I thought so too, especially with linnea safe. I guess I have 2 more weeks that it could still grow in - and possibly even after that it can change...but I don\'t think it\'ll be that drastic (who knows) based on past experience. But, so far, it\'s not looking great...similar to what SLK20003 posted, except he had metacrill.
I\'m just kind of depressed at the moment about this whole thing, with it looking bad on top of the fact it\'s not any bigger. The
Flaccid gain is kind of variable. Sometimes it\'s 4\" sometimes it\'s 5\"... but
Erect, it doesn\'t get any bigger than 5\" because that
PMMA gets stretched out.
I wonder if a lot of the
PMMA got stuck in these big nodules I have on the left...though they are certainly not 15cc big...so I don\'t know what is going on, but I hope something changes in the next few weeks.
Also, I wonder if
Cialis and various
Erection-enhancement supplements (arginine, citrulline) are not a good idea. They are used (off-label, and only theoretically) for reducing the fibrosis in peyronies disease. I\'m going to stop them today. In Peyornie\'s, the goal is to get rid of the fibrosis and extra collagen on the tunica in the penis. Here, the goal is to encourage it (it\'s not on the tunica, it\'s a separate layer)...so definitely (lemperle himself has said) high doses of cortisone are going to be bad. However, viagra /
Cialis has a very minor, tangential effect on collagen building...still, I wonder if this is part of the problem. I thought a lot of guys took these pills after the procedure to get erections, but I could be wrong.
N.F. Gonzalez-Cadavid, J. RajferTreatment of Peyronie's disease with PDE5 inhibitors: an antifibrotic strategyNat Rev Urol, 7 (2010), pp. 215'221AbstractPeyronie\'s disease (PD) is a localized fibrotic condition of the tunica albuginea that is associated with risk factors for corpora cavernosa fibrosis (such as advanced age and diabetes) and Dupuytren contracture, another localized fibrotic process. Most of the current pharmacological treatments for PD are not based on antifibrotic approaches that have shown promising results in animal models and clinical efficacy in other fibrotic conditions, which may explain why they are generally unsuccessful. Evidence gathered in human specimens and animal models of PD have elucidated aspects of its etiology and histopathology, showing that overexpression of transforming growth factor ?1, plasminogen activator inhibitor 1, reactive oxygen species and other profibrotic factors, which are, in most cases, assumed to be induced by trauma to the tunica albuginea, leads to myofibroblast accumulation and excessive deposition of collagen. At the same time, a steady overexpression of inducible nitric oxide synthase, leading to increased nitric oxide and cGMP levels, seems to act as an endogenous antifibrotic mechanism. This process has also been reported in corporal and cardiovascular fibrosis, and has led to the demonstration that long-term continuous administration of phosphodiesterase type 5 inhibitors counteracts the development of a PD-like fibrotic plaque in a rat model, and later extended to the prevention of corporal fibrosis in animal models of erectile dysfunction. ' 2010 Macmillan Publishers Limited. All rights reserved.