Background Previous studies have shown that differential exposure to lifestyle factors may mediate the association between education and coronary heart diseases (CHD). However, few studies have examined the potential roles of allostatic load (AL) or differential susceptibility.
Methods 25 310 men and 26 018 women aged 35–74 and CHD free at baseline were identified from 21 European cohorts and followed for a median of 10 years, to investigate the mediating role of AL, as well as of smoking, alcohol use and body mass index (BMI), on educational differences in CHD incidence, applying marginal structural models and three-way decomposition.
Results AL is a mediator of the association between educational status and CHD incidence, with the highest proportion mediated observed among women and largely attributable to differential exposure, (28% (95% CI 19% to 44%)), with 8% (95% CI 0% to 16%) attributable to differential susceptibility. The mediating effects of smoking, alcohol and BMI, compared with AL, were relatively small for both men and women.
Conclusion Overall, the educational inequalities in CHD incidence were partially mediated through differential exposure to AL. By contrast, the mediation of the educational gradient in CHD by investigated lifestyle risk factors was limited. As differential susceptibility in men was found to have a predominant role in the accumulation of AL in low educational classes, the investigation of AL-related risk factors is warranted.
- cardiovascular diseases
- health inequalities
Data availability statement
No additional data are available from each of the cohorts. Data may be made available to researchers upon reasonable request.
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Contributors Authors’ contributions: GV, FK, MMF and BH conceived the research question. BH, FK, GV drafted the manuscript along with MMF and HF. GV conducted the statistical analyses. KK, TZ and SB are guarantor of the MORGAM/BiomarCaRE database. HT-P, SSa, VS, BT, FK, MMF, BT, SSo, GC, LI, LP are the principal investigators of the cohorts included in the current analyses. MW, FD, KK, HT-P, SSa, VS, BT, AP, TB, AP, SSo, GC, LI, LP, MB, TZ and SB actively contributed to the interpretation of the results and made critical revision of the manuscript.
Funding The BiomarCaRE Project is funded by the EU Seventh Framework Programme (FP7/2007– 2013) under grant agreement HEALTH-F2–2011–278913. The activities of the MORGAM Data Centre have also been sustained by recent funding from EU FP7 project CHANCES (HEALTH-F3–2010–242244). A part of the biomarker determinations in the population cohorts was funded by the Medical Research Council London (G0601463, identification No.80983: Biomarkers in the MORGAM Populations). The MONICA/KORA Augsburg study was initiated and financed by the Helmholtz Zentrum München—German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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