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Hair loss and Sweat glands ...yes, testosterone
James Howard (phis@sprynet.com)
Fri, 20 Sep 1996 15:06:40 GMT
A number of posts have connected hair loss and sweat glands in the
development of Homos sapiens. Often these explanations deal with
temperature. Since I think human evolution is mainly the result of
the increased testosterone in us, I must be able to show that hair
loss is due to increased testosterone and that sweat glands are a
target tissue for testosterone. We have less hair and more sweat
glands. (I have posted some of my explanations of human evolution
resulting from increased testosterone here, but one can read more in
my article on human evolution at http://www.naples.net/~nfn03605 on
the web.)
If I am correct that we produce less hair because of more
testosterone, then reducing testosterone should increase the amount of
hair growth. This has been done in the stumptail macaque. In the
following quotation, note that "finasteride, a 5 alpha-reductase
inhibitor," significantly increases hair growth. Finasteride reduces
the effects of testosterone. That is, 5-alpha-reductase produces
5-alpha-dihydrotestosterone from testosterone in "testosterone target
tissues." If this enzyme product of testosterone is reduced, hair
growth increases.
Rhodes L et al., "The Effects of Finasteride (Proscar) on Hair
Growth, Hair Cycle Stage, and Serum Testosterone and
Dihydrotestosterone in Adult Male and Female Stumptail Macaques
(Macaca arctoides)" J Clin Endocrinol Metab 1994; 79: 991
"Finasteride, a 5 alpha-reductase inhibitor, was administered orally
(1 mg/kg.day) for 6 months to six male and five female stumptail
macaques. Vehicle was given to five male and five female animals over
the same period of time. Hair weights in a defined 1-in.2 area of
frontal scalp were measured periodically every 1-2 months, and serum
was collected for measurement of testosterone and dihydrotestosterone.
In addition, scalp biopsies were taken before and 6 months after
treatment to evaluate the micromorphometry of hair follicles. Results
showed that both male and female serum dihydrotestosterone levels were
significantly reduced (60-70%) by finasteride treatment. Both males
and females showed statistically significant increases in mean hair
weight over the treatment period compared to controls (P = 0.034). In
addition, there was a statistically significant increase in mean
follicle length (measured histologically in scalp biopsies)
compared to baseline in the finasteride-treated animals (P = 0.028)."
In the stumptail macaque, reducing the effects of testosterone
increases hair. So, increases in testosterone in Homo sapiens may be
the reason for reduced hair. Different areas of hair growth respond
to testosterone in differing amounts. "Androgens [testosterone]
stimulate hair growth in some areas, e.g., beard, but may cause
regression and baldness in the scalp." Clin. Endocrinol (Oxf) 1993;
39: 633. My basic principle, of my work, is that the hormone, DHEA,
is used in transcription and replication of genes. (DHEA is used to
"read" genes for gene activity and copy genes for equal distribution
in cell division.) I have suggested that tissues differ in their use
of DHEA; this is how I explain evolution of eukaryotes and
multicellularity. Therefore, tissues will require different levels of
DHEA for specific gene expression. Scalp hair and beard hair are
examples of this. I suggest the differentiating factor is the
availability of DHEA. It has been found that the receptor for DHEA
can bind dihydrotestosterone (the 5 alpha-reductase product)
secondarily. That is, "Bound [3H]DHEA was displaced sensitively by
DHEA and secondarily by dihydrotestosterone, but not effectively by
other steroids, including DHEA sulfate." J. Clin. Endocrinol. Metab.
1995; 80: 2993. This means, to me, that DHEA is absorbed for growth
of hair primarily, but the by-product of testosterone,
dihydrotestosterone, can compete for its receptor. (This should
happen at the cell surface and within the cell.) Therefore,
expression of genes dependent on less DHEA will be adversely affected
by the presence of dihydrotestosterone. This is why increased
testosterone reduces hair over the body, but not the hair producing
tissues of the face.
Hair is present from birth. Since DHEA is at its highest immediately
following birth, some neonates of high DHEA should have hair at birth.
However, since the brain, primarily, and body start to use so much
DHEA for growth and development (gene function and replication), the
DHEA falls quickly after birth and the original hair is lost. (See my
chart of DHEA during the human life-span at my web page.) This is the
same reason that the deciduous teeth form early, then are lost.
I have explained, just above, that tissues differ in their dependence
on DHEA. Testosterone target tissues have their testosterone target
genes "turned on" by testosterone. These genes then use DHEA for
transcription. Following the finalization of brain growth, DHEA
begins to increase in amounts in the blood from late childhood (5-7
years); this is called adrenarche in the textbooks. (The textbooks do
not have an explanation for this.) What this means to this discussion
is that DHEA begins to increase from late childhood to reach a peak
around 20 to twenty-five years. Since sweat gland activity really
begins following puberty, I think this means that the rise in
testosterone in men and women is the cause. Sweat glands are a
phenomenon of testosterone, and this is an affect on gene activity.
Rees J and Shuster S "Pubertal Induction of Sweat Gland Activity"
Clin Sci 1981; 60: 689
"1. To study the difference in sweat rate between men and women the
rates of cholinergic-induced sweating were measured in normal people
before and after puberty and in response to androgens and
anti-androgens. 2. Sweat rate in men was more than double that in
women. 3. This difference did not occur in prepubertal boys and girls
in whom the rate, corrected for surface area, was comparable with that
in women. 4. Application or injection of androgen locally did not
stimulate sweat production in the adult female. 5. Anti-androgen
topically or systemically did not decrease sweat rate in men. 6. It is
concluded that the rate of sweat rate in men is caused by
androgen-induced gene expression at puberty and not by androgen
modulation in adult life."
The next quotation demonstrates that sweat glands have the highest 5
alpha-reductase activity of the entire skin, sebaceous glands have a
high activity, and hair follicles have significantly less activity
than the sebaceous glands. As you read this, think about the
increased activity in males, that may, therefore, increase the
activity of the sweat glands, which could further increase hair loss
in the scalp.
Takayasu S et al., "Activity of Testosterone 5 alpha-reductase in
Various Tissues of Human Skin" J Invest Dermatol 1980; 74: 187
"In order to know the distribution of testosterone 5 alpha-reductase
activity in human skin, we developed a micro-method, in which we used
20-50 micrograms of various tissues microdissected from freeze-dried
sections. The characteristics of this enzyme in the sebaceous
gland are briefly described, as follows: the identified 5
alpha-reduced metabolites are 5 alpha-dihydrotestosterone, 5
alpha-androstane-3 beta, 17 beta-diol and 5 alpha-
androstanedione; the optimal pH is about 7.5; and the apparent Km is
approximately 2.4 x 10(-5)M. The measurement of 5 alpha-reductase
activity of various components of the skin obtained
from 7 men and 5 women revealed that the sweat gland (probably
apocrine) in the axillary skin possessed the highest activity of 5
alpha-reductase: the value was nearly 400 pmoles/mg dry
weight/hr in the standardized condition. The sebaceous gland also
showed a high activity of 85-261 pmoles/mg/hr. The hair follicles
exhibited a significantly lower activity than the sebaceous gland. The
enzyme activity was negligible in the epidermis, while it was detected
in the dermis though the values determined were variable probably
because of contamination with other components such as sweat glands
and hair follicles. Thus, the present study demonstrates that the 5
alpha-reductase activity is mainly located in the apocrine sweat gland
and sebaceous gland. This suggests that 5 alpha-reduction of
testosterone is an important step in mediating the
action of androgens in these tissues."
Testosterone is known to increase sex drive in both males and females.
This would increase the percentage of higher testosterone hominids
with time. Increased testosterone would reduce hair, increase sweat
glands and activity and, in the female would reduce labial displays,
normally dependent upon increased estrogen to testosterone. The
exposed breast, also indicative of sexual maturity, would become the
primary sexual display. This combination would eventually lead to
bipedalism. Other events, dependent upon the hormones DHEA and
melatonin, would, much later, result in an enlarged brain.
So, you see, one does not have to resort to looking for environmental
effects to account for all of these characteristics of hominids. The
single mechanism of increases in testosterone, alone, will cause all
of these changes. That is, increases in testosterone increase the
sexual device. The sexual device is one of most important devices
created by DNA for duplication.
James Howard
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