The anti-cortisol mechanism of trenbolone
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@alfredoolivas What's your take on the infamous tren insanity?
Are such susceptible people, in hindsight, simply not meant to ever take tren?
Or can things like the turning violently homosexual, hysterically hyperemotional or sleepwalking be otherwise avoided by plausible mechanisms? -
@CrumblingCookie excess adrenaline signalling, possible glutamate, combined with high androgen signalling and possibly high estrogen membrane receptor signalling.
Studies show it creates a insomniac, aggressive phenotype with excitable legs.
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@alfredoolivas said in The anti-cortisol mechanism of trenbolone:
excess adrenaline signalling
excitable legsThis almost sounds like... too low dopamine? Restless legs is a symptom of too low dopamine and certain dopamine agonists reduce adrenalin. A match made in heaven?
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@engineer yeah maybe, though it lowers prolactin in these microdoses. I think a better explanation is that it is neurotoxic to dopamine neurons.
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@alfredoolivas said in The anti-cortisol mechanism of trenbolone:
"In conclusion, our findings indicate that while 17-TB mitigates muscle atrophy and enhances motor activity in PD mice, it concurrently exacerbates neuroinflammation, induces neuronal apoptosis, and worsens dopaminergic neuronal death"
https://pubmed.ncbi.nlm.nih.gov/39222261/What dosage?
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@engineer 8mcg / kg.
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Trenbolone increases excretion or metabolism of estrogen massively
https://www.sciencedirect.com/science/article/abs/pii/0039128X76900659 -
@alfredoolivas it is criminal to not include HEDs if available with these studies
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@engineer https://www.pidantuan.com/ to get studies behind paywalls not added to sci hub.
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@alfredoolivas thats not the problem
I can access all articles anyway because my college is good
problem is that I dont want to manually go through the article content to find a dosage
haidut always provided heds for his study reviews if dosages were available
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goldmine of a thread
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In case a chemist is interested in this thread in the future, please develop 18 Methyl Tren thanks
https://www.sciencedirect.com/science/article/pii/0022473180901120 -
2 oxo steroids have much greater affinity for the GR..... 2 oxo methyl tren has around 3x the affinity for the GR as methyl tren.
So anavar could have a greater affinity for the GR, but mestanolone, which is anavar despite the 2 oxo, has poor affinity. But still, it has a really long half life and can mog cortisol in it's blood levels. Interdasting.
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@jamezb46 this expalins why the "clear" had such great affinity for the GR.
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@alfredoolivas Makes sense, but also, if we could choose to have a new steroid developed, why wouldn't we just go with 2-oxa-DHT that my post last year referenced? Haidut's group already synthesized it, and it should be like anavar but sans the potential liver sides (if there even are any with anavar)
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The reason 17a methylated steroids are dosed multiple times lower than non 17a methylated steroids is because their half life is so great, allowing for far more stable blood and tissue concentrations that are greater
Think about it. You give a guy A 10mg of oxandrolobd and guy B 12mg testosterone acetate.
Hour 1:
Guy A: 10mg of Oxandrolone in his system
Guy B: 0.3-0.6mg of testosterone has been released this hourHour 6:
Guy A: 6mg of Oxandrolone in his system
Guy B: 0.28 to 0.35mg of testosterone has been released in hour 6.methylation allows for supraphysiological & stable levels of androgens from low doses.
10mg of 2 oxo DHT will not replicate 10mg of anavar for those reasons
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@alfredoolivas If you check some of the research I posted from last year, the evidence supports 2-oxa steroids (sans 17-A methylation) being quite anabolic, though definitely less than 17-A steroids. I think what the big deal with 2-oxa-tren was that when given orally it significantly outperformed about methyl-test.
https://academic.oup.com/endo/article-abstract/84/2/441/2695192?redirectedFrom=fulltext&login=false
"The 2-oxa analog (III) was 2–9 times as androgenic as MT and 93 times as myotrophic. Activity of this magnitude was surprising in view of the absence of a methyl substituent on C-17 of this compound."
https://en.wikipedia.org/wiki/Tetrahydrogestrinone
BTW: the clear actually has a 17-A ethyl group, not methyl. That probably has something to do with its potency, as ethyl groups are even more lipophilic than methyl groups. Possibly, it makes metabolic deactivation of it even more difficult than with 17-alpha methyl groups.
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@jamezb46 great find
Why do people prefer methyl groups over ethyl groups? Surely there isn't free lunch. Ethyl nandrolone (norethisterone) has less affinity for the AR relative to nandrolone
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@alfredoolivas The methyl groups are probably better for AR binding, as you suggest. Actually, something similar is the case with methamphetamine. Methamphetamine is a better stimulant than ethylamphetamine.
THG has an ethyl group not for some special reason to do with the ethyl being "better" but because of two reasons 1) the precursors PA was working with (norgestrel) 2) even if PA could have made THG with methyl instead of ethyl at 17-A he wouldn't have because he wanted to make something undetectable and I believe the 17-A ethyl group made it undetectable because it was metabolized into compounds that no algorithm at the time analyzing the breakdown products in urine could detect
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@jamezb46 what were the doses of the clear? Idk why methylated steroids were chosen, because you can just take more of the ethyl steroid and have the same endocrine effects without hepatoxicity
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