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I have no idea whether the overall pendulum is swinging back from "race is a purely social construct". I hope so, because it has always seemed absurd to me, for
by cgiles 9y ago
I have no idea whether the overall pendulum is swinging back from "race is a purely social construct". I hope so, because it has always seemed absurd to me, for the very reasons the author cites, just as absurd as the idea that race is a hard determinant of anything.
But what I can say is that in molecular biology, working scientists have completely ignored this politically charged debate and continued to use the concept this whole time. In one example I am directly familiar with, researchers have continued to use and stratify genome-wide association studies by self-reported race/ethnicity in the search for variants causal for lupus. This is important not only because as with many diseases, there is a difference in likelihood of getting the disease between "races" not attributable to lifestyle, but also because it is entirely possible, even probable, that the mechanisms causing the disease are somewhat different between ethnicities.
Actually, therefore, the understanding that there are real differences between "races" in the context of disease is actually helpful for the smaller groups because it means that special attention is paid to the etiology of their disease apart from the general etiology. In the same way that, for many years, most biology research was done on males and it was just assumed that the findings would always apply to females. That was incorrect, and now studies are done to determine gender differences in treatment and disease etiology.
IMO this whole debate has dragged on as long as it has because too many in the public are seemingly incapable -- or unwilling -- to understand basic concepts about population means and variances, and in particular that in a situation like this where population means are very real but usually small, and the variance is high, knowing what "race" you are usually conveys little information about some other attribute of interest. Usually, but not always, as is particularly the case with many diseases.
I have grown particularly tired of the argument that, because a taxonomy, like any clustering, is fuzzy and the number of clusters is somewhat arbitrary, the whole thing conveys no useful information. It is patently false.
- tptacek 9y agoIs it not the case that biologists are simply on firmer ground working on the premise of causal genetic relationships with populations and genes, and far shakier ground when they try to correlate genes to behavior?
- cgiles 9y agoThe typical path to determining causality for a variant is: Variant -> (Gene expression or some other molecular-level phenomenon) -> Phenotype. Actually, associating a variant with a phenotype is the easy part, determining what happens in between is much harder. Another hard part is determining which variant does something since variants are highly correlated with each other. I am not sure I understand your question exactly so I'll give a few different answers. One is that I see no difference whether the phenotype is behavioral or some disease occurring below your neck. It all depends on the statistics and effect sizes of the phenotype and how good a predictor "race" is. Another is that actually it is much more difficult, obviously, to determine causality than a correlation, regardless of what you are correlating with what. And a final answer is that we generally consider a causal relationship between genetics and a phenotype proved with acceptable levels of error if the two are correlated, and we control for all the environmental variables we can, and the correlation remains. You can also look at heritability with twins separated at birth and raised in different environments and other such experiments to control for environment.
- tptacek 9y agoI'd probably start with the question of: isn't it easier to understand the causal relationships in a lot of diseases than it is to understand behavior, the biology of which we barely understand without bringing genetics into it?
- cgiles 9y agoExcept for Mendelian diseases, not really. The sad fact is that for the so-called "complex diseases", we have very little idea what is going on inside the black box. I won't presume to guess whether we know less about them or about behavior, but the ignorance level is very high in both cases. They are called "complex" because we don't understand them, and because they seem to have many causes, both individual genetic loci and environmental variables, each contributing a little bit rather than something like sickle-cell anemia which has one big cause. However, I think our techniques are quite sufficient right now to say X% of the variance in phenotype P is attributable to genetics (i.e., genetics partially cause P). That is a totally different thing from explaining how the genotype causes the phenotype.