Cortisol is actually a glucocorticoid, not an androgen so I'm not really sure if preg would "mimic" it. Preg showed to reduce cortisol by 60% which I believe it does it in an indirect way.
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Pregnenolone & Progesterone Are Both Agonists Of The Androgen Receptor
- Thread starter haidut
- Start date
Cortisol is actually a glucocorticoid, not an androgen so I'm not really sure if preg would "mimic" it. Preg showed to reduce cortisol by 60% which I believe it does it in an indirect way.
OP
While officially a neutral steroid, cortisol is a potent functional androgen antagonist by suppressing androgen synthesis both in the gonads and peripherally. It also stimulates estrogen synthesis through aromatase and that is definitely anti-androgenic as well.
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Pregnenolone is the precursor to all of them, it tends to convert to what is needed if the right dose is taken,a higher does going to allopregenolone it seems. What signals it to convert to cortisol or androgens is open to question I believe.
We all lack knowledge in these areas!
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I am very interested in this topic. I love the complexity of hormones and how they interact with eachother.
I was just reading this paper and it says some interesting things regarding progesterone that seem to be in line with what you're talking about Haidut.
In the study they are testing for lordosis behavior in male and female rats, and seeing which hormones reduce its effect and which contribute to it. The first experiment had groups of males that were gonadectomized, then estrogen primed, then given different hormones. Experiment 2 was the same but without the estrogen priming. Experiment 3 had the males gonadectomized, adrenalectomized and also estrogen primed.
Lordosis behavior in males was lowest in the DHT groups, as is expected. In DHT females, giving them progesterone caused more lordosis behavior, however giving progesterone to the DHT male group had no effect on this behavior. Interestingly, DHT + P males had lower lordosis behavior than DHT + T males. Also, males given T + P had significantly lower lordosis behavior than control group, and also the T only group and the P only group. So testosterone + progesterone seemed to have unique effects that progesterone and testosterone didn't have when given by themselves. (I'm actually finding this hard to summarize so I will just quote some stuff from the study)
Here are some quotes from the discussion portion...
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).
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).
[A] 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, 392 Butler, Mills, and Bloch 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.
The only difference in plasma steroid levels between the T-treated males in Experiments 1 and 2 (no reduction in lordosis) and the T+P-treated males (reduced lordosis) was in plasma levels of P, which were approximately 55% lower in the T-treated males. Thus, the higher levels of P in the T+P-treated males may have been a necessary factor to reduce lordosis, perhaps a threshold effect acting through an upregulation of AR.
In summary, we report a new finding, that a combination of T+P at physiological doses for the male dramatically inhibited estrogen-stimulated lordosis in the Gx [gonadectomized] male rat but not the female, an effect not seen with T or P alone. T+P also inhibited lordosis in males without estrogen and in ADX [adrenalectomized] males. T+P-treated males had normal body weights, and the absence of effects on general locomotor, aggressive, and male sex behaviors indicated that the T+P inhibition was behaviorally specific. DHT at approximately physiological doses for males inhibited lordosis, suggesting the involvement of AR. It is possible that the T+P-induced inhibition involves an upregulation of AR by P, but research is needed to establish this interesting possibility
One effect they didn't talk about was that of progesterones anti-estrogenic effects. Surely, this must also play a role in the behavior observed, right?
I was just reading this paper and it says some interesting things regarding progesterone that seem to be in line with what you're talking about Haidut.
In the study they are testing for lordosis behavior in male and female rats, and seeing which hormones reduce its effect and which contribute to it. The first experiment had groups of males that were gonadectomized, then estrogen primed, then given different hormones. Experiment 2 was the same but without the estrogen priming. Experiment 3 had the males gonadectomized, adrenalectomized and also estrogen primed.
Lordosis behavior in males was lowest in the DHT groups, as is expected. In DHT females, giving them progesterone caused more lordosis behavior, however giving progesterone to the DHT male group had no effect on this behavior. Interestingly, DHT + P males had lower lordosis behavior than DHT + T males. Also, males given T + P had significantly lower lordosis behavior than control group, and also the T only group and the P only group. So testosterone + progesterone seemed to have unique effects that progesterone and testosterone didn't have when given by themselves. (I'm actually finding this hard to summarize so I will just quote some stuff from the study)
Here are some quotes from the discussion portion...
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).
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).
[A] 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, 392 Butler, Mills, and Bloch 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.
The only difference in plasma steroid levels between the T-treated males in Experiments 1 and 2 (no reduction in lordosis) and the T+P-treated males (reduced lordosis) was in plasma levels of P, which were approximately 55% lower in the T-treated males. Thus, the higher levels of P in the T+P-treated males may have been a necessary factor to reduce lordosis, perhaps a threshold effect acting through an upregulation of AR.
In summary, we report a new finding, that a combination of T+P at physiological doses for the male dramatically inhibited estrogen-stimulated lordosis in the Gx [gonadectomized] male rat but not the female, an effect not seen with T or P alone. T+P also inhibited lordosis in males without estrogen and in ADX [adrenalectomized] males. T+P-treated males had normal body weights, and the absence of effects on general locomotor, aggressive, and male sex behaviors indicated that the T+P inhibition was behaviorally specific. DHT at approximately physiological doses for males inhibited lordosis, suggesting the involvement of AR. It is possible that the T+P-induced inhibition involves an upregulation of AR by P, but research is needed to establish this interesting possibility
One effect they didn't talk about was that of progesterones anti-estrogenic effects. Surely, this must also play a role in the behavior observed, right?
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