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Long-term consequences of intrauterine growth retardation
1Metabolic Programming Group,Medical Research Council (University of Southampton), Southampton General Hospital, Southampton, UK.
Insights
Babies born with low birth weight may face higher risks of adult diseases like high blood pressure and diabetes. This suggests fetal growth impacts long-term health, a concept known as the fetal origins hypothesis.
Area of Science:
- Developmental Biology
- Epidemiology
- Endocrinology
Background:
- Low birth weight and abnormal fetal growth are linked to adult diseases.
- The 'fetal origins' hypothesis suggests intrauterine conditions program long-term health.
- Mechanisms underlying this programming are not fully understood.
Purpose of the Study:
- To explore the link between fetal growth and adult disease prevalence.
- To investigate the 'fetal origins' hypothesis.
- To examine potential mechanisms involving neuroendocrine development.
Main Methods:
- Review of recent studies from Europe, North America, and developing nations.
- Analysis of epidemiological data on birth weight and adult health outcomes.
- Consideration of animal studies and preliminary human evidence on neuroendocrine changes.
Main Results:
- Consistent associations found between adverse fetal growth and increased prevalence of hypertension, non-insulin-dependent diabetes, and cardiovascular disease in adulthood.
- Evidence suggests impaired fetal nutrient supply may alter offspring neuroendocrine development.
- Potential for permanent changes in hormonal activity set points (adrenocortical and sympathoadrenal).
Conclusions:
- Adverse fetal growth may program persistent physiological and metabolic changes predisposing to adult chronic diseases.
- Neuroendocrine development alterations due to fetal nutrient supply are a plausible mechanism.
- Further research is needed to elucidate the precise pathways involved in fetal programming.
Abstract:
Recent studies in Europe, North America and the developing world have shown that low birth weight or other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of raised blood pressure, non-insulin-dependent diabetes and cardiovascular disease in late adult life. These findings have led to the 'fetal origins' hypothesis which proposes that fetal adaptations to an adverse intrauterine environment programme persistent physiological and metabolic changes which predispose to these diseases. The mechanisms are unknown, but evidence from animal studies and preliminary evidence in humans suggest that impaired fetal nutrient supply permanently alters neuroendocrine development in the offspring resulting in long-term changes in the set point of adrenocortical and sympathoadrenal hormonal activity.