Population differences are important when working with genome-wide association studies, because a model "trained on" one population won't perform as well against the "test set" of a different population. Suppose you do a big study and find a bunch of SNPs that correlate with a trait, like schizophrenia or liking opera. The frequencies of those SNPs for two populations from the same continent (like Japanese and Chinese) will hugely correlate (Pearson's _r_ ≈ 0.97), but for more genetically-distant populations from different continents, the correlation will still be big but not huge (like _r_ ≈ 0.8 or whatever).
-What do these differences in SNP frequencies mean in practice?? We ... don't know yet. At least some population differences are fairly well-understood: I'd tell you about sickle-cell and lactase persistence, except [then I would have to scream](/2017/Dec/interlude-xi/). There are some cases where we see populations independently evolve different adaptations that solve the same problem: people in Tibet and Peru have both adapted to high altitudes, but the Tibetans did it by breathing faster and the Peruvians did it with more hemoglobin!
+What do these differences in SNP frequencies mean in practice?? We ... don't know yet. At least some population differences are fairly well-understood: I'd tell you about sickle-cell and lactase persistence, except [then I would have to scream](/2017/Dec/interlude-xi/). There are some cases where we see populations independently evolve different adaptations that solve the same problem: people living on the plateaus of Tibet and Peru have both adapted to high altitudes, but the Tibetans did it by breathing faster and the Peruvians did it with more hemoglobin!
Sorry, "the Tibetans did it with ..." is sloppy phrasing on my part; what I actually mean is that the Tibetans who weren't genetically predisposed to breathe faster were more likely to die without leaving children behind. That's how evolution works!
[TODO: link, Cynthia M. Beall, "Two Routes to Functional Adaptation", double-check what "resting ventilation" means]
-The third part of the book is about genetic influences on class structure! Untangling the true causes of human variation is a really hard technical philosophy problem, but behavioral geneticists have at least gotten started on the problem with their simple _ACE_ model.
+The third part of the book is about genetic influences on class structure! Untangling the true causes of human variation is a really hard technical philosophy problem, but behavioral geneticists have at least gotten started with their simple _ACE_ model. It works like this: first, assume that genetic variation for a trait is _additive_ (if you have the appropriate SNP, you get more of the trait), rather than exhibiting epistasis () or Mendelian dominance ().
[p. 212-4: A + C + E model and comparing identical and fraternal twins (different from twins raised apart)]
[ACE model assumes no assortative mating, which leads to an underestimate of A: because it makes fraternal twins resemble each other for non-environmental reasons]
projects / Ultimately_Untrue_Thought.git / blobdiff