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Re: Sounds like a question for CHEMIST! BarbaraCat

Posted by Larry Hoover on July 18, 2004, at 11:23:45

In reply to Re: Sounds like a question for CHEMIST! chemist, posted by BarbaraCat on July 13, 2004, at 14:41:36

> I am going to be delving into methylation land for the next bit. There is a common thread that's appearing to all this, first with the histamine hypothesis and the tie with with possible methyl doner malfunctioning.

Easy enough to supplement to target methyl donation.....betaine and B-12.

> The reason it jangled my bells is that I had a serious reaction to Lamictal all the while I was taking it and eventually stopped. Stevens Johnson developed from taking DMPS, a heavy metal chelator with a high affinitiy to thiol groups (in my case trying to chelate mercury) so there could be a possible tie in with the histimine/methylation relation, if there is one, and a possible breakdown of sulfur/thiol metabolism.

DMPS has a substantial impact on all metal cations. If I recall correctly, it is about 30 times more effective at removing zinc than mercury. Serious business, using chelation therapy. All too often, it is poorly managed, from a medical perspective. If mercury is a potential toxicant, take selenium. It will covalently bond to the mercury, totally inactivating it. The solubility constant for Se-Hg is on the order of ten to the -70. In other words, you would require roughly 10 to 46th power litres of water to dissolve one molecule. In other other words, it is so insoluble that its solubility can't be measured. The mercury will stay in your body, but it will be totally inert.

Thiol/sulphur metabolism is absolutely disturbed in fibromyalgia. That's why I've been pushing taurine. It's the sulphonic acid version of GABA.

> The other clue is that I have fibromyalgia and some recent studies have identified a epithelial mast cell inflammatory involvment which may account for the heightened skin nerve pain response. But also, ta-da, a malfunctioning histamine response at skin receptor sites seems to be involved, which would predispose one towards an inflamed skin pain sensitivity but also a heightened alergic response resulting in the erythema multiforme 'rash' (which is a severe separation of mast cells from the epithelial substrate). Mast cells -> histimine. There it is again.

Niacinamide down-regulates histamine synthesis, and also blocks mast-cell degranulation (histamine release). It also, coincidentally, is an agonist at GABA receptors.

FASEB J. 2003 Aug;17(11):1377-9.

Nicotinamide: a potential addition to the anti-psoriatic weaponry.

Namazi MR.

Dermatology Department, Shiraz University of Medical Sciences, Shiraz, Iran.

Psoriasis is an inflammatory disorder characterized by a T helper type 1 cell cytokine pattern. Increased expression of adhesion molecules, prominent neutrophil accumulation, and increased production of nitric oxide are characteristics of this disorder. Moreover, histamine and proteases are supposed to participate in the pathogenesis of psoriasis. Nicotinamide is an inhibitor of poly (ADP-ribose) polymerase-1 (PARP-1) that, through enhancement of nuclear kappa B-mediated transcription, plays a pivotal role in the expression of inflammatory cytokines, chemokines, adhesion molecules, and inflammatory mediators. Through interaction with CD38 and inhibition of IL-1, IL-12, and TNF-alpha production, nicotinamide produces a mild TH2 bias. Nicotinamide is a potent phosphodiesterase inhibitor and suppresses neutrophil chemotaxis and mast cell histamine release. It inhibits nitric oxide synthase mRNA induction and suppresses antigen-induced lymphocyte transformation. Nicotinamide increases the biosynthesis of ceramides, which upon degradation produce sphingosine. Sphingosine inhibits protein kinase C (PKC) and decreases basal cell proliferation dependent on PKC. Taken together, it can be reasoned that nicotinamide could be a useful addition to anti-psoriatic armamentarium. The combination of nicotinamide and thalidomide or methotrexate provided a powerful synergistic inhibition of murine collagen-induced arthritis. Nicotinamide decreased the methotrexate-induced hepatotoxicity. The above combinations may prove to have a powerful anti-psoriatic effect as well. As PARP inhibitors could exert anti-retroviral effect, nicotinamide could also be of special value in the treatment of HIV-infected psoriatics.

I expect this topic to be redirected, but I hope that a greater audience is exposed to some of these concepts, here on the main Babble board. Alternative medicine is drug-augmentative. There's a lot more you can do than get prescriptions filled.





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