Abstract

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.

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