Anabolic Androgenic Steroids Stimulate DHEA in the same Mechanism as Testosterone
It is my hypothesis that mammalian evolution occurred because of selection for dehydroepiandrosterone (DHEA). ("Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184). Subsequently, I deduced that human evolution is a consequence of selection for testosterone within mammals which produced primates; further selection produced humans. ("Androgens in Human Evolution. A New Explanation of Human Evolution," Rivista di Biologia / Biology Forum 2001; 94: 345-362)
I suggest the benefit of this increase in testosterone, which stimulates androgen receptors through which DHEA enters cells, is increased gene activity. Testosterone increases DHEA, which increases gene function which increases differences in gene activity. For example, our brain activity increases at the expense of our bodies. We have much bigger brains and less robust bodies in the hominid line.
By increasing androgen receptors, the life span production of DHEA is affected. That is, testosterone increases use of DHEA and how long it is readily available. This may explain why men exhibit increases in testosterone-target tissues and, also, why men die sooner.
I suggest anabolic androgenic steroids (AAS)act in the same manner as testosterone. That is, AAS stimulate increases in androgen receptors which act to increase use of DHEA within various tissues. AAS will increase the onset of the natural decline of DHEA.
DHEA naturally begins to decline around the ages of twenty to twenty- five, reaching very low levels in old age. Numerous brain malfunctions begin to occur and increase in intensity with aging. It is my hypothesis that many mental illnesses are caused by low, or disrupted, availability of DHEA. Therefore, early loss of DHEA caused by AAS would increase the probability of mental illness in AAS users.
Conflict of Interest: