Loss of DHEA is the Cause of Menopause
Copyright 2013, James Michael Howard, Fayetteville, Arkansas, U.S.A.
I suggest the unusual characteristic of menopause in humans is caused by an early loss of dehydroepiandrosterone (DHEA) caused by evolutionary selection for testosterone in humans, specifically increased testosterone in females. (“Androgens in Human Evolution. A New Explanation of Human Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 345-362; if your library does not subscribe to “Rivista … ,” http://anthropogeny.com/evolution.html )
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 ) It is also my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA. DHEA affects 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 mother’s 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 primarily but also by estradiol. In the case of menopause, the age reductions of estradiol and DHEA combine to reduce the positive effects of DHEA. (If one desires more detail of this: “DHEA, Estradiol, Testosterone, and the Relevance of Their Ratio …The Androgen Receptor …and the Secular Trend,” at: http://anthropogeny.com/Androgen%20Receptor%20and%20Secular%20Trend.htm )
Maternal testosterone, very much increased in humans compared to the great apes, increases androgen receptors in a fetus which increases competition for DHEA because some tissues will be more affected by testosterone than others. I think the brain is especially affected by maternal testosterone. Therefore, the brain will absorb DHEA at the expense of other tissues. The brain will grow large in humans at the expense of other tissues and produce “gracile” subcranial growth and development. Therefore, as testosterone increases from amounts typical of monkeys, through chimpanzees, to humans, the life span measurable levels of DHEA decline because of absorption by the differences in brain size. (See the second chart in “Dehydroepiandrosterone, Melatonin, and Testosterone in Human Evolution,” at: http://anthropogeny.com/Original%20Theory%20of%20Human%20Evolution.htm ).
If the case that optimal levels of DHEA are necessary for conception is correct, then the chart demonstrates why humans exhibit a menopause. Humans produce less measurable DHEA than monkeys and the great apes. The optimal ages of conception in humans is far less than the DHEA at optimal ages of conception in monkeys and great apes.
DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age. It is well known that ability to conceive declines around age 25 and worsens with age. Therefore, women begin to fail to conceive with aging. Now, back to my contention that DHEA is involved in maintenance of all tissues, the natural loss of DHEA reduces ability to conceive at the same time that support for all tissues begins to fail. It is this combination of loss of reproductive capacity and aging that occurs around age fifty. This combination we call menopause.
Men are attracted to young women because all of their tissues are affected by optimal levels of DHEA. This includes interest in sex. The optimal time of conception is linked to optimal levels of DHEA. Evolution has no interest in us beyond optimal reproduction which appears to end a number of years after the optimal age of reproduction. Menopause is the result of the natural loss of DHEA in women.