HDAC Is a demethylation agent
Can you explain this for the dummies like me?
Mcbbould
I am also a dummie, the point is that it had be done, I mean " Androgen receptor (AR) overexpression and sensitivity to hormones reversed by epigenetic therapy" it mean that if our problem is due sensitivity to hormones, it can be done, our problem can be fixed.
They used histone deacetylase inhibitors (HDACI) to restore the AR sensitivity
HDAC is used as anticancer drug.
But interest is in the brain no the prostate, but seem that they are (HDACI) capable of cross BBB
This is another promising (HDACI)
I don’t understand what kind of epigenetic therapy have they used ?
I don’t know neither, but maybe we can contact the authors of the study and maybe they get interested to help us trough the foundation
I will going to have an appointment with Dr, Khera soon at Baylor College University, please guys if you have any question, let me know.
As I said before, I had an appointment with a geneticist at the same Baylor College University, he told me that it is impossible that Finasteride make any genetic or epigenetic modification specialty at 1mg dosage, I ask him if in case there were any epigenetic change he said that if epiegentic is not permanent.
I really can’t wait to hear what comes of it - MOONCHILD you’re the f-ing don, thanks. <3
He’s accepting pfs patients? I live only 2 1/2 hours away
Thanks you for doing this! 
please also bring up PSSD and PAS etc…
Khera is involved in a stem cell clinic in Mexico
Ask them what could be done, with our diminished neurosteroid levels, to safely restore the ability to sleep throughout the night again.
I think that once that our AR start working properly, those neurosteroids are going back to the normal levels
I think that our AR are deregulated
Ask him how long he personally thinks it is most likely going to take for an effective therapy for our condition to arrive.
I know he’ll say it’s hard to predict, etc. But if he could imagine himself having it right now and wanting to have an internal estimate just for psychological purposes, what would he choose as the estimate?
The Panama cells are US approved at the highest standard I’m just not sure of the delivery.
Stem cells is so fucking powerful that even HVI had been cure with it, I do not have any doubt that it is very possible that stem cell can fix PFS, but stem cell have many problem before get in the market to treat neurological conditions, like delivery method, differentiation in the type of cell that is need it, FDA approval, etc…
https://www.sciencedirect.com/topics/neuroscience/trichostatin-a
HDAC inhibitors such as sodium butyrate (SB), valproic acid, trichostatin A, suberoylanilide hydroxamic acid, and so on have long been studied for their role in normalizing the deleterious consequences of environmental factors including addictive drugs and stress.101 Similarly, recent studies also show the neuroprotective effects of HDAC inhibitors via restoration of histone acetylation in the frontal cortex and hippocampus of TBI-induced animals.
Sodium butyrate : Sodium butyrate, the sodium salt of butyric acid, is a well-known HDAC inhibitor, and competitively binds to the zinc sites in class I and II HDACs. The administration of SB on the 14th day after CCI injury increases global histone acetylation in the hippocampus. In addition, SB also improves CCI-induced deficits in spatial learning and memory, as well as fear conditioning due to TBI.54
And there are a lot more information in this page
Have you tried taking butryic acid/sodium butyrate? If so, did it have any effect?
Don’t want to speak for Moonchild, but I believe he recovered 100%, and I believe he did try this.
Are you aware of anyone else trying it? Seems like a very straightforward, easy and relatively low risk protocol to try, given the ease of buying this supplement.
I have ordered some. Unsure if it will help in the case of PAS, but I will let you know.
People always say HDAC would be about (de)methylation, when in truth it’s literally about (histone) deacetylation, which depending on issue can be just as “powerful” or relevant as methylation, as can phsophorylation, for example. Acetylation and methylation can be linked and take each other’s places, sometimes, I think, i.e. deacetylation is required for methylation to take place, and if HDAC (deacetylation) is inhibited, methylation usually cannot take place.
However, as usual, it’s not as straightforward or simple as that either, since HDAC inhibitors usually show a pattern of demethylation followed by hypermethylation… (E.g. Sodium Butyate as a HDAC inhibitor, or any others, you can read up studies and some will mention such patterns if they are detailed enough. Bacopa is a herbal HDAC inhibitor.)
By the way, the opposite of HDAC is HAT or Histone-Acetyltransferase - this is what causes deacetylation. This is quite common in herbs, and I think the protein p300 is an important factor in it (like SIRT1 might be in demethylation or possibly HDAC). So one can check for either p300 (also often mentioned to be inhibited by various options) or HAT or histone acefyltransferase, instead of HDAC, for interest’s sake. HAT inhibitors I already know: Curcumin, Quercetin, EGCG (mixed, seems to do nearly everything…), Schisandra…
By the way, I am sure HDAC inhibition (for acetylation) is a major factor of Bacopa’s positive effect on memory and mood, and might be behind some of the receptor regulation processes that get most of the attention. I am sure one will also feel “hollow” and more confused after taking high doses of a HAT inhibitor for a while (although it can also be useful to some extent sometimes). These effects are usually said (and I think felt) to just take half a day or so in their onset, by the way.
Just my personal sidenote on the topic, not sure how it will bring anyone further right now.