You and Awor have alluted to knowing some advances in research… So do you KNOW what it is? If you don’t, then your comment is in fact speculation, but you delivered it as fact.
If you do in fact know something that the rest of us dont, then transparency would be greatly appreciated.
It’s been repeated over and over where the potential problem lies. Nothing has been confirmed 100% yet, but we’re in the right direction. iwontgiveup, I thought you were closest to getting to the problem when you suggested PFS was an aquired case of Kennedy’s disease. PFS is not Kennedy’s disease, but the similarities are too remarkable to ignore. PFS is almost certainly a disease of the AR.
Transperancy isn’t possible at this point. The scientists working on the problem are looking to get their names published, disclosing too much info could jeopardize this, and thus the relationship the PFS community has with the scientists.
The scientists seem to know they are on to something big here, from what I gather. I think this research has a lot of scientific and POLITICAL implications.
No. A disease of the AR cannot possibly explain the high percentage of prostatitis in PFS sufferers, bloody stools that many of us have, improvement with antifungals, worsening with immuno-suppressing corticosteroids such as dexamethasone (me, JG) etc ect. Utter and complete nonsense.
Gynecomastia: breast enlargement.
Impotence
Erectile dysfunction
Reduced fertility
Low sperm count
Testicular atrophy: Testicles become smaller and less functional.
Fasciculations: Twitching of muscles when at rest.
Cramps: Large muscle spasms.
Muscular atrophy: Loss of muscle bulk that occurs when the lower motor neurons do not stimulate the muscle adequately.
Differences: PFS cases seem to respond well to testosterone, but poorly to DHT. Reasons should be obvious.
So you repeated the “symptom”, where is the explanation? Plus I dont understand how AR rendered hypersensitive to DHT, but not T, makes us more reactive to T vs DHT, did you mean the opposite?
Second, why not, but another fact is that 5ar is in fact POSITIVELY controlled by DHT and adrogens in general (no negative feedback - the usual thing happening in the HPTA for instance- but the opposite, more DHT actually induces MORE 5ar). This is why some of us (including me, JN, cytochrome…) tryed andractim/proviron to increase DHT. Its did work for JN for a while so I guess he was still sensitive enough to it? Anyway, bottom line, we dont know anything here and any theory is bound to be unscientific speculation based on hints of knowledge, and many of us react so differently to hormones that its impossible to create universal PFS clear-cut laws for everyone.
You mean the 5ar2 reduced DHT, So the problem should be only in 5ar2 areas, right, so everyone should be not experiencing hair loss post fin?
And if DHT cant bind to the receptor properly like T with kennedys patients shouldnt we have high levels of DHT in the blood, like T with kennedys patients?
Also i like others on this board crashed while on finasteride, never to make any sort of brief recovery, that hardly says dht hypersensitivity to me.
edit-also most people’s bloodwork/dht level is taken coming off the drug, so their levels are still low. People who report high DHT might be the ones months/years off the drug. Mew’s DHT was nearly out of range high 19 months off.