Leslie deRosset1, Kelly L Strutz2. 1. Department of Maternal and Child Health, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill. Electronic address: derosset@email.unc.edu. 2. Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing.
Abstract
PURPOSE: The developmental origins of adult disease hypothesis suggests that the intrauterine environment may program postnatal health outcomes through mechanisms such as chronic inflammation. The purpose of this article was to review the literature on the association between infant birth weight and C-reactive protein (CRP), markers of the fetal environment and inflammation, respectively. METHODS: We used PubMed, Google Scholar, Web of Science, ScienceDirect, the citation lists of the reviewed literature, and recommendations from experts in the field to identify potential articles. Inclusion criteria for the studies, regardless of study design, included human subjects, documented or self-reported infant birth weight, and a minimum of one measurement of CRP (during childhood, adolescence, or adulthood). RESULTS: Several studies demonstrated a statistically significant inverse association between birth weight and CRP in adulthood, although in many cases only after controlling for markers of current adiposity. No studies significantly linked birth weight to CRP in childhood or adolescence. CONCLUSIONS: Longitudinal studies, including multigenerational studies, are needed to further understand whether adult CRP has origins in the fetal environment.
PURPOSE: The developmental origins of adult disease hypothesis suggests that the intrauterine environment may program postnatal health outcomes through mechanisms such as chronic inflammation. The purpose of this article was to review the literature on the association between infant birth weight and C-reactive protein (CRP), markers of the fetal environment and inflammation, respectively. METHODS: We used PubMed, Google Scholar, Web of Science, ScienceDirect, the citation lists of the reviewed literature, and recommendations from experts in the field to identify potential articles. Inclusion criteria for the studies, regardless of study design, included human subjects, documented or self-reported infant birth weight, and a minimum of one measurement of CRP (during childhood, adolescence, or adulthood). RESULTS: Several studies demonstrated a statistically significant inverse association between birth weight and CRP in adulthood, although in many cases only after controlling for markers of current adiposity. No studies significantly linked birth weight to CRP in childhood or adolescence. CONCLUSIONS: Longitudinal studies, including multigenerational studies, are needed to further understand whether adult CRP has origins in the fetal environment.
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