DHT and those herbs only work for a select few lucky.
Realistically a cure looks like it might come from crispr. Luckily it won’t actually take decades like people automatically assume when it comes to new tech
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Ok I just read the entire study and I’ve changed my mind after seeing all of the details. I do believe this study has found a strong correlation in PFS sufferers.
The reason being because 100% of non-PFS users in the study (aka control group) did not show a methylated SRD5A2 gene. Actually, there was one person in the non-PFS group who did have the problem with the SRD5A2 gene, and kind of interesting they found out he suffered from normotensive hydrocephalus and should have been excluded from the control group. I looked up the symptoms of normotensive hydrocephalus, a couple of the symptoms are “difficulty concentrating” and “urinary problems”. In any case, this person should have been excluded, so I do see a strong correlation in the studies findings.
So half of the PFS guys in the study had problems with SRD5A2, what about the other half? I would guess that further studies will show they are affected in some other way, maybe their SRD5A2 receptors, or an enzyme that assists with facilitating the creation of DHT is having problems.
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People are affected in so many different ways that I think it would be strange if it all boiled down to a single thing. The variability of symptoms from person to person is just too big.
Baylor is heading to the same mistake because they didn’t tap the spinal to check the genes in the spinal fluid.
Baylor have at this point 6 years trashed.
Give it a rest.
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@Moonchild, your posts are becoming exhausting and even aggressive. Please consider take a break from the forum, or at least refrain from reposting ill-informed assertions about ongoing research over and over. Summarising in your topic “What I believe PFS Is”, you wrote (very quickly, apparently) the following:
You have also clearly stated more than once:
…You posted repeatedly within the past months between your many recoveries that you had spoken to a geneticist in a clinic and his statement of it being impossible made a big impression on you(1,2), and this is clearly the extent of your knowledge on the subject. You have not exhibited any understanding of what epigenetics even means as a conceptual framework.
A year ago when fasting had cured you, you had declared the only hope for us was blood infusions from young people. I understand and appreciate you are very influenced by what you read that day, but this is a very serious issue and your posts are increasingly reading like declarative statements, despite being baseless. After a few weeks ago repeatedly rubbishing discussion of epigenetic modifications, you are now declaring which sites and cells they should be assaying in research. This is risible. Please recognise your own limitations in consideration of this issue and have a little humility. After such a volte face, you have not become expert within a fortnight.
We’ve all heard - a lot - that you think the baylor research is a waste of time, so please now stop spamming variations on this theme and wait until after the publication, as I’m sure you’ll have a lot to explain to us all then. Thank you.
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It is true bro, I will take a rest.
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Why dont just use a DNMT1 inhibitor, reading the study that will un - methylation 5ar2 on CNS, and maybe creation of hormones will follow
Do you know we can undo that metilation with DNMT1 inhibitors that you can take via supplements … people have tried in the past with good results while on them… and also most of them are 5ar2 inhibitors so…
Same here Brother
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Actually the study about methylation seems to show correlation, but not necessarily causation.
Among PFS sufferers we may already have the methylation of the gene. And Finasteride was exactly the wrong drug to take. A drug that may have accelerated apoptosis in the body and other shocks in the brain that take ages to revert.
People with no methylation must be more resistent to that shock.
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I know it’s a pain but if you know where these posts/links are please drop some, I’m interested in reading about these experiences, might want to try.
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has someone used a DNMT1 inhibitor and done that? i dont even know what that is
Guys, this study is worth 0 in my case as well as for PAS patients or Saw Palmetto Syndrome that inhibit 5-type alfareductase 1. In other words, the SRD5A1 gene in our case can be methylated, which with Finasteride is not. This is extremely depressing since the mechanism of the Syndrome in 5AR1 patients can be and is different. It’s not all. Mr. Melcangi denies me being included in the study because those who haven’t taken Finasteride are NOT even considered. Enjoy.
I think that counts for me as well since the stuff I took contained Saw palmetto as well.
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Saw Palmetto inhibits both the enzyme 2 and the enzyme 1. While Rutin inhibits only 1, as does Accutane. I am even worse because I had an inhibition of Aromatase from Vitamin D3. What I’m saying is that nobody will value us.
Stupid question but can I check my 23andme for this gene mutation?
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I would like to know it too, man
I don’t think it would be very useful. It’s all about epigenetics (not a genetic mutation).
And it’s likely that we already had the epigenetic change in ourselves before Finasteride.
Finasteride may have shocked our body and brain (with an imbalance in neurotransmitters, muscle spasms, etc.).
Epigenetic changes can occur at an early age or even in the womb.
It would not matter about which enzymes are blocked if the theory here holds true lowering androgen levels by any means can cause pfs…pfs imo is more common with finastride because it lowers it immediately and greatly which increases the risk of triggering the syndrome…The other inhibitors are much less potent and effective but cause it in some people…
Seems it takes more androgen reduction ti cause the syndrome in certain people where others can have it triggered by a mild inhibitor…Just my thoughts from observation of users.
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