Talk:Abnormal Development - Fetal Origins Hypothesis

• Barker DJ. The fetal and infant origins of adult disease. BMJ. 1990 Nov 17;301(6761):1111.
• Barker DJ, Martyn CN. The maternal and fetal origins of cardiovascular disease. J Epidemiol Community Health. 1992 Feb;46(1):8-11.
• Barker DJ. Fetal nutrition and cardiovascular disease in later life. Br Med Bull. 1997 Jan;53(1):96-108.
• Wilson J. The Barker hypothesis. An analysis. Aust N Z J Obstet Gynaecol. 1999 Feb;39(1):1-7.

• Lucas A, Fewtrell MS, Cole TJ. Fetal origins of adult disease-the hypothesis revisited. BMJ. 1999 Jul 24;319(7204):245-9.
  • Link to full article
  • The hypothesis that adult disease has fetal origins is plausible, but much supportive evidence is flawed by incomplete and incorrect statistical interpretation.
  • When size in early life is related to later health outcomes only after adjustment for current size, it is probably the change in size between these points (postnatal centile crossing) rather than fetal biology that is implicated.
  • Even when birth size is directly related to later outcome, some studies fail to explore whether this is partly or wholly explained by postnatal rather that prenatal factors.
  • These considerations are critical to understanding the biology and timing of "programming," the direction of future research, and future public health interventions.
• Mongelli M, Gardosi J. Fetal growth. Curr Opin Obstet Gynecol. 2000 Apr;12(2):111-5.
  • Recent epidemiological and experimental studies show that abnormal fetal growth can lead to serious complications, including stillbirth, perinatal morbidity and disorders extending well beyond the neonatal period. It is now clear that the intrauterine milieu is as important as genetic endowment in shaping the future health of the conceptus. Maternal characteristics such as weight, height, parity and ethnic group need to be adjusted for, and pathological factors such as smoking excluded, to establish appropriate standards and improve the distinction between what is normal and abnormal. Currently, the aetiology of growth restriction is not well understood and preventative measures are ineffective. Elective delivery remains the principal management option, which emphasizes the need for better screening techniques for the timely detection of intrauterine growth failure.
• Holemans K, Aerts L, Van Assche FA. Fetal growth and long-term consequences in animal models of growth retardation. Eur J Obstet Gynecol Reprod Biol. 1998 Dec;81(2):149-56.
  • Perturbations of the maternal environment involve an abnormal intrauterine milieu for the developing fetus. The altered fuel supply (depends on substrate availability, placental transport of nutrients and uteroplacental blood flow) from mother to fetus induces alterations in the development of the fetal endocrine pancreas and adaptations of the fetal metabolism to the altered intrauterine environment, resulting in intrauterine growth retardation. The alterations induced by maternal diabetes or maternal malnutrition (protein-calorie or protein deprivation) have consequences for the offspring, persisting into adulthood and into the next generation.