At the height of the recent recession around 2.7 million people were unemployed, and youth unemployment accounted for nearly 40% of that total. Given growing evidence that unemployment is linked to long term illness and increased mortality, we can expect health implications for those affected. Amanda Hughes from the ESRC International Centre for Lifecourse Studies, shares new evidence on the links between unemployment and killer diseases such as heart disease.
In 1984 a study was published which had linked census data to mortality records and found that men unemployed in the week of the 1971 census were 36% more likely to have since died than men of the same age who had been in work. Accounting for differences in social background only explained part of the excess, raising the question: can unemployment kill, and if so how?
That unemployment might damage health was not a new idea. Marie Jahoda’s research on unemployment in the 1930s had shown that the non-financial benefits of work, such as defining aspects of status and identity and providing regular social contact, are for many people crucial to mental wellbeing. And since job loss usually brings a sharp drop in income, it is intuitive that unemployment could affect physical health by reducing quality of diet or opportunities for exercise.
But there tends to be more scepticism as to whether serious physical illness or mortality could be causally influenced by the undoubtedly stressful experience of unemployment. Might those unemployed men have developed serious illness when employed, lost their jobs as a result, and then died from their illness? Or might their increased mortality simply be caused by unemployed people smoking and drinking more? In neither case could it be claimed that unemployment itself has caused any deaths.
Since the 1980s, the tools available to scientists researching the health impacts of social conditions have moved on considerably. One new approach involves molecules called ‘inflammatory markers’ which circulate in the bloodstream and appear to be influenced by stressful experiences.
Elevated concentrations have been found in the recently bereaved and caregivers; inflammatory markers are also typically higher for people of disadvantaged socioeconomic position as measured by income or occupational social class. Crucially, raised concentrations of these molecules are linked to atherosclerosis and predict heart disease, presenting a possible causal pathway between a stressful social environment and increased mortality.
It was for this reason that we wanted to see if two inflammatory markers – C-reactive protein and fibrinogen – were elevated in jobseekers compared to employed counterparts.
We used the Health Survey for England and Scottish Health Survey, annual government surveys used to track changes in the health of both countries’ populations. To isolate elevations in these molecules due to unemployment-related stress, we considered a number of additional factors beyond participants’ age and gender.
To rule out elevations due to serious illness predating job loss, we considered whether participants had a long-term illness of any type. To rule out elevations caused by disadvantaged socioeconomic position more generally, we took into account housing tenure and occupational social class from current or most recent job.
Finally, to test whether elevations might be explained by worse health-related behaviours of jobseekers, we took into account participants’ smoking, alcohol consumption and body mass index.
In our sample of over 23,000 men and women of working age, unemployed people had elevated circulating levels of both molecules even after consideration of these factors. These differences were moreover clinically relevant, since unemployed participants were 40% more likely to have C-reactive protein over 3mg/L, the level at which cardiovascular risk becomes elevated.
Effects were not uniform across the population. Firstly, older jobseekers (48-64) were more affected than younger jobseekers. This might indicate that unemployment is more stressful for jobseekers facing age discrimination, or equipped with outdated skills.
Since older jobseekers will have accumulated more unemployment over their lifetimes than younger counterparts, it could alternatively indicate that long-term or repeated unemployment is especially damaging to this aspect of health.
Secondly, we found substantial differences in results by country, with much greater elevations in both molecules for jobseekers in Scotland than in England. Data from the Labour Force Survey and the British Household Panel Study show that during the years of data collection (1998-2010) unemployment was higher in Scotland than England, and unemployment spells on average longer, which suggests two possible explanations.
Firstly, the jobseekers in Scotland may have been unemployed for longer, or had more recent unemployment spells, than English counterparts. Secondly, unemployment could be more stressful in times and places where the background rate is higher, since jobseekers will rationally perceive their prospects for re-employment as worse.
Since these surveys only collect information from people at one point in time, it was not possible in this analysis to investigate effects in the context of people’s employment histories. But unpicking these explanations will be crucial if we are to better understand the conditions under which unemployment is most likely to damage health, and which groups are most at risk.
Crucially, the recession may be over and unemployment down, but policy makers interested in the long term health of the population should not divert their gaze from the wider consequences, especially given that long term or persistent unemployment remains worryingly high at around a million people.
Elevated inflammatory biomarkers during unemployment: modification by age and country in the UK is research by Amanda Hughes, Anne McMunn, Mel Bartley and Meena Kumari and is published in the Journal of Epidemiology and Community Health.
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