Evolutionary Selection of Testosterone


James Michael H

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

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

I suggest increases in testosterone produced the
characteristics of maleness as well as those of primates
and, eventually, humans.