*Deacetylase inhibitors ( HDACs ) reverse CpG methylation by regulating DNMT1*

I not a scientist, but I am trying really hard to find a solution by myself, because I know that if we wait for the scientific community, my grandson will be seat on my grave waiting for the study to be released.

How I am doing it ? Well looking into the medical literature and based in the very little ultra tiny knowledge that I have about our condition and a lot of reading, then I look for supplements and giving it a try. at least is better to try that die waiting, what are your going to choose ?

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Idk if u guys are talking about sodium butyrate here. But i have tried it and it worked a bit for derealization and feeling shitty overall. Did get some tolerance overtime, and I take it now once in a while if i want a better day. It’s also safe as fuck.

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Also. People here are talking about the dangers of HDACs/DNMT inhibitors etc as if they are hazardous. This ofcourse is ok, but let me tell you one thing. I think taking TRT, clomid, antidepressants to cope with the PFS, are just as dangerous and often, in my opinion, even more dangerous. U are literally messing ur already fucked up hormones up again. This in some way is accepted here, but when talked about substances like this, a lot of fear mongering takes place. I think this happens simply because people don’t have knowledge on this subject. Ofcourse, DNMTinhibitors like the chemos Aza and Deca come with risks, but this is mostly not even because of it’s demethylating properties. More because of the cell death they cause. Honoustly, using some safe HDACi etc. is nothing compared to trying TRT, clomid or antidepressants.

Well sodium butyrate is not the same as β - hydroxybutyrate.

Potential Synergies of β -Hydroxybutyrate and Butyrate on the Modulation of Metabolism, Inflammation, Cognition, and General Health

I believe that some of you remember this post, where talk about bicalutamide, well bicalutamide is another HDAC inhibitor, but I prefer β - hydroxybutyrate over bicalutamide in term of safety.

Androgen receptor (AR) overexpression and sensitivity to hormones reversed by epigenetic therapy that restores Purα to a transcriptional repressor complex (RC) of AR deregulated in hormone refractory prostate cancer (HRPC) | Journal of Clinical Oncology

Bicalutamide is literally an antiandrogen.

It is but it doesn’t mean that will kill your androgen forever, as soon it can repair what is damaged the rest doesn’t matter because the androgen restore by then self,
a lot stuff are anti androgen even bananas, soybean, avocado, tomatoes and the list goes on…

All of these conditions (PSSD, PFS, PAS) are literally caused by temporary androgen ablation.

Yes but different molecules, different mechanism, in all those cases seem that occurred methyliation, now it seem that HDAC like Bicalutamide despite of being anti androgen fix what is broke.

Look fasting is anti androgenic, because fasting low LH, then low Testosterone and so on…but at the long run when you break the fasting seem that testosterone peak and you get an increase of T

Just take another HDACi such as beta hydroxybutyrate. An antiandrogen is literally the last thing I would take regardless of whether it has other properties which could help. And also you can’t really compare fasting with antiandrogenic substances. What happens during fasting is caused by mechanisms which have been developed by evolution after millions of years, so there will be no acute androgen ablation that antiandrogenic substances can cause.

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Did you ever read anything about beta hydroxybutyrate ?
What more amazing me is that you dare to take Propecia, and you are afraid to take B-hydroxybutyrate, if you think that you will reverse PFS with a drug without side effects or risk or naturally, do you know what? don’t read anymore about PFS and pretend that you never have it.
It is easy to be critical without even take the time of do any research.

Yes, I’ve ordered it as a supplement.

Are you saying the genetic stuff hasnt even started yet? Who gave you this information?

Did you mean to reply to someone else?

They only had collected the data, by the time that I meet Khera a couple months ago he told me that they were about to start comparing the data to start the second part of the study and the first part of the study was waiting for the approval for publication.
I am sorry guys I will like to have better news.
As I said before, I am 48, my grandsons will be seating in my grave waiting for the result of the study.
If you compare others disease research vs PFS in scale of interest 1- to 10
I will say that PFS is no reaching 1.
PFS is 0.01 or less
Why ? No money involved, cure is not an option for the pharma industry.
And the researching want endless money funding to keep the research forever.

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Seems contradictory to some statements that there was a significant step forward in knowledge regarding PFS achieved by this study. If they had just collected the data a couple of month ago, how can you know that?

Anyway, @axolotl seems to be in the dark about this development (study being published in two parts), or at least isnt revealing anything. :neutral_face:

Lets hope its not true.

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I didn’t said that they collected the data 2 months ago, I said that around 2 months ago when I visit Khera he told me that they just finished to collect the data to start comparing it.
The sample were collected from the skin to analyze the genes, he told me this in a previous appointment.
The Italian study the finding was in the spinal fluid.

Thats what I wanted to say. If they had just finished the process of collecting the data 2 months ago, how can people on here claim many months ago that there was a significant knowledge gain? It seems contradictory.

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thats literally what i said.

last year some guy said there was significant genetics finding that delayed the study.