Impact Of Maternal Diet Research Articles

Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood.

Exposure to environmental factors in early life can influence developmental processes and long-term health in humans. Early life nutrition and maternal diet are well-known examples of conditions shown to influence the risk of developing metabolic diseases, including type 2 diabetes mellitus and cardiovascular diseases, in adulthood. It is increasingly accepted that environmental compounds, including nutrients, can produce changes in the genome activity that, in spite of not altering the DNA sequence, can produce important, stable and, in some instances, transgenerational alterations in the phenotype. Epigenetics refers to changes in gene function that cannot be explained by changes in the DNA sequence, with DNA methylation patterns/histone modifications that can make important contributions to epigenetic memory. The epigenome can be considered as an interface between the genome and the environment that is central to the generation of phenotypes and their stability throughout the life course. To better understand the role of maternal health and nutrition in the initiation and progression of diseases in childhood and adulthood, it is necessary to identify the physiological and/or pathological roles of specific nutrients on the epigenome and how dietary interventions in utero and early life could modulate disease risk through epigenomic alteration.

Sex-specific placental differences as a contributor to sex-specific metabolic programming?

Over the past decades, maternal nutritional intake has been proven to affect the prenatal and post-natal development of the foetus as well as its long-term health (see (Jimenez-Chillaron et al. 2012) and (Lillycrop & Burdge 2015) for recent overviews). In this journal, we have recently shown that maternal Western-style diet gives rise to long lasting programming of the liver in adult mouse offspring (Pruis et al. 2014), affecting mostly the males. Moreover, we demonstrated that several aspects of sex-specific programming are already present in 2-week-old offspring (Mischke et al. 2013), that is, well before puberty. The question arising now is whether this sexual dimorphism was already present during prenatal development, and which factors contributed to its manifestation. One major determinant of development and intrauterine growth is the placental supply of nutrients, which occurs primarily by a combination of diffusion and transporter-mediated transport (Sandovici et al. 2012). The surface area for exchange is a major determinant of these pathways. Despite the important role of the placenta, very few studies have investigated the relation of sex and placental development as a putative explanation of sex-specific programming. Therefore, we here present an overview of the foetal and placental findings in our previously described mouse model (Pruis et al. 2014). To determine the impact of maternal diet and sex on foetal development, C57BL/6J dams were fed either a low-fat diet (10 kcal% from fat, 18 mg cholesterol kg−1) or Western-style high-fat diet (45 kcal% from fat, 196.5 mg cholesterol kg−1) 2 weeks pre-mating and during pregnancy. At gestational day 18.5, dams were killed under isoflurane anaesthesia and foetuses and placentas were characterized. Interestingly, male foetuses exposed to the Western diet during development weighed significantly more than those exposed to low-fat diet, while there was no difference in body length (P = 0.085, not significant) (Fig. 1a,b). In addition, also the placentas of male offspring exposed to Western diet were of a slightly, but significantly larger weight than low-fat diet-fed male offspring (Fig. 1c). In female offspring of these dams, none of these differences due to maternal diet were observed (Fig. 1a–c). Due to the set-up of the experiments, we had only 5 male and 5 female placenta samples for histological examination. However, we observed a distinct difference in placental histology in terms of the ratio between the labyrinth layer and the spongiotrophoblast layer in male offspring (Fig. 1d,e). As mentioned previously, the major determinant of intrauterine growth is the placental supply of nutrients to the foetus. The labyrinthine zone is the main site for nutrient transfer in the mouse placenta during late gestation, and its absolute volume and volume fraction are known to increase progressively during the second half of pregnancy. The estimated depth of the labyrinth layer for the male mice was 872 ± 161 μm, while the measurement for the females was 340 ± 48 μm. As placental layering was affected, mRNA levels of selected transporter genes were measured on gestational day 18.5 by TaqMan real-time PCR. We determined the expression of genes responsible for glucose transport (Glut1 (Slc2a1), Glut4 (Slc2a2), Glut12 (Slc2a12), cholesterol uptake (Ldlr, Scarb1), and cholesterol excretion (Abca1, Abcg1). Neither maternal diet nor sex significantly affected the examined transcription levels (Fig. 1f). In summary, we observed an increase in weight of the male foetuses and their placentas under Western diet conditions. Moreover, there was a distinct difference between the male and female placentas: The larger labyrinth diameter in male placentas compared with the female placentas might lead to a higher transport capacity of nutrients, which let us speculate that the male placenta supports transport of excess maternal nutrients to the male foetus. On the contrary, the female placenta might act as a barrier which limits nutrient supply to the female foetus. As a result, the male foetus shows increased growth under these conditions of maternal surplus nutrients, whereas the female foetus is protected. Our findings are supported by other mouse studies which report that placental changes to prenatal stimuli differ between both sexes, supporting the idea that placentas of female foetuses protect against prenatal insults (Cuffe et al. 2012, 2014, O'Connell et al. 2013). Our findings might contribute to a better understanding of the sex differences observed in many animal studies in the field of long-term metabolic programming. The authors have no conflicts of interest to declare. This research was performed within the framework of CTMM, the Center for Translational Molecular Medicine (www.ctmm.nl), project PREDICCt (grant 01C-104), and supported by the Dutch Heart Foundation, Dutch Diabetes Research Foundation and Dutch Kidney Foundation. TP is supported by the Netherlands Organization for Health Research and Development (ZonMW TOP grant 91211053).

Maternal nutrition during pregnancy is associated with differential expression of imprinted genes and DNA methyltranfereases in muscle of beef cattle offspring.

Maternal diet during pregnancy is a major determinant of the fetal developmental competence and may induce long-lasting epigenetic changes to the offspring. Imprinted genes have important roles in fetal programming, growth, and development. There are, however, limited data available on the influence of maternal diet on the expression of imprinted genes in beef cattle. Therefore, the objective of this study was to analyze the impact of maternal diet during pregnancy on the expression of 5 imprinted genes and 3 DNA methyltransferase genes in longissimus dorsi muscle from Angus calves. A total of 36 Angus-cross cows were inseminated to a single sire and on Day 135 of gestation they were randomly assigned to either low-starch (haylage) or high-starch (corn silage) diets. Diets were initially formulated to provide isocaloric and isonitrogenous intake. The H19, MEG8, IGF2R, and DNMT3a genes showed differential expression in longissimus dorsi muscle in calves between the diet groups. Given that high-starch diet is a source of energy for muscle growth and feed conversion efficiency in postnatal development, the mechanisms by which this diet affected expression of imprinted genes should be further explored.

Maternal–Fetal Nutrient Transport in Pregnancy Pathologies: The Role of the Placenta

Appropriate in utero growth is essential for offspring development and is a critical contributor to long-term health. Fetal growth is largely dictated by the availability of nutrients in maternal circulation and the ability of these nutrients to be transported into fetal circulation via the placenta. Substrate flux across placental gradients is dependent on the accessibility and activity of nutrient-specific transporters. Changes in the expression and activity of these transporters is implicated in cases of restricted and excessive fetal growth, and may represent a control mechanism by which fetal growth rate attempts to match availability of nutrients in maternal circulation. This review provides an overview of placenta nutrient transport with an emphasis on macro-nutrient transporters. It highlights the changes in expression and activity of these transporters associated with common pregnancy pathologies, including intrauterine growth restriction, macrosomia, diabetes and obesity, as well as the potential impact of maternal diet. Molecular signaling pathways linking maternal nutrient availability and placenta nutrient transport are discussed. How sexual dimorphism affects fetal growth strategies and the placenta’s response to an altered intrauterine environment is considered. Further knowledge in this area may be the first step in the development of targeted interventions to help optimize fetal growth.

A pilot study on the impact of maternal diet and preconception body mass index on breast milk macronutrient composition

Materials and methods A cross-sectional study was conducted at the maternity units of the University Hospital of Leuven, Belgium. Postpartum women, who delivered a term (≥37 weeks of gestation), did not smoke, were normoglycaemic and who were not on predefined medication, were invited to participate. Participants completed a 24 dietary recall and donated a breast milk sample of 1.5-2cl at day 4 post-delivery. The samples were collected during the first feeding in the morning by use of a vacuum pump. Each sample was analyzed for macronutrients (carbohydrates, protein, fats) and energy with the MIRIS Human Milk Analyzer. The prepregnancy weight and length were assessed from the online medical patient file to calculate the pre-pregnancy BMI. Further baseline characteristics included maternal age, ethnicity and parity. Pregnancy outcomes included delivery mode, the use of combined spinal epidural, gestational age, birth weight and gender of the baby.

Impact of maternal diet on human milk composition and neurological development of infants

Maternal nutrition has little or no effect on many nutrients in human milk; for others, human milk may not be designed as a primary nutritional source for the infant; and for a few, maternal nutrition can lead to substantial variations in human milk quality. Human milk fatty acids are among the nutrients that show extreme sensitivity to maternal nutrition and are implicated in neurological development. Extensive development occurs in the infant brain, with growth from ∼ 350 g at birth to 925 g at 1 y, with this growth including extensive dendritic and axonal arborization. Transfer of n-6 (omega-6) and n-3 (omega-3) fatty acids from the maternal diet into human milk occurs with little interconversion of 18:2n-6 to 20:4n-6 or 18:3n-3 to docosahexaenoic acid (DHA) and little evidence of mammary gland regulation to maintain individual fatty acids constant with varying maternal fatty acid nutrition. DHA has gained attention because of its high concentrations and roles in the brain and retina. Studies addressing DHA intakes by lactating women or human milk amounts of DHA at levels above those typical in the United States and Canada on infant outcomes are inconsistent. However, separating effects of the fatty acid supply in gestation or in the weaning diet from effects on neurodevelopment solely due to human milk fatty acids is complex, particularly when neurodevelopment is assessed after the period of exclusive human milk feeding. Information on infant fatty acid intakes, including milk volume consumed and energy density, will aid in understanding of the human milk fatty acids that best support neurological development.

Impact of maternal diet on neonatal anthropometry: a randomized controlled trial

Large for gestational age infants are at increased risk of childhood obesity and maternal nutrition impacts birthweight. The aim of this study was to assess the impact of a maternal low glycaemic index (GI) diet on neonatal anthropometry. The ROLO (Randomised Control Trial of Low Glycaemic Index Diet in Pregnancy) study was a randomized controlled trial to assess the impact of a low GI diet versus usual diet on birthweight. It took place in a tertiary maternity hospital in Ireland and women were randomized to receive either a low GI diet or no dietary intervention from early pregnancy to term. Two hundred sixty-five neonates had anthropometric measurements on day 1-2 of life, 126 in the intervention group and 139 in the control group. Measurements included birthweight, length and circumferences of the head, chest, abdominal, thigh and mid-upper arm. A subgroup of 219 (82%) neonates also had skin-fold measurements. Neonates whose mothers had a low GI diet in pregnancy had lower thigh circumference (15.9 ± 1.7 cm vs. 16.6 ± 1.5 cm, P = 0.04). There was no difference between the intervention and control groups in head, chest abdominal or mid-upper arm circumferences. No difference was noted between the two groups for any skin-fold measurements (subscapular, thigh, biceps and triceps). Neonatal thigh circumference was altered by maternal low GI diet in pregnancy. These findings suggest that maternal low GI diet is safe in pregnancy and may positively impact infant adiposity.

Maternal high fat diet programming of the endocrine system

Maternal high fat diet programming of the endocrine system

204: Impact of maternal diet on peripheral vs hepatic insulin resistance in young female offspring

insulin resistance in young female offspring Hye Heo, Howard Slomko, Scarlett Karakash, Fabien Delahaye, Yongmei Zhao, Derek Huffman, Nir Barzilai, Francine Einstein Albert Einstein College of Medicine/Montefiore Medical Center, Obstetrics & Gynecology and Women’s Health, Bronx, NY, Albert Einstein College of Medicine/Montefiore Medical Center, Pediatrics, Bronx, NY, Albert Einstein College of Medicine, Medicine, Bronx, NY, Albert Einstein College of Medicine/Montefiore Medical Center, Obstetrics & Gynecology and Women’s Health, Bronx, NY OBJECTIVE: To characterize body composition and metabolic phenotype of young female offspring exposed to maternal western diet and calorie restriction (CR). STUDY DESIGN: SD female rats were fed 1 of 3 diets: 1) standard chow (Con-M), 2) western diet from 3 wks through gestation/lactation (WD-M) or 3) standard chow from 3 wks until Day 11 of gestation, then calorie restricted (pair-fed 50% kcal/d of Con-M) through lactation (CR-M). Litters were culled to 8pups. Female offspring (n 9/ grp, Con-F, WD-F and CR-F) were given standard chow after weaning. Body composition (microCT) was assessed at 4 and 6 weeks of life. At 9wks, insulin sensitivity was measured by hyperinsulinemic (3mU/ kg/min) clamp technique, using somatostatin (1.5ug/kg/min) and 3H3-glucose (to follow glucose flux). RESULTS: Maternal calorie intake (kcal/d/kg) and weight were similar in Con-M and WD-M. Litter size, pup and placental weight were similar in all groups. At weaning, WD-F weighed more and had greater SC/VF ratio compared to Con-F, but no differences in total fat. CR-F weighed less and had less total fat at weaning and did not catch up in growth. By 6wks, weight and fat distribution normalized in WD-F compared to Con-F. Both WD-F and CR-F consumed more calories for body weight compared to Con-F during the study, but normalized at 9 wks (Fig 1). Clamp results shown in Table 1. Glucose infusion rate was lower in both WD-F and CR-F. While CR-F had greater hepatic insulin resistance (less suppression of hepatic glucose production (HGP)), HGP was similar in WD-F compared to Con-F. Peripheral insulin sensitivity (Rd) was lower in WD-F, but this did not reach statistical significance. CONCLUSION: Western diet alone (i.e. without changes in maternal body weight) leads to insulin resistance in the young female rat offspring similar to the degree seen with severe maternal CR. Unlike offspring of WD dams, offspring of CR dams have greater degree of hepatic insulin resistance. The mechanism for differences in hepatic vs peripheral insulin resistance requires further study. *p 0.05. 205 Sedentary behavior during pregnancy does not alter maternal fat distribution or insulin action Hye Heo, Scarlett Karakash, Derek Huffman, Fabien Delahaye, Yongmei Zhao, Nir Barzilai, Francine Einstein Albert Einstein College of Medicine/Montefiore Medical Center, Obstetrics & Gynecology and Women’s Health, Bronx, NY, Albert Einstein College of Medicine, Medicine, Bronx, NY, Albert Einstein College of Medicine/Montefiore Medical Center, Obstetrics & Gynecology and Women’s Health, Bronx, NY OBJECTIVE: To determine the effects of voluntary exercise on insulin action and body composition in young pregnant and non-pregnant female rodents. STUDY DESIGN: Four groups of lean, age-matched SD rats were studied (n 5/group): non-pregnant controls (NPC), non-pregnant sedentary (NPS), pregnant controls (PC), and pregnant sedentary (PS). PC had continuous voluntary access to running wheels starting Day 1 of a 22 day gestation. PS were housed in similar cages without access to the running apparatus. At day 19, insulin sensitivity was assessed by hyperinsulinemic-euglycemic (3mU/kg/min) clamp technique, using somatostatin (1.5ug/kg/min) and 3H3-glucose (to follow glucose flux). A bolus of 2-[U-14C]deoxyglucose (20 Ci) was administered 30 min before the end of the clamp to determine tissue glucose uptake. To study chronic effects of exercise (as opposed to acute effects), wheel breaks were placed 18 hrs prior to insulin clamps. Animals were sacrificed at end of the clamp and tissues were collected and weighed. RESULTS: NPS had similar food intake, but greater visceral fat (3.0 .3 v 1.7 .4g; p 0.05) compared to NPC. PS and PC also had similar food intake, but no significant differences in visceral fat. PS and PC had no differences in pup weight, litter size, or glucose uptake in placenta, pups or maternal muscle. PC ran approximately 1/4 of the distance that NPC ran (9,434 1,593 v 36,235 11,517m; p 0.059). During insulin clamps (Table 1), overall insulin sensitivity, measured by glucose infusion rate (GIR) was not statistically different in NPS and NPC. In NPS, peripheral insulin sensitivity (Rd) was similar, but hepatic glucose production (HGP) was greater compared to NPC. GIR, Rd and HGP were similar in PS and PC. CONCLUSION: Sedentary behavior in non-pregnant, young female rodents is associated with increased visceral adiposity and hepatic insulin resistance. This effect is not seen in sedentary pregnant animals most likely because voluntary activity is decreased in pregnancy. *p 0.05. www.AJOG.org Clinical Obstetrics, Medical-Surgical-Disease, Neonatology, Physiology-Endocrinology Poster Session I

Impact of maternal diet during pregnancy and breastfeeding on infant metabolic programming: a prospective randomized controlled study

To evaluate the impact of maternal diet and intensive dietary counselling during pregnancy and breastfeeding on the infant's metabolic status. At the first trimester of pregnancy, 256 women were randomized into a control/placebo group and two dietary counselling groups (diet/probiotics and diet/placebo). The counselling, with double-blind randomization to probiotics (Lactobacillus rhamnosus GG and Bifidobacterium lactis) or placebo, targeted excessive saturated fat and low fibre consumption. Maternal diet was evaluated repeatedly during pregnancy and postpartum by means of 3 days' food diaries. Metabolic markers, serum 32-33 split and intact proinsulin, leptin/adiponectin ratio, skinfold thickness and waist circumference were measured of 194 healthy infants at the age of 6 months, and the high levels were taken to mirror adverse metabolic status. The proportion of infants with a high 32-33 split proinsulin was significantly lower in dietary counselling with probiotics (n = 6/62, 9.7%) or placebo (n = 7/69, 10.1%) compared with the control/placebo group (n = 17/63, 27.0%). The high split proinsulin was associated with larger skinfold thickness, waist circumference and higher leptin/adiponectin ratio in the infants (P < 0.05). With respect to maternal diet during pregnancy, the highest and lowest tertiles of fat intake increased the infant's risk of high split proinsulin, whereas those of butter associated correspondingly with the infant's waist circumference. Further, breastfed infants showed a reduced risk of high split proinsulin and leptin/adiponectin ratio compared with formula-fed infants. Modification of maternal diet during pregnancy and breastfeeding may benefit infant metabolic health. High split proinsulin reflects adverse metabolic status in infancy, which can be improved by early dietary counselling.

Maternal Protein Restriction Affects Postnatal Growth and the Expression of Key Proteins Involved in Lifespan Regulation in Mice

We previously reported that maternal protein restriction in rodents influenced the rate of growth in early life and ultimately affected longevity. Low birth weight caused by maternal protein restriction followed by catch-up growth (recuperated animals) was associated with shortened lifespan whereas protein restriction and slow growth during lactation (postnatal low protein: PLP animals) increased lifespan. We aim to explore the mechanistic basis by which these differences arise. Here we investigated effects of maternal diet on organ growth, metabolic parameters and the expression of insulin/IGF1 signalling proteins and Sirt1 in muscle of male mice at weaning. PLP mice which experienced protein restriction during lactation had lower fasting glucose (P = 0.038) and insulin levels (P = 0.046) suggesting improved insulin sensitivity. PLP mice had higher relative weights (adjusted by body weight) of brain (P = 0.0002) and thymus (P = 0.031) compared to controls suggesting that enhanced functional capacity of these two tissues is beneficial to longevity. They also had increased expression of insulin receptor substrate 1 (P = 0.021) and protein kinase C zeta (P = 0.046). Recuperated animals expressed decreased levels of many insulin signalling proteins including PI3 kinase subunits p85α (P = 0.018), p110β (P = 0.048) and protein kinase C zeta (P = 0.006) which may predispose these animals to insulin resistance. Sirt1 protein expression was reduced in recuperated offspring. These observations suggest that maternal protein restriction can affect major metabolic pathways implicated in regulation of lifespan at a young age which may explain the impact of maternal diet on longevity.

The effect of a low-protein diet on physiological adaptations to pregnancy

Figure. The effect of gestational age and maternal diet on plasma volume (A; effect of gestational age P < 0.05) and creatinine clearance (B; interaction gestational age · diet P < 0.05) during pregnancy. Data are means with their standard errors represented by vertical bars. Blood volume (results not shown) and plasma volume (Figure; A) increased significantly with gestational age (P < 0.05), but this outcome was unaffected by diet. There was a significant interaction between the effects of diet and gestational age on creatinine clearance (Figure; B), with low-protein animals exhibiting a decrease in clearance between days 10 and 20 of pregnancy in comparison with the relatively constant levels in controls. The increase in plasma and blood volume observed during gestation agrees with previous investigations (2) . Although the data appeared to show a delay in the increase in plasma volume in low-protein animals, this effect was not significant. These data therefore suggest that plasma volume expansion is not sensitive to the level of maternal protein restriction used in the present study, despite the apparent effects of the low-protein diet on glomerular filtration rate. Further investigation of the impact of maternal diet on the molecular systems controlling maternal and fetal renal function during pregnancy is ongoing, as this effect may have implications for renal development and subsequent blood pressure control in the offspring.

Dietary intake of B-vitamins in mothers born a child with a congenital heart defect

Periconceptional use of multivitamins reduces the risk of a child with a congenital heart defect (CHD). Data on the impact of maternal diet, however, are lacking. We investigated the association between the maternal dietary intake of B-vitamins and having a child with a CHD. A case-control study was performed in 192 mothers of a child with a CHD and 216 mothers of a healthy child. Mothers filled out food frequency questionnaires covering the current dietary intake, and general questionnaires at 17 months after the index-pregnancy. Maternal blood samples were taken to determine B-vitamin and plasma total homocysteine (tHcy) concentrations as nutritional biomarkers. Pregnant and lactating mothers and those with another diet compared with the preconceptional period were excluded for analysis. Case-mothers and controls were compared using the Mann-Whitney U test and logistic regression. The dietary intake of macronutrients and B-vitamins was comparable between both groups, but all mothers had a substantially lower median folate intake (cases 161 microg, controls 175 microg) than the Dutch recommended dietary allowance of 300 microg. Within the case-group, the intake of proteins and vitamin B(6) and the concentrations of serum vitamin B(12) and folate were significantly lower in hyperhomocysteinemics (tHcy > or = 14.5 micromol/l) than in normohomocysteinemics. The maternal educational level was positively associated with B-vitamin intake, except for vitamin B(12) in controls. Low educated case-mothers showed a significantly lower median vitamin B(12) intake than controls (2.8 microg and 3.8 microg, P = 0.01). The CHD risk doubled if vitamin B(12) intake in these mothers reduced by 50% (OR 2.0; 95% CI: 1.1-3.5). A diet low in vitamin B(12) is associated with an increased risk of a child with a CHD, especially in low educated women. A disbalance in the maternal intake of proteins and low folate intake may play a role as well, but needs further investigation. As hyperhomocysteinemia is a strong risk factor for adult cardiovascular disease, these data may imply that the hyperhomocysteinemic mothers and their children should be targeted for nutritional interventions.

Commentary: Maternal diet during pregnancy and blood pressure in the offspring

Like other living creatures, human beings are plastic during development, they are able to adapt to the environment. There is now considerable evidence that coronary heart disease originates in developmental plasticity. Almost 100 studies assessing the link between birth weight and blood pressure have been performed worldwide. Two meta analyses have shown that low birth weight is consistently linked with an increased blood pressure in later life, 1 and that this association is similar for men and women. 2 Birth weight has been a central feature of epidemiological studies because it is a measurement that is readily available and has been recorded for many years. However, there is now evidence that fetal programming may occur in the absence of changes in fetal size. Recent research therefore has sought to identify the nature of the adverse maternal influences that raise blood pressure and alter levels of cardiovascular risk factors in the offspring. In this issue of the International Journal of Epidemiology, Huh et al. describe their study in which they assessed the direct impact of maternal diet during pregnancy on offspring’s blood pressure. 3 They studied the link between maternal protein intake in the first and second trimester and blood pressure of the offspring at the age of 6 months. Although they did confirm the well-described association between low birth weight and raised blood pressure, they could not detect an association between protein intake in the maternal diet during pregnancy and offspring’s blood pressure. The third trimester is thought to be a critical window for programming blood pressure. It is therefore a serious drawback of Huh’s study that the maternal diet was only studied in the first and second, but not third, trimester. Our study of men and women born around the time of the Dutch famine, for instance, has shown that blood pressure was linked to the balance between protein and carbohydrate intake in the maternal diet during the third, but not first and second trimester. 4 Similarly, a study in Aberdeen found that the blood pressures of men and women were related to the balance of carbohydrate and protein in their mother’s diet during late pregnancy. 5 At either extreme of this balance, their blood pressures were raised, even if their growth in utero was not affected. The influence of the maternal diet on offspring’s blood pressure is complex. Animal studies show that the effects of protein restriction in the diet of pregnant rats on the blood pressure of their offspring are stronger than the effects of caloric restriction with a balanced reduction of all macro-nutrients. 6 Moreover, the effects seem to depend not only on the composition of the diet with respect to macro-nutrients in general, but also with respect to the source of macro-nutrients in the diet. Giving low protein diets to pregnant rats raises blood pressure in the offspring if the diets contain fats rich in linoleic acid, 6 whereas no effects on blood pressure are found in similar experiments using a diet containing fats rich in linolenic acid. 7 Furthermore, the blood pressure raising effect of protein restriction can be prevented by supplementing the maternal diet with glycine. 8 Most studies relating maternal diet to offspring’s blood pressure show that blood pressure of the offspring may be programmed through the maternal diet without affecting the size of the baby at birth. 4,5 Evidence from animal studies leads to similar conclusions: the programming of adult physiology can occur as a result of maternal factors that either do not alter fetal growth or result in alterations in organ growth and body composition but have little or no effect on size at birth.

Impact of Maternal Diet on Reproductive Outcome: Foreword

Impact of Maternal Diet on Reproductive Outcome: Foreword

Fat-Soluble Vitamins in the Maternal Diet, Influence of Cod Liver Oil Supplementation and Impact of the Maternal Diet on Human Milk Composition

Background/Aims: To investigate lactating mothers’ intake of fat-soluble vitamins in free-living subjects and to what extent cod liver oil supplementation influences the maternal intake in a population with common intake of cod liver oil. The impact of maternal diet on the concentration of fat-soluble vitamins in human milk was studied. Methods: Dietary intake of 77 lactating women was investigated by 24-hour diet recalls and breast-milk samples were taken at the same occasions. Breast milk samples were analyzed for fat-soluble vitamins. Results: The median intakes were 927 µg/day for vitamin A, 5.5 mg/day for vitamin E and 3.3 µg/day for vitamin D. Maternal vitamin A, E and D intakes were higher when the diet was supplemented with cod liver oil. Icelandic breast milk was found to have high contents of vitamin A and E. Only vitamin D was too low in breast milk to meet the recommended intake for infants. Retinylpalmitate in relation to lipids correlated with maternal vitamin A intake (r = 0.23, p < 0.05). The group with cod liver oil supplementation had significantly lower levels of γ-tocopherol in breast milk (p < 0.01), whereas the supplementation did not affect other fat-soluble vitamins. Conclusion: The recommended intake of fat-soluble vitamins for lactating women can more easily be met with a cod liver oil supplementation than diet alone. Only vitamin D in human milk cannot meet the recommended intakes for infants, with normal breastfeeding. There is a relationship between the content of vitamins A and E in human milk and the maternal diet.

Dietary composition during fetal and neonatal life affects neuropeptide Y functioning in adult offspring

The aim of this study was to examine the impact of maternal diet during the gestation and lactation periods on the neuropeptide Y (NPY) system in adult offspring. Male Long-Evans rats were obtained from dams fed either on a well-balanced diet (C), a high carbohydrate diet (HC) or a high-fat diet (HF) and fed themselves on the well-balanced diet for their whole life. At 6 months of age, their feeding response to various doses of NPY injected in the lateral brain ventricle was measured in one group and NPY concentrations in microdissected nuclei of the hypothalamic were measured in a second group. The HF rats were lighter than the two other groups ( P<0.001). The control rats showed a typical dose-dependent feeding response to NPY. The HC rats showed a continuous increase in the response, starting at the intermediate dose (1.0 μg) only while the HF rats had a maximal response at the lowest dose (0.5 μg). The HF rats ate twice as much as the HC rats at the lowest dose tested 1 h after injection (4.4±0.6 vs. 2.7±0.4 g; P<0.05), showing therefore the greatest sensitivity to NPY. This change in the sensitivity was not related to hypothalamic NPY concentration as it was not modified in the arcuate and paraventricular nuclei. The diet imposed on the mother could have long-lasting effects on body weight regulation of the offsprings and alter the NPY system likely through modifications at the receptor level.

Maternal diet rich in saturated fat during breastfeeding is associated with atopic sensitization of the infant.

To investigate the impact of maternal diet during breastfeeding on atopic sensitization of infants at risk. Prospective cohort study. Turku University Central Hospital, Finland. Altogether 114 infants with a family history of atopic disease were followed during their first year of life. The mothers completed a 4 day food record during breastfeeding just before the infants were 3 months old. Atopic sensitization of the infants was determined by a positive skin prick test result at 12 months. Positive skin prick test reactivity to at least one antigen was detected in 27/114 (24%) infants at 12 months. The energy intake of the mothers was low, mean 8.0 MJ/day (95% CI 7.7-8. 3), and the proportion of energy derived from fat was high, mean 36. 6 E% (95% CI 35.6-37.6). Atopic mothers had a higher intake of total fat and saturated fat and a lower intake of carbohydrate as a percentage of total energy intake than non-atopic mothers; P=0.017, P=0.050, P=0.004 respectively. Maternal intake of saturated fat during breastfeeding was associated with atopic sensitization of the infant, OR=1.16 (95% CI 1.001-1.36); P=0.048 irrespective of the maternal atopic status. Our results show that an unbalanced maternal diet during breastfeeding may be a risk factor underlying the later development of atopic sensitization of the infant regardless of maternal atopic disease. The observation thus extends findings implying that early nutrition programmes the subsequent health of the child to the risk of developing atopic disease. Academy of Finland and National Technology Agency.