Adequate maternal micronutrient and vitamin status is especially critical during pregnancy and lactation. Several micronutrient deficiencies (like iron, iodine, zinc) are well established as contributors to abnormal prenatal development and or pregnancy outcome. But less well-recognized for their importance are deficiencies of vitamins. Evidence is accumulating that maternal antioxidant status is important to prevent abnormal pregnancy outcomes. In lactation, the maternal status of several of these vitamins affects their concentration in breast milk. The main cause of multiple vitamin deficiencies is a poor quality diet, even though gene polymorphism can also impair vitamin absorption or alter their metabolism, and cause vitamin deficiency. In some diets high in unrefined grains and legumes, the amount of nutrients consumed may be adequate, but dietary constituents, such as phytanes and polyphenols, can also limit their absorption.
Since pregnancy and exercise place higher demands on oxygen requirements, women who exercise during pregnancy should be monitored for suboptimal iron status and inadequate intake. Many women enter pregnancy with depleted iron stores, as discussed in Chap. 16 ( Iron Requirements and Adverse Outcomes ). This, along with expansion of maternal blood volume and increased fetal demand for oxygen, makes it more of a challenge for many women to achieve adequate iron status. If a woman enters pregnancy with iron deficiency anemia, repletion of iron stores may be difficult. Prenatal vitamin and mineral supplements are routinely prescribed to provide additional iron and folic acid. However, these should not replace a healthy balanced diet containing a variety of foods from all food groups so as to ensure adequate intake of antioxidants, fiber, and the necessary nutrients to support maternal health and growth of the fetus 46 .
Vitamins C and E improve rat embryonic antioxidant defense mechanism in diabetic culture medium. Teratology 2001 64 33-44. 44. Ornoy A, Zaken V, Kohen R. Role of reactive oxygen species (ROS) in the diabetes-induced anomalies in rat embryos in vitro reduction in antioxidant enzymes and low-molecular weight antioxidants (LMWA) may be the causative factor for increased anomalies. Teratology 1999 60 1-11.
Oxidative stress and antioxidants Many studies implied that the causes of diabetic embryopathy may be secondary cellular damage from overproduction of reactive oxygen species (ROS) or and decreased antioxidant defense mechanism in the embryonic cells.15,22-24 The source of ROS is complex and non-specific. The main question is whether deranged oxidant antioxidant status can occur at this early stage of pre-implantation embryonic development. We found that serum from diabetic women can induce oxidative stress in the mouse blastocysts,15 apparently in a way similar to that induced in post-implantation embryos.22 This was evidenced by reduced concentrations of low molecular weight antioxidants (LMWA) such as glutathione and vitamins C and E. The pre-implantation mouse embryos cultured in serum from diabetic pregnant women had lower concentration of LMWA compared to embryos cultured in serum from nondiabetic women. It seems, therefore, that diabetic metabolic factors may induce...
Previous studies have shown, however, that the uptake of arachidonic acid by embryonic yolk sacs is increased in a hyperglycemic environment.32 This finding would preclude an uptake deficiency of arachidonic acid in the conceptus of diabetic pregnancy, a result supported by the demonstration of unchanged concentration of arachidonic acid in membranes of high glucose cultured embryos in vitro.70 Recent measurements in day-12 embryos indicate a decreased arachidonic acid concentration in offspring from diabetic rats.55 A downregulation of the gene expression of COX-2, the inducible form of the COX enzyme, as well as a GSH-dependent enhancement of the conversion of the precursor PGH2 to PGE2 has also been demonstrated.68 Thus, the PGE2 concentration of day-10 embryos and membranes was decreased after exposure to high glucose in vitro or diabetes in vivo. In vitro addition of NAC to high glucose cultures restored the PGE2 concentration.68 Hyperglycemia diabetes-induced downregulation of...
Rate limiting enzyme of the glycolysis, Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), since this enzyme has displayed sensitivity to ROS in several different conditions of oxidative stress.100 This sensitivity resides in the thiol group of cysteine residue 149 in the active site of the enzyme.101,102 Oxidation of the thiol group by NO or ROS leads to decreased enzyme activity,103 and blocking of this process by antioxidants protects the activity of the enzyme.104 In rat embryos subjected to a diabetic environment in vivo or in vitro, decreased GAPDH activity was found,105 and addition of the antioxidant NAC prevented the decrease in activity.105 In addition, when the enzyme was inhibited by iodoacetate, NAC addition also blocked the inhibition (Figure 24.4).105 The bulk of data implicates oxidative stress and ROS excess as an important component in the etiology of diabetic embryopathy. The data also suggest that long-term exposure to high glucose creates embryonic ROS excess...
The Pax-3 gene expression was found to be reduced in embryos of diabetic mice,159,160 and this transcription factor may regulate the gene expression of the licensing factor cdc-46,161 and a gene, Dep-1,162 as well as p53,163 all of which may be of importance for a correct neural tube closure. Null mutation of the Pax-3 gene yields the Splotch mouse displaying neural tube defects.159,164 It has also been shown that the decreased Pax-3 expression in embryos of diabetic mice could be normalized by treatment of the mother with antioxidants,165 thereby demonstrating a coupling between ROS excess and a teratologically important change in gene expression.
Pr eg na nt women need up to 60g of protein a day, so re member to eat a variety of protein foods to get a ba I a nc e of a I I th e a mino acids. Antioxidant foods are vitally i mportant in the body's fight against free radicals (see pa g e 1 5) . Eat plenty of fruit and vegetables containing c a r ote n o i d s th e s e a r e a sa fe s o u r c e o f vi tamin A, which is important for vision as well as cell division and d i ffe re nti a ti o n . S e I en i u m is an antioxidant trace mineral i mportant to the immune system. Certain B vitamins are n e ed ed at th i s sta g e for th e d evel o pment of the baby's bra i n a nd n ervou s syste m. Choline and iodine are important for bra i n d eve I op ment, as is the essential fatty acid DHA. For food sou rce s of a I I th es e n u tr i e nts see pa g es 1 34-7.
As was stated earlier, there are no well-established methods of primary prevention for preeclampsia, although numerous supplements have been studied regarding their ability to impact its occurrence. Thus far, randomized controlled trials do not support routine prenatal supplementation with magnesium, omega-3 fatty acids, antioxidants (vitamins E and C), or calcium to prevent preeclampsia 21-24 .
Fumaric acid is used as an antioxidant, in small amounts, in the food industry. With increasing dosages, it is prescribed as therapy in cases of psoriasis (several hundred milligrams daily) leukopenia and lymphopenia may occur as adverse reactions. There is no information about effects on the unborn. However, one of the current authors (C.S.) has documented data on 15 pregnancies treated during the first trimester for psoriasis with numeric acid. No embryotoxic or teratogenic effects were found (there was one spontaneous abortion and one stillbirth).
Better understanding of the mechanisms and factors involved in the pathogenesis of diabetic retinopathy (as described earlier) has led to exploration of new drugs directed against these factors, some of which are currently under clinical trials. Examples include aldose reductase inhibitors,33,118-120 protein kinase C inhibitors, antioxidants, inhibition of nonenzymatic glycation of proteins (aminoguanidine),121 VEGF inhibitors,122,123 intraocular gene therapy with the PEDF gene,124,125 and somatostatin analogues (reduce GH and IGF-I levels).126
The sections that follow describe the evidence linking maternal nutritional deficiencies to maternal mortality. Specifically, the association between anemia and maternal mortality and hemorrhage is examined, including the efficacy of iron supplementation and other interventions in reducing maternal anemia. The role of calcium and antioxidants in the prevention of hypertensive disease and preeclampsia, and the efficacy of magnesium sulfate in the prevention of eclampsia is reviewed as well as the link between sepsis and infection and maternal vitamin A and zinc deficiencies. Finally, causes of obstructed labor and nutritional factors related to maternal stunting with focus on growth in childhood and adolescence are discussed.
Oxidative stress has been proposed to have a potential role in the two-stage model of preeclampsia 54, 56, 57 . The first stage in this model is reduced placental perfusion, resulting from abnormal implantation or other pathologies. The second stage involves the maternal hypertensive inflammatory response that may be influenced by environmental factors and oxidative stress 56 . Trophoblastic cells isolated from the placenta of preeclamptic women have increased superoxide generation and decreased superoxide dismutase activity, supporting the hypothesis that increased oxidative stress plays a role in the pathology for preeclamptic placentae 58 . In a small randomized, placebo-controlled trial, daily vitamin C (100 mg) and E (400 IU) from 16 to 22 weeks of gestation significantly reduced the risk of preeclampsia 59 . The plasminogen activator inhibitor ratio (PA1 PA2), which is elevated in preeclampsia, significantly decreased due to supplementation, suggesting a reduction in endothelial...
Human colostrum is particularly rich in vitamin E (tocopherol). Milk of mothers with preterm and term infants have similar levels of vitamin E (3 IU 100 kcal) and carotenoid levels, which are higher than those in bovine milk (Ostrea, 1986) or formula (Sommerburg et al., 2000). A deficiency of vitamin E in infancy can result in he-molytic anemia, especially in the premature infant. Because it is an antioxidant, vitamin E protects cell membranes in the retina and lungs against oxidant-induced injury. The requirement for vitamin E increases with intake of polyunsaturated fatty acids in
This recipe uses oats, which are an excellent source of fiber and folic acid, in addition to the nuts and fruits. Nuts are a great source of protein, fiber (especially almonds), and heart-healthy unsaturated fats. They're also a cholesterol-free snack. Dried fruits are a great source of quick energy and antioxidants.
The whole grain cereal in this recipe provides a good source of essential vitamins. The nuts have omega-3 fatty acids, which are good for your heart and good for your baby's development. The dried fruits contain antioxidants to keep you young. And, last but not least, the peanut butter gives you some extra protein.
In addition to the prevention of scurvy, vitamin C has numerous other functions and is a co-factor for several enzyme systems. For humans, vitamin C is an essential vitamin, with an important antioxidant function. As antioxidant defense systems are important to protect tissues and cells from damage caused by oxidative stress, an imbalance between increased oxidative stress and decreased antioxidant defenses impairs fetal growth.45 Thus, pregnant women utilize a defense mechanism, composed of antioxidant enzymes and nutrients including vitamin C, against oxidative stress and free-radical damage. It is believed that ascorbic acid, through conversion to dehydroascorbic acid, crosses the placenta to enter fetal circulation. Once dehydroascorbic acid is present in the fetal circulation, it is reduced back into ascorbic acid and is maintained in high concentrations on the fetal side of the placenta.46 Maternal serum vitamin C levels during the second trimester of gestation are correlated...
Dietary control is very important not only for GDM patients, but also for normal pregnant women. The incidence of macrosomia is about 5-10 in most Chinese hospitals. If GDM is not detected and managed properly, the incidence of macrosomia could be as high as 50 . But if dietary control is carried out strictly, most patients do not need insulin therapy and the incidence of macrosomia could be greatly reduced. The ideal dietary control should provide the necessary nutrition to both mother and fetus, achieve well-controlled glucose levels, and avoid hypoglycemia and ketosis. The ideal body weight (IBW height - 100) should be calculated first, and the daily calorie requirement is calculated according to the standard of 30-35 kcal kg. The proportions of carbohydrate, protein, and fat are 40-50, 25-30, and 25-30 , respectively. In order to counter-balance the effects of day and night fluctuation of anti-insulin hormones of pregnant women, GDM patients are advised to have five meals a day....
Rodent embryos were exposed to a diabetic environment in vivo and in vitro (high glucose embryo culture) and at the same time subjected to supplementation of folic acid.33,34 The folic acid treatment increased folic acid concentration in the embryos and almost completely abolished the diabetes glucose-induced dysmorphogenesis, i.e. both the growth retardation and somatic maldevelopment in the offspring.33,34 In this context, the reports suggesting that folic acid may act as an antioxidant may offer an explanation for the findings of a marked antiteratogenic effect by folic acid on embryos exposed to a diabetic environment (Figure 24.2).
Selenium (see also Chapter 2.17) is an essential trace element. Selenium poisoning can be caused by high concentrations in drinking water. In this respect, it has been associated with miscarriages (Robertson 1970). No definitive data are available - certainly not to evaluate Lhe use of selenium as an antioxidant.
Cocaine and crack cause more severe heart, circulatory, and neurological effects in pregnant women than in those who are not pregnant. It has been discussed whether the damage to the embryo following decreased perfusion may not in fact be the direct consequence of oxygen deprivation, but rather may be caused by a highly reactive toxic oxygen radical following reperfusion of the ischemic tissue. In the first trimester, the fetoplacental unit does not have sufficient protective antioxidants.