Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status
Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status
复制标题
补充核黄素对核黄素水平低的老年人血浆同型半胱氨酸的影响
DOI:
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发表时间:
2002
影响因子:
4.7
通讯作者:
J. Scott
中科院分区:
文献类型:
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作者:
M. C. McKinley;H. McNulty;J. Mcpartlin;J. Strain;J. Scott
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≥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 µg/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.