The problem is that if the adrenals are shut down supplementing DHEA won’t help. Basically the low DHEA shows that the adrenals are not producing its core hormones. So without getting them going again, supplementing the DHEA won’t do anything for mood, sexual function or fatigue.
Results: Circulating DHEAS and androstenedione rose significantly in both sexes, with testosterone increasing to low normal levels only in females. DHEA reversed ongoing loss of bone mineral density at the femoral neck ( P < 0.05) but not at other sites; DHEA enhanced total body ( P = 0.02) and truncal ( P = 0.017) lean mass significantly with no change in fat mass. At baseline, subscales of psychological well-being in questionnaires (Short Form-36, General Health Questionnaire-30), were significantly worse in Addison’s patients vs. control populations ( P < 0.001), and one subscale of SF-36 improved significantly ( P = 0.004) after DHEA treatment. There was no significant benefit of DHEA treatment on fatigue or cognitive or sexual function. Supraphysiological DHEAS levels were achieved in some older females who experienced mild androgenic side effects.
In men, higher basal testosterone levels are likely to have obscured the relatively small additional effect of administered DHEA. Although DHEA is converted to estradiol, the magnitude of this effect is insufficient to cornify the vaginal epithelium in rats (a sensitive assay) ([42] and by analogy, we suggest that our observed lack of change in circulating estradiol levels in men receiving DHEA is not unexpected.
Yes HCG will help offset adrenal fatigue, and with the adrenals working then supplementing DHEA would be advantageous.
We propose that the adrenal gland of an older higher primate female animal model will respond to a human chorionic gonadotropic (hCG) hormone challenge by secreting additional dehydroepiandrosterone sulfate (DHEAS). Such a response in surgically and chemically-castrated animals will provide proof-of-concept and a validated animal model for future studies to explore the rise of DHEAS during the menopausal transition of women.
These data demonstrate a positive adrenal androgen response to LH/CG in older female higher primates and suggests a mechanism for the rise in adrenal androgen production during the menopausal transition in women. These results also illustrate that the nonhuman primate animal model can be effectively used to investigate this phenomenon.