Evolution of Placental Animals and Enlarged Brains

Copyright ć 1999 by James Michael Howard.


I was presented with the question of why mammalian brains evolved larger than dinosaurs, or extant fish and birds. While trying to answer 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. 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." Encyclopędia 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.