As devil’s advocate, I’m essentially performing a regulatory function. You keep coming up with good ideas, and I keep throwing cold water on them. In an ideal system, that would cause you to sharpen your points and clarify your logic. This can continue iteratively until we can both agree on something. Then we’ll know whether we’ve made any progress.
It’s not that I disagree with you, it’s that I see holes in your logic that I am hoping you will fill in. I don’t have the expertise to do that.
If I’m reading you correctly, the main point of your last post is that damage caused by PE is like the damage caused by Peyronie’s, and is thus susceptible to the same treament:
Sure. Quite possibly, there are similarities between PD and PE-induced toughness. But the scale is entirely different. Whereas PE may cause “micro-tears” and burst capillaries, I do not believe it causes “trama” that rises to the level of “chronic inflammation, excessive collagen deposition and disorganization, and elastin fragmentation” [quoted from the study above].
The body tends to heal small injuries in stride. For example, small cuts don’t leave scars. But fibrosis is an extreme reaction to a chronic problem. I don’t think it’s the normal consequence of wear-and-tear, or even of PE. Feel free to disagree, but please tell me why.
“NO” and other substances have been found effective in reducing the deposition of collagen in PD. But, does this only occur in cases of fibrosis where there is “abnormal wound healing,” or does it occur elsewhere?
Inquiring minds want to know.
Yes, I know you are serving a very important function in the development of working theory. I know that you are knowledgeable, probably understand what I have presented and disagree. I just started school again so time is tight. However, when I get a chance I will try to find published literature that more directly address your concerns.