New Support
This is what all drugs do to people's DHEA. It is the early loss of DHEA that is the problem. (Exercisers may be doing this too.)
Thrombosis may be a natural consequence of low DHEA to stop bleeding.
Possible New Support
Is DHEA the natural ligand of the peripheral benzodiazepine receptor?
(Copyright 2006; support coming)
Newest articles at bottom of page.
New Support May, 2005
Why We Kiss ...transfer of Testosterone!
Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.
Men kiss women to stimulate them. ...well, dah, but do you know why? What is the mechanism? Testosterone levels of saliva and blood are essentially identical (Steroids. 1996 Jun;61(6):374-8). It is known that testosterone improves all aspects of sexuality in low libido women and increases that of normal women even more. This is the reason for the recent decision to sell testosterone to women in patch form.
I suggest men kiss women to transfer testosterone via saliva to excite them. I am not being flippant when I say that a "french kiss" is more exciting for women than "just a kiss." Men kiss women because it increases women's libido and enjoyment.
NEW: "Antibiotic Use in Relation to the Risk of Breast Cancer," C.M. Velicer, et al., Journal of the American Medical Association 2004; 291: 827-835
Velicer, et al., reported that the "Use of antibiotics is associated with increased risk of incident and fatal breast cancer."
It is my hypothesis (1994) that low dehydroepiandrosterone (DHEA) may trigger oncogenes and that high testosterone may reduce DHEA, therefore increasing the probability of cancer. Both of these have since received support. For example, hormone replacement therapy decreases DHEA and HRT has been found to increase the incidence of breast cancer. Also, consumption of ethanol by women increases testosterone; alcohol consumption by women has been connected with increased breast cancer. ("How 'Hormone Replacement Therapy' (HRT) May Cause Breast Cancer" at www.anthropogeny.com/research.html .)
It is known that DHEA exerts protective effects against many forms of infections, including bacteria. I suggest the connection of increased breast cancer in women who have required antibiotics is low DHEA. That is, low DHEA in these women reduced their immune response which subsequently required the aid of antibiotics. I suggest the increased incidence of breast cancer in these women is reduced DHEA, not antibiotics.
Feb 11, 2004: FDA: HRT increases dementia and Alzheimer's. This may be the same mechanism, reduced DHEA, as the increase in breast cancer.
Flavonoids are known to protect against a number of cancers. I suggest this is because flavonoids inhibit sulfonation of DHEA, i.e., flavonoids help maintain levels of the active form of DHEA instead of DHEAsulfate: “Sulfonation of dehydroisoandrosterone (DHEA) via hydroxysteroid sulfotransferase, SULT2A1, was inhibited by higher amounts of the flavonoids (IC(50)s ranging from 34 to 116 micro M).” Xenobiotica. 2003 Dec; 33(12): 1211-20 It has been determined that flavonoids exert weak effects against cancer in the elderly. "We conclude that intake of flavonoids, mainly from tea, apples, and onions, does not predict a reduced risk of all-cause cancer or of cancer of the alimentary and respiratory tract in elderly men." (Nutr Cancer. 1994;22(2):175-84) DHEA naturally begins to decline around the mid-twenties and reaches very low levels in old age. Since I think the effect of flavonoids against cancer is the inhibition of sulfonation of DHEA, the fact that DHEA is so low in the elderly may be the reason flavonoids are ineffective or very weak in the elderly.
“The relationship between testosterone levels and cognitive ability patterns”
The cognitive performance of normal men and women was studied, grouped according to whether the subjects had relatively high or low salivary testosterone (T) concentrations. Men with lower T performed better than other groups on measures of spatial/mathematical ability, tasks at which men normally excel. Women with high T scored higher than low-T women on these same measures. T concentrations did not relate significantly to scores on tests that usually favor women or that do not typically show a sex difference. These results support suggestions of a nonlinear relationship between T concentrations and spatial ability, and demonstrate some task specificity in this respect. Psychoneuroendocrinology. 1991; 16: 323-34
Prematurity
(Strong, new support 2004 and August, 2006)
“The data also suggest that estrogen treatment (OCs and ERT/HRT) suppresses DHEA concentrations in premenopausal and PM [postmenopausal] females, and that DHEA declines with age in PM females regardless of estrogen treatment.” Metabolism. 2001; 50(4): 488-93
Also, alcohol consumption by women has been connected with increased breast cancer. I suggest this is due to stimulation of increased testosterone found in women who consume alcohol.
In 1979, I attempted to explain how transcription of DNA could be controlled by H1 histones and what was called then, "nonhistone chromosomal proteins." This is my explanation from that time, exactly as it was. I suggest this may still explain how chromatin is involved in transcription of DNA. I intend to add new research findings to this soon to demonstrate that this may still be a viable explanation.
Evolution and Ontogeny:
The Impact of Dehydroepiandrosterone and Testosterone Levels
My primary hypothesis is dehydroepiandrosterone (DHEA) is an integral component of evolution because it optimizes transcription and replication of DNA. (DHEA is the major steroid hormone produced by the adrenal glands.) Furthermore, I think events converged to increase production and utilization of DHEA over time; I suggest this produced mammals. Within mammals, it is my hypothesis that testosterone increased utilization of DHEA by "target tissues" of testosterone. Testosterone production and utilization increased; I suggest this produced primates. Testosterone continually increased within primates to produce humans.
Testosterone levels affect the availability of DHEA by directing use of DHEA Additionally, it is my hypothesis that cortisol evolved as the major antagonist of the effects of DHEA. (Cortisol is the second major steroid hormone produced by the adrenal glands.) I suggest the interaction of the ratio of levels of DHEA and cortisol control "pecking order." Testosterone and cortisol evolved as subordinate mechanisms of the effects of DHEA on evolution. The effects of testosterone and cortisol are detectable within modern populations and within individual lives. Our phylogeny and ontogeny are directly connected!
I suggest DHEA is utilized in gene replication and activation. Therefore, levels of DHEA affect our physiology and pathology. The top chart at the right, "normal production / normal length," represents the production of DHEA during the human life span. The other two charts represent basic deviations from "normal" that significantly affect the life span. These deviations from normal may be endogenous or produced by exogenous forces.
This section of my web site deals with new applications of my work as well as new reports of research of relevance to my interpretation of my hypotheses. (As time passes, each of these will be moved to other sections of this web site.) PLEASE SEE LIST BELOW:
it is like a fan
