Confirmed ED is caused by neurosteroid imbalance & NOT actual tissue damage
What do you mean?
At the end it mention peripheral neuropathy
Anybody wanna weigh in on this?
If this is saying that persistent ED is caused by neurosteroid and not structural issues, how come the majority lose nocturnals?
“Separately, he tells us, “We suspect that post-finasteride ED may be related to alterations in neuroendocrine control of sexual desire, rather than physical damage to the genital area. That’s an important distinction when formulating strategies for attacking the problem of developing effective treatments for sexual dysfunction in PFS patients.””
This doesn’t explain losing morning erections, correct? Also, doesn’t this contradict Khera’s study which found structural issues?
What I don’t understand is how you can determine PFS in rats if only a subsection of humans acquire it. Surely the findings would relate across the board for all men who take finasteride. I don’t know whether anyone could clarify my understanding here.
Run the experiment again and see if any of them sign up here.
It’s always good to see more peer reviewed data on finasteride’s effects. However, I still have the sense that measuring so many different parameters without a central guiding hypothesis may be less productive. Sometimes reading these papers feels like hearing blind men describe an elephant…
It’s possible for the drug to have multiple effects, so there’s not necessarily a contradiction.
Also, Khera was looking at human subjects while this study is using rats. It’s also possible that there are effects that appear in humans but not rats (and vice versa), which is a key criticism of the Melcangi rat studies in general.
@mstone, the Mark Twain of PFS.
The semi-final sentence in the 3rd paragraph down towards the end of the Foundation link.
IL-1 and TNF indicate inflammation is involved. Weren’t we (or just I in some cases) talking about this not too long ago? @Jimwildman, @Bigpoppa10040, @Lazarusry, @Dubya_B, @IrishLegend, @Henrique Seems my hunch was not so crazy after all. I’d love to see the studies evolve enough to rule out or rule in autoimmunity at some point in time. Branch out, leave no stone unturned, and exhaust all possibilities. It’s a drug I never took, but progress is progress.
Based on my personal experience, my penis has noticeably become lax, and at its most severe, it presents an ischemic yellowish color. This article is like another blind person touching an elephant.
Again the researchers miss the goal.
This whole study is missing the point due to not measuring AR expression in the penis during/after treatment.
From my POV it looks like what happened to these rats are what happens to people who don’t develop PFS.
What we want to know is if the overexpressed AR is the root cause or not.
Cortisol/glucocorticoids are highly implicated in nocturnal erections, so the lack of nocturnals could still be consistent with neurosteroids/hormones. Based on people’s symptoms and the known role of 5α- and 5β-reductases at metabolizing cortisol, I would think this is a major implicated factor in our symptom profile. Dry eyes, frequent urination, fatigue, brain fog, inhibited sexuality/libido, erections, sleep problems, water retention. On and on, cortisol is implicated in all of that.
You think too much or too little cortisol? I took prednisone and it made me feel worse
I don’t think any of it is as simple as too high or too low. We know in hormones that a lot of ‘good functioning’ distributions are parabolic, with either extremes of too high or too low being detrimental. In addition, there’s also variation in localities, where high levels in one region of the body could be better and in another, worse.
Did you monitor your sodium and potassium levels on prednisone? Prednisone and methylprednisolone as well as the herbal equivalent licorice cause sodium retention and potassium loss. A low (0) sodium diet along with a high potassium diet protects me against side effects. It’s simple and magical! I feel bad if I don’t follow these guidelines. I never took prednisone, but I took licorice and methylprednisolone. The latter 2 feel the exact same to me. Licorice is to corticosteroids what saw palmetto is to finasteride.