Genetics, race, ethnicity, and health

It is my hypothesis that changes in testosterone levels are directly
involved in human evolution and may be identified in modern populations as
the “secular trend.” (“Androgens in Human Evolution,” Rivista di Biologia
/ Biology Forum 2001; 94: 345-362). Changes in testosterone occur more
rapidly than changes in genes. Therefore, the “races” may reflect
different testosterone levels that affect growth and development as well
as maintenance of the adult form. While the data are not complete, as an
example that may produce useful applications, consider that black women
produce more testosterone than white women and, in one study, black males
produce significantly more testosterone than white males. Testosterone
levels may produce differences that significantly impact health. I
suggest the effects of maternal testosterone levels on the fetus are the
driving force of testosterone on populations.

Pearce, et al., considered possible explanations of race and
essentially dismissed race as a factor affecting health. Therefore, race
is “on the table.” Lets examine the most often cited, and most often
dismissed, difference, skin color. It is my hypothesis that skin color is
affected by levels of testosterone. This is also a trait that originates
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). This could account for
the findings of Jablonski and Chaplin that "In all populations for which
skin reflectance data were available for males and females, females were
found to be lighter skinned than males." (J Human Evolution 2000; 39: 57-
106) 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 one study, melanocytes, derived from neonatal foreskins, an
area of skin directly affected by testosterone that has not been
significantly exposed to sunlight exhibit differences. "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). Melanocytes grown in culture, without
testosterone added to the culture media, inherently express a difference
in growth potential between black and white males.

Melanocytes 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).

I think the effects of testosterone on melanocytes first occurs in
utero. In utero, black fetuses are exposed to higher levels of
testosterone. “Black mothers had higher androstenedione and testosterone
concentrations than white mothers.” (Cancer Causes Control 2003; 14: 347-
55) "Serum testosterone was modestly, but significantly, greater in the
black than in the white women." (J Clin Endocrinol Metab 1996; 81: 1023-6.
I suggest melanocytes are stimulated by increased testosterone during
gestation in blacks.

According to my explanation of human evolution, lower testosterone
groups migrated away from the equator. Therefore, lower levels of
testosterone contribute to lighter skin in groups living away from the
equator. This racial difference, skin pigmentation, may be directly
influenced by testosterone levels.

Testosterone may be connected with numerous pathologies.
Testosterone is known to reduce the response of the immune system. In
fact, this may explain the increased levels of HIV infection in blacks,
especially males, compared to whites. Testosterone, in rats, reduces CD4+
T cells and reduces the CD4+/CD8+ ratio as well stimulates as an increase
in CD8+ T cells, which is diagnostic of AIDS in humans (Int
Immunopharmacol 2003; 3: 1853-60). The same pattern exists in black
compared to white children in “infected and uninfected children born to
HIV-infected women.” The pattern exists whether or not HIV infection has
occurred. It is inherent; the HIV more readily infects those with a more
vulnerable immune system and then exaggerates the difference.

“This study investigated whether age-related patterns of immunologic
markers in 1488 uninfected (9789 measurements) and 186 infected (3414
measurements) children differed by gender and race. CD4+, CD8+, and
absolute lymphocytes by HIV infection status, gender, and race were
assessed using linear mixed-effects natural cubic spline models, allowing
for prematurity and maternal CD4+ cell count. In uninfected children,
levels of all 3 markers peaked twice in the first few months of life,
declining to adult levels by around 8 years of age; uninfected boys and
uninfected black children had significantly reduced CD4+ and absolute
lymphocyte counts; the gender difference was especially pronounced in
black children. Infected children had substantially lower levels and
distinctly different patterns; with, e.g., by age 6 months CD4+ cell
counts nearly 1200 per mm3 lower than in uninfected infants. Levels also
significantly differed by gender and race for infected children, although
for gender in the opposite direction. The gender and race differences in
CD4+ levels were not explained by a general lymphocytosis nor were they
confounded by treatment. These substantial differences in immunologic
markers may reflect underlying genetic influence on the cellular immune
system and may have implications for clinical decisions about therapeutic
management.” (J Acquir Immune Defic Syndr 2003; 33: 635-41)

Preeclampsia is definitely connected with testosterone and is
increasing within our populations. (I suggest the secular trend is
actually an increase in the percentage of individuals of higher
testosterone. As they increase, we see their characteristic also
increase. This is human evolution identifiable within modern
populations.) A number of reports connect high levels of testosterone
directly to preeclampsia: "Levels of the potent androgen testosterone were
significantly higher in primigravid women with preeclampsia than in
normotensive women with similar gestational and maternal ages. This
difference may indicate a role for testosterone in the pathogenesis of
preeclampsia." (Acromite, M.T., et al., "Androgens in preeclampsia,"
American Journal of Obstetrics and Gynecology 1999; 180: 60-3) and. "A
history of preeclampsia an average of 17 yr earlier thus appears to be
associated with elevated levels of testosterone, which may contribute to
the increased risk of vascular morbidity in such women." (Laivuori, H., et
al., "Evidence of high circulating testosterone in women with prior
preeclampsia," Journal of Clinical Endocrinology and Metabolism 1998; 83:
344-7)

Prematurity is also a very serious problem that is increasing.
Exposure to testosterone, during pregnancy, results in increased
probability of low birth weight. This has been tested. Prenatal
testosterone exposure reduced body weight of fetuses and newborn rats
(Arzneimittelforschung 1984; 34: 780). Another study in sheep found that
both fetal survival and growth were markedly impaired by prenatal
testosterone administration (Metabolism 1978; 27: 253). Even more ominous
is the finding that alcohol and testosterone, combined, induced low birth
weight in rats (Tetratology 1989; 40: 335).

Pearce, et al., cite the plight of North American Pima Indians as an
example of ill effects of “new white settlers” who imposed negative
environmental stresses upon the Pima population. While it is possible
that the diet imposed on this group “by the United States Government” may
have resulted “in one of the highest rates of prevalence of diabetes in
the world,” Pimas exhibit high testosterone levels (J Endocrinol Invest
1993; 16: 403-6)

Female breast cancer is also an increasing problem. While there is
not a lot of difference in incidence rates between white and black women,
black women present with much larger tumors. While this is attributed to
later exposure to diagnostic situations, it may also be due to the
increased testosterone in black women. It was reported in 2002 that
testosterone may be more directly connected to breast cancer risk than
estradiol. "…androstenedione and testosterone might be more strongly
associated with [breast cancer] risk than estradiol." (J Natl Cancer Inst
2002; 94: 606-616).

There are a number of other disorders that may also be linked to
testosterone levels. I suggest “race” may be directly connected to
testosterone levels. It is my hypothesis that testosterone levels are
involved in race and differences in health between races. History is full
of human malignancy; it occurs every day. We must attempt to identify
racial abuse and try to stop it when it occurs. We must also be careful
that we not find guilt where it does not exist.

Competing interests:
None declared