Five myths of race.

Here are my five myths of race, by Jon Entine. 

It’s an archived cut and paste, none of it is my work, barring a couple of comments.

The complete text is available through the link.

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.

(It’s now 99.7% the same, the figure was corrected recently)

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.