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Dl-Methionine 200 Grams

ADP: $43.99
Price: $9.99
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Manufacturer: *Supplement Direct*
Manufacturer Part No: 734890003215
The body also needs plenty of methionineto produce two other sulfur-containing amino acids, cysteine and taurine, which help support the body's natural elimination of toxins, builds strong, healthy tissues, and supports cardiovascular health. Methionine is a lipotropic, or a chemical substance that helps the liver process fats (lipids). Other lipotropics include choline, inositol, and betaine (trimethylglycine), all of which help ensure normal liver function, which is essential for the elimination of toxins from the body. Methionine also supports liver function by maintaining healthy glutathione supplies; glutathione is needed to help neutralize toxins in the liver.

Methionine is needed to make creatine, a nutrient naturally found primarily in muscle tissue that provides the energy our muscles need to move, and has been found to boost athletic performance during short, intense workouts. Creatine is necessary for all muscular function, and thus supports normal functioning of the heart and circulatory system.

Methionine is essential for the formation of healthy collagen used to form skin, nails, and connective tissue. Methionine is an essential vitamin, which means it must be obtained through dietary sources. It is found in a variety of natural food sources, including beans, eggs, fish, garlic, lentils, meat, onions, soybeans, seeds, and yogurt. It is also available at health food stores and from online distributors in capsule and powder forms.

200 Grams
Supplement Facts
Serving Size1/4Teaspoon(1gram)
Servings Per Container 200
Amount Per Serving
Methionine 1g (1000 mg)
Directions For Supplement Direct Methionine: As a dietary supplement, take 1/4 level teaspoon one or more times daily as needed, preferably on an empty stomach or use as directed by a health care professionals.

Dietary methionine imbalance, endothelial cell dysfunction and atherosclerosis

Nutrition Research (USA), 1996, 16/7 (1251-1266)

Dietary factors can play a crucial role in the development of atherosclerosis. High fat, high calorie diets are well known risk factors for this disease. In addition, there is strong evidence that dietary animal proteins also can contribute to the development of atherosclerosis. Atherogenic effects of animal proteins are related, at least in part, to high levels of methionine in these proteins. An excess of dietary methionine may induce atherosclerosis by increasing plasma lipid levels and/or by contributing to endothelial cell injury or dysfunction. In addition, methionine imbalance elevates plasma/tissue homocysteine which may induce oxidative stress and injury to endothelial cells. Methionine and homocysteine metabolism is regulated by the cellular content of vitamins B6, B12, riboflavin and folic acid. Therefore, deficiencies of these vitamins may significantly influence methionine and homocysteine levels and their effects on the development of atherosclerosis.

Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project.

JAMA (UNITED STATES) Jun 11 1997, 277 (22) p1775-81

CONTEXT: Elevated plasma homocysteine is a known risk factor for atherosclerotic vascular disease, but the strength of the relationship and the interaction of plasma homocysteine with other risk factors are unclear.

OBJECTIVE: To establish the magnitude of the vascular disease risk associated with an increased plasma homocysteine level and to examine interaction effects between elevated plasma homocysteine level and conventional risk factors.

DESIGN: Case-control study.

SETTING: Nineteen centers in 9 European countries.

PATIENTS: A total of 750 cases of atherosclerotic vascular disease (cardiac, cerebral, and peripheral) and 800 controls of both sexes younger than 60 years.

MEASUREMENTS: Plasma total homocysteine was measured while subjects were fasting and after a standardized methionine- loading test, which involves the administration of 100 mg of methionine per kilogram and stresses the metabolic pathway responsible for the irreversible degradation of homocysteine. Plasma cobalamin, pyridoxal 5'-phosphate, red blood cell folate, serum cholesterol, smoking, and blood pressure were also measured.

RESULTS: The relative risk for vascular disease in the top fifth compared with the bottom four fifths of the control fasting total homocysteine distribution was 2.2 (95% confidence interval, 1.6-2.9). Methionine loading identified an additional 27% of at-risk cases. A dose- response effect was noted between total homocysteine level and risk. The risk was similar to and independent of that of other risk factors, but interaction effects were noted between homocysteine and these risk factors; for both sexes combined, an increased fasting homocysteine level showed a more than multiplicative effect on risk in smokers and in hypertensive subjects. Red blood cell folate, cobalamin, and pyridoxal phosphate, all of which modulate homocysteine metabolism, were inversely related to total homocysteine levels. Compared with nonusers of vitamin supplements, the small number of subjects taking such vitamins appeared to have a substantially lower risk of vascular disease, a proportion of which was attributable to lower plasma homocysteine levels.

CONCLUSIONS: An increased plasma total homocysteine level confers an independent risk of vascular disease similar to that of smoking or hyperlipidemia. It powerfully increases the risk associated with smoking and hypertension. It is time to undertake randomized controlled trials of the effect of vitamins that reduce plasma homocysteine levels on vascular disease risk.

Hyperhomocysteinemia induced by folic acid deficiency and methionine load--applications of a modified HPLC method.

Clin Chim Acta (NETHERLANDS) Aug 15 1996, 252 (1) p83-93

The increasing possibility that homocysteine might be involved in atherosclerosis in non-homocysteinuric subjects has required the measurement of low concentrations of this aminothiol in biological samples. The procedure described here represents an improvement of different HPLC methods. We utilized an isocratic HPLC system with fluorescence detection of plasma total homocysteine derivatized after reaction with ammonium 7- fluoro-benzo-2-oxa-1,3-diazole-4-sulphonate. With the help of the rapidly eluting internal standard N-acetyl- cysteine, the method ensures very good recovery (approximately 100%), reproducibility and precision (within-assay 2.31%; day-to-day: 2.8%) in the physiological concentration range. This procedure allowed us to validate various animal models of hyperhomocysteinemia such as dietary folic acid deficiency in rat and acute methionine loads in rat and hamster. Using this method, we also confirmed that men have higher plasma total homocysteine levels than women. Due to its simplicity and reliability, our procedure is suitable for routine analysis of total homocysteine and other aminothiols (cysteine, cysteinyl-glycine and glutathione) in biological samples, as required in clinical and research laboratories.

Male rats fed methyl- and folate-deficient diets with or without niacin develop hepatic carcinomas associated with decreased tissue NAD concentrations and altered poly (ADP-ribose) polymerase activity

Journal of Nutrition (USA), 1997, 127/1 (30-36)

Folate is an essential cofactor in the generation of endogenous methionine, and there is evidence that folate deficiency exacerbates the effects of a diet low in choline and methionine, including alterations in poly (ADP- ribose) polymerase (PARP) activity, an enzyme associated with DNA replication and repair. Because PARP requires NAD as its substrate, we postulated that a deficiency of both folate and niacin would enhance the development of liver cancer in rats fed a diet deficient in methionine and choline. In two experiments, rats were fed choline- and folate-deficient, low methionine diets containing either 12 or 8% casein (12% MCFD, 8% MCFD) or 6% casein and 6% gelatin with niacin (MCFD) or without niacin (MCFND) and were compared with folate-supplemented controls. Liver NAD concentrations were lower in all methyl-deficient rats after 2-17 mo. At 17 mo, NAD concentrations in other tissues of rats fed these diets were also lower than in controls. Compared with control values, liver PARP activity was enhanced in rats fed the 12% MCFD diet but was lower in MCFND-fed rats following a further reduction in liver NAD concentration. These changes in PARP activity associated with lower NAD concentrations may slow DNA repair and enhance DNA damage. Only rats fed the MCFD and MCFND diets developed hepatocarcinomas after 12-17 mo. In Experiment 2, hepatocarcinomas were found in 100% of rats fed the MCFD and MCFND diets. These preliminary results indicate that folic acid deficiency enhances tumor development. Becausetions of NAD in these animals were also low, further studies are needed to clearly define the role of niacin in methyldeficient rats.


* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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