The ectodysplasin A receptor (EDAR) gene has a range of pleiotropic effects, including sweat gland density, incisor shoveling, and mammary gland ductal branching. The frequency of the human-specific EDAR V370A allele appears to be uniquely elevated in North and East Asian and New World populations due to a bout of positive selection likely to have occurred circa 20,000 y ago. The dental pleiotropic effects of this allele suggest an even higher occurrence among indigenous people in the Western Hemisphere before European colonization. We hypothesize that selection on EDAR V370A occurred in the Beringian refugium because it increases mammary ductal branching, and thereby may amplify the transfer of critical nutrients in vitamin D-deficient conditions to infants via mothers’ milk. This hypothesized selective context for EDAR V370A was likely intertwined with selection on the fatty acid desaturase (FADS) gene cluster because it is known to modulate lipid profiles transmitted to milk from a vitamin D-rich diet high in omega-3 fatty acids.
The authors placed my claims about the mouse-to-human model of the EDAR V370A variant back into the context of an evolutionary adaptation. They seem unwilling to accept the fact that the EDAR V370A variant is a nutrient-dependent pheromone-controlled ecological adaptation in mice and in humans. It links energy-dependent changes from angstroms to ecosystems in all living genera via natural selection for energy-dependent codon optimality.
The EDAR V370A allele is also known as rs3827760, 1540T/C, 370A, or Val370Ala. It is a SNP in the ectodysplasin A receptor EDAR gene on chromosome 2.
See the author’s copy of my invited review of nutritional epigenetics, which was returned without review :
In the context of climate change and changes in diet, the story began with what probably was a nutrient-dependent base pair change and a variant epiallele that arose in a human population in what is now central China. Apparently, the effect of the epiallele was adaptive and it was manifested in the context of an effect on sweat, skin, hair, and teeth. In another mammal, such as the mouse, the effect on sweat, skin, hair, and teeth is probably due to a nutrient-dependent epigenetic effect on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones appear to control the nutrient-dependent epigenetically-effected hormone-dependent organization and hormone-activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates and in microbes as previously indicated.
The ecological adaptations, which appear to be manifested in the human population are detailed in these two reports [162-163]. The ecological adaptations are likely to be nutrient-dependent and pheromone-controlled. If so, ecological variation probably leads to ecological, social, neurogenic, and socio-cognitive niche construction, which is manifested in increasing organismal complexity and species diversity. If not, there may be something as yet unknown about mutations and evolution that makes sense in the light of what is known about nutritional epigenetics and the molecular biology of species from microbes to man.
More than four years later, biologically uninformed theorists have again tried to make natural selection something different than environmental selection. Nina G. Jablonski is one of the co-authors. I’m tempted to think that all the others also are biologically uninformed science idiots who cannot link physical and chemistry from subatomic particles to ecosystems via what organisms eat and the physiology of pheromone-controlled reproduction, which biophysically constrains viral latency in all living genera.
Virus-encoded miRNAs in Ebola virus disease (April 24, 2018)