Mutations, Testosterone, and Human Evolution

James Michael Howard jmhoward at arkansas.net
Wed Sep 4 14:23:01 EST 2002


Mutations, Testosterone, and Human Evolution

James Michael Howard
Fayetteville, Arkansas, U.S.A.

I suggest increases in testosterone are directly connected to human evolution
(J. Howard, Rivista di Biolgia / Biology Forum 2001; 94: 345).  Human males
and females produce more testosterone than chimpanzee males and females,
respectively.   Increased testosterone may have increased brain capacity and
reproduction.  However, periodically, negative effects of excessive levels of
testosterone occurred which may have reduced fertility and immunity
sufficiently to threaten survival.  (Increased testosterone reduces
spermatogenesis and immune function.)  Increasing testosterone produced
increasingly large hominids with moderately increased brain capacity,
vulnerable to periodic negative effects of testosterone.  Fortuitously,
testosterone produces an additional effect which counterbalances negative
effects and may have produced modern humans.  

The evolution of Primates from other mammals may be due to increased
testosterone.  Early Primates may have also been affected by negative effects
of excessive testosterone.  The gene, Deleted in AZoospermia, DAZ, first
appears about 30-40 million years ago, the time of the appearance of the
Primates.  (Some think DAZ is necessary / beneficial for spermatogenesis.)  I
suggest DAZ rescued the early Primates from extinction due to reduced
spermatogenesis.  Hominids evolved from Primates, again as a result of
increased testosterone.  With time, this would, again, cause negative effects.
DAZ "doubled" about the same time that "Y Chromosome Adam" appears in human
evolution.  I suggest DAZ increased spermatogenesis a second time and, again,
rescued us from excessive testosterone.  (J. Howard, Rivista di Biologia /
Biology Forum 95 (2) in press; this paragraph inclusive).

I suggest increased testosterone may increase the probability of mutations,
some of which counteracted the negative effects of excessive testosterone.
There is a strong "male-driven" effect on gene mutation in humans and apes
(Kateryna, et al., Nature 2002; 416: 624 and Ebersberger, et al., American
Journal of Human Genetics 2002; 70: 1490).  This effect is greater in Primates
than rodents (Huang, et al., Journal of Molecular Evolution 1997; 44: 463) and
is "particularly pronounced in the human brain," (Enard, et al., Comment in
Science 2002; 296: 233).  

Testosterone's effect of accelerating gene change may have participated in the
change in the human gene, FOXP2.  FOXP2 is thought to participate in human
language, differs from FOXP2 in the chimpanzee, gorilla, orangutan and mouse,
and is "doubled" in humans (Nature 2002; 418: 869).  Humans do not make a
common mammalian sialic acid (Neu5Gc), because the enzyme which makes Neu5Gc,
CAMH, is mutated in humans.  The change in CAMH in hominids occurred a short
time before the "brain expansion began in humankind's ancestry, 2.1 - 2.2
million years ago." (Chou, et al., Proceedings of the National Academy of
Science U.S.A. 2002; 99: 11736).

During times of excess testosterone during human evolution, I suggest
increased testosterone participated in these genetic changes that are thought
to play significant roles in the evolution of the human brain and language.
This effect may also explain increased cancer in humans.




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