The
full text of the article
Homocysteine as a Risk Factor for Vascular Disease is available.
In this paper, the authors find an increase in collagen production in a dose dependent fashion when homocysteine is added to cell cultures. The lowest dose at which this occurred was 50 µmol/L, which many people have but is still quite high (my homocysteine was around 13 a couple of years back but is now around eight).
Like atherosclerosis, Peyronies Disease also has increased collagen deposition, smooth muscle cell defects, and "excessive deposition of extracellular matrix protein".
The paper also stated that "SMC proliferation is stimulated by short-term exposure to Hcy". Plasma homocysteine is usually measured after fasting, so I wonder if it peaks day to day. [Edit: it appears to be fairly steady, actually.]
The interesting part is here: "The addition of aqCbl inhibited the Hcy-induced enhancement of SMC proliferation, collagen synthesis, and total protein synthesis".
Patients with genetically impaired remethylation of Hcy caused by Cbl C, D, and E mutations involving the intracellular metabolism of Cbl can have normal plasma Cbl levels but still be hyperhomocysteinemic. Such patients, when treated with hydroxocobalamin, which is converted to aqCbl at physiological pH, improve clinically.
I have some hydroxocobalamin
on order from RI and will give it a try once it arrives. It would be interesting if it turned out that Peyronies Disease sufferers have a cobalamin mutation.
s&s
