title: Normal and abnormal fetal growth.
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.
authors.affiliation: London Centre of Paediatric Endocrinology and Metabolism, Institute of Child Health, University College London, UK.
authors.forename: S M
authors.initials: SM
authors.lastname: Bryan
authors.forename: P C
authors.initials: PC
authors.lastname: Hindmarsh
mesh_terms: D000328:Adult; D001699:Biometry; D001724:Birth Weight / Q000502:physiology*; D005260:Female; D047109:Fetal Development / Q000235:genetics / Q000502:physiology*; D005317:Fetal Growth Retardation / Q000175:diagnosis*; D006801:Humans; D007328:Insulin / Q000502:physiology; D008297:Male; D008423:Maternal Age; D039382:Maternal Nutritional Physiological Phenomena; D010298:Parity / Q000502:physiology; D010920:Placenta / Q000502:physiology; D011247:Pregnancy; D012727:Sex Characteristics; D012907:Smoking / Q000009:adverse effects; D013002:Somatomedins / Q000502:physiology
chemical_list: D007328:Insulin; D013002:Somatomedins