Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status.

European journal of clinical nutrition. 2002;56(9):850-6

Plain language summary

Riboflavin is a cofactor in the various pathways involving plasma homocysteine. The body has efficient methods of modulating total plasma homocysteine (tHcy) concentration as elevated levels are associated with cardiovascular disease. Riboflavin is frequently lowered in older populations, and while it is possible that riboflavin may be an important determinant of tHcy levels, there is limited information on the effect of riboflavin intake and status on plasma tHcy in humans. The aim of this study was to investigate the effect of riboflavin supplementation on fasting plasma tHCy levels. Healthy adults aged 60 and over were screened and 45 participants with sub-optimal riboflavin status completed the study. The first part of the trial was a placebo-controlled intervention with riboflavin; the second part involved supplementation of folic acid for six weeks followed by folic acid and riboflavin supplementation for a further 12 weeks. The findings of this study indicate that, though riboflavin supplementation significantly improved riboflavin status, it did not affect tHcy concentrations. Despite the metabolic dependence on riboflavin, folic acid supplementation proved to be a more effective homocysteine-lowering agent.

Abstract

OBJECTIVE To investigate the effect of riboflavin supplementation on plasma homocysteine (tHcy) concentrations in healthy elderly people with sub-optimal riboflavin status. DESIGN A double-blind, randomized, placebo-controlled riboflavin supplementation trial. SETTING Community based study in Northern Ireland. SUBJECTS From a screening sample of 101 healthy elderly people, 52 had sub-optimal riboflavin status (erythrocyte glutathione reductase activation coefficient, EGRAC>or=1.20) and were invited to participate in the study. INTERVENTION The intervention had two parts. Part 1 was a 12 week randomized double blind, placebo-controlled intervention with riboflavin (1.6 mg/day). Following completion of part 1, the placebo group went on to part 2 of the study which involved supplementation with folic acid (400 micro g/day) for 6 weeks followed by folic acid and riboflavin (1.6 mg/day) for a further 12 weeks, with a 16 week washout period post-supplementation. The purpose of part 2 was: (a) to address the possibility that homocysteine-lowering in response to riboflavin may be obscured by a much greater effect of folate, and that, once folate status was optimized, a dependence of homocysteine on riboflavin might emerge; and (b) to demonstrate that these subjects had homocysteine concentrations which could be lowered by nutritional intervention. RESULTS Although riboflavin supplementation significantly improved riboflavin status in both parts 1 and 2 of the study (P<0.001 for each), tHcy concentrations were unaffected (P=0.719). In contrast, folic acid supplementation (study part 2) resulted in a homocysteine lowering of 19.6% (P=0.001). CONCLUSION Despite the metabolic dependency of tHcy on riboflavin, it did not prove to be an effective homocysteine-lowering agent, even in the face of sub-optimal riboflavin status.

Lifestyle medicine

Patient Centred Factors : Mediators/Homocysteine
Environmental Inputs : Nutrients
Personal Lifestyle Factors : Nutrition
Functional Laboratory Testing : Blood
Bioactive Substances : tHcy ; Folate

Methodological quality

Allocation concealment : Not applicable

Metadata

Nutrition Evidence keywords : tHcy ; Folate