Hair loss and Sweat glands ...yes, testosterone

James Howard phis at sprynet.com
Mon Nov 11 06:11:10 EST 1996


A number of posts have connected hair loss and sweat glands in the development
of Homos sapiens at other newsgroups.  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




More information about the Mol-evol mailing list