Why gains slow!

Well, your not senile yet like me but you are up there in the years.

Frigging froggin frim. What was special about the GNC arnica? It many not have been clearing old discoloration but preventing new discoloration. Maybe it was the penatrant.

Do you remember anything else about it? Anyone else?

Thanks Hobby

ModestoMan,
There are a lot of publications listed, but I think your referring to one of the later ones. Yes, I think it is the latter, however, we want to limit it everywhere. Within the CC, it will reduce the strength of ones erection. This could very well be why guys have a hard time getting an erection after a long period without a break. Welcome!

>Do you remember anything else about it?

It was in a liquid base, not a gel.

Thanks Hobby. Shit, I just bought some in a gel form but I think I can mix few things I have on hand to get deep penetration.

Alright. I have arnica, Vit E and Acetyl L-Carnitine and DMSO. My goal is to de-fib for maybe a month and then start a (supplemented ;) ) newbie routine.

PS,

I’ve just reread the first publication: “Platelet-derived growth factor (PDGF) and PDGF receptors in rat corpus cavernosum: changes in expression after transient in vivo hypoxia”

The study itself deals only with CC tissue:

“The CC tissues were carefully dissected free from the surrounding tunica albuginea and made available for RT-PCR and immunohistochemical studies.” Page 396.

However, what didn’t register upon my first reading is that the study refers to earlier studies in which PDGF has been found to be overexpressed in the tunica:

“Recently, immunohistochemical and electron microscopy studies showed that PDGF is highly expressed in penile tunica albuginea obtained from patients with veno-occlusive dysfunction and Peyronie’s disease (Gentile et al. 1996), suggesting that it could be involved in the pathogenesis of these two conditions that are frequently associated with erectile dysfunction (ED) in men.” Page 395.

Still, I don’t see a clear statement that the tunica itself becomes fibrotic, even with veno-occlusive dysfunction or Peyronie’s disease. It’s true that PDGF is overexpressed in the tunica, but that may be more of a reflection on what’s happening inside to the smooth muscles and blood vessels of the CCs than on what’s happening to the tunica itself. It’s unclear.

Regardless, I certainly agree that fibrosis is not desirable. The study’s statement that “prompt detumescence of erections that exceed a duration of 2 h should be recommended” (page 401) sort of bounds the problem for us PE’ers, at least in the opinion of the study’s authors. Don’t impair circulation for more than 2 hours, or you risk fibrosis.

… I’ll keep reading.

Hmmmmm,

Great post MM -

That may be why my stretcher manual emphasizes taking the stretcher off at least once per hour (or sooner) and make sure to restore circulation. And, for anybody eager enough to consider wearing a stretcher at night while asleep they had better reconsider.

Thanks,

MrTiPS

This sounds as reasonable an explanation as I’ve heard. Many threads have stated that wrapping (like, with a Thera-P wrist strap) improves flaccid hang. From the first study, which started this thread, it seems that the wrap may impair circulation and create a hypoxic environment, in which fibrosis of the smooth muscles occurs.

I wonder whether these people develop erectile problems.

You can skip to here:
ThunderSS - Nice work
I think you will see a pretty solid argument developing by the time you find yourself at your first post.
I look forward to your thoughts!

I might need you to explain a little more. The question I’m raising is whether hypoxia leads to fibrosis in the tunica, or whether fibrosis is limited to the smooth muscles and blood vessels.

It might be interesting to check out the Gentile reference from 1996. Do you know how to find that?

http://www.ncbi .nlm.nih.gov/en … st_uids=9169352

1: J Bone Miner Res. 1997 Jun;12(6):929-34. Related Articles, Links

Peyronie’s disease is associated with Paget’s disease of bone.

Lyles KW, Gold DT, Newton RA, Parekh S, Shipp KM, Pieper CF, Krishan R, Carson CC 3rd.

GRECC, VA Medical Center, Durham, North Carolina, USA.

Peyronie’s disease is an idiopathic disorder in which an inflammatory fibrosis occurs in the tunica albuginea of the corpora cavernosa which causes the erect penis to become deformed. Peyronie’s disease has a prevalence of 1% in men over age 50 years. Paget’s disease of bone is a chronic skeletal disease with areas of increased bone turnover leading to pain, deformity, and in some cases arthritis. Because of a high rate of Peyronie’s disease in subjects in a Paget’s disease industry-sponsored drug trial, we asked whether there was an association between Peyronie’s disease and Paget’s disease of bone. We evaluated 61 men with Paget’s disease attending our clinic for metabolic bone disease in a tertiary referral hospital, reviewed hospital records of all men discharged from our three hospitals with the diagnosis of Peyronie’s disease, and mailed a validated questionnaire about shape of the erect penis to 1500 male members of the Paget Foundation. In the clinic population of men with Paget’s disease of bone, 51 of 61 (83.6%) reported having normal erections; 10 patients (16.4%) were impotent. Sixteen of the 51 men (31.4%) had developed a bend or deformity in their erect penis which was confirmed by a urologist’s examination to be Peyronie’s disease. When the men with Paget’s disease with and without Peyronie’s disease were compared, there was no difference in their ages, years with Paget’s disease, or serum alkaline phosphatase level. Upon medical record review, 1 patient of 262 (0.4%) with Peyronie’s disease was found to have Paget’s disease of bone. The men with Paget’s disease returned their questionnaires for a response rate of 44.8% and reported Peyronie’s disease with a prevalence of 14.5%. We suggest that Peyronie’s disease is associated with Paget’s disease of bone. Furthermore, we suggest that Peyronie’s disease may be a previously unrecognized complication of Paget’s disease of bone.

PMID: 9169352 [PubMed - indexed for MEDLINE]

From above:

"Peyronie’s disease is an idiopathic disorder in which an inflammatory fibrosis occurs in the tunica albuginea of the corpora cavernosa which causes the erect penis to become deformed."

In Peyronie’s, the plaques are on the tunica as well as elsewhere. The tunica plaques lead to the bend. If you start at the link I listed, I think this will all make a lot more sense!

Here is the whole article:
域名停靠

PS,

Thank you for your PM. The article you cite is interesting because finds a strong corellation between three fibrosising conditions: Peyronie’s Disease, Paget’s Disease, and Dupuytren’s contractures. The reason for the corellation is unclear.

It seems that certain people may be predisposed to these types of fibrosis.

As you suspected, it is not clear from the article whether Peyronie’s or other fibrotic conditions are brought on by hypoxia. In fact, there is no discussion of hypoxia.

Also, the fact that Peyronie’s is a fibrotic condition of the tunica does not automatically imply that it is typical or the natural consequence of PE.

In fact, the article actually suggests the opposite: that Peyronie’s is not a normal condition but a disease. The disease may be caused by a biochemical abnormality that also predisposes people to other diseases.

OK MM,

“Also, the fact that Peyronie’s is a fibrotic condition of the tunica does not automatically imply that it is typical or the natural consequence of PE.”

I am glad you responded because if knowledgeable people like you are not seeing what I am saying, it means I have failed in explaining it.

Yes, I don’t think we are giving ourselves Peyronie’s. It is a complex argument that I am trying to lay out. What we do to are dicks is eerily similar to what they do in the following priapism study. Priapism results in fibrosis. Don’t get too caught up on the oxygen thing. We all know about microhemorages on our penis (the red dots and eventual skin discoloration). It is known that microhemorages trigger the TGF-beta response and the fibrosis that follows. I submit that we get the same fibritic effects that the rats get and that these effects are very likely what slow gains. It makes seance. There are a whole lot more cables to break when we try to expand and lengthen our penises!

So why do I bring Peyronie’s into the picture? It is basicly a disease of localized fibrosis. I talk about it because there are treatments for this fibrosis.

So, the question is, will the treatments that dissolve the plaques in Peyronie’s dissolve the fibrosis that happens in us and the rats in the study below.

Int J Impot Res. 2004 Jul 29 [Epub ahead of print] Related Articles, Links

TGF-beta(1) neutralizing antibodies decrease the fibrotic effects of ischemic priapism.

Sanli O, Armagan A, Kandirali E, Ozerman B, Ahmedov I, Solakoglu S, Nurten A, Tunc M, Uysal V, Kadioglu A.

1Istanbul Faculty of Medicine, University of Istanbul, Istanbul, Turkey.

The objective of this study was to evaluate the possible role of transforming growth factor beta 1 (TGF-beta(1)) antibodies (ab) for the prevention of fibrotic effects of priapism in a rat model. In total, 30 adult Sprague-Dawley rats were divided into five groups. Priapism with 6 h (group 1), priapism with 6 h+ab (group 2), priapism with 24 h (group 3), priapism with 24 h+ab (group 4) and control (group 5). Priapism was induced with a vacuum erection device and a rubber band was placed at the base of the erect penis. At 1 h after the initiation of priapism, TGF-beta1 antibodies were given intracavernosaly. All rats underwent electrical stimulation of the cavernous nerve after 8 weeks. Intracavernous and systemic blood pressures were measured during the procedure. Rats in group 1 showed significantly higher (intracavernosal pressure (ICP) pressures to cavernous nerve stimulation and had higher ICP/BP ratios when compared to other groups. Similarly, histopathologic examination revealed less fibrosis in group 2, compared with the other groups. Consequently, TGF-beta1 antibodies antagonise the fibrotic effects of TGF-beta1, especially in cases with duration of priapism less than 6 h.International Journal of Impotence Research advance online publication, 29 July 2004; doi:10.1038/sj.ijir.3901261

PMID: 15284835 [PubMed - as supplied by publisher]

Is it more clear now?

Mr. Penismith,

I’m deliberately being a bit of a party pooper here to satisfy your request for a devil’s advocate.

Honestly, I think you may be onto something, but it’s important to be very conservative in drawing inferences—especially in such a complicated area.

For example, I believe fibrosis brought about by strangling the penis (priapism, clamping, or other ways of inducing hypoxia) is probably a red herring, because, according to the studies, the fibrosis is observed only within the tissues of the CCs, not in the tunica or ligs. This would not necessarily slow PE. To the contrary, the evidence suggests that the penis generally grows to the extent of its fibrous envelope. Fibrosis of the tissues inside the CCs may be irrelevant (although it’s certainly not to be encouraged). It’s fibrosis of the tunica that concerns us.

(As an aside, it has been proposed that fibrosis of the CC tissues promotes flaccid hang. It would be interesting to know whether people with good flaccid hang are also hard gainers. That would tend to weaken my assertion that fibrosis of the internal CC tissue doesn’t affect gains.)

So, what is the evidence that PE, or even choking the penis for that matter, causes fibrosis of the tunica? I haven’t seen any. (If you want to refute this, please be very specific.)

Your argument that you may have found a treatment for over conditioning relies on the belief that ordinary toughening of the tunica induced by PE can be reversed using treatments that are effective for Peyronie’s disease.

Is there any evidence for this? How does normal connective tissue respond to these treatments? Do all collagenous tissues weaken and thin, or only plaques from Peyronie’s? One does not necessarily follow from the other. For example, in post 35, you quoted a study stating that

DMSO has no effect on normal connective tissue. Perhaps the treatments for Peyronie’s are similar.

In summary, you’ve made some important finds and have certainly expanded the knowledge base on this forum. But more data is needed to know whether your finds can translate into any benefits for PE’ers.

Of course, one of us could just volunteer to be the guinea pig :) .

OK, I don’t think this is an issue of understanding but a disagreement. I think, taken together, the information I have listed is compelling and I am not going to spend more time researching this but I will repost a little. If I find more while doing other studies, I will post it but I am ready to move on unless there are people who don’t understand. Thanks for your thoughts!

Your wrote:

"For example, I believe fibrosis brought about by strangling the penis (priapism, clamping, or other ways of inducing hypoxia) is probably a red herring, because, according to the studies, the fibrosis is observed only within the tissues of the CCs, not in the tunica or ligs.

So, what is the evidence that PE, or even choking the penis for that matter, causes fibrosis of the tunica? I haven’t seen any. (If you want to refute this, please be very specific.)"

I think the what I repost below suffices. I have already demonstrated that Peyronie’s is fibrosis of the tunica. I repost this because it talks about vascular damage and the fibrosis that results. Vascular damage results from the PE we do. That can’t be argued, we see the red dots and thrombosed veins. This is evidence that vascular damage causes fibrosis. I know you disagree.

"Peyronie’s disease (PD) is a localized fibrosis of the tunica albuginea (TA) of the penis

affecting about 2-4% of the male population (1). This fibrosis is assumed to be triggered by

trauma to the erect penis (2,3), followed by vascular damage, fibrin extravasation, recruitment of

inflammatory cells, and release of pro-fibrotic factors like transforming growth factor (TGF-β1)

and other cytokines, as well as reactive oxygen species (ROS), leading to cellular infiltration,

proliferation and differentiation. These processes cause chronic inflammation, excessive

collagen deposition and disorganization, and elastin fragmentation. This can be recognized

clinically as a palpable plaque and/or penile curvature during tumescence (2-4). Although

spontaneous regression of the plaque and the resulting curvature may occur in about 15% of

these cases (1), and some reports suggest that the injection of certain agents like verapamil

may improve the clinical condition, the majority of cases of PD seem to be refractory to

pharmacological therapy.

The recent description of a new rat animal model for PD whereby the injection of fibrin

into the TA produces a lesion indistinguishable histologically from the human condition allows us

to test pharmacological regimens in an attempt to cure or diminish the fibrosis. One approach

was based on the recently recognized antifibrotic effect of nitric oxide (NO), that reduces

collagen deposition and inhibits fibroblast differentiation into myofibroblasts, cells whose

persistence in abnormal wound healing may lead to fibrosis (5). NO was also a potent quencher

of ROS, one of the presumed agents in PD that induce fibrosis. Furthermore, when iNOS

activity was inhibited in a rat model of PD, tissue fibrosis is exacerbated and leads to an

increase in oxidative stress, whereas administration of the NOS substrate L-arginine and certain

phosphodiesterase (PDE) inhibitors exerts an antifibrotic effect (6-8)."

http://www.ncbi .nlm.nih.gov/en … t_uids=15240426

"Your argument that you may have found a treatment for over conditioning relies on the belief that ordinary toughening of the tunica induced by PE can be reversed using treatments that are effective for Peyronie’s disease.

Is there any evidence for this? How does normal connective tissue respond to these treatments? Do all collagenous tissues weaken and thin, or only plaques from Peyronie’s? One does not necessarily follow from the other."

I already posted substances that dissolve plaques. We are causing vascular injury. Vascular injury causes fibrosis. Plaques made of fibrin and collagen result. Look at the effects of NO in the study above.

"Of course, one of us could just volunteer to be the guinea pig :) ."

I am as we write : )

PS,

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.