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The Biology of Race Unraveled

By tdberg

Within the context of the current race debate, the question of whether race is a legitimate term rests on how we define it, and how, in turn, we deploy it. Can we use race to mandate a belief in biological determinism, or should we use it as a genetic surrogate to achieve equality? And, importantly, can we let the second one in without paying homage to the first? Recent developments in the biomedical and genetic fields have only worked to complicate these matters. To the layperson, it may seem that there are very real reasons to embrace the gene as an explanatory precept of race- but within the realm of biology, this conjecture has produced a fierce debate about both its scientific accuracy and social utility. It is clear that genotypes and ancestry do not necessarily correlate with phenotypes and visual traits (skin color, facial features, etc.). And, it is also clear that no one gene can account for the things that we define as being properties of race. As such, it seems that racial concepts, forged not from the natural sciences but from the discourses of law, politics and history, should be abandoned as a biological category altogether. Moreover, it seems that if we wish to legitimize racial terms as proxies, we should ask what they are ultimately doing for us. For, it may be that we are unintentionally diverting attention and money away from the very real socioeconomic problems that are the root cause of many health disparities in the United States and in the Global South.
But before we decide whether or not race is a legitimate proxy for social risk factors, we must first examine the claim’s underlying scientific data. For, if race is not scientifically meaningful, we deny a necessary condition for keeping it as a biological category. Science, as an ideal, has never been in the business of appealing to unnatural categories, whether empirical or prescriptive, and to do so now would only undermine its self-proclaimed foundations of objectivity and universality. Historical attempts at such phrenological claims in the past have all been eventually trumped as illegitimate and bogus, if not racist.
While few modern day biomedical researchers believe in the Platonic notion of a racial essence that was forwarded in the eighteenth century, recent theories have tried to link ancestral populations to these taxonomic categories genetically. As an example, Blumenbach’s taxonomy of 1776 (Caucasian, Mongolian, Ethiopian, American, Malay) seems to eerily reappear in the work of Neil Risch (Caucasian, East Asian, African, Native American, Pacific Islander). As such, Risch’s proposal for reanimating this scheme rests on two central claims. The first is that racial self-identification is a legitimate proxy for use in medical treatment and research. The second is that these scientific racial facts exist separately from politics, and must ultimately trump politics because of their objectivity and truth. But, is that really the case? According to Craig Venter, a prolific contributor to the Human Genome Project, “Race is a social concept, not a scientific one. We all evolved in the last 100,000 years from the same small number of tribes that migrated out of Africa and colonized the world.” So, how does Risch and company get to where they are going if there is no such thing as actual race genes derived via population clusters? And furthermore, if there is no such thing as a specific race gene, how legitimate can this type of proxy be, and why should it trump politics?
New DNA technology allows us to scrutinize the many small differences in the human genome. Scientists are now able to delineate single base pair variations at defined locations on particular chromosomes- and these pairs, known as single nucleotide polymorphisms (SNPs), number close to 30 million in the collective human genome. In general, a SNP occurs when a neutral mutation appears on a chromosome in the midst of an already-existing DNA sequence. Further, these already existing sequences with their new mutation are called haplotypes, because they come from one of the two parentally donated chromosomes. In the course of evolutionary history, new haplotypes have formed by either a new mutation occurring, or by crossing over during meiosis. Since individual SNPs can be found within the same haplotype, and because only a few haplotypes account for most of the genetic variation among members of a particular human population, scientists can assess human variation by looking at all the SNPs that vary within known haplotypes. By snipping the genome in this way, geneticists have confirmed that 85% of human variation occurs in all populations and about 15% between populations. So, ultimately, it is what resides in this 15% that is at the heart of the debate. And, furthermore, any statistic that looks for specific racial differences will be a subset of this 15%. Subsequently, to make a claim of medical importance, the SNP must not only be related to a gene involved with a particular medical condition, but it must also be known to differ in groups that one wants to apply a racial label too. As such, let’s examine what kind of prevalence and statistical rates we are looking at.
In a response to Risch’s argument, a group of medical researchers (Cooper, Kaufman, and Ward) attack his claim that rare alleles for disease are related to racially defined categories. In fact, they claim that the most well known genetic diseases are found in populations that are not considered by Risch to even constitute a race. Specifically, Cooper et al give the examples of hemochromatosis, which is found in 7.5% of all Swedes, and Tay-Sachs, which is found in 4% of the Ashkenazi Jewish population. Tellingly, Risch has lumped these two groups together under the category of Caucasian, even though there is no meaningful incidence of hemochromatosis in the Ashkenazi Jewish population or of Tay-Sachs in Swedes. In spite of this, Risch defines, in his paper, hemochromatosis as a Caucasian disease (pg. 5) even though its prevalence rests mainly with those of a Swedish national origin. As such, Cooper thinks one might make the case that hemochromatosis is a disease prevalent in Swedes, but not the case that it is a disease prevalent in Caucasians. Furthermore, Cooper argues that there is no compelling evidence that links well known SNPs that differ between groups to the most common of debilitating illnesses- such as cardiovascular disease or chronic hypertension. Rather, the diseases that we can link genetics to are rare killers and not necessarily the ones we should be focusing on. Risch, who must realize this, states, “This is an important concern because alleles underlying disease susceptibility, especially deleterious diseases, may be less frequent than randomly selected alleles.” And, “few genes underlying susceptibility to common diseases or influencing drug response have been identified.” (Pg 5) As such, it may be that we are working to avert precious time and money away from the genuine fact of the matter. In other words, if these problems are entirely cultural and socioeconomic in nature, and not biological, then we should address the socioeconomic problems without masking them in the biological sciences. To do otherwise is not only dubious, but an inefficient spend of limited resources.
Another important component of the Risch argument, which we must address, rests upon a discussion of admixture, indigenous populations, and genetic drift. He asserts that there has been little intermixing in the United States, a claim which is based on the self-reporting of individuals in the 2000 census. But clearly, self-reporting is a notoriously flawed measure, and more importantly, the self-reporting of social race masks biological admixture. As such, there are only six options on the census form to choose from, and it should be obvious that individuals may self-identify differently from what they are genetically according to Risch’s five groups, due to social perceptions and pressure. Furthermore, the trend toward higher admixture, which entails the need for more boxes, will only increase as time goes by since more interbreeding will occur. Yet, if Risch cannot preserve his notion of distinct populations that have not interbred, his argument starts to collapse. Why? Because unlike natural selection, which selects for beneficial alleles, genetic drift is a random occurrence that works mainly on previously isolated breeding populations. So by means of mathematical probability, when migration and interbreeding occur, the alleles in question, as an ideal, either eventually die out or become ingrained in 100% of the population. For this reason, it becomes more and more difficult, if not inevitably impossible, to distinguish one group from another group genetically.
As such, let’s explore this issue further by examining one recent admixture study conducted on populations of self-identified African Americans (E. Parra et al.) This study discovered that the proportion of European admixture, within the aforementioned restricted 15%, was the highest in New Orleans (around 23%), and the lowest in South Carolina (around 12%). Yet, whether a subset average of 17% is enough to warrant the validation of a genetic definition of race is definitely arguable. Furthermore, the problem widens when we look at so-called black populations on other continents. In Brazil, for example, the admixture percentage rate can run as high as 50%. As such, the biomedical practices and procedures that Risch condones fail to remain universal because they clearly cannot be applied globally- and universality is generally considered a hallmark of science. This is something that doesn’t escape Risch entirely- he states, “Primary categories that are relevant for the current U.S. population might not be optimal for a globally derived sample.” (Bruchard et al. Pg. 1174)
Most of the studies that follow Risch’s lead render results that stem from a biologically determinist way of thinking. In other words, many of these scientists operate under the assumption that most aspects of our lives are ultimately predetermined by our genetic makeup. And, in the areas where we do not yet have the answers, we can reliably default to what we think is the base cause and use it as a surrogate. Following, the misguided entailment of this argument states, for example, that if one population is at a higher risk for a particular cancer than another group, then it must be that the first group is genetically, and therefore racially, predisposed to that cancer. Yet, often times this way of thinking reduces complex systems, in which genetics and environment interact intimately, to a simple causal chain. Stephen Jay Gould states, “We make a category error in arguing that because [something] has moderate heritability within groups, the causes for average differences must be genetic.” (The Mismeasure of Man, Pg. 33)
So, if this is the case, we must question how effective Risch’s utility argument really is. If there are no alleles or SNPs that differ between populations that are also attached to widespread diseases such as hypertension and diabetes- and only to rare diseases like Tay-Sachs- where is the strength of this utility? And if many of the causal mechanisms that he is relating to genetics are actually environmental, and therefore changeable, what are we really doing here? Stephen Gould states, “The truly salient issues are malleability and flexibility, not fallacious parsing by percentages. A trait may be 90 percent heritable, yet entirely malleable.” (The Mismeasure of Man, Pg. 34) As such, if things like geography, income, diet, exercise, education, and social caste play a far greater role in determining health disparities than race based genetics, than we should abandon the use of race as a surrogate variable; especially if we find that the costs far outweigh the benefits. To encourage the use of race as a genetic proxy ultimately encourages the belief that race is a legitimate genetic, hence biological, category. The danger here is that social prejudice often seeks scientific support, since scientific support can somehow validate beliefs that are otherwise spurious.
Michael Root makes a case for avoiding this proxy in The Use of Race in Medicine as a Proxy for Genetic Differences. Specifically, he targets the administering of drugs to any group based on a phenotypical conception, or rather a possible misconception. In discussing the use of beta-blockers for heart disease he states, “Doctors do not know how an individual patient will respond to each of the different heart drugs, but they know or think they know a patients race.” Yet, “targeting blacks assumes that race is a better predictor than any environmental factor,…but the assumption is not reasonable since the rate at which a drug is metabolized varies as a result of many factors, age, environment and lifestyle as well as genes.” (Pg. 1178) As a result, many blacks might be given the black drug when the white drug, due to interracial differences, might actually be a more effective remedy. Thus, if we treat all black patients the same, we might inadvertently deny some a more efficacious treatment and not give them a better one.
Root additionally highlights a second problem with assuming that a disease is genetically racial- namely, that doctors might be wrongly convinced and thus fail to search for the real cause. Sickle-cell anemia has been historically perceived as a black disease. Root states, “During most of the nineteenth and much of the twentieth century many physicians were so convinced that sickling is a black disease and the sickle-cell gene a black gene that they refused to diagnose the disease in white patients or reasoned that apparently white patients are black.” (Pg. 1176) However, according to Root, these physicians were wrong. We now know that phenotypically white people with origins in the malarial regions of Europe are more likely to carry the sickle-cell gene than blacks from the malarial regions of Africa. Since there are more blacks in the United States from the malarial regions of Africa than whites from the malarial regions of Europe, it became a black disease in the United States. What’s distinctly worse here, is that even after researchers discovered this truth, they continued to use race as a surrogate, propagating a myth that sickle-cell was an exclusively a black disease.
Unfortunately, science has a long history of institutionalizing racism, from Linnaeus’ essentialist taxonomy to Hernstein and Murray’s The Bell Curve. Anthropologists, at the turn of the century, gave up on notions of race because they decided that it was not capable of doing the work they needed it to. So why are biologists, who deal in a natural science, not following suit? And, what types of biases underwrite their objective truths? We must question how deeply the moral consequences of our cultural notions are embedded into our notions of race and the biological sciences. And, additionally, we need to discuss and consider what is at the epistemological center of this rationalization.
The reasoning behind scientific racialism goes something like this- science gives us objective facts, and once we have discovered these facts, we have gained universal knowledge of the world. Since race is a legitimate and objective biological category, using race as a causal mechanism for explanation and prediction is both desirable and legitimate. If it turns out that different some races are less intelligent, less capable, less ambitious, or weak, we should accept this as merely an objective fact of science and nothing more.
Yet, it should be interjected here that the concept ‘all men are created equal’ is not a scientific fact, but rather a political and moral judgment that resides squarely outside of the realm of science. Moreover, epistemically, science cannot provide us with a solid basis for this type of moral judgment because it can never provide us with the necessary certainty. Science is inherently abductive, or inductive at best, so it gives us approximations, probabilities, and contingent statements. And, this does not mean that we should defer to race simply because it gives us an “elegant” explanation. For, are we ultimately willing to subjugate entire populations because of the way we parse our percentages? If it turns out that this is the case, then nature becomes nothing more than an accomplice to political inequality, and our scientist’ end-up currying the favor of bigots by providing them with apparently useful data. This is very dangerous ground. In the past, this type of manifesto, has led to poverty, social rioting, and genocide. As Gould admonishes, “Those who cannot remember the past, are condemned to repeat it” (Ibid, 371).
In closing, I do not believe that we can let a race proxy for genetics into the biomedical sciences without letting in a whole lot of undesirable consequences. We need to think of genes as merely a small part of a complex environmental system- not the simple root cause of race. To do so is not only bad science; it is politically and socially dangerous. Uneducated laymen all too often look to science for a justification of their beliefs, and it is our responsibility if we allow our objectivity to be clouded or misread. By using race as a proxy for genetics, we are implying that there is a legitimate biological connection between race and genes when there is little evidence of one. And, in so doing, we are wrongfully promoting a policy of scientific racism. Biology devised a taxonomic racial structure in the eighteenth century to justify the political and social institutions of slavery and white dominance. Now, it is time for science to acknowledge this and eradicate it. To quote Charles Darwin, “If the misery of our poor be caused not by the laws of nature, but by our institutions, great is our sin.”

3 Responses to The Biology of Race Unraveled

  1. Didier

    The answer is both, praobbly?Ten years ago I believed there had to be a genetic disposition in order to develop type 2 diabetes, now I believe that lifestyle and/or genetics can bring the disease on. There are numerous studies that show people who have no history of diabetes in their families are developing the disease but to be fair it isn’t always possible to know if their is a family history of diabetes since many are never diagnosed and/or are not telling anyone they have it.That site that Mz Lamb gave is outdated, it hasn’t changed or been updated in 6 years that I know of.

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