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1 Cardiovascular Sciences Research Group, Wales Heart Research Institute, and
3 Department of Epidemiology, Statistics and Public Health, University of Wales College of Medicine, Cardiff, Wales CF14 4XN, United Kingdom.
2 Centre for Human Nutrition, Division of Clinical Sciences, Northern General Hospital, University of Sheffield, Sheffield S5 7AU, United Kingdom.
aAuthor for correspondence. Fax 44-29-2074-3500; e-mail moatsj{at}cardiff.ac.uk
Background: Riboflavin (vitamin B2) is the precursor for FAD, the cofactor for methylenetetrahydrofolate reductase (MTHFR). MTHFR catalyzes the formation of 5-methyltetrahydrofolate, which acts as a methyl donor for homocysteine remethylation. Individuals with the MTHFR 677C
T mutation have increased plasma total homocysteine (tHcy) concentrations, particularly in association with low folate status. It has been proposed that riboflavin may act together with folate to lower plasma tHcy, particularly in individuals with the thermolabile MTHFR T variant.
Methods: We measured B-vitamin status and plasma tHcy in 126 healthy individuals 20–63 years of age (42 CC, 42 CT, and 42 TT MTHFR genotypes) at baseline and after three interventions (4 months): placebo plus natural diet; daily 400 µg folic acid supplement plus natural diet; and increased dietary folate to 400 µg/day.
Results: At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 µmol/L higher in the lowest plasma riboflavin quartile compared with the highest (P <0.02) and was 4.2 µmol/L higher in the highest erythrocyte glutathione reductase activation coefficient (EGRAC) quartile compared with the lowest (P <0.001). This effect was not restricted to those with the T allele. Folic acid given as a 400 µg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC 
1.4 from 52% to 65% after supplementation (P <0.05).
Conclusions: Folate and riboflavin interact to lower plasma tHcy, possibly by maximizing the catalytic activity of MTHFR. The effect may be unrelated to MTHFR genotype.
The following articles in journals at HighWire Press have cited this article:
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J. R Dainty, N. R Bullock, D. J Hart, A. T Hewson, R. Turner, P. M Finglas, and H. J Powers Quantification of the bioavailability of riboflavin from foods by use of stable-isotope labels and kinetic modeling Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1557 - 1564. [Abstract] [Full Text] [PDF]
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H. J. Powers Interaction among Folate, Riboflavin, Genotype, and Cancer, with Reference to Colorectal and Cervical Cancer J. Nutr., December 1, 2005; 135(12): 2960S - 2966S. [Abstract] [Full Text] [PDF]
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V. Ganji and M. R Kafai Frequent consumption of milk, yogurt, cold breakfast cereals, peppers, and cruciferous vegetables and intakes of dietary folate and riboflavin but not vitamins B-12 and B-6 are inversely associated with serum total homocysteine concentrations in the US population Am. J. Clinical Nutrition, December 1, 2004; 80(6): 1500 - 1507. [Abstract] [Full Text] [PDF]
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S. Narayanan, J. McConnell, J. Little, L. Sharp, C. J. Piyathilake, H. Powers, G. Basten, and S. J. Duthie Associations between Two Common Variants C677T and A1298C in the Methylenetetrahydrofolate Reductase Gene and Measures of Folate Metabolism and DNA Stability (Strand Breaks, Misincorporated Uracil, and DNA Methylation Status) in Human Lymphocytes In vivo Cancer Epidemiol. Biomarkers Prev., September 1, 2004; 13(9): 1436 - 1443. [Abstract] [Full Text] [PDF]
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H. J Powers Riboflavin (vitamin B-2) and health Am. J. Clinical Nutrition, June 1, 2003; 77(6): 1352 - 1360. [Abstract] [Full Text] [PDF]
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