MtDna has a very profound impact on "fitness" and "health", so much so that there was a concern that in places like the U.S. where pre-existing conditions or hereditary traits could make acquiring health insurance difficult, people should be wary of making their complete mtDna genome public.
This 2015 paper provides a good summary of the mitochondria and its role in these matters
See:
https://academic.oup.com/humupd/art...tionary-defined-role-of-the-mitochondrial-DNA
"
mitochondrial evolutionary mechanisms have had a profound effect on human adaptation, fertility, healthy reproduction, mtDNA disease manifestation and transmission and ageing. An understanding of these mechanisms might elucidate novel approaches for treatment and prevention of mtDNA disease."
I hate the title of this, but whatever...
See: Mother's curse: the effect of mtDNA on individual fitness and population viability.
https://www.ncbi.nlm.nih.gov/pubmed/16701262
"there is increasing evidence that mitochondrial DNA (mtDNA) is an important contributor to viability and fecundity. Some of this evidence is now well documented, with mtDNA mutations having been shown to play a causal role in degenerative diseases, ageing, and cancer. However, most research on mtDNA has ignored the possibility that other instances exist where mtDNA mutations could have profound fitness consequences. Recent work in humans and other species now indicates that mtDNA mutations play an important role in sperm function, male fertility, and male fitness. Ironically, deleterious mtDNA mutations that affect only males, such as those that impair sperm function, will not be subject to natural selection because mitochondria are generally maternally inherited and could reach high frequencies in populations if the mutations are not disadvantageous in females. "
MtDna "H", in particular, has been associated with increased resistance to sepsis, which is a huge deal in a world without antibiotics, and also with increased resistance to viral infections, including AIDS. That's why I have speculated for a long time on these boards and even on the old dna forums that mtDna frequencies may be the result of selection, especially in periods of extreme stress, as in the face of plague, which has been a repeated scourge.
See:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699618/
My U2e seems to rather be a loser in this regard, probably contributing to the fact that it is now so rare.
As for natural selection in terms of both skin pigmentation and lactase persistence, the papers are too numerous to post. Anybody interested can easily find them using the search engine.
Just generally, we see these de-pigmentation snps popping up here and there, but I don't think it's a coincidence that the place that suddenly seems to sprout a number of them all together should be in a place in Europe with very low levels of sunlight. The same thing happened in northern East Asia, although they have their own snps, not associated with SLC 24A5 or 42A5, for example.
Anyway, that doesn't mean that once present in a population in good numbers it wouldn't have spread with that population or that selection is only natural when it's probably social as well. There are a lot of factors involved.
I also have a hunch, although that's all it is, that LP and de-pigmentation are somehow connected in later periods. You need Vitamin D to process dairy if I understand it correctly, so having pale skin in a low light environment would be very beneficial.
Ed. @Fire-Haired,
I agree with you generally, but pre-steppe arrival people of central Europe were not "dark skinned". Remember the Gamba et al paper, and Otzi even further south with both his copies of derived SLC24A5 and SLC42A5. Also remember the people in Neolithic Anatolia who also had both derived copies. It's just that it wasn't in the high percentages of later periods.
I don't think this all happened in the Bronze Age to Iron Age. I think it's been an ongoing process. However, I also don't think this is all the result of migrations.