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Related Experiment Videos

Normal and abnormal fetal growth.

S M Bryan1, P C Hindmarsh

  • 1London Centre of Paediatric Endocrinology and Metabolism, Institute of Child Health, University College London, UK.

Hormone Research
|April 14, 2006
PubMed
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Poor intrauterine growth may increase cardiovascular disease risk. However, studies show growth patterns are unpredictable and sex-specific, not distinct phenotypes, challenging the fetal origins hypothesis.

Area of Science:

  • Obstetrics and Gynecology
  • Developmental Biology
  • Cardiovascular Disease Research

Background:

  • The fetal origins of adult disease hypothesis links poor intrauterine growth to adult cardiovascular disease.
  • Specific growth phenotypes, like disproportionate growth, are thought to influence disease type.

Purpose of the Study:

  • To analyze antenatal growth patterns in a low-risk population.
  • To determine if distinct growth phenotypes, as predicted by the fetal origins hypothesis, are present.
  • To investigate the role of growth predictability and sexual dimorphism in fetal development.

Main Methods:

  • Analysis of antenatal growth data from a low-risk pregnancy cohort.
  • Examination of growth predictability and centile crossing.

Related Experiment Videos

  • Assessment of sexually dimorphic growth patterns.

    • Main Results:

    • Distinct growth phenotypes were not identified in the general low-risk population.
    • Intrauterine growth showed poor predictability of subsequent size, with centile crossing being common.
    • A sexually dimorphic pattern in fetal growth was observed.

    Conclusions:

    • The fetal origins of adult disease hypothesis, in its current form implicating specific phenotypes, may not be supported by growth patterns in low-risk populations.
    • Centile crossing and sexual dimorphism are key features of intrauterine growth that require further investigation.
    • Future research should consider these complex growth dynamics when testing the fetal origins hypothesis.