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Editorial
June 26, 2017

The Persisting Challenge of Socioeconomic Inequalities in Health Across the Life Course

Author Affiliations
  • 1Medical Research Council Unit for Lifelong Health and Ageing at University College London, London, England
JAMA Pediatr. Published online June 26, 2017. doi:10.1001/jamapediatrics.2017.1370

Social inequalities in a range of health outcomes, including cardiovascular disease (CVD), are well documented. The pathophysiological process of atherosclerosis that ultimately leads to CVD is initiated in early life, highlighting the importance of a life-course approach to cardiovascular aging. There is a need to understand the factors from childhood and across life that may influence the development and progression of the disease process,1 considering not just disease onset as an outcome but also life-course trajectories of cardiovascular risk factors and subclinical markers of disease. Socioeconomic position (SEP) in childhood, usually indicated by parental occupational social class, has consistently been shown to be associated with CVD.2 The term SEP is used here instead of socioeconomic status because SEP encompasses various dimensions of inequality including status (ie, hierarchy of prestige or social honor), class (ie, occupation), and material circumstances (ie, indexed by income or other measure of living standards).3 The mechanisms underlying childhood SEP differences in CVD largely remain to be elucidated. There may be developmental, behavioral, and psychosocial pathways, and several studies highlight the importance of education as a mediator.4 In this issue of JAMA Pediatrics, Laitinen et al5 extend existing knowledge and add to the evidence of persisting socioeconomic inequalities across age, time, and place. Using data from the Cardiovascular Risk in Young Finns Study, the authors5 provide evidence that greater childhood socioeconomic disadvantage, as characterized by annual income of the family (and, in a sensitivity analysis, by parental occupation), is associated with poorer left ventricular (LV) structure (measured by LV mass index) and diastolic function (measured by E/e′ ratio) in adulthood. Outcomes are thus measured before disease onset, and most participants have measures of LV mass index and E/e′ ratio within the normal range. The associations persist after adjustment for a host of factors from childhood and adulthood, including SEP, suggesting that effects are not entirely mediated through continuing disadvantage in adulthood.

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