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Author Topic: Defining Peyronies Disease - The struggle to understand the disease  (Read 109317 times)

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Liam

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Re: Specifics
« Reply #50 on: July 28, 2007, 03:48:39 PM »

Quote
Liam - I reject your criteria for Peyronies Disease.  You started by expressing the fact that if it gets better that it can be assumed it was not Peyronies Disease.  Now you seem to expand that to say that you think if it ever stabilizes that it was not Peyronies Disease.

I was speaking of this one case that started, apparently, at puberty.  So, in a nutshell, part one is my view.  Part two, nuh uh (no).  :D

Tim,  I agree about black and white thinking only because most people don't consider enough blacks and enough whites.  Grey thinking promotes he status quo.  Green thinking promotes Al Gore ;D.

One other thought is when a shoulder adhesion is "torn free" during a manipulation under anesthesia, the adhesion (plaque, thickening, nom du jour) is freed (my word) from the joint.  How does this compare to the Leriche technique?
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Liam

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Re: Question Yet Unanswered
« Reply #51 on: July 28, 2007, 04:35:18 PM »

In Peyronies Disease, what causes the curve if not plaque?  If a person has a knife wound resulting in scar tissue and a curve, is this Peyronies Disease?  This is not rhetorical.  I would like for someone to explain how this is possible.
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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #52 on: July 28, 2007, 07:17:49 PM »

Liam,

I think, or thought that it is widely accepted that Peyronies Disease is an abnormal scaring. 

Normal scaring is a normal immune response to a wound.  All scars both normal and abnormal are much less elastic than the soft tissue they replace.  Either could cause a bend or deformity in a penis in large enough quantities.

A main difference between abnormal scaring and normal scaring is that with
Abnormal scaring the mechanism for turning the scar tissue off, never occurs.  Some mechanism signals the less flexible collagen III scar tissue to began production.  It could be real trauma, microtrauma, or unknown events. This abnormal process goes unchecked and replaces totally healthy undamaged tissue.  Abnormal scaring includes keloids, hypertropic scars, and Peyronies Disease  plaque

Obviously a severe burn or cut into the penis can cause the immune system to just patch the wound and then turn the normal scaring process off at the edge of the wound..  That would require not be Peyronies Disease.  It would not be progressive, it would not calcify.  For this normal scaring to be sufficient to cause a bend it would require a very significant injury to  preceded the normal scarring event.  This type of injury would not go unnoticed by the recipient.

Even significant injuries of the penis can result in either normal scaring that just fixes the wound or they can result in Peyronies Disease that continues onto healthy tissue laying much more scar tissue than is needed.  Which of these two processes happens depends on a host of factors.  Many of these factors remain unknown to anyone. 

Insignificant or non-existent injuries could never create enough normal scarring to cause deformity.  They can however innate Peyronies Disease if the conditions are suitable for the process.
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Tim468

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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #53 on: July 30, 2007, 09:46:34 AM »

Attached are two images of the wound healing process - hope this is of help in descrihbing the differences between normal and abnormal wound healing.
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Tim468

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Figure Captions too!
« Reply #54 on: July 30, 2007, 09:49:25 AM »

Figure 1. (top image) Normal wound healing following trauma or microtrauma to the penis does not lead to scar formation or fibrosis.
In a simplified view of a complex process, fibrin deposits and other factors attract macrophages and, via release and activation of cytokines (mainly transforming-growth-factor 1) induce fibroblasts to differentiate into myofibroblasts. Both cell types actively synthesize collagen and other extracellular matrix components. Myofibroblasts also facilitate closing of the wound, before being degraded via apoptosis; fibrin is removed by fibrinolysis. In the Peyronie's disease plaque, inhibition of fibrinolysis by plasminogen activator inhibitor-1, release of transforming-growth-factor 1, myofibroblast differentiation with reduced apoptosis, and accumulation of matrix metalloproteinase inhibitors (plasminogen activator inhibitor-1 and tissue inhibitors of matrix metalloproteinases) lead to excessive collagen deposition and disorganization (fibrosis) and abnormal healing (scar). Fibroblasts also contribute to collagen deposition. Arrows indicate stimulation or increase; bars indicate inhibition or decrease. MMPs, matrix metalloproteinases; PAI-1, plasminogen activator inhibitor 1; TGF-1, transforming-growth-factor 1.

Figure 2.  Peyronie's disease plaques result from dynamic interplay between profibrotic and antifibrotic factors in cells such as fibroblasts and myofibroblasts of the tunica albuginea
One of the antifibrotic mechanisms in the Peyronie's disease plaque is increased levels of nitric oxide and cyclic GMP resulting from sustained expression of inducible nitric oxide synthase. Fibrosis in smooth muscle of the corpora cavernosa and in penile arteries may be associated with aging and diabetes, contributing to corporal veno-occlusive dysfunction. Corporal fibrosis, like tunical fibrosis, seems to be counteracted by inducible nitric oxide synthase. Arrows indicate stimulation or increase; bars indicate inhibition or decrease. cGMP, cyclic GMP; iNOS, inducible nitric oxide synthase; MCP-1, monocyte chemoattractant protein 1; MMP, matrix metalloproteinase; nNOS, neuronal nitric oxide synthase; NO, nitric oxide; Peyronies Disease, Peyronie's disease; TGF-1, transforming-growth-factor 1.


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Hawk

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Re: Normal Vs Abnormal Scaring - apoptosis
« Reply #55 on: July 30, 2007, 10:09:12 AM »

I started to refer to apoptosis in my post but Decided to keep it simple.  I am glad Tim's post refers to it,  One could read over that fact in the technical text.

Apoptosis is the normal (not traumatic) cell death.  It regulates all normal tissue as far as I know. It is why we are literally rebuilt bone, skin, and muscle (and more) many times in our lives.  Cells die and are replaced by other like cells.  It can also help us remodel scar tissue if, as the scar tissue dies it is replaced by more normal tissue.  Some cells do not readily relinquish life such as cancer cells that grow uncontrollably.  It is my understanding that cells making up Peyronies Disease plaque have longevity and resist apoptosis.
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George999

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Re: Tim's Charts ...
« Reply #56 on: July 30, 2007, 10:34:23 AM »

Tim,

Thanks for posting the flow charts!  The are really helpful in understanding the process to some degree.  They should be archived somewhere on this site for future reference.

From the "abnormal" chart, one can rather quickly deduce the potential value of the following:

1)  Anti-Oxidants (from Vitamin E to OPCs)  to attack the Reactive Oxygen Species at the head of the process

2)  TGF-Beta-1 inhibitors (like Pentox) to attack at the next level down regulating Collagen Synthesis

3)  NO precursors (like Arginine) to increase NO thus down regulating Collagen Sythesis via multiple paths

4)  cGMP up regulators to (like Forskolin) to down regulate Collagen Synthesis

Also, once again we see mention of Diabetes and Aging with potential anomalies in the underlying corpora cavernosa and in penile arteries possibly stimulating abnormal processes portrayed.  This, linked with research data suggesting poorer outcomes for those with Diabetes would tend to indicate that aggressively attacking insulin resistance with DIET, EXERCISE, and key supplements (CLA/Sesamin, ALC, etc) might contribute to improved outcomes.  If insulin resistance is known to make it worse in the case of diabetics, it would certainly seem helpful to attack sub clinical insulin resistance in the case of non-diabetics.  BUT, make no mistake that NO AMOUNT of supplements can make up for unhealthy diet and exercise patterns.  Diet (avoiding all refined sugars AND sugar substitutes AND using things like cinnamon and grapefruit to stabilize glucose uptake) and Exercise (daily) are essential to knocking down insulin resistance.  Supplements can then add fuel to that process.

Anyone see any other possibilities here?

- George
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Liam

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Re: Cool stuff
« Reply #57 on: July 30, 2007, 08:58:20 PM »

Great stuff.  Love the flow charts.

My first question,however, was the one I really wanted addressed.  In Peyronies Disease, what causes the curve if not plaque

This is asked because of the continuing theme of Peyronies Disease without plaque (which  have a hard time accepting).  If the explanations are half as good as what I just read, you may make me a believer. ;)
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George999

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Re: Plaque
« Reply #58 on: July 30, 2007, 09:48:42 PM »

Liam,  I think the problem is with the definition of "plaque", which few people seem able to agree on.  Certainly, if it can be palpitated, just about everyone will agree that it is "plaque".  The problem comes when it can't be detected in the traditional manner.  But that does not mean that the tissue is not compromised.  What you will find down deep is tissue that is devoid of elastin AND consists of CHANGED collagen, with other aberrant processes going on in an ongoing fashion as portrayed by Tim's flow chart.  REMEMBER, there are multiple types of collagen that vary in degree of elasticity EVEN in the case where they are devoid of elastin.  And there is one type of collagen that meets the definition of "scar tissue", "plaque" or whatever name you want to call it, and it may not vary much in thickness from normal tissue, if at all.  And it tends to contract and stiffen.  While I know some of my views are controversial and probably a number of them are just plain off the wall (disclaimer), I see the tendency of tissue to "contract" as simply the inverse of "elasticity" which is typical of NORMAL collagen populated by a typical amount of elastin.  If you haven't experienced non-palpable plaque, you probably won't understand, but the common denominator is that if you were to put any of this tissue under a microscope, palpable or not, it would exhibit precisely the properties described above.  And if there is enough of it, in the right place, and at the right degree of 'maturity', it will result in deformity ("curve", etc.)  Now Tim can come and tear this apart and we will all learn more as a result.  I simply can't express emphatically enough what a great asset Tim is to this forum.  We are all blessed to have him here with his unique insights and expertise.  - George
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Hawk

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Re: What causes Curve
« Reply #59 on: July 30, 2007, 09:59:32 PM »

In my not so humble opinion, curve is caused by ONE THING.  One side of the penis not expanding at the same rate as the other.  This in turn can only be caused by one thing, normal "elastic" tissue on that side has been replaced by scar tissue (plaque).

Subtleties like location (tunica or cavernosa) can determine whether the plaque can be felt with the fingers (palpable) or not but it has to be there.  Also distribution, as in one large area or many lesser areas on the same side may effect palpability.  Finally it could be that in the inflammatory stage some plaque just develops faster and is more inflamed, and is therefore more palpable.  We all know plaques tends to reduce in size as it matures.

Bottom line, there may be a host of things that determine if we can actually feel the plaque but if there is a curve, we don't have to wonder it is there.
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Hawk

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PS: To last post
« Reply #60 on: July 31, 2007, 07:27:04 AM »

For new members I want to make it clear we are talking about the onset of a curve that was never there, not a congenital curve that always existed (from birth or puberty) because of the hereditary structure of the penis.
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Larry H

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Hawk and "What Causes Curve"
« Reply #61 on: July 31, 2007, 07:36:23 AM »

Hawk:

Great Job! Easy for all to understand and to the point.

Larry
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Liam

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Re: At Last
« Reply #62 on: July 31, 2007, 08:23:27 AM »

Quote
Bottom line, there may be a host of things that determine if we can actually feel the plaque but if there is a curve, we don't have to wonder it is there.

This is all I've been saying.  I conceded a long time ago that maybe in some circumstances someone may not recognize the plaque by touch.  But it has to be there.

I said:
Quote
What causes the bend if not plaque (palpable or otherwise)?

I must say, however, if I had a curve and could not feel the plaque, I would have imaging done until I found out for sure what was causing it.

I can even live with what George said.  But there has to be something there.

I feel some closure.   :)

Two exceptions on which all will agree, though:

1)Congenital Curves -No plaque;  No Peyronies Disease (as Hawk said)

2)Trauma that directly compromised tissue of the penis causing a curve. - Lacerations, abrasions, burns, body modification (art) etc. - no Peyronies Disease


Now if you guys could find me that miracle case of a documented spontaneous recovery, I might start singing Kumbaya and ask for a group hug..............On second thought... ;)
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Hawk

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Re: Liam - At Last (hmmmmm!)
« Reply #63 on: July 31, 2007, 09:12:56 AM »

2)Trauma that directly compromised tissue of the penis causing a curve. - Lacerations, abrasions, burns, body modification (art) etc. - no Peyronies Disease

The injury in the above quote could lead to Peyronies Disease or it could cause a curve without Peyronies Disease if the injury and resulting natural scar tissue were very significant.
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Tim468

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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #64 on: July 31, 2007, 09:43:11 AM »

The tissue of Tunica from men with Peyronies Disease is abnormal elsewhere - not just in the plaque (remember the article?).

Plaque is heaped up and thickenedscar tissue with elements of collagen, fibroblasts, osteoclasts, etc. If it is not heaped up, it may not be easy to feel, but that does not mean it is any more or less stretchable.

Therefore, one can have no palpable plaque, but be histologically, and "elastically" abnormal, and thus not stretch out as well. That leads to a curve.

Think of taping a wad of paper to a balloon with duct tape, versus applying a thin piece of scotch tape. In both circumstances, the balloon will bend when inflated because the tissue is not stretchy right there.

The only thing that is remarkable about plaque is that it is palpable (ie thickened). That does not mean that non-palpable tissue is normal. If one develops a bend in the penis, or a dent, without a plaque, that is still Peyronie's Disease.

I am baffled why this seemingly simple concept gets so much debate.

Tim
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Re: Tim
« Reply #65 on: July 31, 2007, 12:36:54 PM »

Tim,

Can I impose on you about the location of that article?  I do remember that there are identifiable abnormalities in the general tunica tissue of Peyronies Disease patients separate from the plaque.  I specifically do not recall if it clarified what those abnormalities were.  In other words did it more or less state that these changes include a lack of elasticity?

Any response other than  Duh! will be appreciated.  ;D
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George999

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Re: Plaque ...
« Reply #66 on: July 31, 2007, 12:50:00 PM »

Tim,

I am convinced that the confusion here ALL revolves around the definition of the term "plaque".  Some define plaque as "scar tissue on the tunica", some define it as "any abnormal tunica tissue", and others like you, define it as "palpable thickened tissue".  I think that if we could get past this whole semantic struggle, it would really help us to find common ground in this discussion.  Since I think you have more insight in this area than most of the rest of us, I would suggest that we follow your lead and define plaque as:

"heaped up and thickened scar tissue with elements of collagen, fibroblasts, osteoclasts, etc."

All the while realizing that other non-thickened abnormal tissue in the tunica could be causing deformity.  In the case of congenital issues, the differentiating factor is that the tissue in question is NOT abnormal.  Rather it is ONLY asymmetric in dimension.

Thus what marks Peyronies is the abnormality of the tissue composition, not whether or not it is palpable or whether or not it is considered to be "plaque".  I suppose that it could all be classified as some form of "scar tissue", perhaps Tim could comment further on that.

Hopefully this explanation will satisfy Hawk and Liam and we can all achieve the same page on this issue.

- George

PS - Just to demonstrate how quickly medical science is moving these days, researchers have just announced that they have discovered what is potentially an extremely simple and effective crackerjack cure for juvenile onset type 1 diabetes:
http://www.healthday.com/Article.asp?AID=606783
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Tim468

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All Tunica involved
« Reply #67 on: July 31, 2007, 01:19:53 PM »

Here is the abstract - I have not gotten the entire article (it is in a Serbian Journal, written in Serbian)(and the translation of the abstract is poorly done. But the message is clear. In about 67 percent of patients where they excised "normal looking" tunica opposite of the lesion to do a NEsbit procedure, it abnormally stained for "fibrosis". Presumably, the H and E stain was for fibroblasts or similar cell types (it is not a stain used for collagen generally). The take home, though, is that it is not normal when it looks normal macroscopically. It might go without saying, but shall not, that if it looks normal, it would palpate as normal through the skin as well!

Authors: Nale D., Mii S., Vukovi I.,  Radosavljevi R.

Institute: Institut za urologiju i nefrologiju, Klinicki centar Srbije,  Beograd.

Titile: [Induratio penis plastica--localized or diffusive fibromatosis of tunica albuginea penis?]. [Serbian]

SO Vojnosanitetski Pregled.  63(11):939-44, 2006 Nov.

Abstract:

BACKGROUND/AIM: The part of the tunica albuginea that is not affected by localized pathological fibrosis is excised by the Nesbit contralateral excisional corporalplasty in patients with induratio penis plastica (IPP). The aim of this study was to find out if there were any histological changes of the macroscopically normal tunica albuginea excised during the Nesbit corporalplasty.

METHODS: A total of 31 patients, mean age 45 +/- 7.65 years, were surgical treated for extensive penile curvature (impossible or difficult penile imission in the vagina), using the Nesbit surgical technique. The tunica albuginea tissue was manipulated by Allis's clamps and excised in the shape of a diamond and placed in the 4% formaldehyde solution for histological analysis. The excised tunica albuginea was not wider than 1 cm, while the histological preparations were 3 to 5 microm thick, and they were stained with hematoxylin-eosin. The excised tunica albuginea tissue appeared macroscopically (anatomically) normal in all of the operated patients. In 28 (90.3%) patients opperated for dorsal curvature of the penis, the tissue of the tunica albuginea was excised from the urethral ridge, while in 3 (9.7%) patients operated for lateral curvature, the tissue was excised from the lateral corpus cavernosum.

RESULTS: The histological results were normal in 12 (38.7%) patients, while in 19 (61.3%) cases the findings indicated fibrosis of tunica albuginea.  No significant difference in the patients age was found between these two groups (p = 0.09). The analysis of a total number of histological results of the patients with tunica albuginea fibrosis in relation to the patients with normal results showed that there was no significant difference (chi2 = 1,2; df = 1; p > 0.05), suggesting that the macroscopically normal tunica albuginea is not always expected to yield normal histological result.

CONCLUSION: Significantly more reported histological results of tunica albuginea fibrosis in the location that appeared normal macroscopically (chi2 = 27.5; df = 1; p < 0.01) indicated that, in the majority of IPP patients (61.3%), pathological lesion was diffusive with localized phenotypic expression plaque in the tunica albuginea, showing that, in the majority of cases noxa acted diffusely.
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Hawk

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Re: Tim -
« Reply #68 on: July 31, 2007, 01:39:54 PM »

Thanks Tim,

I needed that second read.  I do not think I gave it careful attention the first time.  While it does clarify some things, like every answer, it raises a question or two.  If the abnormal tissue was taken from the opposite side of the plaque/curve, it would have to be concluded that it must stretch more than the plaque side thus the curve.  This may or may not mean it has normal expansion.

I was also a bit puzzled because in the case of dorsal curves they took tunica tissue from the opposite side (to be expected). But for
Quote
patients operated for lateral curvature, the tissue was excised from the lateral corpus cavernosum.
  That must be the opposite side but why the corpus cavernosum and not the tunica?

That last question does not require an answer, just thinking out loud.
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Re: What is the article telling me?
« Reply #69 on: July 31, 2007, 03:19:18 PM »

Tim:

Although I don't like what the article says, it is interesting. The question is then, what is it telling me, how do Peyronies Disease patients apply this information to the treatment of their condition? To use my case as an example, I have a very well defined thick band aid size strip of plaque on the top of the shaft causing a 70 degree upward bend. I always thought that my tunica was only diseased in the area of palpable plaque, now the article seems to indicate that perhaps all of my tunica albuginea is diseased.

So again, what is the practical application of this new information? For instance, if I was planning to run over to Norfolk to have surgery by Dr. Jordan should I now reconsider because the condition most likely will reappear in another location? If I have plaque incision or excision will it result in a bend in another direction because of the diseased un-palpable plaque in other areas?

All information is good (if it is correct) because it is educational. However, the best information has a practical application. Do you see a practical application for this information?

My Best,

Larry
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Tim468

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Hopefully a clarification
« Reply #70 on: July 31, 2007, 03:50:32 PM »

Hawk - I think this is a translation issue - that the tissue was the tunica over the corpus cavernosum, and the tunica over the urethral ridge. In the Nesbit, the plication is taken in the tunica - the tissue tolerances of the other tissue is such that it does not hold suture well (I think).

Larry - good questions - no answers.

I am not sure that there is "practical" value in this information. The point of sharing it is to remind us that what we can see and palpate is not always the entire story. Rather, there may be microscopic changes or physiological changes that are more generalized (a handful of articles show increased autoimmune markers in men with Peyronies Disease; increased evidence of other related diseases and so on).

I can't give you advice about what to do for you. For me, though, I know that if I had gone and gotten surgery at 25, I would be bending in other places by now, since the disease has continued to progress. It is more likely that someone like me has a more diffuse problem than someone with a history of injury during sex, development of scar/plaque, and a stable lesion. So I might avoid surgery, and the other fellow might be a perfect candidate.

What this goes to IMO is characterizing WHY some of us are different. Hopefully it can also help us understand why some of us might heal, while others do not, or understand why some get piled up plaque whereas others do not. And if it helps end the seemingly endless debate about plaque and what it is like (as if we are all the same), well then, all the better!

Tim
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Re: Yet another question ...
« Reply #71 on: July 31, 2007, 04:29:52 PM »

Amazing how every new piece of research seems to create more questions than answers.  Well here goes.  If indeed areas of the tunica unaffected by obvious disease, in fact, test out to be abnormal, then could it be possible that the abnormal histology was actually present PRIOR to the manifestation of Peyronies and in fact could have been a precursor to the Peyronies?  In other words, could it be that a man with an outwardly normal penis is actually extremely vulnerable from any tiny degree of trauma due to preexisting abnormalities in his tunica?  How is that for a question?  Any thoughts?  - George

PS - Why am I asking this question?  Well, because it seems like much of the effort in treating Peyronies is directed at treating the "plaques".  I see this as perhaps trying to treat and correct the symptoms rather than the underlying problem.  If the abnormal tunica that APPEARS outwardly to be normal is indeed a preexisting condition, and I have yet to see any evidence that would demonstrate it is not, it would seem that THAT is the physiological aberration we should be targeting and attempting to correct.  And, in fact, this is why I think that Larry is asking a VERY good question here.  On the other hand, Hawk makes a very good argument that the abnormal tissue is simply tissue that is left behind AFTER it has been over run by the moving line of plaque.  This would also make sense, in which case one would have to not only look at what could be done to treat the plaque, but also consider what might be able to be done to deal with the abnormal tissue left in its wake.  BUT in this case, Larry's fears might be unfounded, since the abnormal tunica might be the end result of Peyronies rather than a breeding ground for it.  My own personal history actually seems to support Hawk's theory as opposed to the theory of preexisting abnormalities since all of my deformations have had there locus in an area at one time affected by palpable plaque.  But I would certainly be interested in hearing how the experiences of others resonate with these two theories.  And then of course there is always the possibility that BOTH statements are true and that abnormal tunica can be either a precursor OR a product of Peyronies.  (more questions than answers ???)
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Re: Tim
« Reply #72 on: July 31, 2007, 04:38:20 PM »

Tim,

A bit off topic, but I was just reflecting on your long history with this condition and how it began at an abnormally young age with no injury (as I recall).  I was interested enough that I went looking for your history and found you had not posted one.  I know with such a long history it would take some time but it would be some rich information for many of us, especially the young guys just registering on the forum.  You have way to many posts for a member to try to piece it together.
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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #73 on: July 31, 2007, 04:45:44 PM »

tim468, what is the actual medical definition of the term "plaque"?  I I also have Dupuytren's contracture, which as I understand it is essentially the same thing in a different location - the tissue changes are identical.  The word "plaque" is never used in describing Duputyren's. 

I hear for example of "plaques" in the brains of people with Alzheimer's, an unrelated condition; so it seems like "plaque" is just a synonym for bad stuff, or maybe for unwanted accumulations of tangled proteins.
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Re: Yet another question ...
« Reply #74 on: July 31, 2007, 04:53:10 PM »

In other words, could it be that a man with an outwardly normal penis is actually extremely vulnerable from any tiny degree of trauma due to preexisting abnormalities in his tunica? 

George,

I recall an old study where the tunica of some small number of men dying from accidents were examed postmortem and many with no clinical signs of Peyronies Disease were found to have  some sort of Peyronies Disease like changes to the tunica.  It may have been a French study. Sorry to be so vague but it raises the question of was Peyronies Disease just developing or would these tunica abnormalities be there for years prior to Peyronies Disease. 

At what age do would the abnormalities present through tissue samples?
Would they appear from puberty, only as the disease is manifesting, or is the onset of the disease very slow and the symptoms only manifest at the last stages?

Just a few more reasons we need widespread awareness and research.

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Re:Peyronies Disease in Women
« Reply #75 on: July 31, 2007, 06:58:29 PM »

George said
Quote
All the while realizing that other non-thickened abnormal tissue in the tunica could be causing deformity.  In the case of congenital issues, the differentiating factor is that the tissue in question is NOT abnormal.  Rather it is ONLY asymmetric in dimension.

Thus what marks Peyronies is the abnormality of the tissue composition, not whether or not it is palpable or whether or not it is considered to be "plaque".  I suppose that it could all be classified as some form of "scar tissue", perhaps Tim could comment further on that.

Fibrosis may be a better term.  So, if the curve is caused by fibrotic tissue, it is Peyronies Disease.

Tim said:
Quote
The only thing that is remarkable about plaque is that it is palpable (ie thickened). That does not mean that non-palpable tissue is normal. If one develops a bend in the penis, or a dent, without a plaque, that is still Peyronie's Disease.

I assume you meant without plaque but with fibrotic tissue. 


Guys,  the reason this has been an issue is because of a large group young men with no palpable plaque and nebulous symptoms (atypical at best).  All of these pointing away from Peyronies Disease, at least by traditional definitions. 

Hell we can be real open.  Lets include women.  If we don't need plaque, why does the patient need a penis.

Quote
Diabetes mellitus produces significant adverse effects on the hemodynamic mechanism of clitoral engorgement and leads to diffuse clitoral cavernous fibrosis in a rabbit model.[22]
Source:  http://www.medscape.com/viewarticle/488894_4    - Sildenafil and Clitoral Arterial Blood Flow

My point is...sometimes it is NOT Peyronies Disease.

I know, I know... I'm a little over the top on this one.  My exaggeration is to make a point.  But, I will not be surprised when someone says they are probably related (maybe they are).  ??? ;) ???
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Liam - Women with Peyronies Disease
« Reply #76 on: July 31, 2007, 07:11:30 PM »

Liam,

I have to say this.  To me you almost seem to have an obsessive compulsive desire to narrow the definition of Peyronies Disease to limits that few if any can support.  Are you vying for some exclusive status as the world's only Peyronies Disease patient.  PDMAN What a chick magnet that is. ;D

Also, on your clitoris post.  I have actually wondered that since a clitoris has erectile tissue and the embryonic origins are the same, why women don't get Peyronies Disease.  I concluded they might well get it but who would notice or really care since it would have no impact on functionality.  You just verified it for me.  It may add a whole new dimension to the Ladies Room.
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Re: Abstract - Histological Changes
« Reply #77 on: July 31, 2007, 07:12:42 PM »

Quote
RESULTS: The histological results were normal in 12 (38.7%) patients, while in 19 (61.3%) cases the findings indicated fibrosis of tunica albuginea.  No significant difference in the patients age was found between these two groups (p = 0.09). The analysis of a total number of histological results of the patients with tunica albuginea fibrosis in relation to the patients with normal results showed that there was no significant difference (chi2 = 1,2; df = 1; p > 0.05), suggesting that the macroscopically normal tunica albuginea is not always expected to yield normal histological resultAre these just biomarkers for Peyronies Disease?

Are these possibly just biomarkers?

Biomarkers-Substances in the blood whose levels can indicate the presence or extent of disease.
www.dcri.duke.edu/patient/glossary.jsp

Biomarkers-Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers.
www.spineuniverse.com/community/cancerdictionary.html
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Re: Defining Peyronies Disease - Words Have Meanings
« Reply #78 on: July 31, 2007, 07:42:40 PM »

My search is for truth.  I know your statement is as exaggerated as mine.  I might get on "Who Wants to be a Superhero", though.  Just add SUPER PDMAN  ;)

I said:
Quote
So, if the curve is caused by fibrotic tissue, it is Peyronies Disease.

By anyone's definition, this is pretty inclusive.  How can you or anyone find fault with this statement?


It is just when I read about someone using drugs and alcohol and over masturbating and noticing a dent that comes and goes and an erection that is not as firm as it once was and two doctors said it wasn't Peyronies Disease but he didn't trust them, I have a hard time defining that as Peyronies Disease.  Granted that was an amalgam of several posts.  it does serve to illustrate my point.

I have softened my view about palpable plaque, although noone here with Peyronies Disease has said they have NON palpable plaque.  Hard to find was the strongest descriptor I've seen.  With the feeling going away in my fingertips, though, I can imagine....maybe....someone couldn't feel the altered tissue. 

Think about my questions for a minute.

What causes the curve?

Has spontaneous recovery been clinically documented?

These are two BASIC questions.  The answer to these is absolutely essential if we hope to find a cure.  So, I reject the implication (although done in jest) my querries are somehow self serving.

Also, if it is not important to understand what the plaque or fibrosis is and we accept the view that trauma leads to Peyronies Disease, we can just tell men, "It is just a callous from over use." ;)
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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #79 on: July 31, 2007, 08:33:07 PM »

I like to keep coming back to comparisons to Dupuytren's disease.  As per this paper (and others I've seen), the tissue changes are essentially identical - given the large number of men who have both, they may be just 2 expressions of the same disease. 

http://cat.inist.fr/?aModele=afficheN&cpsidt=16035818


As far as I know, the incidence of spontaneous resolution of Dupuytren's is zero.  Absolutely unheard of.  And I've been following this closely for about 10 years.

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Re: Dupuytrens and Peyronies Disease
« Reply #80 on: July 31, 2007, 10:01:42 PM »

Quote
they may be just 2 expressions of the same disease.
 

Expressed well :)
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Defining the Clinical Characteristics of Peyronie’s Disease in Young Men
« Reply #81 on: August 01, 2007, 09:13:46 AM »

Defining the Clinical Characteristics of Peyronie’s Disease in Young Men
Serkan Deveci, MD , Carin V. Hopps, MD , Keith O’Brien, MD , Marilyn Parker, RN , Patricia Guhring, RN , and John P. Mulhall, MD Department of Urology, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, NY, USA
Serkan Deveci, MD, Department of Urology, Weill Medical College of Cornell University, New York Presbyterian Hospital, 525 E 68th Street, New York, NY 10021, USA. Tel: +1-212-746-5653; Fax: +1-212-746-0403; E-mail: drdevecitr@yahoo.com
ABSTRACT
 
Introduction. Peyronie’s disease (Peyronies Disease) is usually seen in men in their fifth decade of life.

Aim. In this study, we investigated the characteristics of the disease in young men.

Main Outcome Measures. The demographics, clinical features, and associated comorbidities of the patients with Peyronies Disease were retrospectively reviewed.

Methods. The findings were compared between men with the disease who were under 40 years of age with those over 40 years. Statistical analyses were conducted to define differentiating features between these two groups.

Results. Of the 296 patients, 32 were under the age of 40 years and 264 over 40 years. The mean duration of the disease was 2 ± 4 and 6 ± 8 months in the respective age groups. Fifty-six percent of the patients under the age of 40 years and 75% of the patients over this age presented with curvature (P < 0.01). Thirty-seven percent under 40 years and 12% men over 40 years had more than one plaque at presentation (P < 0.01). Dupuytren’s contracture was seen only in patients over 40 years of age. Pain at presentation was found in 75% under the age of 40 years and in 65% over 40 years (P = 0.03). Trauma history was found in 18% under 40 years and in 5% over this age (P < 0.01). Statistical significant differences were found between the groups under and over the age of 40 years for hypertension (P < 0.01) and dyslipidemia (P < 0.01). Diabetes was noted in 50% of the patients under the age of 40 years and in 18% of the patients over this age (P < 0.001). Multivariate analysis of conditions associated in men with Peyronies Disease under 40 years of age showed statistical significant differences for diabetes (P = 0.015), presentation within 6 months (P = 0.004), and having multiple plaques (P = 0.008).

Conclusions. Young men with Peyronies Disease are more likely to present at an earlier stage of the disease, to have diabetes, and to have more than one plaque at the time of presentation. Deveci S, Hopps CV, O’Brien K, Parker M, Guhring P, and Mulhall JP. Defining the clinical characteristics of Peyronie’s disease in young men. J Sex Med 2007;4:485– 490

Source:  http://www.blackwell-synergy.com/doi/abs/10.1111/j.1743-6109.2006.00344.x?journalCode=jsm
The Journal of Sexual Medicine
Volume 4 Issue 2 Page 485-490, March 2007

Can't remember if this had been posted here or not.
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Re: Study/Hawk
« Reply #82 on: August 01, 2007, 09:43:04 AM »

Hawk:

The study you mentioned to George goes back almost 40 years. It was in an article by B.H. Smith called Subclinical Peyronie's Disease and published in the American Journal of Clinical Pathology. It was a study of autopsy's done one 100 men who had no known Peyronie's Disease. Out of the 100 men, 22 were found to have "asymptomatic fibrotic lesions of the tunica albuginea".

Larry
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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #83 on: August 01, 2007, 10:55:33 AM »

Liam,

In your quote that refers to biomarkers, I am not sure what you are quoting. The article I referenced did not mention or use the term biomarkers.

I think it would be very useful, and in fact I consider it inevitable, that biomarkers will eventually be used to identify those at risk for developing Peyronies or other fibrosing disorders.

I still do not get it with the your (Liam's) perseveration about plaque. All that it is is palpable fibrotic tissue. The tissue may be non-palpable, and yet be fibrotic. One could say it is "not as advanced", but if you have a bent penis and pain, what is the difference? Why is limiting either the definition, or the discussion, to "palpable" helpful? I do not see it that way.

Having looked at such tissue under the microscope, I cannot fathom the difficulty in accepting that some abnormalities of tissue structure may not be palpable through a layer of skin by a human finger. Is the digital dexterity of a urologist to be the defining diagnostic characteristic of a disease!? Maybe when the disease was first described, but not now. That is why they use ultrasound, or MRI - to see if they can extend their diagnostic accumen such that men can be helped.

Finally, the study that described the increased frequency of "asymptomatic" plaque is intriguing, for it suggests not that such men had no problem, but that they did not ask for help. I believe that onereason for an increased reporting of Peyronie's (according to a talk at a national conference) is due to increased willingness for men to seek help, and an increased expectation that sexual activity is their right, even in later middle age. We owe a lot of that to the "sexual revolution" and the release of Viagra on the market.

Tim
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Re: Autopsy Study
« Reply #84 on: August 01, 2007, 12:08:49 PM »

Tim:

If you are referring to the autopsy study that Hawk mentioned some posts back, I have also found it most intriguing. My take has always been that the men in the study didn't know they had a problem so of course they didn't seek help. However, after reading your comments and looking at it in a different light perhaps some or all knew they had a problem but concealed it and didn't seek help. With the study going back to the less enlightened time of the late '60's that certainly could be the case.

Of course the 22% incidence is what really caught my attention. I first saw reference to the study in a Peyronie's review article authored by several urologists including Tom Lue and printed in The Journal of Urology in 2003. They went on to say that the study suggested that these asymptomatic lesions may develop in the natural course of aging and sexual activity.

Larry
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Re: Asymptomatic fibrosis ...
« Reply #85 on: August 01, 2007, 12:18:07 PM »

The assumption that these men DID NOT ask for help is also suspect.  My experience with uros tells me that back in those days those men may well have complained only to be told by their docs that the problem is "just a part of the aging process and there is nothing to be done for it", end of complaint.  Those days were just so different from the time in which we live now in which we all tend to EXPECT solutions to our afflictions and we are very put out when medical technology fails to deliver.  Back then we were all just thankful that our hearts were continuing to beat for another day.  We would mention things to our docs and would rejoice at the answer "well ... it won't kill you".   ;)  - George
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Re: Plaque
« Reply #86 on: August 01, 2007, 02:57:50 PM »

Tim,

I was raising the point that these may well indeed be (used as, I'm not sure of the grammer) biomarkers even though the author of the paper did not label them such.

As for the plaque issue, here is what I previously said.
Quote
So, if the curve is caused by fibrotic tissue, it is Peyronies Disease.
and
 
Quote
I have softened my view about palpable plaque, although no one here with Peyronies Disease has said they have NON palpable plaque.  "Hard to find" was the strongest descriptor I've seen.  With the feeling going away in my fingertips, though, I can imagine....maybe....someone couldn't feel the altered tissue. 
I added the quotes to hard to find to help readability.


Here is what you said,
Quote
I cannot fathom the difficulty in accepting that some abnormalities of tissue structure may not be palpable through a layer of skin by a human finger.

Seems I extended that possibility.  You just don't hear of it happening very often.  I do think if it is hard or thick enough to bend a penis, a good physician should be able to feel it.  But, if they can't, they can get an ultrasound.  Not that it will change anything other than a few bucks for the procedure. 

I found this in a paper you submitted.  I bring it up to substantiate why I could think a person with a curve should be able to feel something.
Quote
Definition
Peyronie’s disease is a primary and progressive
fibroblast proliferation of the albuginea of the
penis. It could also involve the corpus cavernosum
and the septum in the later stages. Collagen and
calcium deposition are accompanying patterns.
This last phenomenon provokes penile curving
,
which may affect vaginal penetration.
I think your views and George's views on the autopsy study may be dead on.  The guys died, for goodness sake.  Maybe a few of them were sick and had bigger worries than a knot or thickening in their penis.  More than a few probably had Erectile Dysfunction and may not have even known.  The possibilities are numerous.

Now my one remaining outlier view is there is no spontaneous recovery.  FIRE AWAY!!! ;D
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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #87 on: August 01, 2007, 03:23:42 PM »

George:

That is also a real possibility as times have certainly changed, and in some respects it's a hell of a shame, but that's the way it is. I remember several years ago my urologists asked me if I knew of any history of Peyronie's on either parents side. I laughed and told him that my parents and my wife's parents wouldn't even discuss cancer much less a bent penis. I wasn't about to know if my father or uncles had Peyronies Disease.

We are talking about a study that came out in 1969, an autopsy study, so you would assume that when these folks were among the living their Peyronies Disease went back to the '50's and possibly beyond.

Of course we are doing a lot of speculating in this area of the study. However, there is one solid fact of importance and that is that the study indicated that 22% of the cadavers autopsied had tunical lesions. Now when I first read this my take was that these 22 men had undiagnosed Peyronies Disease, but when thinking about what asymptomatic, fibrotic lesions means I'm not so sure. My laymans simplistic definition would be "a non-diseased abnormal change to the tunica caused by trauma" (this also squares with the Lue paper suggesting the lesions developed from the natural course of aging and sexual activity). I stand to be corrected if I'm off base with my definition, but if I'm substantially correct does it mean that these men did in fact have undiagnosed Peyronies Disease, or the precursor to Peyronies Disease. Any thoughts?

Larry
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Re: Where is the Smith Paper
« Reply #88 on: August 01, 2007, 03:39:34 PM »

Is there a copy I can read?  I know I've read it in the past.  Its nowhere to be found on my computer now :(
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Re: Smith Paper
« Reply #89 on: August 01, 2007, 04:04:46 PM »

I have never read the actual paper, I've only seen it referenced in several more recent papers in discussions about the incidence of the disease. Since it's 38 years old it may be hard to get a copy.
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Re: Plaque
« Reply #90 on: August 01, 2007, 04:16:38 PM »

Now my one remaining outlier view is there is no spontaneous recovery.  FIRE AWAY!!! ;D

Well Liam my friend, let me take that first shot.  My contention is that there are, in fact, plenty of known cases where men suffer severe penile trauma and heal flawlessly.  This fact alone should call into question your position on spontaneous remission.  NEVER say NEVER, remember that old standby?  If people can heal flawlessly from major trauma, that is an indication that there is some underlying condition causing a FAILURE to heal properly in some cases.  So from that one can deduce:

No underlying condition = Complete healing
Severe underlying condition = Peyronies

But what about:

Mild occasional underlying condition = Potential Peyronies followed by remission?

You yourself are digging up stuff that points in that direction.  Many people have speculated that TGF-beta-1 is the driving force behind Peyronies.  Now BMP7 is being credited with being the antidote to TGF-beta-1.  But BMP7 occurs naturally in tissues just like TGF-beta-1.  So perhaps the question that needs to be asked is not why Peyronies exhibits excessive TGF-beta-1 activity, but rather why Peyronies is typified by insufficient BMP7 activity.  Here again, this all points to a MAJOR metabolic imbalance with far ranging ramifications that go far beyond Peyronies.

So do we just pump the patient full of BMP7 like we give insulin to a diabetes patient or do we ask WHY is the patient BMP7 deficient in the first place?  What could be the major metabolic imbalance causing it?  I would once again suggest that all roads somewhere lead back to the major medical plague of our modern era - Metabolic Syndrome typified by insulin resistance and lipid overflow in the liver.  And here again, rather than pumping people full of insulin and Lipitor, we need to be asking what it is that is causing this whole cascade in the first place and how can we poke a stake in that wheel.  We have to start thinking about CURING people instead of just treating symptoms.  Once you get in that mode, you see the potential for INDUCING remission.

One of the first laws of troubleshooting is that you first fix what you KNOW is wrong and then you deal with the stuff you don't understand.  But that somehow doesn't translate over to the medical profession.  So we have people that we know are walking around with excessive levels of insulin, cortisol and serum lipids, but they don't get treated until AFTER the problem manifests itself and then they only get treated with a maintenance objective rather than looking toward a cure.

Widespread remission in the case of a whole slew of diseases is only going to come when we start at the basic metabolic level and fix the underlying problems and believe me, they CAN be fixed.  I have experienced that to the point of a complete cure of my 20yr+ affliction with hypertension and I plan to drive it even further to the point that I see some response at the Peyronies level.  If one can literally drive their hypertension into complete and full remission, it should certainly be possible to do the same with Peyronies.

Modern medicine has achieved great technology and skill, but it is also very myopic.  Example:  I had hypertension, so I was advised to follow a "low fat diet" and everything was pointed toward looking at LDL/HDL levels and ratios.  And it was suggested that I should be sure to consume foods with the endorsement of the Heart Association.  Well, part of achieving a "remission" with the hypertension was in realizing that much of that advice was simply wrong.  In the first place much of the food endorsed by the Heart Association was low fat, but loaded with sweeteners, everything from artificial no calorie ones to even corn syrup of all things.  WRONG ... WRONG ... WRONG!  These things just cause me to add weight which increased physical stress on my kidneys and cardio-vascular system which further drives up my blood pressure.  So you say, well that may be true of corn syrup, but not the artificial sweeteners.  WRONG again!  While artificial sweeteners contain no calories, they DO make people hungry.  Hunger not only causes you to eat more stuff which DOES contain calories, it also slows down your metabolism and so triggers two paths of weight gain right there.  It also feeds certain bacteria in the gut which stimulate weight gain.  And then there are the hypertension drugs that actually cause weight gain and just add to the problem.  EVERY hypertension patient, with rare exception, should be on a strict low glycemic (NOT low carb!) diet AND should be encouraged to consume selected fats since cutting the wrong kind of fats can also actually induce weight gain.  And docs should not be measuring progress just by fasting LDL/HDL, but rather also by lipid overflow, in other words non-fasting serum triglycerides which give a much more accurate picture of Metabolic Syndrome risks.  And weight objectives should not be measured on the old scale in pounds, but rather with a tape measure in terms of hip to navel circumference differentials.  At that point you would see a lot of people making some real progress toward health and you would see our current medical crisis begin to fade away.  And then I could repeat the same rant on the diabetes side where the whole myopic focus is on glucose rather than a holistic approach leading to research driven weight loss and restoral to health.  I have not mentioned exercise recommendations because the docs generally get that right.  So there.  Fire back!  ;D  - George
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Liam

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Re: George - Spontaneous recovery
« Reply #91 on: August 01, 2007, 06:19:37 PM »

I agree with most of what you say.  It's the conclusion I differ on.  What would happen to diseased tissue if a spontaneous recovery happened?  Would it detach from the healthy tissue and then get absorbed.  What chemical does the body produce that breaks this altered tissue down?  How long does the process take?  These are some of the questions that cause me to doubt spontaneous recovery.

I believe a cure can be found.  It may even be a "natural" cure.  I just can't believe the body goes haywire enough to produce this hateful fibrosis, then stabilizes, then corrects all the damage done and eliminates the fibrotic tissue.

I wish it would happen.

This does not mean I don't believe Peyronies Disease can and does stabilize.  Its the reversal I have problems with.
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George999

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Re: Plaque, etc.
« Reply #92 on: August 02, 2007, 11:33:48 AM »

Liam, remember that collagen is the "glue" that holds tissue together.  It is constantly being broken down and replaced by new collagen.  When the addition of new collagen occurs faster than the breaking down of the old collagen and/or when the new replacement collagen is the wrong type, fibrosis is advancing.  When the breakdown is exceeding the accumulation and/or when the replacement collagen is of the appropriate type, fibrosis is being eliminated.  Remember, this is all happening on the cellular level.  Its not like on one side you have perfectly normal tissue and on the other it is fibrotic.  It happens in degrees and the whole process is very dynamic even when it appears to our senses to be stable.  There is constant turnover of collagen even in scar tissue.  And somewhere there is a metabolic key that tells the body that scar tissue is no longer appropirate and that it is time to begin laying down normal collagen.  That is what needs to be identified and BMP7 begins to look very interesting from that perspective.  TGF-beta-1, on the other hand, plays a key role in encouraging the never ending process of generating scar tissue, even when it is no longer needed.  But I understand your skepticism.  I had a difficult time believing that I could reverse my hypertension until I discovered the keys and was finally able to pull it off.  At this point, I believe that most if not all hypertensives and diabetics can achieve "remission" if they are willing to address the root of the problem.  But it was hard to see it that way before when numerous experts were telling me that it was impossible to achieve.  I experienced grave doubts and times where I wondered if I was just fantasizing.  But now I see things from a whole different perspective.  The human body is truly amazing and its recuperative capacity is beyond belief.  But to capitalize on that, basic dysfunction has to be addressed and corrected and we know enough these days to achieve that.
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Tim468

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Another intriquing paper
« Reply #93 on: August 02, 2007, 01:52:09 PM »

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=14996430&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

Again, the better stuff seems to come out of his (Gonzalez-Cadavid) lab - this is the paper that got others like Lue into looking at Pentox, I believe.

Tim
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52, Peyronies Disease for 30 years, upward curve and some new lesions.

Liam

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Re: Spontaneous
« Reply #94 on: August 02, 2007, 06:07:24 PM »

George,

If you have to alter your diet and take supplements, we are talking about a cure (which is a GOOD thing  :) ) not a spontaneous recovery.  I know that seems what some would call playing semantic games.  My point is it ain't gonna get better on its own.  We will have to do something.  This may be surgery, injections, pills, creams, regulating diet, supplements or a combination of the aforementioned. 

One of my favorite sayings, which supports your views is:

If you always do what you've always done, you're always going to get what you've always gotten.



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percival

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Re: Another intriguing paper
« Reply #95 on: August 02, 2007, 06:11:47 PM »

Tim
This makes interesting and encouraging reading. However the doses given to the rats would, for a 13 stone guy, scale up to 186g/day arginine; 827 mg/day pentox or sildenfal. A bit on the high side!
Regards
Percival
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George999

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Re: Spontaneous Recovery
« Reply #96 on: August 02, 2007, 06:26:43 PM »

Liam,

This whole thing is most definitely a matter of semantics.  I really doubt if anybody recovers from anything for no reason.  But sometimes people recover for no apparent reason.  This IS a reason, we just can't put our finger on it.  And those are the cases that get referred to as spontaneous recovery.  So if you don't like that definition, thats OK because we are both on the same page in terms of concept even though we can't find agreement as to the words to express it.

- George
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percival

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Re: Spontaneous recovery
« Reply #97 on: August 02, 2007, 06:32:58 PM »

Current discussions on spontaneous recovery have made me recall the very first time I noticed a problem with my unit. 24 years ago at the age of 33 I discovered a small lump underneath in the spongiosum tissue around the urethra. It caused an indentation underneath when erect, but it was localised and not really visible from above and there was no pain or bend. Although concerned at the time, I was working overseas and left it alone. It disappeared completley after about 3 months - a spontaneous recovery.
Unfortunately, a year or so later plaque appeared on the side near the glans causing a 30 degree bend to the left. This plaque has never disappeared, but the bend has more or less gone because plaque also appeared on the right side. 7 years ago more plaque formed on top causing a 90 degree upward bend. I had surgery (incision and graft) to cure this.
So there is some truth in spontaneous recovery, but in my case it was fairly short lived and the Peyronies Disease returned with vengeance.
Regards
Percival
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Tim468

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Re: Defining Peyronies Disease - The struggle to understand the disease
« Reply #98 on: August 02, 2007, 07:03:53 PM »

Thanks for sharing Percival,

That is a perfect example of spontaneous resolution of a lesion. It happens, but some doctors hold onto theories so hard that if something happens that doe not support their theory, they claim it must be something else. Your example is good because it shows that it can appear in different places, with different effects, and different outcomes.

Tim
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52, Peyronies Disease for 30 years, upward curve and some new lesions.

Liam

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Re: We Should be More Spontaneous
« Reply #99 on: August 02, 2007, 09:36:45 PM »

Quote
...but some doctors hold onto theories so hard that if something happens that does not support their theory, they claim it must be something else

Wait!  I'm not a doctor.  I just play a cynical, arrogant one on the forum.   :)  I'm really a Teddy Bear.  ;)

If SR happens so often, why is there no case study out there.  Many doctors love writing that kind of paper.  I've seen phychics and ghost chasers with more clinical evidence.

Percival, 

Anytime someone notices improvement, no matter how short lived, I'm happy for them.  Don't think I'm criticizing you.  Your story is interesting.  It is not proof of spontaneous recovery, though.  The initial condition was in an unusual place for Peyronies Disease.  Could it have been another condition?  If it was, maybe there is a relationship to the Peyronies Disease.  If it was Peyronies Disease, it obviously didn't really go away.   BTW, did the lump get smaller and smaller or was it just gone one day (serious question)? 

This is the closest thing I've heard, though.   :)

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