Another waste of money in my opinion.
I might be biased when it comes to this tho so I didn’t want to comment. I only put into my body stuff that is proven to give results. I’m big on efficiency and the risk/reward system. I’m not going to spend money on stuff like these two things that are really not necessary on accomplishing a goal that can better be met with more efficient drugs.
Do you have a link to this study. I cant find it anywhere.
Sorry for the typo I meant hexadrone, not hexedrone which is a stimulant club drug haha, what would you recommend instead in terms of efficiency?
So here’s the problem, and it comes up frequently: prohormones are kind of lousy, but…
Some genuine steroids (designer steroids is the name we’ve collectively chosen for some reason) like superdrol, epistane, and methylstenbolone actually work really, really well. And they work because they’re real steroids. But they were sold/marketed as prohormones back in the day. So people think that because X worked well, and X is a “prohormone”, then Y must work well too. These things were not created equally.
You’re better off saving your money on those two products and investing it in either A.) a more proven oral, or B.) something entirely unrelated to steroids, like high quality food.
Epistane is notorious for shutting you down hard. Of all the people I have been around who haven taken this - it tanked their hormones like a mofo. Stay away imo
This assumes it’s being run within a larger cycle and testosterone is being used.
Full text isn’t available, if you give me an email (in profile desc) I can probably gain access to the full paper and send it to you in screenshots.
The Role of PPAR-δ in Metabolism, Inflammation, and Cancer: Many Characters of a Critical Transcription Factor (study in PDF) shows highlights a potential role with regard to PPAR agonsts and cancer progression
Should say that (papers on this) a lot of “epistane” isn’t actually epistane. Epi in itself is a DHT derivative absent of progestognenic or estrogenic activity. Thus, in theory the unesterified, non progestogen/aromatising nature of the hormone should indicate the suppressive nature of the hormone would be less than, say that of an aromatising testosterone derivative or an aromatising or nonaromatising 19-nortestosterone derivative with regard to the sheer level of gonadotropin suppression mg for mg. However shut down is shut down, once one gets shut down there is no difference between “suppressiveness” or hormones as when one uses AAS with the intent to enhance performance/muscle mass in a non medical setting, they’re always using enough to achieve near full gonadotropin suppression, all that matters is how LONG will the hormone shut them down for.
Given the structure and properties of epistane (2a 3a epitio c17aa methyl dihydrotestosterone) the time to bounce back (given epi is the sole drug used) wouldn’t be much, however it should be suspected to nearly fully suppress gonadotropins and thus measurable androgen concentrations in the blood when used solo would be nearly zero. Hell, even oxandrolone is suppressive, anyone who says it’s less so is talking out of their ass.
Studies on oxandrolone demonstrating a lack of suppression show 1-2 mg/day to not cause significant issues… when 15mg/day is used, TT tanks by about 45 percent in THREE DAYS
Short-Term Oxandrolone Administration Stimulates Net Muscle Protein Synthesis in Young Men1 | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic (download the PDF)
as soon as one takes an amt of hormones equivalent to more than what the body would naturally produce, hormonal production is almost entirely shut off (with the exception of t produced via adrenal glands). Take less than that, only partial suppression will occur, but then you aren’t going to get much of an anabolic response, if any at all. Maybe in a clinical setting this might be of relevance to someone who is so far wasted away that any boost in anabolism would help, but I’d argue that if someone is that wasted away you’d want to initiate a more aggressive treatment protocol to reduce the chance of the patient suddenly dying due to such severe atrophy of skeletal muscle.