DHT Stimulates Its Own Synthesis

haidut

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The stress hormone estrogen is well-known for its ability to stimulate its own synthesis, resulting in a vicious circle. Some of the beneficial steroids like pregnenolone do the same, but for pretty much all others like T, cortisol, aldosterone, and even progesterone there is a feedback mechanism that prevents excess if working properly.
This study shows that DHT is another one of the protective steroids that have a positive feedback loop - i.e. it stimulates its own synthesis. So, the more androgenic your steroid profile is the more it will continue to be so. As far as I know, unless supplemented exogenously in very high doses, endogenous DHT will not downregulate its own synthesis even if its levels reach several times beyond the upper limit of the "normal" range.

Feed-forward control of prostate growth: dihydrotestosterone induces expression of its own biosynthetic enzyme, steroid 5 alpha-reductase. - PubMed - NCBI

"...Dihydrotestosterone, the primary mediator of prostate growth, is synthesized in target tissues from the circulating androgen testosterone through the action of steroid 5 alpha-reductase (EC 1.3.99.5). The expression of 5 alpha-reductase and the level of 5 alpha-reductase messenger RNA in rat ventral prostate are regulated by androgens. To determine whether this control is mediated by dihydrotestosterone or testosterone, we investigated the effect of finasteride, a potent inhibitor of steroid 5 alpha-reductase, on the expression of 5 alpha-reductase in the prostate. The administration of finasteride to intact rats for 7 days caused a 55% decrease in prostate weight and an 87% decrease in 5 alpha-reductase enzyme activity. Furthermore, the restoration of prostate growth after castration and the enhancement in 5 alpha-reductase enzyme activity and 5 alpha-reductase messenger RNA level by testosterone administration were blocked by finasteride, whereas the inhibitor had no effect on dihydrotestosterone-mediated increases in 5 alpha-reductase activity or messenger RNA level. These findings indicate that dihydrotestosterone itself controls prostate growth and 5 alpha-reductase activity. They further suggest that prostate growth is controlled by a feed-forward mechanism by which formation of trace amounts of dihydrotestosterone induces 5 alpha-reductase, thereby increasing dihydrotestosterone synthesis and triggering a positive developmental cascade."
 

Area-1255

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Jul 12, 2016
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and then all the online retailers of Proviron sold out...
There's plenty of Proviron suppliers/retailers. Just to let you know, Proviron has a fairly low protein binding/oral bioavailability, most will find that Masteron is much more effective. Pansterone and other pregnenolone solutions might be one of the best instances for increasing DHT long-term.
https://www.old.health.gov.il/units/pharmacy/trufot/alonim/3368.pdf
http://www.anabolic-bible.org/Profile.aspx?callpage=Proviron®
Response of serum testosterone and its precursor steroids, SHBG and CBG to anabolic steroid and testosterone self-administration in man. - PubMed - NCBI
 

Wagner83

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The stress hormone estrogen is well-known for its ability to stimulate its own synthesis, resulting in a vicious circle. [...]

Feed-forward control of prostate growth: dihydrotestosterone induces expression of its own biosynthetic enzyme, steroid 5 alpha-reductase. - PubMed - NCBI

"...Dihydrotestosterone, the primary mediator of prostate growth, is synthesized in target tissues from the circulating androgen testosterone through the action of steroid 5 alpha-reductase (EC 1.3.99.5). The expression of 5 alpha-reductase and the level of 5 alpha-reductase messenger RNA in rat ventral prostate are regulated by androgens. To determine whether this control is mediated by dihydrotestosterone or testosterone, we investigated the effect of finasteride, a potent inhibitor of steroid 5 alpha-reductase, on the expression of 5 alpha-reductase in the prostate. The administration of finasteride to intact rats for 7 days caused a 55% decrease in prostate weight and an 87% decrease in 5 alpha-reductase enzyme activity. Furthermore, the restoration of prostate growth after castration and the enhancement in 5 alpha-reductase enzyme activity and 5 alpha-reductase messenger RNA level by testosterone administration were blocked by finasteride, whereas the inhibitor had no effect on dihydrotestosterone-mediated increases in 5 alpha-reductase activity or messenger RNA level. These findings indicate that dihydrotestosterone itself controls prostate growth and 5 alpha-reductase activity. They further suggest that prostate growth is controlled by a feed-forward mechanism by which formation of trace amounts of dihydrotestosterone induces 5 alpha-reductase, thereby increasing dihydrotestosterone synthesis and triggering a positive developmental cascade."

How can they make the difference between testosterone and dht mediated increase in 5ar activity ?
Also ain't they suggesting things like BPH could be triggered by excessive dht levels ?
 
Last edited:

IhateFin

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Can proviron be taken sublimgually? Like just letting the pill desolve under the tongue.
 

cdan1

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The stress hormone estrogen is well-known for its ability to stimulate its own synthesis, resulting in a vicious circle. Some of the beneficial steroids like pregnenolone do the same, but for pretty much all others like T, cortisol, aldosterone, and even progesterone there is a feedback mechanism that prevents excess if working properly.
This study shows that DHT is another one of the protective steroids that have a positive feedback loop - i.e. it stimulates its own synthesis. So, the more androgenic your steroid profile is the more it will continue to be so. As far as I know, unless supplemented exogenously in very high doses, endogenous DHT will not downregulate its own synthesis even if its levels reach several times beyond the upper limit of the "normal" range.

Feed-forward control of prostate growth: dihydrotestosterone induces expression of its own biosynthetic enzyme, steroid 5 alpha-reductase. - PubMed - NCBI

"...Dihydrotestosterone, the primary mediator of prostate growth, is synthesized in target tissues from the circulating androgen testosterone through the action of steroid 5 alpha-reductase (EC 1.3.99.5). The expression of 5 alpha-reductase and the level of 5 alpha-reductase messenger RNA in rat ventral prostate are regulated by androgens. To determine whether this control is mediated by dihydrotestosterone or testosterone, we investigated the effect of finasteride, a potent inhibitor of steroid 5 alpha-reductase, on the expression of 5 alpha-reductase in the prostate. The administration of finasteride to intact rats for 7 days caused a 55% decrease in prostate weight and an 87% decrease in 5 alpha-reductase enzyme activity. Furthermore, the restoration of prostate growth after castration and the enhancement in 5 alpha-reductase enzyme activity and 5 alpha-reductase messenger RNA level by testosterone administration were blocked by finasteride, whereas the inhibitor had no effect on dihydrotestosterone-mediated increases in 5 alpha-reductase activity or messenger RNA level. These findings indicate that dihydrotestosterone itself controls prostate growth and 5 alpha-reductase activity. They further suggest that prostate growth is controlled by a feed-forward mechanism by which formation of trace amounts of dihydrotestosterone induces 5 alpha-reductase, thereby increasing dihydrotestosterone synthesis and triggering a positive developmental cascade."


Haidut, at what exonegous dose do you feel this would start to Happen? Particularly with something such as transdermal pure dht?
 

Madato

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Haidut, at what exonegous dose do you feel this would start to Happen? Particularly with something such as transdermal pure dht?

I’ve taken Andractim 3 pumps a day + 50mg proviron for a few weeks.

Got off everything for a few months.

My DHT results came back just as before Andractim and proviron, like if i hadn’t taken anything.

Only my T + e2 got slightly surpressed
 

cdan1

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I’ve taken Andractim 3 pumps a day + 50mg proviron for a few weeks.

Got off everything for a few months.

My DHT results came back just as before Andractim and proviron, like if i hadn’t taken anything.

Only my T + e2 got slightly surpressed

Thank you for the insight. But in regards to suppresion i guess im more speaking towards at what dose of DHT would Testosterone* start to drop (via releasing glands) so this could possibly be avoided.
 

Madato

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Thank you for the insight. But in regards to suppresion i guess im more speaking towards at what dose of DHT would Testosterone* start to drop (via releasing glands) so this could possibly be avoided.

What’s your goal with higher DHT anyways?
 

cdan1

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Jan 16, 2018
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What’s your goal with higher DHT anyways?
Well noted benefits it provides(ive used before higher doses along with other dht derivatives). But i dont need drastic effects so longer term lower dose desirable that does not negatively effect Test levels.
 

trogers38

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Jan 19, 2021
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Well noted benefits it provides(ive used before higher doses along with other dht derivatives). But i dont need drastic effects so longer term lower dose desirable that does not negatively effect Test levels.
For almost 3-4 weeks I’ve had symptoms of low dht. It was very miserable. I also tried everything to increase my dht levels like glycine, sorghum, butea Superba. Butea superba actually made it worse as it can be toxic to some people. The only thing that worked to increase my dht levels and 5 a reductase to baseline was a big dose of epiandrosterone(epi-andro) which was probably equivalent to a 2-5mg dose of pure dht. Now when I take my test boosters like shilajit and tongkat Ali I can feel the conversion to dht.
 
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