Vitamin A in pregnancy and lactation.
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Animals↗
Biomedical subjects
C J Bates
Publications and source records attributed to C J Bates.
Efficacy of a riboflavin supplement given at fortnightly intervals to pregnant and lactating women in rural Gambia.
Thirty-seven women living in two rural Gambian villages, who were either pregnant or lactating at the outset of the study, received a tablet containing 15 mg riboflavin, or a placebo, at fortnightly intervals for 10 weeks at a time of year when riboflavin status was deteriorating. Clinical assessments were carried out once a week, with particular attention to signs and symptoms of riboflavin deficiency, and blood samples were taken at the beginning of the study and after 4 and 10 weeks supplementation for the assessment of riboflavin status by the activation coefficient of erythrocyte glutathione reductase. The overall incidence of lingual papillary atrophy increased significantly during the course of the study, but the increase was significantly smaller in the supplemented than in the placebo group. More complaints of sore mouths were encountered in the placebo group. Biochemical evidence of deficiency was very marked at the outset, and showed some improvement after supplementation, but values within the normal range were not achieved. It is concluded that a riboflavin supplement given at spaced intervals can be clinically beneficial, despite failure to achieve normal biochemical indices. This may have practical implications for intervention programmes.
Atrophy↗
Effects of riboflavin deficiency in rats on some aspects of iron metabolism.
Female Norwegian Hooded rats were given a diet low in riboflavin prior to pregnancy and during gestation and lactation. Each animal had a pair-fed control receiving a diet adequate in riboflavin. The ability of liver mitochondrial preparations to mobilise iron from ferritin was measured in the dams and their pups. The rate of mobilisation was reduced in the deficient animals relative to their controls and significantly so for the pups. The data support the hypothesis that riboflavin is an important factor in controlling iron utilisation.
Animals↗
The relative effectiveness of iron and iron with riboflavin in correcting a microcytic anaemia in men and children in rural Gambia.
Adult males and children between 4 and 12 years in a subsistence farming community in The Gambia were screened for haematological status. 80 men and 80 children with initially poor status were identified and allocated to three treatment groups comprising: a placebo, ferrous sulphate, and ferrous sulphate with riboflavin. Over a period of 6 weeks of supplementation there was a general improvement in haematological status in the two supplemented groups. The inclusion of riboflavin in the supplement enhanced recovery, particularly in those individuals with strikingly low levels of haemoglobin at the outset.
Adolescent↗
Analytical versus food table values for vitamin C in foods: the effect on calculated vitamin C intake of elderly subjects.
During a longitudinal study of vitamin C nutrition in 23 healthy elderly people, samples of cooked vegetables and liver, canned meats, canned vegetables and fruit drinks were analysed for vitamin C content. The analytical data are presented here and the effect on calculated daily intake of vitamin C of using the analytical values in place of food table values is assessed. For cooked foods the analysed values were close to food table values; exceptions were spring cabbage, cauliflower and canned potatoes. Fortified fruit drinks contained 20-60 mg vitamin C per 100 ml and made an important contribution to intake. Canned meats contained 0.3-61.4 mg per 100 g (mean 14.9 mg), but their contribution to intake was considered small. The difference between daily intakes calculated using analytical and food table values was greater than 5 mg in 37 per cent of 1-day periods and in 17 per cent of 7-day periods. These differences were not sufficient to significantly alter the correlations between intake and biochemical indices found in the original study. Nevertheless, given the discrepancies between calculated and analysed vitamin C intakes reported in the literature, analytical work is probably essential in studies of vitamin C nutrition.
Aged↗
The effect of vitamin C supplementation on lactating women in Keneba, a West African rural community.
A study of vitamin C requirements was undertaken in the village of Keneba, The Gambia, during the rainy season, when the intake of vitamin C-rich foods is very low. The effect of four supplementary levels of vitamin C (0, 24, 47 and 60 mg/day), together with a milk and biscuit food supplement which provided 34 mg vitamin C/day, was studied for a five-week period. Plasma ascorbate increased from 0.25 to 0.72 mg/dl; buffy coat ascorbate increased from 14.7 to 24.3 micrograms/10(8) cells and breast milk ascorbate increased from 3.4 to 5.5 mg/dl as intake increased from 34 to 103 mg/dl. Breast milk ascorbate approached a plateau at the high intakes. A fasting plasma ascorbate of at least 0.3 mg/dl in 97.5% of the population of lactating women in Keneba would require a daily vitamin C intake of about 117 mg. No differences between vitamin C supplementation levels were observed with respect to changes in plasma iron, total iron-binding capacity or its percentage saturation. Whole blood histamine levels showed a slight downward trend as the vitamin C intake increased.
Adult↗
Seasonal variations in ascorbic acid status and breast milk ascorbic acid levels in rural Gambian women in relation to dietary intake.
Vitamin C intakes from mangoes and oranges, and plasma and breast milk ascorbic acid concentrations were measured at regular intervals in a cohort of pregnant and lactating women in Keneba and Manduar, two neighbouring rural Gambian villages. Extremely wide seasonal variations in plasma ascorbic acid levels were observed, the peak during the mango season in May and June attaining mean levels of 1.4 mg/dl, while the lowest levels, averaging only 0.2 mg/dl, were observed during the rainy season, during September and October. Parallel, but less pronounced variations were observed in breast milk ascorbate levels. A vitamin-fortified milk and biscuit supplement, given first to the lactating, and later to the pregnant, mothers in Keneba, which provided about 35 mg ascorbic acid per day, failed to produce any major improvement in plasma ascorbic acid levels during the rainy season, although there was some evidence for an improvement in breast milk levels. It is therefore likely that considerably greater intakes are required to maintain satisfactory maternal circulating levels and biochemical status during this critical period.
Ascorbic Acid↗
Riboflavin status in infants born in rural Gambia, and the effect of a weaning food supplement.
Riboflavin status was measured in infants between birth and two years of age, by the erythrocyte glutathione reductase (NAD(P)H2: glutathione oxidoreductase, EC 1.6.4.2) test on finger-prick blood samples. The infants were living in three rural Gambian villages: Keneba, Manduar and Kanton Kundar; those in Keneba were receiving a weaning food supplement between three and 12 months, which provided 0.15 to 0.20 mg riboflavin per day, in addition to their normal intake from breast milk and locally available weaning foods, which provided 0.13 to 0.21 mg/day over the same age range. On the basis of currently accepted criteria of biochemical normality, the unsupplemented infants were born deficient and, in the absence of a supplement, remained so throughout their first two years of life, with only a minor, short-lived improvement during the first few months. In the supplemented group, however, riboflavin status fell within normal limits for the duration of the supplement, but rapidly deteriorated again once the supplement was withdrawn. It is concluded that infants born to deficient mothers are usually deficient at birth, and remain so throughout suckling and weaning on to locally available foods. The daily requirement, to achieve satisfactory biochemical status, is thus greater than 0.13 to 0.21 mg/day, and probably approaches 0.4 mg/day, for most individuals up to the age of one year.
Child, Preschool↗
Lipid metabolism in riboflavin-deficient rats. 1. Effect of dietary lipids on riboflavin status and fatty acid profiles.
1. The increase in activation coefficient (stimulated: basal activity) of erythrocyte NAD(P)H2: glutathione oxidoreductase (EC 1.6.4.2) and reduction in hepatic flavin concentration which occurred in riboflavin-deficient weanling rats were not markedly or consistently affected by differences in the concentration of lipid in the diet nor by differences in the total proportion of saturated or polyunsaturated fatty acids in the dietary lipid. 2. Their gain in body-weight was, however, reduced when the dietary lipid concentration was increased from 30 to 200 g/kg and liver: body-weight and hepatic triglyceride content were correspondingly increased, suggesting a functionally-deleterious effect of high fat intake in the deficient animals. This was especially severe when the diets contained cottonseed oil, which appeared to be toxic for the deficient animals. 3. Comparisons between fatty acid profiles of hepatic phospholipids of deficient, pair-fed and ad lib,-fed control animals indicated that the increase in proportion of 18:2 omega 6 and the decrease in proportion of 20:4 omega 6 observed in deficient animals were due specifically to riboflavin deficiency, whereas certain other changes were probably caused by inanition. The changes in 18:2 omega 6 and 20:4 omega 6 were observed at both low and high levels of lipid intake and at both low and high levels of dietary lipid polyunsaturation. Similar changes in fatty acid profiles were observed in renal, erythrocyte membrane, and plasma phospholipids, but were not seen in cardiac phospholipids, 4. A consistent increase in proportion of 18:2 omega 6 was also observed in the hepatic triglycerides, together with a decrease in proportion of 16:0. 5. It is concluded that acute riboflavin deficiency affects lipid metabolism in a characteristic manner, probably by interfering with beta-oxidation of fatty acids, but that diets of high lipid content do not significantly increase the extent of flavin depletion.
Animals↗
Lipid metabolism in riboflavin-deficient rats. 2. Mitochondrial fatty acid oxidation and the microsomal desaturation pathway.
1. Oxygen consumption was measured by means of an O2 electrode in mitochondrial suspensions from riboflavin-deficient and pair-fed control rats, using six different substrates. Whereas consumption of O2 by glutamate was only slightly depressed in mitochondria from deficient animals, the consumption of O2 by hexanoate and by palmitoyl-L-carnitine was depressed to approximately half the control value: a highly significant difference. A comparable magnitude of depression was observed for stearoyl-, oleoyl-, and linoleoyl-L-carnitine. There were no major or consistent differences between groups of animals receiving two different types, and two different levels, of fat in their diet. 2. The activity of acyl coenzyme A dehydrogenase (EC 1.3.99.3) in hepatic mitochondrial fragments, measured by cytochrome c reduction with palmitoyl-coenzyme A as substrate, and expressed as maximum velocity (Vmax) with respect to phenazine methosulphate, was also reduced to approximately half the control value in deficient animals. 3. In hepatic microsomes, cytochrome b5 reductase (EC 1.6.2.2) activity was unaffected by riboflavin deficiency, although NADPH-cytochrome c reductase (EC 1.6.2.4) and microsomal flavin content were diminished to approximately half the control values. Acyl CoA (delta 9) desaturase activity (EC 1.14.99.5) was virtually identical in deficient, pair-fed, and ad lib.-fed control groups. 4. It is concluded that the depression of mitochondrial beta-oxidation of fatty acids which is observed in riboflavin-deficient animals is not a secondary result of inanition, and may account for the observed changes in fatty acid profiles of triglycerides and phospholipids. Failure of the microsomal fatty acid desaturation system is less likely to be a major consequence of riboflavin deficiency.
Acyl-CoA Dehydrogenase↗
Riboflavin requirements of lactating Gambian women: a controlled supplementation trial.
As part of a study to determine the minimum allowance of riboflavin which is adequate for lactating women in a rural African environment, 60 subjects living in two Gambian villages were given either 2 mg riboflavin or a placebo daily on a double-blind basis for 12 wk. Their riboflavin intake from dietary sources was about 0.5 mg/day. In the supplemented group, the mean activation coefficient (AC) of erythrocyte glutathione reductase fell from 1.62 to 1.19 within 3 wk, and 90% had mean AC's below 1.3 throughout supplementation, whereas the placebo group maintained mean AC's between 1.6 and 1.9. Clinical signs associated with riboflavin deficiency improved more rapidly in the supplemented group; their breast milk riboflavin levels increased, and their infants' AC's were reduced, compared with those of the placebo group. After withdrawal of the supplement, the maternal and infants' AC's rose toward those of the placebo group. Thus a total riboflavin intake of about 2.5 mg/day during lactation is sufficient to maintain normal biochemical status in most Gambian women.
Adult↗
Physiological tests during an improvement in riboflavin status in lactating Gambian women.
During several weeks riboflavin supplementation of lactating African women, which reduced their mean activation coefficient of erythrocyte glutathione reductase (EGRAC) from 1.65 to 1.21 and initiated an improvement in clinical deficiency signs, measurements were made of physiological functions which may be connected with riboflavin status. No specific response to the supplement could be detected in body weight, grip strength, haematological parameters, osmotic fragility and resistance to oxidative stress of erythrocytes, plasma iron levels and related indices, or plasma hormone levels. There was a cross-sectional relationship between erythrocyte distribution on Percoll density gradients and EGRAC before supplementation, and between the Percoll pattern and total haemoglobin concentration. It is not yet known, however, whether a direct causal relationship exists between these variables.
Adult↗
The relationship between plasma ascorbate and lipid concentrations in fasting men.
A study was undertaken to investigate the relationship between vitamin C status and plasma lipid concentrations in 97 fasting men. Plasma ascorbate was found to be negatively associated with total cholesterol and positively associated with both high-density lipoprotein (HDL) cholesterol concentration and the HDL/total cholesterol ratio (P less than 0.05 in each case). There was no association between ascorbate and triglyceride levels. In view of the relevance of HDL cholesterol to ischaemic heart disease these associations may have some clinical importance, although they were all rather weak.
Adult↗
The discrepancy between normal folate intakes and the folate RDA.
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Adult↗
Plasma ascorbate and HDL-cholesterol in women.
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Adolescent↗
A biochemical evaluation of the erythrocyte glutathione reductase (EC 1.6.4.2) test for riboflavin status. 1. Rate and specificity of response in acute deficiency.
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Acute Disease↗
A biochemical evaluation of the erythrocyte glutathione reductase (EC 1.6.4.2) test for riboflavin status. 2. Dose-response relationships in chronic marginal deficiency.
1. Chronic marginal riboflavin deficiency was induced in groups of weanling rats by feeding a deficient diet supplemented with 0, 0.5, 1.0 and 1.5 mg riboflavin/kg diet. Ad lib.- and pair-fed controls received 3.0 and 15 mg riboflavin/kg diet respectively. 2. Serial measurement of erythrocyte NAD(P)H2 glutathione oxidoreductase (glutathione reductase; EC 1.6.4.2) and its activation coefficient revealed that after 12 weeks a steady-state of deficiency had been reached following initial fluctuations in status; the animals were then killed, and their tissues analysed. 3. Food intake, growth rate and the appearance of pathological signs were directly proportional to riboflavin content; however relative liver weight was increased above control levels only in the most-severely-deficient group, and anaemia was not detected in any group. 4. The activation coefficient of glutathione reductase in erythrocytes and liver was closely related to dietary riboflavin content; that of skin responded maximally even in the least-severely-depleted animals. 5. Hepatic and renal flavin contents were directly proportional to dietary riboflavin, FAD being conserved at the expense of riboflavin and FMN. ATP:riboflavin 5-phosphotransferase (flavokinase; EC 2.7.1.26) activity was reduced, even in the least-severely-deficient animals; ATP:FMN adenylyltransferase(FAD pyrophosphorylase; EC 2.7.7.2) was increased in liver, but only in the most-severely-deficient animals. 6. Hepatic succinate:(acceptor) oxidoreductase (succinate dehydrogenase; EC 1.3.99.1) activity fell sharply between 1.5 and 0.5 mg riboflavin/kg diet, producing an S-shaped dose-response curve; it showed smaller or less specific changes in other tissues such as brain, skin and intestine. NADH:(acceptor) oxidoreductase (NADH dehydrogenase; EC 1.6.99.3) activity declined in liver and intestine, but not in skin or brain. 7. The activation coefficient of glutathione reductase was correlated strongly with nearly all the riboflavin-sensitive variables measured, once equilibrium had been reached in this chronic deficiency model, and it was particularly strongly correlated with hepatic and renal FAD levels. Under equilibrium conditions, therefore, it appears to represent a good index of the extent of riboflavin deficiency, and significant changes in flavin levels and enzymes in the internal organs were detected even under conditions of marginal deficiency, associated with relatively small increases in the activation coefficient.
Animals↗
Riboflavin status in Gambian pregnant and lactating women and its implications for Recommended Dietary Allowances.
Riboflavin status by the erythrocyte glutathione reductase (NAD(P)H2:glutathione oxidoreductase EC1.6.4.2) test, and dietary riboflavin intake, were measured in 156 pregnant and lactating women in Keneba, a rural Gambian village, and in 59 pregnant and lactating women in Cambridge, England. The Keneba women were studied longitudinally, for up to 19 months. In Keneba, where the mean daily riboflavin intake was 0.5 mg, the mean erythrocyte glutathione reductase activation coefficient was 1.78 and there was a marked deterioration of biochemical status near parturition. In Cambridge, where the mean intake was 2.3 mg/day, the mean activation coefficient was 1.19. A vitamin fortified diet supplement, given to lactating women in Keneba for 8 months, raised their mean riboflavin intake for 0.5 to 1.5 mg/day and reduced the mean activation coefficient to 1.42. It is therefore likely that an intake even greater than the current United Kingdom or United States recommended daily amounts would be needed to achieve biochemical 'normality' in these women.
Adolescent↗