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Background: Whilst prevention of growth faltering has both short- and long-term health benefits, whether too fast or accelerated infant growth adversely affects later health outcomes is controversial and a major focus of research. Summary: Many observational studies suggest that rapid weight gain in infancy (upward centile crossing) increases the long-term risk of obesity and non-communicable disease. This association has been seen in infants from low- and high-income countries, in infants born preterm or at term, and those born with normal or low birth weight for gestation. Experimental (randomized) studies in both breast- and formula-fed infants support a causal link between early growth acceleration and infant nutrition and later risk of obesity. These observations suggest that strategies to optimize the pattern of infant growth could make a major contribution to stemming the current global epidemic of non-communicable disease. Key Messages: The optimal pattern of infant weight gain is likely to differ in different populations. The benefits of rapid infant weight gain for later neurodevelopment favors the promotion of rapid growth in infants born preterm. However, growth acceleration in healthy infants born at term (either normal or low birth weight for gestation) is likely to have adverse effects for long-term health.

Catch-up growth in the first few months of life is seen almost ubiquitously in infants born small for their gestational age and conventionally considered highly desirable as it erases the growth deficit. However, recently such growth has been linked to an increased risk of later adiposity, insulin resistance and cardiovascular disease in both low income and high-income countries. In India, a third of all babies are born with a low birth weight, but the optimal growth pattern for such infants is uncertain. As a response to the high rates of infectious morbidities, undernutrition and stunting in children, the current policy is to promote rapid growth in infancy. However, with socio-economic transition and urbanization making the Indian environment more obesogenic, and the increasing prevalence of type 2 diabetes and cardiovascular disease, affecting progressively younger population, the long term adverse programming effect of fast/excessive weight gain in infancy on later body composition and metabolism may outweigh short-term benefits. This review discusses the above issues focusing on the need to strike a healthy balance between the risks and benefits of catch-up growth in Indian infants.

Evidence that early nutrition can influence (program) later cardiovascular health was first obtained for the long-term effects of overfeeding in animals. This concept is now supported in humans by evidence for a beneficial effect of breast-feeding on the major components of the metabolic syndrome (obesity, blood pressure, cholesterol metabolism, and insulin resistance) that affect cardiovascular risk. The size of this effect is large and relevant for public health. The potential mechanisms involved include a benefit of slower weight gain in breast-fed compared with formula-fed babies.Evidence that early nutrition can influence (program) later cardiovascular health was first obtained for the long-term effects of overfeeding in animals. This concept is now supported in humans by evidence for a beneficial effect of breast-feeding on the major components of the metabolic syndrome (obesity, blood pressure, cholesterol metabolism, and insulin resistance) that affect cardiovascular risk. The size of this effect is large and relevant for public health. The potential mechanisms involved include a benefit of slower weight gain in breast-fed compared with formula-fed babies.

Objectives: An increase in food portion size offered to children over recent decades has been suggested to contribute to the rise in childhood obesity. This review investigated the effect of interventions that manipulated portion size on energy intake and risk of obesity in school-aged children. Methods: A systematic search was performed using MEDLINE, Embase, and Cochrane Library databases (from inception to 2025). Included studies were original articles in English, involving children aged 5–17 years, that focused on portion size interventions using an experimental or controlled study design, with energy intake, body weight, or body mass index (BMI) as the study outcome. The risk of bias was evaluated using the Quality Criteria Checklist (QCC). Results: From 514 articles identified, 10 met the inclusion criteria, including a total of 1765 participants. Larger portion sizes increased food intake (grams) and/or energy intake (kcal) in eight studies but did not affect energy intake in one study. Another study focusing on fruit and vegetable portions found inconsistent results. The meta-analysis found that larger portion sizes were associated with higher energy intake compared to the reference portion (mean difference = 86.0 kcal/meal, 95% CI [62.2, 109.9], p < 0.00001). Conclusions: Offering children larger portions increases energy intake. However, this finding was limited by being based mainly on studies which manipulated portion size at a single meal, in a laboratory setting, and with only short-term measures of energy intake. Future studies need to investigate the long-term effects of portion size interventions on energy intake and risk of childhood obesity.

Background To evaluate the efficacy and safety of upadacitinib monotherapy versus methotrexate (MTX) monotherapy over 5 years among MTX-naïve patients with moderately to severely active rheumatoid arthritis (RA) in the long-term extension (LTE) of the phase 3 SELECT-EARLY trial. Methods Patients were randomized to receive upadacitinib 15 mg or 30 mg or MTX. Patients who did not achieve CDAI remission and had < 20% improvement in tender and swollen joint counts at week 26 received rescue therapy (addition of MTX in the upadacitinib group and addition of upadacitinib in the MTX group). Efficacy assessments were evaluated over 5 years and are reported as observed (AO) for patients who received continuous monotherapy with upadacitinib 15/30 mg or MTX and by randomized group applying non-responder imputation (NRI). Treatment-emergent adverse events (TEAEs) per 100 patient-years were summarized over 5 years. Results Of 945 patients randomized and treated, 775 (82%) completed week 48 and entered the LTE on study drug. Higher proportions of patients consistently achieved disease activity targets over 5 years with upadacitinib than MTX. In AO analyses, 53%/59% of patients attained CDAI remission with upadacitinib 15/30 mg versus 43% with MTX at week 260. NRI analyses showed better CDAI, DAS28(CRP), and ACR responses with upadacitinib relative to MTX at week 260 (all comparisons, nominal P  < .001). Upadacitinib treatment also resulted in numerically greater inhibition of structural joint progression through week 260 compared to MTX. Most TEAEs, serious AEs, and AEs leading to discontinuation were numerically higher in patients receiving upadacitinib 30 mg. Rates of serious infections, herpes zoster, creatine phosphokinase elevation, nonmelanoma skin cancer, and neutropenia were numerically higher with upadacitinib than MTX. The observed safety profile of upadacitinib over 5 years was consistent with earlier trial results and integrated phase 3 safety analyses. Conclusions Upadacitinib showed better clinical responses versus MTX in patients with RA throughout the 5-year trial. Higher rates of several AEs were observed with upadacitinib, especially in the 30 mg group, compared to MTX. When used as monotherapy in MTX-naïve patients, the approved upadacitinib 15 mg dose showed better long-term efficacy versus MTX and an overall favorable benefit-risk profile. Trial registration NCT02706873.

Atherosclerotic CVD is the most common cause of death in the West. Yet, its pathogenesis and early development are only partially understood. Central to the early atherosclerotic process is impairment of vascular endothelial function. Endothelial dysfunction can be measured non-invasively and is evident in children before clinical manifestations of atherosclerosis in adulthood. Factors in early life, such as conventional cardiovascular risk factors, or programming by perinatal growth and nutrition strongly affect endothelial function and hence the development of atherosclerosis and CVD. For instance, low birth weight and faster growth early in infancy have a detrimental effect on vascular structure and function. Childhood obesity, a key independent risk factor for CVD, also adversely affects early vascular health. Obesity is associated with endothelial dysfunction and greater arterial stiffness from as early as the first decade of life, while weight loss is beneficial. This effect on vascular function is probably mediated in part by low-grade inflammation and insulin resistance associated with obesity or by the production by adipose tissue of cytokine-like molecules, collectively termed adipokines. A high leptin concentration, in particular, is found in obese individuals and is strongly associated with vascular changes related to early atherosclerosis. The present review focuses on the early origins of endothelial dysfunction, emphasising the role of obesity. It also considers the mechanisms by which obesity impairs endothelial function, understanding of which will be important to further scientific knowledge and to improve public health.

Non-communicable diseases (NCD) and atherosclerotic CVD in particular, are the most important health problems of the 21st century. Already in every world region except Africa, NCD account for greater mortality than communicable, maternal, perinatal and nutritional conditions combined. Although modifiable lifestyle factors in adults are the main determinants, substantial evidence now suggests that factors in early life also have a major role in the development of NCD; commonly referred to as the Developmental Origins of Health and Disease hypothesis. Factors in utero, early postnatal life and throughout childhood, have been shown to affect NCD by influencing risk factors for CVD such as obesity, diabetes, hypertension and dyslipidaemia. Infant nutrition (e.g. breastfeeding rather than bottle feeding) and a slower pattern of infant weight gain have been shown to be particularly protective against later risk of obesity and CVD in both low- and high-income countries. The mechanisms involved are poorly understood, but include epigenetic changes; effects on endocrine systems regulating body weight, food intake and fat deposition; and changes in appetite regulation. As a consequence, strategies to optimise early life nutrition could make a major contribution to stemming the current global epidemic of NCD. This review will consider the role of early life factors in the development of NCD, focusing on the impact of infant nutrition/growth on obesity and CVD. The review will highlight the experimental (randomised) evidence where available, briefly summarise the underlying mechanisms involved and consider the implications for public health.

Background & objectives: The tribal population in India is considered as one of the vulnerable groups with respect to their achievements in health and other developmental issues. In this context, this mapping review attempted to understand the health profile of the Tharu tribal community residing in the northern State of Uttar Pradesh, India through literature mining. Tharu tribe is one of the indigenous groups living in the Terai plain on the Indo-Nepal border. In 1967, this tribe was documented as a Scheduled Tribe by the Government of India. The present review aimed to map the health-seeking behaviour of the Tharu population and review other factors pertaining to their health such as socioeconomic, developmental, employment, education, etc. Methods: Online data search was carried out on PubMed and Google Scholar using search terms 'Tharu' AND 'India'. In addition, official reports avaibale in public domain and grey literature was also searched. Results: Twenty seven studies including reviews, articles, books/book chapters were evaluated along with 13 reports (including reports from government organizations and grey literature) were retrieved and analyzed. Of the 27 published reports, 16 were found relevant to Tharu tribe in India. A total of 29 (16 articles + 13 reports) were included in this review. Interpretation & Conclusions: This mapping review highights the health seeking behaviour of the Tharu tribe in India that can help inform future interventions to improve the health status of the Tharu tribe as well as other aspects of their development.

In animals, acceleration of neonatal growth is thought to increase the later propensity to insulin resistance and non-insulin-dependent diabetes, whereas slow growth as a consequence of undernutrition is thought to have a beneficial effect. To test this hypothesis in people, we measured fasting concentrations of 32–33 split proinsulin, a marker of insulin resistance, in adolescents born preterm who had participated in randomised intervention trials of neonatal nutrition, and in adolescents born at term. We determined fasting 32–33 split proinsulin concentration in participants aged 13–16 years born preterm and randomised to receive a nutrient-enriched or lower-nutrient diet (n=216) or in a reference group born at term (n=61). Fasting 32–33 split proinsulin concentration was greater in children given a nutrient-enriched diet (geometric mean 7·2 pmol/L, 95% CI 6·4–8·1) than in those given the lower-nutrient diet (5·9 pmol/L [5·2–6·4]; mean difference 20·6% [5·0–36·3]; p=0·01). Healthy babies born at term had similar fasting 32–33 split proinsulin concentrations (6·9 pmol/L; 6·0–8·2) to the nutrient-enriched group. In non-randomised analyses, fasting 32–33 split proinsulin concentration was associated with greater weight gain in the first 2 weeks of life (13·2% [5·4–20·9] change per 100 g weight increase; p=0·001) independent of birthweight, gestation, neonatal morbidity, and demographic, anthropometric, and socioeconomic factors. Our results suggest that relative undernutrition early in life in children born preterm may have beneficial effects on insulin resistance.

BackgroundVitamin B12 deficiency is common in populations with limited animal-source foods and has been linked to delayed infant neurodevelopment and adverse pregnancy outcomes. Evidence on the benefits of maternal B12 supplementation for improving infant neurodevelopment remains mixed, particularly in low-income and middle-income countries where deficiency is prevalent.MethodsThis double-blind, randomised controlled trial was conducted in two tertiary maternity care centres in India and Nepal. Pregnant women in their first trimester, following a vegetarian diet, were enrolled and randomised to receive either a daily oral supplement of 250 µg (group A) or 50 µg (group B) of methyl-cobalamin from enrolment to 6 months post partum. The primary outcomes were infant neurodevelopment assessed at 9–12 months using the Development Assessment Scale of Indian Infants and biochemical B12 status in mothers and infants measured through blood tests.Results531 mothers completed the study (group A n=255; group B n=276). There were no significant differences in baseline characteristics between mothers at both centres or in groups A and B. Mental developmental quotients (DQs) were higher in the infants of group A: 103.7 (7.7) than group B: 101.7 (8.8); p=0.008). This corresponds to a mean difference of 7.8 centiles (p=0.007). Mean motor DQs were not significantly different between the groups. Maternal vitamin B12 levels rose from the first to third trimester in both groups, with a larger increase in group A (104.9 pg/mL (SD 159.1)) than group B (47.5 pg/mL (SD 118.0)), p<0.001. Holotranscobalamin levels improved similarly (p<0.001). All infant levels of vitamin B12 were within the normal range. Newborn anthropometry, APGAR scores and morbidity profiles were similar in both groups (p>0.05). Serum ferritin, vitamin D and folate were similar (p>0.05).ConclusionsDaily supplementation with 250 µg of vitamin B12 during pregnancy in vegetarian mothers significantly improved infant mental DQ and maternal B12 status compared with a 50 µg dose.