Why gains slow!

After you distinguished gentlemen find the answer, can we, the unblessed, have a dumbed down version to look over?

Also, I know it is a pain in the ass to cut and paste entire articles, but doing so saves possible problems if the links eventually go bad. Two or more links in a thread and we can call it research. :D

In my acrobat reader the page numbers differ to those of the actual text, so I’m not sure I’m looking at the correct text. However, page 26 (as Acrobat sees it) had this to say:

“They describe how denatured collagen and frayed fibril ends in tendons are readily removed by proteolytic enzymes produced by macrophages. The ruptured fibril ends may then be rejoined by the synthesis of new collagen materials.105 A Scandinavian study reports the regeneration of Achilles tendons after necrosis.133”

Unfortunately this copy of the document does not appear to contain the references cited. Still, it mentions Proteolytic enzymes (read: Bromelain) and its ability to scavenge fibril ends. It also appears to reduce bruising, and speed healing by around 400%! (some good reading here: ). I can vouch first hand that bromelain prevented edema almost completely while pumping, as well as making bruising and discolouration a very transient event.

Off to read the rest of the thread now…

I’m not sure if we all agree or disagree on most of this :) but my own interpretation so far is that whether the injury response is beneficial or not to our goals is determined by whether the immune response is overwhelmed or not. Minor trauma and stress response seems to lead to healthy new cell generation (good), whereas major trauma seems to lead to an emergency response to shore up the damage at any cost (bad). The elusive trick seems to be in modulating the degree of response.

My money would be on rate limiting the response and/or optimising the nutritional environment. I personally will be going for a positive NO environment (tadalafil/arginine etc), and high turnover cleanup and repair (Bromelain, Papain etc).

I wonder if any of the big gainers bruise easily?

Yes. As I said, I’m playing the role of devil’s advocate. I’m hoping it will encourage a more rigorous analysis.

I really, really want to get to the bottom of this, but I know that that doesn’t happen if everybody just agrees with everybody else’s good ideas. Somebody has to be the asshole, and I volunteer for this round.

It looks like you may be volunteering for the next round:

I’ll try, but this may be very hard to find. Thus, my emphasis on critical logical analysis of the papers we’ve found. PE is not scientifically studied. THe studies relate to diseases (ED, PD, and VOD).

Believe it or not, this devil’s advocate stuff is a lot of work as well. But it’s for a good cause :) . I’ll do my best to find something, but I wouldn’t hold my breath if I were you.

I’m referencing the page numbers as printed at the bottom of each page, not the page numbers reported by Acrobat Reader.

BTW, after re-reading my post above, I got the impression I was calling you an asshole. That was not my intention, and I hope you didn’t take offense.

Anyway, I think you understand that by “asshole,” I just mean the person playing the unpopular and skinky, yet necessary role. I didn’t mean to insult myself either.

So regarding the enzymes, I assume this means “take your enzymes everyday,” correct? Would you suggest taking the enzymes once a day, or taking them perhaps three times a day, with every meal, to really keep your system “saturated?” Should a person focus only on papain and bromelain, or would it be ok to take a “blend” with other enzymes in it. And finally, would it be best to take the enzymes on ALL days, just on workout days, or just on rest days?
[/stupid questions] :)

If it would help, I could PM a few folks and invite then over here to comment, I don’t know… horsehung, Big Girtha? Make me a little list of people, and I can do that if it would help.

“Never give up… never surrender.”

Electron,

I used Bromelain only, but I mentioned papain to avoid implying that Bromelain somehow had the proteolytic market cornered. I take 1000mg 3 times a day, but that is over the label recommendation. I would take it all the time that there would be inflammation otherwise, which if you’re doing PE at least every other day would probably be all the time. It is suggested that if they are taken at meal times then they may be used up in the stomach to break down proteins rather than being available for other uses, but there seems little evidence to suggest this actually happens, so if meal times are more convenient for you then that should be fine.

I want to point out that there is no evidence or feedback from anyone on this forum that Bromelain will do anything for your PE. I don’t know of anyone other than myself who actually takes it, and since I’m not in a hardcore PE program at the moment, even that doesn’t amount to much. I just noticed a vastly improved response with the occasional use of a vacuum pump, which normally produces unsightly edema when not using bromelain.

It looks like you have quite a complex stack of supplements already, so it might be worth rotating just a couple of them to see what works for you. Personally I would thin it out quite a lot unless you have other reasons for taking them (not that I think the’ll do any harm - it’s just the expense and hassle).

Modesto,

I’ve read the proper pages now, which has raised another question. They talk about Type III collagen deposition being replaced later with Type I. The tunica as I understand it is mostly Type II, so I’m wondering if this process is valid for us, or if it simply means Type III is replaced with Type II(?). The compression/adhesion/nodules/fibrosis etc. that are the complications they discuss all seem to step from circular inflammation. Whilst it is probably not possible or desirable to stop inflammation altogether, it may slow the process down enough so that the next PE session is done before the final strength related remodelling is overly advanced.

If we can slow down the ‘911’ (or 999) emergency response call of the inflammation to a regular “we’ll call round in the next day or so” response, then we might have a chance to keep extending the scaffolding and framing without the brickies/cladding getting built up (if that makes sense).

Nothing to extreme. I am using:

a loofah soap once every two days
Arnica Gel (Boiron brand) 2 applications over entire penis/day

At night:
Vitamin E 1000 IU
L-Arginine 1g

Morning:
Alpha Lipoic Acid 300mg
Acetyl L-Carnitine 500mg
L-Carnitine Tartrate 500mg

I am not super quantitative with this. Some days I forget to take stuff which I don’t worry about because I think one should give their bodys a break every few days at least.

I am also doing a lot of semi erect deep tissue penile massages for about 10 min. in the shower under the hot water. No constriction or pain, just very much loosing up the tissue. These are interesting and I think a new PE exercise might develop out of it. If you get hard enough, you are actually stretching the tunica as you push in, however, you are not forcing fluids across barriers or causing trauma so fibrosis is less likely. I am nowhere near ready to call it a PE exercise although I do hang fuller afterward.

I am thinking of using DMSO but I want to see where I can get with this other stuff first because I know it is all healthy and safe as long as I don’t overdo it.

Although I hang fuller during my shower massages, I am loosing flaccid gains. This is a little disappointing, however, I am not loosing erect gains and fsl is still the same. My penis seems harder erect than it has in a long time. Also, oddly enough, I have regained some of my erection angle without a loss in length. This is of course all very anecdotal and I don’t know what is doing what or if anything is doing anything and how much is in or stimulated by my mind.

It is not fading uniformly. This is a little disconcerting at first because I have pink, brown, yellow and black patches now. The circumcision scar is still black, the ridge on the head looks brand new but there are brown and yellow areas between the pee hole and the ridge. The area immediately around the pee hole is pink, which suggests the acid in the urine might be speeding up the turnover of skin. Rich and famous people get acid peels for the same reason, to speed the turnover. Disgusting I know, but someone might consider peeing in a condom and letting my shaft soak in it (not for me). The shaft is white at the base. This is my shaft point of reference, I have a distinct line separating the coloring of the base and the rest of the shaft behind the head.

IOW, my penis is starting to look really weird but I am heading in the right direction. This is nothing quantitative, just an update on my supplements and perceptions.

“I am also doing a lot of semi erect deep tissue penile massages for about 10 min. in the shower under the hot water. No constriction or pain, just very much loosing up the tissue. These are interesting and I think a new PE exercise might develop out of it. If you get hard enough, you are actually stretching the tunica as you push in, however, you are not forcing fluids across barriers or causing trauma so fibrosis is less likely. I am nowhere near ready to call it a PE exercise although I do hang fuller afterward.”

I have noticed that the tissue is harder in some places that others. I know this sounds like crap and I am hesitant to post it but I have some tough regions in the tissue immediately adjacent to my urethra. On the right side, it is very noticeably harder to depress than on the right side. I am not claiming this is fibrosis, I have no way of knowing what it is. I have to be pretty close to fully erect to feel this.

Uploaded excellent article on PD (in case link dies).

PEYRONIE’S DISEASE
TULIO M. GRAZIOTTIN, JULIO RESPLANDE, SHAHRAM S. GHOLAMI, TOM F. LUE Department of Urology, University of California School of Medicine, San Francisco, California, USA

Abstract on Gentile article mentioned many times above:

JOURNAL ARTICLE

Ultrastructural and immunohistochemical characterization of the tunica albuginea in Peyronie’s disease and veno-occlusive dysfunction

V. Gentile, A. Modesti, G. La Pera, F. Vasaturo, A. Modica, G. Prigiotti, F. Di Silverio and S. Scarpa
Urology Department, University of Rome La Sapienza, Italy.

The tunica albuginea and corpus cavernosum from patients with Peyronie’s disease (PD), patients with veno-occlusive dysfunction (VOD), and those from normal control subjects were studied by transmission electron microscopy and immunohistochemical staining for type I, III, and V collagens, platelet-derived growth factor (PDGF) AA and BB homodimers, and PDGF alpha and beta receptors. Ultrastructural modifications resembling a fibrotic reaction were detected in the two pathological tunica albuginea, but not in those from control subjects. Ultrastructural data demonstrated a general increase in fibrous and amorphous extracellular matrix material in the pathological tunica albuginea. The amorphous material probably represents glycoproteins and proteoglycans. The fibrous material, representing collagen, appears disorganized in the tissue and does not display the typical and homogeneous diameter, size, and spatial arrangement. Large areas of extracellular and intracytoplasmic, partially degraded, fibers are visible. An increased type I/III collagen ratio was detected by immunohistochemistry in the two pathological tunica albuginea. Moreover, a strong expression of type V collagen, correlated to fibroblasts, was revealed. Fibroblasts from control tissues, on the other hand, were totally negative. Finally, PDGF AA and BB were positive in fibroblasts from pathological tunica albuginea but were negative in control tissues. PDGF beta receptor was positive in pathological and normal tissue fibroblasts. Tunica albuginea from PD and VOD show similar ultrastructural and immunohistochemical alterations, whereas the corpus cavemosum shows no visible modifications.

Text of study linking VOD to PD:

Journal of
Islamic Academy of Sciences
Volume 6, No.4

M. ÇELI?KTAS¸*, M. OG<breve>UZ*

*From Department of Radiology, School of Medicine, Çukurova University, Balcal?, Adana, Türkiye.

SUMMARY : Color Doppler sonographic evaluations of penile vascularity of 50 impotent patients, 24 of them were known to have the Peyronie’s disease, were done. Eight (33.2%) of the patients with Peyronie’s disease had abnormal blood flow parameters consistent with the arterial insufficiency. One patient (3.8%) had normal results but prolonged erection. The remaining 15 (62.5%) had venous leakage. Whereas, 14 (53%) of the 26 impotent patients without Peyronie’s disease had arterial pathology, 7 (26.9%) with venous insufficiency and 5 (19.6%) with psychogenic or neurogenic impotence. Our results indicate that veno-occlusive dysfunction is the principal cause of impotence.

Key Words : Peyronie’s disease, ultrasonographic diagnosis.

INTRODUCTION

Peyronie’s disease is characterized by formation of palpable plaques in the corpora cavernosa, generally seen in the fourth to fifth decade (3). There is no tendency toward malignancy (3). Clinical manifestations include penile curvature, pain associated with erection and induration at the site of the fibrotic plaques.

Most of these patients are known to be potent. The reported prevalence varies from 4% to 48% (3). Although attempts have been made to clarify the etiology of impotence in this group of patients, the results are still controversial. In order to assess the etiology of erectile dysfunction in Peyronie’s disease; color Doppler penile vascular evaluations of impotent men with and of normal controls without Peyronie’s disease were done.

MATERIALS AND METHODS

Fifty impotent patients underwent color Doppler penile vascular evaluation. Peyronie’s disease was clinically diagnosed in 24 of them. GE Sonochrome Color Doppler Ultrasound device was used with a 7.5 MHz probe. The color imaging examination was performed with the patient supine and penis in the anatomic position. The sonographic probe was placed on the ventral surface at the base of the penis. The initial scan was obtained with the penis in the flaccid state; high resolution real time imaging was used to show anatomic detail of the corpora cavernosa. Color Doppler imaging was then performed to display blood flow through cavernosal arteries. Maximum values of velocity of each cavernosal artery were measured before and after the intra-cavernosal injection of 60 mg papaverine.

Maximum velocity values >40 cm/sec was accepted as a normal arterial response. An erectile angle of <90 with Vmax values of >40 cm/sec was accepted as an indirect finding of venous incompetence (Figure 1a and b). Values between 30 and 40 cm/sec correlated with the erectile angle. An erectile angle of >90 was accepted as normal. Vmax values between 25 and 30 cm/sec indicated arterial insufficiency.

Dynamic infusion cavernosometry and cavernosonography, was performed on 4 impotent and 7 Peyronie’s disease patients with impotence as a part of preoperative assessment of erectile dysfunction. Because of the invasiveness of the procedure, it was not routinely performed.

Dynamic infusion cavernosometry and cavernosonography were performed 15 minutes after the injection of 60 mg intra-cavernosal papaverine by placement of 21 gouge needle into the cavernosal body and infusing saline by an automatic perfusion pump. The pump was adjusted to perfuse 1 cc/sec saline. When full erection was established at this speed (in 3 minutes with 180 cc saline), it was concluded that the patients had veno-occlusive dysfunction (Figure 2). In this group of patients, the same procedure was repeated with contrast added to the saline (1/5) for radiologic demonstrations of the leakage. Angiography was done on one patient with Vmax <25 cm/sec (Figure 3). It was performed by introducing an 4F Simmons catheter through the femoral artery.

RESULTS

Of the 50 impotent patients whose color Doppler penile vascular evaluations were done, 24 of them had concomitant Peyronie’s disease. The mean age of the patients with Peyronie’s disease was 55 and that of the control impotent patients, 51. There were no significant risk factors for impotence other than Peyronie’s disease such as hypertension, smoking, diabetes, trauma and atherosclerotic heart disease.

Color Doppler Sonography was performed on all the patients after the patients were classified as having arterial insufficiency and venous incompetence according to the criteria explained previously. Eight patients (33.3%) of the 24 impotent patients with Peyronie’s disease had abnormal blood flow parameters consistent with arterial insufficiency. One patient (3.8%) had normal findings and prolonged erection (psychogenic or neurogenic impotence). The remaining 15 patients (62.5%) had normal arterial flow but insufficient tumesance indicating veno-occlusive dysfunction. Whereas 14 (53%) patients of the 26 in the impotent group without Peyronie’s disease had arterial pathology; 7 (26.9%), venous insufficiency and 5 (19.2%), neurogenic or psychogenic impotence. In both groups the existence of veno-occlusive dysfunction was confirmed by dynamic cavernosometry.

DISCUSSION

The studies that we have done on Peyronie’s disease by Color Doppler Sonography and dynamic cavernosometry suggest that veno-occlusive dysfunction played an important role in the impotence seen in these patients. In our study, we found the ratio between venous incompetence and arterial insufficiency to be 62.5% which is consistent with other reports using different modalities.

Color Doppler Ultrasonography is not a direct way of testing venous leakage (1,2,4,6,7). Since we know the demonstration of high blood flow in the deep dorsal vein is not a reliable indicator of venous leakage, it is possible that some of our patients with arterial insufficiency might have had concomitant veno-occlusive dysfunction.

Between these two groups there is no significant difference between risk factors for impotence. In the general population the tendency toward impotence among patients with Peyronie’s disease is a reality. Our study and other previous similar investigations show that veno-occlusive dysfunction is the major factor responsible from impotence in Peyronie’s disease. Therefore, there is a causative relationship between Peyronie’s disease and venous dysfunction. The pathogenesis of this correlation is still unknown. Fibrosis of the tunica albuginea may disrupt the normal veno-occlusive mechanism. Histopathologic studies should be the next step in clarification of the pathogenesis.

REFERENCES

1. Benson CB and Vickers MA : Sexual impotence caused by vascular disease: Diagnosis with duplex ultrasonography. AJR, 153:1149-1153, 1989.

2. Lee B, S?kka SC, Randrup ER, Villemarette P, Baum N, Hower JF and Hellstrom WJ : Standardization of penile blood flow parameters in normal men using intra-cavernous prostaglandin El and visual sexual stimulation. Jour Urol, 149:49-52, 1993.

3. Lopez JA and Jarow JP : Penile vascular evaluation of men with Peyronie’s disease. Jour Urol, 149:53-55, 1993.

4. Pickard RS, Oates CP, Sethia KK and Powell H : The role of color duplex ultrasonography in the diagnosis of vasculogenic impotence. BJU, 68:537-540, 1991.

5. Quam JP, King BF, James EM, Lewis RW, BRakke DM, Ilstrup DM, Parulkar BG and Hattery RR : Duplex and Color Doppler Sonographic evaluation of vasculogenic impotence. AJR, 153:1141-1147, 1989.

6. Schwartz AN, Wang KY, Mack LA, Low M, Berger RE, Cyr DR and Feldman M : Evaluation of normal erectile function with color flow Doppler. AJR, 153:1155-1160, 1989.

7. Valji K and Bookstein JJ : Diagnosis of arteriogenic impotence: Efficacy of duplex sonography as a screening tool. AJR, 1993: 65-59, 1993.

*Correspondence

Medih Çeliktas¸
Çukurova Üniversitesi,
T?p Fakültesi,
Radyoloji Bölümü,
Balcal?, Adana, TÜRKI?YE.

I am also taking 4-6 mg of Melatonin each night to sleep but I see it also has effects on collagen by inself and fibrosis.

J Pineal Res. 2004 Sep;37(2):78-84. Related Articles, Links

Melatonin reduces dimethylnitrosamine-induced liver fibrosis in rats.

Tahan V, Ozaras R, Canbakan B, Uzun H, Aydin S, Yildirim B, Aytekin H, Ozbay G, Mert A, Senturk H.

Dpeartment of Internal Medicine, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey. veytahan@yahoo.com

Increased deposition of the extracellular matrix components, particularly collagen, is a central phenomenon in liver fibrosis. Stellate cells, the central mediators in the pathogenesis of fibrosis are activated by free radicals, and synthesize collagen. Melatonin is a potent physiological scavenger of hydroxyl radicals. Melatonin has also been shown to be involved in the inhibitory regulation of collagen content in tissues. At present, no effective treatment of liver fibrosis is available for clinical use. We aimed to test the effects of melatonin on dimethylnitrosamine (DMN)-induced liver damage in rats. Wistar albino rats were injected with DMN intraperitoneally. Following a single dose of 40 mg/kg DMN, either saline (DMN) or 100 mg/kg daily melatonin was administered for 14 days. In other rats, physiologic saline or melatonin were injected for 14 days, following a single injection of saline as control. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) levels were evaluated in blood and tissue homogenates. DMN caused hepatic fibrotic changes, whereas melatonin suppressed these changes in five of 14 rats (P < 0.05). DMN administration resulted in increased hydroxyproline and MDA levels, and decreased GSH and SOD levels, whereas melatonin reversed these effects. When melatonin was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that melatonin functions as a potent fibrosuppressant and antioxidant, and may be a therapeutic choice.

PMID: 15298665 [PubMed - in process]

http://www.ncbi .nlm.nih.gov/en … t_uids=15298665

I don’t even want to think about listing everything in my multi vitamin and protein powders: Trader Joe’s milk and egg protein powder. All one people multi vitamin powder. Cliff Bar soy protein bars.

“Clinical manifestations include penile curvature, pain associated with erection and induration at the site of the fibrotic plaques.”

I am still not claiming it is fibrosis, but the main hard spot on my shaft next to the urethra is a little sore if I press too hard while doing my deep tissue massages. The same spot on the other side of the urethra is not.

I have done some ridiculously extreme PE in the past and may have penile side effects that very few of us share. Anyone else up for a deep tissue massage to see if they have tender hard spots? Oh no, I am not offering to do it for you, you have to get into the shower and do it yourself : )