The future of oral testosterone
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i formally retract my condescending and incorrect comments about science nerds and instead am recognizing the valuable and worthwhile discussion in this thread
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@dht
@dht said in The future of oral testosterone:
it likely inhibits LH transiently (a non issue if you take androgens with it, like i suggested) while the high doses of progesterone are active, it doesn't inhibit FSH at all.
@dht said in The future of oral testosterone:
this is a non issue if you take androgens with it (like i suggested)
Yes, but neither of these things are useful for anabolism nor increasing androgens.
@dht said in The future of oral testosterone:
isn't it almost as powerful of a GR antagonist as tren per that study haidut had posted?
No. Tren itself is a weak GR antagonist, and binds to the GR with an affinity of 3% compared to dexamethasone.
Tren blocks glucocorticoids effects via another mechanism, such as reduced glucocorticoid receptor expression hence it lowers the amino transferases / the transfer of amino acids out of the muscle / catabolism
Progesterone has 8-20% of the affinity of the GR compared to dexamethasone (from what I have read and remember), and activatives it, and therefore increases the amino transferases, such as tyrosine amino transferase (TAT), increasing the transfer of amino acids out of the muscle / catabolism.
https://en.wikipedia.org/wiki/Pharmacodynamics_of_progesterone
https://digicomst.ie/wp-content/uploads/2020/05/1985_04_70.pdf
As you see progeserone increased tyrosine transferase in vitro.
And in vivo it increased the expression of tyrosine amino transferase, decreased liver protein content mildly and increased muscle proteien mildy in ewes.
This was an experiment done over 2 days with a single 50mg of progesterone injection in ewes.
I must preferace, that I don't think progesterone's catabolism is significant nor is it's anabolism but my point is that it isn't laughable that James thinks it isn't useful in promoting anabolism.
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@alfredoolivas https://www.google.com/search?q=progesterone+tyrosine+aminotransferase&sca_esv=a55453b1a2e256c7&rlz=1C5CHFA_enIE1125IE1125&sxsrf=AE3TifMJdy148J2Tj4Z-xXaFpxc7CS6Aqw%3A1749071173656&ei=RbVAaLvmJ62QhbIPiIDO8AQ&oq=progesterone+t&gs_lp=Egxnd3Mtd2l6LXNlcnAiDnByb2dlc3Rlcm9uZSB0KgIIADIEECMYJzIEECMYJzIKEAAYgAQYQxiKBTIFEAAYgAQyBRAAGIAEMgUQABiABDIFEAAYgAQyBRAAGIAEMgUQABiABDIKEAAYgAQYQxiKBUiYClBBWP0BcAF4AZABAJgBMKABW6oBATK4AQHIAQD4AQGYAgKgAmjCAg0QABiABBixAxhDGIoFmAMAiAYBkgcBMqAH1BKyBwEyuAdowgcDMi0yyAcM&sclient=gws-wiz-serp
A google search, shows lots of studies show progesterone alone increases tryosine amino transferasee, but blocks the stimulation of tyrosine amino transferase when adminstered with corticosteroids.
So endougenously it may act as a partial agonist of the GR, blocking cortisol, a stronger agonist, effects, but when delivered in high quanitities, it may act as a GR as it binds to and activates the GR.
For example; we produce 5-15mg of cortisol a day, and therefore per hour, we produce around 0.5mg of cortisol an hour. If you endogenously produce 0.1mg of progesterone it would act as a functional antagonist to cortisol, but adminstering 15mg of progesterone exogenously would cause progesterone to act as an agonist independently.
Messy stuff, I wouldn't consider exogenous progesterone pro anabolic
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@dht
What role is progesterone supposed to play exactly? If you're using it as an AI, why not just use aromasin or proviron or masteron instead?
I don't think you're correct that it prevents shutdown and in fact I think it directly causes it.
I don't think progesterone is a male hormone. It's for women. We have DHT. We need it for sure in small quantities but I would not be looking to raise it much as a man
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@dht I respect your opinion but Haidut is not a bodybuilder. Show me the athletes/bodybuilders who followed this progesterone advice and I will take it more seriously. Just because he said it doesn't make it true.
As far as I am concerned, it is at best a theory with some evidence in rats or mice. There is plenty of evidence against it.
Consider this study which shows argues that progesterone causes gyno in hyperthyroid men who again according to Haidut have LOW estrogen
https://pubmed.ncbi.nlm.nih.gov/3335607/
I largely agree that excess aromatization is probably what largely contributes to HPTA shutdown.
But the solution I think should be low dose test, an AI if necessary, and plenty of DHT or Mast.
I guess I neither see the need for elevating progesterone in men nor do I see any evidence that it actually works in practice. I am more than happy to believe in it if people want to come forward with their actual progress and experience but until then I'm skeptical of it.
Even Peat would sometimes say on podcasts/radio shows that 20 mg progesterone for men could give them a numb penis so I think he understood the risks.
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@dht I promise I'm not joking I'm just telling you what I think.
I still don't understand what role is being filled by progesterone that isn't filled by simply blocking estrogen.
Some people for example think that progesterone has a unique role in regulating myelin production.
But I haven't really heard a good argument for the necessity of progesterone as an exogenous hormone for men but if you have one I am curious.
BTW I think that the smartest way to use gear is to use DHT or non-aromatizing- based compounds for cycles of about 4-6 weeks followed by abating for a couple weeks at minimum before going back on. There are studies showing that DHT does not cause HPTA shutdown, especially if it isn't allowed to convert to 3 beta androstanediol, which is an estrogenic metabolite.
I don't think I'm necessarily cherry picking studies. To the best of my knowledge there aren't more studies showing that progesterone itself causes shutdown of the HPTA because pharma companies instead fund studies investigating synthetic progestins as male contraceptives. There are plenty of studies showing that those are effective at shutting down the HPTA.
https://pubmed.ncbi.nlm.nih.gov/11585019/
"Testosterone (T) and other hormones such as progestins suppress circulating gonadotropins and spermatogenesis and have been studied as potential male contraceptives"
https://pubmed.ncbi.nlm.nih.gov/20933120/
"All hormonal male contraceptives use testosterone, but only in East Asian men can testosterone alone suppress spermatogenesis to a level compatible with contraceptive protection. In Caucasians, additional agents are required of which progestins are favored. Clinical trials concentrate on testosterone combined with norethisterone, desogestrel, etonogestrel or depot-medroxyprogesterone acetate."
https://pubmed.ncbi.nlm.nih.gov/12641635/
"Both progesterone and desogestrel administration resulted in decreases in the concentration of both LH and FSH secretion, as well as testosterone. Analysis of the pulsatile nature of LH secretion indicated that both treatments reduced LH pulse amplitude, and that progesterone reduced LH pulse frequency. Progesterone, but not desogestrel, treatment also reduced the increase in LH secretion in response to GnRH."
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@dht
I agree that keeping the steroid cascade going in important, even critical.
If you HPTA is shut down, then even if you are using exogenous androgens, if you aren’t producing p5 and p4 then you aren’t getting any of the benefits that they or their metabolites turn into.
My idea was to use a non-aromatizing compound like masteron or proviron and tbol or whatever else fits the bill with the idea being that your HPTA stays in tact, thus you never lose testicular steroidogenesis completely, thus you still get the youth hormones.
If you were going to use progesterone for this purpose, would you try to inject it or go with oral in tocopherols?
And even if you’re right about progesterone not shutting down HPTA, what do you think about the possibility that it will have anti-androgenic effects at the transcriptional level or even cause lack of libido because of how it affects the male brain?
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