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American Journal of Clinical Nutrition, Vol. 80, No. 4, 1050-1057, October 2004
© 2004 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

Phenotypic expression of the methylenetetrahydrofolate reductase 677C->T polymorphism and flavin cofactor availability in thyroid dysfunction1,2,3

Steinar Hustad, Bjørn G Nedrebø, Per Magne Ueland, Jørn Schneede, Stein Emil Vollset, Arve Ulvik and Ernst A Lien

1 From the LOCUS for Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway (SH, PMU, JS, SEV, AU, and EAL), and the Hormone Laboratory, Haukeland University Hospital, Bergen, Norway (BGN and EAL).

Background: The 5,10-methylenetetrahydrofolate reductase gene (MTHFR) 677C->T polymorphism modifies the risk of coronary artery disease and colon cancer and is related to plasma concentrations of total homocysteine (tHcy). Riboflavin status modifies the metabolic effect of the polymorphism, and thyroid hormones increase the synthesis of flavin cofactors.

Objective: The aim of the study was to investigate the phenotypic expression of the MTHFR 677C->T polymorphism in terms of plasma tHcy concentrations in patients with thyroid dysfunction.

Design: The study population consisted of 182 patients with hyperthyroidism. We studied plasma tHcy in relation to MTHFR genotype, riboflavin, and folate before and during 6 mo of treatment with antithyroid drugs.

Results: Before treatment, tHcy was higher in patients with the mutant enzyme than in those with the wild-type enzyme. A genotype effect was observed only at low riboflavin or folate concentrations (P ≤ 0.05). During treatment, concentrations of flavin cofactors in plasma decreased (P < 0.001), and tHcy increased (P < 0.001). The overall tHcy increase was greatest in patients with the T allele, particularly at low riboflavin concentrations (P = 0.004).

Conclusion: Thyroid status affects the phenotypic expression of the MTHFR 677C->T polymorphism, possibly by modifying the availability of flavin cofactors.

Key Words: Flavin adenine dinucleotide • flavin mononucleotide • Graves disease • polymorphism • genetics • riboflavin




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[Abstract] [Full Text] [PDF]


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