Name: James Michael Howard
Testosterone and Evolution of Skin Color in Humans
Testosterone and Evolution of Skin Color in Humans
James Michael Howard
Fayetteville, Arkansas, U.S.A.
In October of 1996, I first posted (to some internet news groups) my hypothesis that skin color evolved as a result of testosterone. It was entitled "Skin color …perhaps Testosterone." My explanation of human evolution suggests increased testosterone in human males and females, compared to chimpanzee males and females, is directly involved in human evolution. Therefore, I decided testosterone could be linked to skin color. (If you wish to explore my explanation of human evolution in more detail, please read "New Theory of Human Evolution Involving DHEA, Melatonin, and Testosterone" ( http://www.naples.net/~nfn03605/dheamela.htm )and "Androgens in Human Evolution: A New Explanation of Human Evolution," (http://www.naples.net/~nfn03605/dheaandr.htm ). In 1996, I found limited support of a connection, so I left further work on this connection for later. The July, 2000, issue of "The Journal of Human Evolution," included an article, "Evolution of Human Skin Coloration," which caused me to look again at a connection between testosterone and human skin color (Jablonski, NG and Chaplin, G, J Human Evolution 2000; 39: 57-106). Jablonski and Chaplin state: "Here we present new evidence indicating that variations in skin color are adaptive, and are related to the regulation of ultraviolet (UV) radiation penetration in the integument and its direct and indirect effects on fitness." The article concerns UV light and skin color. They also state: "In all populations for which skin reflectance data were available for males and females, females were found to be lighter skinned than males." This indicates to me that testosterone, as I first suggested in 1996, may be directly involved in skin color.
July 12, 2000, I posted "Evolution of Skin Color" to some news groups. This consisted of "Long ago, I decided skin coloration is due to levels of testosterone. Blacks produce more testosterone than other races, hence, blacks have darker skin. (I derived this from my explanation of human evolution.) Jablonski and Chaplin just found that 'In all populations for which skin reflectance data were available for males and females, females were found to be lighter skinned than males.' This would support my hypothesis." The obvious question quickly returned in response at the news group. Why are black women darker than white men? The following is my answer to the question and is an extension of my original hypothesis that testosterone is directly involved in skin color and human evolution. I suggest the difference results from effects of testosterone on melanocytes in utero.
It is known that testosterone and ultraviolet light work together in stimulating melanocyte structure and function. "Cultured skin receiving both UVL [ultraviolet light] and testosterone illustrates a synergistic effect." (J Exp Zoo 1978; 204: 229, "Organ culture of mammalian skin and the effects of ultraviolet light and testosterone on melanocyte morphology and function," Gilmcher, ME, et al.). This could account for the findings of Jablonski and Chaplin, mentioned in my July 12 post that "In all populations for which skin reflectance data were available for males and females, females were found to be lighter skinned than males." This may be a tanning effect, however, testosterone is definitely involved in melanocyte function.
Healthy black males produce significantly more testosterone than healthy white males (J Nat Cancer Instit 1986; 76: 421). Melanocyes from black males grow differently from melanocytes from white males, in culture. In this study, melanocytes are derived from foreskins, an area of skin directly affected by testosterone. "At the ultrastructural level, cultured melanocytes derived from black (negroid) neonatal skin (B-M) had numerous mature rod-shaped stage IV melanosomes, while white (caucasoid) skin-derived melanocytes (W-M) in culture contained no mature melanosomes. Growth rate, cell yield, and in vitro lifespan for B-M were more than twice that for W-M in pure melanocyte cultures in the presence of MGF [melanocyte growth factor]. Our results suggest that MGF-dependent growth of B-M differs from that of W-M." (J Cell Physiol 1988; 135: 262-8, "Growth characteristics of human epidermal melanocytes in pure culture with special reference to genetic differences," Hirobe, T, et al.). Melanocytes grown in culture, without testosterone added to the culture media, inherently express a difference in growth potential between black and white males.
Melanocytes derived from neonates already exhibit differences in growth rate according to race. "Differences in size and number of melanosomes attributable to race of the tissue donor were readily apparent, and pigment content of melanocytes from both black and Caucasian donors appeared to increase with time in culture. Newborn melanocytes proliferated more rapidly and survived longer than did adult melanocytes, but there were no consistent morphologic differences as a function of donor age." (J Invest Dermatol 1984; 83: 370-6, "Selective cultivation of human melanocytes from newborn and adult epidermis," Gilchrest, BA, et al.).
I think the effects of testosterone on melanocytes first occurs in utero. In utero, black fetuses are exposed to higher levels of testosterone. "Serum testosterone was modestly, but significantly, greater in the black than in the white women." (J Clin Endocrinol Metab 1996; 81: 1023-6, "Demonstration of a lack of racial differences in secretion of growth hormone despite a racial difference in bone mineral density in premenopausal women—a Clinical Research Center study," Wright, NM, et al.). Therefore, I suggest melanocytes are stimulated by increased testosterone during gestation in blacks. In respect to the specific question, this would result in increased melanocyte stimulation in female, black fetuses. Male fetuses are exposed to testosterone, from the fetal gonads, at a critical period in utero that exerts effects on reproductive development. I make the assumption that this period of exposure of male, fetal-derived testosterone does not coincide with the constant supply of maternally-derived testosterone that stimulates melanocytes. If that is the case, then it is possible that black women exhibit darker skin than white males because of a difference in timing of exposure of developing melanocytes to testosterone in utero. The color of offspring of interracial unions would depend upon testosterone levels of the mother and embryonic/fetal melanocytes, that is, the propensity of melanocytes for producing melanin and the stimulation of melanocytes by testosterone during the critical period.
According to my explanation of human evolution, lower testosterone groups migrated away from the equator. Therefore, it is the lower levels of testosterone that resulted in lighter skin in groups living away from the equator. Advantages of darker skin near the equator and advantages of lighter skin away from the equator are simply secondary advantages.