Until recently, undernourished children were usually assessed using simple anthropometric measurements, which provide global assessments of nutritional status. There is increasing interest in ...obtaining more direct data on body composition to assess the effects of undernutrition on fat-free mass (FFM) and its constituents, such as muscle and organs, and on fat mass (FM) and its regional distribution.
Recent studies show that severe-acute undernutrition, categorised as 'wasting', is associated with major deficits in both FFM and FM that may persist in the long-term. Fat distribution appears more central, but this is more associated with the loss of peripheral fat than with the elevation of central fat. Chronic undernutrition, categorised as 'stunting', is associated with deficits in FFM and in specific components, such as organ size. However, the magnitude of these deficits is reduced, or - in some cases - disappears, after adjustment for height. This suggests that FFM is largely reduced in proportion to linear growth. Stunted children vary in their FM - in some cases remaining thin throughout childhood, but in other cases developing higher levels of FM. The causes of this heterogeneity remain unclear. Several different pathways may underlie longitudinal associations between early stunting and later body composition. Importantly, recent studies suggest that short children are not at risk of excess fat deposition in the short term when given nutritional supplementation.
The short- and long-term functional significance of FFM and FM for survival, physical capacity and non-communicable disease risk means that both tissues merit further attention in research on child undernutrition.
The capacity-load model is a conceptual model developed to improve understanding of the life-course aetiology of non-communicable diseases (NCDs) and their ecological and societal risk factors. The ...model addresses continuous associations of both (a) nutrition and growth patterns in early life and (b) lifestyle factors at older ages with NCD risk. Metabolic capacity refers to physiological traits strongly contingent on early nutrition and growth during the first 1000 days, which promote the long-term capacity for homeostasis in the context of fuel metabolism and cardiovascular health. Metabolic load refers to components of nutritional status and lifestyle that challenge homeostasis. The higher the load, and the lower the capacity, the greater the NCD risk. The model therefore helps understand dose-response associations of both early development and later phenotype with NCD risk. Infancy represents a critical developmental period, during which slow growth can constrain metabolic capacity, whereas rapid weight gain may elevate metabolic load. Severe acute malnutrition in early childhood (stunting, wasting) may continue to deplete metabolic capacity, and confer elevated susceptibility to NCDs in the long term. The model can be applied to associations of NCD risk with socio-economic position (SEP): lower SEP is generally associated with lower capacity but often also with elevated load. The model can also help explain ethnic differences in NCD risk, as both early growth patterns and later body composition differ systematically between ethnic groups. Recent work has begun to clarify the role of organ development in metabolic capacity, which may further contribute to ethnic differences in NCD risk.
Increases in the prevalence of noncommunicable diseases (NCDs), particularly cardiometabolic diseases such as cardiovascular disease, stroke and diabetes, and their major risk factors have not been ...uniform across settings: for example, cardiovascular disease mortality has declined over recent decades in high-income countries but increased in low- and middle-income countries (LMICs). The factors contributing to this rise are varied and are influenced by environmental, social, political and commercial determinants of health, among other factors. This Review focuses on understanding the rise of cardiometabolic diseases in LMICs, with particular emphasis on obesity and its drivers, together with broader environmental and macro determinants of health, as well as LMIC-based responses to counteract cardiometabolic diseases.
Malnutrition has historically been researched and addressed within two distinct silos, focusing either on undernutrition, food insecurity, and micronutrient deficiencies, or on overweight, obesity, ...and dietary excess. However, through rapid global nutrition transition, an increasing proportion of individuals are exposed to different forms of malnutrition during the life course and have the double burden of malnutrition (DBM) directly. Long-lasting effects of malnutrition in early life can be attributed to interconnected biological pathways, involving imbalance of the gut microbiome, inflammation, metabolic dysregulation, and impaired insulin signalling. Life-course exposure to early undernutrition followed by later overweight increases the risk of non-communicable disease, by imposing a high metabolic load on a depleted capacity for homoeostasis, and in women increases the risk of childbirth complications. These life-course trajectories are shaped both by societal driving factors—ie, rapidly changing diets, norms of eating, and physical activity patterns—and by broader ecological factors such as pathogen burden and extrinsic mortality risk. Mitigation of the DBM will require major societal shifts regarding nutrition and public health, to implement comprehensive change that is sustained over decades, and scaled up into the entire global food system.
Worldwide variation in human stature and limb proportions is widely accepted to reflect thermal adaptation, but the contribution of population history to this variation is unknown. Furthermore, ...stature and relative lower limb length (LLL) show substantial plastic responses to environmental stressors, e.g., nutrition, pathogen load, which covary with climate. Thus ecogeographic patterns may go beyond temperature-based selection. We analysed global variation in stature, sitting height and absolute and relative LLL using large worldwide samples of published anthropometric data from adult male (n = 571) and female (n = 268) populations in relation to temperature, humidity, and net primary productivity (NPP). Population history was modeled using spatial eigenvector mapping based on geographic distances reflecting the hypothesized pattern for the spread of modern humans out of Africa. Regression models account for ~ 50% of variation in most morphological variables. Population history explains slightly more variation in stature, sitting height and LLL than the environmental/climatic variables. After adjusting for population history, associations between (usually maximum) temperature and LLL are consistent with Allen's "rule" and may drive similar relationships with stature. NPP is a consistent negative predictor of anthropometry, which may reflect the growth-limiting effects of lower environmental resource accessibility (inversely related to NPP) and/or pathogen load.
Hominin evolution saw the emergence of two traits—bipedality and encephalization—that are fundamentally linked because the fetal head must pass through the maternal pelvis at birth, a scenario termed ...the ‘obstetric dilemma’. While adaptive explanations for bipedality and large brains address adult phenotype, it is brain and pelvic growth that are subject to the obstetric dilemma. Many contemporary populations experience substantial maternal and perinatal morbidity/mortality from obstructed labour, yet there is increasing recognition that the obstetric dilemma is not fixed and is affected by ecological change. Ecological trends may affect growth of the pelvis and offspring brain to different extents, while the two traits also differ by a generation in the timing of their exposure. Two key questions arise: how can the fit between the maternal pelvis and the offspring brain be ‘renegotiated’ as the environment changes, and what nutritional signals regulate this process? I argue that the potential for maternal size to change across generations precludes birthweight being under strong genetic influence. Instead, fetal growth tracks maternal phenotype, which buffers short-term ecological perturbations. Nevertheless, rapid changes in nutritional supply between generations can generate antagonistic influences on maternal and offspring traits, increasing the risk of obstructed labour.
The emerging discipline of evolutionary medicine is breaking new ground in understanding why people become ill. However, the value of evolutionary analyses of human physiology and behaviour is only ...beginning to be recognised in the field of public health. Core principles come from life history theory, which analyses the allocation of finite amounts of energy between four competing functions—maintenance, growth, reproduction, and defence. A central tenet of evolutionary theory is that organisms are selected to allocate energy and time to maximise reproductive success, rather than health or longevity. Ecological interactions that influence mortality risk, nutrient availability, and pathogen burden shape energy allocation strategies throughout the life course, thereby affecting diverse health outcomes. Public health interventions could improve their own effectiveness by incorporating an evolutionary perspective. In particular, evolutionary approaches offer new opportunities to address the complex challenges of global health, in which populations are differentially exposed to the metabolic consequences of poverty, high fertility, infectious diseases, and rapid changes in nutrition and lifestyle. The effect of specific interventions is predicted to depend on broader factors shaping life expectancy. Among the important tools in this approach are mathematical models, which can explore probable benefits and limitations of interventions in silico, before their implementation in human populations.
Human diseases in adulthood are increasingly associated with growth patterns in early life, implicating early‐life nutrition as the underlying mechanism. The thrifty phenotype hypothesis proposed ...that early‐life metabolic adaptations promote survival, with the developing organism responding to cues of environmental quality by selecting an appropriate trajectory of growth. Recently, some authors have proposed that the thrifty phenotype is also adaptive in the longer‐term, by preparing the organism for its likely adult environment. However, windows of plasticity close early during human development, and subsequent environmental changes may result in the selected trajectory becoming inappropriate, leading to adverse effects on health. This paradox generates uncertainty as to whether the thrifty phenotype is indeed adaptive for the offspring in humans. The thrifty phenotype should not be considered a dichotomous concept, rather it refers to the capacity of all offspring to respond to environmental information during early ontogenetic development. This article argues that the thrifty phenotype is the consequence of three different adaptive processes ‐ niche construction, maternal effects, and developmental plasticity ‐ all of which in humans are influenced by our large brains. While developmental plasticity represents an adaptation by the offspring, both niche construction and parental effects are subject to selection on parental rather than offspring fitness. The three processes also operate at different paces. Human offspring do not become net calories‐producers until around 18 years of age, such that the high energy costs of the human brain are paid primarily by the mother, even after weaning. The evolutionary expansion of human brain volume occurred in environments characterised by high volatility, inducing strong selective pressure on maternal capacity to provision multiple offspring simultaneously. The thrifty phenotype is therefore best considered as a manipulation of offspring phenotype for the benefit of maternal fitness. The information that enters offspring phenotype during early development does not predict the likely future environment of the offspring, but rather reflects the mother’s own developmental experience and the quality of the environment during her own maturation. Offspring growth trajectory thus becomes aligned with long‐term maternal capacity to provision. In contemporary populations, the sensitivity of offspring development to maternal phenotype exposes the offspring to adverse effects, through four distinct pathways. The offspring may be exposed to (1) poor maternal metabolic control (e.g. gestational diabetes), (2) maternally derived toxins (e.g. maternal smoking), or (3) low maternal social status (e.g. small size). Adverse consequences of these effects may then be exacerbated by (4) exposure either to the “toxic” western environment in postnatal life, in which diet and physical activity levels are mismatched with metabolic experience in utero, or at the other extreme to famine. The rapid emergence of the epidemic of the metabolic syndrome in the 20th Century reflects the rapid acceleration in the pace of niche construction relative to the slower physiological combination of developmental plasticity and parental effects.
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