1,721,434 research outputs found
The role of the placenta in fetal programming-a review
No full textThe fetal origins hypothesis proposes that adult cardiovascular and metabolic disease originate through developmental plasticity and fetal adaptations arising from failure of the materno-placental supply of nutrients to match fetal requirements. The hypothesis is supported by experimental data in animals indicating that maternal nutrition can programme long term effects on the offspring without necessarily affecting size at birth. There is now evidence linking body composition in pregnant women and the balance of nutrient intake during pregnancy with raised levels of cardiovascular risk factors in the offspring. Maternal body composition and diet are thought to affect fetal development and programming as a result of both direct effects on substrate availability to the fetus and indirectly through changes in placental function and structure. Alterations in placental growth and vascular resistance, altered nutrient and hormone metabolism in the placenta, and changes in nutrient transfer and partitioning between mother, placenta and fetus all have important effects on the fetal adaptations thought to be central to programming. Future interventions to improve placental function are likely to have lifelong health benefits for the offspring
The role of the placenta in the developmental origins of health and disease: implications for practice
No full textThe placenta is actively involved in transporting nutrients to the fetus, it has both direct and indirect effects on fetal cardiovascular function and has endocrine influences on the mother and fetus. As such, a properly functioning placenta is crucial for normal fetal development and plays a central role in mediating effects of the maternal environment on the fetus. An altered external environment or abnormal placental function can induce developmental changes in the fetus and may have important consequences for the risk of cardiovascular and metabolic disease in adult life.The developmental origins hypothesis proposes that the early environment, from the periconceptional period until early childhood, can predispose an individual to adult cardiovascular and metabolic disease. This hypothesis is supported by epidemiological studies and by work in animals. These effects do not just act in low birth weight babies but have been shown to occur within the normal range of birth weight. It is thought that fetal adaptations to an impaired intra-uterine environment may enhance survival in early life but have deleterious effects in later life.Experimental studies suggest that maternal diet and body composition can alter placental structure and function, and we have recently demonstrated associations between a woman's nutritional state before pregnancy and placental function at term. To elucidate these relationships, further work is needed to define markers of placental function and to characterize their relation to rates of fetal growth.Understanding how the placenta mediates maternal influences will be crucial in determining the mechanisms underlying developmental programming. This will allow the design of targeted public health interventions, both before and during pregnancy, to enhance placental function and thereby improve the health of the offspring throughout life
Developmental origins of metabolic disease: life course and intergenerational perspectives
No full textRecent evidence demonstrates important maternal effects on an offspring's risk of developing metabolic disease. These effects extend across the full range of maternal environments and partly involve epigenetic mechanisms. The maternal effects can be explained in evolutionary terms, and there is some evidence for their transmission into succeeding generations. Unbalanced maternal diet or body composition, ranging from poor to rich environments, adversely influences the offspring's response to later challenges such as an obesogenic diet or physical inactivity, increasing the risk of disease. Adopting a life course approach that takes into account intergenerational effects has important implications for prevention of non-communicable diseases, particularly in populations undergoing rapid economic transitio
Umbilical cord plasma lysophospholipids and triacylglycerols associated with birthweight percentiles
No full textDysregulated transplacental lipid transfer and fetal-placental lipid metabolism affect birthweight, as does maternal hyperglycemia. As the mechanisms are unclear, we aimed to identify the lipids in umbilical cord plasma that were most associated with birthweight. Seventy-five Chinese women with singleton pregnancies recruited into the GUSTO mother-offspring cohort were selected from across the glycemic range based on a mid-gestation 75 g oral glucose tolerance test, excluding pre-existing diabetes. Cord plasma samples collected at term delivery were analyzed using targeted liquid-chromatography tandem mass-spectrometry to determine the concentrations of 404 lipid species across 17 lipid classes. The birthweights were standardized for sex and gestational age by local references, and regression analyses were adjusted for the maternal age, BMI, parity, mode of delivery, insulin treatment, and fasting/2 h glucose, with a false discovery-corrected
p < 0.05 considered significant. Ten lysophosphatidylcholines (LPCs) and two lysophosphatidylethanolamines were positively associated with the birthweight percentiles, while twenty-four triacylglycerols were negatively associated with the birthweight percentiles. The topmost associated lipid was LPC 20:2 [21.28 (95%CI 12.70, 29.87) percentile increase in the standardized birthweight with each SD-unit increase in log
10-transformed concentration]. Within these same regression models, maternal glycemia did not significantly associate with the birthweight percentiles. Specific fetal circulating lysophospholipids and triacylglycerols associate with birthweight independently of maternal glycemia, but a causal relationship remains to be established.
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The long-term effects of prenatal development on growth and metabolism
No full textPeople who were small at birth and had poor infant growth have an increased risk of adult cardiovascular disease, osteoporosis, and type 2 diabetes, particularly if their restricted early growth was followed by increased childhood weight gain. These relations extend across the normal range of birth size in a graded manner, so reduced size is not a prerequisite. In addition, larger birth size is associated with risks of obesity and type 2 diabetes. The associations appear to reflect developmental plastic responses made by the fetus and infant based on cues about the environment, influenced by maternal characteristics including diet, body composition, stress, and exercise levels. These responses involve epigenetic processes that modify the offspring's phenotype. Vulnerability to ill health results if the environment in infancy, childhood, and later life is mismatched to the phenotype induced in development, informed by the developmental cues. This mismatch may arise through unbalanced diet or body composition of the mother or a change in lifestyle factors between generations. These insights offer new possibilities for the early diagnosis and prevention of chronic disease.<br/
Effortful control mediates associations of fetal growth with hyperactivity and behavioural problems in 7- to 9-year-old children
No full textBackground: Inverse associations of fetal growth with behavioural problems in childhood have been repeatedly reported, suggesting long-term effects of the prenatal developmental environment on behaviour later in life. However, no study so far has examined effects on temperament and potential developmental pathways. Temperamental traits may be particularly susceptible to neurodevelopmental alterations, and they are linked to behavioural problems. Therefore, we tested for associations of fetal growth with behavioural problems in children and tested if temperament mediated such effects. Methods: 139 mother-child pairs were recruited in early pregnancy. Weight, head circumference and gestational age were measured at birth, and the mother reported on their child’s behavioural problems and temperament at age 7 to 9 years. Results: Birth weight and head circumference at birth adjusted for gestational age (i.e. fetal growth) were inversely associated with hyperactivity and total behavioural problems, and positively associated with the temperamental trait Effortful Control. Path analyses showed that Effortful Control mediated the effects of fetal growth on hyperactivity and total behavioural problems. Conclusions: Our results suggest that an adverse fetal environment is associated with behavioural problems in childhood, in particular in those children that show a low capacity for attentional and behavioural regulation. An adverse fetal environment might induce vulnerability for behavioural problems, or it might induce changes in temperament and behavioural problems independently, representing a common cause. Pathways are likely to be based on long lasting neurodevelopmental alterations due to prenatal adversity
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