elitefitness.com/forum/anabo … 18281.html
(Read under functions of aromasin here
en.m.wikipedia.org/wiki/Exemestane
Article on dht below, the similarities of the actions of aromasin and dht are quite interesting, it may explain why it is so effective with pfs (at the correct dose).
Old 07-Mar-2003, 04:27 PM
clobro
Good Broly
Join Date: Sep 2002
Posts: 282
Canada
Anyone know how DHT affects T levels/muscle mass?
I’m a little confused about how dihydrotestosterone acts on T levels/muscle mass. One study on people on Andractim dihydrotestosterone gel for HRT showed a decrease in free and bound T yet the main use for Andractim is HRT.
Would dihydrotestosterone have any effect on muscle mass? I would think it would have positive effects (like Masteron does), but how does it work if it lowers T? dihydrotestosterone seems to lower estrogen (see below from Pat Arnold) I’m taking it because it has helped me for my gynecomastia symptoms and for it’s anobolic effects.
Study for dihydrotestosterone as HRT:
endo-society.org/pubrelat…ember_jcem.pdf
This is from Patrick Arnold:
Anti – Estrogen effects of dihydrotestosterone
One important function of dihydrotestosterone 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 dihydrotestosterone’s protection against estrogen in the body, these men have fallen victim to its most dreaded ramification – !
How does dihydrotestosterone protect against estrogen? There are at least three ways that this likely occurs. First of all, dihydrotestosterone 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 receptor binding.
Second of all, dihydrotestosterone 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 dihydrotestosterone, 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 the least.
Lastly, dihydrotestosterone 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 (dihydrotestosterone itself cannot aromatize into estrogens). This property of dihydrotestosterone comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section.
dihydrotestosterone, 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 dihydrotestosterone. The inaccurate and overly simplistic attitude that dihydrotestosterone 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 prostate growth.
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 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 dihydrotestosterone 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 (dihydrotestosterone related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. 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 the 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 dihydrotestosterone 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. As I started to explain before, dihydrotestosterone 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 dihydrotestosterone, 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 illustrates the results:
"In 27 subjects in which the plasma dihydrotestosterone 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 50%.
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 dihydrotestosterone (P=0.01)."
This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?
Conclusion
People have a natural tendency to classify things as either good or bad, with no gray areas. dihydrotestosterone (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. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give dihydrotestosterone a break. I now pronounce June “dihydrotestosterone Appreciation Month”. Thank you.
by Pat Arnold