Human species-specific genetic mutation enhances atherosclerosis
pnas.org
pnas.org
2 to 3 million years ago, a gene in early humans was permanently inactivated (perhaps due to a malaria-like outbreak targeting a cell-surface molecule that the protein the gene coded for helped to build). That cell-surface molecule is found in most other mammals (excepting humans, ferrets, platypuses, and New World monkeys) so consumption of certain meats can cause it to be taken up and incorporated into human cell membranes, as the genes that allow for this are still functioning. But the immune system becomes sensitized to it, as a foreign antigen, and produces antibodies that subsequently cause chronic inflammation in the cells that took it up and exposed it on their surfaces.
I'm curious how those findings relate to this.
Since this is a prehistoric alteration to the genome, cutting across all humans, it's more than likely a result of natural selection via merciless and deadly contagion. Every early human predecessor with the gene died without offspring, and only the last remaining children of those ancestral origins lacking the gene lived long enough to evade death by the disease.
So, before any or all humans even emerged as a species, something came along and cut down common ancestors, only leaving behind survivors that disused the related genes.
There was a lot of research that showed smoking didn't cause cancer and we all know how that came about.