Evidence of Ongoing Evolution: Evidence of Increasing Testosterone and the
Increase in Preeclampsia
James Michael Howard
Fayetteville, Arkansas, U.S.A.
This is intended to demonstrate that an ongoing, pathological phenomenon ma=
y
be directly connected to my explanation of human evolution. That is, human
evolution is directly influenced by levels of testosterone within
populations. It is my hypothesis that testosterone is rising in society.
More specifically, it is my hypothesis that the percentage of individuals
who produce more testosterone is increasing compared to people who produce
less. I suggest the increase in percentage of individuals of higher
testosterone is identifiable as a change in children known as the "secular
trend." The secular trend is the increase in height and weight and earlier
puberty in children. (That is, children of higher testosterone are bigger
and reach puberty earlier.) The secular trend is real and was recently
documented in the United States (Freedman, D.S., et al., "Secular trends in
height among children during 2 decades, The Bogalusa heart study," Archives
of Pediatric and Adolescent Medicine 2000; 154:155-161). A secondary
hypothesis suggests increased testosterone causes a number of problems
within groups of higher testosterone. This may be occurring at this time.
Among these problems may be an increase in a severe complication of
pregnancy called preeclampsia. The Associated Press reported March 13, 2001=
,
in: "Dangerous pregnancy complication on the rise," that preeclampsia is on
the rise in the United States: "The NIH [National Institutes of Health] jus=
t
sounded an alarm that the pre-eclampsia rate rose by nearly a third during
the 1990s." The rise in the percentage of individuals of higher
testosterone increases the fecundity of humans as well as specific
characteristics of the hominid line. However, excessive amounts of
testosterone produce characteristic negative phenomena within the hominid
line and humans. This periodic cycling of high versus low levels of
testosterone within populations has produced periodic shifts in hominid and
human populations. Preeclampsia may be one of these negative consequences
of excessive testosterone; the increase may represent a consequence of high
levels of testosterone.
This may be identifiable in the effects of testosterone on an enzyme,
epoxide hydrolase, associated with preeclampsia. Steegers, E.A., et al., "=
A
polymorphism in the gene for microsomal epoxide hydrolase is associated wit=
h
pre-eclampsia," (Journal of Medical Genetics 2001; 38: 234-237) report a
connection between genotype variability of the gene for "epoxide hydrolase"
and the incidence of preeclampsia. "Microsomal epoxide hydrolase is an
important enzyme involved in the metabolism of endogenous and exogenous
toxicants." The "high activity genotype" occurs more often (29%) in
preeclampsia than in controls (16%). They conclude that: "Women with the
high activity genotype in exon 3, which could reflect differences in
metabolic activation of endogenous or exogenous toxic compounds, may have
enhanced susceptibility to pre-eclampsia."
Exposure to testosterone is directly involved in expression of epoxide
hydrolase in the livers of adult rats (Denlinger, C.L. and Vesell, E.S.,
"Hormonal regulation of the developmental pattern of epoxide hydrolases.
Studies in rat liver," Biochemical Pharmacology 1989 Feb 15;38(4):603-10).
Treatment of castrated mice with testosterone increases soluble epoxide
hydrolase activity between 49% and 400% depending upon the tissue examined
(Pinot, F., et al., "Differential regulation of soluble epoxide hydrolase b=
y
clofibrate and sexual hormones in the liver and kidneys of mice,"
Biochemical Pharmacology 1995; 50(4): 501-8). Testosterone activates
soluble and mitocondrial expoxide hydrolase activity, while "=85estradiol
treatment showed a suppressive effect on both subcellular activities in
males, but had no effect on female activities." (Inoue, N., et al., "Sex
hormone-related control of hepatic epoxide hydrolase activities in mice,"
Biological and Pharmaceutical Bulletin 1993 Oct;16(10):1004-7).
A number of reports connect high levels of testosterone directly to
preeclampsia: "Levels of the potent androgen testosterone were significantl=
y
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=85 "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)
It is my hypothesis that testosterone is rising in society. More
specifically, it is my hypothesis that the percentage of individuals who
produce more testosterone is increasing compared to people who produce less=
=2E
I suggest the increase in percentage of individuals of higher testosterone
is identifiable as a change in children known as the "secular trend." The
secular trend is the increase in height and weight and earlier puberty in
children. (That is, children of higher testosterone are bigger and reach
puberty earlier.) The secular trend is real and was recently documented in
the United States (Freedman, D.S., et al., "Secular trends in height among
children during 2 decades, The Bogalusa heart study," Archives of Pediatric
and Adolescent Medicine 2000; 154:155-161).=20
Preeclampsia is increasing in the United States. I suggest this increase
results from an increase in the percentage of women who produce increased
levels of testosterone. Increased levels of testosterone may activate the
"high activity genotype" of epoxide hydrolase in women of higher
testosterone. This may account for the increase in preeclampsia.
