Most likely it is the former. Finasteride has been out since what the early to mid 90’s? Propecia for hairloss not until 98… Even if someone took it right when it came out and very shortly after popped out a kid that kid would barely be getting to age which hairloss occurs right now. It is far more likely (and logical) that a father son dou took the drug and both got side effects.
I meant the first. The second question is one of the hottest research subjects currently going on in basic science and is termed “Epigenetics and Transgenerational Inheritance” (or variation thereof). This area of research is basically about learning in what ways the epigenome is inherited from one generation to the next. This is truly cutting edge, and much is still unknown in this area. Hence, any discussions about potential epigenetic changes in our cells (which needs to be proven first) can potentially be inherited, would be pure speculation at this point.
Thank you for putting this clearly, far too many people here seem to have somehow been led to think this is already an established fact.
Established fact is that we have found a change at the AR level which is a logical and documented consequence of reducing DHT levels inside the cell (i.e. result of taking 5AR inhibitors). The change we found has the potential of explaining most if not all aspects of PFS. Research must verify this in detail now. What we don’t know at this point, is WHY it has become persistent in our case. It is plausible that some epigenetic mechanism is involved (methylation, acetylation, etc.), because epigenetic changes are a reasonable explanation for the persistency of this problem and are known to be induced by environmental changes (including pharmaceutical products).
So, to sum it up: There is fact and there is hypothesis. But hypothesis comes in various shades of gray, from very uncertain to highly likely. Epigenetic changes (methylation, acetylation) fall into the “very likely” category, but we still need to prove it. The interesting effects of antibiotics/antifungals and GHB some people have reported are an indication that epigenetic changes may be involved (all of these substances have strong epigenetic effects). I will also try to post some more educational videos on epigentics. It is becoming increasingly clear to science that epigenetics are just as important as genetics (or even more imporant). It also is increasingly aparent that environment (i.e. chemicals, substances and events outside the cell) have a massive influence on our epigenetic code.
What aspects of PFS may it not explain?
GHB is a known strong HDACi. No problem finding info on that,
But PLEASE provide us with proofs to back up the statement that “antibiotics/antifungals” (which represent a VERY broad range of different compounds with very different modes of action and properties) have “strong epigenetics effects” as a whole.
Ive asked you about this already there viewtopic.php?p=53840#p53840
Ill say it again here : all azoles (includes fluconazole, miconazole, ketoconazole, voriconazole etc…) and nystatin, amphotericin B (=the major antifungals) + penicillin, streptomycin, gentamicin (major antibiotics) have NO HDACi properties. So WHICH antifungals (besides Trichostatin A) and antibiotics are you talking about, and why (please provide a scientific paper about it)? Epigenetics modifications is a (maybe the main) mechanism of fungi/bacteria acquired resistance to antibacterial/antifungals, but this has nothing to do with what you are stating above.
Your belief (or for now, theory) that everything that has some effect (like procaine viewtopic.php?p=53780#p53780, or antifungals) have so because of a hidden/alternate epigenetics mechanism has to be proven before spreading it around the forum as a fact. Your words have a weight here that you may not realize. Notice how forum members will just quote your posts and PMs without the slightest scrutiny, as if there were established facts.
Awor, are you stating that this change is “permanent” genetic change? Or an expression of the effects of finasteride consumption?
In other words, would you expect that those who recovered from PFS had this marker? Or are you saying they never likely had this marker and fall into a different category? Thanks for clarifying.
I’m also curious for your response to Venceremos’ question. Thanks.
Also
It would definitely seem to me more reasonable and accurate to say that
GHB
ncbi.nlm.nih.gov/pubmed/20456291
About inflammatory pudendal neuropathy
viewtopic.php?p=53632#p53632
Its now 7 out of 7 and counting french PFS sufferers positive for this test.
I am not discounting the epigenetics PFS theory at all (although its more on the “incertain” side of the spectrum in my eyes), but I just want to be sure that you are not categorically excluding an “immune PFS” theory in the presence of many hints showing its plausibility. Your word seems to be extremely important to many people in this forum and they seem to have been lead to beleive by the forum administrators that anything else than the epigenetics theory is a waste of time.
The studies your people are conducting are NOTHING but good news but the way things are presented on this forum is not.
I am just speculating here but I’m thinking it has to do with an imbalance (or lack of) in neurosteroids/allopregnanolone etc. that is causing these results with the pudendal issues ( i.e. inflammatory issues of nerves), which maybe Awor can give some input on?
Why would you expect awor to be able to answer this? His study focuses on molecular level defects of the androgen receptor of penile skin biopsies, and his underlying theory/area of interest is epigenetic modification…
Not my own speculation, but the theory of the specialists behind the pudendal neuropathy diagnosis (which is based on echo-doppler observation of the vessels on the traject of the pudendal nerve in addition to modified EMG + ESSP) is that its an inflammation (edema) that is the cause of the compression of the nerve (leading to a form of entrapment syndrome). That theory is coherent with the observations by echo-doppler of the area. So most probably nothing to do with neurosteroids, allopregnanolone etc. Now I will stop hijacking awor’s thread, this topic is about his study first and foremost.
Can we still expect know the full details of the first study (change at AR level?) and have that published within a few months? Or has that been delayed till the other studies are finished as well?
Somewhere on this site, is a very very good chart on how different hormones in the body are metabolized. If you look at it you will see that many hormones are not only metabilized by the same enzymes but also that one hormone being metabolized will alter the amount of another hormone circulating and also being metabolized. Many neurosteroids and allopregnanolone are metabolized or affected by the same 5AR2 that finasteride targets. It was already stated that the problem that has been identified could potentially be the cause of all PFS side effects. A problem identified at the AR level is a huge step for us, as it can prove that it is the source of our altered hormone metabolism which can have numerous effects on all of our bodily systems.
Needle in a hay stack. Good luck to you awor.
OK, I don’t think anybody ever denied that on this forum? And yes it’s been “already stated” over and over again by the admins and repeated by others all over the forum, so it’s pretty clear by now. But if anything awor in his last post seems to have moderated his claims by saying the identified problem could potentially explain “most if not all the symptoms of PFS”. For the moment only awor knows exactly what is the identified problem and why and how it would be able to explain PFS, so we’ll have to wait for divulgation of the results before speculating on all this. Repeating the admin’s line is for the moment is just as useless as saying it has to be wrong without factual bases.
Maybe I’m missing something but I dont get how finding defects at the AR level can prove than THIS could be THE SOURCE, and not another CONSEQUENCE of a problem located more “upstream” (and I have personally NO theory for that in case you wanted to ask).
Like I said awor’s study, and his plan on investigating further following the epigenetics theory, is nothing but great news for all of us, the more research the better, obviously!
What is NOT great news for all of us is deciding that this is the one and final theory to be pursued to the exclusion of any others. NOTHING allows us to adopt such a stance yet but this is definitely what is in the minds of the administrators, just look at mew’s interventions in IHP’s “theoretical discussion” thread.
Games of “gotcha” semantics are even more useless. I’ve never seen Awor alter his statement that the current findings explain most all side effects of PFS. The range of sides of PFS are so broad of course he would qualify with “most all” as we do not know now which sides to attribute to the core PFS problem.
It’s fine to disagree with the direction of the research but it’s just begun and certainly will evolve over time. The ball has just started rolling and I don’t think it’s unreasonable at all to guess that this could lead to future studies investigating other theories. The admins here give miles of latitude to allow for a very broad discussion here nearly to a fault. I have zero doubt that anyone here would gladly eat their words to find a cure for PFS if the research pointed another direction.
About a year ago a member posted that maybe it’s “a bit fanciful” to suggust one of us will come up with a cure for PFS. He was more right than I understood at the time. It’s fine to research the literature and educate ourselves but at the end of the day the only way we are going to get some answers is for each one of us here to continue to promote media awareness (as I know many have) and to support any and all research no matter our opinions.
I don’t see what the problem with this questioning is.
Awor is making a repeated broad assertion that antifungals are strong HDACIs.
Venceremos has in multiple threads, supplied strong evidence to the contrary. Even quoting the very research paper that one poster used to (falsely) claim that Nysatin was an HDACI. Read this thread. It absolutely BLOWS MY MIND! viewtopic.php?p=53706#p53706 Do you guys realize the implications here???
Venceremos is asking for Awor’s sources in making his assertions. Assertions which get repeated as truth all too frequently.
Why would you take a statement on faith and not require the same burden of proof no matter who the poster?
“Constant TROLLING”???
“Disagreeing with the direction of the research”? Have you actually read what I wrote?
“The admins here give miles of latitude to allow for a very broad discussion here nearly to a fault”??? Have you read the exact content of mew’s intervention in IHP’s theoretical discussion thread? His plan to close down the “theories” section because “theorizing” from any other ppl than him and awor is “useless” or “worthless” now that their research has allegedly identified the only path worth pursuing?
Boston, you’ve obviously become just another robot repeating and enforcing the admin’s line like too many people here.
You win. I quit, I will not post in this thread anymore.
I hope that more people will keep their mind awake and maintain critical thinking alive in this thread.
Kind of off topic, but this thread is anyways. Has cgj1 really recovered? He says complete recovery but then he was looking into buying that damiana herbs. I PMed him but he didn’t respond. Has anyone spoken to him?
Vene,
I was responding to the discussion on neurosteroids and allopregnanolone being related to a AR problem. Which in my opinion could account for many of the PFS side effects being that hormones help our body maintain homeostasis and when there is a disruption in these pathways it can effect many areas of the body. I am not discounting anyones evidence of other problems but I believe this is the root problem that the other problems stem from. Like boston said other areas of research should be pursued and I will gladly contrubute to other studies in whatever way I can and I think most on here would.
I think the problem is that here is an actual study going on to help us, why try to shift opinions away from here? Especially if there is no official undertaking going on to research other potential targets. The problem with the theories section is simple, its just a bunch of us debating various ideas and citing linked studies from the internet which are only potentially linked to PFS as opposed to actual research, like this study that is focused specifically on PFS and not other things.
If, like Awor said, a problem has been found at the androgen receptor level, a problem that we have but other people do not then this in fact could be important to understanding our condition even if it leads to something else so why try to discount it? At this time we need all the research we can get, because god knows we are not getting the attention we deserve and any is welcome in my opinion.
Broken_Pecker, I would agree with most of the spirit of what you said, except for:
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This is not the only study on PFS subjects.
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Nobody is attacking Awor’s study. We’re ALL for it. Some people are prematurely spreading conclusions from this unpublished study, however, which is irresponsible.
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Some assumptions or assertions posted by Awor and others have been challenged with factual references that contradict those statements. This is troubling and fair to point out. One can’t keep saying that all antifungals and antibiotics are HDAC inhibitors without any sources or proof.
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I have many genuine, fair questions that I’ve posted that have not been addressed. Again, this is concerning: viewtopic.php?p=51275#p51275
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In a perfect world, none of the theories or clinical observations would be competing with each other. There is value to putting together the PFS puzzle from as many different angles as possible. The frequency of varicoceles, prostatitis, potentially pudendal neuropathy, dysbiosis, thyroid issues, etc. point to this being a multi-faceted problem. We shouldn’t put all our hopes into a singular smoking gun.