Essential fatty acids in mothers and their neonates.
(57/2033)
Essential fatty acids (EFAs) and their long-chain polyenes (LCPs) are indispensable for human development and health. Because humans cannot synthesize EFAs and can only ineffectively synthesize LCPs, EFAs need to be consumed as part of the diet. Consequently, the polyunsaturated fatty acid (PUFA) status of the developing fetus depends on that of its mother, as confirmed by the positive relation between maternal PUFA consumption and neonatal PUFA status. Pregnancy is associated with a decrease in the biochemical PUFA status, and normalization after delivery is slow. This is particularly true for docosahexaenoic acid (DHA) because, on the basis of the current habitual diet, birth spacing appeared to be insufficient for the maternal DHA status to normalize completely. Because of the decrease in PUFA status during pregnancy, the neonatal PUFA status may not be optimal. This view is supported by the lower neonatal PUFA status after multiple than after single births. The neonatal PUFA status can be increased by maternal PUFA supplementation during pregnancy. For optimum results, the supplement should contain both n-6 and n-3 PUFAs. The PUFA status of preterm neonates is significantly lower than that of term infants, which is a physiologic condition. Because the neonatal DHA status correlates positively with birth weight, birth length, and head circumference, maternal DHA supplementation during pregnancy may improve the prognosis of preterm infants. In term neonates, maternal linoleic acid consumption correlates negatively with neonatal head circumference. This suggests that the ratio of n-3 to n-6 PUFAs in the maternal diet should be increased. Consumption of trans unsaturated fatty acids appeared to be associated with lower maternal and neonatal PUFA status. Therefore, it seems prudent to minimize the consumption of trans fatty acids during pregnancy. (+info)
New standard for dietary folate intake in pregnant women.
(58/2033)
The Institute of Medicine Panel for Folate and Other B Vitamins and Choline considered data from population-based and metabolic studies to revise the dietary intake standards for pregnancy. The recommended dietary allowance (RDA) for pregnant women is the average daily dietary intake sufficient to meet the requirements of 97-98% of pregnant women. The RDA is derived from the amount estimated to meet the requirement of half of healthy pregnant women, or the estimated average requirement (EAR). Maintenance of red cell folate was selected as the primary indicator of adequacy of folate status during pregnancy. The dietary folate equivalent (DFE) was used to interpret studies in which folate was provided as a combination of food folate and synthetic folic acid because folic acid is more bioavailable than is food folate. Many population-based studies confirmed that approximately 680 nmol (approximately 300 microg) folic acid/d consumed in conjunction with a low-folate diet prevented folate deficiency in pregnant women. Additional studies showed that 227 nmol (100 microg) folic acid/d was inadequate to maintain normal folate status in a significant percentage of the groups assessed. The EAR was derived by adding the DFE of this quantity [454 nmol (200 microg)/d] to the EAR for nonpregnant women [725 nmol (320 microg)/d] to provide an EAR of 1178 nmol (520 microg)/d. The RDA of 1362 nmol (600 microg) DFE/d was derived by multiplying the EAR by 1.2 to account for an estimated 10% CV. Data from the metabolic studies support an RDA of 1362 nmol (600 microg) DFE/d on the basis of the maintenance of normal red cell folate concentrations and agree with the findings from the population studies that 1362 nmol DFE/d is adequate to maintain normal folate status in pregnant women. (+info)
Response of red blood cell folate to intervention: implications for folate recommendations for the prevention of neural tube defects.
(59/2033)
Committees worldwide have set almost identical folate recommendations for the prevention of the first occurrence of neural tube defects (NTDs). We evaluate these recommendations by reviewing the results of intervention studies that examined the response of red blood cell folate to altered folate intake. Three options are suggested to achieve the extra 400 microg folic acid/d being recommended by the official committees: increased intake of folate-rich foods, dietary folic acid supplementation, and folic acid fortification of food. A significant increase in foods naturally rich in folates was shown to be a relatively ineffective means of increasing red blood cell folate status in women compared with equivalent intakes of folic acid-fortified food, presumably because the synthetic form of the vitamin is more stable and more bioavailable. Although folic acid supplements are highly effective in optimizing folate status, supplementation is not an effective strategy for the primary prevention of NTDs because of poor compliance. Thus, food fortification is seen by many as the only option likely to succeed. Mandatory folic acid fortification of grain products was introduced recently in the United States at a level projected to provide an additional mean intake of 100 microg folic acid/d, but some feel that this policy does not go far enough. A recent clinical trial predicted that the additional intake of folic acid in the United States will reduce NTDs by >20%, whereas 200 microg/d would be highly protective and is the dose also shown to be optimal in lowering plasma homocysteine, with possible benefits in preventing cardiovascular disease. Thus, an amount lower than the current target of an extra 400 microg/d may be sufficient to increase red blood cell folate to concentrations associated with the lowest risk of NTDs, but further investigation is warranted to establish the optimal amount. (+info)
Maternal calcium metabolism and bone mineral status.
(60/2033)
Human pregnancy is associated with major changes in calcium and bone metabolism and in bone mineral status before and after gestation. The changes are compatible with the uptake and mobilization of calcium by the maternal skeleton to meet the high requirement for fetal growth and for breast-milk production. Breast-feeding is accompanied by decreases in bone mineral status, increases in bone turnover rate, and reductions in urinary calcium excretion. These effects are reversed during and after weaning, and, in several skeletal regions, bone mineral content ultimately exceeds that measured after delivery. By 3-6 mo after lactation, the postpartum changes in bone mineral status of women who breast-feed largely match those of women who do not, regardless of the duration of lactation. No consistent picture has emerged of the effect of pregnancy on bone mineral status, although increases in bone turnover, calcium absorption, and urinary calcium excretion are well recognized. Events before conception may modify the bone response, particularly if conception occurs within a few months of a previous pregnancy or lactation. There is no evidence that the changes observed during lactation reflect inadequacies in calcium intake. Supplementation studies have shown that neither the bone response nor breast-milk calcium secretion is modified by increases in calcium supply during lactation, even in women with a low calcium intake. The situation in pregnancy is less clear. Calcium nutrition may influence the health of the pregnant woman, her breast-milk calcium concentration, and the bone mineralization and blood pressure of her infant, but these possibilities require formal testing. (+info)
Vitamin A in pregnancy: requirements and safety limits.
(61/2033)
Most of the functions of vitamin A are mediated through the binding of retinoic acid to specific nuclear receptors that regulate genomic expression. Recent experimental work in transgenic mice showed clearly that normal embryonic development depends on the correct spatial and temporal expression of the receptors in the differentiating cells and on the binding of specific forms of retinoic acid. This implies that the parent compound, vitamin A, is available in adequate forms and quantities. Excessive dietary intake of vitamin A has been associated with teratogenicity in humans in <20 reported cases over 30 y. However, caution must be exercised to avoid unnecessary supplementation of women of childbearing age. Hypovitaminosis A affects millions of women and children worldwide. The main consequence of a poor vitamin A supply during pregnancy is a low vitamin A status at birth and in the next few months. Vitamin A deficiency is strongly associated with depressed immune function and higher morbidity and mortality due to infectious diseases such as diarrhea, measles, and respiratory infections. Vitamin A deficiency is often associated with an increased mother-to-child transmission of HIV-1. The initiation of vitamin A supplementation should be carefully examined in each case according to the risk-to-benefit ratio. The final decision should take into account the estimated vitamin A status of the woman, the availability of vitamin A-rich foods in her diet, and whether supplementation can be supervised. (+info)
Determinants of maternal zinc status during pregnancy.
(62/2033)
Zinc deficiency in pregnant experimental animals limits fetal growth and, if severe, causes teratogenic anomalies. Although the data from human studies are not consistent, similar outcomes have been observed and were associated with poor maternal zinc status. This paper reviews humans studies of zinc status and pregnancy outcome, describes the physiologic adjustments in zinc utilization during pregnancy to meet fetal needs while maintaining maternal status, and identifies dietary and environmental conditions that may override those physiologic adjustments and put the health of the mother and fetus at risk. Adjustments in intestinal zinc absorption appear to be the primary means by which zinc retention is increased to meet fetal demands. However, transfer of sufficient zinc to the fetus is dependent on maintenance of normal maternal serum zinc concentrations. Conditions that could interfere with zinc absorption include intake of cereal-based diets that are high in phytate, high intakes of supplemental iron, or any gastrointestinal disease. Conditions that may alter maternal plasma zinc concentrations and the transport of zinc to the fetus include smoking, alcohol abuse, and an acute stress response to infection or trauma. Supplemental zinc may be prudent for women with poor gastrointestinal function or with any of these conditions during pregnancy. (+info)
Dietary copper influences reproduction in cats.
(63/2033)
The objective of this study was to determine the copper requirement of female cats (queens) for gestation. Cuproenzyme activities were evaluated to identify a noninvasive indicator of copper status. This study used a depletion-repletion model. Specific pathogen-free queens (n = 28) were adapted to a purified diet; after consuming a copper-depletion diet (0.8 mg Cu/kg diet) for 4 mo, they were randomly allocated to three dietary treatment groups receiving copper sulfate at 4.0, 5.8 or 10.8 mg Cu/kg diet. Four queens underwent liver biopsies at two time points during the study. Plasma samples were analyzed for copper concentrations, extracellular superoxide dismutase, ceruloplasmin and diamine oxidase activities. Only liver copper concentrations were responsive to dietary copper intake. The dietary concentration of copper had a significant effect on the time taken for queens to conceive (P = 0.04). There was a negative linear relationship between dietary copper (x = Cu mg/kg diet) and the mean time (y = days) for queens to conceive (y = 43.38-2.87x; R(2) = 0.97). The current NRC recommendation of 5 mg/kg diet copper for cats appears marginal for optimal reproduction. (+info)
Human zinc deficiency.
(64/2033)
The objective of this paper is to provide a current overview of the significance of zinc in human nutrition. To achieve this, the following issues are addressed: (1) the biochemistry and biology of zinc in the context of their relevance to zinc in human nutrition and to our understanding of the complexity and practical importance of human zinc deficiency; (2) the history of our understanding of human zinc deficiency with an emphasis both on its brevity and on notable recent progress; (3) the clinical spectrum of severe zinc deficiency; (4) the lack of ideal biomarkers for milder zinc deficiency states, with the consequent dependence on randomized, placebo-controlled intervention studies to ascertain their prevalence and clinical consequences, including growth delay, diarrhea, pneumonia, other infections, disturbed neuropsychological performance and abnormalities of fetal development; (5) the public health significance of human zinc deficiency in the developing world; (6) reasons for concern and unanswered questions about zinc nutriture in the United States; (7) the need for better understanding of human zinc metabolism and homeostasis (including its limitations) at a molecular, cellular, organ-system and whole body level and of factors that affect zinc bioavailability; and (8) potential strategies for the prevention and management of human zinc deficiency. This review concludes with an emphasis on the immediate need for expanded research in directions that have become increasingly well demarcated and impelling as a result of recent progress, which is summarized in this overview. (+info)