Are microdoses of mifeprestone the ultimate receptor level anti-glucorticoid?
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@sunsunsun cortisol le bad
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Took me some time to realize this is RU486. I don't think there was any Haidut podcast where he didn't mention RU486
So at the dosages you propose what would the effect on progesterone be ?
Do you know where it can be obtained ?
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Can you tell me please what we're trying to accomplish here? I haven't followed that thread. Does this lower inflammatory cytokine effects?
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@Ecstatic_Hamster
At first I thought Alfredo's eying the incredibly anabolic effects of tren without it turning him gay and into an overemotional, overdramatic wuss. He may secretly be thinking about that. It would be counteracting the progesteron receptor agonism of tren.
Here, however, he really focussed in on the anticortisol action: So suppression of cortisol equals suppression of catabolism, i.e. less muscle wasting.
Don't know to what scenario this will apply, though.
To old people to retain muscle and prevent sarcopenia? Or to young and healthy guys to improve gains and to retain them for longer without overconsumption of protein and AAS? To anyone of any age to simply fully independent of muscle but to chill down and override elevated stress from whatever origin?@Ecstatic_Hamster said in Are microdoses of mifeprestone the ultimate receptor level anti-glucorticoid?:
Does this lower inflammatory cytokine effects?
Since it lowers cortisol, I reckon it would enhance inflammatory cytokines' effects by lowering the endogenous break on them.
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@CrumblingCookie said in Are microdoses of mifeprestone the ultimate receptor level anti-glucorticoid?:
He may secretly be thinking about that.
I will hopefully be running parabolan next month if my blood work is okay. 75mg. 25mg is sufficient to lower cortisol receptors by 50% and the IC50 for ru486 is a few mg a day, so I thought the pair would synergise
@CrumblingCookie said in Are microdoses of mifeprestone the ultimate receptor level anti-glucorticoid?:
Don't know to what scenario this will apply, though.
To mog
@mauritio it would likely occupy all progesteorone receptors, it's birth control, you can get it through online pharmacies I think.
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@alfredoolivas antagonizing progesterone? what good is it if gainers the world but antagonizes the progesterone?
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@sunsunsun that's why you have tren, which is a progesterone receptor agonist
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@sunsunsun lets see...
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Is the goal here to increase muscle mass? Because if so, I think the effects of steroids are actually quite simple and don’t have that much to do with GR directly in this way. Actually, if you consider it in the context of muscle, saying that the effects work that way doesn't really explain much.
Anyway, it reminded me of that study where they say that a heterodimer forms between AR and GR
Oxandrolone blocks glucocorticoid signaling in an androgen receptor-dependent manner
Conversely, experiments in cell culture systems demonstrated significant antagonism of cortisol-induced transcriptional activation by oxandrolone in cells expressing both the AR and GR. Inhibition(of oxandrolone antagonism) was not overcome by increased cortisol concentration, and no inhibition by oxandrolone was observed in cells expressing GR alone, confirming that non-competitive mechanisms were involved.
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@TexugoDoMel The goal is to MOG and transform into a low cortisol FREAK
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@alfredoolivas said in Are microdoses of mifeprestone the ultimate receptor level anti-glucorticoid?:
it would likely occupy all progesteorone receptors, it's birth control, you can get it through online pharmacies I think.
Then I don't think it's really worth the hassle.
Id still be curious to hear how something like this feels and affects a person...
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I SHOULD OF FUCKING TRIED THIS, THE SELF SABOTAGE IS UNREAL.
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That's really interesting about the thymus, it makes you wonder about the effects of so much estrogenic substance starting in childhood. But any stress related situation could increase it I think.
But when it comes to muscle, the ability to bind to GR isn't even among the top two ways that counteract catabolism IMO
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You’ll see that, in addition to any androgen binding to GR, you’ll have two potent anti-catabolic factors:
mTOR and PGC-1α; GR negatively regulates both
To put it very simply, REDD1 negatively regulates mTOR, and FOXO1 is largely regulated by PGC-1α. Although they function “separately,” they can converge since REDD1 not only inhibits mTOR but also increases FOXO1.
You can make them resistant to catabolism by inhibiting FOXO1, and abolish the effects of GCs by inhibiting REDD1.
Not surprisingly, type 1 fibers—rich in mitochondria and OXPHOS—are resistant to stress-induced atrophy (glucocorticoids, energy deprivation, etc.) but are also resistant to hypertrophy.
Glycolytic fibers, on the other hand, which are prone to energy deficits because they have few mitochondria and rely on glycolysis, are sensitive to stress but are also sensitive to hypertrophy due to greater GR and AR density.
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