227 resultados para maternal diet

em Deakin Research Online - Australia


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The prenatal environment can influence development of offspring blood pressure (BP), which tracks into adulthood. This prospective longitudinal study investigated whether maternal pregnancy dietary intake is associated with the development of child BP up to age four years. Data are from 129 mother-child dyads enrolled in the Women and Their Children's Health study. Maternal diet was assessed using a validated 74-item food frequency questionnaire at 18 to 24 weeks and 36 to 40 weeks, with a reference period of the previous three months. Child systolic and diastolic BP were measured at 3, 6, 9, 12, 24, 36 and 48 months, using an automated BP monitor. Using mixed-model regression analyses adjusted for childhood growth indices, pregnancy intakes of percentage of energy (E%) polyunsaturated fat (β coefficient 0.73; 95% CI 0.003, 1.45; p = 0.045), E% omega-6 fatty acids (β coefficient 0.89; 95% CI 0.09, 1.69; p = 0.03) and protein-to-carbohydrate (P:C) ratio (β coefficient -14.14; 95% CI -27.68, -0.60; p = 0.04) were associated with child systolic BP trajectory up to 4 years. Child systolic BP was greatest at low proportions of dietary protein (<16% of energy) and high carbohydrate (>40% of energy) intakes. There may be an ideal maternal macronutrient ratio associated with optimal infant BP. Maternal diet, which is potentially modifiable, may play an important role in influencing offspring risk of future hypertension.

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Objective
We hypothesized that elevating creatine in the maternal diet would reach fetal and placental tissues and improve fetal survival after acute hypoxia at birth.
Study Design
Pregnant spiny mice were fed a control or 5% creatine-supplemented diet from day 20 of gestation (term, approximately 39 days). On days 37-38, intrauterine hypoxia was induced by placement of the isolated uterus in a saline solution bath for 7.5-8 minutes, after which fetuses were expelled from the uterus and resuscitation was attempted by manual palpation of the chest. Total creatine content (creatine + phosphocreatine) of placental, fetal, and maternal organs was measured.
Results
The maternal creatine diet significantly increased total creatine content in the placenta, fetal brain, heart, liver, and kidney and increased the capacity of offspring to survive birth hypoxia. Maternal creatine improved postnatal growth after birth hypoxia.
Conclusion
This study provides evidence that creatine has potential as a prophylactic therapy for pregnancies that are classified as high risk for fetal hypoxia.

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Objective Maternal nutrition knowledge has frequently been identified as an important target for nutrition promotion interventions. The aim of the present study was to investigate whether maternal nutrition knowledge is more strongly associated with the mother's own diet or that of her child.

Design Cross-sectional multivariate linear regression with interactions analyses of survey data.

Setting
Socio-economically disadvantaged neighbourhoods in Victoria, Australia.

Subjects Five hundred and twenty-three mothers and their children who participated in the Resilience for Eating and Physical Activity Despite Inequality (READI) study, a cross-sectional survey study conducted in 2009 among women and their children residing in socio-economically disadvantaged neighbourhoods.

Results In adjusted models, for three (vegetable, chocolate/lollies and soft drink consumption) out of the seven dietary outcomes assessed, there was a significant association between maternal nutrition knowledge and maternal diet, whereas for the children's diets none of the seven outcomes were associated with maternal nutrition knowledge. Statistical comparison of regression coefficients showed no difference between the maternal nutrition knowledge–maternal diet association and the maternal nutrition knowledge–child diet association.

Conclusions Promoting maternal nutrition knowledge may represent an important avenue for improving diet in mothers from socio-economically disadvantaged neighbourhoods, but more information is needed on how and when this knowledge is translated to benefits for their children's diet.

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Over the past 100 years, advances in pharmaceutical and medical technology have reduced the burden of communicable disease, and our appreciation of the mechanisms underlying the development of noncommunicable disease has broadened. During this time, a number of studies, both in humans and animal models, have highlighted the importance of maintaining an optimal diet during pregnancy. In particular, a number of studies support the hypothesis that suboptimal maternal protein and fat intake during pregnancy can have long-term effects on the growing fetus, and increase the likelihood of these offspring developing cardiovascular, renal, or metabolic diseases in adulthood. More recently, it has been shown that dietary intake of a number of micronutrients may offset or reverse the deleterious effects of macronutrient imbalance. Furthermore, maternal fat intake has also been identified as a major contributor to a healthy fetal environment, with a beneficial role for unsaturated fats during development as well as a beneficial impact on cell membrane physiology. Together these studies indicate that attempts to optimise maternal nutrition may prove to be an efficient and cost-effective strategy for preventing the development of cardiovascular, renal, or metabolic diseases.

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In rats, a maternal diet rich in lard is associated with reduced Na+,K+-ATPase activity in adult offspring kidney. We have addressed the role of different fatty acids by evaluating Na+,K+-ATPase activity in offspring of dams fed diets rich in saturated (SFA), monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids. Female Sprague–Dawley rats were fed, during pregnancy and suckling, a control diet (4% w/w corn oil) or a fatty acid supplemented diet (24% w/w). Offspring were reared on chow (4% PUFA) and studied at 6 months. mRNA expression (real-time PCR) of Na+,K+-ATPase α subunit and protein expression of Na+,K+-ATPase subunits (Western blot) were assessed in kidney and brain. Na+,K+-ATPase activity was reduced in kidney (P < 0.05 versus all groups) and brain (P < 0.05 versus control and MUFA offspring) of the SFA group. Neither Na+,K+-ATPase α1 subunit mRNA expression, nor protein expression of total α, α1, α2, α3 or β1 subunits were significantly altered in kidney in any dietary group. In brains of SFA offspring α1 mRNA expression (P < 0.05) was reduced compared with MUFA and PUFA offspring, but not controls. Also in brain, SFA offspring demonstrated reduced (P < 0.05) α1 subunit protein and increased phosphorylation (P < 0.05) of the Na+,K+-ATPase modulating protein phospholemman at serine residue 63 (S63 PLM). Na+,K+-ATPase activity was similar to controls in heart and liver. In utero and neonatal exposure to a maternal diet rich in saturated fatty acids is associated with altered activity and expression of Na+,K+-ATPase in adulthood, but mechanisms appear tissue specific.

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BACKGROUND: While maternal nutrition during pregnancy is known to play a critical role in the health of both mother and offspring, the magnitude of this association has only recently been realized. Novel, epigenetic data suggest that maternal dietary intake has permanent phenotypic consequences for offspring, highlighting the potency of antenatal diet. To date, the relationship between poor antenatal diet and maternal mental health specifically, remains poorly understood. Therefore, we aimed to systematically review evidence that has examined associations between antenatal diet quality and the experience of depressive, anxiety and stress symptoms during the perinatal period.

METHODS: A search for peer-reviewed papers was conducted using Medline Complete, PsycINFO, CINAHL, Academic Search Premiere and Psychology and Behavioral Science Collection.

RESULTS: Nine studies (cohort = 4, cross-sectional = 5) published between 2005 and 2013 were eligible for inclusion in this review. A synthesis of findings revealed positive associations between poor quality and unhealthy diets and antenatal depressive and stress symptoms. Healthy diets were inversely associated with antenatal depressive and anxiety symptoms. Postnatal depressive symptoms demonstrated inconsistent results.

CONCLUSIONS: Given the paucity of research examining diet quality and mental health in women during the perinatal period, further sufficiently powered studies are urgently required to examine this association.

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Using a model of birth asphyxia, we previously reported significant structural and functional deficits in the diaphragm muscle in spiny mice, deficits that are prevented by supplementing the maternal diet with 5% creatine from mid-pregnancy. The long-term effects of this exposure are unknown. Pregnant spiny mice were fed control or 5% creatine-supplemented diet for the second half of pregnancy, and fetuses were delivered by caesarean section with or without 7.5 min of in-utero asphyxia. Surviving pups were raised by a cross-foster dam until 33±2 days of age when they were euthanized to obtain the diaphragm muscle for ex-vivo study of twitch tension and muscle fatigue, and for structural and enzymatic analyses. Functional analysis of the diaphragm revealed no differences in single twitch contractile parameters between any groups. However, muscle fatigue, induced by stimulation of diaphragm strips with a train of pulses (330 ms train/sec, 40 Hz) for 300 sec, was significantly greater for asphyxia pups compared with controls (p<0.05), and this did not occur in diaphragms of creatine + asphyxia pups. Birth asphyxia resulted in a significant increase in the proportion of glycolytic, fast-twitch fibres and a reduction in oxidative capacity of Type I and IIb fibres in male offspring, as well as reduced cross-sectional area of all muscle fibre types (Type I, IIa, IIb/d) in both males and females at 33 days of age. None of these changes were observed in creatine + asphyxia animals. Thus, the changes in diaphragm fatigue and structure induced by birth asphyxia persist long-term but are prevented by maternal creatine supplementation.

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The fetal origins theory of adult disease suggests that term infants who are small for their gestational age have an increased susceptibility to chronic disease in adulthood as a consequence of physiologic adaptations to undernutrition during fetal life. Consistent evidence for an influence of women's dietary composition during pregnancy on growth of their babies is lacking, despite robust effects in animal experiments. We undertook a prospective observational study of 557 women aged 18-41 y, living in Adelaide, South Australia. Diet was assessed in early and late pregnancy using an FFQ. In early pregnancy, medians for energy intake, the proportion of energy derived from protein and from carbohydrate were 9.0 MJ, 17 and 48%, respectively. In late pregnancy the corresponding medians were 9.2 MJ, 16 and 49%. In early pregnancy, the percentage of energy derived from protein was positively associated with birth weight (P = 0.02) and placental weight (P = 0.07), independently of energy intake and weight gain during pregnancy, and after adjustment for potential confounders, including maternal age, parity, and smoking. Effects were stronger among women (n = 429) who had reliable data, based on prespecified criteria including the plausibility of dietary data when referenced against estimated energy expenditure. In addition, for this subgroup, the percentage of energy from carbohydrate in early and late pregnancy was negatively associated with ponderal index of the baby, and a specific effect of protein from dairy sources was identified. These data support the proposition that maternal dietary composition has an effect on fetal growth. Maternal diet in Western societies may therefore be important for the long-term health of the child.

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Objective: To investigate the effect of maternal dietary ω-3 polyunsaturated fatty acid (PUFA) deficiency and repletion on food appetite signaling.
Research Methods and Procedures: Sprague-Dawley rat dams were maintained on diets either supplemented with (CON) or deficient in (DEF) ω-3 PUFA. All offspring were raised on the maternal diet until weaning. After weaning, two groups remained on the respective maternal diet (CON and DEF groups), whereas a third group, born of dams fed the DEF diet, were switched to the CON diet (REC). Experiments on food intake began when the male rats reached 16 weeks of age. Food intake was stimulated either by a period of food restriction, by blocking glucose utilization (by 2-deoxyglucose injection), or by blocking β-oxidation of fatty acids (by β-mercaptoacetate injection).
Results: DEF animals consumed more than CON animals in response to all stimuli, with the greatest difference (1.9-fold) demonstrated following administration of 2-deoxyglucose. REC animals also consumed more than CON animals in response to food restriction and 2-deoxyglucose but not to β-mercaptoacetate.
Discussion: These findings indicate that supply of ω-3 PUFA, particularly during the perinatal period, plays a role in the normal development of mechanisms controlling food intake, especially glucoprivic (i.e. reduced glucose availability) appetite signaling. Dietary repletion of ω-3 PUFA from 3 weeks of age restored intake responses to fatty acid metabolite signaling but did not reverse those in response to food restriction or glucoprivic stimuli.

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Background : Dietary ω-3 fatty acid deficiency can lead to hypertension in later life; however, hypertension is affected by numerous other dietary factors. We examined the effect of altering the dietary protein level on blood pressure in animals deficient or sufficient in ω-3 fatty acids.

Methods : Female rats were placed on one of four experimental diets 1 week prior to mating. Diets were either deficient (10% safflower oil; DEF) or sufficient (7% safflower oil, 3% flaxseed oil; SUF) in ω-3 fatty acids and contained 20 or 30% casein (DEF20, SUF20, DEF30, SUF30). Offspring were maintained on the maternal diet for the duration of the experiment. At 12, 18, 24, and 30 weeks, blood pressure was assessed by tail cuff plethysmography.

Results : At both 12 and 18 weeks of age, no differences in blood pressure were observed based on diet, however, by 24 weeks hypertension was evident in DEF30 animals; there were no blood pressure differences between the other groups. This hypertension in DEF30 group was increased at 30 weeks, with systolic, diastolic, and mean arterial pressure all elevated.

Conclusions : These results indicate that the hypertension previously attributed to ω-3 fatty acid deficiency is dependent on additional dietary factors, including protein content. Furthermore, this study is the first to plot the establishment of ω-3 fatty acid deficiency hypertension over time.

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The aim of this project was to investigate the effects of oral contraceptives on the nutrient composition of breast milk. The design of the study also allowed the effects of stage of lactation and maternal diet on milk composition to be observed. A prospective study was designed to measure maternal dietary intake and vitamin and trace element concentration in milk and plasma. Vitamin A, ascorbic acid and iron, copper, zinc, manganese, selenium, cobalt, chromium, rubidium and caesium were measured. Two groups of women participated, oral contraceptive users and controls. Fasting milk and blood samples and 24-hour food records were collected from the women once a week for 20 weeks commencing 3-8 weeks post-partum, and 1-2 weeks before they began to take oral contraceptives. Fifteen women participated in the study; 5 took progestogen-only oral contraceptives, 1 took an oestrogen-progestogen oral contraceptive and 9 acted as controls. Progestogen-only oral contraceptives did not affect the milk or plasma concentration of the vitamins and trace elements measured. As only 1 subject took an oestrogen-progestogen preparation no conclusion could be drawn as to its effect. The mean milk and plasma concentration of all nutrients studied did not change significantly with the progression of lactation, with the exception of iron and zinc. The mean milk iron concentration was significantly higher at 16 weeks post-partum than at 8 and 23 weeks post-partum. The mean milk zinc concentration was significantly lower at 23 weeks post-partum than at 8 and 16 weeks post-partum. The infants1 mean estimated daily intakes of ascorbic acid and vitamin A from breast milk were above the U.S. and British Recommended Dietary Allowance for those vitamins. However, their mean estimated intakes of iron, zinc, copper, manganese and selenium were well below the U.S. recommendations. Effects of the maternal dietary intake on milk and plasma composition were variable. Implications of these findings have been discussed.