Addressing your points respectively,
-
Exactly. That’s a major reason for bringing it up. My understanding of evolution has played an enormous role in my work, but I’ve never actually studied it.
-
Meyer’s assertion is truly mind-bogglingly wrong, both from the work I’ve started to present here, and in my more recent work on inherited cardiomyopathies. The cardiomyopathies have the advantage of being natural, but the literature is so granular that it’s harder to get the big picture. The gross generalization is, for all but the most severe single-amino acid residue changes in cardiac cytoskeletal proteins, for every teenager who dies suddenly and tragically from cardiac arrest caused by hypertrophy, the half of her/his family members carrying the same disease allele will not have any problem for decades or will die from something else while never showing any symptoms. I suspect that there’s more tolerance for these mutations in the heart over skeletal muscle because of the plasticity of cardiac physiology. The bottom line is that cardiac cytoskeletal genes are pretty darn polymorphic, we knew that in 2010, and more so now.
-
I found your analysis to be compelling, so I thought that adding a more empirical approach might stimulate more discussion. We’ll see…