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.