What’s the point? There’s no evidence to suggest he has a rat model of PFS.
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No… Preper a rat with finasteride and after give a allopregnanolone.
Right, but a rat that’s been fed Finasteride isn’t the same as a rat with PFS.
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Understand but this is a study. Roberto melcangi study… All rest the world… Nothing.
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Do we know if he got the money needed for the study ? If so, when the study is scheduled ?
Where can we donate ? 
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On the Italian post finastride italia website. The kids are raising the money for this study obviously the more money we collect the better it will be for the study. Donations are welcome if you want.
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If we join forces we can create something positive. It is up to us to try to organize ourselves in a studio. The only one currently available is melcangi. Maybe his study will not be the definitive resolution of the problem but it is also being studied for multiple sclerosis for parkinson’s for alzaimer for epilepsy and in every study that I have seen published for these diseases it has positive effects. Allo is pro-sexual calming anti-anxiety. It is not known if it will work but because we do not join the forces of the Italian and American communities and let’s try to come out of what has happened to us. Suffice it to consider that in Italy the best studies have been done so far on this disease. The examination of the cerebrospinal fluid was done in Italy by melcangi. Trust him.
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Melcangi studied the cerebrospinal fluid did the analysis of the neuropathy of the pudendal blood analysis the neurosteroid analysis of the cerebrospinal fluid the study on the intestinal microbiota is about to come out in short I believe that he is one of the most active doctors on this issue and has been studying for now more than 10 years.
He is the doctor. If we find even 1 treatment that can benefit our bad condition it would already be a huge step forward to how we are today I don’t understand who is reluctant in this … What other options do we have? The proviron the tribulus antidepressants … None of this will make us feel better. Because if a neurosteroid is so markedly missing none of these can be raised again … I ask the administrators of this American community to join forces with the Italian one and to speak with the professor and see in a scientific way to seek at least a partial resolution of this serious problem that afflicts us. If we join forces then we can find a solution together.
So far a study that you paid a lot for Baylor has not paid off at the moment … It didn’t take a well of science to understand that in some subjects the blood flow in the penis is not good. But who has neuropathies Tremors depression Muscles pains etc etc So I say if we have given a chance that we Italians are 30 and obviously we can do limited things, we must join forces and stop watching. Let’s join together in this battle, let’s collect the money in a study done by those who have studied for its understanding this nasty disease that afflicts us and let’s trust it … What it costs us … Nothing
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Read this article. Allo is one key for us. Peaple wake up… Please
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I took 5a-DHP and did not get better. Others took 5a-DHP and did not get better as well.
Prog converts to 5a-DHP via 5AR
5a-DHP converts to allopregnanolone via 3a-HSD
so the question becomes was the 5a-DHP converting to allopregnenolone via 3a-HSD. I think I am low in 3a-HSD and 3b-HSD enzyme activity.
my recent testing shows that I have flagged high serum DHT. so I do have 5AR activity to be able to have flagged high serum DHT. but for some reason i have low normal allopregnenlone in saliva, flagged low 3b-diol in blood and low normal 3a-diol in blood. 3a-diol and 3b-diol are metabolites of DHT that convert to 3a-diol and 3b-diol via 3a-HSD and 3b-HSD. So I appear to have low 3a-HSD and 3b-HSD activity. low normal allopregnenlone is another sign of low 3a-HSD enzyme activity. So i’m low in these neurosteroids with high blood DHT. My money is not on low 5AR ten years post Dut and Saw-P. I think we need to source these neurosteroids and experiment with them. 3a-diol, 3b-diol, allopregnenlone. Any metabolite that inhibiting 5AR has the potential to impact we could be doing experiments with.
I am trying to source 3b-diol seeing that this is what I am flagged low in. It is an estrogen receptor agonist. I got worse from inhibiting estrogen while already in PFS. This is my best bet. Low
3b-diol is also a possibly explanation for why some men who take DHT inhibitors get high grade prostate cancer. I am very curious about this metabolite and why I am low in it. To bad the PFS foundation could not enroll us in funded supervised studies where we can be giving these things. We know what we need to try.
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Quoting Wikipedia:
Androgens, including testosterone and DHT, are known to downregulate the hypothalamic-pituitary-adrenal axis, and this has been found to be due in part or full to their conversion into 3β-androstanediol rather than to activation of the AR.
Interesting. Is the lack of this steroid common amongst PFS sufferers?
unfortunately it does not look like it is
spstriken’s results:
3b-diol: 7.0 (4.0-20.2)
3a-diol-4.0 (2.3-10.5)
scaredoutofmymind’s results:
3b-diol: 13.1 (4.0-20.2)
3a-diol: 6.4 (2.3-10.5)
scaredoutofmymind got PFS from finasteride i believe
spstriken got PFS from Saw-P
So low 3b-diol or 3a-diol does not appear to be common in finansteride induced PFS or Saw-P induced PFS. We would need more members getting this test done to know for sure but based on this info it appears that we don’t have the same imbalances. I think it will take a more customized approach for each of us. Seeing that I am low in 3b-diol increasing 3b-diol seems like the most logical thing to do in my own case.
Agonists of estrogen receptor beta can prevent negative feed back production of cortisol.
3b-diol is a potent agonist of estrogen receptor beta. I also have low free saliva cortisol in the morning when cortisol should be at it’s highest. My low free saliva cortisol in the morning could be because I don’t have enough 3b-diol binding to estrogen receptor beta when it should be in order to prevent negative feed back of cortisol production. Because again cortisol should be at its highest in the morning . “Mother natures” get up and go if you will. Mine is at it lowest in the morning. Agonists of estrogen receptor beta are required to keep cortisol in the morning high and I am clearly low in “mother natures” estrogen receptor beta’s agonist 3b-diol.
So what I am trying to do is piece together my personalized imbalance protocol. I am looking at mineral levels in my hair, hormone levels in saliva, urine, blood and neurotransmitter levels in urine. I think all of this is required to know exactly where our own imbalances lie.
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