Health is a well-known inequality issue. While aging is inevitable and most of us will get sick at some point, the rate of your decline is likely to be faster the lower down the socioeconomic ladder you started.
The intriguing thing is, nobody knows exactly why. Tempting though it is to blame the usual suspects – poor diet, obesity, smoking – they don’t account for the whole story.
“If you exactly knew somebody’s diet, exercise level, smoking habit or alcohol consumption, you would be about 30 to 40% likely to accurately predict how long they are going to live,” says Mel Bartley, professor emerita of medical sociology at University College London, who has dedicated her career to understanding the links between society and health. “But what’s the rest? That’s the big question.”
Unpicking the biological connections between external socioeconomic forces and an individual’s health is no easy task. But Bartley and others in her field believe important clues can be found in the very lifeblood of a nation.
The idea that measurable biological markers (“biomarkers”) in the bloodstream can reflect an individual’s underlying health status – and even offer some kind of prediction of their life expectancy – gained popularity in the 1950s, as scientists started searching for tell-tale markers linked to the epidemic of heart disease spreading through the US.
High blood pressure was the obvious one, but they also discovered that the level of “bad” cholesterol in the bloodstream was a good indicator of risk. By monitoring blood cholesterol levels in healthy people before they show any outward signs of heart disease, doctors can predict who is most at risk. The resulting medical interventions, such as dietary changes and statin drugs, can demonstrably improve those people’s long-term health.
Now, researchers are using the same approach to measure the impact of social status on the body, in the hope of developing policies that can reduce the health toll on society’s most deprived section (on average, the poorest people in the UK miss out on more than a decade of life compared with the richest).
One of the most ambitious projects, currently being undertaken by the University of Essex’s Institute for Social and Economic Research (ISER), is looking at blood biomarkers from some of the 40,000 UK households taking part in its Understanding Society study, which covers the entire socioeconomic spectrum.
“A biomarker is an objective measure of health,” explains Professor Meena Kumari, the epidemiologist leading the study along with health economist Dr. Apostolos Davillas. “These chemicals are like molecular flags: they allow us to see what happens inside people as they’re going through their life course – which they themselves might not be so aware of.”
According to Kumari, “What’s happened historically is that social scientists have tended to measure health in a simple way – just asking people: ‘How do you rate your health right now?’ But we wanted to bring together the biology and the social science.”
Published in the journal Scientific Reports, the ISER team’s initial analysis focused on measuring the levels of two molecules, fibrinogen and C-reactive protein (CRP), that are produced by inflammation – the body’s response to infections, stress and other harmful stimuli. Chronic long-term inflammation is linked to poorer health outcomes including heart disease, diabetes, and cancer.
According to Davillas and Kumari, measuring an individual’s CRP and fibrinogen levels and matching them against their socioeconomic position starts to reveal the hidden mechanisms connecting social inequality and health. And the missing link appears to be stress.
The impact of chronic stress
When we experience something stressful, we activate the “hypothalamic pituitary adrenal axis”: a convoluted network involving the brain and the pituitary and adrenal glands. This results in the release of cortisol and other stress hormones such as adrenaline, which have a range of effects on the body.
The complex biological conversation between this stress response and the body’s inflammatory processes actually damps down inflammation in the short term. But this careful balance seems to shift in the face of chronic stress, resulting in more inflammation over time. Thus the levels of CRP and fibrinogen, as markers of chronic inflammation, are a proxy for the impact of long-term stress on a person’s body.
For Kumari and Davillas’s biomarker study, blood samples were gathered from nearly 8,000 adults in the Understanding Society cohort. While CRP and fibrinogen levels increase in all of us as we age, the ISER team found that differences in the levels of CRP and fibrinogen between socioeconomic groups begin to show relatively early in life – and on average rise faster and peak sooner in poorer people.
“The research shows differences in CRP levels start around 30 years old and peak around the age of 55,” Davillas says. “Then the gap starts to narrow again – there’s not so much difference between the lowest and highest socio-economic groups in later life, although of course, the social inequalities are still there.” People in both groups end up with similar CRP readings by their mid-70s.
The analysis suggested people in lower socioeconomic groups have a demonstrably longer exposure to chronic inflammation – with all its knock-on impacts on long-term health – even once the team corrected for the “usual suspects” of health inequality, including diet and smoking. There’s clearly something else at work.
“If you ask people about their health, you don’t really see differences early in life – people tend to become unhealthy later in life,” Kumari says. “But we’re starting to see these underlying biomarker differences in people in their 30s; so what’s that about?”
Kumari and Davillas are now considering the causes of chronic stress that might contribute to the patterns they have found, starting with employment – or lack of it – and the associated issues of poor pay, job insecurity, long hours and the burgeoning gig economy.
“You have stressful life events such as bereavement or divorce, but we’re talking about understanding chronic long-term stresses,” Kumari says. “One of the things we think about is why is disadvantage stressful? For something like low income, it could be because you don’t have the same levels of control over your life. Maybe you can manage it for a little while, but over the long term, it becomes a chronic stress. These things are hard to measure and capture.”
Bartley agrees more needs to be done to understand the financial causes of stress across society. “Debt is deadly for people – it’s the ultimate lack of control,” she says. “Housing is also a huge issue and it doesn’t get researched enough – living in poor situations is depressing, especially if you’re bringing up children. People in poverty can end up in social isolation, and that’s known to be associated with all kinds of unhealthy outcomes.”
Changes in policy
It’s all very well to be able to measure levels of inflammatory biomarkers, and link them to stress and worse health outcomes – but the big question is what to do about it. If it’s as simple as lowering inflammation, then maybe we should just hand out anti-inflammatory drugs such as aspirin to poorer people?
“I don’t believe that’s the answer,” says Bartley. “We need to understand what it is about living in a tougher social and economic situation that causes this underlying stress, in order to argue for more effective changes in policy.”
“From a policy perspective, if you know when health inequalities begin and when they peak, this can help you target these age groups and allocate resources more effectively,” says Davillas, pointing to the example of retirement timing. “If you’re doing a stressful job and this impacts your health more compared to someone in a less stressful occupation, this is an important issue to consider from a public health perspective. Perhaps people in more stressful jobs should retire earlier.”
Measuring biomarkers across society could also give researchers a way of monitoring the impact of policy interventions. But to do that effectively will require a lot more data. While the ISER team’s findings suggest a link between inflammation, stress and poor health outcomes in the most disadvantaged sectors of society, the study is only a snapshot of biomarker levels in individuals of different ages at one point in time. What’s really needed is detailed, long-term research, monitoring and following people over decades as their lives change.
“If we have 30-year-olds with high CRP, we want to know what happens to them five years later,” says Bartley. “We need to study people over their whole life course to find out if that early high CRP reading is fixed, and does high CRP at age 30 condemn someone to get sicker faster later on – or does their health outcome change if they improve their situation and lower their stress levels?”
The challenge with this long-term approach is finding ways of measuring biomarkers in large numbers of people across the full spectrum of society. “It would be good if we could collect them by some electronic means, instead of having to stick needles in people for blood samples,” Bartley speculates. “There’s a lot of scope for improvements in technology such as mobile phones, in terms of understanding how society gets under the skin.”
The ISER study also highlights another striking issue: the general lack of research
focuses on people in midlife – a time when life paths can become entrenched.
“There are a lot of studies looking at older age groups because that’s when people get sick, and lots involving children because child development is interesting, but there’s not a lot going on in the middle of the age span,” Kumari says. “And yet we found the difference between biomarker levels was biggest in working age groups, where we have the least amount of data.
“Understanding the underlying biological pathways will help us to target what it is we should be focusing on. Our data suggest that it might be stress that we need to be thinking about, particularly for working-age people. But this is just the beginning – there’s still a lot to do.”
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