Abstract
BackgroundGiven the broad spectrum of health and wellbeing outcomes that are patterned by socioeconomic position (SEP), it has been suggested that there may be common biological pathways linking SEP and health. Allostatic load is one such pathway, which aims to measure cumulative burden/dysregulation across multiple physiological systems. This study aimed to determine the contextual and demographic factors (age, sex and place) that may be important in better understanding the links between lower SEP and higher allostatic load.MethodsData were from a nationally representative sample of adults (18+): the Scottish Health Survey (2008–2011). Higher SEP (‘1’) was defined as having ‘Higher’-level, secondary school qualifications versus having lower level or no qualifications (‘0’). For allostatic load, a range of 10 biomarkers across the cardiovascular, metabolic and immune systems were used. Respondents were scored “1” for each biomarker that fell into the highest quartile of risk. Linear regressions were run in STATA, including SEP, age (continuous and as a 7-category variable), sex (male/female), urbanity (a 5-category variable ranging from primary cities to remote rural areas) and geographical location (based on 10 area-level healthboards). Interactions between SEP and each predictor, as well as stratified analyses, were tested.ResultsLower SEP was associated with higher allostatic load even after adjusting for age, sex and place (b = −0.631, 95 % CI −0.795, −0.389, p < 0.001). There was no significant effect moderation between SEP and age, sex or place. Stratified analysis did show that the inequality identified in the baseline models widened with age, becoming significant at ages 35–44, before narrowing at older ages (75+). There was no difference by sex, but more mixed findings with regards place (urbanity or geographical location), with a mix of significant and non-significant results by SEP that did not appear to follow any pattern.ConclusionsInequalities in allostatic load by educational attainment, as a measure of SEP, are consistent with age, sex and place. However, these stratified analyses showed that these inequalities did widen with age, before narrowing in later life, matching the patterns seen with other objective and subjective health measures. However, effect moderation analysis did not support evidence of a statistically significant interaction between age and SEP. Context remains an important feature in understanding and potentially addressing inequalities, although may be less of an issue in terms of physiological burden.Electronic supplementary materialThe online version of this article (doi:10.1186/s12889-016-2796-4) contains supplementary material, which is available to authorized users.
Highlights
Given the broad spectrum of health and wellbeing outcomes that are patterned by socioeconomic position (SEP), it has been suggested that there may be common biological pathways linking SEP and health
Allostasis is beneficial in the short-term, chronic, high levels result in cumulative damage, known as allostatic load [9, 10]
This study has explored in further detail the relationship between lower SEP and higher allostatic load across the lifecourse using a large, nationally representative population sample, finding that inequalities widen with age, before narrowing in later life through stratified analysis
Summary
Given the broad spectrum of health and wellbeing outcomes that are patterned by socioeconomic position (SEP), it has been suggested that there may be common biological pathways linking SEP and health. Allostatic load is one such pathway, which aims to measure cumulative burden/dysregulation across multiple physiological systems. Sustained exposure results in dysregulation and desensitisation to the stress response (reviewed by McEwen, 2002 [6]) These exposures manifest in a reduced capacity to adapt [7], inducing a recalibration process to restore the normative environment, known as allostasis [8]. High allostatic load, which is typically measured using a number of the body’s physiological biomarkers (primarily constructed using secondary outcomes of the stress pathway, as described above) as indicators of regulation/dysregulation [13], is predictive of an increased risk of a number of adverse medical conditions [14,15,16], and all-cause mortality [13]. Subsequent reduction in allostatic load is associated with a reduction in risk of dying [17]
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