Fetal Nutrition Research Articles

Possible role of birth weight on general and central obesity in Chinese children and adolescents: a cross-sectional study

PurposeAccording to the developmental origins of health and disease theory, fetal nutrition is associated with obesity and chronic diseases in children and adults. However, previous findings regarding the association between birth weight and childhood obesity have been inconsistent. The aim of the present study was to investigate the relationship between birth weight and childhood obesity in China. MethodsThe 16,580 subjects (8477 boys and 8103 girls) aged 7–17 years, who participated in this study were recruited from a cross-sectional study in six cities in China. Epidemiological data, including birth information, were collected through face-to-face interviews, and anthropometric indices were measured by trained physicians. Overweight and obese cases were defined using sex-specific and age-specific 85th and 95th percentile body mass index (BMI) cutoffs for Han children and adolescents. Central obesity was defined using sex-specific waist-to-height ratio (WHtR) cutoffs (WHtR ≥0.48 in boys and WHtR ≥0.46 for girls). ResultsThe overall rate of overweight status and obesity was 20.3% in the Chinese children and adolescents and that of central obesity was 18.9%. Subjects were stratified into eight groups according to weight at birth. J-shaped relationships were observed between birth weight and BMI for age Z-score and WHtR. After adjusting for confounders such as gender, gestational age, parental factors, and dietary factors, the risk of overweight and obese status was still higher in the children with higher birth weights than in children with birth weights of 3000–3499 g (3500–3999 g: odds ratio [OR] = 1.14, 95% confidence interval [CI] = 1.02–1.28; 4000–4499 g: OR = 1.39, 95% CI = 1.19–1.63; and 4500–4999 g: OR = 1.36, 95% CI = 1.06–1.76). Moderately high birth weight also increased the risk of central obesity. Relative to the children with normal birth weights (3000–3499 g), the adjusted OR and 95% CI were 1.33 (1.13–1.56) in children with birth weights of 4000–4499 g. Children with very low birth weight (lower than 1500 g) had the highest risk of central obesity. The adjusted OR was 2.30 (95% CI: 1.03–5.14) relative to children with birth weights of 3000–3499 g. ConclusionsBirth weight was associated with obesity in Chinese children and adolescents. J-shaped relationships were observed between birth weight and BMI and WHtR in childhood, and very low birth weight was associated with a mild increase in the risk of central obesity in Chinese children and adolescents.

The effect of intraumbilical fetal nutrition via subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses

The effect of intraumbilical fetal nutrition via subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses

Placental Transport of Nutrients and Fetal Metabolism in Intrauterine Growth Restricted Rats

Previous studies show that reduced uterine perfusion results in intrauterine growth restriction and impaired fetal nutrition. However, the mechanisms involved are not totally understood. The objective of this study was to investigate whether reduced uterine perfusion alters placental transport of glucose and fatty acids in growth‐restricted fetuses. We used a rat model of growth‐restricted offspring induced by reduced uterine perfusion at 14 days of gestation. At 19 days of gestation fetuses and placentas were excised by cesarean section followed by collection of fetal and maternal blood and tissue. GraphPad software was used for statistical analysis with significance set at P<0.05. Reduced uterine perfusion resulted in male and female growth‐restricted fetuses with lower body weight and placental size compared to controls (P<0.05); and greater placental efficiency in female fetuses. Protein concentration and gene expression of placental glucose transporters GLUT2 and GLUT3 and fatty acids transporter FATP1 were elevated in growth‐restricted fetuses compared to controls (P<0.05). Glucose levels were elevated in female growth‐restricted fetuses compared to male and controls (P<0.05). Analysis of correlation between placental efficiency and fetal glucose level showed negative correlation (Pearson r=‐0.7939) in controls and positive correlation (Pearson r= 0.0747) in growth‐restricted fetuses. These results suggest that reduced uterine perfusion induces compensatory changes in glucose and fatty acids placental transporters to ensure fetal survival and also results in changes on glucose homeostasis in growth‐restricted fetuses

Leptin intake in suckling rats restores altered T3 levels and markers of adipose tissue sympathetic drive and function caused by gestational calorie restriction

Maternal calorie restriction during gestation in rats has been associated with altered white adipose tissue (WAT) sympathetic innervation and function in offspring. Here, we aimed to investigate whether supplementation with oral leptin (a breast milk component) throughout the lactation period may revert the aforementioned adverse programming effects. Three groups of male and female rats were studied at the postnatal day 25: the offspring of control dams, the offspring of 20% calorie-restricted dams during pregnancy (CR) and CR rats supplemented with physiological doses of leptin throughout lactation (CR-Leptin). Tyrosine hydroxylase (TH) levels and its immunoreactive area, and mRNA expression levels of lipid metabolism-related genes and of deiodinase iodothyronine type II (Dio2) were determined in WAT. Triiodothyronine (T3) levels were determined in the blood. In CR males, leptin treatment restored the decreased TH levels and its immunoreactive area in WAT, and partially normalized expression levels of genes related to lipolysis and fatty acid oxidation (adipose triglyceride lipase, hormone-sensitive lipase, carnitine palmitoyltransferase 1b and peroxisome proliferator-activated receptor gamma coactivator 1-alpha). Leptin treatment also reverted the decreased T3 plasma levels and WAT lipoprotein lipase mRNA levels occurring in CR males and females, and the decreased Dio2 mRNA levels in CR females. Leptin supplementation throughout the lactation period reverts the malprogrammed effects on WAT structure and function induced by undernutrition during pregnancy. These findings support the relevance of the intake of leptin during lactation, bearing clear characteristics of essential nutrient, and provide a strategy to treat and/or prevent the programmed trend to obesity acquired by inadequate fetal nutrition.

Relationship between Foetal Growth Restriction and Maternal Nutrition Status Measured by Dual-Energy X-Ray Absorptiometry, Leptin, and Insulin-Like Growth Factor

Aims: The aim of this study was to determine if maternal nutritional status, as defined by body composition, leptin, and insulin-like growth factor (IGF)-I levels, relates to foetal growth. Methods: In this prospective study, mothers of foetuses with foetal growth restriction (FGR; cases; n = 46) and mothers of appropriate-for-gestational-age (AGA) foetuses (controls; n = 81) were consecutively recruited over a 14- month period. A maternal blood sample was obtained during the third trimester (between 32 and 34 weeks of gestation) for the assessment of IGF-I and leptin. Body composition was assessed by dual-energy X-ray absorptiometry within the first 15 days after delivery. The study used the SPSS-PC statistical package, version 19.0, and p < 0.05 was considered statistically significant. Results: Mean serum IGF-I levels were lower in the cases than in the controls (p < 0.05), whereas leptin concentrations were higher in the cases after adjusting for age, body mass index and cigarette consumption (p < 0.05). Cases had less lean and fat tissue than controls (p < 0.05) but a relatively higher fat percentage. Conclusions: The mothers of foetuses with FGR have a body composition pattern characterized by a slightly increased fraction of fat mass, lower IGF-I concentrations, and increased serum leptin levels. Optimization of maternal nutritional status should be considered, as the nutritional status may be involved in the pathogenesis of FGR.

Three-dimensional growth dynamics of the liver in the human fetus.

PurposeThe fetal liver is indubitably the earliest and the most severely affected organ by abnormal fetal growth. The size of the fetal liver assessed by three-dimensional ultrasonography is indispensable in determining the status of fetal growth, nutrition and maturity, and in the early recognition and monitoring fetal micro- and macrosomias. The aim of the present study was to measure the human fetal liver length, transverse and sagittal diameters to establish their age-specific reference intervals, the 3rd, 10th, 50th, 90th, and 97th smoothed centile curves, and the relative growth of the liver calculated for the 50th centile.Materials and methodsUsing anatomical, digital (NIS-Elements AR 3.0, Nikon) and statistical methods (one-way ANOVA test for paired data and post hoc RIR Tukey test, Shapiro–Wilk test, Fisher’s test, Student’s t test, the Altman-Chitty method), length, transverse and sagittal diameters of the liver for the 3rd, 10th, 50th, 90th, and 97th centiles were assessed in 69 human fetuses of both sexes (32 males and 37 females) aged 18–30 weeks, derived from spontaneous abortions or stillbirths.ResultsNo male–female differences (P > 0.05) concerning the three parameters studied were found. During the study period, the fetal liver increased tri-dimensionally: in length from 19.51 ± 1.02 to 39.65 ± 7.05 mm, in transverse diameter from 29.44 ± 3.73 to 53.13 ± 5.31 mm, and in sagittal diameter from 22.97 ± 3.79 to 43.22 ± 5.49 mm. The natural logarithmic models were found to fit the data with gestational age (P < 0.001) in the following five cutoff points: 3rd, 10th, 50th, 90th and 97th centiles. The values of liver parameters in relation to gestational age in weeks were calculated by the following logarithmic regressions: y = −82.778 + 35.752 × ln(age) ± Z × (−2.778 + 0.308 × age) for liver length, y = −123.06 + 52.668 × ln(age) ± Z × (3.156 + 0.049 × age) for liver transverse diameter, and y = −108.94 + 46.052 × ln(age) ± Z × (−0.541 + 0.188 × age) for liver sagittal diameter. For the 50th centile, at the range of 18–30 weeks, the growth rates per week were gradually decreasing from 1.93 to 1.21 mm for length, from 2.85 to 1.79 mm for transverse diameter, and from 2.49 to 1.56 mm for sagittal diameter of the liver (P < 0.05). During the study period both the length-to-transverse diameter ratio and the sagittal-to-transverse diameter ratio of the liver changed little, attaining the values of 0.71 ± 0.11 and 0.87 ± 0.12, respectively.ConclusionsThe fetal liver does not reveal sex differences in its length, transverse and sagittal diameters. The fetal liver length, transverse and sagittal diameters grow logarithmically. The regression equations for the estimation of the mean and standard deviation of liver length, transverse and sagittal diameters allow for calculating any desired centiles according to gestational age. The three-dimensional evolution of the fetal liver follows proportionately. The age-specific reference intervals for evolving liver length, transverse and sagittal diameters constitute the normative values of potential relevance in monitoring normal fetal development and screening for disturbances in fetal growth.

Birth weight, malnutrition and kidney-associated outcomes--a global concern.

An adverse intrauterine environment is associated with an increased risk of elevated blood pressure and kidney disease in later life. Many studies have focused on low birth weight, prematurity and growth restriction as surrogate markers of an adverse intrauterine environment; however, high birth weight, exposure to maternal diabetes and rapid growth during early childhood are also emerging as developmental risk factors for chronic diseases. Altered programming of nephron number is an important link between exposure to developmental stressors and subsequent risk of hypertension and kidney disease. Maternal, fetal, and childhood nutrition are crucial contributors to these programming effects. Resource-poor countries experience the sequential burdens of fetal and childhood undernutrition and subsequent overnutrition, which synergistically act to augment the effects of developmental programming; this observation might explain in part the disproportionate burden of chronic disease in these regions. Numerous nutritional interventions have been effective in reducing the short-term risk of low birth weight and prematurity. Understanding the potential long-term benefits of such interventions is crucial to inform policy decisions to interrupt the developmental programming cycle and stem the growing epidemics of hypertension and kidney disease worldwide.

Variation of Placental and Neonatal Weight in Normal Pregnancy and Pregnancy with Hypertension in Western Maharashtra

Placenta is an organ for foetal nutrition and continuation of pregnancy. Morphological changes are observed in hypertensive disorder of pregnancy. Weight of placenta affects neonatal weight, and the predisposing factor for this is maternal age.

Prenatal Exposure to Sodium Arsenite Alters Placental Glucose 1, 3, and 4 Transporters in Balb/c Mice.

Inorganic arsenic (iAs) exposure induces a decrease in glucose type 4 transporter (GLUT4) expression on the adipocyte membrane, which may be related to premature births and low birth weight infants in women exposed to iAs at reproductive age. The aim of this study was to analyze the effect of sodium arsenite (NaAsO2) exposure on GLUT1, GLUT3, and GLUT4 protein expression and on placental morphology. Female Balb/c mice (n = 15) were exposed to 0, 12, and 20 ppm of NaAsO2 in drinking water from 8th to 18th day of gestation. Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy. NaAsO2 exposure induced a significant decrease in fetal and placental weight (P < 0.01) and increases in infarctions and vascular congestion. Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased. In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm. The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

The Evolution of the Primate, Hominid and Human Brain

Human evolution involved four brain enhancement steps. The first step of brain size enhancement occurred in lower simian primates (brain size 0.17%-0.19% of body weight). The second step occurred in advanced simian primates (brain size 0.66%-0.78% of body weight). The third step occurred among early hominids (brain size 1.0%- 1.2% of body weight), and the fourth of final step occurred among humanoids (brain size 2.1%-2.7% of body weight). This brain enhancement occurred in response to brain growth genes or brain growth factor proteins. Brain growth was very much limited by the efficiency of fetal nutrition or placentation. In many respects it was the efficiency of placentation and implantation that controlled brain growth genes expanding brain growth to the limit that placentation could allow. Brain growth was initially blocked by inefficiency of epitheliochorial placentation. It was the initial evolution of chorionic gonadotropin (CG) and hyperglycosylated CG that promoted the creation of hemochorial placentation, and the implantation of the placenta. This occurred in lower simian primates and so was followed by initial implantation and hemochorial placentation. This permitted the first step in brain growth. The CG gene underwent mutation with advanced simian primates and a higher biological activity CG and hyperglycosylated hCG resulted. This drove more efficient implantation and placentation and so primates developed a bigger brain, the second step in brain growth. The CG gene underwent further mutation with early hominids and a higher biological activity CG and hyperglycosylated hCG resulted. This drove even more efficient implantation and placentation and so early hominids developed a bigger brain, the third step in brain growth. The CG gene underwent mutation with humanoids and a higher biological activity CG and hyperglycosylated hCG resulted. This drove the most efficient implantation and placentation and so humanoids developed the biggest brain, the fourth step in brain growth.

Effect of Perinatal Protein Malnutrition Under Serotonergic Control on Feeding Behavior: A Systematic Review

malnutrition during the perinatal period leads to several morphological and physiological changes in the central nervous system whose main purpose is to prepare the body for environmental conditions. Several studies have been developed to explain the effects that malnutrition causes over feeding behavior in adults, and in particular on the role of the serotonergic system in this control. Thus, the objective of this systematic review was to assess emerging literature on the effects of perinatal malnutrition on the control of feeding behavior and the role of the serotonergic system in this control. The articles were researched in the virtual libraries Pubmed, Lilacs and Medline using as keywords: Protein Malnutrition, Feeding Behavior, Serotonin Receptors, Gestational malnutrition, Perinatal undernutrition, Fetal Nutrition Disorders and Serotonin. 261 articles in total were found. However, after excluding duplicates and analysis of the criteria for inclusion and exclusion 8 articles remained. Analysis of the articles showed that malnutrition in the perinatal period leads to changes in food preference in rats, in addition to delaying the point of satiety of these animals. It was also found that there is increased protein expression of c-fos groups forebrain neurons, increased expression of 5HT-1A receptors and increase in brain serotonin levels. These findings suggest that changes in eating behavior in malnourished animals can be brought about due to changes in the serotonergic system.

Potential of the application of epigenetics in animal production

Our many current environmental challenges, including worldwide abnormal weather, global warming, and pollution, necessitate a new and innovative strategy for animal production for the next generation. This strategy should incorporate not only higher-efficiency production, but also advanced biological concepts and multi-functional agricultural techniques, into environmentally friendly systems. Recent research has discovered a unique phenomenon referred to as ‘foetal and neonatal programming’, which is based on ‘the developmental origins of health and disease (DOHaD)’ concept. These studies have shown that alterations in foetal and early postnatal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology and metabolism of affected animals during adult life. Ruminants fill an important ecological niche that capitalises on the symbiotic relationship between fibre-fermenting ruminal microbes and the mammalian demand for usable nutrients. The timing of the perturbation in maternal nutrient availability plays an important role in determining the effect that the foetal and neonatal programming will have on the developing placenta or foetus and offspring performance. Developmental programming through nutritional manipulations may help the ruminant, as an effective grass–protein converter, fulfil its production potential.

114 ASYNCHRONOUS EMBRYO TRANSFER AFFECTS THE EXPRESSION OF IMPRINTED GENES IN EQUINE TROPHECTODERM

Gene imprinting is a form of epigenetic modification that results in parent-of-origin specific monoallelic expression. Imprinted genes play important roles during fetal-placental growth with paternally imprinted genes generally promoting and maternally imprinted genes suppressing fetal growth. Imprinted genes are therefore believed to have important effects on trophoblast differentiation and placental development, and in adjusting fetal nutrition to maternal supply. The horse is an interesting model of early placental development because of its unusually long pre-implantation period (40 days), during which the conceptus is dependent on uterine secretions for nutrient provision. Moreover, horse embryos tolerate a wide range of uterine asynchrony following embryo transfer (ET), offering a unique tool to study maternal influences on conceptus development. This study examined the effect of asynchronous ET on the expression of imprinted genes in equine trophectoderm. Twenty Day 8 embryos were transferred to recipient mares that either ovulated on the same day (synchronous; n = 10) or 5 days after (asynchronous; n = 10) the donor mare. The conceptuses were recovered 6 or 11 days after ET (Day 14 or 19 of conceptus development; n = 5 per group). Bilaminar trophectoderm was isolated and mRNA expression for a range of genes known to be imprinted in equine trophectoderm (H19, PHLDA2, IGF2R, IGF2, PEG3, PEG10, SNRPN, INSR, and INS) was investigated by RT-qPCR. The effects of asynchronous ET and stage of pregnancy on gene expression were analysed by two-way ANOVA followed by independent-samples t-tests. IGF2, PEG3, PEG10, INSR, H19, and PHLDA2 all showed a significant up-regulation in gene expression between Days 14 and 19 of pregnancy; however, expression was higher in synchronous than asynchronous pregnancies at Day 19 (P &lt; 0.05). IGF2R expression increased significantly from Day 14 to 19 in the synchronous pregnancies (P &lt; 0.05), but did not differ between treatments at Day 19. SNRPN expression increased from Day 14 to 19, and was unaffected by asynchrony. INS mRNA was not detectable in trophectoderm. In conclusion, asynchronous ET had a significant effect on gene expression at Day 19 of gestation that was not evident at Day 14. This may be either a contributor to the delayed development that is observed in asynchronous pregnancies or a result/response; in either case, it may affect subsequent development. This study was founded by EpiHealthNet (Project number 317146).

Late gestation under- and overnutrition have differential impacts when combined with a post-natal obesogenic diet on glucose-lactate-insulin adaptations during metabolic challenges in adolescent sheep.

To determine whether late gestation under- and overnutrition programme metabolic plasticity in a similar way, and whether metabolic responses to an obesogenic diet in early post-natal life depend on the foetal nutrition history. In a 3 × 2 factorial design, twin-pregnant ewes were for the last 6 weeks of gestation (term = 147 days) assigned to HIGH (N = 13; 150 and 110% of energy and protein requirements, respectively), NORM (N = 9; 100% of requirements) or LOW (N = 14; 50% of requirements) diets. The twin offspring were raised on high-carbohydrate-high-fat (HCHF; N = 35) or conventional (CONV; N = 35) diets from 3 days to 6 months of age (around puberty). Then intravenous glucose (GTT; overnight fasted), insulin (ITT; fed) and propionate (gluconeogenetic precursor; PTT; both fed and fasted) tolerance tests were conducted to evaluate (hepatic) metabolic plasticity. Prenatal malnutrition differentially impacted adaptations of particularly plasma lactate followed by glucose, cholesterol and insulin. This was most clearly expressed during PTT in fasted lambs and much less during ITT and GTT. In fasted lambs, propionate induced more dramatic increases in lactate than glucose, and HIGH lambs became more hyperglycaemic, hyperlactataemic and secreted less insulin compared to the hypercholesterolaemic LOW lambs. Propionate-induced insulin secretion was virtually abolished in fasted HCHF lambs, but upregulated in fasted compared to fed CONV lambs. HCHF lambs had the greatest glucose-induced insulin secretory responses. Prenatal malnutrition differentially programmed glucose-lactate metabolic pathways and cholesterol homeostasis. Prenatal overnutrition predisposed for hyperglycaemia and hyperlactataemia, whereas undernutrition predisposed for hypercholesterolaemia upon exposure to an obesogenic diet. Prenatal overnutrition (not undernutrition) interfered with pancreatic insulin secretion by non-glucose-dependent mechanisms.

Oral cadmium exposure during rat pregnancy: assessment of transplacental micronutrient transport and steroidogenesis at term.

Diet is the main source of cadmium (Cd) exposure. Gastrointestinal absorption increases during pregnancy. Cadmium accumulated in the placenta may interfere with nutrient transport to the foetus. Data on the potential of Cd to act as a steroid disruptor of pregnancy are limited. We evaluated the effects of oral Cd exposure during pregnancy on placental function in micronutrient transfer to the foetus and steroidogenesis in Wistar rats (regular 4-day cyclers) that mated with unexposed males. Pregnant rats were randomly assigned to a Cd group exposed orally to 50 mg Cd l(-1) (CdCl(2)xH2O dissolved in demineralized water), ≈ 7.5 mg Cd kg(-1) a day, during 20 days of gestation and control (supplied with demineralized water). Non-pregnant rats were treated under the same experimental conditions. On day 20, all of the rats were killed and samples were taken for element analyses (by electrothermal atomic absorption spectrometry). Progesterone and testosterone were measured in serum and placenta-derived samples (by immunoenzymometric assay and/or enzyme-linked immunosorbent assay). In the exposed rats, Cd increased in blood and organs, more in pregnant rats, and in placenta and foetus whereas zinc increased in liver. Iron decreased in maternal organs and in foetus, whereas zinc decreased in maternal kidney and placenta. Liver copper was lower and kidney copper higher in all pregnant vs. non-pregnant rats. Steroids in serum and placenta did not change. In conclusion, oral Cd exposure during rat pregnancy does not affect progesterone and testosterone at term. Transplacental iron and zinc handover are disrupted, which may put at risk the maintenance of foetal nutrition and viability.

Intrauterine nutrition: long-term consequences for vascular health.

There is a growing body of evidence that improper intrauterine nutrition may negatively influence vascular health in later life. Maternal malnutrition may result in intrauterine growth retardation and, in turn, metabolic disorders such as insulin resistance, diabetes, hypertension, and dyslipidemia, and also enhanced risk of atherosclerosis and cardiovascular death in the offspring. Energy and/or protein restriction is the most critical determinant for fetal programming. However, it has also been proposed that intrauterine n-3 fatty acid deficiency may be linked to later higher blood pressure levels and reduced insulin sensitivity. Moreover, it has been shown that inadequate supply of micronutrients such as folate, vitamin B12, vitamin A, iron, magnesium, zinc, and calcium may contribute to impaired vascular health in the progeny. In addition, hypertensive disorders of pregnancy that are linked to impaired placental blood flow and suboptimal fetal nutrition may also contribute to intrauterine growth retardation and aggravated cardiovascular risk in the offspring. On the other hand, maternal overnutrition, which often contributes to obesity and/or diabetes, may result in macrosomia and enhanced cardiometabolic risk in the offspring. Progeny of obese and/or diabetic mothers are relatively more prone to develop obesity, insulin resistance, diabetes, and hypertension. It was demonstrated that they may have permanently enhanced appetites. Their atheromatous lesions are usually more pronounced. It seems that, particularly, a maternal high-fat/junk food diet may be detrimental for vascular health in the offspring. Fetal exposure to excessive levels of saturated fatty and/or n-6 fatty acids, sucrose, fructose and salt, as well as a maternal high glycemic index diet, may also contribute to later enhanced cardiometabolic risk.

Intergenerational effects of early life nutrition: maternal leg length predicts offspring placental weight and birth weight among women in rural Luzon, Philippines.

Leg length is the component of stature most sensitive to early life nutrition; as such, it provides an opportunity to retrospectively evaluate the relationship between a woman's infancy and early childhood nutrition and offspring birth weight (BW). Here we explore the relationship between maternal leg length and offspring BW in a rural Philippine community, while also investigating the potential role of placental size as a pathway. Anthropometric and questionnaire data were obtained among pregnant women (ages 17-42 years) at a birthing clinic in Antipolo City, Philippines (n = 80). Offspring BW and placental weight were collected upon delivery. Maternal leg length, but not trunk length, was a positive predictor of infant BW. This relationship was strengthened after adjusting for gestational age and maternal body mass index (BMI). Further adjustment for placental weight attenuated the relationship between leg length and BW, while placental weight was unrelated to maternal trunk length. The relationship between maternal BMI and BW was also attenuated after adjustment for placental weight. Maternal leg length is the component of stature that most strongly predicts offspring placental weight and BW in this sample. These findings suggest that fetal nutrition and growth in the present generation are influenced, in part, by the mother's own early life growth conditions. Our results add to evidence that fetal nutrition tracks the mother's past nutritional experiences, while also suggesting that ensuring favorable growth conditions during infancy and early childhood may benefit not only the present generation, but future offspring.

Higher systolic blood pressure with normal vascular function measurements in preterm‐born children

Preterm birth, low birth weight and poor foetal nutrition have been linked to cardiovascular disease, but the underlying mechanisms remain unclear. We explored prematurity and vascular function by studying a UK cohort of 14 049 children and conducting a systematic review. Systolic blood pressure was higher in subjects born preterm than term, but there were no differences in endothelial dysfunction or arterial stiffness. The systematic review revealed no clear association between prematurity and vascular function.

Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child.

Some breastfed infants with atopic eczema benefit from elimination of cow milk, egg, or other antigens from their mother's diet. Maternal dietary antigens are also known to cross the placenta. To assess the effects of prescribing an antigen avoidance diet during pregnancy or lactation, or both, on maternal and infant nutrition and on the prevention or treatment of atopic disease in the child. We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (6 July 2012). All randomized or quasi-randomized comparisons of maternal dietary antigen avoidance prescribed to pregnant or lactating women. We excluded trials of multimodal interventions that included manipulation of the infant's diet other than breast milk or of non-dietary aspects of the infant's environment. We extracted data from published reports, supplemented by additional information received from the trialists we contacted. The evidence from five trials, involving 952 participants, does not suggest a protective effect of maternal dietary antigen avoidance during pregnancy on the incidence of atopic eczema during the first 18 months of life. Data on allergic rhinitis or conjunctivitis, or both, and urticaria are limited to a single trial each and are insufficient to draw meaningful inferences. Longer-term atopic outcomes have not been reported. The restricted diet during pregnancy was associated with a slightly but statistically significantly lower mean gestational weight gain, a non-significantly higher risk of preterm birth, and a non-significant reduction in mean birthweight. The evidence from two trials, involving 523 participants, did not observe a significant protective effect of maternal antigen avoidance during lactation on the incidence of atopic eczema during the first 18 months or on positive skin-prick tests to cow milk, egg, or peanut antigen at one, two, or seven years. One crossover trial involving 17 lactating mothers of infants with established atopic eczema found that maternal dietary antigen avoidance was associated with a non-significant reduction in eczema severity. Prescription of an antigen avoidance diet to a high-risk woman during pregnancy is unlikely to reduce substantially her child's risk of atopic diseases, and such a diet may adversely affect maternal or fetal nutrition, or both. Prescription of an antigen avoidance diet to a high-risk woman during lactation may reduce her child's risk of developing atopic eczema, but better trials are needed. Dietary antigen avoidance by lactating mothers of infants with atopic eczema may reduce the severity of the eczema, but larger trials are needed.

Evolution of vertebrate viviparity and specializations for fetal nutrition: A quantitative and qualitative analysis

Phylogenetic analyses indicate that viviparity (live-bearing reproduction) has originated independently in more than 150 vertebrate lineages, including a minimum of 115 clades of extant squamate reptiles. Other evolutionary origins of viviparity include 13 origins among bony fishes, nine among chondrichthyans, eight in amphibians, one in Paleozoic placoderms, six among extinct reptiles, and one in mammals. The origins of viviparity range geologically from the mid-Paleozoic through the Mesozoic to the Pleistocene. Substantial matrotrophy (maternal provision of nutrients to embryos during pregnancy) has arisen at least 33 times in these viviparous clades, with most (26) of these origins having occurred among fishes and amphibians. Convergent evolution in patterns of matrotrophy is widespread, as reflected by multiple independent origins of placentotrophy, histotrophy, oophagy, and embryophagy. Specializations for nutrient transfer to embryos are discontinuously distributed, reflecting the roles of phylogenetic inertia, exaptation (preadaptation), and constraint. Ancestral features that function in gas exchange and nutrition repeatedly and convergently have been co-opted for nutrient transfer, often through minor modification of their components and changes in the timing of their expression (heterochrony). Studies on functional and evolutionary morphology continue to play a central role in our attempts to understand viviparity and mechanisms of fetal nutrition.