A considerable chunk of my workday is
always spent answering people's questions
about prohormones and steroids. Of course,
one of the biggest concerns people have is
about estrogen and estrogen related side
effects. Right behind that however are questions about DHT. It seems that people have
the misconception that DHT is some evil
androgen byproduct that serves no purpose in
the body but to make our prostates blow up
and our hair fall out.
The real situation is of course much more
complex. DHT is one of those good guy/bad guy hormones that is sorely misunderstood. For many people, it is NOT something that you want to reduce or eliminate
in the body. For some others though, keeping DHT levels under control is probably a
prudent course of action. Knowing the facts
about DHT will help you decide just which
group you belong to.
Testosterone Is A Prohormone?
The main androgen secreted by the testes is of
course testosterone. However, in most of the body, the
androgenic signal is not carried through by testosterone. In these tissues, which include the brain
(CNS), skin, genitals—practically everything but muscle—the active androgen is actually DHT.
Testosterone in this case simply acts as a prohormone
that is converted to the active androgen DHT by the
action of the enzyme 5alpha reductase (5-AR).
5-AR is concentrated heavily in practically every
androgen dependent area of the body except for skeletal muscle. This results in very little testosterone
actually getting through to these parts of the body to
bind to androgen receptors. Instead, it is quickly
transformed into DHT, which then interacts with
This transformation serves a very important biological function in these tissues. You see, DHT is a
much stronger androgen than testosterone - it binds
about 3-5 times more strongly to the androgen receptor. If you took away 5-AR from these tissues and
blocked the formation of DHT, then you would see
some dramatic changes in physiology.
A good case in point is demonstrated in male
pseudohermaphroditism due to congenital 5-AR deficiency. This is a relatively rare disorder, however it is
actually quite common in the Dominican Republic. In
this disorder, males are born with little or no 5-AR
enzyme. They have ambiguous genitalia and are often
raised as girls. When puberty occurs, their testosterone levels elevate normally although their DHT
levels remain very low. Their musculature develops
normally like that of other adults, however, they end
up with little or no pubic/body hair and underdeveloped prostate and penis. Their libido and sexual function is often disrupted also.
Testosterone Is The Active Androgen In Muscle
Skeletal muscle is unique from other androgen
dependent tissues in the body. It actually contains little
or no 5-AR, so little or no DHT is actually formed in
the muscle. In addition to this, any DHT that is formed,
or that is already present in the blood and travels to
the muscle, is quickly deactivated by an enzyme called
3alpha-hydroxysteroid reductase (3a-HSD).
So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to
say that administering exogenous DHT is not without any anabolic effect. It actually does have some
anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone.
This is due to its quick breakdown by 3a-HSD into
the weak metabolite 5alpha-androstan-3a, 17b-diol. If
this enzyme were somehow blocked, it is likely that
DHT would exhibit very potent anabolic effects on
It is important to understand that even though
testosterone is the active androgen in muscle, and
DHT exhibits relatively little direct anabolic effects on
muscle in men, DHT is still very important for the
full performance enhancement effects from testosterone. What I specifically mean here are the effects
of DHT on the central nervous system that lead to
increased neurological efficiency (strength), and
increased resistance to psychological and physical
stress—not to mention optimal sexual function and
I have heard several anecdotal reports of individuals
who have stacked testosterone with Proscar (a 5-AR
inhibitor) and have noticed significantly reduced performance enhancement effects. What's going on here?
We know it couldn't be due to the inhibition of the
direct anabolic activity of testosterone on muscle
anabolism. Most likely it is due to the reduction of
androgenic effects in other parts of the body that contribute to the ergogenic effects. Specifically the CNS, which is stimulated by androgens to increase neural
output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors
(such as IGF-1), since DHT is an important androgen
in the liver.
Anti-Estrogen Effects Of DHT
One important function of DHT in the body that
does not get much discussion is its antagonism of estrogen. Some men that take Proscar learn this the hard
way—by developing a case of gynecomastia. By reducing
DHT's protection against estrogen in the body, these
men have fallen victim to its most dreaded ramification-bitch tits.
How does DHT protect against estrogen? There are
at least three ways that this likely occurs. First of all,
DHT directly inhibits estrogens activity on tissues. It
either does this by acting as a competitive antagonist to
the estrogen receptor or by decreasing estrogen-induced
RNA transcription at a point subsequent to estrogen
Second of all, DHT and its metabolites have been
shown to directly block the production of estrogens
from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue
showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone
from androstenedione. 5alpha-androstandione was
shown to be the most potent, while androsterone was
Lastly, DHT acts on the hypothalamus/pituitary to
decrease the secretion of gonadotropins. By decreasing
the secretion of gonadotropins you decrease the production of the raw materials for estrogen production testosterone and androstenedione (DHT itself cannot
aromatize into estrogens). This property of DHT comes
into particular utility when it is administered exogenously, and this is to be discussed in further detail in
the next section.
DHT, Estrogen, And The Prostate
When it comes to sex hormones, few things are as
misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly
simplistic attitude that DHT is responsible for prostate
hypertrophy, and even prostate cancer predominates
amongst most people.
The real situation is, of course, much more complex.
One must understand that there are marked differences
between healthy prostate growth (developmental
growth), prostate growth due to BPH, and cancerous
The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate
from its prepubertal dormancy to the normal sized,
healthy, and functional prostate gland of an adult.
During the early and mid adult years the prostate
stays at this stage, despite the constant levels of high
levels of androgens in the body. However, if androgens
are blocked in the body then the adult prostate will
shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active
androgen in the prostate).
Later in life, there is often a second stage of
growth. This growth is deemed benign prostate
hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen/androgen ratio—a condition
common in older men—is highly correlated to the
development of BPH.
Experimental studies have shown the inability of
androgens with saturated A rings (DHT related) to
induce an initial condition of prostate hypertrophy.
These compounds are non-aromatizable. While,
aromatizable androgens on the other hand, such as
testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but
these effects are reversed by addition of an aromatase inhibitor.
So apparently, estrogen is a
causative factor in BPH. Or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.
None of this may come as news to many of you,
but I bet that very few of you know that DHT can
actually be used to treat BPH!! How can it do that?
It basically does this by replacing the testosterone
in the body, which then has the effect of reducing
the amount of estrogen in the body.
"DHT can actually be used to treat benign
prostate hypertrophy (BPH)!"
As I started to
explain before, DHT is a strong androgen that will
signal the pituitary to decrease the production of
gonadotropins. The decrease in gonadotropins will
then cause less testosterone to be produced which
will in turn cause the estrogen levels to drop. The
resulting change in the hormonal milieu (high DHT,
low estrogen) then apparently results in a regression of BPH.
The clinical application of this theory is discussed in US patent 5,648,350 Dihydrotestosterone
for use in androgenotherapy.
The following two
paragraphs taken from the patent study illustrates
In 27 subjects in which the plasma DHT
level was controlled, so as to modulate the
administered doses, said levels have been
increased to 2.5 to 6 ng/ml. There resulted
a decrease in gonadotrophy as well as in
the plasma levels of testosterone which
exceeded at least 1.5 ng/ ml (from 0.5 to
1.4 according to the case); as to the estradiol plasma levels, these decreased by
Among this group of subjects, the volume
of the prostate diminished significantly, as
was evaluated by ultrasound and by PSA
(Prostate Specific Antigen). The mean
volume of the prostates was from 31.09. + .16.31 grams before treatment and
from 26.34. + -. 12.72 grams after treatment,
for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years
with DHT (P= 0.01).
The information from this study kind of flies in the
face of the traditional thinking concerning BPH now
Unfortunately, people seem to have a natural
tendency to classify things as either good or bad,
black or white with absolutely no gray areas. DHT
(like estrogen) has recently been on everyone's bad
list, and is often considered to be a hormone that
serves no function in the body except to cause
harm. Now that you have all the necessary facts
you can ultimately see, this view is far from the
In my opinion, the widespread use of 5-AR
inhibitors such as Proscar as a prophylactic agent
for people that don't really need it should be highly
reconsidered. After reading this I hope you'll agree
with me or at least keep an open mind on this sensitive subject. In other words, why don't you just
give DHT a break.
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