1,721,240 research outputs found
Maternal nutrition: effects in health in the next generation
No full textNearly 20 years ago, it was discovered that low birthweight was associated with an increased risk of adult
diabetes and cardiovascular disease (CVD). This led to the hypothesis that exposure to undernutrition
in early life increases an individual’s vulnerability to these disorders, by ‘programming’ permanent
metabolic changes. Implicit in the programming hypothesis is that improving the nutrition of girls and
women could prevent common chronic diseases in future generations. Research in India has shown that
low birthweight children have increased CVD risk factors, and a unique birth cohort in Delhi has shown
that low infant weight, and rapid childhood weight gain, increase the risk of type 2 diabetes. Progress
has been made in understanding the role of specific nutrients in the maternal diet. In the Pune Maternal
Nutrition Study, low maternal vitamin B12 status predicted increased adiposity and insulin resistance
in the children, especially if the mother was folate replete. It is not only maternal undernutrition that
causes problems; gestational diabetes, a form of foetal overnutrition (glucose excess), is associated with
increased adiposity and insulin resistance in the children, highlighting the adverse effects of the ‘double
burden’ of malnutrition in developing countries, where undernutrition and overnutrition co-exist.
Recent intervention studies in several developing countries have shown that CVD risk factors in the
offspring can be improved by supplementing undernourished mothers during pregnancy. Results differ
according to the population, the intervention and the post-natal environment. Ongoing studies in India
and elsewhere seek to understand the long-term effects of nutrition in early life, and how best to translate
this knowledge into policies to improve health in future generation
Birthweight, weight in infancy and risk of coronary heart disease in adult life
No full textFrom 1911 the birthweight, weight at one year, and type of feeding in infancy were recorded routinely for all babies born in Hertfordshire. These records have been used to trace men and women born in the county during 1911-1930. An initial study showed that men who were lighter at birth and one year had higher death rates from coronary heart disease (CHD). This thesis describes further work in Hertfordshire.Men who were exclusively bottle-fed from birth or breast-fed but not weaned at one year had higher death rates from CHD than men who were breast-fed and weaned within a year. Women of lower birthweight had higher mortality from cardiovascular disease and CHD, though the trend for CHD was not statistically significant. There were no associations in women between mortality and weight at one year or feeding in infancy.In both sexes, lower birthweight was associated with a more adverse risk factor profile, including shorter adult height, and higher waist/hip ratio, systolic blood pressure, and 120-minute glucose concentrations. In women, lower birthweight was also associated with increased insulin resistance and lower serum HDL-cholesterol and apolipoprotein A1 concentrations. In men, there were similar relationships with weight at one year, and lower weight at one was also associated with increased insulin resistance and higher concentrations of apolipoprotein B, fibrinogen and factor VII. In women, low weight at one year was not associated with increased risk factors. Men who were bottle-fed from birth, or breast-fed but not weaned at one year, had higher serum LDL-cholesterol and apolipoprotein B concentrations than men who were breast-fed and weaned at one. These associations with birthweight, weight at one year and infant feeding were independent of adult body size, social class and smoking.</p
The fetal and early life origins of adult disease
No full textThe fetal origins of adult disease (FOAD) hypothesis is based on the observation that men and women who were small at birth (low birthweight) have an increased risk of atherosclerotic cardiovascular disease (CVD) and the related diseases hypertension, type 2 diabetes and the Insulin Resistance Syndrome. Risk is increased further if they showed rapid weight gain in childhood or become obese. The hypothesis proposes that CVD is ‘programmed’ by under nutrition during critical periods of early development and that ‘poverty’ during early life creates a permanent vulnerability to ‘diseases of affluence’. This concept is arguably of greatest relevance to developing countries, where fetal growth restriction still affects large numbers of people, where economic progress is leading to the emergence of childhood and adult obesity, and where CVD and type 2 diabetes are rising rapidly. Its implication is that the prevention of adult disease should include strategies to improve maternal health and fetal growth. This paper reviews work leading to the FOAD hypothesis and the results of FOAD research in India. It also discusses some of the controversies surrounding the hypothesis, notably the debate as to whether the link between fetal growth restriction and adult CVD is mediated by environmental factors (such as maternal nutrition) or by genes
Fetal programming and the risk of noncommunicable disease
No full textThe "developmental origins of health and disease" (DOHaD) hypothesis proposes that environmental conditions during fetal and early post-natal development influence lifelong health and capacity through permanent effects on growth, structure and metabolism. This has been called 'programming'. The hypothesis is supported by epidemiological evidence in humans linking newborn size, and infant growth and nutrition, to adult health outcomes, and by experiments in animals showing that maternal under- and over-nutrition and other interventions (e.g., glucocorticoid exposure) during pregnancy lead to abnormal metabolism and body composition in the adult offspring. Early life programming is now thought to be important in the etiology of obesity, type 2 diabetes, and cardiovascular disease, opening up the possibility that these common diseases could be prevented by achieving optimal fetal and infant development. This is likely to have additional benefits for infant survival and human capital (e.g., improved cognitive performance and physical work capacity). Fetal nutrition is influenced by the mother's diet and body size and composition, but hard evidence that the nutrition of the human mother programmes chronic disease risk in her offspring is currently limited. Recent findings from follow-up of children born after randomised nutritional interventions in pregnancy are mixed, but show some evidence of beneficial effects on vascular function, lipid concentrations, glucose tolerance and insulin resistance. Work in experimental animals suggests that epigenetic phenomena, whereby gene expression is modified by DNA methylation, and which are sensitive to the nutritional environment in early life, may be one mechanism underlying programming
Metabolic programming in early life in humans
No full textAn association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently ‘programmes’ organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomized trials of maternal nutritional interventions during pregnancy have so far had limited follow-up of the offspring. Moreover, interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high-risk individuals in mid-life, DOHaD concepts offer a ‘primordial’ preventive strategy to reduce disease in future generations by improving fetal and infant development
Non-industrialised countries and affluence: relationship with Type 2 diabetes
No full textThe prevalence of type 2 diabetes is rising rapidly in all non-industrialised populations. By 2025, three-quarters of the world's 300 million adults with diabetes will be in non-industrialised countries, and almost a third in India and China alone. There is strong evidence that this epidemic has been triggered by social and economic development and urbanisation, which are associated with general improvements in nutrition and longevity, but also with obesity, reduced physical exercise and other diabetogenic factors. There is evidence too that fetal growth retardation and growth failure in infancy, both still widespread in non-industrialised populations, increase susceptibility to diabetes. An additional factor may be intergenerational effects of gestational diabetes occurring in mothers who grew poorly in early life and become obese as adults. Prevention of type 2 diabetes will require measures to promote exercise and reduce obesity in adults and children, alongside programmes to achieve healthy fetal and infant growth
Maternal vitamin D deficiency and GDM risk: evidence for the case of investing more attention in antenatal clinics
No full textGestational diabetes mellitus (GDM) is a global public health problem, and in India, it affects about 20% of pregnancies. India, despite being a tropical country with abundant sunshine has a high prevalence (80%) of vitamin D deficiency (VDD) among reproductive-aged women. Global and Indian evidence links VDD with a higher risk of hyperglycaemia in pregnancy and GDM. VDD has also been implicated in gestational hypertension, preterm birth and poorer offspring health. Global scientific consensus acknowledges the need for maternal vitamin D screening and supplementation, but knowledge gaps exist about optimal blood levels (50-100 nmol/l), and the required vitamin D dosage (400-4000 IU). Diet can provide <10% of the vitamin D requirements, food fortification can deliver limited amounts, and hence optimal antenatal supplementation is key. Prenatal calcium supplements containing 400 IU of vitamin D may be sufficient for calcium absorption and bone health, but may not provide immunomodulatory benefits, including GDM prevention. Increasing evidence calls for higher maternal vitamin D requirements (2000-4000 IU) for skeletal, metabolic and immune health benefits. Current screening and supplementation for maternal VDD in India is low. We need to invest in future studies to determine optimal maternal vitamin D requirements and formulate policies for vitamin D supplementation to prevent GDM. Improving the maternal vitamin D status is an important nutritional priority for policymakers to reduce the large economic burden of non-communicable diseases (10% of India's gross domestic product), and eventually achieve the 2030 UN sustainable development goals.</p
Infant nutrition and later health: a review of current evidence
No full textThere is a growing recognition of the need for a lifecourse approach to understanding the aetiology of adult disease, and there is now significant evidence that links patterns of infant feeding to differences in health outcomes, both in the short and longer term. Breastfeeding is associated with lower rates of infection in infancy; in high-income populations, it is associated with reductions in blood pressure and total blood cholesterol, and lower risks of obesity and diabetes in adult life. Breastfeeding rates are suboptimal in many countries, and strategies to promote breastfeeding could therefore confer important benefits for health at a population level. However, there are particular challenges in defining nutritional exposures in infancy, including marked social gradients in initiation and duration of breastfeeding. In recent studies of low and middle-income populations of children and young adults, where the influences on infant feeding practice differ, beneficial effects of breastfeeding on blood pressure, BMI and risk of diabetes have not been confirmed, and further information is needed. Little is currently known about the long-term consequences of differences in the timing and nature of the weaning diet. Future progress will depend on new studies that provide detailed prospective data on duration and exclusivity of breastfeeding together with appropriate characterisation of the weaning diet
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