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Published on: December 7, 2013
Early growth and later atherosclerosis
1Childhood Nutrition Research Centre, University College London, Institute of Child Health, London, UK. a.singhal@ich.ucl.ac.uk
Insights
Accelerated infant growth is linked to long-term health risks, including cardiovascular disease. Early life interventions are crucial for primary prevention of cardiovascular disease (CVD).
Area of Science:
- Developmental biology
- Cardiovascular health
- Public health
Background:
- Long-term biological effects of early growth are well-established in animal models.
- Emerging human studies demonstrate a significant influence of early growth on later health outcomes.
Purpose of the Study:
- To review evidence linking infant growth patterns to cardiovascular disease (CVD) risk factors.
- To explore the biological mechanisms and public health implications of early growth on later health.
Main Methods:
- Review of existing scientific literature and experimental data.
- Analysis of prospective randomized controlled trials on infant growth and cardiovascular risk.
Main Results:
- Accelerated infant growth is associated with increased risk of obesity, glucose intolerance, hypertension, and dyslipidemia.
- These factors collectively predispose individuals to atherosclerotic cardiovascular disease (CVD).
- Evidence strongly supports a causal link between infant growth and later cardiovascular risk.
Conclusions:
- Primary prevention of CVD should commence in early infancy.
- Understanding early growth's impact is vital for public health strategies targeting cardiovascular disease.
Abstract:
The concept that early growth has long-term biological effects is based on extensive studies in animals dating from the 1930s. More recently, compelling evidence for a long-term influence of early growth on later health has also emerged in humans. Substantial data now support the hypothesis that 'accelerated', or too fast infant growth, increases the propensity to obesity, glucose intolerance, raised blood pressure, dyslipidaemia and endothelial dysfunction, the clustering of risk factors which predispose to the development of atherosclerotic cardiovascular disease (CVD). The association between infant growth and these risk factors is strong, consistent, shows a dose-response effect, and is biologically plausible. Moreover, experimental data from prospective randomized controlled trials strongly support a causal link between infant growth and later cardiovascular risk. These observations suggest, therefore, that the primary prevention of CVD should begin from as early as the first few months of life. The present review considers this evidence, the underlying mechanisms involved, and its implications for public health.
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