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Developmental antecedents of cardiovascular disease: a historical perspective
David J P Barker1, Susan P Bagby
1Developmental Origins of Health and Disease Division, University of Southampton, Southampton General Hospital, Southampton, United Kingdom. david.barker@mrc.soton.ac.uk
Insights
Low birth weight increases the risk of cardiovascular disease and type 2 diabetes. Fetal development, particularly altered kidney development, may explain this increased risk later in life.
Area of Science:
- Developmental biology
- Epidemiology
- Cardiovascular science
Background:
- The link between low birth weight and later cardiovascular disease (CVD) risk has been established for two decades.
- Recent research indicates that individuals with low birth weight, or those who were thin or short at birth, face elevated risks for both CVD and type 2 diabetes.
Observation:
- Epidemiological studies across different countries consistently demonstrate this association, ruling out confounding variables.
- Clinical and animal studies are beginning to elucidate the biological mechanisms driving these observed associations.
Findings:
- Altered fetal development, specifically reduced nephron numbers in the kidneys, is identified as a key biological process.
- This diminished nephron endowment may be an initiating factor for hypertension.
Implications:
- Understanding fetal origins of disease is crucial for developing preventative strategies.
- Postnatal growth and environmental factors significantly modify the long-term health consequences of early-life conditions.
Abstract:
Knowledge of the fetal antecedents of cardiovascular disease has increased rapidly since the association between low birth weight and the disease was demonstrated 20 yr ago. It now is known that individuals who had low birth weight or who were thin or short at birth are at increased risk for both cardiovascular disease and type 2 diabetes. This has been shown in studies in different countries and cannot be explained by confounding variables. Through clinical and animal studies, the biologic processes that underlie the epidemiologic associations and how their effects are modified by postnatal growth and by living conditions in childhood and adult life are beginning to be understood. One such process is altered renal development, with reduced nephron numbers, which may initiate hypertension.
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