The early origins of atherosclerosis.

Atherosclerosis has a long pre-clinical phase with development of pathological changes in arteries of children and young adults decades before overt clinical manifestations of disease. Nutritional factors in both infancy and childhood have been shown to be important in this process and affect lifetime cardiovascular disease risk. Breast-feeding in particular is associated with benefits for long-term cardiovascular risk factors possibly as a consequence of a slower pattern of growth in breast-fed compared to formula-fed infants. In fact, the benefits of slower growth for later health and longevity, appears to be a fundamental biological phenomenon conserved across diverse animal species. The nutritional programming of atherosclerosis could therefore be regarded as a specific example of programming of human ageing as seen previously in programming of lifespan and telomere length in animals. The critical window for these effects is unknown, but evidence is accumulating for programming effects of growth from very early in infancy.

Understanding and acting on the developmental origins of health and disease in Africa would improve health across generations.

Data from many high- and low- or middle-income countries have linked exposures during key developmental periods (in particular pregnancy and infancy) to later health and disease. Africa faces substantial challenges with persisting infectious disease and now burgeoning non-communicable disease.This paper opens the debate to the value of strengthening the developmental origins of health and disease (DOHaD) research focus in Africa to tackle critical public health challenges across the life-course. We argue that the application of DOHaD science in Africa to advance life-course prevention programmes can aid the achievement of the Sustainable Development Goals, and assist in improving health across generations. To increase DOHaD research and its application in Africa, we need to mobilise multisectoral partners, utilise existing data and expertise on the continent, and foster a new generation of young African scientists engrossed in DOHaD.

Refeeding Low Weight Hospitalized Adolescents With Anorexia Nervosa: A Multicenter Randomized Controlled Trial.

BACKGROUND: Refeeding patients with anorexia nervosa (AN) is associated with high morbidity and mortality. A lack of evidence from interventional studies has hindered refeeding practice and led to worldwide disparities in management recommendations. In the first randomized controlled trial in this area, we tested the hypothesis that refeeding adolescents with AN with a higher energy intake than what many guidelines recommend improved anthropometric outcomes without adversely affecting cardiac and biochemical markers associated with refeeding. MATERIALS AND METHODS: Participants aged 10-16 years with a body mass index (BMI) <78% of the median (mBMI) for age and sex were recruited from 6 UK hospitals and randomly allocated to start refeeding at 1200 kcal/d (n = 18, intervention) or 500 kcal/d (n = 18, control). RESULTS: Compared with controls, adolescents randomized to high energy intake had greater weight gain (mean difference between groups after 10 days of refeeding, -1.2% mBMI; 95% confidence interval, -2.4% to 0.0%; P = .05), but randomized groups did not differ statistically in QTc interval and other outcomes. The nadir in postrefeeding phosphate concentration was significantly related to percentage mBMI at the start of refeeding (baseline; P = .04) and baseline white blood cell count (P = .005) but not to baseline energy intake (P = .08). CONCLUSIONS: Refeeding adolescents with AN with a higher energy intake was associated with greater weight gain but without an increase in complications associated with refeeding when compared with a more cautious refeeding protocol-thus challenging current refeeding recommendations.

Prevention of obesity in preschool children.

Obesity is a serious problem that affects children from diverse ethnic backgrounds in both industrialised and developing countries. Worldwide, an estimated twenty-two million children <5 years of age were overweight in 2007. In the UK if current trends continue an estimated one-quarter of all children <16 years of age will be obese by 2050. Recent evidence suggests that most obesity is established during the preschool years, and because one in five obese 4 year olds will become obese adults this situation has major implications for public health. The causes of obesity in preschool children are complex and multifactorial. Although 30-50% of the predisposition towards obesity in preschool children can be explained by genetic factors, environmental influences also play a crucial role. The preschool period in particular is a pivotal time during which long-term dietary and physical activity habits are established, with potential lifelong effects on health. However, research in this age-group is limited. Previous studies have aimed to improve diet, increase physical activity and achieve behavioural change. However, few of these studies have been successful and there is an urgent need, therefore, for the development of evidence-based interventions aimed at the prevention of preschool obesity.

Nutrition in infancy and long-term risk of obesity: evidence from 2 randomized controlled trials.

BACKGROUND: Growth acceleration as a consequence of relative overnutrition in infancy has been suggested to increase the risk of later obesity. However, few studies have investigated this association by using an experimental study design. OBJECTIVE: We investigated the effect of early growth promotion on later body composition in 2 studies of infants born small for gestational age (weight <10th percentile in study 1 and <20th percentile in study 2). DESIGN: We reviewed a subset of children (n = 153 of 299 in study 1 and 90 of 246 in study 2) randomly assigned at birth to receive either a control formula or a nutrient-enriched formula (which contained 28-43% more protein and 6-12% more energy than the control formula) at 5-8 y of age. Fat mass was measured by using bioelectric impedance analysis in study 1 and deuterium dilution in study 2. RESULTS: Fat mass was lower in children assigned to receive the control formula than in children assigned to receive the nutrient-enriched formula in both trials [mean (95% CI) difference for fat mass after adjustment for sex: study 1: -38% (-67%, -10%), P = 0.009; study 2: -18% (-36%, -0.3%), P = 0.04]. In nonrandomized analyses, faster weight gain in infancy was associated with greater fat mass in childhood. CONCLUSIONS: In 2 prospective randomized trials, we showed that a nutrient-enriched diet in infancy increased fat mass later in childhood. These experimental data support a causal link between faster early weight gain and a later risk of obesity, have important implications for the management of infants born small for gestational age, and suggest that the primary prevention of obesity could begin in infancy.