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Maternal Weight Gain is Caused by Fetal use of DHEA which is Increased by Male Fetuses

Posted by jamesmhoward on 15 Dec 2014 at 10:09 GMT

I suggest this ratio of maternal weight gain to male fetal mortality is caused by the male fetus. This relationship impacts the effects of maternal dehydroepiandrosterone (DHEA). A viable male fetus should produce more maternal weight gain than a male fetus exhibiting less robust growth and development or female fetus. This is caused by fetal testosterone.

It is my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA, that is, genes. Therefore, DHEA levels affect all tissues and all tissues compete for available DHEA, especially the brain. (I think evolutionary selection of DHEA produced mammalia. “Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184). DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. When DHEA is low or decreasing, all tissues are adversely affected.

It is also my hypothesis of 1985 that the “fight or flight mechanism” is based on the ratio of DHEA to cortisol. That is, I think DHEA levels determine the amount of motivation an organism brings to a confrontation and cortisol evolved to counteract the effects of DHEA. If cortisol is high enough, then an organism avoids the consequences of a confrontation such as loss of blood, infection, ...death. Evolution would quickly select this mechanism as it would promote future reproduction of more organisms and fighting would reduce reproduction.

This is derived from my examination of the adrenal hormone pathways in 1984. It became apparent to me quickly that there really are mainly two pathways of major amounts of hormone production, that is, DHEA and cortisol. This ratio directly affects gene activation, so, physiology and behavior are affected.

A high cortisol to DHEA ratio reduces the effects of DHEA and causes weight gain. It is known that stress, cortisol, increases weight gain.

Male, fetal testosterone will also reduce the availability of maternal DHEA. A mother produces DHEA for herself and her fetus until the onset of fetal DHEA production which causes birth.

As a fetus grows, it relies on maternal DHEA. Depending upon the mother's DHEA and the use of that DHEA by a fetus, maternal weight gain will occur according to the reduction in maternal DHEA caused by the fetus.

It is my hypothesis that mammals evolved because of selection for DHEA. (Hormones in Mammalian Evolution, Rivista di Biologia / Biology Forum 2001; 94: 177-184 ) This is based on my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA. DHEA affects expression of genes. Therefore DHEA levels affect all tissues and the life span. A case may be made that optimal amounts of DHEA are necessary for conception. Since a mother produces DHEA for herself and her fetus, she must have an optimal level of DHEA for conception and maintenance of a fetus until near birth when fetal production of DHEA combines with the mothers DHEA to signal and initiate birth. Selection pressure within Mammalia for testosterone produced primates and, with exaggeration, humans. I think testosterone increases cellular absorption of DHEA by increasing androgen receptors through which DHEA enters cells. The selection is basically selection for additional cellular DHEA because of testosterone. (If you, et al., desire more detail of this: DHEA, Estradiol, Testosterone, and the Relevance of Their Ratio The Androgen Receptor and the Secular Trend, at: http://anthropogeny.com/A... .)

Therefore, a male fetus will access increased maternal DHEA because of increased fetal testosterone. Therefore, a viable male fetus will cause increased maternal weight more than a female fetus or a male fetus which is not producing optimal testosterone levels for optimal growth and development.

If a male fetus is not producing optimal testosterone, it will cause less “reduced DHEA maternal weight gain,” and exhibit some form of reduced growth and development. This will increase the probability of morbidity and mortality in male fetuses.

No competing interests declared.