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The article comments on a study on riboflavin deficiency and vitamin B-6 status. It identifies strengths of the study including its use of erythrocyte glutathione reductase activation (EGRac), inclusion of data on dietary intake and riboflavin marker and determination of the effect of methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism on riboflavin requirements. Also noted is the significance of the study to defining nutrient reference intake.

Background: Moderate riboflavin deficiency is prevalent in certain population groups in affluent countries, but the functional significance of this deficiency is not clear. Studies have indicated a role for riboflavin in the absorption and use of iron. Objective: We investigated the effect of riboflavin supplementation on hematologic status in a group of moderately riboflavin-deficient women aged 19-25 y in the United Kingdom. Design: One hundred twenty-three women with biochemical evidence of riboflavin deficiency [erythrocyte glutathione reductase activation coefficient (EGRAC) >1.40] were randomly assigned to receive 2 or 4 mg riboflavin or a placebo for 8 wk. Measurements of hematologic status were made pre- and postsupplementation, and dietary intakes were also assessed; iron absorption was measured in a subgroup of women. Results: One hundred nineteen women completed the intervention. The use of a riboflavin supplement for 8 wk elicited a significant improvement in riboflavin status with a dose response (P < 0.0001). For women who received supplemental riboflavin, an increase in hemoglobin status correlated with improved riboflavin status (P < 0.02). Women in the lowest tertile of riboflavin status at baseline (EGRAC >1.65) showed a significantly greater increase in hemoglobin status in response to the supplement than did women in the first and second tertiles (P < 0.01). Dietary iron intake and iron absorption did not change during the study. Conclusions: Moderately poor riboflavin status can affect iron status: the lower the riboflavin status, the greater the hematologic benefits of improving status. The results also suggest that consideration should be given to raising the currently accepted EGRAC threshold for deficiency. This trial was registered at controlled-trials.com as ISRCTN35811298. [ABSTRACT FROM AUTHOR]

The article presents a study which aims to identify whether dietary deficiencies of choline and riboflavin in pregnant mice affect embryonic development. It mentions the collection of embryos of 14.5 d postcoitum and the examination for reproductive outcomes and cardiac defects. It concludes that low dietary choline and riboflavin affect cardiac development and embryonic growth in mice.

The article presents a study which investigates the use of stable-isotope labels and kinetic modeling in the quantification of bioavailability of riboflavin from foods. Topics discussed include discrepancies in the estimates of the prevalence of riboflavin deficiency in Great Britain based on riboflavin consumption, result of urinary monitoring which suggest that riboflavin from spinach is bioavailable as in riboflavin in milk, and absorbed riboflavin in plasma and urine.

The article presents a study which examines the effect of supplemental riboflavin and iron on plasma retinol and pupillary threshold (PT) in nightblind, pregnant Nepali women taking vitamin A-fortified rice. Authors of the study measured erythrocyte riboflavin, hemoglobin, plasma ferritin and retinol before and after the intervention. Results showed that the deficiency in iron might limit the efficacy of vitamin A to normalize dark adaptation in pregnant Nepali women.

Background: Current data suggest that physiologic doses of vitamin B-6 have no significant homocysteine-lowering effect. It is possible that an effect of vitamin B-6 was missed in previous trials because of a much greater effect of folic acid, vitamin B-12, or both. Objective: The aim of this study was to investigate the effect of low-dose vitamin B-6 supplementation on fasting total homocysteine (tHcy) concentrations in healthy elderly persons who were made replete with folate and riboflavin. Design: Twenty-two healthy elderly persons aged 63-80 y were supplemented with a low dose of vitamin B-6 (1.6 mg/d) for 12 wk in a randomized, double-blind, placebo-controlled trial after repletion with folic acid (400 g/d for 6 wk) and riboflavin (1.6 mg/d for 18 wk); none of the subjects had a vitamin B-12 deficiency. Results: Folic acid supplementation lowered fasting tHcy by 19.6% (P < 0.001). After folic acid supplementation, baseline tHcy concentrations ranged from 6.22 to 23.52µ mol/L and 10 subjects had suboptimal vitamin B-6 status (plasma pyridoxal - P < 20 nmol/L). Two-way analysis of variance showed that the significant improvement in vitamin B-6 status in response to vitamin B-6 supplementation (on the basis of both pyridoxal-P and the erythrocyte aspartate aminotransferase activation coefficient) was reflected in a significant reduction in plasma tHcy of 7.5%. Conclusions: Low-dose vitamin B-6 effectively lowers fasting plasma tHcy in healthy subjects who are both folate and riboflavin replete. This suggests that any program aimed at the treatment or prevention of hyperhomocysteinemia should include vitamin B-6 supplementation. [ABSTRACT FROM AUTHOR]

Several abstracts are presented including on erythrocyte lipid peroxidation during riboflavin deficiency, electron microscopy study of lungs and role of magnesium deficiency in the pathogenesis.

Assesses vitamin B-6 and riboflavin intake and status in healthy, elderly in Northern Ireland. Percent of individuals who showed abnormal riboflavin and vitamin B-6 coefficients; Ability of low dose riboflavin supplementation to correct biochemical abnormalities.

Six groups of elderly subjects from central Guatemala were assessed for riboflavin status by using the erythrocyte glutathione reductase activity coefficient (EGRAC). The prevalence of riboflavin deficiency ranged from 50% to 76% among the free-living rural elderly subjects. Milk intake data that were collected from some of the subjects showed a significant correlation (P < 0.0001) between frequency of milk intake and riboflavin status. In a short-term riboflavin supplementation experiment in which nine riboflavin-deficient subjects were given 10 mg riboflavin/d for 3 d. all the subjects' EGRACs were normalized by the supplementation. However, they returned to a state of deficiency within 2 wk while consuming their usual diets without supplementation. It appears that the high prevalence of riboflavin deficiency in elderly Guatemalan people is caused by inadequate intake of riboflavin-rich foods such as dairy products, and that sufficient amounts of riboflavin need to be ingested regularly to maintain satisfactory riboflavin status. [ABSTRACT FROM AUTHOR]

This study was designed to confirm that low dietary riboflavin does not contribute to the flavin-deficient red blood cells commonly found in subjects in Ferrara Province, northern Italy. In this area it is primarily an inherited characteristic believed to have been selected for by malaria, which was endemic from the 12th century. In parallel with assessment of daily riboflavin intake (DRI), flavin adenine dinucleotide-dependent glutathione reductase (EGR) and flavin mononucleotide-dependent pyridoxine phosphate oxidase (PPO) were measured in β-thalassemic heterozygotes, their normal relatives, and normal spouses (representative of the normal population). In all of these groups there is a high incidence of deficiency of these flavin enzymes. We found that the majority had an adequate riboflavin intake and there was no significant correlation of EGR and PPO activities with DRI. Thus, interpretation of low EGR activity is discussed with reference to studies of EGR done to detect nutritional riboflavin deficiency in countries where there is malnutrition and endemic malaria. [ABSTRACT FROM AUTHOR]

To determine the effect of riboflavin deficiency on the rat pancreas, one-third of a group of rats was fed a purified riboflavin-sufficient diet ad libitum and two-thirds were fed isocaloric amounts of riboflavin-deficient diet for 13 wk; one-half of the latter group was replenished with daily intraperitoneal injections of riboflavin for the last 3 wk. Body weight, pancreas weight, DNA, protein, amylase, chymotrypsinogen, and trypsinogen decreased in riboflavin-deficient animals. In vitro basal secretion of chymotrypsinogen decreased and basal and bethanechol-stimulated secretions of trypsinogen increased in riboflavin-deficient rats. These changes were considered to be caused by relative inanition resulting from decreased food consumption. On replenishment of niboflavin, amylase content reverted to that of animals fed ad libitum whereas increases in body weight, pancreas weight, DNA, protein, chymotrypsinogen, and trypsinogen were not statistically significant. Both basal- and bethanechol-stimulated secretions of chymotrypsinogen increased. These data indicate that riboflavin deficiency, which commonly accompanies chronic alcoholism, may contribute to the pancreatic injury in chronic alcoholism. [ABSTRACT FROM AUTHOR]

In the hypothyroid rat the flavin adenine dinucleotide (FAD) content of the liver is similar to that observed in rats maintained on a riboflavin-deficient diet. Thyroxine regulates the enzyme flavin kinase. Human adults with hypothyroidism have levels of erythrocyte glutathione reductase (EGR), an FAD-containing enzyme, in the range indicative of riboflavin deficiency, which can be corrected with thyroxine therapy. In the present study six newborns with severe congenital hypothyroidism because of athyrosis, ectopic thyroidism, or congenital hypothyroidism with Down's syndrome had normal levels of EGR, and treatment with thyroxine had no effect on these levels. [ABSTRACT FROM AUTHOR]