Methionine Introduction

Methionine is the least abundant of all amino acids. Despite this verity, methionine is essential, and is an important chelating agent that assists in both metabolic and growth processes. Along with cysteine and cystine, methionine is also a sulfur-containing amino acid. Cysteine and methionine are the only sulfur-containing amino acids readily coded for by DNA.

Methionine (along with choline and inositol) is included in a group of compounds referred to as lipotropics. Lipotropic literally means “fat loving”, and these specialized compounds aid the liver in processing fats by increasing the production of lecithin. Choline and methionine work in union to detoxify the body of amines resulting from protein synthesis, and protecting the liver from damage that is the result of fat accumulation. Methionine serves as a catalyst for choline and inositol functioning. It actively participates in the formation of D-glucose, the primary energy source of living organisms, as well.

In addition to the aforementioned roles, methionine in included in a number of biochemical reactions. Methionine is an integral element in the production of L-cysteine, glutathione, taurine, sulfate, and perhaps most notably, S-adenosylmethionine (SAMe). The varying forms of methionine include:

• L-methionine
• Ademethionine
• S-Adensyl-L-methionine

The most plentiful sources of methionine include beef, eggs, chicken, fish, sardines, pork, liver, milk products, sunflower and sesame seeds, and lentils. Vegetarians are more likely to obtain the majority of their intake through whole grains, as beans are a relatively poor source of this amino acid. Serving sizes below are based upon 100 grams of a given food source and are expressed in milligrams, representing the amount of methionine contained.

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Being a lipotropic, methionine may reduce the liver-toxic affects of hepatoxins. Hepatotoxins are chemicals which are toxic to the liver and include medications such as acetaminophen and methotrexate. Methionine supplementation may prove especially useful in cases of acetaminophen poisoning. Methionine, given within ten hours of poisoning from either acetaminophen or methotrexate, has proven affective in the treatment and prevention of severe liver damage, and even death. [2, 3]

Methione’s most important function in human physiology may be its antioxidant activities. Both the L- and D- forms of this amino have been shown to protect the body’s cells from harmful free radical damage. [4] The protection against free radicals and toxic compounds may coincide to the sulfur which methonine possesses in its chemical makeup. [5] This may also provide a feasible explanation as to why methionine is ascribed as an anti-hepatotoxic agent.

Methionine may also reduce histamine levels in the body. Histamines are amino acids that cause the dilation of capillaries, a stimulation of gastric secretion, constriction of bronchial smooth muscle, and a decrease blood pressure. The reduction of histamine levels, by supplemental methionine, may prove useful for individuals suffering from depression, as it is linked to elevated histamine levels, and certain allergies. [6]

Schizophrenia is another cognitive disorder which has also been linked to excessive blood histamine levels. Methionine has shown great promise in the reduction of symptoms associated with this condition. [7]

Persons suffering from HIV/AIDS often exhibit dangerously low levels of methionine. Research suggests that this deficiency may have a direct impact on severity of the disease process, especially in the deterioration of the nervous system. [8] Methionine may improve cognitive functioning and prevent nervous system degeneration in these persons. [9]

Ongoing and future clinical application into the benefits of methionine supplementation include; the treatment of endometriosis (condition in which white patches of endometrial tissue from the uterine lining grow outside the uterus), Parkinson's disease, pancreatitis, osteoarthritis, and migraine headaches. [10, 11]

The established Recommended Daily Allowance (RDA) for methionine is listed under the heading ‘S-containing amino acids,’ because it provides the body with an abundant supply of Sulfur (S-). The average consumption in adults ranges from 800 - 1000 milligrams of methionine per day. The RDA of methionine is easily achieved in western diets and is often times exceeded.

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The U.S. National Academy of Sciences recommends that healthy people achieve .36 grams of highly bioavailable protein for each pound of bodyweight - equaling 0.8 grams of protein, per kilogram of bodyweight.

Methionine Deficiencies

Lesser deficiencies of methionine may be characterized by symptoms of inhibited growth, edema, fatty liver, and skin lesions. Prolonged and severe deficiencies of methionine may lead to dementia in certain individuals.

Persons suffering from liver problems, HIV/AIDS, pancreatitis, and Parkinson’s disease, may be at an elevated risk for the development of a methionine deficiency. Lowers levels of methionine have also been observed in women who are pregnant. This may be of special importance due to the complications arising from an inadequacy of methionine, referred to as neural tube defects, in newborns. [13]

Toxicities

Excessive amounts of supplemental methionine for an extended period of time may be correlated with an upset stomach and/or vomiting. [14] Persons with diets high in methionine should also be aware of the potential for an increased risk of increasing blood levels of cholesterol and the oxidant homocysteine. [15] This may be especially important due to research indicating an association between elevated homocysteine levels and the amplified risk for heart disease and stroke. There have also been studies highlighting the relation between excessive dosages of supplemental methionine to the growth of certain types of cancers. [16] More research is necessary to validate these claims.

1. Nutrition Data. “999 Foods; Highest in Serine.” (2004) http:// www.nutritiondata.com/foods-000084000000000000000-w.html

2. Vale JA, Meredith TJ, Goulding R. Treatment of acetaminophen poisoning. The use of oral methionine. Arch Int Med. 1981; 141(3 Spec No.)

3. Kroger H, Hauschild A, Ohde M, et al. Nicotinamide and methionine reduce the liver toxic effects of methotrexate. Gen Pharmacol. 1999; 33; 203-206.

4. Sha S-H, Schacht J. Antioxidants attenuate gentamicin-induced free radical formation in vitro and ototoxicity in vivo: D-methionine is a potential protectant. Hearing Res. 2000;142:34-40.

5. Donaldson WE, Leming TK. Effect of Dietary Methionine and Lysine on the Toxicity of Ingested Lead Acetate in the Chick. J Nutr. 1984;114:2155-59.

6. Braverman E, et al. The Healing Nutrients Within. New Canaan, CT: Keats Publishing Inc; 1997:189-190.

7. Braverman E, et al. The Healing Nutrients Within. New Canaan, CT: Keats Publishing Inc ;1997:191-92.

8. Singer P, Katz DP, Dillon L, et al. Nutritional aspects of the Acquired Immunodeficiency Syndrome. Am J Gastroenterol . 1992;87:265-273.

9. Dorfman D, DiRocco A, Simpson D, et al. Oral methionine may improve neuropsychological function in patients with AIDS myelopathy: results of an open-label trial. AIDS 1997;11:1066-7.

10. Smythies JR, Halsey JH. Treatment of Parkinson’s disease with l-methionine. South Med J. 1984;77:1577.

11. Uden S, Bilton D, Nathan L, et al. Antioxidant therapy for recurrent pancreatitis: placebo-controlled trial. Aliment Pharmacol Ther 1990;4:357-71.

12. Zest for life information page. “RDA of amino acids.” (1999-2003) http://www.anyvitamins.com/amino-acids/rda-amino-acids.htm (14 Sept. 2004).

13. Shaw GM, Velie EM, Schaffer DM. Is dietary intake of methionine associated with a reduction in risk for neural tube defect-associated with pregnancies? Teratology 1997;56: 295-9.

14. Murray MT, Pizzorno J: Encyclopedia of Natural Medicine 2nd ed. Prima Publishing, Rocklin, CA; 1998.

15. Toborek M, Hennig B. Is methionine an atherogenic amino acid? J Optimal Nutr 1994;3;80-3.

16. Duranton B, Freund JN, Galluser M, et al. Promotion of intestinal carcinogenesis by dietary methionine. Carcinogenesis. 199;20:493-497.