Tongue roll, please…: Part Four of The Evolutionary Biology of Race

In my last post on the evolutionary biology of ‘race’ I spent considerable time on skin colour and its variability. I hope it’s obvious that I chose skin colour to begin this part of the discussion because of its long history of use as a ‘racial’ determinant. I’m also hoping I was thorough enough to have persuaded you that, at least as far as skin colour goes, ‘racial’ categories are specious.
     There’s a very large number of heritable traits, like skin colour, that are the product of more than one gene, resulting in continuously variable characteristics. Height is a good example. Look deeper and you see that there’s no single superficial trait, such as hair type, skin colour, nose shape, stature, ear shapeyou name itthat distinguishes one so-called race from another. Moreover, looking at the superficial qualities of people’s skin, hair, and noses ignores the very large numbers of other genetically determined traits that you can’t see, or may not be aware of even if you can see them. 
     Here are a few examples. How many of you can roll your tongue lengthwise in your mouth? You might be surprised, as I was, to learn that some people can’t. The ability to roll the tongue is genetically determined, and variable across the human species, within and between the traditional ‘racial’ categories. 
     Did you also know that there are two types of ear wax? About 98 percent of northern Chinese have dry ear wax, while about 84 percent of pale-skinned Americans have a waxy substance in their ears? My partner from the United States didn’t even know that the waxy stuff existed, because her entire family has dry ear wax. It’s a recessive gene variant, and it requires one copy from each parent. If two such persons have babies, all of the babies will have dry ear wax. 
     If you used ear wax to define your races instead of skin colour think of the consequences! Instead of racialist-inspired studies purporting to show the link between skin colour and IQ, you might find studies showing a link between dry ear wax and lower IQ.
     But these are all examples of ‘neutral’ traits, that probably don’t contribute to an individual’s survival. Is there any more or less variability in potentially lethal genes or gene combinations? The relationship between the disease malaria and one known as sickle-cell anemia is one well-known example. 
     Malaria is a deadly disease that’s prevalent in the warmer latitudes. It’s caused by a very hardy parasite that destroys healthy red blood cells, those that transport oxygen throughout the body. Sickle-cell anemia is caused by a gene variant that directs the body to make abnormal, sickle-shaped, red blood cells.

A ‘sickled’ red blood cell

     Carrying one normal and one sickling gene variant means that, when infected with malaria, the parasite is unable to find enough normal red blood cells to allow it to flourish and debilitate the host. Carriers display no symptoms of anemia, and they are not significantly debilitated. In a malaria area, having one copy of the sickling variant is  advantageous. For offspring to develop sickle-cell anemia, they must inherit one copy of the sickling variant from each parent. The odds of this happening are about 1 in 4.
     In areas where malaria is common, the sickling variant occurs in a high proportion of the population because those without it tend to die before they’re able to produce offspring, leaving more carriers to pass on their sickling genes. Where malaria has little or no effect on populations, that sickling variant settles in the population at a very low frequency, perhaps as a commonly recurring, usually non-lethal mutation.

Piel, et al. Nature Communications, 1:104, 2010 (DOI: 10.1038/ncomms1104)

     Map b, above, illustrates the percentage of people in the population who have at least one copy of the sickling variant. Map c shows the level of malaria occurrence. Central equatorial Africa has the highest incidence. Compare the two distributions, and notice how the areas of high gene frequency ‘map’ on to the pattern of malaria prevalence. 
     The further away you get from the areas of highest incidence, the lower the frequency of the sickling variant in the population. Note, also, that this sickling gene variant is present, in small proportions, across the traditionally defined races. And it even occurs, in very small numbers of people, in areas where malaria is not endemic. It is only seen in higher frequencies in the presence of malaria. 
     The take-home message here is that there’s much more variability in the human genome than can be accounted for by racial classifications. Genetic traits just won’t behave according to the prescriptions of a racial worldview. 

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