ArticleBrain, behavior, and immunity2025
A Phenome-Wide association study (PheWAS) of genetic risk for C-reactive protein in children of European Ancestry: Results from the ABCD study.
Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- A decade of discovery: Leveraging genomic data in the ABCD study to illuminate adolescent neurodevelopment.Developmental cognitive neuroscience · 2026Review
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Abstract
backgroundC-reactive protein (CRP) is a moderately heritable marker of systemic inflammation that is associated with adverse physical and mental health outcomes. Identifying factors associated with genetic liability to elevated CRP in childhood may inform our understanding of variability in CRP that could be targeted to prevent and/or delay the onset of related health outcomes.
methodsWe conducted a phenome-wide association study (PheWAS) of genetic risk for elevated CRP (i.e. CRP polygenic risk score [PRS]) among children genetically similar to European ancestry reference populations (median analytic n = 5,509, range = 120-5,556) from the Adolescent Brain and Cognitive Development
resultsNine phenotypes were positively associated with CRP PRS after multiple testing correction: five weight- and eating-related phenotypes (e.g. BMI, overeating), three phenotypes related to caregiver somatic problems (e.g. caregiver somatic complaints), as well as weekday video watching (all ps = 1.2 x 10 DISCUSSION: Genetic liability to elevated CRP is associated with higher weight, eating, and weekday video watching during childhood as well as caregiver somatic problems. These associations were consistent with direct genetic effects (i.e., not solely due to confounding factors like passive gene-environment correlations) and were independent of measured BMI. The majority of associations with weight and eating phenotypes were attributable to shared genetic architecture between BMI and inflammation. The relationship between genetics and heightened inflammation in later life may be partially attributable to modifiable behaviors (e.g. weight and activity levels) that are expressed as early as childhood.
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