
What is it?
Methionine is one of the essential amino
acids (building blocks of protein), meaning that it cannot be produced by the body, and
must be provided by the diet. It supplies
sulphur and other compounds required by the body for normal metabolism and growth.
Methionine also belongs to a group of compounds called lipotropics, or chemicals that help the
liver process fats (lipids). Others in this group include choline,
inositol, and betaine
(trimethylglycine).
People with AIDS have low levels of
methionine. Some researchers suggest this may explain some aspects of the disease
process,1 2 3 especially the deterioration that occurs in the
nervous system that can cause symptoms, including
dementia.4 5 A preliminary study has suggested that methionine (6
grams per day) may improve memory recall in people with AIDS-related nervous system
degeneration.6
Other preliminary studies have suggested that methionine (5 grams per day) may help treat
some symptoms of Parkinson’s
disease.7 However, another form of methionine, S-adenosylmethionine (SAMe) may worsen the symptoms of Parkinson’s
disease and should be avoided until more is known.8 9 10
11 12
Methionine (2 grams per day) in combination with several antioxidants, reduced pain and recurrences of attacks of pancreatitis in a
small but well-controlled trial.13
Where is it found?
Meat, fish, and dairy are all good sources of methionine. Vegetarians can obtain methionine from whole grains,
but beans are a relatively poor source of this
amino acid.
Methionine has been used
in connection with the following conditions (refer to the individual
health concern for complete information):
Who is likely to be deficient?
Most people consume plenty of methionine through a typical diet. Lower intakes during pregnancy have been associated with neural tube defects in newborns, but the significance
of this is not yet clear.14
How much is usually taken?
Amino acid requirements vary according to
body weight. However, average-size adults require approximately 800–1,000 mg of
methionine per day—an amount easily obtained or even exceeded by most Western diets.
Are there any side effects or interactions?
Animal studies suggest that diets high in methionine, in the presence of B-vitamin
deficiencies, may increase the risk for
atherosclerosis (hardening of the arteries) by increasing blood levels of cholesterol and a compound called homocysteine.15 This idea has not yet been
tested in humans. Excessive methionine intake, together with inadequate intake of folic acid, vitamin B6, and vitamin B12, can increase the conversion of methionine
to homocysteine—a substance linked to heart
disease and stroke. Even in the absence of
a deficiency of folic acid, B6, or
B12, megadoses of methionine (7 grams per day) have been found to cause elevations in
blood levels of homocysteine.16 Whether such an increase would create a significant
hazard for humans taking supplemental methionine has not been established. Supplementation of
up to 2 grams of methionine daily for long periods of time has not been reported to cause any
serious side effects.17
At the time of writing, there were no well-known drug interactions
with methionine.
References
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1. Muller F, Svardal AM, Aukrust P, et al. Elevated plasma concentration
of reduced homocysteine in patients with Human Immunodeficiency Virus infection. Am J Clin
Nutr 1996;63:242–6.
2. Revillard JP, Vincent CM, Favier AE, et al. Lipid peroxidation in
Human Immunodeficiency Virus infection. J Acquir Immune Defic Syndr
1992;5:637–8.
3. Singer P, Katz DP, Dillon L, et al. Nutritional aspects of the
Acquired Immunodeficiency Syndrome. Am J Gastroenterol 1992;87:265–73.
4. Tan SV, Guiloff RJ. Hypothesis on the pathogenesis of vacuolar
myelopathy, dementia, and peripheral neuropathy in AIDS. J Neurol Neurosurg
Psychiatry 1998 65:23–8.
5. Keating JN, Trimble KC, Mulcahy F, et al. Evidence of brain
methyltransferase inhibition and early brain involvement in HIV-positive patients.
Lancet 1991;337:935–9.
6. 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.
7. Smythies JR, Halsey JH. Treatment of Parkinson’s disease with
l-methionine. South Med J 1984;77:1577.
8. Charlton CG, Mack J. Substantia nigra degeneration and tyrosine
hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain. Support for an
excess methylation hypothesis for parkinsonism. Mol Neurobiol
1994;9:149–61.
9. Crowell BG Jr, Benson R, Shockley D, Charlton CG.
S-adenosyl-L-methionine decreases motor activity in the rat: similarity to Parkinson’s
disease-like symptoms. Behav Neural Biol 1993;59:186–93.
10. Benson R, Crowell B, Hill B, et al. The effects of L-dopa on the
activity of methionine adenosyltransferase: relevance to L-dopa therapy and tolerance.
Neurochem Res 1993;18:325–30.
11. Cheng H, Gomes-Trolin C, Aquilonius SM, et al. Levels of L-methionine
S-adenosyltransferase activity in erythrocytes and concentrations of S-adenosylmethionine and
S-adenosylhomocysteine in whole blood of patients with Parkinson’s disease. Exp
Neurol 1997;145:580–5.
12. Charlton CG, Crowell B Jr. Parkinson’s disease-like effects of
S-adenosyl-L-methionine: effects of L-dopa. Pharmacol Biochem Behav
1992;43:423–31.
13. Uden S, Bilton D, Nathan L, et al. Antioxidant therapy for recurrent
pancreatitis: placebo-controlled trial. Aliment Pharmacol Ther
1990;4:357–71.
14. Shaw GM, Velie EM, Schaffer DM. Is dietary intake of methionine
associated with a reduction in risk for neural tube defect-associated pregnancies?
Teratology 1997;56:295–9.
15. Toborek M, Hennig B. Is methionine an atherogenic amino acid? J
Optimal Nutr 1994;3:80–3.
16. McAuley DF, Hanratty CG, McGurk C, et al. Effect of methionine
supplementation on endothelial function, plasma homocysteine, and lipid peroxidation. J
Toxicol Clin Toxicol 1999;37:435–40.
17. Leach FN, Braganza JM. Methionine is important in treatment of
chronic pancreatitis. Br Med J 1998;316:474 [letter].
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