Stop being ungratefull little whiny brats, noone forced finasteride down your throat and noone promised that melcangi will cure you…
The fact alone that a scientist took up on our illness and researches what happened and why it happened gives me hope for the future… You wanna see real shit? Search permanent damage from fluoroquinolones, after suffering both from pfs and FQ toxicity I can safely say FQs are WAY more harmfull than finast, you cant ever imagine and guess what; theres not even a fucking foundation to help fund studies or research the damage done. So be grateful, hope and donate
BS. They announced researching 5ar epigenetic changes. They didn’t do it.
This results don’t even help us.
It is like promising researching genetic changes in cancer patients but researching instead what cancer causes in rats.
You ordered a computer in order to get online and work, but you get a book about computers.
A friend of mine is biologist: He said those results and researches are completely gone the wrong direction. And he is convinced that based on that results, they will go further in the wrong direction re epig. changes or mutation re 5ar in humans.
Conclusion: In the next studies, you get a new book about the last book and never a computer to work with.
Ridiculous. As I predicted. No results re pfs. BS.
This is nonsensical. It’s clear you have a very loose grasp of the concepts your discussing, often completely wrong, and seemingly are not aware of or have misinterpreted the science that already exists on PFS. That should give you pause before shouting your head off constantly. I can’t talk about unpublished research, but you have zero idea what Baylor are doing and why so stop repeating it’s delayed.
I agree, it is not the same. However, that doesn’t matter as he did not claim it was. He published a paper showing treatment with finasteride induces long lasting effects on the mentioned biological systems in rats. I personally don’t think this is much use in isolation as I’ve posted above, but it adds to the volume of published literature establishing finasteride’s interaction with such systems in mammals, even if this isn’t PFS. Every brick laid in such a way helps lay groundwork for our issue and ultimate aims. Furthermore, this was unbelievable value considering Melcangi’s entire current phase of research cost a collective $20k in donations. Being involved with the scientific side and in contact with professors, I can assure you this is extraordinarily cheap.
Scientists can and do publish more than one paper. As @Sugarhouse said science is a process and this is Melcangi’s angle of research. I don’t personally believe 5ar to be the key issue, rather a dysregulated gene amongst others, and have expressed misgivings about his papers mischaracterising the profile of PFS. However, he is a good and intelligent man, wants to look into our issue and it’s useful and worthwhile angle as there is clearly an issue with 5a reduction in PFS. Melcangi is recognised as a world leading authority on 5 alpha reductase, which neither you nor your biologist friend are.
You keep going on about a mutation, disproven already, and you provide absolutely zero reasoning for this. While it’s basically certain there’s gene(s) involved in predisposing us to this, that gene is not relevant and has been sequenced in PFS patients already - there is no mutation and no rationale for believing there would be anyway. It is pointless to equate PFS with genetic 5ar2 deficiency or chronic inhibition in a “normal” non-PFS patient. You only have to read @Demon’s severe penile atrophy and look at his sky high DHT levels to write this one off. As Melcangi recently said, “[W]hen you stop treatment, [ligand] should in theory function as it did before, which is absolutely not the case" in PFS patients.
We absolutely do not have the same issues. Observations of this are what led to the development of finasteride, but the conclusion you are drawing is completely wrong. You’re referring to Imperato-Mcginley’s research on 46XY subjects in eastern Papua New Guinea which she published observations regarding in “A cluster of male pseudohermaphrodites with 5α‐reductase deficiency in Papua New Guinea”, and further in “Androgens and male physiology the syndrome of 5alpha-reductase-2 deficiency”. The head of development of finasteride, Stoner, used this to claim that the clinical features here serve as a predictor of the biological effects of chronic inhibition of this enzyme in the adult male. Which it may be, but PFS is not that and is not remotely the same as genetic 5ar2 deficiency. Merck would not have cited these men as a model for chronic inhibition of 5ar2 if they were all housebound, depressed, cognitively damaged, sexually dysfunctional with a myriad of chronic health problems. The profile of these subjects includes late virilisation, elevated LH, less body hair, no hair line recession, no acne and a small prostate. This is not the symptom profile of PFS and you can see severe patients with the opposite. Nor is PFS the same as chronic inhibition of 5 alpha reductase 2 in a normal male. Scientific measurements from men using finasteride did not find any sign of problems in areas that are frequently affected and sometimes secondarily diagnosed in pfs. This study concluded “1 year does not adversely impact bone, serum lipoproteins or hemoglobin, and has a minimal, reversible effect on serum prostate specific antigen and sexual function in normal men”. Many PFS patients have had diagnosis related to these androgen-mediated systems - including osteopenia - and significant shifts in lipid (awor pointed this out about 8 years ago reviewing bloods) and psa readings after very short exposure to the drug.
I think you should leave the scientific thought to those of us bothered to put the work in rather than repeating the same incorrect assertions over and over - usually including things that are inaccurate or already disproven. It gives out an extremely negative and pessimistic message to sufferers with no justification. If you personally don’t want to donate, don’t donate. If you want to keep making claims, provide citation and stop making the same post over and over.
You can defend the results if you like.
As I said, nothing re results as promised.
This project failed completely.
But it is difficult to communicate this I guess. And my friend confirmed me that this kind of research brings nothing re our issues. It even makes pfs shining less scientific due to non comparable parameters.
Re 5ar and pseudohermaphrodites I am right. And I have these information from a doc.
I never said 5ar is the root but was promised to be researched. Right?
Instead of not reading properly my clear statements, you could ask yourself if those results were what ppl invested their money in.
You are not right, and I just gave you several citations as to why. The SRD5A genes have been sequenced in PFS patients already with no finding of mutation. You have provided, as ever, nothing.
That Melcangi has published this paper is not a basis for this not being looked into.
The foundation have made an announcement about the study:
I found this quote really interesting, but i’m not sure what they mean:
“This research marks the completion of Phase II of Prof. Melcangi’s ongoing investigation into post-finasteride syndrome at the molecular level, aimed at determining the root causes of the condition, while possibly setting the stage for the development of effective therapies.”
Reading the posts of someone constantly berating people that are actually DOING something about our problem, whether you agree with it or not, feels to me completely counter to that: sucking both life and energy. If you don’t agree, do something about it. Going on about it here has little value.
Hey @diffi. No, this was a study on rats after 20 days of finasteride, so not PFS per se. However it did indicate long lasting changes. Melcangi is quite focused on the cognitive/central symptoms but there is other research going on into the broader epigenetic profile at Baylor, and I believe Melcangi is also looking into possible epigenetic changes to the 5ar enzyme in PFS patients so I would expect further publications along this line from his team.
Just that this is his second phase of investigation, but that his investigation is ongoing and has the eventual aim of therapeutic options.
Well this seems positive, lets hope that Baylor provides more answers and further research from Melcangi:
“This is yet another example of the excellent research being conducted by Professor Melcangi and his team. It brings us one critical step closer to better understanding the underlying biochemistry of PFS and—hopefully—to an effective treatment. We already know how to prevent the condition,” said John Santmann, MD, CEO of the Post-Finasteride Syndrome Foundation, which co-sponsored both studies.
The Big question is why do some people get away with it and some people suffer persistently after being exposed to 5ar inhibitors
From what I can make of it all male rats had the same outcome not a select few …
So a persistent effect has been demonstrated in rodents and a variety of noteworthy changes have been observed. I always preface my posts with clearly stating that I am NOT a biologist. I am NOT an expert and will never profess to be one, unlike many ‘armchair biologists’ who seem to think they can solve this issue like solving a jigsaw puzzle. They think all it takes is a ‘eureka’ moment. I urge people not to overestimate their understanding of this complicated issue. Attempting to do so is a disservice to both yourself as well as anybody who is unlucky and desperate enough to follow your lead. Thus this is not meant to be an analysis which stands on solid ground by any means but merely a rumination.
I get the feeling that PFS is showing itself to be one of two things:
System-wide alterations which are due to damage caused by the cessation of Finasteride treatment. These alterations in the hippocampus, gut and HPTA axis lead to the symptoms we know as PFS. Damage is permanent and thus symptoms persist as a result.
There is a root cause to these problems, perhaps singular (which itself is a form of damage or dysregulation), and the problems persist because of this root cause. The alterations can be reversed or at least somewhat reverted back to a more normal state once this single issue is addressed.
My suspicion is that the second scenario is more convincing, whereby the function of AR signalling or the 5-AR enzyme causes these system-wide effects, ranging from the brain to the skin to the gut. Melgangi pays particular focus to gut microbiota and theorises that ‘an alternative possibility is a direct action of finasteride on gut microbiota’ which is related in some fashion to the function and neurogenesis in the hippocampus as well as neurosteroid levels and GABA expression in the brain. So in essence, he’s entertaining the possibility that in some way Finasteride affected the gut microbiota which caused all of this to happen as a consequence.
He then states that people with major depressive disorder have similar changes in gut microbiota, which would make one feel that it’s more of a brain->gut phenomena rather than a gut->brain. However he then states that a particular strain of bacteria introduced to the gut can alleviate depression.
Is PFS’s manifestation of depression the reason for this altered gut microbiota or did Finasteride change the flora itself? I’d posit that the former is more likely than Finasteride having altered the microbiota which then brought about depressive symptoms. Why? Because the millions around the world suffering from depression and exhibiting altered gut flora are on the most part unlikely to have taken any singular substance to disturb them sufficiently. So I feel that the change in microbiota of the gut in PFS sufferers is due to the depressive markers in the brain rather than the other way round
I’m still mystified as to why myself as well as several (perhaps many) others have observed a near-total remission of symptoms for a period of days to weeks. How can systems, ranging from the gut to the brain suddenly ‘flip a switch’ and revert to a seemingly normal state? This is strange. I suppose those with depression often have ‘windows’ of improvement, so the idea of a damaged system returning to normal for a period of time isn’t unprecedented, however the multifaceted nature of PFS and it’s transient but very real alleviation of each of the facets is more surprising than the temporary improvements of the more homogeneous symptoms in the case of those with MDD.
Years ago I proposed to use Rat model to see the effects of Finasteride but some idiots and dumb heads here ridiculed me. Few years back I contacted a university who were ready to use rate modes to see the effects of fin and possibly find a treatment. I did not have needed funds for this study so contacted pfsfoundation who not only declined the funds but also did not contact the university on my repeated request.
interesting. one striking side-effect of taking transdermal DHT (andractim) is extreme flatulenzia. mabe there is a link. i dont eat different foods when takin DHT…maybe its efect on gut flora is happeing.
