• Malnutrition has long been researched and addressed in two distinct silos, focusing either on chronic 2 or acute undernutrition, energy inadequacy and micronutrient deficiencies, or on overweight, obesity 3 and dietary excess. The contemporary reality of the double burden of malnutrition is different, making it 4 impossible to separate these issues, but also indicating shared opportunities to address them. 5 • Malnutrition harms health throughout the life-course, but its emergence early in life has particularly 6 pernicious consequences. A variety of physiological mechanisms propagate effects of early-life 7 malnutrition across the life-course, while adolescent and adult malnutrition can transmit effects to the 8 next generation. 9 • Different forms of malnutrition can interact through the life-course and across generations. In some 10 settings, early stunting may predispose to a more central distribution of adiposity at later ages, while 11 the extent to which maternal obesity adversely affects early growth and development of the offspring 12 may be exacerbated if the mother herself was under-nourished in early life. 13 • Life-course exposure to the double burden of malnutrition (early undernutrition followed by later 14 overweight) increases the risk of non-communicable disease, by imposing a high metabolic load on a 15 depleted capacity for homeostasis. The health costs of adult obesity are therefore exacerbated among 16 those who previously experienced undernutrition. In women, life-course exposure to the double burden 17 of malnutrition increases the risk of childbirth complications. 18 • Exclusive and appropriate breast-feeding protects infants against all forms of malnutrition, and 19 protects mothers against diabetes and breast cancer, in part through healthy-weight benefits. However, 20 maternal obesity, diabetes and micronutrient deficiencies alter the biology of lactation, and should be 21 addressed to maximise the success of breast-feeding. 22 • Exposure to the double burden of malnutrition can only be fully understood in the context of broader 23 societal drivers acting across culture, behaviour and technology. Various groups are at high risk of the 24 double burden through elevated exposure to these drivers, often exacerbated by biological 25 susceptibility. 26 • Developmental responses to malnutrition in early life are shaped by ecological factors, such as 27 pathogen burden and extrinsic mortality risk. An evolutionary perspective, focusing on how our 28 biological plasticity was shaped in ancestral environments to promote survival and reproduction, may 29 help design interventions that promote linear growth and lean tissue accretion rather than excess 30 adiposity. 31 • Inter-generational cycles of malnutrition have proven difficult to disrupt through public health 32 interventions. Major societal shifts are required regarding nutrition and public health, in order to 33 implement comprehensive change that is sustained over decades, and scaled up into the entire global 34 food system.

Children can be stunted and wasted at the same time. Having both deficits greatly elevates risk of mortality. The analysis aimed to estimate the prevalence and burden of children aged 6–59 months concurrently wasted and stunted. Data from demographic and health survey and Multi‐indicator Cluster Surveys datasets from 84 countries were analysed. Overall prevalence for being wasted, stunted, and concurrently wasted and stunted among children 6 to 59 months was calculated. A pooled prevalence of concurrence was estimated and reported by gender, age, United Nations regions, and contextual categories. Burden was calculated using population figures from the global joint estimates database. The pooled prevalence of concurrence in the 84 countries was 3.0%, 95% CI [2.97, 3.06], ranging from 0% to 8.0%. Nine countries reported a concurrence prevalence greater than 5%. The estimated burden was 5,963,940 children. Prevalence of concurrence was highest in the 12‐ to 24‐month age group 4.2%, 95% CI [4.1, 4.3], and was significantly higher among boys 3.54%, 95% CI [3.47, 3.61], compared to girls; 2.46%, 95% CI [2.41, 2.52]. Fragile and conflict‐affected states reported significantly higher concurrence 3.6%, 95% CI [3.5, 3.6], than those defined as stable 2.24%, 95% CI [2.18, 2.30]. This analysis represents the first multiple country estimation of the prevalence and burden of children concurrently wasted and stunted. Given the high risk of mortality associated with concurrence, the findings indicate a need to report on this condition as well as investigate whether these children are being reached through existing programmes.

Background The etiologic relationship between wasting and stunting is poorly understood, largely because of a lack of high-quality longitudinal data from children at risk of undernutrition. Objectives The aim of this study was to describe the interrelationships between wasting and stunting in children aged <2 y. Methods This study involved a retrospective cohort analysis, based on growth-monitoring records spanning 4 decades from clinics in rural Gambia. Anthropometric data collected at scheduled infant welfare clinics were converted to z scores, comprising 64,342 observations on 5160 subjects (median: 12 observations per individual). Children were defined as “wasted” if they had a weight-for-length z score <–2 against the WHO reference and “stunted” if they had a length-for-age z score <–2. Results Levels of wasting and stunting were high in this population, peaking at approximately (girls–boys) 12–18% at 10–12 months (wasted) and 37–39% at 24 mo of age (stunted). Infants born at the start of the annual wet season (July–October) showed early growth faltering in weight-for-length z score, putting them at increased risk of subsequent stunting. Using time-lagged observations, being wasted was predictive of stunting (OR: 3.2; 95% CI: 2.7, 3.9), even after accounting for current stunting. Boys were more likely to be wasted, stunted, and concurrently wasted and stunted than girls, as well as being more susceptible to seasonally driven growth deficits. Conclusions We provide evidence that stunting is in part a biological response to previous episodes of being wasted. This finding suggests that stunting may represent a deleterious form of adaptation to more overt undernutrition (wasting). This is important from a policy perspective as it suggests we are failing to recognize the importance of wasting simply because it tends to be more acute and treatable. These data suggest that stunted children are not just short children but are children who earlier were more seriously malnourished and who are survivors of a composite process.

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Objectives To construct growth curves for mid-upper-arm circumference (MUAC)-for-age z score for 5-19 year olds that accord with the World Health Organization growth standards, and to evaluate their discriminatory performance for subsequent mortality. Design Growth curve construction and longitudinal cohort study. Setting United States and international growth data, and cohorts in Kenya, Uganda, and Zimbabwe. Participants The Health Examination Survey (HES)/National Health and Nutrition Examination Survey (NHANES) US population datasets (age 5-25 years), which were used to construct the 2007 WHO growth reference for body mass index in this age group, were merged with an imputed dataset matching the distribution of the WHO 2006 growth standards age 2-6 years. Validation data were from 685 HIV infected children aged 5-17 years participating in the Antiretroviral Research for Watoto (ARROW) trial in Uganda and Zimbabwe; and 1741 children aged 5-13 years discharged from a rural Kenyan hospital (3.8% HIV infected). Both cohorts were followed-up for survival during one year. Main outcome measures Concordance with WHO 2006 growth standards at age 60 months and survival during one year according to MUAC-for-age and body mass index-for-age z scores. Results The new growth curves transitioned smoothly with WHO growth standards at age 5 years. MUAC-for-age z scores of −2 to −3 and less than−3, compared with −2 or more, was associated with hazard ratios for death within one year of 3.63 (95% confidence interval 0.90 to 14.7; P=0.07) and 11.1 (3.40 to 36.0; P<0.001), respectively, among ARROW trial participants; and 2.22 (1.01 to 4.9; P=0.04) and 5.15 (2.49 to 10.7; P<0.001), respectively, among Kenyan children after discharge from hospital. The AUCs for MUAC-for-age and body mass index-for-age z scores for discriminating subsequent mortality were 0.81 (95% confidence interval 0.70 to 0.92) and 0.75 (0.63 to 0.86) in the ARROW trial (absolute difference 0.06, 95% confidence interval −0.032 to 0.16; P=0.2) and 0.73 (0.65 to 0.80) and 0.58 (0.49 to 0.67), respectively, in Kenya (absolute difference in AUC 0.15, 0.07 to 0.23; P=0.0002). Conclusions The MUAC-for-age z score is at least as effective as the body mass index-for-age z score for assessing mortality risks associated with undernutrition among African school aged children and adolescents. MUAC can provide simplified screening and diagnosis within nutrition and HIV programmes, and in research.