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The Basis of Redelsperger, et al., may be Increased dehydroepiandrosterone (DHEA)

Posted by jamesmhoward on 06 Sep 2016 at 09:07 GMT

I suggest the basis of the findings of Redelsperger, may reside in increased availability of dehydroepiandrosterone (DHEA) caused by a retrovirus.

It is my hypothesis that evolution selected dehydroepiandrosterone (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 known that prolactin is a specific and direct stimulator of DHEA production. In: "The regulation of mammary prolactin receptor metabolism by a retroviral envelope protein," (Journal of Molecular Endocrinology (1997) 19, 131–136), it is stated: "In summary, the MMTV [mouse mammary tumor virus] increases the PRL sensitivity of mouse mammary epithelium by elevating PRLRs through both enhanced synthesis and recruitment from microsomes."

In 1999, I suggested that placental animals evolved because an evolutionary selection for prolactin and DHEA: "Evolution of Placental Animals and Enlarged Brains," at: http://anthropogeny.com/E... .

It is possible that a retrovirus was involved in this evolution of mammals but, I suggest, it is the increase in DHEA that is the basis of this evolution (""Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184. If your library does not subscribe to "Rivista ... ," you may find this at: http://anthropogeny.com/e... .)

Also, in 1985, I first suggested that low DHEA would increase vulnerability to the HIV (not called this at the time). The first reports of decreased DHEA in HIV / AIDS appeared years later. It is known that DHEA peaks subsequently to HIV infection but declines severely. It is my hypothesis that it is this loss of DHEA that causes the symptoms of AIDS. It has been determined that reduction in DHEAS, the precursor of DHEA, is lower in men who progress to AIDS: "DHEA levels in the progressors ∼5 months before the diagnosis of AIDS were lower than the levels in the nonprogressors after the same follow-up (median, 5.6 vs. 8.8 nmol/l; P = .007). DHEA levels <7 nmol/l and CD4+ cell counts <0.5 × 109/l both proved to be independent predictors for disease progression in HIV-1-infected men." (J Infect Dis. (1992) 165 (3): 413-418).

So, it is possible that ancient retroviruses triggered increased DHEA upon infection in animals in which DHEA did not subsequently decline, as does DHEA in HIV infection. This would produce various DHEA-induced positive changes which resulted in evolutinary selection of mammals.

No competing interests declared.
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