DetailNazi
Member
- Joined
- May 6, 2020
- Messages
- 14
I'm currently running the following every day:
50 mg IM testosterone propionate
100 mg oral pregnenolone
100 mg oral DHEA
600 mg Ashwagandha
250 mg magnesium
2 pills of Thorne Multivitamin
As of now I'm experimenting with the Peat DHEA Pregnenolone stuff and I've noticed a bit better sleep after my first couple days of DHEA, then had my first T injection and I had knockout sleep last night. It seems now I'm incapable of sleeping less than 12h (before when I was super sleep deprived I couldn't sleep for more than 6h even if I wanted to). My concern here is that test isn't androgenic enough to accomplish voice deepening and beard growth after puberty, hence why I want to run a tren cycle. The topic of this post is, if test doesn't work and I end up doing tren, how do I do it and remain fertile and in good health on cycle? @haidut 's post here provides a clue:
Pregnenolone (P5) Fully Prevents Testicular Atrophy Due To Steroid (ab)use Or High Estrogen
I'm hoping the discussion here will address the questions I posed to @haidut on the below thread, as well as some other things I will mention now:
Estrogen Is NOT Needed For Muscle / Bone Growth And Anabolism
Why does tren suppress your testosterone if:
1. We established that estrogen is responsible for negative feedback to the hypothalamus, and thus we use an AI as part of PCT,
2. Tren is non-aromatizable, non-estrogenic, highly androgenic and thus suppresses estrogen, and has progestogenic effects (I don't know if it acts like a 'progestin' poison like medroxyprogesterone acetate... but it may very well be the case since people DO complain of 19-nor (tren) **** and gyno from elevated prolactin, which is an estrogenic effect, not progesteronic)
3. Progesterone is anti-estrogenic, and so tren's PR activation suggests that it shouldn't produce prolactin effects, so you shouldn't even need to run a dopamine agonist like cabergoline with it,
4. In another thread you stated the following:
"The estrogen role in gonadal atrophy caused by T is suggested by one of the studies showing that while "lower" doses T (in the range of HED 1mg/kg daily) were suppressible and caused gonadal atrophy, VERY high doses (equivalent to 1g+ daily in humans) increased gonadal size. .... It will also be recalled that small doses of testosterone cause a testis atrophy which is not seen at high dose levels (1 1). This fact could best be explained by the assumption that comparatively low doses of testoids inhibit the gonadotropic hormone secretion of the pituitary and thus cause a secondary testis involution which, in the case of high doses, is over-compensated by the direct testis-stimulating effect of these compounds."
The only explanation I can think of that reconciles some of this is that testosterone / AR activation ALSO feeds back to the hypothalamus (edit: to the Leydig cells). Otherwise past a certain threshold of AR activation estrogen would become totally suppressed forever and the release of androgens would become a positive feedback loop. "VERY high doses increased gonadal size"... so if it turns out that the progesteronic effect of tren is actually progesteronic and not estrogenic, why doesn't blasting tren give you massive balls? Even if there is some estrogenic effect from tren (there must be if there's gyno and tren ****) then doesn't the same logic apply - just run it in a high enough dose and the androgenicity will beat the estrogenicity into submission?
So I will go through the above and list my further questions:
5. @haidut has said that there may be a secondary feedback loop in cases of pituitary unresponsiveness in the case of a tumor. This exists inside the Leydig cells and keeps test levels in a physiological range by responding directly to AR receptor activation. However, he also says what I quoted above about low dose T causing testicular atrophy but super high dose T increasing testicle size. So how does super high dose exogenous T have a "direct testis-stimulating effect" that makes your balls bigger if there's an AR feedback loop internal to the Leydig cells themselves? It's reasonable to surmise that the former idea is true, i.e., being a strong dominant masculine man is called "being ballsy" for a reason. High T = big balls. But the suppression and atrophy people see doing highly androgenic/antiestrogenic AAS like tren stumps me.
6. I've also seen @haidut say progesterone at low doses is androgenic but at higher doses is antiandrogenic. Why, if at all doses it acts as an antiestrogen/antiserotonin/anticortisol agent?
7. Let's assume progesterone is somewhat antiandrogenic at higher doses. If so, why does using 12-15x the oral dose of pregnenolone as injected testosterone prevent atrophy? I know administering DHEA pushes most coadministered pregnenolone to become progesterone, so I'd imagine the same would be true for at least T and DHT since they're part of Route C (endogenous androgens and estrogens), if not for any androgenic steroid. My potential explanation is progesterone inhibits the Leydig cell feedback by acting as an antiandrogen there, allowing the testicles themselves to produce their own testosterone. But if that were the case, then estrogens, which act as systemic antiandrogens, should make your balls bigger and improve sperm count, which we know to be false - or at least this should counteract the negative feedback estrogen has on the HPGA.
8. @haidut also mentions in the P5 article that pregnenolone administration in 12-15x the dose of an androgen it is coadministered with should potentiate the effects of that androgen. I can see this making sense if progesterone, its main metabolite under such conditions, is a pure antiestrogen at all doses. But as we see above, it isn't that simple. If it's true that progesterone is an antiandrogen at high doses (which we would inevitably achieve by taking 12-15x the dose of pregnenolone as of the androgen in question) then shouldn't it cancel out, instead of potentiate, the effects of the androgen? I know progesterone itself is half as anabolic as testosterone, so that would pick up some of the slack, but as people have figured out, tren turns you into a ******* beast, so it appears the idea that PR activation is antiandrogenic might be wrong. And if it's wrong, see questions 2 and 3 again.
9. Finally, for those of you who do run gear while incorporating Peat concepts, have any of you experienced the effects I'm looking for (voice deepening, filling out the beard)? If so, could you please share your stack?
TLDR for my most important question: how do I do (and maybe even potentiate the effects of) tren and keep my balls plump and healthy at the same time using Peat technology?
50 mg IM testosterone propionate
100 mg oral pregnenolone
100 mg oral DHEA
600 mg Ashwagandha
250 mg magnesium
2 pills of Thorne Multivitamin
As of now I'm experimenting with the Peat DHEA Pregnenolone stuff and I've noticed a bit better sleep after my first couple days of DHEA, then had my first T injection and I had knockout sleep last night. It seems now I'm incapable of sleeping less than 12h (before when I was super sleep deprived I couldn't sleep for more than 6h even if I wanted to). My concern here is that test isn't androgenic enough to accomplish voice deepening and beard growth after puberty, hence why I want to run a tren cycle. The topic of this post is, if test doesn't work and I end up doing tren, how do I do it and remain fertile and in good health on cycle? @haidut 's post here provides a clue:
Pregnenolone (P5) Fully Prevents Testicular Atrophy Due To Steroid (ab)use Or High Estrogen
I'm hoping the discussion here will address the questions I posed to @haidut on the below thread, as well as some other things I will mention now:
Estrogen Is NOT Needed For Muscle / Bone Growth And Anabolism
Why does tren suppress your testosterone if:
1. We established that estrogen is responsible for negative feedback to the hypothalamus, and thus we use an AI as part of PCT,
2. Tren is non-aromatizable, non-estrogenic, highly androgenic and thus suppresses estrogen, and has progestogenic effects (I don't know if it acts like a 'progestin' poison like medroxyprogesterone acetate... but it may very well be the case since people DO complain of 19-nor (tren) **** and gyno from elevated prolactin, which is an estrogenic effect, not progesteronic)
3. Progesterone is anti-estrogenic, and so tren's PR activation suggests that it shouldn't produce prolactin effects, so you shouldn't even need to run a dopamine agonist like cabergoline with it,
4. In another thread you stated the following:
"The estrogen role in gonadal atrophy caused by T is suggested by one of the studies showing that while "lower" doses T (in the range of HED 1mg/kg daily) were suppressible and caused gonadal atrophy, VERY high doses (equivalent to 1g+ daily in humans) increased gonadal size. .... It will also be recalled that small doses of testosterone cause a testis atrophy which is not seen at high dose levels (1 1). This fact could best be explained by the assumption that comparatively low doses of testoids inhibit the gonadotropic hormone secretion of the pituitary and thus cause a secondary testis involution which, in the case of high doses, is over-compensated by the direct testis-stimulating effect of these compounds."
The only explanation I can think of that reconciles some of this is that testosterone / AR activation ALSO feeds back to the hypothalamus (edit: to the Leydig cells). Otherwise past a certain threshold of AR activation estrogen would become totally suppressed forever and the release of androgens would become a positive feedback loop. "VERY high doses increased gonadal size"... so if it turns out that the progesteronic effect of tren is actually progesteronic and not estrogenic, why doesn't blasting tren give you massive balls? Even if there is some estrogenic effect from tren (there must be if there's gyno and tren ****) then doesn't the same logic apply - just run it in a high enough dose and the androgenicity will beat the estrogenicity into submission?
So I will go through the above and list my further questions:
5. @haidut has said that there may be a secondary feedback loop in cases of pituitary unresponsiveness in the case of a tumor. This exists inside the Leydig cells and keeps test levels in a physiological range by responding directly to AR receptor activation. However, he also says what I quoted above about low dose T causing testicular atrophy but super high dose T increasing testicle size. So how does super high dose exogenous T have a "direct testis-stimulating effect" that makes your balls bigger if there's an AR feedback loop internal to the Leydig cells themselves? It's reasonable to surmise that the former idea is true, i.e., being a strong dominant masculine man is called "being ballsy" for a reason. High T = big balls. But the suppression and atrophy people see doing highly androgenic/antiestrogenic AAS like tren stumps me.
6. I've also seen @haidut say progesterone at low doses is androgenic but at higher doses is antiandrogenic. Why, if at all doses it acts as an antiestrogen/antiserotonin/anticortisol agent?
7. Let's assume progesterone is somewhat antiandrogenic at higher doses. If so, why does using 12-15x the oral dose of pregnenolone as injected testosterone prevent atrophy? I know administering DHEA pushes most coadministered pregnenolone to become progesterone, so I'd imagine the same would be true for at least T and DHT since they're part of Route C (endogenous androgens and estrogens), if not for any androgenic steroid. My potential explanation is progesterone inhibits the Leydig cell feedback by acting as an antiandrogen there, allowing the testicles themselves to produce their own testosterone. But if that were the case, then estrogens, which act as systemic antiandrogens, should make your balls bigger and improve sperm count, which we know to be false - or at least this should counteract the negative feedback estrogen has on the HPGA.
8. @haidut also mentions in the P5 article that pregnenolone administration in 12-15x the dose of an androgen it is coadministered with should potentiate the effects of that androgen. I can see this making sense if progesterone, its main metabolite under such conditions, is a pure antiestrogen at all doses. But as we see above, it isn't that simple. If it's true that progesterone is an antiandrogen at high doses (which we would inevitably achieve by taking 12-15x the dose of pregnenolone as of the androgen in question) then shouldn't it cancel out, instead of potentiate, the effects of the androgen? I know progesterone itself is half as anabolic as testosterone, so that would pick up some of the slack, but as people have figured out, tren turns you into a ******* beast, so it appears the idea that PR activation is antiandrogenic might be wrong. And if it's wrong, see questions 2 and 3 again.
9. Finally, for those of you who do run gear while incorporating Peat concepts, have any of you experienced the effects I'm looking for (voice deepening, filling out the beard)? If so, could you please share your stack?
TLDR for my most important question: how do I do (and maybe even potentiate the effects of) tren and keep my balls plump and healthy at the same time using Peat technology?
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