Childhood Adversity and Self-Reported Rheumatoid Arthritis: A Structural Equation Modeling Analysis of the Canadian Longitudinal Study on Aging
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Keri J West1, Lin Fang2, Eleanor Pullenayegum3
1K.J.W. West, PhD, Assistant Professor, School of Social Work, California State University, San Bernardino, CA, USA.
Objective:
The purpose of this study was to examine the association between adverse childhood experiences (ACEs) and self-reported rheumatoid arthritis (RA), and to investigate potential psychosocial and behavioural mediators of this relationship.
Methods:
Exploratory and confirmatory factor analyses (EFA; CFA) were conducted to assess the dimensionality of ACEs. Hypothesized direct and indirect pathways from a latent ACEs construct to RA were tested using structural equation modeling (SEM) with data (N = 44,142) from the Canadian Longitudinal Study on Aging. Putative mediation through depression, anxiety, obesity, and smoking was examined. Analyses adjusted for sociodemographic factors, asthma, and childhood passive smoking. Moderation by birth sex was tested with multigroup SEM.
Results:
EFA and CFA supported a higher-order latent childhood adversity factor with three first-order factors (physical abuse, sexual abuse, household dysfunction). SEM showed a small but significant direct ACEs-RA association, as well as significant associations operating through depression, obesity, and smoking. Birth sex appeared to moderate the indirect pathway through obesity, with a stronger association for men. An indirect association through smoking was observed only in men, though the between-group difference was not statistically significant.
Conclusion:
ACEs were significantly associated with self-reported RA, partially through indirect pathways involving depression, obesity, and smoking, with evidence of sex-specific effects on the obesity pathway. Targeted screening and intervention for ACEs-affected individuals with psychosocial and behavioural risk factors may help reduce RA burden. Prospective mediation research examining gene-environment interactions (e.g., smoking × RA risk alleles) and sex-specific mechanisms is warranted.
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