Evolution of Placental Animals and Enlarged Brains

James Howard jmhoward at sprynet.com
Thu Sep 9 13:33:20 EST 1999


Evolution of Placental Animals and Enlarged Brains

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

I was presented with the question of why mammalian brains evolved larger
than dinosaurs, or extant fish and birds.  While trying to answering that
question, I also deduced a potential explanation for evolution of placenta
animals; they occur together.  My work with dehydroepiandrosterone (DHEA),
testosterone, and human evolution immediately made me look to these for an
explanation.  I think the hominid brain evolved because of the effects of
testosterone on brain growth.  That is, I think the slow, steady increase in
brain size that started with the Australopithecines, and which continues
today as an increase in “IQ” identified as the “Flynn Effect,” is due to
slow, steady increases in testosterone in the hominid line.  Human males and
females produce more testosterone than male and female chimpanzees,
respectively.  (Further explanation of this and supporting citations may be
found primarily in my explanation of human evolution at
http://www.naples.net/~nfn03605 on the net.)  The secondary increase in
brain size that resulted in Homo sapiens, I attribute to increases in use of
DHEA by the brain.  I recently found direct support that DHEA, indeed, may
be directly involved in brain growth.  “These studies provide evidence of
mechanisms by which DHEA and DHEAS exert biological actions, show that they
have specific functions other than as sex steroid precursors, and suggest
that their developmentally regulated synthesis in vivo may play crucial and
different roles in organizing the neocortex.”  Compagnone NA and Mellon SH,
Proceedings of the National Academy of Science USA 1998; 95: 4678.

Since DHEA increases heat production and, I think, is directly related to
brain growth and function, I decided that the enlarged brains of placenta
animals, as well as the evolution of  placentae are tied together around the
time of the demise of the dinosaurs.  That is, a change occurred which
increased the probability of survival of an animal during a time of cold,
and or dark, that increased the production/availability of DHEA.  The extra
DHEA would increase heat production; the extra DHEA would increase brain
size.  DHEA increases resting metabolism (Journal of Nutrition 1987; 117:
1287).

During my work trying to link DHEA with various phenomena, I found that the
hormone, prolactin, is directly connected to DHEA production.  This is what
provided the key to explaining the evolution of placenta animals.  The usual
neurohormone given credit for stimulating DHEA production is
adrenocorticotropic hormone (ACTH), but it may be shown that not only is the
prolactin (PRL) more effective in stimulating DHEA, but PRL may be specific
for stimulating DHEA.  “Dehydroepiandrosterone formation was increased
(p<0.05) 3.5 fold and five [fold] by adrenocorticotropic hormone and
prolactin respectively [in baboon fetus].” (American Journal of Obstetrics
and Gynecology 1987; 156: 1275)  “These findings indicate that the majority
of serum androgens in young baboons is of adrenal origin.  Therefore, we
conclude that PRL, in addition to ACTH, may also be an adrenocorticotrophic
factor in baboon infants.  However, in contrast to ACTH, the action of PRL
on the adrenal is apparently specific of androgen [DHEA] production.”
(Endocrinology 1985; 117: 1968).  So, I suggest an event occurred that
selected for an increase in prolactin production in an animal at a time when
increased metabolism would be a great advantage.

The hormone melatonin is produced by the pineal gland.  Melatonin is known
to reduce prolactin production.  “Melatonin treatment appeared more
efficient than an artificial photoperiod in reducing plasma prolactin
concentrations.” (Journal of Endocrinology 1986; 108: 287).  So animals that
have “better developed …pineal complexes” may produce, or rely more on
melatonin production for physiological phenomena.  “In fishes, amphibians,
and reptiles, the pineal complex is better developed than in mammals. The
nonmammalian pineal functions as both a photoreceptor organ and an endocrine
source for melatonin. Effects of light on reproduction in fishes and
tetrapods are mediated at least in part through the pineal, and it has been
implicated in a number of daily and seasonal biorhythmic phenomena.”
Encyclopædia Britannica, “CD99”  The explanation I want to draw from this is
that an animal derived from creatures of this sort, i.e., “fishes,
amphibians, and reptiles” and, maybe dinosaurs, might have a survival
advantage if it was a low melatonin producer during a time of cold and dark.
The advantage would be a reduction in the prolactin “brake,” melatonin,
which would increase prolactin production.  Increased prolactin would
increase DHEA.  These individuals would have an advantage in heat production
and brain growth.

Now, increased prolactin may be tied to not only the advantage just
described, but directly to “why” placenta animals would no longer rely on an
egg case around an embryo. It occurred to me that if increases in prolactin
are the key, then, perhaps, increased prolactin should reduce levels of
calcium.  My idea was that the egg shell might be so reduced, at the same
time, that the placenta might evolve from structures already designed for
oxygen transfer within the egg itself.  There is direct support that
increased prolactin adversely affects calcium deposition, naturally and
experimentally.  (While the actual cause reduced bone calcium is debated as
secondarily a result of reduced estrogen, the primary effect results from
increased prolactin.)  “Therefore, the present data indicate that the
osteoporosis of hyperprolactinemia is likely due to PRL-induced
hypogonadism, rather than a direct effect of PRL on calcium homeostasis.”
(Metabolism 1998; 47:425).  The osteoporosis of increased prolactin can be
“experimentally” induced, i.e., antipsychotic drugs increase prolactin.
“The major effects of hyperprolactinemia in women are amenorrhea, cessation
of normal cyclic ovarian function, loss of libido, occasional hirsutism, and
increased long-term risk of osteoporosis.”  (Schizophrenia Research 1999; 35
Suppl: S67)  These are extreme cases of hyperprolactinemia, but the
direction of the effects supports my hypothesis.  That is, increasing
prolactin, as a result of reduced melatonin, might result in decreased egg
case production.

I suggest placenta animals and their enlarged brains evolved from an
increase in prolactin.  Increased DHEA, due to the increased stimulus of
prolactin, immediately provided an advantage in heat.  Secondarily,
reduction in egg shell production, also due to increased prolactin, would
increase the probability of internal growth and development of embryos.  The
trigger for this advantage in survival may have resulted from decreased
melatonin production in some animals during a time of prolonged cold and
dark.






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