Thoughts on the mechanism of Post-Drug Syndrome

Straight from the bottle soy sauce mixed with green tea can’t really taste it also using some curcumin.

Are you sure soy sauce contains a decent amount of flavonoids? I think it’s the flavonoids that have the antiandrogenic effect.

This would be a good question for @skorpio88. @Papasmurf I did have good benefit from soy but I took soy flour. Only negative was it gave me pretty bad shits on the day I took a lot. Penile sensitivity felt a little improved and I’ve been having a little better energy as of late

I’m really not sure it was just lying up the cupboard so thought why not

When did you start taking?

Like a month ago for about a week and a half.
One tablespoon a day but did two on the day I got the shits

So you’ve seen improvements then

I support your answer. You have a point here

Hey @fixit, could you fill out the survey please.

Hello Greek. Page 14.

Theory: selective androgen receptor degraders (SARDs) could cure PFS. Currently there is only one, dimethylcurcumin, and it’s still in phase 2 clinical trials. I’ve thought about trying curcumin however I believe the AR degrading effect is much less reliable than the one induced by dimethylcurcumin.

Very interesting indeed.

How is selective degradation different from receptor antagonism?

A degrader binds to a receptor and degrades it significantly faster than it would have degraded without being exposed to the degrader.

Is castration resistant prostate cancer (CRPC) the opposite of PFS? This type of cancer means that androgenic genes continue to be expressed even in the absence of androgens if I’ve understood the condition correctly. But in CRPC the androgen receptor is often overexpressed, and this leads to the question of how AR is able to function in CRPC?

Hi, sorry I do not get it.

Could you please explain ?
What is the point to target the receptor ? Is not the issue is repression of receptor’s gene (by methylation of promoter) ?

Thank you.

The Di Loreto study found that AR was overexpressed in people with PFS and this is often believed to be a possible cause of PFS, so here I was thinking about how overexpressed AR in CRPC is able to function. I personally think it’s unlikely that the cause of PFS is a type of AR methylation given that AR is overexpressed in PFS. However I think a possible cause would be methylation of an androgen signaling gene, which would cause the body to overexpress AR in an attempt to compensate for the methylation.

1 Like

Thank you very much, Arkaeik.

In this case, if AR is overexpressed should not DHT bind even more than in normal state and increase sexuality/sensitivity/muscle mass ? However most of patients report opposite symptoms. Is it correct ?

That’s what would seem intuitive and I think it’s also what the body is trying to do, however it seems like when you increase AR to a certain degree it becomes less sensitive, in fact it can become completely non-functional.

1 Like

I was thinking about the term androgen insensitivity syndrome, currently this is only used to describe the genetic disorder in which the AR is flawed. But doesn’t this syndrome describe PADS quite well? We have symptoms which are known to be caused by low androgen levels and yet we do not improve upon taking exogenous androgens. In fact I believe most of us are not affected by exogenous androgens at all. So we are literally insensitive to androgens, at least in certain regions of our bodies. Our bodies have obviously undergone profound changes. At the moment there is most likely not enough information about PADS to scientifically state that it is a form of androgen insensitivity, but perhaps when more research is published this will be possible. I think it’s possible that when we refer to our condition as a form of androgen insensitivity syndrome it will be taken more seriously than “post __ syndrome”, because the latter is unfortunately more likely to be considered a fabricated disease.