Background:

Social inequalities in health, with people experiencing progressively worse health with increasing deprivation, are present throughout the world. Inequalities in health are not limited to mortality and life expectancy, with the incidence of physical and mental conditions being higher for individuals with lower socioeconomic position (SEP), including most cancers, heart disease, diabetes, depression and multimorbidity. However, the pathways, and particularly the underlying biological processes, linking poorer SEP and ill health are not well understood. Understanding the causal links between SEP and health are essential if inequalities are to be reduced in the UK and elsewhere.

Given the wide range of conditions that vary by SEP, it has been proposed that there are some common biological pathways in how SEP can 'get under the skin'. Through the exposure to environmental, psychosocial and behavioural factors that SEP results in, the body is put under demands that it can adapt to in the short-term (normal system regulation). However, if these exposures persist, dysregulation can occur. The 'wear and tear' on the body that will occur over long spells of such dysregulation is typically irreversible, eventually increasing the risks of poor health and functioning.

Cumulative physiological burden and dysregulation that occurs across multiple physiological systems throughout the lifecourse can be captured using the concept of allostatic load. The most widely used construct of allostatic load has been developed by Seeman and colleagues, where it is conceptualised using biomarker measures across an array of systems including the cardiovascular, metabolic and inflammatory systems. Allostatic load has been shown to predict the risk of major health outcomes including heart disease and all-cause mortality. Importantly, many of the individual components of allostatic load are not risk predictors for the same health outcomes associated with allostatic load. Assessing these biomarkers together as allostatic load helps us to understand the synergistic nature of the physiological burden on the body imposed by exposure to damaging environmental stressors. To date, there has been consistent (albeit small in number) evidence for lower SEP to be associated with higher allostatic load. Given the associations identified between SEP and allostatic load, and allostatic load and health, it is hypothesised that allostatic load is a mediator in the pathway between SEP and health. However, we are missing evidence for how SEP and allostatic load are associated throughout the lifecourse, how these associations can differ over time and place and if allostatic load is indeed a link between SEP and health. If allostatic load is a predictor of health, it would be expected that similar patterns of inequality would be seen in allostatic load as those seen with life expectancy and diseases like CHD. Greater knowledge on the relationship between SEP and allostatic load (and subsequent risk prediction of ill health) could be important for targeting interventions aimed at reducing inequalities in health that will have the broadest impact across the population. Understanding how the relationship between SEP and allostatic load differs according to factors such as age, gender and geographical location could be an important step in ensuring that these interventions are targeted correctly and efficiently.

Preliminary work:

I have recently led on a study paper looking at the relationship between SEP over the lifecourse and allostatic load (to be submitted April 2013). This study used a structured modelling approach comparing various theoretical models of the influence of SEP on health across the lifecourse that encompass the accumulation of risk, critical/sensitive periods and social mobility models. We found that the accumulation model of lifecourse SEP had the best model fit for the association with allostatic load in men and women aged approximately 35, 55 and 75 from the West of Scotland Twenty-07 Study (although the results were less convincing at older ages). However, the results also indicated that childhood was a particularly important time-point for the link between SEP and allostatic load. Since March 2013 I have also been leading on a study investigating some of the potential mediators (behavioural, psychosocial and material factors) between SEP and allostatic load using the Twenty-07 Study. This work has been funded by a six-month MRC Centenary Award.

Aims:

The overall aim of the fellowship is to examine if allostatic load, as a measure of cumulative physiological burden, is a mediator in the association between lower SEP and poorer health outcomes, including physical and mental health and mortality. The specific aim of the project using ALSPAC data is to examine allostatic load inequalities by SEP in children. Very little evidence exists in the development of allostatic load in childhood and its association with SEP, although there is good evidence for social patterning in adolescence. In addition, our preliminary work above has indicated the importance of childhood as a possible critical period in the development of adult allostatic load. Other data on childhood circumstances will also help answer if any patterning is driven by factors such as disease in infancy.

Hypotheses:

Lower SEP (based on a latent parental SEP construct) will be associated with higher allostatic load scores in children aged 9 from the ALSPAC study. This association will be partly mediated by disease in infancy and poorer conditions at birth (e.g. low birth weight, small for gestational age).

Exposure variables:

Parental SEP (education, income, social class, housing tenure, financial difficulties and area deprivation)

Outcome variables:

Allostatic load - a score produced from several bookmarkers (blood pressure, pulse rate, cholesterol, glycated haemoglobin (diabetes marker), waist-hip ratio, C - reactive protein (inflammation marker) and IL-6 (inflammation marker))

Confounding variables:

Sex, disease, birth weight, gestational age, ethnicity

Please note, any data provided will be stored on secure drive spaces at SPHSU, which only I have access to.