Evolutionary Selection of Testosterone
Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that mammals evolved because of increases in
dehydroepiandrosterone (DHEA) (Hormones in Mammalian Evolution, Rivista di
Biologia / Biology Forum 2001; 94: 177-184.) I think increased testosterone in
mammalia produced the primates (Rivista di Biologia / Biology Forum 2002; 95:
319-326) which culminated, as a result of further increases in testosterone,
with humans (Androgens in Human Evolution, Rivista di Biologia / Biology Forum
2001; 94: 345-362.).
I suggest estradiol and testosterone direct the use of DHEA. That is, target
tissues of estradiol and testosterone are affected by these two hormones to
increase absorption of DHEA. My principal hypothesis is that DHEA optimizes
replication and transcription of DNA. Therefore, DHEA affects growth and
development and later, maintenance, of all tissues. I suggest testosterone
increases the use of DHEA more than estradiol, therefore, testosterone produces
more robust growth. Men produce more testosterone than women; men grow bigger
and differently than women. I suggest this is what determines sex. Increased
testosterone determines growth and development of tissues more robustly than
estradiol. This robust growth produced the characteristics called "male" from
the same primordial structures that produce "female."
Heat increases testosterone formation. (I anticipate your reaction here, please
wait for the full explanation.) In a study of the effects of exercise-induced
increases in body heat, it was determined that plasma testosterone increases 33%
while sperm counts were not affected (Med Sci Sports Exerc 1984; 16: 51-5). I
suggest the accident that started this selection was connected with the loss of
part of one X chromosome. This may have produced individuals that increased
testosterone at the expense of steroids down stream. This would have been
maximized in mammalia due to constant body temperature. This would have
produced "male" offspring of high testosterone.
In my work with testosterone in evolution, it has become clear to me that excess
testosterone is detrimental. For example, increased testosterone reduces the
immune response and wound healing; very negative characteristics. Individuals
of high testosterone are at a selective disadvantage. Therefore, the second
"accident" of evolution, external gonads, would be selective in reducing
excessive testosterone levels.
I am aware that undescended testes produce sterility, that is, poor sperm
counts. It is my hypothesis that excessive testosterone reduces sperm count.
This characteristic is currently being studied. That is, testosterone is
currently being considered as a male contraceptive because excess testosterone
decreases sperm count. Early in evolution, those individuals without external
gonads would be sterile, I suggest as a result of their increased testosterone
resulting from increased body heat. I suggest evolution selected those
individuals whose gonads were external because of the increased growth and
development which, eventually produced sperm in greater quantities, among other
characteristics, and whose testosterone was not so detrimental.
I suggest increases in testosterone produced the characteristics of maleness as
well as those of primates and, eventually, humans.