Elsevier

Social Science & Medicine

Volume 165, September 2016, Pages 19-27
Social Science & Medicine

Mediating pathways between parental socio-economic position and allostatic load in mid-life: Findings from the 1958 British birth cohort

https://doi.org/10.1016/j.socscimed.2016.07.031Get rights and content

Highlights

  • Parental SEP at birth was linked with allostatic load at 44 years.

  • Parental SEP was mediated by an educational, material and health behaviors paths.

  • The educational path shows a major role in these relationships.

  • Allostatic load may allow a better understanding of social-to-biological transitions.

Abstract

Understanding how human environments affect our health by “getting under the skin” and penetrating the cells, organs and physiological systems of our bodies is a key tenet in public health research. Here, we examine the idea that early life socioeconomic position (SEP) can be biologically embodied, potentially leading to the production of health inequalities across population groups. Allostatic load (AL), a composite measure of overall physiological wear-and-tear, could allow for a better understanding of the potential biological pathways playing a role in the construction of the social gradient in adult health. We investigate the factors mediating the link between two components of parental SEP, maternal education (ME) and parental occupation (PO), and AL at 44 years. Data was used from 7573 members of the 1958 British birth cohort follow-up to age 44. AL was constructed using 14 biomarkers representing four physiological systems. We assessed the contribution of financial/materialist, psychological/psychosocial, educational, and health behaviors/BMI pathways over the life course, in mediating the associations between ME, PO and AL. ME and PO were mediated by three pathways: educational, material/financial, and health behaviors, for both men and women. A better understanding of embodiment processes leading to disease development may contribute to developing adapted public policies aiming to reduce health inequalities.

Introduction

Redressing the social stratification of ill health is a major concern in public health research. Classic determinants of non-communicable disease, which are mainly behavioral, are insufficient for explaining the large disparities observed in morbidity and mortality (Gallo et al., 2012). The concept of embodiment (Krieger, 2005) and biological embedding (Hertzman, 2012) are similar, and may be useful tools for formulating hypotheses on how health inequalities are produced over the lifecourse. In both concepts, how human environments affect our health by penetrating the cells, organs and physiological systems of our bodies, is a key tenet. We conceptualize embodiment as a dynamic process that summarizes how we become altered by our past experiences and are responding to the present, from how well we feel, down to the molecular modifications in our bodily structures. The process of embodiment being socially stratified (Hertzman and Boyce, 2010) may contribute to explaining the production of social gradients in health.

Growing evidence supports the idea that exposure to stressful conditions over life contributes to physiological dysregulation, subsequently translated into disease, through prolonged activation of stress response systems (McEwen and Stellar, 1993). Allostasis is the process where our body adapts to environmental challenges or stressful conditions in order to maintain physiological stability. The repeated activation of compensatory physiological mechanisms as a response to chronic stress can lead to a physiological wear-and-tear, known as allostatic load (AL) (Juster et al., 2010, McEwen and Stellar, 1993). AL has been strongly correlated with subclinical conditions, cardiovascular events, physical and functioning decline and mortality (Juster et al., 2010, Karlamangla et al., 2002, Karlamangla et al., 2006). As a composite measure, AL performs as a better predictor of subsequent morbidity and mortality over and above each constituent biomarker when analyzed individually (Karlamangla et al., 2002). These findings suggest that AL could represent a global physiological state and perhaps even a proxy for an outcome of the embodiment process.

Growing evidence suggests that early life socioeconomic position (SEP) is a distal determinant of AL (Gruenewald et al., 2012), suggesting that poor socioeconomic circumstances early in life could set different population subgroups on life trajectories that are unfavorable for health, increasing their probability of being exposed to unhealthy environmental stressors and lifestyles. Early SEP is often measured using parental education and occupation at birth or in childhood, both of these measures being generally available in birth cohort studies. Education and occupation may operate through both similar and unique mechanisms to influence offspring health. In the current analysis, measures of parental education were limited to maternal education (ME), and occupation to paternal occupation (PO), due to variables availability and due to the historical context in which measures were assessed. Literature suggests that education and occupation do not impact health through the same pathways and should be analyzed separately (Galobardes et al., 2006, Galobardes et al., 2007). PO may affect health through: i) material resources (that determine material leaving standards), ii) work privileges (i.e. social security), iii) social standing (determining work control/autonomy and work based stress), and iv) toxic occupational exposures (Bartley et al., 1996, Galobardes et al., 2006). ME could affect health through: i) higher score of knowledge/skills and thus cultural capital, ii) material resources, iii) increasing the odds of acquiring better positions in occupation and higher income (Galobardes et al., 2006).

The lifecourse pathways linking early SEP to AL deserve to be disentangled, in particular the specific pathways involving ME and PO respectively. We aim to address this question by exploring four pathways through which ME and PO may be differentially embodied during childhood, adolescence and early adulthood leading to physiological wear-and-tear, as measured by AL. (a) A material/financial pathway: we hypothesize that living in poor material/financial circumstances could increase the risk of exposure to stressful and harmful situations relate to housing, work conditions, neighborhood, etc. (toxins, allergens, overcrowding) (Gustafsson et al., 2012, Lannero et al., 2002, Robertson et al., 2015). (b) A psychosocial/psychological pathway: parental SEP could influence parenting and the creation of a secure social environment buffering toxic stress responses, as well as the set-up of stress responses systems (Repetti et al., 2002, Shonkoff et al., 2012). (c) An educational pathway: higher parental SEP may influence educational outcomes in childhood, impact cognitive functions (Dubow et al., 2009, Kaplan et al., 2001) and later adult SEP (d) a health behaviors & BMI pathway: the accumulation of social disadvantage over life could contribute to adopt risky behaviors, impacting physiological functioning (Adler and Stewart, 2010, Stringhini et al., 2011).

We selected these four pathways based on epidemiological evidence and on empirical studies suggesting a link between SEP and each path. Lynch et al. (Lynch et al., 2000) suggested that health is the result of an accumulation of experiences and exposures due to the material world. Biological (viruses, bacteria) and chemical hazards, are more likely in more deprived homes and neighborhoods, and in some occupational statuses. An inverse relation between SEP and risky health behaviors has been largely demonstrated in empirical research (Stringhini et al., 2011). The adoption of health behaviors may be explained by complex psychological processes (e.g. self-regulation, self-efficacy, locus of control) (Bandura, 1991). Other explanations relate to social norms, tradition, and customs since lifestyle depends on social characteristics established by community social standards (Bartley, 2003). Concerning the psychosocial path, previous research (Marmot and Wilkinson, 1999) suggests that SEP may relate to health through the perception individuals have of their position in a social hierarchy. These perceptions may produce negative emotions resulting in poorer health, through psycho-neuroendocrine mechanisms (Brunner and Marmot, 1999) linked to stress responses (and/or stress-related behaviors such as smoking). Regarding the educational path, Hackman & Farah, showed in a recent review that SEP is linked with neurocognitive performance, such as language and executive function. Cognitive ability appears to be affected by poverty, especially during childhood. Different mechanisms have been suggested (e.g. cognitive stimulation, nutrition, parenting styles).

Section snippets

Study population

The National Child Development Study (NCDS) is a birth cohort that includes all children born during one week in 1958 (N = 18,558) in Great Britain. Subsequent data collection was carried out on cohort members between 7y and 50y. At age 44-45y a biomedical survey was conducted including a self-reported questionnaire, physical measurements, blood and saliva samples (Power and Elliott, 2006). The sample used for this study is described in Fig. S1. Details about ethics and data are given in

Results

Descriptive statistics of the nonimputed sample are presented in Table 1 for the subsample (n = 3782 for men; n = 3791 for women). Fig. 2, Fig. 3 represent the path analyses results, showing only the mediating variables explaining >5% of the total effect for men and women respectively, first between ME and AL, and second between PO and AL. The sum of all pathways are not equal to 1 due to other small or negative pathways not presented in the figures (Tables S5 and S6).

The path analyses for ME

Discussion

Lower maternal education and manual paternal occupation were associated with a higher allostatic load at 44 years, mainly via the educational, material/financial, and health behaviors pathways for both men and women. For the relationship between ME and AL, more than 60% of the link in women and 45% in men, remained unexplained by the mediators. Around 50–60% of the relationship between PO and AL remained unexplained by the mediators in men and in women. In both relationships these pathways may

Acknowledgments

C.B.S. is supported by the University of Costa Rica and funded by the European Commission (Horizon 2020 grant no 633666). The present work is part of the Incorporation Biologique et Inégalités Sociales de Santé (IBISS) project supported by funds from Agence Nationale de la Recherche (ANR-12-DSSA-0004).

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