If I recall correctly, prostate cancer is a possible side effect from Propecia. Some cancers involve HDAC recruitment which then silence tumor suppressing genes. I know this is just another theory but the more I think about it the more likely than all the other theories it seems. The fact that Propecia can cause cancer brought on by HDAC recruitment and the improvements some people have seen on some antibiotics and IHPs recovery via Nystatin makes me think that some of our genes were silenced by epigenetic changes. Now I’m not sure that the antibiotics and nystatin are HDACi but some anti-fungals are in fact HDACis. The possible high dosing of nystatin over a long period of time may have resulted in the unwinding of DNA around histones that then resulted in proper gene expression.

Here’s an interesting article: mct.aacrjournals.org/content/2/2/151.full

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I don’t beleive that nystatin is an HDACi (source? I think you got this from Second Amendment, LOL). But all HDACi are in effect antifungals.

Safe, easy to find HDACi are nicotinamide aka niacinamide (vit B3) and butyrate (sodium or calcium-magnesium butyrate can be easily found).

Also this article
Has great tables


Thanks for clarifying that up. For now I guess I’ll increase my intake of spinach, basil, garlic, ginger, eggs, soy, and wasabi until I can get some more potent HDACis.


I wouldnt increase consumption of soy if I were you, it’s a known phytoestrogen. You can do without it, just use all the others.


LOL Taking prostate and antiobiotic lessons from solonjk LOL

Nystatin its used for purposes other than anti-fungals due to its HDAC inhibition properties.



Where does it say nystatin is a hdaci?

Please post any info about oral (not absorbed by the gut) being a hdaci.


Please try to think a little bit more and actually read the studies before posting shit like this.
If you dont understand anything, then dont bother sharing your erroneous deductions (here you’ve obviously made a dumb shortcut because youve located the 2 words you were looking for thinking that should be enough).
Solonjk has at least extensive medical knowledge, and although he is obsessed with intraprostatitc bacteria, and giving him too much credit harmed me very gravely (because as most doctors he doesnt know much about the actual toxicity of antibiotics), he actually gave the much needed impulse for us to finally think outside of the hormonal and “molecular level” box.
You on the other side have not made a single constructive post in this forum. NONE. Please stop misleading people with your flawed reflexions. Its dumb pseudo-scientific hasty conclusion from less than clever minds, such as the quoted sentence above, that is slowing down the collective “research” and makes us look like fools.

Nowhere in this study is nystatin said to have HDACi properties.

Now maybe nystatin has indeed HDACi properties (I have yet to find info on this) but this study has nothing to do with this.
The HDACi used in this research are the “classic” Trichostatin A (TSA) and Sodium Butyrate (NaBy)
Nystatin and amphotericin B are used in some in vitro studies to permeate cells to the actions of other agents.
Now in this particular study its being used with antibiotics most probably because of its antifungal properties only, as part of a protocol to culture cartilage cells :

DMEM = Dulbecco’s modified Eagle’s medium, is a variation of Eagle’s minimal essential medium (EMEM), a cell culture medium that can be used to maintain cells in tissue culture.
The adjunction of antibiotics and antifungals is made to keep the culture sterile.

The part of the study quoted by Scnd A relevant to all this : (the word “nystatin” appears only once in this study, the relevant part is quoted there after)

I cant beleive I just wasted my precious time only to prove you wrong (nothing of interest to us in that study), but some people are easily misled and will beleive any written statement without looking too hard for the elements behind it, especially if a study is linked.
I hope that now people will understand how much faith (hint:none) they have to put in your “findings” and theories as of now.

Here is a post you quickly made in IHPs thread, where no one even scrutinized your statements.

(IHP also took 1 dex pill years before he had any improvements, which started with nystatin.)
Great job giving scientific reasoning lessons and displaying the worst example of pseudo-sci BS in the same post.
And you dare saying that solonjk sent us years behind by sending us to Kos (a 100% useful experience for PFSers as a whole, while being extremely detrimental to some us of whom went there, ask me about it).
Someone please point me to one positive, constructive, valuable or interesting post from 2ndA. Noone can be that useless


Here is a quote from a personal message Awor sent to me:

“Various people have reported some degree of success with antibiotics / antifungals in the past. Just about all of these substances have HDAC inhibiting properties.”


I guess we now have to ask awor to give some proof behind this assertion.
Unless awor is some kind of HDAC specialist scientist, I have no reason to beleive such a thing without some scientific source to back it up.
Also it might be useful to remember that (not just about)ALL of antibiotics and antifungals have antiinfectious properties (duh), before looking at exotic properties.
I hope you wont ask for proofs for this last sentence :wink:


Just checked back to see if awor had posted a reply, and it struck me : although not relevant to PFS at all the above study at least tells us that antibiotics and nystatin actually can only have very negligible HDACi properties if at all.

Congratulations to 2nd amendment for providing a study proving the exact opposite of what he was claiming with such impressive certitude!

Just read the parts of the study that I quoted above, think a little bit, and the evidence should be jumping at you :
Streptomycin, penicillin, and gentamicin (antibiotics), and nystatin (an antifungal) DO NOT HAVE SIGNIFICANT HDACi PROPERTIES.
And you can quote me on that.

People are giving way too much credit to awor in this forum.


OK, I realize many ppl will not put the effort or find the time to understand exactly why the above study proves that streptomycin, penicillin, gentamicin, and nystatin cannot possibly have any signifiacnt HDACi properties.
So Il explain briefly :
That study, called “Histone deacetylase inhibitors modulate metalloproteinase gene expression in chondrocytes and block cartilage resorption” purpose is to show the effect of HDACi (Trichostatin A and Sodium Butyrate) on cartilage cells.
Cartilage cells are cultured then in a culture medium (DMEM) with antibiotics (streptomycin, gentamicin, penicillin) and an antifungal (nystatin) obviously to keep the cultures sterile. The cultures are then divided in two groups, one where HDACi are added, another (control) where no HDACi are added. The results are then compared and conclusions are drawn on the effect of HDACi on these cultures. Obviously, if any of the antibiotics or nystatin had any relevant HDACi activity at all, the results would have been completely screwed and that study would be a worthless experiment by ignorant or even plain moronic “scientists”. I personally give them the benefit of the doubt and think they knew what they were doing.

Also, azoles antifungals (fluconazole, ketoconazole, miconazole, oxiconazole, voriconazole, econazole etc) cannot have significant HDACi property as the studies I have posted above seem to show, here s why:
HDACi are being used in addition to azoles to potentiate their effect BECAUSE development of resistance to azole antifungal drugs may occur by an HDAC mediated mechanism! The studies show us that enhanced activity and potency of current azole treatments fungi occurs when these drugs are co-administered with HDAC inhibitors, and that HDAC inhibitors enhances the azole susceptibility of otherwise drug-resistant fungi.
If azoles were HDACi in the first place this would NOT happen or any of these researches be necessary!


For those who liked the tables Ive posted above (about the nutritional epigenetics effects of dietary foods), Ive uploaded the full article in pdf format there. It is excellent and I encourage EVERYONE here to read it. The tile says it all : Nature or nurture: Let food be your epigenetic medicine in chronic inflammatory disorders. Thanks to DatBtrue btw.


I’ve looked through the pdf and I’ve found several foods I can incorporate into my diet without any difficulty at all. I do have a question though, one to which I’m pretty sure I already know the answer. Would orange juice have any HDACi properties or is it too processed to have them? I love clementines but I haven’t purchased any that have lasted more than a few days and it would get quite costly to keep buying them every week (though I wouldn’t hesitate to eat them every week).


7 years later. Melcagi study confirmed your theory


What theory?


Awor’s theory. :wink: