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OP30 How do adversities predict onset of rheumatoid arthritis? Evidence from the English Longitudinal Study of Ageing
  1. CC Hammond
  1. Institute of Social and Economic Research, University of Essex, Colchester, UK

Abstract

Background Socioeconomic inequalities in prevalence of rheumatoid arthritis (RA) indicate that adverse exposures such as financial hardship, family difficulties, and traumatic events contribute to its onset. We investigate: (1) Whether adversities predict RA onset (2) How adversities at different life stages combine to predict RA onset (3) Whether adversities associated primarily with material and psychosocial pathways independently predict RA onset, after adjustment for health behaviours.

Methods The English Longitudinal Study of Ageing is representative of adults aged 50+ living in private households. Data collected bi-annually between 2002 and 2012 were used to measure age of RA onset. Retrospective life-history information was used to measure a wide range of adversities and smoking history. Indices of adversity were created for each life stage, to measure adversity accumulated over life stages, and for different types of adversity.

Multiple imputation with chained equations was used to impute missing values. Cox regression analyses were estimated of RA with onsets from 45 and 60 on adversity, adjusting for birth cohort and gender. Stata14 was used.

RA onset was regressed on total life course adversity, number of life stages (childhood, youth, early adulthood) during which adversity was reported, adversity during each life stage with mutual adjustment, and material and psychosocial adversities with mutual adjustment and adjustment for smoking.

Sensitivity analyses excluded respondents reporting pain, depression, and with poor cognitive function at the time of the life-history interview.

Results 6,663 respondents were included; 208 developed RA from age 45.

For onset from age 45, each additional adversity up to a maximum of 8 predicts RA onset; hazard ratio HR = 1.086, 95% confidence interval 95% CI: = 1.004–1.174. Evidence is weak that adversities at each life stage combine cumulatively to predict RA onset; for each additional life stage with adversity (maximum three life stages), HR = 1.155, 95% CI: = 0.937–1.424. After adjustment for adversity during other life stages, adversity during youth (maximum three adversities) is salient; HR = 1.253, 95% CI: = 1.052–1.492. Evidence is weak that after adjustment for smoking, adversities associated with material (maximum two adversities) and psychosocial (maximum three adversities) pathways independently predict RA onset; HR = 1.34, 95% CI: = 0.894–2.018, HR = 1.28, 95% CI: = 1.043–1.577, respectively.

Results for onset from age 60 and for all sensitivity analyses provide similar findings.

Conclusion Evidence about adversity and RA onset is sparse, our numbers are small, and these findings require replication. Nevertheless, they indicate the importance of adversity in the development of RA, and raise questions about the mechanisms involved.

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