This is an old post, but some good points still. Receptors have always been the most promising theory, I just can’t believe 10 years later we still haven’t been able to test the methylation of these genes and regulating genes.
Because Andrew, if it were as simple as that a vast majority of people would’ve gotten better from Testosterone or DHT supplementation. And that hasn’t happened. For every guy who said he’s benefitted from it on this website, there are 10 who’ve either gotten worse or had no therapeutic benefit.
We need to unite under a single front. I’m not asking you to blindly have faith in it, but to look at all the information we have at hand and decide accordingly, so we can all live better lives sooner rather than later. If you look at the history of this place, you’ll see this debate has been going on forever. There’s people who believe in a theory because it’s convenient or because it happens to fit into one person’s symptom profile, and it causes more divide amongst the community.
We need more people to make this happen faster, but we all need to work towards a common goal. I see some members posting random studies and discussing the science like it’s going to make a difference. We’re past that stage, we have one strong theory that has so far, been supported by studies done on PFS patients and I think it would be prudent to apply Occam’s razor here. What we need to do is figure out what is different in us genetically/epigenetically compared to normal people. And the way to do that, is to conduct studies. The way to conduct studies is to get researchers interested in our problem, and the best way to do that is to strengthen the data set we have (i.e. the survey).
I know a lot of you have been ambivalent about the survey at best. Trust me, in the beginning, I was too. I didn’t even really understand the point of it besides, well, why not? But it’s what gets scientists/official bodies interested, so if you guys want to make this progress faster, figure out how we can get more people to take it. @Sibelio @Andrew35
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The simple reason is the Foundation studies were geared towards proving the existence of PFS with the goal of taking Fin off the market. We are simply spectators watching the latest episode of Foundation vs Merck.
We donated towards the Foundation studies because they cleverly tacked on a sentence or two saying they hope therapies would come from the studies. I feel like we got played on numerous levels.
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I have left out references to Dr’s and studies on Dht and T it’s been done enough already. While we don’t know for certain why the majority dont respond we could start with receptor expression and Methylation as a probable cause. Those who do respond to treatment likely have functioning receptors that can utilise Dht and T. We could run tests on these patients.
Sibelio has shown by applying dht to certain tissue that he was able to improve symptoms. So can we assume there is also a tissue problem that needs addressing which goes beyond the limitations of Melcangis study.
All of this costs money, money which we frankly, as a community, aren’t in abundance of. Which means that we’ve probably don’t have a ton of shots at getting this right, so we need to go with what’s most likely, and what makes the most sense.
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That’s seems like a lifetimes work. Before we took these androgen inhibitors I believe many of us functioned normally and well. Who is to say that we cannot function like that again if we restore methylation and receptor expression. We may have a genetic weakness to these drugs and nothing has really changed within us. So we restore the necessary functions, and continue living and obviously don’t take any substances that could recreate the effects of Finasteride. How many here would prefer that option over waiting a possible lifetime for the answer.
The first goal should be to restore health. The second is to achieve this following the path of least resistance.
I think we are all pretty much in alignment with our main theories on PFS. However some of us want to start addressing a possible solution while others want to know the route cause. It sounds like the testing for methylation will be cheaper than finding the route cause which requires 7 figure investment that can only be conducted by a limited number of researchers.
They are codependent goals Andrew.
There are plenty of supplements/drugs that people take that lower AR expression as a direct effect or a consequence, and that clearly does not fix the problem (permanently) for majority of people on this website. A lot tend to get some degree of relief temporarily, followed by a loss of efficacy, or some relief followed by a worsening of their condition.
Let’s make this very clear, I haven’t spoken to the other moderators but I believe they feel the same way. If there was a solution right now, we would take that. None of us want to go through PFS, and the main reason we want to understand it is because that is a prerequisite for safely treating it (or treating it at all). Not because we have a deep passion for steroid biology.
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I don’t know how methylation or demilitarization is related to brain damage.
I just don’t understand the connection.
We don’t know specifically how much AR expression is altered using supplements or we’re exactly is this being affected in the body. We don’t know how many receptors are affected it could be too many at once which the body cannot handle. So we’d look to focus on one receptor and have control over what we target.
We would be restoring normal function to the receptor this is not the same as using a supplement that could be influencing other parts of the body. It’s a blunt instrument. People get PFS in stages by going on and off the drug so it’s possible we could recover in stages.
We could also be sat here in 10 years time still discussing PFS theories. Progress has been slow over the past decade. That’s no attack at people here doing their best. People sat back and put their faith in others. That simply hasn’t worked and the community won’t get those 10 years back. We can go back and forth but I will leave it here, enough information has been exchanged for people to think about.
Thanks Borax for taking the time to respond you are a good guy and I always appreciate your help and support 
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I feel extremely annoyed and bored that I have to explain the same things a hundred times. I may do that, again, if and when I have the time and am in the mood. @borax
I don’t know why are you arguing here about something you don’t understand 
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It’s not because no one understands Sibelio, it’s because your hypothesis doesn’t hold up to scrutiny. It REQUIRES US TO SPECULATE A LOT MORE than the predominant one, and has literally ZERO EVIDENCE (no studies done on PFS patients to support it), which would’ve been fine if it at least supported all anecdotal experiences, but it doesn’t.
I’ve capitalized the important parts so hopefully, you don’t miss them.
You seem like a smart guy, and I don’t know how the issues I’ve raised haven’t changed your mind.
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Article discusses recent methods to improve safety.
Russia announces 1.7billion investment in gene editing.
Yi Li, a plant scientist at the University of Connecticut in Storrs, says that the programme’s launch is “a significant move” both for Russia and the world. He says that it could prompt China to invest more in gene-editing technologies, and help to fuel growing enthusiasm for such technologies in the United States. “For European countries, this can be a very interesting development in the light of the European court of justice ruling on genome editing,” he adds.
Exactly. I would even go for a bit of a gamble right now, but I have lost all of those bets I made in the past.
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Ok, that’s lovely. I see an ad hominem element is peeking up as well, which is always fun.
But before I waste time addressing each one of your points, even though I have done it in detail before, I would like to have only one question answered please.
How does the theory you support explain getting PFS from a single (the first) pill of Finasteride, within an hour of taking the pill and before having discontinued the drug? Or - while taking the drug, before having reduced the dose or having quit the drug.
I did not intend for it to come across that way, but I apologize since it did.
Maybe it’s best if I establish what I think based on the evidence presented. I think our Androgen Receptor isn’t functioning as it should (because it is overexpressed, which is supported by a study done on PFS patients, as I’ve mentioned before), and there is an epigenetic component behind that. As for what is driving that, I don’t know because I don’t know what every single gene in the genome does, and you can’t either. As for how we got there, I’m not sure either and I don’t think any of us can say conclusively. Which is why I believe the way to get out of this is to find out what it is that (on a genetic level), that ALL of us have in common, that makes us different from the rest of the population. Without that information, I don’t believe there’s much we can do with CRISPR.
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You did not answer my question so let me ask you another question, which may be harder to get out of.
How does PFS happen, roughly, according to the theory you have adopted? In other words, what is the theory?
Roughly: http://www.protocol-online.org/forums/uploads/monthly_07_2010/msg-19273-074754700%201280151401.ipb
What do YOU have to offer?
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