History of socioeconomic disadvantage and allostatic load in later life
Highlights
► In a US sample, life course patterns of socioeconomic adversity were examined as predictors of a multi-system allostatic load index. ► Greater cumulative life course socioeconomic adversity is linked to higher allostatic load in later adulthood. ► Findings also suggest a potential protective effect of upward mobility on allostatic load levels in adulthood.
Introduction
A voluminous literature documents an inverse association between socioeconomic status (SES) and health, such that occupation of a lower SES position is associated with greater risk of a wide array of adverse health outcomes (Adler et al., 1994, Kaplan and Keil, 1993). This includes risk of development of infectious illness, as well as chronic health conditions, such as heart disease, diabetes, and poor cognitive and physical functioning (see Cohen, 1999, Kaplan and Keil, 1993, Strike and Steptoe, 2004, Tamayo et al., 2010). Those of lower SES are also at greater risk of disease-specific and all-cause mortality (e.g., Lynch et al., 1994, Turrell et al., 2007).
That the potential ill effects of low SES can be observed across such a wide range of conditions suggests common biological mechanisms through which SES adversity is linked to health. A general conceptualization of the mechanisms, offered by many theorists (e.g., Gallo and Matthews, 2003, Seeman and Crimmins, 2001, Williams, 1990), through which SES variations may be linked to variations in biological functioning is provided in Fig. 1. SES-patterned environmental exposures, and psychological, social and behavioral processes, are hypothesized to affect the functioning of various biological regulatory systems important to health. These include primary regulatory systems, such as the neuroendocrine and nervous systems which respond to internal and external demands and which, in turn, affect the activity of secondary regulatory systems, such as the immune, cardiovascular and metabolic systems, that carry out biological activities to meet such demands. The underlying hypothesis of this general conceptual model is that those of lower SES are subject to environmental, psychological and behavioral characteristics and experiences that more often put demands on these biological systems, leading to greater system wear and tear over time, and subsequently enhancing risk for poor health and functioning.
Evidence for SES gradients in biomarkers of these potential physiological pathways to disease is accumulating. Lower SES, assessed by a variety of indicators (education, income, occupational status, financial strain), has been linked to more “risky” patterns of biological functioning, including higher levels of hormones hypothesized to be elevated under conditions of stress (e.g., sympathetic nervous system and hypothalamic-pituitary-adrenal hormones, e.g., Cohen et al., 2006, Janicki-Deverts et al., 2007, Rosmond and Bjorntorp, 2000, Steptoe et al., 2003), poorer metabolic profiles (e.g., greater body mass index, higher fasting glucose and insulin and glycosylated hemoglobin, poorer lipid profiles; Danese et al., 2009, Loucks et al., 2007, McLaren, 2007, Senese et al., 2009), and other indicators of cardiovascular disease risk (e.g., high blood pressure, low heart rate variability; Colhoun et al., 1998, Hemingway et al., 2005, Sloan et al., 2005). Circulating levels of C-reactive protein, fibrinogen and other indicators of inflammatory burden, have also been found to be greater in those of lower SES (e.g., Brunner et al., 1996, Gruenewald et al., 2009, Hemingway et al., 2003, Koster et al., 2006).
A number of investigations have also documented SES gradients in multi-system physiological indices, often referred to as measures of allostatic load (AL) (McEwen, 1998, McEwen and Stellar, 1993, Seeman et al., 1997), which assess risk across a wide array of biomarkers or across multiple biological systems. Given that the experiential and behavioral correlates of SES likely affect, and risk for most major morbid conditions is affected by, the functioning of multiple physiological systems, multi-system AL indices may provide a better picture of the physiological toll that SES adversity experience imparts on the body. AL levels, assessed with a variety of scoring methodologies, have been found to be higher in those of lower SES (Crimmins et al., 2009, Geronimus et al., 2006, Kubzansky et al., 1999, Seeman et al., 2004, Singer and Ryff, 1999, Weinstein et al., 2003).
Increasing interest is also being accorded to the time course of such associations, that is, how experience of SES adversity across the life course is linked to biological functioning in adulthood. A number of models have been advanced to explain the potential association between life course SES and health, which may be applicable to the study of physiological pathways to disease, including the accumulation of risk, status mobility, and sensitive or critical periods models (Ben-Shlomo and Kuh, 2002, Pollitt et al., 2005). The accumulation of risk model posits that greater exposure to SES adversity (e.g., low levels of educational attainment, low occupational status, financial strain) accumulates across the life course to have a more negative impact on physiological functioning and health in later adulthood. This accumulative process is also captured in theories of the aging or weathering of biological systems under conditions of chronic adversity (e.g., Geronimus et al., 2006). An additive process is also acknowledged in the status mobility framework, in which those who persistently experience a low status position across the life course are expected to fare the worst, while the upwardly mobile are expected to benefit physiologically from status improvements over the life course. Sensitive or critical periods models suggest that SES adversity experience may have a differential effect on physiological functioning depending on the life course phase in which adversity is experienced (e.g., early life SES adversity experience may permanently ‘tune’ developing biological systems).
Several studies provide support for the accumulation of risk hypothesis in that cumulative measures of SES adversity across childhood and adulthood are stronger predictors of physiological risk, such as high inflammatory burden (e.g., Loucks et al., 2010, Pollitt et al., 2008) and weight gain (e.g., Baltrus et al., 2005, Senese et al., 2009), than measures from single points in the life course. Support has been less consistent for the protective effects of upward mobility (Pollitt et al., 2005), and adult SES measures often have greater explanatory power than childhood measures, although some investigations find significant associations for childhood SES independent of adult SES (e.g., Pollitt et al., 2005, Pollitt et al., 2007, Tamayo et al., 2010). To date, research on associations between AL indices and life course SES experience is limited, although Singer and Ryff (1999) demonstrated that AL levels were highest in those of low income in adolescence and midlife, lowest in those with persistently high income, and of intermediate levels in the upwardly and downwardly mobile, in a small subsample of participants from the Wisconsin Longitudinal Study.
The goal of the present investigation is to further explore the cumulative risk hypothesis, by examining whether AL levels in adult Americans are greater in those with greater experience of SES adversity across the life course, as measured in childhood and two points in adulthood. The multiple time periods for which SES information is available also allows for explorations of the social mobility and sensitive periods hypotheses, that is, whether specific patterns of SES mobility, or the experience of SES adversity at certain life course phases (e.g., childhood versus adulthood), are differentially correlated with biological functioning in later adulthood.
Section snippets
Sample
Data come from the Biomarker Substudy of the Study of Midlife in the U.S. (MIDUS), a longitudinal study of psychosocial, behavioral, and sociodemographic correlates of healthy aging. In 1994–1995, a national sample of 3487 individuals were surveyed via telephone using random digit dialing, with 3034 of the respondents completing an additional mail survey. Samples of siblings of randomly dialed respondents (n = 950) and twins (n = 1914) were also included in the baseline cohort. The original
Results
Descriptive statistics for individual biomarkers and the multi-system AL score are detailed in Table 1. Sample-derived high-risk quartile cutpoints for the biomarkers were similar to standard clinical risk cutpoints or “borderline” or “moderate” risk clinical cutpoints (see Table 1). Average AL level was rather moderate in the sample (M = 1.72, SD = 1.02; range 0–4.8; possible range of 0–7), although there was considerable variability in the range of scores. Descriptive statistics for
Discussion
Findings indicate higher levels of allostatic load in middle and later adulthood in individuals who have experienced a greater level of SES adversity across the life course from childhood to adulthood. Greater AL in those with greater life course SES adversity was observed whether cumulative SES adversity was assessed as higher scores on a summary measure incorporating SES adversity information from childhood and two points in adulthood, or when assessed as persistent SES adversity in both
Acknowledgments
This work was supported by the National Institute on Aging (grant numbers K01-AG028582 to T.G., R01-AG032271 to T.S., R01-AG033067 to A.K. and C.C., and P01-AG020166 which funded MIDUS II data collection); and the MacArthur Foundation Network on Midlife (which funded MIDUS I data collection).
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