Since all humans are less than 1 percent different, many people take this to mean that “Race is a social construct“. The stranglehold that race-denying individuals have had on our society for the past fifty years has had huge implications for our society. This egalitarian notion that “we are all the same” together with affirmative action has already begun its devastating effects on our society with this “Blank Slate“, “ghost in the machine” way of thinking.
However, when they engage in this fallacious reasoning, they fail to realize that we are 96 percent genetically similar to chimpanzees. They also don’t know that cats have 90 percent homologous genes with humans; 82% with dogs; 80% with cows; 79% with chimpanzees; 69% with rats and 67% with mice. 90% of the mouse genome could be lined up with a region on the human genome. 99% of mouse genes turn out to have analogues in humans. We share 97.5 percent of our DNA with mice (which is why lab tests get carried out on them). All of this data makes it clear: what causes phenotypic differences between species that are so genetically similar is not how much genetic distance (Fst) is between them, but how those genes that differ are expressed between these populations. Knowing this, it doesn’t seem so crazy now that with less than a 1 percent difference in the genome on average between the races that there are ways to see that race exists genetically. Moreover, the fact that geneticists estimate that there is a difference of 3 million base pairs between two humans on average, shows that there are enough genetic differences between human populations to produce phenotypic differences to be able to differentiate human populations and that since genotype is the cause for the phenotype, due to the physical diversity between human populations that it doesn’t matter how “small” these differences are, but, as mentioned previously, how those differing genes are expressed is the proof that race exists.
Cheung and Speilman collected the gene sequence of a particular white blood cell in 82 Asians and 60 Europeans. They found that the amount of genetic differences was minute, though the two races had differing amounts of gene expression. 25 percent of the overall genes tested showed differing expression between the Asians and Europeans in the sample. It was noticed on one gene that Europeans expressed it at 22 times the strength that Asians did! Since Asians and Europeans split off around 40 kya, I wonder what a study done on Europeans and Africans would show in regards to gene expression strength along with overall differing genetic expression between those two races.
Hicks et al (2013) compared gene expression levels in 4 populations (whites, blacks, Asians and ‘Hispanics’). The gene expression data consisted of 126 whites, 51 ‘Hispanics’, 13 blacks and 8 Asians. They discovered that there were 300 significantly identified genes that showed differing expression in the four populations tested. Some of the genes were: PHF6 (“Mutations affecting the coding region of this gene or the splicing of the transcript have been associated with Borjeson-Forssman-Lehmann syndrome (BFLS), a disorder characterized by mental retardation, epilepsy, hypogonadism, hypometabolism, obesity, swelling of subcutaneous tissue of the face, narrow palpebral fissures, and large ears.”, BRD3 (observed to be implicit in some forms of leukemia, as well as performing cell overlapping functions), CRLF2 (“. . . which control processes such as cell proliferation and development of the hematopoietic system. Rearrangement of this gene with immunoglobulin heavy chain gene (IGH) on chromosome 14, or with P2Y purinoceptor 8 gene (P2RY8) on the same X or Y chromosomes is associated with B-progenitor acute lymphoblastic leukemia (ALL) and Down syndrome ALL.”) and finally RNF135 (known to be involved in protein-protein and protein-DNA interactions). All though this study had an extremely small sample size for Asians and blacks, with further study in the future, we will see bigger sample sizes to better test these predictions.
Analysis of 639 tumor samples (270 black, 369 white), showed that 95 genes were overexpressed involving prostate cancer from blacks relative to whites and 132 were overexpressed in whites relative to Asians. This seems like testosterone is correlated with this as well. Since blacks are twice as likely to get prostate cancer than white men, this shows another reason why there is a disparity in disease acquisition between races: genetic differences, not any allegations of racism people attempt to use.
Still, there are differences in gene expression that account for more disease rate differences between blacks and whites. Huang et al (2011) observed gene expression differences between blacks and whites that lead to atherosclerosis. They discovered 409 differently expressed genes. Genes expressed lower in black Americans also tended to express lower in blacks with lower CAC. Ontological analysis also verified that of the 409 race-associated genes, a significant amount of them “revealed significant enrichment in mobilization of calcium and immune/inflammatory response”.
With differences in testosterone, estradiol and other hormones between the races, as well as looking at disease rates between human populations and studying what genes correlate with what disease, we can better understand human evolution as well as develop new and specific drugs for individuals based on their genotype.
The gene ACTN3 has been linked to athletic performance, specifically sprinting. Those descended from West African populations have it, i.e., Jamaicans and other Caribbean Islanders along with West Africa. 70 percent of those individuals have this gene variant, so, due to this, the all-time record holders in sprinting are all descended from West African populations. This holds true for Europeans as well. This is seen in World’s Strongest Man (WSM) competition wins by country, seeing as the countries with the most wins have majority white populations. A white man has also won the WSM every year since its inception, which is yet another example of gene expression in action. Whites and Asians have more slow twitch fibers (along with Kenyans) and West African descended blacks have more fast twitch fibers, accounting for these genetic differences which then manifest themselves in our athletic competitions.
Race does exist, and average phenotypic variation is the proof that there is a biological reality to race. The races differ in disease acquisition, as well as muscle fiber typing, which then accounts for disparities in professional championships won along with racial differences in the racial mix of certain sports. As we begin to fully understand the human genome, we will then begin to understand how and why the races differ genetically. The fact that the races differ, on average, on genetic expression shows that there is a reality to what we call “race”. Yes, race is a “social construct”, but it is a social construct of a biological reality. To put it simply, everything is a social construct, and if race doesn’t exist because it’s a social construct then nothing exists, since everything is socially constructed in our minds. But, we know this is not the case. There is a reality, and we use science to test that reality and confirm it with the scientific method.