Only few PFS guys can get (way) better with the use of 5ARis like saw, progesterone or zinc. I was also one of the lucky guys, used prog cream 2 years ago and then tomato juice cycles for 4 weeks and improved from 0 to 70%.
But then i wanted even more and bought more and more supplements to raise androgens. My AR changed somehow and now I need to inject huge amounts of Testosterone, take 20g creatine and bulgarian tribulus daily to feel OK.
This shows how much the AR can change over time. I went from totally intolerant to androgens to oversensitive and then finally to almost insensitive (I need at least 300mg t/week + DHT boosting supplements to have decent libido).
So I continued the regimen and it did not worsen conditions nor improve them after continued use. It provided a few days worth of sexual enhancements which tapered off and then returned to normal (post fin) state. Thanks for reading and I am done with this little trial.
I tried saw palmetto for about a year after crashed due to saw palmetto. (at the time I didn’t know pfs)
During saw palmetto I had absolutely no interest in sex and no erections. My stamina however was pretty good and capacity of problem solving and memory were good. I had no anxiety, no racing heart or depression. Stopped saw palmetto for the second time I developed insomnia, extreme anxiety, racing heart and depression. Take it carefully. It’s not a candy.
Currently my T level dropped by 22% after discontinuing saw palmetto.
In my case saw palmetto and finasteride boosted my T level like steroids.
My body shape now is awful. I developed huge pot belly, thin arms, thin neck and double chin.
I react immediately well to clomiphene/hCG/anastrozole with amazing improvements in physical, mental and sexual sides but for a while (I was able to achieve a full recovery for 8 days).
Despite all hormonal therapies (not AAS) my T level is unmovable and fixed at 4.0 ng/mL (immediately after discontinuing saw palmetto was 5.1 ng/mL and body shape and cognition were a lot better than now).
Hi @axolotl. I have a question which may have been discussed and answered before. So as far as I understand, we have over-expressed androgen receptors following prolonged DHT deprivation. Now that DHT is back up, presumably, ARs are being overwhelmed and rendered dysfunctional for some reason. Wouldn’t it make sense, at least theoretically, to try to down-regulate ARs by raising DHT, T, etc way up for a period of time? Then once the treatment is discontinued, ARs would have theoretically returned to a more normal state. That of course is likely to be dangerous vis-a-vis cancer risk and additional side effects, but speaking strictly theoretically, doesn’t it make sense? Also, I know something like that has been tried by many and it doesn’t seem to work. Are there any theories as to why?
What you suggest appears to make sense. If lowering androgens increases ARs, then increasing androgens should lead to a decrease in ARs. However, when we quit Fin, our androgens increase significantly compared to Fin-levels back to baseline without an equivalent decrease in ARs back to baseline. Now it would be interesting to know whether AR density remains unchanged between on Fin and post-Fin periods, or whether the density decreases after quitting Fin, but just not enough to reach pre-Fin levels. I don’t know if this data is available. I think there is even a rat study where ARs density continues to increase post-Fin.
Anyway, it is crucial to find our why AR density does not return to baseline when androgens do. Clearly, at least for us the connection between AR density and androgens is not linear. It would also be interesting to know why the negative feedback loop that silences the androgen signal (when after quitting Fin baseline androgens connect to the overexpressed AR) is so massive that it overcorrects the signal. And, of course, it would be interesting to know how we can safely decrease AR density.
Coming back to your original question: Quitting Fin already results in an increase in androgens without decreasing AR density (at least not enough), Now one could argue that the level were just not high enough to make an impact. But many people here have already tried supplementation of DHT and T (incl. supraphysiological amounts). A few had success, most did not, and a lot got worse. The risk is that you make the problem even worse. Remember, apparently, our problem is that our AR signal is silenced in the presence of overexpressed ARs and baseline androgen levels. Increasing androgens may just silence your AR signal even more. Plus, people get problems from using aromatase inhibitors with T.
I think we need to figure out another way to decrease ARs.
Take what I write with a grain of salt. I have litle clue about biology and just try to get the big picture ideas from the studies and the people here who are more versed in this field.
As far as I understand androgens are pro-proliferative, meaning they lead to increased rate of cell self-replication, etc, which is what happens in cancer. Presumably finasteride decreases prostate cancer while you are on it by reducing the proliferative effect of DHT on prostate tissue. In our case, post finasteride, ARs are super sensitive so we may already be getting a high proliferative signal with the DHT we normally have. Should we raise DHT even further, the proliferative effect would be even higher. Prof. Traish talks about cancer in the context of DHT in one of his papers. Not sure how relevant it is but check it out.
Basically I developed pfs from Saw Palmetto and not from finasteride.
However I didn’t know about pfs at the time.
With Saw Palmetto I had no mental sides after discontinuing finasteride.
After discontinuing Saw Palmetto I developed racing heart, insomnia and depression for several months. Now I’m better.
Paradoxically Saw Palmetto seems to mimic finasteride and prevent some side effects.
I have achieved three complete recoveries with hCG and anastrozole, insulin and the last with levothyroxine (and also with selenium combination).
All my recoveries last about a week and also T4 half-life is about a week.
Metabolism is strictly involved in pfs state however with my dad and the endos we are under investigation about an hypothetical abnormal immune response to stimuli.
I tried saw palmetto before I tried Finasteride as i thought its a natural product so would be a better road to try.
For me all it did was give me a bad stomach i had cramps and didn’t feel like eating.
So i switched over to the miracle drug Finasteride but now I’m waiting on another miracle drug to end the damage finasteride did.
Talk about swings and roundabouts
The next miracle will be the Baylor studies
Anyone who’d even consider taking finasteride again after developing pfs, I would think they are actually insane. It can get so much worse. After I got off fin, in my brain fogged state i actually convinced myself it was all in my head and to take another pill. Thankfully I didn’t.
Honestly I’ve thought about it. I took finasteride for 2 months and then quit COLD TURKEY. In hindsight I feel this might be what has cause some of the persistent side effects. The flooding back of neurosteroids (Allo,DHT etc) could have damaged the receptors and/or the over expression of the receptors never had a chance to acclimate back to their original state. When I think about how my body reacted to the cold turkey quitting, I recall my penis doing all kinds of weird things and just feeling bizarre in general for a few weeks after. Then persistent side effects just kicked in.
I wonder if we would have slowly tapered off over a long period of time it would have given our neuro/endo system time to slowly adapt back to normal.
I’ve often wondered what would happen if we went back on fin for a week and then slowly slowly tapered off. And if Saw Palmetto could be used to the same effect.
I agree with your hypothesis of flooding brain chemicals. If you look at people who did too much mdma, the same thing happens. They take too much, their neurosteriods flood their brain and damage neurons and axons. I don’t think getting back on the drug is a good idea because the damage is done. I really don’t think their is a “switch” to be flipped. I think the ppl who recover simply have some neuro plasticity left and their brain repairs slowly over time. Some people and some parts of the brain simply don’t recover. So going back on the drug would basically produce the same result, but it’s operating an already damaged brain, so I can only assume it would do even greater damage than the first time. All just a theory.