CAUSES of Peyronie's Disease - started 2005

[DannyOcean]

Hi George,
I think there is some kind of link out there with stress and Peyronies Disease? Now that when I look back I was under a tremendous amount of stress. I don't remember injuring my penis and I was not having wild sex but I do remember having a lot of stress during the time when I discovered I had Peyronies Disease. Interesting...

If I were to map out stress levels for the last decade of my life the peak of my stress came at almost exactly the same time I contracted Peyronies Disease.  At least in my case I'd say there was a correlation.

[George999]

Perhaps one of the largest benefits I've derived thus far in terms of my Peyronies Disease has to do with attacking inflammation.  Both directly with anti-inflammatory supplements and with anti-oxidants that have an anti-inflammatory effect.  But a big question hanging out there is where does all this inflammatory environment come from in the first place?  Well, there are some leading edge researchers that believe they have the answer to that question.  They believe that answer lies in a little know organ known as the Omentum which is turning out to be a major potential source of toxic chemistry in the body.   And part of that toxic effect is a sub clinical systemic inflammation syndrome.  But the good news is that there are things that can be done to normalize it in terms of diet and exercise.  I am now well along in that process and am hopeful that by getting systemic inflammation out of the picture, I will be able to better get a handle on the localized inflammation that is causing my Peyronies.

PS - The book I am deeply into right now is:

http://www.amazon.com/You-Owners-Manual-Waist-Management/dp/0743292545/sr=8-1/qid=1168638078/ref=pd_bbs_sr_1/102-4473680-5252927?ie=UTF8&s=books

It is quite an eye opener!

- George

[DannyOcean]

My gut tells me you're on to something George.  I'm reading Fantastic Voyage (highly recommended) and it talks a lot about inflammation in terms of aging and a factor in disease.  I think there's a very good chance that Peyronies and inflammation in the body are highly correlated.  I'm going to dive deeper into this stuff too and will post what I find.

Subject added by forum moderator.

[Hawk]

A lot of members discuss inflammation.  Sed rate is a blood test marker for some inflammatory conditions but probably not all such conditions (my knowledge is limited on this topic).  Have any members tested their sed rate or monitored the effect of supplements and diet on sed rate?  

[DannyOcean]

I'm planning on going to see a doc soon who believes in using Western medicine as a diagnostic tool in addition to the "Houston we have a problem" approach that most docs employ after a condition has already reached visible proportions.  I'm going to have a bunch of tests run and so I'll hadd this to the list.  I plan to do the tests on a regular basis going forward to monitor how my health improves.

A lot of members discuss inflammation.  Sed rate is a blood test marker for some inflammatory conditions but probably not all such conditions (my knowledge is limited on this topic).  Have any members tested their sed rate or monitored the effect of supplements and diet on sed rate?

[scott]

I recently had my sedimentation rate checked, along with a battery of other lab tests for a condition other than Peyronie's.  My sed. rate was normal.  This is intriguing, however, and it would be interesting if others have had theirs checked.

[mark501]

George 999, Thanks for bringing this to our attention. One of the authors of the book you are reading, Mehmet C. Oz MD, was on the Oprah Winfrey show recently discussing the Omentum. Hopefully this will be repeated sometime this year. You can type in OMENTUM in the search engine on her website www.oprah.com  OR  http://www.oprah.com/health/yourbody/slide/numberone/slide_yourbody_numberone_206.jhtml   to see photo of oprah w/Dr. Oz holding up an omentum. Hopefully Dr. Oz will inspire some of us to lose our excess fat & at same time reduce inflammation.

[George999]

There are currently a handful of serum inflammation markers.  Sed rate, C-Reactive protein, Homocystine, etc.  My personal opinion is that they are not able to present a totally accurate picture of systemic inflammation.  They do a better job of picking up acute inflammation, but chronic extremely low level systemic inflammation is very difficult to detect and its potential effects on general health are very disturbing.  I think a number of researchers and top docs have been onto this process for a long time, but it has taken until recently to pinpoint its source.  And pinpointing its source is leading to a revolution in terms of acceptable waistline measurements, height/weight ratios, daily caloric excess, etc. and even acceptable blood pressure numbers and blood sugar levels.  It has the potential to redefine health care in America and in the world.  It is that big a thing.  It points out why simply 'losing weight' is largely ineffective and why caloric based dieting has proved to be a disaster.  Americans have worse height/weight ratios and larger waistlines than ever before in our nations history, and all of this is happening in the face of more weight loss surgeries and diet plans than Carter has pills.  Something is clearly wrong and there is ever increasing evidence that it is affecting our general health and making us ever more prone to strange maladies like Peyronies.  And I am not asserting that this is a new problem, it is just becoming more widespread as the US and the rest of the world move from subsistence living to relative prosperity.  It is, at its root, a lifestyle problem, and I know that the purpose of this forum is not to discuss lifestyle issues.  But when there is growing suspicion that they are directly related to Peyronies and our purpose is to focus on that link, at that point, I believe the issue takes on validity for this forum.  Certainly there is no one magic pill to cure Peyronies and even lifestyle changes are not likely to do the job on their own.  I am convinced that it will take an orchestra of finely tuned vectors to take down this and other 'incurable' diseases.  And I have a real problem with the term 'incurable' that is often tossed around.  I believe that the more correct expression would be 'We do not yet currently know of a RELIABLE cure'.  The fact that at least a few cases of Peyronies and even Cancer spontaneously 'go away' should indicate that a cure is possible, it is just a matter of discovering and orchestrating as many of those potential vectors as possible simultaneously.  I am discovering more of those potential vectors all of the time and I am not planning to leave any stone unturned in my quest for health.  I am also EXTREMELY optimistic that most of us can get this disease under control and perhaps even eliminate it if we simply follow the relevant research and take appropriate action and have the patience for the time it takes to turn around a very big ship.

Best wishes to all of you for this New Year, may it be a new beginning for us all,

Sincerely,

George

[stillsearcin]

Beta blocker....Many plants have this effect...Have you ben taking anny...For a long time.../?
http://www.ars-grin.gov/cgi-bin/duke/activity.pl

[Liam]

An article I copied:

1: J Urol. 2007 Jan;177(1):179-82; discussion 183.
Brant WO, Bella AJ, Garcia MM, Tantiwongse K, Dean RC, Lue TF.
Department of Urology, University of California-San Francisco, San Francisco, California 94143-0738, USA. panditah@hotmail.com

PURPOSE: Classically Peyronie's disease presents with penile curvature and/or pain, and is associated with a palpable penile plaque. We frequently examine patients with suspected Peyronie's disease ultrasonographically and have noted a subset of patients in whom we could identify only a circumscribed septal lesion. We identified characteristics of these patients. MATERIALS AND METHODS: Of our series of approximately 650 patients with Peyronie's disease 47 were identified with these lesions. RESULTS: Of the 47 patients 22 presented with penile curvature with or without accompanying or preceding pain. Of the 47 patients 17 had a significant history of trauma, although only had the classic stigmata of penile fracture. A total of 16 patients had no history of curvature, 7 presented with only penile shortening or focal lack of rigidity and 5 were incidentally found to have lesions during assessment for other complaints. Three patients presenting after trauma were noted to have septal liquefied hematomas, which we aspirated under ultrasound guidance. Followup ultrasound revealed minimal septal thickening. In 1 of these patients the hematoma was adjacent to more typical-appearing septal fibrosis. CONCLUSIONS: We theorize that these hematomas are due to septal fractures and may represent a forme fruste or possibly a precursor lesion of more typical septal fibrosis. Ultrasonographic evaluation may allow earlier identification and treatment of occult septal injuries or lesions and prevent subsequent fibrosis and its associated symptoms.

PMID: 17162033 [PubMed - in process]

Source:  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17162033

More:

J Sex Med. 2007 Jan;4(1):226-30. Epub 2006 Oct 11.  Links
Nonpalpable Scarring of the Penile Septum As a Cause of Erectile Dysfunction: An Atypical Form of Peyronie's Disease.Bella AJ, Sener A, Foell K, Brock GB.
Department of Urology, University of California, San Francisco, CA, USA.

Introduction. Men with nonpalpable isolated septal scars (ISS) identified with color duplex ultrasonography (CDU) comprise a group of previously unrecognized patients with wide-ranging sexual concerns. Aim. We aim to identify the clinical characteristics of patients presenting with this atypical form of Peyronie's disease characterized by the absence of palpable deformity. Materials and Methods. Of 482 consecutive patients who presented to a tertiary care erectile dysfunction (ED) clinic and underwent CDU after satisfying inclusion criteria, 27 (5.6%) men with nonpalpable ISS and no dorsal or ventral plaque were identified. Main Outcome Measures. International Index of Erectile Function (IIEF), CDU, and clinical characteristics. Results. The median age of the men with nonpalpable ISS was 49 years. The length of time from onset of symptoms to presentation was 22 months, and the pretreatment IIEF score was 14. The remaining 455 men who underwent CDU were of similar age (48 years) but had a markedly lower IIEF score of 9.5 (statistical median). ISS patients presented with decreased penile rigidity (20), penile shortening (13), chronic pain with erection (13; mean 33 months), and the inability to maintain an erection (7). Fourteen men had failed phosphodiesterase-5 inhibitor therapy, and four reported unsatisfactory results. Management options included retrial with oral agents, intracavernous pharmacotherapy, verapamil injections, and surgery. Conclusions. The clinician should be suspicious for nonpalpable ISS in men with sexual concerns who present with decreased penile rigidity, length loss, and chronic pain with erection. Our findings support the use of CDU for this patient group, particularly when previous treatment has failed, because men with ISS had a greater likelihood of having no palpable deformity or curvature and ongoing penile pain. Bella AJ, Sener A, Foell K, and Brock GB. Nonpalpable scarring of the penile septum as a cause of erectile dysfunction: An atypical form of Peyronie's disease. J Sex Med 2007;4:226-230.

PMID: 17034410 [PubMed - in process]

Source:  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=search&db=pubmed&term=Sener+A[au]&dispmax=50

[George999]

Thanks Liam for those fascinating excerpts.  It is just so good to see that someone cares about finding treatments and solutions for this long neglected disease.  The more I have read lately, the more I am convinced that Tom Lue and his team at UCSF Medical Center are leading this charge.  Hopefully, they will not relent until they have come up with a cure.

- George

[George999]

I would suggest that it is useful, when one explores the causes of Peyronies Disease, to consider the causes of Fibrosis in general.  Unfortunately, for various reasons, the causes of most types of Fibrosis have received comparatively little attention from the research community.  But there is one form of Fibrosis that is currently challenging modern medicine to the point that it is receiving extensive research efforts in terms of both resources and sheer dollar investment.  That would be CKD or Chronic Kidney Disease which unlike Pulmonary Fibrosis (avoid tobacco and asbestos dust, etc.) and Liver Fibrosis (avoid alchohol and drugs, etc.), has no easy answers.  So much effort has gone into finding answers to this stubborn affliction and I believe there is much that we can learn from those answers.  The end result of all of this research is that Renal Fibrosis is caused by:

1)   Inflammation - Yes inflammation is number one on the list of causal issues for Renal Fibrosis.  And that is why inflammation should be a number one target for Peyronies sufferers.  How?
  A) By eliminating inflammatory foods.  Some foods, including red meats and saturated fats are highly inflammatory and should be eliminated from the diet as much as possible.  On the other hand, anti-inflammatory foods should be emphasized.
  B) By avoiding inflammatory supplements.  Some supplements have an inflammatory effect.  Whenever possible, choose supplements that are anti-inflammatory
  C) By avoiding inflammatory drugs if possible. Some drugs use inflammation as a means of therapy.  Whenever possible choose drugs that are anti-inflammatory.
  D) By making it a priority to get ALL localized infections and inflammation under control.  This includes dental issues, chronic low level urinary tract infections, etc.
  E) By maintaining a healthy waist size.  Excess fat within the abdominal wall is now known to cause inflammation.  How does this happen?  It happens because this specific fat releases unique and harmful substances into the blood which alter blood chemistry in a way that is favorable to fibrosis.  It also happens because the this fat causes physical pressure on other organs and  the arteries supplying their blood flow that causes them to also alter blood chemistry in a detrimental way.  If you have Peyronies, you need to do whatever is possible to deal with this issue.
  F) By getting sufficient and regular sleep.  Unhealthy sleep patterns can contribute to low levels of serotonin.  Serotonin levels that are either too high or too low can contribute to inflammation.
  G) By getting sufficient exercise.  Sensible exercise is known to lower inflammation.

2)   Reactive Oxygen-Nitrogen Species - This has to do with oxidation within the body.  It is strongly associated with faulty NO synthesis.  Some refer to it as the 'rusting away of the body'.  In any case, it has been identified specifically as a major contributor to Fibrosis.  This would indicate that oxidative foods should be avoided and foods and supplements with anti-oxidant qualities employed.  This would also indicate that healthy NO activation should be sought after.

3)   Vasoactive Peptides (ANG II, ET-1) and Aldosterone -  If these levels are out of range (typically with hypertension), they should be brought under control with appropriate drugs or lifestyle changes.  My suspicion is that even if these levels are mildly out of their normal range even with no overt hypertension, they could still be a problem for Peyronies sufferers.  Therefore, unless your blood pressure is below 115/75, you should be taking appropriate steps to get it down.

4)   Fibrotic Pathways Activated by ANG II (TGF-beta, PAI-1) - This is the basis for claims regarding products like Neprinol.  But attacking PAI-1 directly has proven problematic, since doing so can result in unintended side effects and may not be practical, but one proven method of attacking PAI-1 has proven safe and effective and that is Nattokinaise.  And as we know, there ways to attack TGF-beta and these should be utilized.

5)   Receptors of Tyrosine Kinase Growth Factors - I don't know of any way to deal with this one, but its on the list, so I throw it in.  On the other side of the coin, Hepatic Growth Factor has been shown to cause a regression of Renal Fibrosis.

6)   Extracellular Matrix Stabilizers (Integrins, Transglutaminases -  Here again, this is on the list, I don't know how one would deal with it except for the fact that there are known Extracellular Matrix destabilizers which should be employed whenever possible.

With this I think I have covered all the known issues in a nutshell regarding Renal Fibrosis.  I find it interesting to note the similarities here with what we already know about dealing with Peyronies.  I would suggest that we could learn much from Renal Fibrosis research that would be helpful in the treatment of Peyronies which is at its core simply Penile Fibrosis.

Hopefully, the above will serve as a springboard for more discussion on some of these issues.  Some of you out there may have insights as to some of the missing pieces of the puzzle, so feel free to build on this concept.

- George

[scott]

George,

Pulmonary fibrosis does not have any "easy answers."  There are five or six different forms of pulmonary fibrosis, depending upon what categorization scheme one considers.  Asbestosis is but one form.  There is an *association* with tobacco smoke exposure in two forms of pulmonary fibrosis, but  cause and effect has not been demonstrated; in fact, many people with idiopathic pulmonary fibrosis (IPF), the most elusive form (and the most common), have no history of known exposure to tobacco smoke.

What is interesting, in light of your post, is that most experts on IPF accept that inflammation is NOT a causal factor (they have come to this conclusion because prednisone, an extremely potent anti-inflammatory, has no "healing" effect on IPF).  Rather, it seems to be a problem with dysregulation of cytokines, including TGF-b1 and TNF-alpha, leading to proliferation and migration of fibroblasts and myofibroblasts, which in turn leads to production of extracellular matrix, or fibrosis.

If all this sounds familiar in terms of Peyronie's Disease and your post on Renal Fibrosis, it is because, in my opinion, they are all the same root problem.  Further, I am convinced that what will help one of these, will help all the others.  I am keenly interested in what is found to work on this forum because I suffer from both Peyronie's and IPF.  So, I do hope this leads to some good discussion.

Anyone else?

[George999]

Scott,

Thanks for the first hand insights on Pulmonary Fibrosis.  I had no idea that IPF was the most common form.  I wish you the very best in your battle against both IPF and Peyronies.

As for the inflammation issue.  I would suggest that the fact that Prednisone is unable to stop IPF in its tracks, but rather only seems to slow it down, is not necessarily an indication that inflammation is not a causative factor, or even the main causative factor.  It is only an indication that 1) Once the process starts, it is extremely difficult to reverse due to biological feedback mechanisms that are by nature degenerative, and 2) That it is possible that Prednisone, as good as it is, is not a perfect defense against inflammation.  Thus, in my opinion, it takes more than Prednisone to bring down inflammation AND it takes more than bringing down inflammation to bring fibrotic diseases to heel.  It takes literally attacking EVERY vector of this process simultaneously via multiple techniques to achieve even the slightest bit of headway.  And we are just now in the process of seeing those vectors identified.  I believe that the best model at this point is CKD because CKD seems to have a far higher profile in terms of research funding than any other fibrotic disease, and they at least have achieved a laundry list of sorts in terms of all the various factors (vectors) that go into promoting and inhibiting fibrosis.  I believe that what needs to happen is for every one of those vectors to be attacked simultaneously, and, I am not sure that even that is enough.  But it would certainly be interesting to see what sort of results could be gotten by doing so.

Again, I wish you the very best, and thanks for the great insights.  Surely we can learn a lot by merging the data on things like CKD and IPF and Hepatic Fibrosis as well.  There is just so much commonality here and I am convinced that most of what applies to one, applies to the others.  I also believe that it is really tricky sorting out what is genetic from what is environmental.  And even genetic diseases can require environmental triggers.  It all gets just so complex.  But the more we discuss it, the more we are learning from each other.

Sincerely,

George

[Tim468]

Thanks George and Scott for your very cogent posts. I just got my internet connections up a running, so will ponder this as I head off to bed.

Tim

[Hawk]

Great exchange guys.  I can add little except a to shine a light on a posible breakdown of communication on one point.  George replied to Scott

I would suggest that the fact that Prednisone is unable to stop IPF in its tracks, but rather only seems to slow it down, ...

Scott had said in part

prednisone, an extremely potent anti-inflammatory, has no "healing" effect on IPF).

A small difference but maybe one with significant implications in this discussion.

[scott]

I intended to respond to George on this point, but wanted to do a little more research on inflammation and IPF (on Google Scholar, which I learned about on this forum, and it is an excellent tool!).  I want to stress again the relevance of this discussion to Peyronie's, because it is my opinion that the processes in play in Peyronie's and IPF appear to be the same, or at the very least, quite similar.

The researchers in IPF are heading to the conclusion that prednisone alone not only does nothing for IPF, but may actually do more harm than good.  Prednisone does not "slow down" IPF, although prednisone given concurrently with azathioprine (a cytotoxic agent), *and* N-acetyl cysteine (NAC) at the same time, does appear to slow down the deterioration in some measures of pulmonary function.  Note that this does not represent improvement, but rather the slowing of what seems to be an inevitable decline in function.  It is unknown at this point whether it is the combination of the three agents, or the NAC alone, that causes this slowing in decline.  I am unable to find any conclusive studies on NAC alone, because well-designed clinical trials on dietary supplements are few and far between.

Returning to the issue of inflammation, I should have noted in my post that it is not only the lack of efficacy of prednisone leading to the conclusion that IPF is not an inflammatory process.  Tissue samples taken during open lung biopsies in IPF patients show little or no indication of inflammation going on.  All this has sort of turned IPF research on its ear, and this takes us back to the role of cytokines.

Reading about IPF research and Tim's posts on the role of cytokines in Peyronie's, I have been struck by the fact that the descriptions of the factors involved are almost exactly the same.  That is, TGF-b1 and TNF-alpha are a kind of on/off switch in the process of fibrosis.  A host of other factors are involved, but these appear to be at the beginning of the cascade leading to abnormal wound repair, or fibrosis.  Both cytokines are essential for normal wound repair, including microvascular injury, but the "switch" is in the always-on mode.  It is intriguing to consider, then, that if the cytokines could be reduced (inhibited) to normal levels, it might then stop the cascade leading to fibrosis dead in its tracks.  This is the hoped-for outcome with pentoxifylline, which inhibits TGF-b1 and TNF-alpha.  Tim also recently mentioned pirfenidone, a drug currently in IPF clinical trials around the country.  The best I can tell, pirfenidone would be a much more powerful inhibitor of TGF-b1 and TNF-alpha than pentoxifylline is, but the reality is that it is some time away from approval for IPF, and wouldn't be approved for Peyronie's anyway.  For personal reasons, I declined to participate in the clinical trials for pirfenidone.  So at this time, pentoxifylline is my best bet.  I'm taking pentox, hoping that it will stop the progression both of my IPF and my Peyronie's.  Note that I said, "stop the progression", because nothing I have read leads me to believe that either pentox or pirfenidone will reverse damage already done.  I'm also throwing NAC into the mix as a "can't hurt" intervention.

I'm still not sure about inflammation, and am interested in knowing more about any role it might have in Peyronie's and/or IPF.  I'm sure Tim will be checking in here pretty soon.  I hope to God he's not going to eat me alive for a simplistic rendering of IPF!!

[Tim468]

Because I see kids with lung problems, I don't have much experience with IPF. I have seen several progressive cases of pulmonary fibrosis after lung irradiation, a process with some similarities to IPF (and Peyronies Disease).

I agree with George that only a multi-pronged attack will help (may be the only) find a way to fixing Peyronies or IPF. All of the proposed avenues towards inflammation that could be addressed are also, in turn, affected by "upstream" mediators. A recent article in Peyronies research showed that the TGF may be induced by platelet activating factor (PAF1) - so going further up the stream to find the source is where we might be able to best affect the course of this process.

I am too tuckered out to go into why Steroids might not help, but physiologically, it may be more of a matter of closing the barn door after the cows get out (horses??). So steroids may not be specific enough to stop the pathologic processes, and their general helpfulness is also their curse - they act generally and also cut off function of a lot of good stuff (like your immune function) so use of steroids comes at a great cost. There is no good data that steroids (oral or injected) help in Peyronies, either.

Tim

[George999]

First of all, I have some real issues as to how the medical community defines 'inflammation'.  It was not that long ago that inflammation was only detectable in acute cases.  Now we have some pretty straightforward tests that can detect much more subtle forms of inflammation.  But I am not sure that we have reached the root of the problem just yet.  I, rather, believe that extremely low level inflammation can be localized, contained, and encapsulated by tissue in such a way that it is virtually undetectable by current technology (I am not even convinced that extremely low level systemic inflammation can be detected by current technology).  I also believe that ischemia and inflammation go hand in hand.  I would suggest that in the case of fibrosis, you end up with a localized area of contained inflammation and toxic pathology that is, by its very nature, putting out toxins that are poisoning adjacent tissue.  This is the process that therefore must be addressed.  And this abnormal tissue is going to be so atrophied and ischemic that you are simply not going to get any anti-inflammatory (or immune suppressive) substance into it via bloodflow in any amount that can be effective.  And you have to remember that as this fibrosis is expanding, it is causing that same ischemia in surrounding tissue.  Part of the effect of Pentoxifylline is its ability to make red cells more flexible, thus oxygenating areas that would otherwise be ischemic.  As for Prednisone, although I really did not want to get into this area because some people really need to be taking it, I have to agree with Tim, that like most other drugs (and supplements), Prednisone is far more than simply an anti-inflammatory.  It carries a pretty broad and extremely potent payload that may or may not be helpful in the case of fibrosis.  Actually, I am very familiar with Prednisone as I have taken it before myself for ITP, another one of those idiopathic (how I hate that word) things that has an autoimmune component.  The two substances that are the most interesting to me in terms of fibrosis at this point are in fact Pentoxifylline and broad spectrum Vitamin E.  But I remain convinced that it is extremely important to knock out systemic inflammation in ANY case of fibrosis, but I don't necessarily believe that Prednisone is the best tool to accomplish that, despite its massive potency.  I believe that ANY degree of systemic inflammation, even at a subclinical level, will only feed the cytokine furnace that is slowly, but progressively, burning through our remaining healthy tissues.  But I would be the first to agree that that is only one step.  Every other facet on the list should be addressed with concerted and unyielding effort and if one looks at the research, there are drugs out there that address most if not all of those specific processes effectively.  This is why I posted the list because it points out a concise inventory of potential targets that can be exploited to drive stakes into the heart of these syndromes, and I believe very strongly that that is going to take as many stakes as we can muster.  And I once again point out that reversing any form of fibrosis is akin to making water flow up hill, but I am also extremely convinced that it can be done IF the information we already have is sufficiently exploited.

- George

[KuMe988]

When I was in 6th grade (I am in 12th now, 18-years old), I had a disease called Pancreatitis, which is an inflammation of the pancreas.  My gastrointerologist had no idea what could've caused this b/c I had no external forces or blows to the abdomen that could damage my pancreas.  He considered some sort of pancreas-attacking virus, but who knows...  maybe a genetic screw up?  lol   i shall never know.  Anyways, my gastrointerologist also said that it was very possible my Pancreatitis could lead to some form of Diabetes (I don't remember if it was type 1 or 2)...  I was wondering if my 6 month bout with Pancreatitis could be tied with Peyronie's Disease.  Alright, thanks for the time.
                                                                      -Kume988

[Tim468]

Although I barely remember being 12 years old, I do recall that I masturbated back then.  

Do you recall whether or not, if you masturbated then (or even just got erections and looked at them) if you had the bend before then? That should answer your question. If you always recall bending downwards, then it is probably congenital.

Tim

[Tim468]

I am routinely emailed an updated literature search for Peyronie's Disease (Peyronies Disease). This floated in last week. It suggests that although we have or see a lesion in one place, that those with Peyronies Disease have a generalized inflammatory change happening in the Tunica Albuginea (TA).

*********************************************

AU Nale D.  Mii S.  Vukovi I.  Radosavljevi R.
FA Nale, Dorde.  Mii, Sava.  Vukovi, Ivan.  Radosavljevi, Radoslav. IN Institut za urologiju i nefrologiju, Klinicki centar Srbije,
 Beograd.
TI [Induratio penis plastica--localized or diffusive fibromatosis of tunica albuginea penis?]. [Serbian]
SO Vojnosanitetski Pregled.  63(11):939-44, 2006 Nov.

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.

***********************************************
Tim

[George999]

Tim, that would seem to provide all the more reason to go after systemic inflammation aggressively!  It would seem likely that the plaques themselves exude inflammatory agents that incite inflammation in the surrounding tissues.  If this can be controlled or even suppressed it will likely greatly diminish or even halt the progression of Peyronies, independent of any therapy directed at the plaque itself (Pentox, etc.).  These are my observations (and this strategy has worked well for me and has seemed to keep my disease state fairly well contained).

- George

[DocSavage]

I would like to see a doctor that would work with me in trying to get to the bottom of this, looking into a collegen disorder or insulin resistance, or ... I don't think a urologist would be interested, a rheumatologist perhaps? indocrinologist perhaps? I am a difficult patient for most doctors because I am so participative in my treatment.

[Tim468]

George I agree with you completely. Like many here, i look to your experience with great hopefulness, because it leads me to hope that the same outcome could come my way. I similarly look to Old Man for his wisdom in use of the VED. Interesting that personal testimonials count for so much more than data!

But I think this is the right thing to do - and it is the right thing to do whether it works or not! Because it is good for so many other aspects of life in general, and one's overall health.

I think that the rheumatologic, genetic or immunologic components will be shown someday to play huge roles in this - not simple "injury". For now, we are left t our own devices to figure out what works for us. I have found that a micronutrient approach that reduces inflammation and the VED (I use a modified protocol and focus on the narrower chambers for now) is most helpful at keeping things at bay. The good news is that my basic curve is better now. I do not think I have ever measured it accurately, but would estimate it has gone from an about 30 degree to a 10-15 degree curve over the past six months. The bad news is that the waisting is still going on and is not better. For that I am starting to focus on a slightly larger cylinder and am about to start the pentox, cialis (works better for me) and arginine (using vasoflow) cocktail.

Tim

PS to DocSavage. If you like to participate and you cannot find a doctor who likes to work with you, then keep on looking. If you have seen over 5 to 10 doctors and found the same result, then it might be you, not them. Maybe what you see as participation they see as something different.

[George999]

Tim, I do think that the improvement in your curve is a very good sign that things are going in the right direction.  And you have to remember that the "waisting" is being caused by the very same process that is responsible for the curve.  I'm assuming that by "waisting" you mean as in hour glass.  In that case, I think that in a physiological sense, it is very likely that you would notice improvement in the curve long before you would be able to detect the same improvement in the waisting.  One of the problems I have observed in dealing with this disease is an issue which I have mentioned before.  We all would like to see quick results, so we tend to move from one remedy to another.  Unfortunately, it is going to take years of dedicated effort for most of us to make progress with Peyronies and that means going with things that are supported by external evidence and sticking with the plan.  As time passes we will see not only progress, but also times of regression.  It is just the nature of the thing.  I still maintain that the important part is keeping a handle on inflammation so that the stuff doesn't spread and at the same time try to whittle away at the entrenched plaques.  This strategy is definitely working for me and I highly recommend  it, but I want to make it clear that I do not intend that to convey that I am promising any miracle cures.  This stuff is tenacious and you have to be just as tenacious and aggressive in attacking it.  I think you are doing all the right things and headed in the right direction.  The main enemy you have to watch out for is discouragement and depression.  It has been helpful to me to concentrate on my general state of health and the You On A Diet book has helped me lose 25lbs effortlessly which has had a huge effect on my overall health.  My blood pressure is staying down continually at this point, even when I am under stress, and I am in the process of tapering back my medication which is going well so far.  I find that really exciting and am planning to try to drop off another 20lbs as soon as we can get the 'evil' foods cleaned out of the fridge and I suspect that will lower my levels of systemic inflammation and thus have a significant, though not major, positive impact on my Peyronies situation.

- George

[roadblock]

Not sure exactly where to put this post, but guess this is as good as any...

Came across this link and found it to be one of the most comprehensive looks at causes of Peyronies Disease I have seen...and notice, the date is 2002! I can only hope that there is research taking place out there investigating every one of these possible etiologies. Maybe there are researchers out there involved with Peyronies Disease research who may come across this and take a new approach that might result in a new therapy or new drug. One can only hope...

http://www.nature.com/ijir/journal/v14/n5/full/3900873a.html

[Hawk]

Roadblock,

I would have to agree with you.  That link is definitely a cut above.  Great find Roadblock!

[George999]

Roadblock, that is a great link!  The Cavidad team has done a lot of good research on Peyronies.  I don't know whether they are still continuing it, but I do know that it is related to a lot of stuff that Dr. Lue is applying in his Pentoxifyline treatment approach, which I believe is the best treatment going and is one of the only treatments that is showing signs of success.  There is now something out there that has been mentioned on this forum that is similar to Pentoxifyline in attacking TGF-beta, but significantly more effective.  It is so good that it is being tested against several different fibrotic diseases and once approved for treatment for any one of those, will be available for off-label use against Peyronies by doctors like Lue.

- George

[roadblock]

What is it?

[Tim468]

It's Pirfenidone, and it might not be THAT much better than pentox, but it seems to have promise.

Tim

[Liam]

One must even ask if there is enough data to know whether it is the actual catheterising that is the causative factor, or the associated surgical procedure and the resulting inflammatory response that occurs.

The longer I have Peyronies Disease, the more I "sense" a correlation to inflammation.  Inflammation may not be the "engine" of Peyronies Disease.  But, it seems, it may be the "throttle".  

[Kimo]

Thought i'd throw this info in here....I do remember being catherterised not to long before i came down with peyronies disease,,,,,but just not sure if that's what brought it on,,,,I know i had bent it bad a couple of times when younger during intercourse with my wife and remember it hurting.....And then when i had taken my first dose of viagra, 100mg,,,,about 8yrs ago i knew something was happening right away and with in a few weeks i was bent real bad...Through all these years i have continued to use viagra and believe it has helped to bring it back somewhat straight along with the use of TV and vita-E.......Hope this might add to the info....

kimo

[Rico]

I have to agree with you Liam on inflammation being the throttle.... I think George made some good points with the dash diet and inflammation and life style changes, seems diet can be corrected faster than say a ex smoker..... up to five years to change your blood back to where it was........http://www.eurekalert.org/pub_releases/2005-06/plos-sai062205.php

[Hawk]

Good link Rico!  

I was unaware of some of that information about smoking.  It almost makes me wish I smoked so I could quit

[Liam]

Very Interesting and Promising

Isolated Septal Fibrosis Or Hematoma - Atypical Peyronie's Disease?
01 Feb 2007

UroToday.com- Classically, Peyronie's disease (Peyronies Disease) presents with penile curvature and/or pain, and is associated with a palpable penile plaque. Often these cardinal symptoms are accompanied by a constellation of other issues, including penile shortening and/or narrowing, loss of erectile rigidity throughout the penis or distal to the plaque, and decreased penile sensation.

A recent report from Tom Lue's group in San Francisco describes a subset of patients with suspected Peyronies Disease who were found to have only a circumscribed septal lesion (CSL) on penile ultrasonography. In the review, published in the January 2007 issue of the Journal of Urology, the characteristics of this subset of patients are reviewed.

Of a series of 650 patients with Peyronie's disease, 47 patients were identified with isolated septal fibrosis on ultrasound. Patients with any additional lesions, such as peripheral plaques, were excluded from the group. Of the group of 47 patients, 33 presented with classic findings of Peyronie's disease including penile pain or curvature. Four men presented with erectile dysfunction. Seven men presented with a primary complaint of penile shortening or distal softening, of whom 3 reported a lump in the mid shaft of the penis. A total of 17 patients had a significant history of penile trauma, but not a penile fracture. The event occurred within 6 months of presentation in all men. In three men presenting soon after their traumatic injuries, a well-defined cystic area in the septal region was found on ultrasound. These areas were found to be liquefied hematomas and were aspirated under ultrasound guidance. In one case, the hematoma was adjacent to a smaller, more typical appearing CSL, and in one patient, a follow-up ultrasound demonstrated evolution to a smaller but otherwise typical CSL. All of these men, who had complained of ED after their traumatic injuries, had complete resolution of their erectile dysfunction within 4 weeks of aspiration.

The authors believe that these septal lesions may actually represent septal fractures and that early intervention with ultrasonographic aspiration may prevent formation of a typical Peyronie's plaque, albeit in the septum, and prevent the complication of fibrosis, penile curvature and other stigmata of Peyronie's disease. The authors also discuss their use of the anti-inflammatory Pentoxifyline in divided doses of 800 to 1,600 mg daily to fight the inflammatory component of Peyronie's disease.

Brant WO, Bella AJ, Garcia MM, Tantiwongse K, Dean RC, Lue TF
J Urol. 2007 Jan; 177(1): 179-183

Reviewed by UroToday.com Contributing Editor Michael J. Metro, MD

UroToday - the only urology website with original content written by global urology key opinion leaders actively engaged in clinical practice.

To access the latest urology news releases from UroToday, go to:
www.urotoday.com

Copyright © 2006 - UroToday

http://www.pharma-lexicon.com/medicalnews.php?newsid=62103

[George999]

This is indeed truly fascinating!

- George

[George999]

The study referenced by Liam makes and interesting point, specifically that the general purpose of Pentox is to control inflammation.  This, once again, brings uncontrolled inflammation to center stage in the list of causes of Peyronies.  One paper that I have found interesting in this regard is this one:

http://obssr.od.nih.gov/Content/Conferences_And_Workshops/Conference_FY2003/allostatic_load.htm

Note particularly:

The stress experienced by socially subordinate female macaques that are fed an atherogenic diet to induce development of the metabolic syndrome has produced a remarkable model of modern life[29],[30]. Similar to chronically stressed humans, these animals over-secrete cortisol, are insensitive to cortisol negative feedback, accumulate visceral fat, and have poorer ovarian function, more coronary artery atherosclerosis and depression as compared to dominant females. Preliminary data suggest that animals with the greatest allostatic load may have relatively short survival times.

In other words, the body's response to stress is to secrete Cortisol.  Cortisol is the body's natural 'cure' for inflammation.  But when Cortisol is chronically secreted due to chronic stress load, it is no longer effective in suppressing inflammation and inflammatory diseases run rampant.  This is referred to as "Adrenal exhaustion".  One has to wonder if this type of syndrome plays a significant role in the development and progression of Peyronies.

Also note this article on the subject:

http://www.usatoday.com/news/health/2005-03-08-heart-happy_x.htm

Upset adults might produce more of the stress hormone cortisol. In the short term, cortisol lowers inflammation, but there's some evidence that chronically high levels make receptors for it less sensitive over time. Then they no longer take in the cortisol, so inflammation can run rampant.

This is the kind of research that is really pointing the way to a global solution to fibrosis.  We are attacking the superficial issues while ignoring the root causes and the resulting therapeutic approaches are less effective as a result.

- George

[George999]

I don't know how many of you made the connection on this one:

http://www.reuters.com/article/healthNews/idUSN1643513920070416

Those who ate cured meat products at least 14 times a month were 78 percent more likely to develop chronic obstructive pulmonary disease than people who did not eat these meats, even after the researchers sought to account for many other risk factors including smoking, overall diet and age.

Chronic obstructive pulmonary disease, also called COPD, refers to emphysema and chronic bronchitis, which interfere with normal breathing.

We are talking about pulmonary fibrosis here and the keyword is fibrosis.  If the nitrites in cured meats are able to stimulate pulmonary fibrosis, one can only wonder if the might not have something to do with penile as well as other forms of fibrosis.

- George

[Liam]

I have found a high correlation between people who eat cured meat and people who attend Monster truck shows.  Now, there is also a higher concentration of Axe Body Spray in the air at said shows mixed with truck emissions and body odor.  All of these are introduced to the body through inhalation.  Therefore, possibly, Monster Truck Shows lead to COPD and P D.

Something to ponder  

Liam

Jiang could not rule out, for example, that people who eat a lot of cured meats -- hot dogs, cold cuts, sausage, bacon, cured hams and the like -- may be more likely to have an unhealthful diet and lifestyle that might account for the higher lung disease risk.

http://www.reuters.com/article/healthNews/idUSN1643513920070416?pageNumber=2

Just having some fun, George.  But, seriously, it is hard to discount lifestyle.  Also, this may be pointing to the link between hypercholesterolemia and other diseases as well.

George,
BTW, I have learned a ton from your posts.  I appreciate your knowlege and your willingness to share.

[Doug]

The anti arrhythmic is called flecainide, which I take for atrial fibrillation. I've also taken propafenone and verapamil. None of them are beta blockers (I have heard about the connection between beta blockers and Peyronies Disease). I also take warfarin for stroke prevention. The anti arrhythmics didn't help my sex life, so I started taking a small dose of Viagra. About a year later, I noticed some curvature and a sort of indentation. Since then it has got much worse, over the course of about 3 years. So I've always had a sneaking suspicion that the Peyronies Disease was caused by either the anti arrhythmics (which definitely slow down blood flow to the "area"), or the Viagra (which maybe stretches things beyond where they are supposed to be stretched).

Regarding the "congenital" Peyronies Disease, I think what he means is that I have a fibrous lump on my foot, some bumps on my hands (ie Dupreytens and Lederhosen), and that I am prone to scarring in these areas, and that there is a connection to what is happening with my penis. I didn't have a real trauma, very little bending or curving, but am developing a "waisting" pattern. He is a real Uro, not a GP, and is the only guy locally who deals with Peyronies Disease by treating it with verapamil injections. He also does surgery, but I'm hoping to avoid that solution.

[Hawk]

So I've always had a sneaking suspicion that the Peyronies Disease was caused by either the anti arrhythmics (which definitely slow down blood flow to the "area"), or the Viagra (which maybe stretches things beyond where they are supposed to be stretched).

....I have a fibrous lump on my foot, some bumps on my hands (ie Dupreytens and Lederhosen), and that I am prone to scarring in these areas, and that there is a connection to what is happening with my penis.

Doug,

It is hard to pin your Peyronies Disease on one of these drugs when they did not cause your other fibrotic diseases.  It seems you definitely have a hereditary predisposition for these disease to develop as you age.  That seems to be the biggest single factor.  A hereditary connection however has nothing to do with the term congenital.  Congenital has one clear meaning, something that was present at birth.  It does not mean a tendency was there at birth.  There simply is no such thing as congenital Peyronies Disease.  No competent doctor would use that term.  There would be no excuse for an MD to misuse such a specific term that is so common to the profession. There is congenital curvature which is not fibrotic, not progressive, and not Peyronies Disease.

[Liam]

Doug,

>>>>>Hawk and I are on the same page on this one<<<<<<

I understand the connections and what you mean.

The question of the "disease" being present at birth (congenital) is troubling.  Having genetic markers means congenital?  Are there genetic markers?

The term congenital (con genital) is troubling.  Two burritos con genital, por favor.    Maybe I'm just troubled.

Good Luck!  Hope you avoid the knife, too.

Liam

BTW, I've have/had adhesive capsulitis in both shoulders, Dupuytren's in both hands, Peyronies Disease (of course) and just found (ouch!) a lump on the bottom of my foot on the "margin" between the ball of the foot and the arch in line with the fourth little piggy.

[Old Man]

Liam and Hawk:

I have no reason to take issue with you guys about congenital conditions, but have one for you to think about.

My mother and father both, had Duputren's and Lederhose conditions. My father has Peyronies Disease as far as I remember. Not bad, but did have a curve to the right about 30 degrees. They used to joke about it when they thought I was not listening.

So, just stating the above to relate that since I have Dupuytren's, Lederhose and Peyronies Disease that there might be a hereditary situation in my case. Who knows since so little is known about all three of these maladies.

Old Man

[Liam]

No.  I agree there is at least a genetic predisposition.  My only problem is a predisposition doesn't mean the disease itself is congenital.  You may have the predisposition without the disease manifesting itself.

I think all of us agree on that.  

[Hawk]

Oldman,

Your point is valid but the term is incorrect.

Congenital means that the CONDITION actually existed at birth.  Congenital Peyronies Disease would mean that at the first diaper change the infant actually had Peyronies Disease.  Many of us (maybe most of us) may have been born with a genetic marker or predisposition to Peyronies Disease.  Many people are born with a genetic marker or predisposition for Peyronies Disease, baldness, breast cancer, prostate cancer.  Those are not congenital diseases however.

[Old Man]

Hawk:

Point taken, but does not a male penis start forming at some stage pregnancy prior to actual birth? If the baby is born with a congenital penis, it would have occurred prior to actual birth. We know that congenital curves usually cannot be corrected short of surgery, right? So then, if a persons forebears have Peyronies Disease, Duputrens and Lederhose conditions, would it not be possible for their offspring to have the genetic background to produce these in the offspring?

The above are just questions that have entered my mind while reading all the prior discussions.

Give me more information relative what the answers could be. Thanks.

Old Man

[George999]

Hawk, Old Man,  I think Hawks point here is that the term 'genetic' is NOT interchangeable with 'congenital'.  'Congenital' refers to a PHYSICAL defect present at birth while 'genetic' refers to a GENE defect present at birth.  Thus a 'congenital' defect may OR may not be related to a 'genetic' issue, while a 'genetic' issue may OR may not cause a 'congenital' defect.  For example many people have 'birthmarks'.  These are by definition 'congenital', but there is no evidence that they are related to 'genetics'.  On the other hand, many people develop certain diseases later in life that ARE the result of a 'genetic' issue, but since they were not present at birth, they are not considered 'congenital' although I suppose you could refer to the underlying 'genetic' problem itself as being congenital.  In the case of the conditions that Old Man is referring to, I would suspect that there is an underlying genetic PREDISPOSITION to developing a 'toxic' metabolic state that in turn predisposes one to developing these diseases that are commonly seen occurring together.  But I suspect there is just a whole lot of stuff happening in between the genetics and the manifestations and that there are probably numerous points at which this process could be short circuited IF we just knew more about the pathways involved.  At this point, I think that we are only barely scratching the surface in that regard.  We know about TGF-beta-1 and the like, but none of those factors really explains what precipitates this endless loop in the first place.  That, like the root causes of metabolic syndrome, involves a deeper set of factors, that eventually results in a metabolic environment that just spins off all of these afflictions.  And that is what makes treatment so difficult.  It is not enough to just treat the afflictions themselves, nor is it enough to just treat the root cause.  You really have to treat everything in perfect sync in order to make progress against the end disease.  This is because you have an underlying condition that is causing continuous damage.  No matter how successful you are at repairing that damage, that underlying condition just keeps pouring on fuel faster than you can dowse the flames with water.  On the other hand, even if you are successful in controlling the underlying condition, the damage it has caused will not only persist, but will continue to worsen, as it has, in effect, taken on a life of its own.  ONLY by precisely addressing both issues can progress be made, and at this point, I think it is safe to say that we just don't know enough yet to reliably make that happen.  I think that in some cases this just happens by chance or serendipity and the result is what we refer to as a spontaneous remission.  But I suspect that if we were able to look closely and analytically, we would see that most cases of spontaneous remission are a result, as it were, of an 'alignment of the stars' in the sense that by sheer good fortune or the grace of God, the underlying condition AND the resulting affliction are able to resolve in sync.  

[Hawk]

Good clarification George.

If the doctor referred to congenital Peyronies Disease when he meant hereditary, that means that he not only used the wrong term, but that he is showing his lack of knowledge by even suggesting he knows the root cause of a specific case of Peyronies Disease.

First, the patient would have to know the Peyronies Disease and fibrotic history of his family, and he would have to cover this in detail with the doctor.  Even then, the doctor would be speculating that this case of Peyronies Disease was hereditary (not congenital)

[Liam]

Another example of the forum at its best!!!