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Updated: Aug 9, 2026
Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Size at birth, postnatal growth and risk of obesity
1MRC Epidemiology Unit, Strangeways Research Laboratory, Cambridge, UK. ken.ong@mrc-epid.cam.ac.uk
Insights
Birth size and early growth impact adult cardiovascular disease and type 2 diabetes risk. Understanding these early life factors is key to preventing childhood obesity and related health issues.
Area of Science:
- Pediatric Health
- Metabolic Disease Research
- Epidemiology
Background:
- Epidemiological studies link birth size, postnatal growth, and childhood weight gain to adult cardiovascular disease and type 2 diabetes.
- Rising childhood obesity rates necessitate identifying early risk factors for targeted interventions.
- Higher birth weight correlates with greater lean mass, while lower birth weight is associated with increased fat mass and insulin resistance.
Purpose of the Study:
- To investigate the complex relationship between birth weight, early growth patterns, and subsequent obesity risk.
- To explore the critical early periods for weight gain that influence long-term fat deposition and insulin resistance.
- To identify genetic factors influencing fetal growth and postnatal energy metabolism for early obesity risk prediction.
Main Methods:
- Analysis of epidemiological data correlating birth size and growth with adult health outcomes.
- Examination of body composition (lean vs. fat mass) in relation to birth weight and postnatal growth.
- Review of existing literature on critical windows for early life influences on obesity and metabolic health.
Main Results:
- Higher birth weight is linked to greater lean mass, not necessarily increased fat mass.
- Lower birth weight is associated with a higher fat-to-lean mass ratio, central adiposity, and insulin resistance.
- Rapid postnatal catch-up growth in infants with in utero growth restriction contributes to central fat deposition.
Conclusions:
- Early life factors, including birth size and rapid postnatal growth, significantly influence long-term metabolic health and obesity risk.
- Understanding the paradoxical effects of birth weight on body composition is crucial for effective early intervention strategies.
- Identifying genetic predispositions for fetal nutrition, growth, and energy partitioning can enhance early detection and prevention of childhood obesity.
Abstract:
Epidemiological studies over the last 15 years have shown that size at birth, early postnatal catch-up growth and excess childhood weight gain are associated with an increased risk of adult cardiovascular disease and type 2 diabetes. At the same time, rising rates of obesity and overweight in children, even at pre-school ages, have shifted efforts towards the identification of very early factors that predict risk of subsequent obesity, which may allow early targeted interventions. Overall, higher birth weight is positively associated with subsequent greater body mass index in childhood and later life; however, the relationship is complex. Higher birth weight is associated with greater subsequent lean mass, rather than fat mass. In contrast, lower birth weight is associated with a subsequent higher ratio of fat mass to lean mass, and greater central fat and insulin resistance. This paradoxical effect of lower birth weight is at least partly explained by the observation that infants who have been growth restrained in utero tend to gain weight more rapidly, or 'catch up', during the early postnatal period, which leads to increased central fat deposition. There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infancy, childhood or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early identification of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth.
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