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Clinical Chemistry 49: 1416-1417, 2003; 10.1373/49.8.1416
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(Clinical Chemistry. 2003;49:1416-1417.)
© 2003 American Association for Clinical Chemistry, Inc.

Letters to the Editor

Folic Acid Supplementation and Riboflavin Status

Michelle M. Murphy1,a and Joan D. Fernandez-Ballart1

1 Unit of Preventive Medicine and, Public Health, Faculty of Medicine, Universitat Rovira i Virgili, Reus NA 43201, Spain

aAuthor for correspondence. Fax 34-977-759-322; e-mail mm@fmcs.urv.es.

The first 20% of the full text of this article appears below.


To the Editor:

Flour in the US is fortified with folic acid and riboflavin. Folic acid reduces mean plasma total homocysteine (tHcy) concentration (1). Riboflavin has been associated with reduced tHcy in homozygotes for the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism (2).

In a study that investigated the effect of riboflavin status on the tHcy-lowering response of folate interventions, Moat el al. (3) reported that riboflavin status is compromised after folic acid supplementation. Subjects were assigned to three interventions (each lasting 4 months) using a crossover design: (a) usual diet but avoiding folic acid-fortified foods, plus a daily placebo tablet; (b) usual diet plus additional folic-acid-fortified and folate-rich foods to achieve at least 400 µg of folic acid/day; (c) usual diet but avoiding folic-acid-fortified foods, plus a folic acid supplement of 400 µg/day.

Moat el al. (3) reported that suboptimal riboflavin status [erythrocyte glutathione reductase activation coefficient (EGRAC) >=1.4] increased from 52% at baseline to 62% after intervention 3. The authors suggested that this was attributable to supplementation with folic acid and proposed two possible mechanisms in which circulating flavins would be reduced as a consequence of the effect of enhanced folate . . . [Full Text of this Article]

Stuart J. Moat2,b, Pauline A.L. Ashfield-Watt2, Hilary J. Powers3, Robert G. Newcombe4 and Ian F.W. McDowell2

2 Cardiovascular Sciences, Research Group, Wales Heart Research Institute, University of Wales, College of Medicine, Cardiff, Wales, CF14 4XN, United Kingdom

3 Centre for Human Nutrition, Division of Clinical Sciences, University of Sheffield, Northern General Hospital, Sheffield S5 7AU, United Kingdom

4 Department of Epidemiology, Statistics, and Public Health, University of Wales College of Medicine, Cardiff, Wales CF14 4XN, United Kingdom

bAddress correspondence to this author at: Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff, Wales CF14 4XN, United Kingdom. Fax 44-29-2074-3500; e-mail: moatsj@cardiff.ac.uk.






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