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Developmental programming of health and disease

Simon C Langley-Evans1

  • 1School of Bioscience, University of Nottingham, Loughborough, UK. Simone.Langley-Evans@Nottingham.ac.uk

The Proceedings of the Nutrition Society
|January 31, 2006
PubMed

Insights

Early life nutrition significantly impacts adult health, influencing conditions like obesity and hypertension. Nutrient imbalances during fetal development can lead to lasting physiological changes and disease risk.

Area of Science:

  • Developmental biology
  • Nutritional science
  • Epidemiology

Background:

  • Fetal and neonatal environments profoundly affect adult physiological function and disease risk.
  • Epidemiological data links impaired fetal growth with rapid infant catch-up to adult obesity, hypertension, non-insulin-dependent diabetes, and coronary heart disease (CHD).
  • While nutritional factors in pregnancy are suspected, direct human evidence is limited.

Discussion:

  • Animal studies confirm a direct link between fetal nutrient imbalance and later-life diseases (hypertension, diabetes, obesity, renal disease), independent of growth rates.
  • Experimental rodent studies reveal mechanisms connecting fetal nutrition to permanent physiological changes.
  • Early life exposure to glucocorticoids, a consequence of nutrient imbalance, may alter gene expression affecting tissue development and function.

Key Insights:

  • Nutrient imbalances during critical developmental windows can program long-term health outcomes.
  • Epigenetic mechanisms, such as DNA methylation, are implicated in early-life programming of disease risk.
  • Animal models provide crucial insights into the molecular pathways linking fetal nutrition to adult disease.

Outlook:

  • Further research is needed to elucidate specific molecular mechanisms in humans.
  • Understanding these early-life influences can inform preventative strategies for chronic diseases.
  • Interventions targeting maternal nutrition may mitigate long-term health risks.

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