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
Newest articles at bottom of page.
New Support May, 2005; New idea, April, 2010
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.
"Antibiotic Use in Relation to the Risk of Breast Cancer," C.M.
Velicer, et al., Journal of the American Medical Association 2004; 291:
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.
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 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
(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
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
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