DHT Is The Primary Driver Of Male Sexual Activity And Is Crucial For Male Orgasm

[haidut]

Yet another study pointing out that DHT is quite the good guy, for both men and women alike.

Contribution of dihydrotestosterone to male sexual behaviour. - PubMed - NCBI

"...RESULTS: Serum dihydrotestosterone concentration was the only independent hormonal predictor of the frequency of orgasms; an increase in concentration of 1.36 nmol/l (about 2 SD) corresponded to an average increase of one orgasm a week.
CONCLUSIONS: Differences in concentrations of circulating dihydrotestosterone within the normal range may represent a major predictor of sexual activity in healthy young men."

 

[johnwester130]

how do you recover from blocking dht ?

I think the dumbest thing I read on a hair loss forum was titled "my war with DHT " .

 

[haidut]

how do you recover from blocking dht ?

I think the dumbest thing I read on a hair loss forum was titled "my war with DHT " .

Well, progesterone and DHEA both convert into DHT. Yes, you read that right - progesterone also feeds into the DHT precursor pools when given in smaller doses (~50mg daily). Pregnenolone does the same. Basically pregnenolone metabolizes into progesterone and prolesterone primarily metabolizes into allopregnanolone. Allopregnanolone is a 5-alpha reduced steroid just like DHT and recent studies show that it is convertible into DHT in humans. DHEA is preferentially converted into DHT anyways, when given in smaller doses. DHEA also upregulates both the levels and activity of 5-AR, so it is a dual benefactor for people with low 5-AR levels (i.e. Finasteride users or prostate cancer patients treated with drugs like flutamide).
TLDR: Take a combination of lower doses pregnenolone + DHEA, or porgesterone + DHEA.
Thyroid hormone (T3) also restores 5-AR activity and levels, as does lowering estrone sulfate using AI drugs of supplements like aspirin and vitamin E. Anti-prolactin drugs also upregulate 5-AR activity and lower estrogen. So, there are tons of ways to do it. It's just a matter of choosing what works best for the specific person.

 

[milk_lover]

TLDR: Take a combination of lower doses pregnenolone + DHEA, or porgesterone + DHEA

I understand the lower doses of DHEA (5 mg to 15 mg a day with no more than 5 mg in one dose preferably) but what would a low dose of pregnenolone be?

 

[Dante]

Yet another study pointing out that DHT is quite the good guy, for both men and women alike.

Contribution of dihydrotestosterone to male sexual behaviour. - PubMed - NCBI

"...RESULTS: Serum dihydrotestosterone concentration was the only independent hormonal predictor of the frequency of orgasms; an increase in concentration of 1.36 nmol/l (about 2 SD) corresponded to an average increase of one orgasm a week.
CONCLUSIONS: Differences in concentrations of circulating dihydrotestosterone within the normal range may represent a major predictor of sexual activity in healthy young men."

Hi @haidut , new member here. Great study. I also read somewhere in an endo book that while E2 and Dht were both required for male rats sexual behaviour , thats not the case with rhesus macaques and humans. a little E2 might be required though. So doesn't that mean whatever masculinization that estradiol causes in male rats would not hold true for rhesus monkeys and humans. So , ideally rhesus monkeys studies correspond more with human neuroendocrinology than rats .
Also . this study says that DHT good prostate effects are due to it's metabolite 3β-diol

The androgen derivative 5alpha-androstane-3beta,17beta-diol inhibits prostate cancer cell migration through activation of the estrogen receptor bet... - PubMed - NCBI

Also wikipedia says - " 3β-diol, is an endogenous steroid hormone. It is a 5α-reduced and 17β-hydroxylated metabolite of dehydroepiandrosterone(DHEA) as well as a 3β-hydroxylated metabolite of dihydrotestosterone (DHT). 3β-Diol is a selective, potent, high-affinity full agonist of the ERβ, and hence, an estrogen.
3β-Diol appears to be the endogenous ligand of ERβ in the prostate gland, and as a result of activation of the ERβ, 3β-diol has antiproliferative effects against prostate cancer cells. "

So, can two compounds ,say 3-beta diol and estradiol , act via same receptors(proteins) , ER-beta here and have different effects? Though DHT can't be aromatized but still can be turned into potent estrogens, so doesn't that make DHT dangerous also ?

I have seen other studies which says the benefits of DHT are due to its action or binding with ER receptors/proteins. Getting so confused here. Can you explain this ?

 

[haidut]

Hi @haidut , new member here. Great study. I also read somewhere in an endo book that while E2 and Dht were both required for male rats sexual behaviour , thats not the case with rhesus macaques and humans. a little E2 might be required though. So doesn't that mean whatever masculinization that estradiol causes in male rats would not hold true for rhesus monkeys and humans. So , ideally rhesus monkeys studies correspond more with human neuroendocrinology than rats .
Also . this study says that DHT good prostate effects are due to it's metabolite 3β-diol

The androgen derivative 5alpha-androstane-3beta,17beta-diol inhibits prostate cancer cell migration through activation of the estrogen receptor bet... - PubMed - NCBI

Also wikipedia says - " 3β-diol, is an endogenous steroid hormone. It is a 5α-reduced and 17β-hydroxylated metabolite of dehydroepiandrosterone(DHEA) as well as a 3β-hydroxylated metabolite of dihydrotestosterone (DHT). 3β-Diol is a selective, potent, high-affinity full agonist of the ERβ, and hence, an estrogen.
3β-Diol appears to be the endogenous ligand of ERβ in the prostate gland, and as a result of activation of the ERβ, 3β-diol has antiproliferative effects against prostate cancer cells. "

So, can two compounds ,say 3-beta diol and estradiol , act via same receptors(proteins) , ER-beta here and have different effects? Though DHT can't be aromatized but still can be turned into potent estrogens, so doesn't that make DHT dangerous also ?

I have seen other studies which says the benefits of DHT are due to its action or binding with ER receptors/proteins. Getting so confused here. Can you explain this ?

Ray said that in humans estradiol is also the masculinizing factor in the fetus. As far as DHT being protective by metabolizing into estrogenic substances - that is the excuse medicine came up with then they found that most men with prostate cancer over 60 had hypogonadism and low DHT, and benefited from androgen replacement. So, they said androgens are still bad but their conversion into estrogens is what makes these older men feel good and helps their prostate. A very twisted view of reality. The conversion of DHT into the 3-diols usually occurs when high, unphysiological doses of DHT or its precursors are taken, which is not what people should be doing anyways. In people using 3mg - 5mg DHT daily, the hormones stay as such for hours/days and do not activate the excretion mechanisms.

 

[Dante]

Ray said that in humans estradiol is also the masculinizing factor in the fetus.
.

Oh . I thought it was gender dependent atleast in humans ( masculinizes women and feminizes men)

As far as DHT being protective by metabolizing into estrogenic substances - that is the excuse medicine came up with then they found that most men with prostate cancer over 60 had hypogonadism and low DHT, and benefited from androgen replacement. So, they said androgens are still bad but their conversion into estrogens is what makes these older men feel good and helps their prostate. A very twisted view of reality.

Though this is just a dissertation
http://dspace.library.colostate.edu..._items/csu01_storage/2012/03/01/file_1/123369

Quoting some of the contents.

"DHT appears to be protective against cerebrovascular inflammation via conversion to 3β-diol and subsequent activation of ERβ in human brain VSM cells.
DHT metabolite/ERβ selective agonist 3β-diol also decreased cytokine-induced COX-2 expression in human brain VSM cells. Furthermore, DHT’s ability to reduce cytokine-induced COX-2 expression in human brain VSM cells was inhibited by the non-selective estrogen receptor antagonist ICI 182,780 and the selective ERβ antagonist PHTPP".

"DHT‘s anti-inflammatory effects during cytokine or HGD-induced inflammation in human brain VSM cells were not blocked by the AR antagonist iv bicalutamide, indicating that they were not AR mediated."

If these are AR mediated instead of ER-β, then this lady is committing a fraud but then again Ray has pointed to a lot of frauds in the past century. I will see if non-US studies come to same conclusion.

 

[Dizzryda]

Strange that I experienced a bizarre phenomenon of no orgasm when I tried dht. I'm not complaining about the product. I just think my body doesn't work properly. Could be I used to much.

 

[sladerunner69]

Well, progesterone and DHEA both convert into DHT. Yes, you read that right - progesterone also feeds into the DHT precursor pools when given in smaller doses (~50mg daily). Pregnenolone does the same. Basically pregnenolone metabolizes into progesterone and prolesterone primarily metabolizes into allopregnanolone. Allopregnanolone is a 5-alpha reduced steroid just like DHT and recent studies show that it is convertible into DHT in humans. DHEA is preferentially converted into DHT anyways, when given in smaller doses. DHEA also upregulates both the levels and activity of 5-AR, so it is a dual benefactor for people with low 5-AR levels (i.e. Finasteride users or prostate cancer patients treated with drugs like flutamide).
TLDR: Take a combination of lower doses pregnenolone + DHEA, or porgesterone + DHEA.
Thyroid hormone (T3) also restores 5-AR activity and levels, as does lowering estrone sulfate using AI drugs of supplements like aspirin and vitamin E. Anti-prolactin drugs also upregulate 5-AR activity and lower estrogen. So, there are tons of ways to do it. It's just a matter of choosing what works best for the specific person.

What advice would you give to someone who experiences depersonalization on pregnenelone or DHEA? It gets pretty bothersome when I run both pregnenelone and DHEA together, maybe 50mg preg plus 5 mg topical DHEA will make it basically impossible for me to concentrate or feel any emotions. The mental experience itself is actually quite scary. I stopped the preg for this reason because I read others who have ahd similar problems with it. Have you heard of anything like this before?

 

[haidut]

What advice would you give to someone who experiences depersonalization on pregnenelone or DHEA? It gets pretty bothersome when I run both pregnenelone and DHEA together, maybe 50mg preg plus 5 mg topical DHEA will make it basically impossible for me to concentrate or feel any emotions. The mental experience itself is actually quite scary. I stopped the preg for this reason because I read others who have ahd similar problems with it. Have you heard of anything like this before?

I'd lower the pregnenolone dose. When taken with DHEA, you need less as DHEA by itself raises both pregnenolone and progesterone production. I think 10mg pregnenolone for every 5mg DHEA is optimal.

 

[CKA]

if 10mg/5mg is optimal, why is pansterone 5mg/5mg?

 

[haidut]

if 10mg/5mg is optimal, why is pansterone 5mg/5mg?

Because it is meant for topical use and because some people repoted manic symptoms from higher doses pregnenolone and DHEA, and I wanted to play safe.

 

[Giraffe]

I separated the discussion about hair loss from this thread. New thread: Hair Loss: Hormones Or Genetics?

 

[sladerunner69]

I'd lower the pregnenolone dose. When taken with DHEA, you need less as DHEA by itself raises both pregnenolone and progesterone production. I think 10mg pregnenolone for every 5mg DHEA is optimal.

Okay I will surely try that. I am considerring ordering the pansterone product and taking that with a nibble of pregnenelone tablet. And I assume that would be safe to take with DHT (I have a bottle of 11-keto) the only thing I am genuinely concerned with DHT is the possibiltiy of testosterone suppression which is documented in a few studies, albeit those use doses of like 25mg of DHT daily.

I was wondering if you have looked into the possibility of t3 raising progesterone or being anti-androgenic? Why is it that bodybuilding juicer forums generally recommend only to take t3 with androgenic steroids, because according to them t3 is "estrogenic" and "catabolic" and will decrease muscle mass. I dont beleive it is estrogenic personally, but I thought perhaps thyroid influence the progesterone cascade preferentially.

If there was any water to that,t hen t3 would indirectly oppose DHT and that should be noted especially for post-finasteride syndrome dudes (like myself).

 

[CKA]

Maybe they think t3 is "catabolic" because it makes it easy to be in a caloric and nutritional deficit? idk about estrogenic

 

[haidut]

Okay I will surely try that. I am considerring ordering the pansterone product and taking that with a nibble of pregnenelone tablet. And I assume that would be safe to take with DHT (I have a bottle of 11-keto) the only thing I am genuinely concerned with DHT is the possibiltiy of testosterone suppression which is documented in a few studies, albeit those use doses of like 25mg of DHT daily.

I was wondering if you have looked into the possibility of t3 raising progesterone or being anti-androgenic? Why is it that bodybuilding juicer forums generally recommend only to take t3 with androgenic steroids, because according to them t3 is "estrogenic" and "catabolic" and will decrease muscle mass. I dont beleive it is estrogenic personally, but I thought perhaps thyroid influence the progesterone cascade preferentially.

If there was any water to that,t hen t3 would indirectly oppose DHT and that should be noted especially for post-finasteride syndrome dudes (like myself).

Actually T3 is a genuine aromatase inhibitor and dramatically upregulates production of androgens, and especially the strong 5-alpha reduced androgens like DHT. So, not sure why the bodybuilding forums talk about T3 in a bad light. I posted a thread on the effects of thyroid hormone on steroid metabolism, and that study confirms the knowledge from 50-60 years ago - i.e. thyroid hormone lowers estrogens and increases androgens.
Effects of thyroid hormone on steroid metabolism

 

[lvysaur]

Danny Roddy thinks it is because they have higher levels of progesterone, which protects against estrogen while also feminizing the individual.

The problem with that reasoning is that DHT is also antiestrogenic, and men who lack the ability to make this antiestrogenic hormone somehow keep all of their hair.

it's the decline of testosterone and the rising of estrogen which contributes to hair loss.

Balding young males tend to have lower testosterone and higher estrogen, but this is consistent with the idea of an adaptive process that increases DHT production to deal with high estrogen and/or high aromatase activity. DHT synthesis from testosterone simultaneously opposes estrogen and prevents aromatization to estrogen. I've still seen zero evidence from Peat or Roddy that nullifies the idea that DHT is a (not necessarily the only, and definitely not the root) cause of hair loss, at least in men who eat a PUFA-containing diet.

I think a good way of testing this would be to slap some DHT cream on a few dozen male scalps for a few months, and look at the results.

 

[natedawggh]

The problem with that reasoning is that DHT is also antiestrogenic, and men who lack the ability to make this antiestrogenic hormone somehow keep all of their hair.




Balding young males tend to have lower testosterone and higher estrogen, but this is consistent with the idea of an adaptive process that increases DHT production to deal with high estrogen and/or high aromatase activity. DHT synthesis from testosterone simultaneously opposes estrogen and prevents aromatization to estrogen. I've still seen zero evidence from Peat or Roddy that nullifies the idea that DHT is a (not necessarily the only, and definitely not the root) cause of hair loss, at least in men who eat a PUFA-containing diet.

I think a good way of testing this would be to slap some DHT cream on a few dozen male scalps for a few months, and look at the results.

Applying DHT to the scalp would not alleviate baldness, because baldness is a down-stream effect from other processes inside the body. Locally, baldness is caused by a decrease in circulation caused by elevated serotonin, which in turn is caused by elevated estrogen, which in turn is caused by any number of things but to which, as you pointed out, DHT is an antagonist, thus reversing the down-stream effect of baldness. Also, hair as one of the least important biological functions of the body, is very sensitive to these changes, and is the first to go and the last to return, so regrowth of hair is a sign that body systems are finally on their way to healing. Unless real healing is achieved, hair restoration is unlikely to happen from quick tricks or local therapies.

Yes, as you pointed out DHT elevates in response to elevated estrogen, the body tries to combat high estrogen with higher testosterone products, but as long as estrogen remains elevated to that degree, hair will continue to be lost.

 

[haidut]

The problem with that reasoning is that DHT is also antiestrogenic, and men who lack the ability to make this antiestrogenic hormone somehow keep all of their hair.




Balding young males tend to have lower testosterone and higher estrogen, but this is consistent with the idea of an adaptive process that increases DHT production to deal with high estrogen and/or high aromatase activity. DHT synthesis from testosterone simultaneously opposes estrogen and prevents aromatization to estrogen. I've still seen zero evidence from Peat or Roddy that nullifies the idea that DHT is a (not necessarily the only, and definitely not the root) cause of hair loss, at least in men who eat a PUFA-containing diet.

I think a good way of testing this would be to slap some DHT cream on a few dozen male scalps for a few months, and look at the results.

HYPER-thyroidism causes elevated levels of 5-AR derived androgens like DHT. Hyperthyroid people are known to almost never go bald, even well into their 80s. If DHT was the cause, it would have manifested itself in that population. But I fully agree with you that it is long overdue to have an actual trial with DHT. However, I am pretty sure it would be deemed unethical and thus won't happen in the USA at least.
Balding is undeniably linked to adrenal hyperactivity, and while this may result in local excess of DHT from the surge in DHEA produced by the adrenals, to blame DHT without taking the account the systemically elevated prolactin, cortisol, estrogen, serotonin, and histamine is cherry-picking. So, the currently correct statement would be that DHT is one among MANY of the steroids found elevated in bald people and DHT itself is actually only elevated in a small sub-population of the balding people. People with high DHT and T but normal DHEA, cortisol, prolactin, etc do NOT go bald. High serum T and DHT are symptoms of good testicular function and thus good metabolism. When the adrenals kick into overdrive to compensate for the low metabolism that is when things go bad.
Hypothyroidism (Cortisol, Prolactin And Adrenal Hyperactivity) Causes Balding
Effects of thyroid hormone on steroid metabolism

 

[Elephanto]

When DHT is suppressed, estrogen raises greatly and this itself promotes higher libido or even sexual obsession. From my experience with finasteride, I was masturbating way more on it (also while smoking weed which suppresses dht even more), so it is really not required for human male sexual activity. Though I will agree with the "male orgasm" part, they were very light and mostly unsatisfying except for the cortisol reduction.