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The term 'optimum nutrition' has evolved from a perceived need to base recommendations for nutrient intakes firmly in the context of function. It follows that 'optimum nutritional status' for individual nutrients should be defined in terms of biochemical or physiological markers having some functional value but also showing an appropriate relationship to nutrient intake. The present short review considers the current position regarding such markers for riboflavin, pyridoxine and niacin. It is concluded that whilst there are several biochemical measures which respond to changes in intake of each of these vitamins, no single measure is wholly satisfactory as a marker of optimum status. [ABSTRACT FROM AUTHOR]

The effects of maternal intake and gestational age on materno-fetal transport of vitamin C were investigated in female Dunkin-Hartley guinea-pigs. Twenty-four time-mated dams were fed on either a moderate-vitamin C (group A) or a high-vitamin C (group B) diet, throughout pregnancy. At days 49, 63 and 66 of gestation, and at term, three animals from each group were killed and fetuses removed by hysterectomy. Plasma, liver, kidney, lungs, heart, placenta and amniotic fluid were collected from dams and fetuses and subsequently analysed for vitamin C. Fetal plasma and amniotic fluid concentrations showed negative associations with gestational age for both dietary groups, independent of an effect of dam (P < 0.001). A similar, though not significant, effect of gestational age was observed on placental vitamin C and group A fetal tissue concentrations. Fetal plasma, placental and amniotic fluid vitamin C concentrations were significantly higher in group B than group A (P < 0.001), suggesting the influence of maternal diet. Although the level of maternal vitamin C intake can influence the circulating concentration in the fetus, there is a decrease associated with increasing gestational age, independent of the maternal diet. The gestational age-dependent change in the fetal accumulation of vitamin C may reflect changes in the rate of placental transfer. [ABSTRACT FROM PUBLISHER]

Abstract:The impaired absorption and metabolism of Fe seen in riboflavin defiaency is attributed, at least in part, to a hyperproliferative response in the small intestine, associated with an altered morphology. Studies were conducted in female weanling Wistar rats to explore further the effect of riboflavin deficiency on the cytokinetics and structure of the small intestine. Feeding a riboflavin-deficient diet for 8 weeks from weaning resulted in a significantly lower villus number, a significant increase in villus length and an increased rate of transit of enterocytes along the villi, compared with weight-matched controls. A second experiment focused on the 3 weeks after weaning and showed that riboflavin deficiency inhibits the increase in villus number observed in control animals over this period. We suggest that riboflavin deficiency induced at weaning impairs the normal increase in villus number and that prolonged deficiency leads to an adaptive increase in length of villi and depth of crypts. [ABSTRACT FROM PUBLISHER]

Female Wistar rats were weaned onto a diet deficient in riboflavin and compared with weight-matched and ad lib.-fed controls. The effects of riboflavin deficiency on villus morphometry and enterocyte number on the villi in the upper small intestine were studied. Riboflavin depletion was associated with increased villus length and a proportional increase in the number of cell positions along the villi. The total DNA, RNA and protein contents in the intestinal mucosa were not significantly different between any of the groups. Villus hypertrophy in the absence of increased cell number in the small intestine suggests that villus number may be reduced in riboflavin deficiency. Riboflavin deficiency did not influence the number of mucus-producing goblet cells or the amount of mucosal glycoprotein in the small intestine. Impaired production of mucus appeared not to be involved in the structural and functional changes seen in riboflavin deficiency. [ABSTRACT FROM PUBLISHER]

Objective: To provide the informed health professional with an up to date evaluation of the current thinking regarding requirements for vitamins in infant feeds. ESTABLISHING CRITERIA FOR ADEQUACY: Vitamin adequacy in the neonate is currently defined in terms of circulating levels of a vitamin or of the activity of a vitamin dependent enzyme in the erythrocytes. Although these measurements have their value there is a need to develop biochemical, physiological or clinical markers of well defined specific function. For some vitamins there is a risk of deleterious effects of very high intakes: risk of toxicity needs to be taken into consideration when making recommendations for inclusion in infant formulae. BREAST MILK AS THE 'GOLD STANDARD': Breast milk concentrations of vitamins have been used as the criteria of adequate intake by neonates. This may not always be justified. Greater consideration needs to be given to differences in bioavailability of vitamins from breast milk compared with formula feeds, of the influence of season, and of stage of lactation, on the stated composition., Experimental Approaches: Animal studies have provided limited information regarding effects of different levels of intakes on current status indices in the neonatal period. There are few reports of randomized controlled studies into the effects of different levels of vitamins and these rely heavily on biochemical criteria of adequacy., Recent Developments: The inclusion of beta-carotene into formula feeds for premature babies is an issue of current interest. What is the justification for this? Are there potential benefits for the term infant? Riboflavin deficiency in the period around weaning may affect the normal structural and functional development of the gastrointestinal tract; some of these effects may be permanent. RESEARCH TO BE DONE: A greater understanding of the absorption and metabolism of vitamins during infancy is required in order to help establish dietary requirements. The relative bioavailability of vitamins in human milk and formulae needs to be investigated. Criteria for vitamin adequacy should be extended to include measures of function. Information regarding the conversion factor from tryptophan to niacin in infancy would allow us to set niacin requirements with greater confidence. There is a particular lack of information about concentrations of biotin and pantothenic acid in breast milk and the relative biochemical status of infants receiving breast milk and formulae. Benefits of including beta-carotene into infant formulae need to be evaluated. The role of individual micronutrients in the structural and functional development of the gastrointestinal tract should be explored.