A bereaved man suffers a heart attack. An unemployed graduate is plagued by eczema. A divorced woman develops high blood pressure. Are these situations connected… or mere coincidences?
Of all the influences on our health and well-being, chronic stress is among the most ubiquitous. And because the misery of stress is often experienced as much in the body as the mind – tiredness, headaches, tense muscles and the like – common sense tells us that psychological stress leaves us prone to physical illness.
While most people outside medicine happily accept this view, it has been viewed with a much greater degree of scepticism within the field. And that’s partly on account of the difficulty in proving exactly how stress might work, not to mention understanding why some people succumb to it but others do not. There are plenty of ideas and intuitive hunches, but rather less incontestable evidence.
But a recent finding from a team led by Sheldon Cohen at Carnegie Mellon University in Pittsburgh could finally have revealed a link, offering perhaps the best evidence so far of how stress operates at the biological level. What Cohen thinks stress is doing – a surprise, perhaps, to many of us – is undermining the body’s capacity to deal with inflammation.
It’s not the only possible stress mechanism; nor is it likely to be the whole truth. But the work represents an important step in understanding the mechanism of stress. It not only adds plausibility to claims about its role in promoting ill health, it’s a mechanism that fellow researchers find plausible and convincing.
Seeking proof
Cohen has been working on stress for 30 years, and despite a fair amount of epidemiological evidence accumulated during this time, he and other professionals have been cautious about accepting a link without firm evidence about a possible mechanism. In a 2007 review of psychological stress published in the Journal of the American Medical Association, Cohen said: “Despite widespread public belief that psychological stress leads to disease, the biomedical community remains [sceptical] of this conclusion.” But speaking now, little more than half a decade later, he takes a rather more positive view. There’s been a shift, he says. A plausible mechanism to explain the effects stress will reinforce it.
The issue is how you design an experiment that proves any ill-effects are caused by stress. Up until now, the real hard evidence has had to come from animal studies. “With humans you can bring them to a lab and expose them to stress, and you can get elevations in heart rate and blood pressure,” he says. Physiological changes, in other words, that often play a role in disease. But, for ethical reasons what you can’t do is give human subjects an illness and see if stress makes it worse.
Well, not quite. An upper respiratory tract infection like a cold is an illness, but it is mild enough to make it ethically acceptable to break the rule, and do human experiments.
Cohen began the research that propelled him to the forefront of this field back in the early 1990s. His approach, originally developed at Britain’s (now defunct) Common Cold Research Unit, relied on giving measured doses of cold virus to volunteers and checking to see if they developed symptoms. Before infecting his subjects with the virus Cohen rated their stress levels using standard questionnaires. The higher his subjects’ stress scores, he found, the greater the likelihood they would catch a cold.
Further studies showed that the principal enduring and stressful life events that rendered people susceptible to the cold virus were problems with family and friends, overwork, and unemployment. The longer these events lasted, the greater the susceptibility.
