Long-term consequences of intrauterine growth retardation

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Updated: Oct 1, 2026

Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
14:19

Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction

Published on: June 29, 2013

R M Reynolds1, D I Phillips

  • 1Metabolic Programming Group,Medical Research Council (University of Southampton), Southampton General Hospital, Southampton, UK.

Hormone Research
|September 8, 1998
PubMed

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.

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