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Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Normal and abnormal fetal growth
1London Centre of Paediatric Endocrinology and Metabolism, Institute of Child Health, University College London, UK.
Insights
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.
- 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.
Abstract:
The fetal origins of adult disease hypothesis suggests that poor intrauterine growth is associated with an increased risk of cardiovascular disease. The hypothesis goes on to implicate different growth 'phenotypes', particularly disproportionate growth, in the determination of the type of cardiovascular disease that develops. Analysis of the antenatal growth of a low-risk pregnancy population does not identify such growth phenotypes within the general population. Rather, intrauterine growth is characterized by poor predictability of subsequent size, suggesting that centile crossing is a common feature of intrauterine growth. Furthermore, there is a sexually dimorphic pattern to this growth that needs to be considered in further work to test the fetal origins hypothesis.
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