The anti-cortisol mechanism of trenbolone

alfredoolivas

"The results conclude that nandrolone decanoate, but neither testosterone decanoate nor trenbolone decanoate, caused impaired recognition memory in the NOR-test, indicating an altered cognitive function. The behavioral profile and stress hormone level of the rats were not affected by the AAS treatments. Furthermore, the study revealed diverse AAS-induced somatic effects i.e., reduced body weight development and changes in organ weights. Of the three AAS included in the study, nandrolone decanoate was identified to cause the most prominent impact on the male rat, as it affected body weight development, the weights of multiple organs, and caused an impaired memory function."
https://pmc.ncbi.nlm.nih.gov/articles/PMC8974338/

alfredoolivas

"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/

CrumblingCookie

@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?

alfredoolivas

@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.

engineer

@alfredoolivas said in The anti-cortisol mechanism of trenbolone:

excess adrenaline signalling
excitable legs

This 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?

alfredoolivas

@engineer yeah maybe, though it lowers prolactin in these microdoses. I think a better explanation is that it is neurotoxic to dopamine neurons.

engineer

@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?

alfredoolivas

@engineer 8mcg / kg.

alfredoolivas

Trenbolone increases excretion or metabolism of estrogen massively

https://www.sciencedirect.com/science/article/abs/pii/0039128X76900659

engineer

@alfredoolivas it is criminal to not include HEDs if available with these studies

alfredoolivas

@engineer https://www.pidantuan.com/ to get studies behind paywalls not added to sci hub.

engineer

@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

sunsunsun

goldmine of a thread

alfredoolivas

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

alfredoolivas

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.

alfredoolivas

@jamezb46 this expalins why the "clear" had such great affinity for the GR.

jamezb46

@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)

alfredoolivas

@jamezb46

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 hour

Hour 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

jamezb46

@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.

alfredoolivas

@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