Size at Birth, Postnatal Growth and Risk of 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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Fetal undernutrition or small birth size interacts with childhood weight gain as predictors of diabetes risk.
“Studies report interactions between fetal undernutrition or small birth size and childhood weight gain as predictors of diabetes risk”
From Metabolic costs and evolutionary implications of human brain development (2014) · cites this paper as [62]
Childhood energetics and substrate availability play an important role in diabetes development.
“suggesting an important role for childhood energetics and substrate availability in diabetes development (62,63).”
From Metabolic costs and evolutionary implications of human brain development (2014) · cites this paper as [62]
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- Authors
- Ong, K. K.
- Affiliations
- MRC Epidemiology Unit (GB)
- Corresponding author
- Ong, K.K.
- ORCID
- Ong, K.K.
- Venue
- Hormone Research in Paediatrics
- Publisher
- S. Karger AG
- Published
- 2006
- Volume
- 65
- Issue
- Suppl. 3
- Pages
- 65-69
- ISSN
- 1663-2818 (ISSN-L)
- 1663-2826
- OpenAlex
- W1963539752
- Cited by
- 274
- References
- 1
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 8 · 2020: 8 · 2019: 11 · 2018: 11 · 2017: 5 · 2016: 8 · 2015: 20 · 2014: 23 · 2013: 15 · 2012: 31
- FWCI
- 17.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hormone Research in Paediatrics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- birth weight, postnatal growth, childhood obesity, catch-up growth, child weight gain, insulin resistance, fetal growth restriction, type 2 diabetes risk, cardiovascular risk, energy allocation
- MeSH terms
- Birth Weight, Child Development, Female, Humans, Infant Nutritional Physiological Phenomena, Infant, Newborn, Obesity, Pregnancy, Risk Factors, Weight Gain, Body Size
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