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Does anyone have a reliable source of DHT?
Yes personally it didn't settle well with me. Also, andractim is hard to dose and easy to overdoDid you try 11Keto?
Weed is lagalized but androgens are still illegal (in America)...Lol maybe we need all the bodybuilders to be as outspoken as pot users.Yes personally it didn't settle well with me. Also, andractim is hard to dose and easy to overdo
What about a DHT precursor?Yes personally it didn't settle well with me. Also, andractim is hard to dose and easy to overdo
In light of your ideas on anabolic compounds and how they just oppose cortisol effects, have you ever looked into nivelar ?
From what I see it was developped specifically to keep the anabolic properties of T but not its androgenic ones. It may have nasty side effects on the liver but I thought it could be interesting to study given its properties and the theory in your OP.
Count me as one who's having trouble with the Metergoline; I got my sugar up some but that stuff really gets cortisol down, gives me energy but that sugar drop is something else.I think I will release progesterone + DHEA as supplement. This way people can try either stack and if needed modulate it with either extra pregnenolone (StressNon) or progesterone (Progestene).
Count me as one who's having trouble with the Metergoline; I got my sugar up some but that stuff really gets cortisol down, gives me energy but that sugar drop is something else.
So I'm thinking of back-tracking and trying the anti- stress chemicals. Even if I take thyroid for the sugar, it's still going to bump up against all my stress hormones. I have very high stress with considerable muscle wasting now.
I've searched all the threads and see all the combinations. The one I can't do is Pansterone. That combo just make me nuts. I get totally estrogenic. I'm interested in trying all the preg/prog stacks and the one you're talking about here, the prog/DHEA.
Grinding up some DHEA is doable and I have some Progestene. But that prog/DHEA sounds good. The only thing I'd have to pick up is some StressNon.
Are you still thinking of bringing that out?
Yes, we will probably have the prog/DHEA combo out before the end of this month, and separate vitamin D as a supplement as well.
Are you planning on making a seperate Vitamin E product as well? I know you have TocoVit, but something more affordable and less niche. Perhaps the one used in EstroBan?Yes, we will probably have the prog/DHEA combo out before the end of this month, and separate vitamin D as a supplement as well.
Are you planning on making a seperate Vitamin E product as well? I know you have TocoVit, but something more affordable and less niche. Perhaps the one used in EstroBan?
Do you have any experiences regarding potency?Lol. I can't speak for Haidut here, but why would he do that :)? Tocovit isn't exactly expensive and is more potent. Just take a smaller amount if cost is a concern?
Vitamin D in DMSO, please? Would be amazing to stack with DMSO KuinoneYes, we will probably have the prog/DHEA combo out before the end of this month, and separate vitamin D as a supplement as well.
I think the dose matters a lot. If you notice, the dose used for RU486 in the PFS thread is also quite a bit lower than the one used for Cushing syndrome. If you use 600mg+ of RU486 as it is used in that condition I think the pro-libido effects will disappear. In that dose RU486 behaves like a progestin and starts to oppose estrogen as well as much as gbolduev does not want to admit it. Same with progesterone - a dose of under 50mg for a male seems to be best. In higher doses because it can also bind the androgen receptor, progesterone can compete with endogenous androgens and become anti-androgenic. A weaker androgen agonist (aka progesterone) competing with stronger androgens for receptor binding behaves as an antiandrogen. Here is an example related to DHEA but the same applies to proegsterone as it is also an AR agonist.
Dehydroepiandrosterone - Wikipedia
"...Although it functions as an endogenous precursor to more potent androgens such as testosterone and DHT, DHEA has been found to possess some degree of androgenic activity in its own right, acting as a low affinity (Ki = 1 μM), weak partial agonist of the androgen receptor (AR). However, its intrinsic activity at the receptor is quite weak, and on account of that, due to competition for binding with full agonists like testosterone, it can actually behave more like an antagonist depending on circulating testosterone and dihydrotestosterone (DHT) levels, and hence, like an antiandrogen. However, its affinity for the receptor is very low, and for that reason, is unlikely to be of much significance under normal circumstances."
So, again, the dose makes the poison. Progesterone dose should probably stay under 50mg for a male unless combined with a strong androgen like DHT, androsterone, etc. gbolduev said to combine progesterone + T but there is no need to do that actually as T is a progestin itself. As I mentioned in a few other threads arguing with tyw, most synthetic progestins are 19-nortestosterone derivatives and are agonist at PR. So is T for that matter. See below for more info.
Wooo's "Progesterone, The Master Hormone Myth"
In summary, if progesterone is used I would stay at a lower dose for a male and combine with a strong androgen when possible, to avoid behaving like an anti-androgen. DHT would be best for stacking with it (IMO) but even adding DHEA or androsterone should work. In fact, IMO an optimal OTC stack would be progesterone + dhea + androsterone as I mentioned in the original thread.
This could be interesting: https://raypeatforum.com/community/threads/progesterone-is-androgenic.21164/#post-294515Another possibility aside from progesterone occupying androgen receptors - progesterone can compete with testosterone for the activity of 5a-reductase in higher doses.
Another possibility aside from progesterone occupying androgen receptors - progesterone can compete with testosterone for the activity of 5a-reductase in higher doses.
"It is doubtful, however, that T+P inhibits lordosis directly through increased levels of DHT, or a product of DHT, because the formation of DHT from T is actually decreased in the presence of P due to competition by T and P for the 5a-reductase enzyme (Massa, Stupnicka, Kniewald, and Martini, 1972)."
The transformation of testosterone into dihydrotestosterone by the brain and the anterior pituitary
"Although there are many possibilities, the inhibition of lordosis by DHT most likely requires binding to androgen receptors (Coyotupa et al., 1972; Blasberg et al., 1998). Estrogen increases androgen receptor (AR) levels and the duration of AR occupation by DHT in the male (Handa, Roselli, Horton, and Resko, 1987; Roselli and Fasasi, 1992), but this action of estrogen does not appear to explain the T+P-induced inhibition because lordosis was still significantly reduced in T+P- compared to T-treated males when no estrogen was administered Another possibility is that the P treatment in some manner upregulated ARs, resulting in a greater responsiveness to DHT. Since the upregulation of ARs would not have been expressed as a reduction of lordosis unless DHT was also present, this hypothesis is consistent with the fact that both T (as a substrate for DHT) and P were required to observe an effect. As pointed out by Crews, Godwin Hartman, Grammer, Prediger, and Sheppherd (1996), at first glance this hypothesis seems to contradict studies showing that T and P can compete with each other for binding with receptors, that P can have anti-androgenic actions, and that P can deplete nuclear ARs, but the doses of P used in these studies were pharmacological (Connolly and Resko, 1989). Indeed, although studied in a different context (that of T and P acting alone or in synergy to elicit male-typical behaviors in lizards and rats (Lindzey and Crews, 1988; Young, Greenberg, and Crews, 1991; Witt et al., 1995)), intracranial implants of P can increase the abundance of AR mRNA in the brain of male whiptail lizards (Crews et al., 1996), and male progesterone receptor knockout mice are less responsive to testosterone replacement on measures of male copulatory behavior (Phelps, Lydon, O’Malley, and Crews, 1998). To our knowledge, no other research pertinent to this issue has been performed."
Inhibition of lordosis behavior in male and female rats by androgens and progesterone.
Thanks. Actually you bring up a great point - that progesterone does NOT inhibit 5-AR but rather has a much higher affinity for it than T, so progesterone will outcompete T even at lower doses and thus raise allopregnanolone levels at the expense of DHT. It is allopregnanolone that is known to have anti-gonadotropic and anti-libido effects, so progesterone gets blamed while in reality that steroid by itself is rather pro-male when used in the proper dose.
Hey @Wagner83 did you see the part about progesterone actually upregulating AR? I think it throws a bit of a wrench in the theory about finasteride actually making cells insensitive to DHT. Not sure if the PFS guys on the other forum would be interested in this, but it caught my eye.