Enden had found this other study:
Have you had any issues at all with hydrocortisone or has it been all positive? What symptoms have you noticed that have been reduced as a result?
Thats interesting but i have not the time today to research this so much again.
I just want to ask you if the analysis you made on those metabolites was through the same method and were the exact same metabolites as in the study. Also, were people taking hydrocortisone or something else when doing those exams? Because i see lots of people here do not give a couple weeks between stopping supps/medication and reevaluating hormones
Instead of inducing the enzyme cyp3a4 have you tried inhibiting it?
Tomorrow i will follow your thread closely
edit: dont forget finasteride inhibits 5ARIII in vitro with the same potency as 5ARIIā¦ that could play a role on your symptoms too
Over the first few years I had ups and downs, but things were gradually progressing upwards. 4 months ago I went ULTRA strick paleo. No soda, no coffee, no sugar, no breads, no carbs, tons of vegetables, and tons of nuts. Everything just clicked into place, like a light switch turned back on. Dizzyness, bloating, brain fog all vanished. I played around with my metabolism and it seems to have worked
We should probably forward this study to Dr. Bhasin.
Does masteron cross the blood brain barrier?
Drugbank says it and DHT do, but elsewhere I read different?
I sent it to Mew, heāll prob take care of that when he sees my PM
I think the Discussion section may answer some of your questions for the treatment, especially the last 5 paragraphs. I gather from it that the cancer drug is more like dutasteride than finasteride since it seems to have a higher affinity for 5ar type1. Or at least they suspect it does. It also mentions the hc doses needing to be higher than they normally would be to work. Given the broad scope of inhibition that suppression of 5ar seems to play, masteron might only be one part of the puzzle of 5a reduced steroids. Iām only speculating here based on the wording of the sudy though.
This honestly tells us very little we didnāt know, in fact we also know neurosteriods are also low post treatment. Treatment wise, replacing all 5a reduced metabolites is an option but to arrange a cocktail like that isnāt going to happen tomorrow.
The one key question for me has not even been touched in this paper, and I believe it is the focus of the specific pfs research, is why the side effects during treatment are different from post treatment. Yes 5ar2 and 3 did not return to baseline, we know that via the Italian release, why have they not returned to baseline?
Agreed. We also dont know if finasteride has the same enzyme induction effect that mitotane has as mentioned in the study. That is the reason hc replacement is effective for that specific treatment in the first place, since it affects cortisol metabolism. Unfortunately, no matter how similar the symptoms caused by the 2 drugs are, their methods of action could be completely different.
why are you looking at this research as if it was tailor made for us?! Why do you expect that this study gives you a solution to your problems? that makes no sense!
You are so focused on finding a study exactlt the way you want that you are missing the whole picture! I will show you a connection between all this tomorrow and you will see i have a good reason to believe this study is very important
Italian study told you the enzyne has not returned to baseline? Can you Quote me that please
The most important conclusion of this study IMO is not on the 5ar enzyme but on the cyp
Im also theorizing here that, Regarding the inhibition by finasteride of the 5ar1, the affinity is high enough that a difference in the enzymes cyp or liver damage, would assure you higher concentrations of the drug that would lead to inhibition of 5ar 2 and 1 .
My only real issue with this study is it only addresses the the method of action of side effects while on the drug. While it still could contribute to further understanding PFS, it isnt a study based on long-term persistent side effects after stopping the drug as in our case. Please correct me if i have that part wrong.
Iām sorry but Iām not sure I follow you or if I follow you but you havenāt read the study? Maybe itās late and Im too tired to follow you.
Anyway, the conclusion suggests long term effects of having used the drug, and the drug is also inhibiting the 5ar.
you need to stop looking at it as if it was funded by the foundation. this was NOT TAILOR MADE FOR US! this study is a clue! a bit clue IMO
These guys found that 2 years after taking a drug which shares some of the same effects of finasteride, the 5AR and CYP3A4 do not return to baseline! They even talk about innefectiveness of TRT in these patientsā¦this is the most interesting study iāve seen around, if you want to think these conclusions are coincidence, go ahead.
tomorrow i will post a connection i found between this and our condition
My symptoms post treatment are identical to my sides during treatment. I had a 6 week recovery in between, but I seem to be an unusual case.
No one sees the real problem?? I told you Iām almost cured now, 3 straight months of zero numbness and full libido and no one cares to inquire. I honestly think many of you hold on to this syndrome as a crutch. I was so fucked up for so long. Itās so sad
Has anyone taken testosterone and cortisol together by any chance? Or used T boosters with cortisol supplementation?
Reduced 5ar is a symptom of the problem.
But i believe you, i know that by supplementing cortisol all the other hormones may fall in place. We arr siffering from adrenal fatigue but adrenal fatigue is almost always a symptom. Do you just take HC or something more?
Everyone on here needs to check their salivary cortisol, dhea and maybe even zinc and copper
A problem in thebliver coild explain AF.
And yes, theres jqd using cortisol with i think its test or dht or both and other stuff and getting better than pre pfs
I am not doubting long-term effects while on the drug. I just didnāt see anywhere where it was they were studying people after the drug was stopped and who still had persistent side-effects. That said, if it turns out Fin has the same action on the cyp enzyme, then i would be inclined to agree. Im not arguing that this isnt promising, just that we need to keep level heads.