes, so that, from only a few genes, each made up of a few subsections, a very large number of combinations of different amino acid sequences could be made by mixing and matching.” Lewontin’s reasonable conclusion: the mere sequencing of the human genome doesn’t tell us very much about what distinguishes a human from a weed, let alone a Kenyan from a Korean.

Significant between group differences have been identified in the harder-to-study regulatory genes. This tiny fraction of the human genome controls the order and make-up of proteins, and may be activated by obscure environmental triggers. For instance, the presence of an abnormal form of hemoglobin (hemoglobin S) can lead to sickle-cell anemia, which disproportionately afflicts families of African descent. But the genetic factors that actually lead to the disease operate at a much finer level. Just one change in the base pair for hemoglobin, can trigger the disease. However, the genetic factors involved are even subtler in part because of gene-gene and gene-environment interactions. For example, a separate set of genes in the genome–genes that code for fetal hemoglobin–can counteract some of the ill effects of the adult hemoglobin S genes if they continue to produce into adulthood. This range of possibilities, encoded in the genome, is found disproportionately in certain populations, but do not show up in the gross calculations of human differences that go into the misleading 99.9 percent figure.

Francois Jacob and Jacques Monod, who shared the Nobel Prize for Medicine in 1965 for their work on the regulator sequences in genes, have identified modules, each consisting of 20-30 genes, which act as an Erector Set for the mosaics that characterize each of us. Small changes in regulatory genes make large changes in organisms, perhaps by shifting entire blocks of genes on and off or by changing activation sequences. But, whether flea or fly, cocker spaniel or coyote, Brittany Spears or Marion Jones, the genetic sequences are different but the basic materials are the same. Minute differences can and do have profound effects on how living beings look and behave, while huge apparent variations between species may be almost insignificant in genetic terms.

3. Human differences are superficial because populations have not had enough evolutionary time to differentiate.

Stephen Jay Gould has periodically advanced an equally flawed argument: Human differences are superficial because populations have not had enough evolutionary time to differentiate. “Homo sapiens is a young species, its division into races even more recent,” Gould wrote in Natural History in November 1984.This historical context has not supplied enough time for the evolution of substantial differences. … Human equality is a contingent fact of history.” In other words, our relatively recent common heritage–differentiation into modern humans may have occurred as recently as 50,000 years ago, an eye blink of evolutionary time–renders the possibility of “races” absurd.

This view has made its way into the popular media as fact. Yet, it’s difficult to believe that Gould believes his own rhetoric, for his own theory of punctuated equilibrium, which argues that swift genetic change occurs all the time, demolishes this assertion. A quarter century ago, Gould and American Museum of Natural History curator Niles Eldredge addressed the controversial issue of why the fossil records appeared to show that plants and animals undergo little change for long periods of time and then experience sudden, dramatic mutations. They argued that new species do not evolve slowly so much as erupt, the result of a chain reaction set off by regulatory genes. Their theory, though controversial and still widely debated, helps explain the limited number of bridge, or intermediary, species in the fossil record (as Creationists never fail to point out). Either as a mutation or in response to an environmental shock, these regulators could have triggered a chain reaction with cascading consequences, creating new species in just a few generations.

The evolutionary record is filled with such examples. A breakthrough study by University of Maryland population geneticist Sarah Tishkoff and colleagues of the gene that confers malarial resistance (one known as the G6PD gene) has concluded that malaria, which is very population specific, is not an ancient disease, but a relatively recent affliction dating to roughly 4,000-8,000 years ago. When a variant gene that promotes its owner’s survival is at issue, substantial differences can occur very rapidly. The dating of the G6PD gene’s variants, done by a method worked out by a colleague of Dr. Tishkoff’s, Dr. Andrew G. Clark of Pennsylvania State University, showed how rapidly a life-protecting variant of a gene could become widespread. The finding is of interest to biologists trying to understand the pace of human evolution because it shows how quickly a variant gene that promotes its owner’s survival can spread through a population. Genes that have changed under the pressure of natural selection determine the track of human evolution and are likely to specify the differences between humans and their close cousin the chimpanzee.

This new understanding of the swiftness of genetic change may ultimately help solve numerous evolutionary puzzles, including the origins of “racial differences.” For instance, there has been contradictory speculation about the origins of the American Indian population. Excavations have pushed the date of the initial migration to the Americas as far back as 12,500 years ago, with some evidence of a human presence as far as 30,000 years. The 1996 discovery of Kennewick Man, the 9,300-year-old skeleton with “apparently Caucasoid” features sparked speculation in the possibility of two or more migrations, including a possible arrival of early Europeans.

Using computer analysis of skeletal fragments, University of Michigan anthropologist C. Loring Brace argues that most American Indians are the result of two major migratory waves, the first 15,000 years ago after the last Ice Age began to moderate and the second 3,000-4,000 years ago. The first wave were believed to be members of the Jomon, a prehistoric people who lived in Japan thousands of years ago. Similar to Upper Paleolithic Europeans 25,000 years ago as well as the Ainu in Japan today and the Blackfoot, Sioux and Cherokee in the Americas, these populations have lots of facial and body hair, no epicanthic eyefold, longer heads, dark hair and dark eyes. Brace argues that the first waves was followed by a second migration consisting of a mixed population of Chinese, Southeast Asians, and Mongolians–similar in some respects to current populations of Northeast Asia–and are likely ancestors of the Inuits (Eskimo), Aleut, and Navajo.

Brace’s data does not resolve whether the two migratory waves consisted of distinct populations or rather different “samples” over time of the same population, whose physical appearance had changed as a result of selection pressures specific to that region, notably the cold, harsh climate. According to Francisco Ayala of the University of California at Irvine, co-author with Tishkoff of the malaria study, the genetic data suggests the remains represent a similar population at different evolutionary points in time. By this reasoning, various American Indian populations are the result of differing paces of evolution of various sub-pockets of populations. “We are morphologically no different in the different continents of the world,” he contends. This research may help explain how “racial” differences could occur so quickly after humans began their expansion from Africa, as recently as 50,000 years ago, Ayala adds.

These findings reinforce those of Vince Sarich. “The shorter the period of time required to produce a given amount of morphological difference, the more selectively important the differences become,” he has written. Sarich figures that since the gene flow as a result of intermingling on the fringes of population pockets was only a trickle, relatively distinct core races would likely have been preserved even where interbreeding was common.

Stanford University geneticist Luigi Cavalli-Sforza has calculated the time it could take for a version of a gene that leads to more offspring to spread from one to 99 percent of the population. If a rare variant of a gene produces just 1 percent more surviving offspring, it could become nearly universal in a human group in 11,500 years. But, if it provides 10 percent more “reproductive fitness,” it could come to dominate in just 1,150 years.

Natural selection, punctuated equilibrium, and even catastrophic events have all contributed to what might loosely be called “racial differences.” For example, University of Illinois archaeologist Stanley Ambrose has offered the hypothesis that the earth was plunged into a horrific volcanic winter after a titanic volcanic blow-off of Mount Toba in Sumatra some 71,000 years ago. The eruption, the largest in 400 million years, spewed 4,000 times as much ash as Mount St. Helens, darkening the skies over one third of the world and dropping temperatures by more than 20 degrees. The catastrophe touched off a six-year global winter, which was magnified by the coldest thousand years of the last ice age, which ended some fourteen thousand years ago. It is believed to have resulted in the death of most of the Northern Hemisphere’s plants, bringing widespread famine and death to hominid populations. If geneticists are correct, some early humans may have been wiped out entirely, leaving no more than 15,000 to 40,000 survivors around the world.

What might have been the effect on evolution? “Humans were suddenly thrown into the freezer,” said Ambrose. Only a few thousand people in Africa and a few pockets of populations that had migrated to Europe and Asia could have survived. That caused an abrupt “bottleneck,” or decrease, in the ancestral populations. After the climate warmed, the survivors resumed multiplying in what can only be described as a population explosion, bringing about the rapid genetic divergence, or “differentiation” of the population pockets.

This hypothesis addresses the paradox of the recent African origin model: Why do we look so different if all humankind recently migrated out of Africa? “When our African recent ancestors passed through the prism of Toba’s volcanic winter, a rainbow of differences appeared,” Ambrose has said. The genetic evidence is in line with such a scenario. Anna DiRienzo, a post-doctoral fellow working out of Wilson’s lab at Berkeley in the early 1990s, found evidence in the mitochondrial DNA data of a major population spurt as recently as thirty-thousand years ago.

What’s clear is that little is clear. Human differences can be ascribed to any number of genetic, cultural, and environmental forces, including economic ravages, natural disasters, genocidal pogroms, mutations, chromosomal rearrangement, natural selection, geographical isolation, random genetic drift, mating patterns, and gene admixture. Taboos such as not marrying outside one’s faith or ethnic group exaggerate genetic differences, reinforcing the loop between nature and nurture. Henry Harpending and John Relethford have concluded “human populations are derived from separate ancestral populations that were relatively isolated from each other before 50,000 years ago.” Their findings are all the more convincing because they come from somewhat competing scientific camps: Harpending advocates the out-of-Africa paradigm while Relethford embraces regional continuity.

Clearly, there are significant genetically-based population differences, although it is certainly true that dividing humans into discrete categories based on geography and visible characteristics reflecting social classifications, while not wholly arbitrary, is crude. That does not mean, however, that local populations do not show evidence of patterns. The critical factor in genetics is the arrangement of gene allele frequencies, how genes interact with each other and the environment, and what traits they influence. This inalterable but frequently overlooked fact undermines the notion that gene flow and racial mixing on the edges of population sets automatically renders all categories of “race” meaningless. As Frost points out, human characteristics can and do cluster and clump even without reproductive isolation. Many so-called “species” are still linked by some ongoing gene flow. Population genetics can help us realize patterns in such things as the proclivity to diseases and the ability to sprint fast.

4. “There are many different, equally valid procedures for defining races, and those different procedures yield very different classifications.”

This oft-repeated quote, written by Jared Diamond in a now-famous 1994 Discover article titled “Race Without Color”, was technically accurate, to a point. Many phenotypes and most complex behavior that depends on the brain–fully half of the human genome–do not fall into neat folkloric categories. In fact, there has been little historical consensus about the number and size of human “races”. Charles Darwin cited estimates ranging from two to sixty-three.

The problem with this argument, however, and the clumsy way it was presented, revolves around the words “equally valid.” Diamond appeared to embrace the post-modernist creed that all categories are “socially constructed” and therefore are “equally valid,” no matter how trivial. To make his point, he served up a bouillabaisse of alternate theoretical categories that cuts across traditional racial lines, including a playful suggestion of a racial taxonomy based on fingerprint patterns. A “Loops” race would group together most Europeans, black Africans and East Asians. Among the “Whorls,” we would find Mongolians and Australian aborigines. Finally, the “Arches” race would be made up of Khoisans and some central Europeans. “Depending on whether we classified ourselves by anti-malarial genes, lactase, fingerprints, or skin color,” he concluded, “we could place Swedes in the same race as (respectively) either Xhosas, Fulani, the Ainu of Japan, or Italians.”

Throughout the piece (and indeed throughout Guns, Germs, and Steel), Diamond appeared to want it both ways: asserting that all population categories, even trivial ones as he puts it, are equally meaningful, yet suggesting that some are more meaningful than others. In discussing basketball, for instance, he writes that the disproportionate representation of African Americans is not because of a lack of socio-economic opportunities, but with “the prevalent body shapes of some black African groups.” In other words, racial categories based on body shape may be an inexact indicator of human population differences–as are all categories of human biodiversity–but they are demonstrably more predictive than fingerprint whorls or tongue-rolling abilities.

It’s one thing to say that race is in part a folk concept. After all, at the genetic level, genes sometimes tell a different story than does skin color. However, it’s far more problematic to make the claim that local populations have not clustered around some genetically based phenotypes. However uncomfortable it may be to Diamond, some “socially constructed” categories are more valid than others, depending upon what phenotypes we are discussing. Moreover, geneticists believe that some of the traditional folkloric categories represent major human migratory waves, which is why so many characteristics group loosely together–for instance, body type, hair texture, and eye and skin color.

5. Documenting human group differences is outside the domain of modern scientific inquiry.

Even suggesting that there is a scientific basis for “racial” differences is baseless speculation, according to some social scientists. University of North Carolina-Charlotte anthropologist Jonathan Marks cavalierly dismisses evidence of patterned differences. “If no scientific experiments are possible, then what are we to conclude? he wrote to me in 1999. “That discussing innate abilities is the scientific equivalent of discussing properties of angels.”

From one perspective, Marks appears to be taking the road of sound, verifiable science: we can only know what we can prove. But he casts the issue in misleading terms, for no one familiar with the workings of genes refers to “innate abilities.” Our personal set of genes no more determines who we are than the frame of a house defines a home; much of the important stuff is added over time. There is no such thing as “innate ability” only “innate potential,” which has an indisputable genetic component. No amount of training can turn a dwarf into a NBA center, but training and opportunity are crucial to athletes with anatomical profiles of NBA centers.

Marks’s corollary assertion that truth rests only in the laboratory presents the antithesis of rigorous science. If every theory had to be vetted in a laboratory experiment, then everything from the atomic theory of matter to the theory that the earth revolves around the sun could be written off as “speculative”. As Steve Sailer writes, “you can’t reproduce Continental Drift in the lab. You can’t scoop up a few continents, go back a billion years, and then see if the same drift happens all over again.”

Ironically, the extremist position taken by Marks and parroted by many journalists mirrors the hard right stance of Darwin’s most virulent critics. While microevolution has been verified, the weakest link of evolutionary theory has always been the relatively meager evidence of transitional fossils to help substantiate macroevolution. “Evolution is not a scientific ‘fact,’ since it cannot actually be observed in a laboratory,” argued the Creation Legal Research Fund before the Supreme Court in an unsuccessful attack on evolution theory. “The scientific problems with evolution are so serious that it could accurately be termed a ‘myth.’” Arguing for the teaching of Creationism in schools, anti-evolution Senator Sam Brownback (R-Kansas) has said “we observe micro-evolution and therefore it is scientific fact; … it is impossible to observe macro-evolution, it is scientific assumption.”

Does the lack of scientific experiments substantiating macroevolution render all talk of evolution theory “the scientific equivalent of discussing properties of angels”? This ideological posturing disguised as science, whether it emanates from the fundamentalist right or the orhodox left, demonstrates a fundamental misunderstanding of the process of scientific reasoning, which rarely lends itself to “smoking guns” and absolute certainty. It also confuses function with process. We may not yet know how genes and nature interact to shape gender identity but that does not mean, as Marks would have it, that stating that genetics play a role is “speculative.” We have yet to find the genetic basis for tallness, yet we can be quite certain that it is more likely to be found in the Dutch, now the world’s tallest population, than in the Japanese. The search for scientific truth is a process. It may be years before we identify a gene that ensures that humans grow five fingers, but we can be assured there is one, or a set of them. There are patterned human differences even though the specific gene sequences and the complex role of environmental triggers are elusive.


Science does require a theory to be predictive and supported by empirical evidence even when laboratory tests remain elusive. So, how do we test the theory that there are some patterned group differences? Certainly, we cannot automatically infer innate abilities from observed performances. As I noted in Taboo, Jews dominated basketball in the 1930s. One of the era’s great sports journalists, New York Daily News sports editor Paul Gallico, ascribed this to the “alert, scheming mind, flash trickiness, artful dodging and general smart aleckness” of Jews. Whatever reality there may be to such a stereotype, the fact that many Protestants avoided the sport in its infancy and blacks were banned from the white semi-pro leagues undermines the biological explanation. Today, however, the playing field is a lot flatter, which means that the empirical, on-the-field evidence actually means something.

What’s distinguishes such assertions from the wrongheaded, and racist, claims that Jews had some “natural” advantage in basketball? An increase in alternatives for Jews and more opportunity in basketball for other ethnic groups has demonstrated the absurdity of Gallico’s assertions. In the 1930s, blacks were banned from participation in the all-white semi-pro leagues dominated by inner city athletes. As the game became more popular, it attracted a more competitive athlete.

The twenty-year reign of Jews in basketball does underscore the importance of cultural factors and the danger of post hoc reasoning when nature and nurture are being discussed. After all, there are no Texans, white, black or Latin, starring in the National Hockey League or great American cricketers. The success of each individual is a product of that person’s ambition, creativity, and intelligence matched with the serendipity of life–the X factors that make sports so compelling. But opportunity alone doesn’t guarantee success. The national sport of Mexico is baseball, yet they are not generally good enough to make much of a mark in the Major Leagues: their ancestral body type works against them. If the roulette wheel of genetics does not land on an athlete’s number, hard work alone will not turn clay into marble. So, though individual success is about fire-in-the-belly and opportunity, the pattern of success in many sports are somewhat circumscribed by population genetics.

“Differences among athletes of elite caliber are so small … they are very, very significant,” says Robert Malina, Michigan State University anthropologist and editor of the Journal of Human Biology, who has studied anatomical differences of Olympic level athletes over more than 30 years. “The fraction of a second is the difference between the gold medal and fourth place.”

Some skeptics claim that any genetic differences that may exist between population groups are, in the end, utterly swamped by environmental influences. That statement reflects the enduring legacy of Cartesian dualism that sees environment and genes as polar opposite forces. “As scientists continue to study the complex interactions between genes and the environment, population-based genetic differences will continue to surface,” notes Michael Crawford, University of Kansas professor of biological anthropology and genetics, president of the Human Biology Association, and former editor of the journal Human Biology. “We need to dispense with the notion that athleticism is entirely due only to biology or only to culture. Biological variation in complex traits is always a result of their interaction.”


Today, with basketball played throughout the world, there is a far more level playing field. Although opportunities remain meager for poverty-riddled Africa, there are more elite basketball players from Nigeria than from Nebraska. In running, the trends are even more startling: athletes of African ancestry hold every major running record, from the 100 meters to the marathon. What is the driving force behind this phenomenon?

Competitive running is nature’s laboratory. “A scientist interested in exploring physical and performance differences couldn’t invent a better sport than running,” wrote Amby Burfoot, executive editor of Runner’s World. “It’s a true world-wide sport, practiced and enjoyed in almost every country around the globe. Also, it doesn’t require any special equipment, coaching or facilities. [Ethiopia’s] Abebe Bikila proved this dramatically in the 1960 Olympic Games when–shoeless, little coached and inexperienced–he won the marathon. Given the universality of running, it’s reasonable to expect that the best runners should come from a wide-range of countries and racial groups. This isn’t, however, what happens. Runners of West African descent win nearly all the sprints. Nearly all the distance races are won, remarkably, by runners from just one small corner of one small African country [Kenya].”

Running provides the most persuasive prima facie case suggesting that sports success cannot be explained by cultural and environmental factors alone. Kenya, a Texas-sized nation with a population of approximately 16 million people, is the world epicenter of distance running. East African runners almost exclusively come from the Nandi Hills, the 6,000-8,000 foot highlands that snake along the western edge of the Great Rift Valley of Kenya, Ethiopia, and Tanzania. Home to roughly 1.5 million people, this region has produced more than 60 percent of the best times ever run in distance races. Kenyans, almost all of them Kalenjin, win 40 percent of top international events.

The Kalenjin represent roughly three-quarters of Kenya’s world-class runners. Hundreds of years ago, what African historians refer to as a proto-Kalenjin population migrated from the Nilotic core area northwest of Lake Turkana to the Mt. Elgon area, where the group fragmented and moved to its present locations in the highlands. This is the home of the Nandi district of 500,000 people. One-twelve-thousandth of Earth’s population sweeps an unfathomable 20 percent, marking it as the greatest concentration of raw athletic talent in the history of sports.

According to socially acceptable wisdom, the sure explanation for Kenya’s success can be found in Kenyan culture. After all, the country’s national sport is the passion of the masses. Little boys dream that one day, they might soak up the cheers of the adoring fans that regularly crowd the stands at the National Stadium in Nairobi. Coaches comb the countryside for the rising generation of stars, who are showered with special training and government perks. It’s no exaggeration to call Kenya’s national sport a national religion.

There’s only one problem: The national sport, the hero worship, the adoring fans, the social channeling–that all speaks to Kenya’s enduring love affair with soccer, not running. Despite the enormous success of Kenyan runners in the past 15 years, running remains a relative afterthought in this soccer-crazed nation. Unfortunately, Kenyans are among the world’s worst soccer players. They are just terrible. In fact, there is no such thing as an East African soccer powerhouse. Clearly, cultural channeling, the lure of privilege, and hero worship, bedrock components of the environmentalist argument, have not done much to make East Africa competitive in soccer.

The East African edge, if you will, reflects the impact of evolution on body type and physiology. “Africans are naturally, genetically, more likely to have less body fat, which is a critical edge in elite running,” notes Joseph Graves, Jr., an evolutionary biologist at Arizona State University and author of The Emperor’s New Clothes: Biological Theories of Race at the Millenium. “Evolution has shaped body types and in part athletic possibilities. Don’t expect an Eskimo to show up on an NBA court or a Watusi to win the world weightlifting championship,” adds Graves, who is African American. “Differences don’t necessarily correlate with skin color, but rather with geography and climate. Endurance runners are more likely to come from East Africa. That’s a fact. Genes play a major role in this.”

Neither science nor the empirical evidence supports the default myth widely peddled by the media that Kenyans dominate because of social factors. “I lived right next door to school,” laughs Kenyan-born Wilson Kipketer, world 800-meter record holder, dismissing such cookie-cutter explanations. “I walked, nice and slow.” Some kids ran to school, some didn’t, he says, but it’s not why we succeed. And for every Kenyan monster-miler, there are others, like Kipketer, who get along on less than thirty. “Training regimens are as varied in Kenya as any where in the world,” notes Colm O’Connell, coach at St. Patrick’s Iten, the famous private school and running factory in the Great Rift Valley that turned out Kipketer and other Kenyan greats. O’Connell eschews the mega-training so common among runners in Europe and North America who have failed so miserably in bottling the Kenyan running miracle.

“Very many in sports physiology would like to believe that it is training, the environment, what you eat that plays the most important role in sports. But based on the data, the genes are what counts most,” states the top scientist in t human performance research, Bengt Saltin, director of the Copenhagen Muscle Research Center. Saltin outlined his widely embraced findings in “Muscles and Genes,” the September 2000 cover story in Scientific American. “The extent of the environment can always be discussed but it’s less than 20, 25 percent. It is ‘in your genes’ whether or not you are talented or whether you will become talented.”


Sport success is a bio-social phenomenon, with cultural factors such as opportunity amplifying small but meaningful differences in performance related to heredity. Genetically linked, highly heritable characteristics such as skeletal structure, the distribution of muscle fiber types, reflex capabilities, metabolic efficiency, lung capacity, and the ability to use energy more efficiently are not evenly distributed among populations and cannot be explained by known environmental factors. Scientists are just beginning to isolate the genetic links to those biologically-based differences (though the fact that this patterned biology is grounded in genetics is unequivocal).

A glance at a world map of athletic pockets or hothouses highlights places where evolution and accidents of culture play a key role in the patterns of excellence we see in sports: The domination of endurance running by East Africans, sprinting by blacks of primarily West African ancestry, Eurasian white supremacy in weightlifting and power events, etc., are explained, in part, by patterned anatomical differences.

East Africans have a near perfect biomechanical package for endurance: lean, ectomorphic physiques, huge natural lung capacity, and a high proportion of slow twitch muscle fibers. It’s also a poor combination for sprinting, which undoubtedly helps explain East Africa’s dismal sprinting history. Kenya has tried desperately over the past decade to replicate its wondrous success in distance running at the sprints, but to no avail. The best Kenyan time ever in the 100 meters–10.28 seconds–ranks somewhere near 5,000th on the all-time list.

The pool of potential great sprinters (and athletes with fast burst, anaerobic skills) is deepest among athletes of West African descent. Claude Bouchard, geneticist at the Pennington Biomedical Research Center at Louisiana State University, found that such populations have a higher percentage of “energy efficient” fast twitch muscle fibers to complement their naturally more mesomorphic physiques. “West Africans have 70 percent of the fast type muscle fibers when they are born,” adds Saltin. “And that’s needed for a 100-meter race around 9.9 seconds.”

Some critics have noted that there have been a few great white sprinters, such as Valery Borzov, the Russian who won Olympic gold in 1972. Borzov’s moment of glory, although an Olympic win, was pedestrian in historical terms. It doesn’t even rank in the top 500 sprints of all time. Athletes of primarily West African origin, including African Americans, hold the top 200 and 494 of the top 500 times. No white, Asian or East African has ever cracked ten seconds in the 100. In fact, there are more elite sprinters from any one of the largest West African countries–Senegal, Cameroon, Ivory Coast, Nigeria, Ghana–then from all of Asia and the white populations of the world combined.

In fact, the old Eastern bloc countries provided a unique laboratory to evaluate the radical environmentalist’s canard that humans are infinitely plastic. The world’s most elaborate sports factory combined with state-supervised illegal drug supplements still could not turn even one East German or Soviet sprinter into the world’s fastest human. The vaunted Eastern European sporting machines lavished much of their efforts, which included sophisticated use of performance enhancing drugs, on its female athletes, where the drug cocktails had the most impact.

This is not evidence that blacks are “superior” athletes. Genetics does not confer rank. There are no Master Races. Populations with naturally less body fat, such as Africans, who are the world’s best runners, quickly find that advantage a huge negative when attempting a cross channel swim or the Iditarod. And for all their achievements in running, athletes of African ancestry are notable underperformers in strength events, from weightlifting to the shot putt.

Eurasians are more likely to have the endomorphic physique of the best strength athletes. The world’s top weightlifters and wrestlers live in or trace their ancestry from a swath of Eurasia, from Bulgaria through upper Mongolia. The original inhabitants of this mostly northern region likely arrived no more than 25,000 years ago. Evolutionary forces shaped a population that is large and muscular, particularly in the upper body, with relatively short arms and legs and thick torsos–for example, Naim Suleymanoglu, the 4-foot, 11-inch Turkish weightlifter, considered the greatest in the history of the sport. Forty-six of the top 50 male hammer throwers of all time and 43 of the top 50 female shot-putters trace their primary ancestry to this region.

Where flexibility is key, East Asians shine, such as in diving and some skating and gymnastic events. Their body types tend to be small with relatively short extremities, long torsos, and a thicker layer of fat–a scaled down mixture of mesomorphic and endomorphic characteristics As a result, athletes from this region are somewhat slower and less strong than whites or blacks, but more flexible on average. “Chinese splits,” a rare maneuver demanding extraordinary flexibility, has roots in this anthropometric reality. It’s a key skill set for martial arts, which of course also are rooted in Asian traditions. Those anthropometric realities circumscribe Asian possibilities in jumping: not one Asian male or female high jumper makes the top 50 all-time. Many scientists believe this distinctive body type evolved as adaptations to harsh climes encountered by bands of Homo sapiens who migrated to Northeast Asia about 40,000 years ago. The excavation of an abundance of precise tools in Asia, including needles for sewing clothes to survive cold winters, has led scientists to speculate that Asians were “programmed” over time to be more dexterous. Studies indicate that East Asians do have the quickest reaction time, which some have speculated may play a role in Asian domination of Ping-Pong.


The thorny reality is that if there were no “racial” differences, the entire Human Genome Project would be meaningless. Frequencies of many polymorphic genes vary with population clusters and can have powerful health consequences. The great paradox of human biodiversity research, which is focused on finding the genetic basis to many diseases, is that the only way to understand how similar humans are is to learn how we differ.

Genetic factors help explain the prevalence of Tay-Sachs, a neurological disease, among European Jews and their Diaspora descendants and the proclivity to skin cancer and cystic fibrosis among Northern Europeans. The presence of the gene apolipoprotein E allele, E-4 allele is a potent risk factor of Alzheimer’s in Caucasians but not for blacks of West African ancestry. The Pima Indians have one of the highest rates of diabetes in the world. A condition called primaquine sensitivity is responsible for the intensity of the reaction to certain drugs among African, Mediterranean, and Asian men. Another mutated gene accounts for the sensitivity of the Japanese to alcohol. Other genetic polymorphisms found in specific population groups are associated with sensitivity to certain foods, type one diabetes, QT syndrome (a heart disease), asthma, thrombophilia (bleeding disorder), and an inability to metabolize common drugs like codeine, beta-blockers and antidepressants. These are all “racial” differences of a kind; potentially thousands more remain to be identified.

Most geneticists dispute the sociological orthodoxy that racial classifications are best represented as an infinite spectrum of overlapping and inseparable populations. Maps of gene frequencies of different characteristics, such as those found in The History and Geography of Human Genes, by Stanford University geneticist Luigi Cavalli-Sforza and colleagues Paolo Menozzi and Albert Piazza belie such a notion. Human differences sometimes, but not always, correlate with broad social categories defined by pigmentation, hair form, blood component reactions such as clotting, disease susceptibility, and the like. Somewhat distinct “racial” groups are frequently the product of geographic cul-de-sacs, where populations remained relatively insular and phenotypic differences emerged.

“The classification of human ethnic or racial groups remains a viable, important feature in understanding the nature and mechanism of human evolution,” writes Ranajit Chakraborty, a population geneticist at the University of Texas Health Science Center at Houston. Chakraborty distinguishes between the popular concept of race (which includes cultural dimensions, such as self-definition) and the term now used by geneticists and evolutionary biologists to mean a common biological inheritance. The precise number and grouping of races will always be somewhat arbitrary–race is in part a social construct. Typology, the typing of humans into categories, is akin to wrestling an octopus into a shoe box: no matter how hard you fight with it, you still have something dangling out somewhere. Modern typologists cannot even agree whether it is more meaningful to lump races into large fuzzy groups or to split them into smaller units of dozens or even hundreds of populations.

Rather than identify “races” by facial characteristics or geography, most scientists now isolate groups based on genotypic patterns, which show up in allele frequencies and proteins. Cavalli-Sforza calls them “populations” while Loring Brace prefers the term “clusters.” They are “fuzzy sets” to Vincent Sarich and “extended families” for Steve Sailer. Their meanings are very similar: waves of migrations and intense evolutionary pressures have shaped identifiable if fuzzy groupings. Cavalli-Sforza and his colleagues have identified 491 world populations. Although they go out of their way to note that “the concept of race has failed to obtain any consensus,” their research breaks down the world populations into 42 smaller groups, and then nine clusters: Africans (sub-Saharans), Caucasians (Europeans), Caucasians (extra-Europeans), Northern Mongoloids (excluding Arctic populations), Northeast Asian Arctic populations, Southern Mongoloids (mainland and insular Southeast Asians), New Guineans plus Australians, Inhabitants of Minor Pacific islands, and Native Americans. Other geneticists have mapped similar racial taxonomies.

“The fact that monolithic racial categories do not show up consistently in the genotype does not mean there are no group differences between pockets of populations,” agrees Graves. “There are some group differences. We see it in diseases. But that’s a long way from reconstructing century old racial science. It varies by characteristic.”


Why do we so readily accept that evolution has turned out blacks with a genetic proclivity to contract sickle cell and colorectal cancer, Jews of European heritage who are one hundred times more likely than other groups to fall victim to the degenerative neurological disease Tay-Sachs, Asians who are genetically more reactive to alcohol, and Northern European whites who are most vulnerable to cystic fibrosis and multiple sclerosis, yet find it racist to acknowledge that the success of East African distance runners, Eurasian white power lifters, and sprinters of West African ancestry can be explained, in part, by genetics?

The elephant in the living room, of course, is the irresolvable controversy over race and intelligence. Although racial labels are occasionally helpful terms–geneticists often study specific ethnic groups to get a handle on the ways commonly shared genes lead to specific diseases–they can leave misconceptions. Some traits are correlated, such as dark skin color and the presence of the sickle cell gene. But such links are not absolute. Blacks who have evolved in cooler climates are no more likely to contract sickle cell than anyone else while other Mediterranean populations have high incidences of sicklemia.

Are there “intelligence” differences between populations? The only honest answer is that this issue is complex and depends on how one defines “population” and “intelligence”. Certainly there is massive empirical evidence demonstrating statistically significant IQ differences between sub-populations. But IQ is only one (albeit a critically important) dimension of intelligence. Moreover, much of the intelligence testing data sweepingly aggregates genetically diverse populations under the banner of folkloric notions of race.

Gould, among others, rightly questions “the propensity to convert an abstract concept (like intelligence) into a hard entity (like an amount of quantifiable brain stuff). After all, the length of the femur bone, an individual’s muscle fiber type, or the presence of the allele frequency for malaria each involves a miniscule amount of genes. Most expressed behaviors, including and especially the complex notion of “intelligence,” engage fully half of the 30,000 genes of the human genome. These genes interact with each and are turned off and on by obscure environmental triggers. We can objectively measure the world’s fastest human over 100 meters; devising a test to measure the world’s “smartest” person is an altogether different enterprise.

With those important caveats, it is scientifically naïve to state that there is no evidence of brain functioning differences between local populations. Humans clearly have developed different physical features; the brain is part of the body and as susceptible to evolutionary forces as any other part. Although this is a relatively virgin area of research (in part, scientists say, because of the sordid history of race science and racist eugenics), intriguing studies are in the works. For example, Professor Clive Harper, a neuropathologist at the of the University of Sydney Hospital, claims to have found that among Aborigines, the area of the brain responsible for visual processing is 25 percent larger than average. Harper’s studies, the last of which was published in the Journal of Hirnforschung (Brain Research), indicates that Aboriginal children have near photographic memories, an evolutionary gift from their ancestors, who “had to master the vast landscape to survive.” IQ tests have shown that Aborigines test lower than some other populations. Are these preliminary findings an indication of a different form of “intelligence”?

As any forensic scientist or anthropology 101 student can confirm, there are disparities in the morphology of the crania (and brains) of different populations, even after adjusting for social and economic factors. The meaningfulness of such data is in dispute, however. The extreme position, advanced by Gould in his polemic The Mismeasure of Man, challenges the veracity of the studies on “racial” cranial disparities. That position, widely cited in the popular media, is contradicted by unassailable studies, many quite recent. Although gross brain size does correlate with one measure of intelligence, IQ, there are caveats about what that means. Graves points out that modern humans have smaller crania than Neanderthals, who they supplanted 30,000 years ago, presumably because of our superior intelligence. Psychologist and intelligence theorist Arthur Jensen of the University of California at Berkeley has noted that women have proportionately smaller brains then do men, even after adjusting for body weight, yet they score the same as men on intelligence tests. However, men and women do appear to express their reasoning skills quite differently, which biologists believe is linked to structural sex-linked differences within the brain (such as the difference in the size and shape of the corpus callosum, the fibers uniting the cerebral hemispheres) caused by hormones.

Any or all of such factors as gross brain size, component structures, and the density of receptors may play roles in how mental capacity is expressed. Clearly, it is fallacious to claim that there is no evidence of any genetically-based “intelligence” differences (whether in abstract reasoning, practical, linguistic, musical, or some other form) between some local human populations.


Some race realists seduce themselves into believing that they are being intellectually honest in pointing out the “natural” advantages of certain “races”, but they reach beyond limited data to speculative and sweeping conclusions. Anti-race ideologues, on the other hand, posture that the public cannot grasp the nuances of population differences so they deny them altogether. As Steven Sailer has written, Darwin has enemies on the right and the left. Unfortunately, the leftwing demagogues have long gotten a pass in the media and in some corners of the academic world. The consequences of such disingenuity are serious and mounting.

Such hypocrisy was on display earlier this year in New York at a conference on race and sports. Gould, renowned for his political correctness as much as for his scientific acumen, declared that there is no “running gene,” as if that somehow resolved the debate over the causes of black domination of running. Such bluster is a classic straw man. No scientist claims there is a “running gene.” That’s a dodge of the real question: Do genes proscribe possibility in some sports, running most specifically, and are there some population-based patterns? The answer is an indisputable ‘yes. Scientists have already identified specific genes linked to athletic performance. In one of numerous such studies, Steven Rudich, a transplant surgeon then at the University of California at Davis, demonstrated that a single injection of the EPO gene into the leg muscles of monkeys produced significantly elevated red blood cell levels for 20 to 30 weeks. EPO is a key factor in endurance and is found in some populations more than in others.

Researchers isolating a gene responsible for muscle weakness caused by the debilitating effects of muscular dystrophy may even have stumbled upon a “smoking gun” that bolsters the genetic case for population-linked differences in sprinting capacity. While, researchers at the Institute for Neuromuscular Research in Sydney, Australia found that 20 percent of people of Caucasian and Asian background have what they called a “wimp gene,” a defective gene that blocks the body from producing ?-actinin-3, which provides the explosive power in fast-twitch muscles. Samples drawn from African Bantus, specifically Zulu tribal members showed that only 3 percent had the wimp gene. Kathryn North, head of the Neurogenetics Research Unit at the New Children’s Hospital speculate that the need for a “speed gene” is dying out because the speed to hunt animals or flee from enemies is no longer necessary for our survival–although it certainly helps in sprinting.

“It is possible that an athlete could be genetically engineered to have a gene so you could increase muscle strength, train with it and shut it off when you want to,” says Helen Blau, professor of molecular pharmacology at Stanford Medical School.

Was Gould unaware of this burgeoning area of genetic research or was he massaging the debate to support what he believes are larger societal values? His contention that there is “no running gene” certainly played to the popular myth that everyone is born as a tabula rasa for the environment to inscribe. The Reuters reporter fell for this doublespeak, headlining his article “Athletic Achievement Isn’t in the Genes.” Yet, even Gould didn’t say something that silly. In his speech, he noted that sports success is a complex combination of social, environmental, and biological factors. Unfortunately, such nuances were buried beneath the screaming headline that implied just the opposite.

This is not just a theoretical concern, for it threatens work on disease research tied to the human genome project. In a spring New York Times article, “Skin Deep: Shouldn’t a Pill Be Colorblind?” Sheryl Gay Stolberg juxtaposed the long-documented fact that “race” can be a strong predictor of health and drug efficacy against the nostrum, espoused by none other than Craig Venter of Celera Genomics, “there is no basis in the genetic code for race. It is disturbing to see reputable scientists and physicians even categorizing things in terms of race,” he told her. Venter was merely engaging in the parlor game of recognizing differences that frequently break out along traditional racial lines without appearing to acknowledge that race exists. Yet, in the same conversation, Venter offered an example of why “race,” redefined as patterned biology, does matter: Caucasians, he said, are much more likely than Africans to have a genetic mutation that provides resistance against the virus that causes AIDS.

Splitting rhetorical hairs to preserve ideological purity (and head off a potential public backlash) already has serious consequences. “Here we have the black community accepting the concept that African-Americans need to be studied as a group, and then we have the scientific community claiming that race is dead,” says Jay Cohn, a professor of medicine at the University of Minnesota. “It seems to me absolutely ludicrous to suggest that this prominent characteristic that we all recognize when we look at people should not be looked at.”

Caricaturing the rhetorical use of folk categories of race is not going to make the patterned biological variation on which some differences are based disappear. “We may believe that most differences between races are superficial, but the differences are there, and they are informative about the origins and migrations of our species,” responds Alan Rogers, a population geneticist and professor of anthropology at the University of Utah in Salt Lake City. “To do my work, I have to get genetic data from different parts of the world, and look at differences within groups and between groups, so it helps to have labels for groups.”

“I believe that we need to look at the causes of differences in diseases between the various races,” agrees Claude Bouchard, who is also one the world’s leading experts in obesity, in the American Journal of Human Biology. “In human biology…it is important to understand if age, gender, and race, and other population characteristics contribute to phenotype variation. Only by confronting these enormous issues head-on, and not by circumventing them in the guise of political correctness, do we stand a chance to evaluate the discriminating agendas and devise appropriate interventions.”

A case might be made that the ideologically-driven perspectives of Gould, Lewontin, Marks and others make some sense as a tactical response to the adaptionist, genetic-centered arguments that looms in the background in evolutionary theory. Indeed, the environment and the complex interrelationship of genes, individuals, and groups of populations can explain much in life. But they have staked out the most extreme and least credible position with ad hominem attacks on even those who articulate a nuanced understanding of the inseparability of genes and culture.

As Barbara Ehrenreich and Janet McIntosh wrote in the liberal weekly Nation in 1997, “What began as a healthy skepticism about misuses of biology [has become] a new form of dogma,” they wrote. “[Like the religious fundamentalists, the new academic Creationists defend their stance as if all of human dignity–and all hope for the future–were at stake. [But] in portraying human beings as pure products of cultural context, the secular Creationist standpoint not only commits biological errors but defies common sense.”

This unrelenting assault on the strawman of race has been directed at some of the most respected researchers in the world. Cavalli-Sforza, who helped establish the Human Genome Diversity Project in 1991, has come under relentless attack by Jonathan Marks and others for “encouraging racist thinking,” “stealing” the genes of developing countries, “destroying” their culture and even “contributing to genocide.” At a recent symposium on the HGDP, Marks and Debra Harry, a Northern Paiute Indian, co-authored an attack that combined misleading statements about genetics with a blatant agenda. “The vast majority of human genetic variation is known to be within-group variation, …” they write. “Thus the value of such a project would appear to be quite minimal, especially given the ill will it has managed to generate.”

Their analysis is scientifically nonsense but politically potent. To underscore their point, Marks and Harry cleverly mock the disingenuity of the HGDP scientists, who waffle about the existence of “race” to protect their left flank (and to keep the research dollars flowing) while publishing research that clearly shows population differences. “We learn, on the one hand, that races do not exist,” he writes, citing public statements by HGDP scientists, “and on the other hand, we learn in widely publicized color-coded maps [of genetic variation] in which Africans are yellow, Australians red, [Mongoloids blue] and Caucasoids green. … Perhaps, then, the project ought to be sandbagged,” he jibes, “until the people writing about it have thought more clearly about the actual nature of the diversity they wish to study.” And Marks is right, if for the wrong reasons.

The irony in this soft-censorship is immense, since a taboo on open discussion on the grounds that it encourages racism is the exact and entirely cynical position proffered by Creationists who oppose the teaching of Darwin. It’s at this point that the views of the far right and demagogic left become virtually indistinguishable. The consequences of following their radical prescription is enforced ignorance, which will only fracture even more the fragile support for genetics research. As UCLA’s Jared Diamond has noted, “Even today, few scientists dare to study racial origins, lest they be branded racists just for being interested in the subject.” Moreover, by encouraging censorship for fear that this data will be misused, righteous social thinkers unwittingly legitimize the taboo that traditional races can be ranked from superior to inferior (“if we shouldn’t talk about racial differences for fear of causing offense, maybe there is some truth to it”).

Folkloric notions of race have come into being because a host of phenotypes are correlated. That does not mean that the folkloric categories (whichever ones are used) are distinct and discrete. They are not and their explanatory powers are limited. That understood, it’s without question that some population groups do resemble ethnic or “racial” groups. The radical cant that groupings based on relatively isolated phenotypic traits such as fingerprint markings are as “equally valid” as population clusters based on genetic alleles is totally fallacious. Some fuzzy-edged population groups do resemble folkloric groupings; pretending that they do not defies logic and undermines the credibility of those whose motives otherwise appear noble.

It might be nice if there were no innate differences of any kind among population groups, at least besides the obvious cosmetic ones. But genes do not confer equality, for without differences, evolution would be impossible. Humans are different, the consequence of thousands of years of evolution in varying terrains. Society, and science in particular, pay a huge price for not discussing this openly, if carefully. We are within a decade of perfecting tools that could make humans run faster, jump higher and throw farther–and most importantly live longer and healthier lives, as the result of gene therapy for diseases. Caricaturing population genetics as pseudo-science just devalues legitimate concerns about how this information will be put to use. It ends up emboldening the anti-evolution cabal that stretches from Bishop Wilberforce to Creationists to Darwin’s enemies on the left.

Science is not an assertion of inalterable facts but a method of interrogating reality. The question is no longer whether these inquiries will continue but in what manner and to what end. If we do not welcome the flowering of this more complex appreciation of human nature with open minds, if we are scared to ask and to answer difficult questions, if we lose faith in science, then there is no winner; we all lose.

© COPYRIGHT Jon Entine Sept 2001

[NOTE: The article above is a revised version of the original]

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