Posted by McPac on May 30, 2003, at 20:52:49
In reply to L-Methionine Undermethylated, posted by samplemethod on May 30, 2003, at 1:44:31
Methionine
Claims for methionine in medicine were initiated by Adelle Davis (1970), who suggested that methionine was deficient in toxemia of pregnancy, childhood rheumatic fever and hair loss. Today, we see a more defined role for methionine as a treatment for some forms of depression, schizophrenia and Parkinson's disease.
Methionine is one of the essential amino acids needed by humans and higher animals; bacteria can make it from aspartic acid. Some methionine may be absorbed from the bacteria of the gut flora under starvation conditions. The average human needs about 10 mg/kg of methionine and cysteine or as much as 700 mg a day of methionine. This minimal daily requirement is significantly less than the optimal need for methionine.
Methionine-deficient diets in experimental animals result in impaired growth and elevated blood spermidine. Normal methionine metabolism depends on the utilization of folic acid which can be elevated in the serum of methionine deficient patients. Some foods are rich in methionine. A cup of low-fat cottage cheese can contain up to a gram of methionine. Most cheeses contain 100 to 200 mg per ounce.
Methionine supplements lower blood histamine by increasing the breakdown of histamine. It is also a useful treatment for copper poisoning and for lowering serum copper. Methionine's three major metabolic roles are as methyl and sulfur donor and a precursor to other sulfur amino acids such as cysteine and taurine.
Methionine supplementation is unusual because the D, L form is probably more effective than just the L form. This is probably due to D-L salt formation. Methionine is well absorbed in the brain where it is converted into SAM, which can increase adrenalin-like neurotransmitters in the brain. Methionine, the methyl donor, may produce active brain stimulants and degrade blood histamine. Methionine supplementation has been particularly useful in depressing the high histamine type (histadelia). It has been found to be more effective than MAO inhibitors in depression.
Methionine is a useful adjunct therapy in some cases of Parkinson's disease, because it can stimulate the production of dopa. Methionine may be of value in acrodermatitis enteropathica, a rare disease of zinc deficiency. Methionine, like other sulfur amino acids, protects against the effects of radiation.
Methionine supplementation may help patients with heroin addiction, who often are unusually high in histamine and have a low pain threshold. Detoxification and withdrawal from barbiturates or amphetamines may also be assisted by methionine. Methionine may be useful for patients with chronic pain and is thought to lower blood cholesterol.
At present, we use methionine for patients with high blood histamine, depression, high copper, high cholesterol and chronic pain, allergies and asthma. Measurement of plasma levels is useful for guiding therapy. Doses of 1 to 2 g of methionine can raise plasma methionine levels 2 to 4 times above normal.
There are usually small elevations in other amino acids. We have had one case where taurine levels were raised as high as the methionine levels and other cases where taurine was not significantly elevated. Elevated levels of taurine, a methionine metabolite, are a hidden benefit of methionine therapy. These elevations may be the basis of methionine's therapeutic effects.
Homocystine – Worse Than Cholesterol
Homocystine is a natural amino acid metabolite of the essential amino acid methionine, but it occurs only transiently before being converted to the harmless cystathionine via a vitamin B6-dependent enzyme. Homocystine is the double-bonded form of homocysteine. Homocysteine metabolism is related to sulfur amino acid metabolism (methionine, taurine and cysteine) and is dependent on vitamin B12, folic acid, vitamin B6 and betaine as primary cofactors. Homocysteine metabolism is relevant to the understanding of psychosis, arteriosclerosis and the biochemical basis of all nutrient therapies.
Homocysteine excess is still another metabolic cause of psychosis and mental retardation. Nutrients-vitamin B6, folic acid, betaine, cysteine and vitamin B12 can help various inborn errors of homocysteine metabolism. We've identified a similar form of psychosis, called pyroluria, which accounts for about 30 percent of psychotic patients (Pfeiffer, 1975). These patients are vitamin B6 and zinc dependent.
Furthermore, S-adenosyl homocysteine can be a useful therapy in certain forms of psychosis. Homocysteine, which presumably accumulates as a result of insufficient vitamin B6, is identified as a chief culprit in initiating the vascular lesions leading to arteriolosclerosis. Zinc deficiency also may have a role in this process. With this knowledge, the nutrient basis of heart disease prevention is expanded beyond the simplistic theory related to cholesterol and the restricted consumption of eggs. Beyond the treatment of arteriosclerosis by reduction of cholesterol is treatment by reduction of homocystine. Homocystine excess is related to vitamin B6 deficiency and probably a zinc deficiency, which has a role in the body's ability to repair cells. Marginal deficiency of vitamin B6 and zinc is widespread in this country (Pfeiffer, 1975).
poster:McPac
thread:230142
URL: http://www.dr-bob.org/babble/20030530/msgs/230349.html