The shallowness of white identity politics, (cont., see my earlier blog entry,) as if the color of one’s skin was something more than just skin deep.
The text below is from The Human Odyssey, a publication of Scientific American. The writer is John Hawks, an associate professor of anthropology at the University of Wisconsin–Madison and the author of a widely read paleoanthropology blog.
What is perhaps most extraordinary about our recent evolution is how many common physical features are completely new to human anatomy. The thick, straight black hair shared by most East Asians, for example, arose only within the past 30,000 years, thanks to a mutation in a gene called EDAR, which is crucial for orchestrating orchestrating the early development of skin, hair, teeth and nails. That genetic variant traveled with early colonizers of the Americas, all of whom share an evolutionary past with East Asians.
Most are new mutations that have emerged in one population or another: a change in a gene named TYRP1, for instance, that makes certain Solomon Islanders blond; the HERC2 mutation that results in blue eyes; changes to MC1R that causes red hairs to sprout instead of black ones; and a mutation in the SLC24A5 gene that lightens skin color and that is now found in up to 95 percent of Europeans.
As in the case of lactase, ancient DNA is giving clear information about the antiquity of such mutations. Blue eyes seem to have appeared in people who lived more than 9,000 years ago, but the massive change to SLC24A5 is not found in the DNA of ancient skeletons from the same time period. Skin, hair and eye color evolved with stunning speed. Variations in pigmentation are some of the most obvious differences between the races and, in some ways, the easiest to study.
Scientists have also investigated much odder and less evident features of human anatomy. Consider the variations of earwax. Most people in the world today have sticky earwax. In contrast, many East Asians have dry, flaky earwax that does not stick together. Anthropologists have known about this variation for more than 100 years, but geneticists did not uncover the cause until recently. Dry earwax results from a relatively new mutation to a gene called ABCC11. Only 30,000 to 20,000 years old, the mutation also affects the apocrine glands, which produce sweat.
If you have stinky armpits and sticky earwax, chances are you have the original version of ABCC11. If you have dry earwax and a little less need for deodorant, you probably have the newer mutation. A few thousand years before dry earwax first appeared among East Asians, another seemingly simple mutation started saving millions of Africans from a deadly disease. A gene called DARC produces a starchy molecule on the surface of red blood cells that mops up excess immune system molecules known as chemokines from the blood. About 45,000 years ago a mutation in DARC conferred remarkable resistance to Plasmodium vivax, one of the two most prevalent malaria parasites infecting humans today. The vivax parasites enter red blood cells through the DARC molecule encoded by the gene, so hindering the expression of DARC keeps the pathogens at bay. The absence of DARC also increased the amount of inflammation-causing chemokines circulating in the blood, which has in turn been linked to an increase in prostate cancer rates in African-American men. Yet on the whole, the mutation was so successful that 95 percent of people living below the Sahara now have it, whereas only 5 percent of Europeans and Asians do.