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Human Genetic Variation, Race, and Medical Research
Posting my homework on Blurty allows me to fulfill my academic and social needs:
In Brown’s chapter on “Human Genetic Variation” (and elsewhere), he echoes a common paradox throughout the genetics literature: the meaning and significance of common sense racial typing (phenotypes) are simultaneously denied and shored up. How do you see that happening? Would there be a way to address human genetic variation without falling into this paradox?
Brown rejects the concept of race, that is, of a simplistic and essentialist idea of human genetic variation, by agreeing that “human races do not exist in any meaningful genetic context.“ Yet he does so briefly. Without even explaining what he means by “meaningful,” he fills the rest of the paragraph with terms like “group characteristics,” “obvious traits,” “isolated populations,” and “human sub-population[s].” What does Brown mean by a “human sub-population” if he doesn’t intend it as a byword for “race?”
Brown certainly writes as if a mere substitution of terms is all he intends. Take the following sentence as an example:
In other words, two individuals who share a variant allele have a single common ancestor who was the source of that mutation, even if those two individuals are members of different modern subpopulations.
Whatever his credentials as a scientist, he shows a limited grasp of logic. If two individuals share this allele, what justifies their categorization into a “subpopulation” besides the very physical traits which are not significant enough to provide a genetic justification for the concept of “race?” Brown’s motivation in advocating the search for correlations between risk factors for disease and “subpopulations,” i.e. socially-constructed identities which are loosely based on phenotype, is to provide a context for selective testing which does not involve the expensive and laborious process of searching entire genomes for risk-factor SNPs, which, unlike racial and ethnic identities, are both present on the genome in concrete form and numerous enough to be medically useful. Using racial and ethnic identities to guess about risk factors is lazy and is just as likely to result in self-identitified members of “subpopulations” not thought to be particularly at risk from a certain disease to not be tested as it is to result in a higher percentage of cases in more at-risk “subpopulations” being detected.
It is necessary to put “subpopulations” in quotes, because when it comes to the spread of alleles through human populations during recorded history, Brown’s information is as limited as his logic. His statement that “by chance, the founders of each subgroup had a higher frequency [of] some variant alleles than the rest of the human population, but overall, they shared no more genetic similarities with each other than with other humans” misses the point entirely. “Subgroups” have not been static. Haplotypes with relatively recent origins, i.e. from the last 2 millennia, are spread with remarkable range around the world because of historical mixing. For instance, 30% of African-Americans males have Y-chromosomes which come from Europeans. Frequencies of mixing are lower in some places and higher in others, but even in Europe, significant portions of the supposedly pure European population have mitochondrial DNA with relatively recent origins in places like southern Africa and eastern Asia. The use of “races” and “subgroups” in medicine will just not work. It is a poor substitute for real research into the causes of disease, may result in more disease, not less, and will become less viable than it already is as the the small number of traits that Brown considers useful for determining “subpopulations” continue to mix at a historically unprecedented rate.
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