How social factors can shape our health through inflammation

People living in more disadvantaged social and economic conditions, especially in young adulthood, are more likely to experience higher levels of inflammation, which in turn can lead to serious health issues like atherosclerosis or coronary heart disease. This connection between social and health inequalities has been revealed by a study published on Nature Communications by researchers of the Lifepath project, an EU-funded consortium that investigates the biological pathways underlying social differences in healthy ageing.

Inequalities in socioeconomic position (SEP) lead to inequalities in health. In order to tackle such a problem, one key step is to unravel how social and economic factors become biologically embodied.

Inflammation is a set of responses that may be caused by a number of processes such as the presence of an infection or tumour cell development, but also occur as a consequence of the chronic solicitation of the stress response system. A higher level of basal inflammation has consequences for overall health and has been linked to mortality across various causes.

Socioeconomic conditions may be a powerful trigger for chronic inflammation since socially disadvantaged populations are disproportionately exposed to environments that can be characterized as pro-inflammatory, such as exposure to infections due to overcrowded conditions, poor housing quality, or insufficient access to sanitation. Moreover, disadvantaged socioeconomic groups are more likely to display adverse health behaviours that may expose them to factors like tobacco smoking as well as nutritional behaviours leading towards obesity, which in turn can trigger inflammation processes. Finally, cumulative social disadvantage may also push individuals towards experiencing adversities, or exacerbate such situations, thus resulting in psychosocial stress and, as a consequence, heightened basal inflammation. 

Lifepath researchers analysed data from six big studies conducted between 1958 and 2013 in Italy, Switzerland and United Kingdom, to investigate several important aspects of the social-to-biological transition. They focused on the chronology of exposures to disadvantaged socioeconomic conditions over the life course, in order to understand how they are associated with inflammation.

The participants’ socioeconomic position (SEP) was evaluated based on three parameters: father’s occupation, educational attainment, and participant’s last occupation. As a marker of overall inflammatory response, the researchers measured the concentration of C-reactive protein (CRP), a protein synthesized by the liver in response to systemic effects of inflammation. They also investigated the potential impact of behavioural factors and body mass index (BMI) on the relationship between CRP and SEP, in order to elucidate their possible role as intermediate factors.

What they found is that disadvantaged socioeconomic position at each life stage was associated with increased inflammation assessed using CRP, and that behavioural factors like alcohol consumption, smoking status and a sedentary life style can explain part but not all of the observed SEP differences in inflammation.

One of the most consistent and important upstream risk factors for elevated inflammation was shown to be educational attainment. «One of the likely mechanisms involved here is the stress response system, where higher educational attainment may act as a physiological stress-regulating buffer», said Raphaële Castagné, research fellow at the Université Toulouse III Paul Sabatier of Toulouse and co-leading author of the study. «A higher educational attainment may provide increased sense of control, which is a suggested pathway linking education to health».

Lifepath researchers also found that body-mass index (BMI) seemed to be the most relevant intermediate factor between SEP and inflammation – which means that the accumulation of body fat among more socially disadvantaged populations could be a mechanism leading to higher levels inflammation – and observed some differences between men and women, which may come down to differences in immunological and inflammatory responses influenced by both sex and gender.

Another critical element is the time of exposure to disadvantaged social and economic conditions: in fact, chronic inflammation is the result of a prolonged wear-and-tear effect on physiological systems, and the earlier this is triggered, the bigger its consequences might be.

«Taken together, our findings highlight the important role that social factors play in health beyond behaviours and lifestyle factors», concluded Michelle Kelly-Irving, researcher in lifecourse epidemiology at the Inserm and Université Toulouse III Paul Sabatier of Toulouse and coordinator of the study. «By documenting how social disadvantages exert their influence on our biology through inflammation, we highlight the need to intervene from early life to reduce the embodiment of social disparities in health».

Further work integrating social-to-biological perspectives will be needed to better understand the mechanisms through which the social environment shapes physiological processes that are important for complex health outcomes. However, this study further confirms that the conditions in which we live and grow can play a relevant role in how our wellbeing is shaped, since they influence our chances of having a longer and healthier life. Investigating the social-to-biological transition is thus a key step towards developing health policies capable of tackling in a precise way the roots of socioeconomic-based health inequalities.

Publication date: 
Wednesday, February 27, 2019