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(5) Glutathione (GSH) is an important component of the anti-oxidant defense against free radical-induced tissue damage. Dietary glutathione is not well absorbed, so that considerable quantities may be found throughout the gut lumen following supplementation[144]. Hepatic GSH is a key substrate for reducing toxic oxygen metabolites and oxidized xenobiotics in the liver. Depletion of hepatic glutathione is a common occurence in Leaky Gut Syndromes contributing to liver dysfunction and liver necrosis among alcoholics and immune impairment in patients with AIDS. The most effective way to raise hepatic glutathione is to administer its dietary precursors, cysteine or methionine. Anti-oxidant supplementation for Leaky Gut Syndromes should therefore include both GSH and N-acetyl cysteine. Because protozoa are more sensitive to oxidant stress than are humans and because most anti-parasitic drugs and herbs work by oxidative mechanisms, high dose anti-oxidant supplementation should be witheld during the treatment of protozoan infection, especially during treatment with Artemisia.
(6) Flavonoids are potent, phenolic anti-oxidants and enzyme inhibitors with varied effects depending on the tissues in which they act. Quercetin and related flavonoids inhibit the release of histamine and inflammatory mediators. Taken before eating, they may block allergic reactions which increase permeability. Catechins have been used in Europe to treat gastric ulcerations. The flavonoids in milk thistle (silymarin) and in dandelion root (taraxacum) protect the liver against reactive oxygen species[145].
Carnitine exists in the body in two forms, either L-carnitine or the acetylated form known as Acetyl-L-Carnitine (ALCAR).[7] The synthesis of these molecules can occur endogenously from the two dietary amino acids L-methionine and lysine, where a peptide-bound lysine is converted to e-N-trimethyllysinevia donation of S-adenosylmethionine
16 patients with liver disease (both alcoholic and non-alcoholic) were given 1,200 mg of oral SAMe per day for six months. Liver biopsies showed a significant increase in glutathione,
yes, but if you dont recycle homocysteine, what is SAME going to do, create more homocysteine and keep atherosclerosis going?
you need to cycle homocysteine further into methionine or into CBS pathway with magnesium b6 into cysteine
or SAME will be broken down by GNMT not to create more homocysteine
remember all those test that I posted. they have high homocysteine
the problem is either with methionine synthase or methionine synthase reductase. IMO OR with SERINE, b6 magnesium for CBS pathway, if you have low cysteine
and low cysteine will cause low androgen binding. cortisol binding. etc
this is why Orion was doing great on vitamin b2. since methionine synthase reductase which recycled vitamin b12 is FAD enzyme
and then recycled b12 turns methionine synthase and lowers homocysteine.
and SAME starts going up and not being broken down by GNMT
Methyl deficiency causes a reduction in SAMe levels, and an elevation in S-adenosylmethionine homocysteine (SAH). SAH is what's left over after SAMe donates a methyl group for biochemical reactions. An enzyme, SAH hydrolase, turns SAH into homocysteine. Homocysteine can be toxic if it builds up within the body, but is converted into cysteine (and eventually glutathione) if enough SAMe is present.
If SAMe is super-deficient, nothing gets converted, and SAH and homocysteine back up like a clogged drain. This is when cancer gets its toehold. A low SAMe-to-SAH ratio is step-one in the development of liver cancer. Maintaining SAMe can reverse the early changes in the process.