PHYSIOLOGY

As part of my explanation of schizophrenia, I have suspected that the "hyperprolactinemia" induced by many antipsychotics meant that this probably increased DHEA. Since prolactin stimulates DHEA, I thought this meant that the increased prolactin probably increased the DHEA. Since I produced my explanation of "panic disorder," I have changed this view. I think hyperprolactemia occurs when DHEA is reduced. That is, DHEA in proper amounts feeds back to shut down prolactin production. So, the antipsychotics produce their effect by reducing DHEA. This helps because it decreases DHEA activation of the over active structures in schizophrenics. This fits with the FDA report about "clozapine" causing diabetes and hyperglycemia of today's date. DHEA is useful against diabetes and hyperglycemia so clozapine also works by reducing DHEA. Therefore, I have to change my explanation of how antipsychotic drugs help with schizophrenics with that of this post of April 9, 2004.

The Influence of Parturition on the Level and Synthesis of Sulfated and Free Neurosteroids in Rats.

Alterations in neurosteroid levels may play a role in affective disorders including those related to changes in the levels of ovarian steroids. The effects of pregnancy and delivery on circulatory and brain levels of dehydroepiandrosterone (DHEA), pregnenolone (PN), their sulfate esters and the enzymatic activities of sulfatase and sulfotransferase were examined in rats. Our findings indicate an increase, not reflected in the brain cortex, in serum DHEA levels, at the end of pregnancy with a partial decrease following delivery. DHEA sulfate levels in the cortex and PN levels in both serum and cortex decreased following delivery with no changes in its sulfated form. Sulfatase levels were high both before and after delivery with no changes noted in sulfotransferase levels, compared to controls. We speculate that changes in the level or ratio of sulfated and free neurosteroids may play a role in postpartum behavioral disorders due to their antagonistic GABA(A) modulatory effect. Copyright 2004 S. Karger AG, Basel Neuropsychobiology. 2004; 49(1): 17-23.

New Support: Two articles add support to my hypothesis regarding testosterone in women and breast cancer. That is, I suggest increased testosterone is involved in triggering cancer. In the first article from the January, 2004, Journal of the National Cancer Institute, U.S.A., you will read the finding that "active smoking may play a role in breast cancer etiology." The second article demonstrates that smoking in women is connected with increased testosterone. "Current smokers had the highest testosterone concentrations with decreasing values in former and nonsmokers (p = 0.0001)." (The abstracts of these two articles are available at my explanation of breast cancer; click on the link, above.) Again, I suggest this adds support to my explanation of the mechanism of cancer.

Also: Radiology 2004; 232: 735-738
It is my hypothesis that low DHEA may trigger oncogenes (1994). It is known that total or full body irradiation prior to bone marrow
transplantation reduces DHEA (Bone Marrow Transplant 1997; 20: 561-5 and Horm Res 1995; 43: 279-85). I suggest the findings of Brenner, et al., may represent increased cancer initiation as a result of low DHEA caused by the irradiation of full body CT screening.

“DHEAS concentrations increased after melatonin therapy. Moreover, a tendency towards a higher DHEAS/cortisol ratio was found after 6 months of treatment.”
Neuroendocrinology Letters 2002 Apr; 23 Suppl 1: 17-9

“This work shows that DHEA-S but not DHEA was able to stimulate melatonin secretion by adrenergic-stimulated pineals removed during the light phase.” Steroids. 2000; 65: 491-6

Cancer "...the incidence of this disease [cancer] in nonhuman primates is very low." (X.S. Puente, et al., BMC Genomics 2006; 7: 15). My explanation of cancer is based on high testosterone and low DHEA in humans. Nonhuman primates produce much less testosterone and much more DHEA.