all hormones inhibited by steroids. take pregnenolone

[All Nats McGee]

Progesterone (P4) & allopregnanolone are positive allosteric modulators of GABA-A receptors: they are potently anxiolytic & antidepressant, on par with benzodiazepines and barbiturates (drug-like efficacy). DHEA is another, though less potent; and with broader spectrum action. GABA-A positive allosteric modulators are subject to reinforcement (addiction) and withdrawal symptoms.

Pregnenolone, conversely, is a negative allosteric modulator of GABA-A receptor; it would follow that it would tend to promote anxiety and depression-like symptoms.

Is it possible that pregnenolone is one system part of a complex balance of neurosteroids?

 

[Type-IIx]

Is it possible that pregnenolone is one system part of a complex balance of neurosteroids?

It certainly is. Yet the clinical relevance of changes in neurosteroid concentrations and activities has never been demonstrated (the most interesting and compelling data I've seen is a small study of 5α-reductase inhibitors that show decreases in some neurosteroid levels, that may implicate similar changes in post-finasteride syndrome). Serum concentrations (a la exogenous supplementation) do not reflect brain activity. It's something understood far less than T's role in men; quite less than T's role in women. Anyone who claims to have expertise in this - not science - but FEELZ, is a bullshit artist. Anyway, as used - exogenous progesterone and allopregnanolone have drug-like efficacy on par with benzodiazepines and barbiturates; carry all the implications of GABAergic drugs (tolerance; withdrawal); as well as exerting antiandrogenic effects in men. Even DHEA is a potent estrogen that dose-dependently increases E2 in men. If you're swayed by the logic of these misfits from the ExcelMale forums, just let me know straight up, so I don't bother with these screeds in the future.

 

[Deleted member 59947]

It certainly is. Yet the clinical relevance of changes in neurosteroid concentrations and activities has never been demonstrated (the most interesting and compelling data I've seen is a small study of 5α-reductase inhibitors that show decreases in some neurosteroid levels, that may implicate similar changes in post-finasteride syndrome). Serum concentrations (a la exogenous supplementation) do not reflect brain activity. It's something understood far less than T's role in men; quite less than T's role in women. Anyone who claims to have expertise in this - not science - but FEELZ, is a bullshit artist. Anyway, as used - exogenous progesterone and allopregnanolone have drug-like efficacy on par with benzodiazepines and barbiturates; carry all the implications of GABAergic drugs (tolerance; withdrawal); as well as exerting antiandrogenic effects in men. Even DHEA is a potent estrogen that dose-dependently increases E2 in men. If you're swayed by the logic of these misfits from the ExcelMale forums, just let me know straight up, so I don't bother with these screeds in the future.

DHEA administered transdermally mostly converts to androgens, unlike oral DHEA.

When I apply 200mg DHEA transdermally / day and my joints crack after 2 days, my libido is through the roof and I shed all the water in my body, effects that I've had with Proviron and Masteron, I can confidently say that the net effect is androgenic.
Those look nothing like e2 effects.

In the end what really matters is how we feel in life. It's important to be self-aware and notice the mental and physical impact of hormones and reassess.

If I were to trust NCBI and science, I'd probably be popping pregnenolone every day :

Memory-enhancing effects in male mice of pregnenolone and steroids metabolically derived from it - PMC

Immediate post-training intracerebroventricular administration to male mice of pregnenolone (P), pregnenolone sulfate (PS), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, dihydrotestosterone, or ...

www.ncbi.nlm.nih.gov

Neuroprotection by the steroids pregnenolone and dehydroepiandrosterone is mediated by the enzyme aromatase - PubMed

Pregnenolone and dehydroepiandrosterone (DHEA) are sex hormone precursors and neuroprotective steroids. Effects of pregnenolone and DHEA may be in part mediated by their conversion to testosterone and by the consecutive conversion of testosterone to estradiol by the enzyme aromatase. This enzyme...

pubmed.ncbi.nlm.nih.gov

 

[Type-IIx]

DHEA administered transdermally mostly converts to androgens, unlike oral DHEA.

When I apply 200mg DHEA transdermally / day and my joints crack after 2 days, my libido is through the roof and I shed all the water in my body, effects that I've had with Proviron and Masteron, I can confidently say that the net effect is androgenic.
Those look nothing like e2 effects.

In the end what really matters is how we feel in life. It's important to be self-aware and notice the mental and physical impact of hormones and reassess.

If I were to trust NCBI and science, I'd probably be popping pregnenolone every day :

Memory-enhancing effects in male mice of pregnenolone and steroids metabolically derived from it - PMC

Immediate post-training intracerebroventricular administration to male mice of pregnenolone (P), pregnenolone sulfate (PS), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, dihydrotestosterone, or ...

www.ncbi.nlm.nih.gov

Neuroprotection by the steroids pregnenolone and dehydroepiandrosterone is mediated by the enzyme aromatase - PubMed

Pregnenolone and dehydroepiandrosterone (DHEA) are sex hormone precursors and neuroprotective steroids. Effects of pregnenolone and DHEA may be in part mediated by their conversion to testosterone and by the consecutive conversion of testosterone to estradiol by the enzyme aromatase. This enzyme...

pubmed.ncbi.nlm.nih.gov

There are far worse things than transdermal DHEA. I'm glad that it helps. E2 is actually what helps joints in particular (I've looked a lot at this topic) & I'd be surprised if your reduced joint cracking wasn't ERα- modulated, directly by DHEA & by its aromatic products (aromatizes at 67% the rate of T to E2 & E1). DHEA's enhancing libido, well-being, is probably modulated by estrogens in part, at least. I think very high DHEA intakes - (not what you're doing here with your transdermal use, though I won't prognosticate as to the blood concentrations this leads to) - can create problems associated with estrogens. Anyway, I think that some supplemental DHEA as we age (due to its age-related decline) is probably good for immune function, at the very least.

 

[connoristiny]

Do you need to take both DHEA and pregnenolone?

 

[Deleted member 59947]

There are far worse things than transdermal DHEA. I'm glad that it helps. E2 is actually what helps joints in particular (I've looked a lot at this topic) & I'd be surprised if your reduced joint cracking wasn't ERα- modulated, directly by DHEA & by its aromatic products (aromatizes at 67% the rate of T to E2 & E1). DHEA's enhancing libido, well-being, is probably modulated by estrogens in part, at least. I think very high DHEA intakes - (not what you're doing here with your transdermal use, though I won't prognosticate as to the blood concentrations this leads to) - can create problems associated with estrogens. Anyway, I think that some supplemental DHEA as we age (due to its age-related decline) is probably good for immune function, at the very least.

You misunderstood my post,
I don't have "reduced joint cracking".
I have induced joint cracking by transdermal DHEA, proving the fact that transdermal DHEA mostly converts to androgens and very minorly to estrogens.

 

[Type-IIx]

You misunderstood my post,
I don't have "reduced joint cracking".
I have induced joint cracking by transdermal DHEA, proving the fact that transdermal DHEA mostly converts to androgens and very minorly to estrogens.

Sure yeah, your joints cracking is solid proof of this. No weight should be given to mammalian receptor luminscence data showing DHEA to be a potent estrogen itself with no potency to transactivate AR, PR, or GR; human placental microsome data showing that DHEA aromatizes at 67% the rate of testosterone; or the human data from Endotext showing that the main effect of DHEA in men is a dose-dependent increase in estradiol. I'm sure that your confidence in DHEA sulfate's potency as a steroid did not affect the loading used in your training whatsoever, nope.

 

[janoshik]

Sure yeah, your joints cracking is solid proof of this. No weight should be given to mammalian receptor luminscence data showing DHEA to be a potent estrogen itself with no potency to transactivate AR, PR, or GR; human placental microsome data showing that DHEA aromatizes at 67% the rate of testosterone; or the human data from Endotext showing that the main effect of DHEA in men is a dose-dependent increase in estradiol. I'm sure that your confidence in DHEA sulfate's potency as a steroid did not affect the loading used in your training whatsoever, nope.

But the joints crack!

 

[Deleted member 59947]

E2 is actually what helps joints in particular (I've looked a lot at this topic) & I'd be surprised if your reduced joint cracking wasn't ERα- modulated

Your words ...

 

[Type-IIx]

Your words ...

Sure, I'd expect that an anticipated effect actually followed from the mechanistic actions supported by data for a drug. Once the opposite is claimed I am surprised to say the least, and I begin thinking about confounding variables like training load.

 

[Deleted member 59947]

Sure, I'd expect that an anticipated effect actually followed from the mechanistic actions supported by data for a drug. Once the opposite is claimed I am surprised to say the least, and I begin thinking about confounding variables like training load.

Your syntax is as confused as your thought, no matter how much you think it conveys relevant ideas and concepts, it doesn't.