If you asked parents of school-age children for an example of a stressful day, shopping for shoes and new school kit in the dog days of August would be right up there at the top. You fight with your kids about what’s “suitable”, endure queue-jumping mothers from hell and spend a ridiculous amount of money while getting zero gratitude from anyone.

The curious thing about stress, however, is that someone, somewhere, will adore the frenetic chaos that is John Lewis’s uniform department in late August. We all react very differently to stress, with one person’s stress being another’s energiser. Understanding why this is so forms part of the work of a unique stress research facility in the Henry Wellcome laboratories for integrative neuroscience and endocrinology at the University of Bristol.

One of the biggest problems in researching stress is finding a way to standardise a stress response. The Bristol stress research team, led by Professor Stafford Lightman, have developed a physiological stress test to which we all react in a standard way because our response to it is automatic. It involves recording someone’s blood pressure and heart rate, and then getting them to breathe — for just four seconds — an air mix containing 35 per cent of carbon dioxide. Normal air contains 0.03 per cent of this gas. And, while making a programme, Stressed Out, on the science of stress for Radio 4, that’s what I found myself doing.

At the start my heartbeat was 54 beats a minute and my blood pressure a healthy 110/65. Although my head said I was safe, when I began to breathe that mixture, my body disagreed violently. It thought I was being suffocated. My blood pressure instantly shot through the roof, to 193/65. My face, apparently, took on an expression of horror, I felt sick, my heart felt as if it were racing (although it wasn’t) and a wave of panic engulfed me. It was horrible. But as I gulped normal air again, my blood pressure returned to 110/65 within a couple of minutes. The point of this test is not the initial response, which is normal, but what happens after. In those who are chronically stressed, the return to prior values is much slower. Long-term stress has blunted their response to acute stress.

The acute stress response generated by this test is good news. A bear in the woods or a dark shadow in an alleyway will prompt a flood of the stress hormones — first adrenalin and then cortisol — preparing you for a fight, flight or fright. Robert Sapolsky, a professor of biological sciences at Stanford University, summarised it: “Your body is turning off all the long-term building and repair projects. It’s do it tonight, if there is a tonight.” So blood pressure soars, enabling blood to be pumped at great speed to muscles for a quick getaway, energy stores are mobilised as glucose, you become more alert, the immune system is enhanced. It’s a wonderful adaptation should you come across a bear. “But too much of a good thing,” says Sapolsky, “and you’re in trouble.”

We have known for years that constant high levels of cortisol generated by stress take your body’s eye off the ball. Repairs aren’t done. Patrols for invaders aren’t sent out. You tire more easily. You can become depressed. Reproduction gets downgraded. The glucose and fatty acids on the loose in the bloodstream gum it up, increasing (along with high blood pressure) the risk of cardiovascular disease. And stress also makes body cells deaf to messages from the glucose-control hormone insulin, increasing the risk of diabetes. And there’s another big effect: the immune system is suppressed.

Recent work done at Bristol clearly demonstrates this, for instance, in the poor response of long-term carers to flu vaccines. Researchers have also turned their attention to the effect that chronic stress has on wound healing, in particular those with diabetic leg ulcers. If such an effect can be quantified, it may mean that interventions to alleviate stress may be the most effective way to prevent hard-to-heal ulcers ending in amputation.

But why are some people more affected by stress than others? “There are three main reasons,” says Lightman. “Our genes, our experiences in early life, and what’s happened to us recently.” We understand the latter. Bereavement, losing a job and divorce are all highly stressful events. Of great scientific interest are our stress “thermostats”, which switch our responses on and off again. Understanding how the “off” switch works is an important strand of the work in Bristol. The settings for our thermostats are partly inherited (our genes) but they can be reset during childhood and, indeed, during pregnancy. Work with animals suggests that emotional deprivation in early life causes heightened stress responses as adult animals. It’s likely that this is the case for people, too.

Resetting the stress thermostat in childhood is an important adaptation. It allows a child born into a difficult world to be constantly on the alert. But this alertness comes with a long-term price: heart disease, diabetes, obesity and depression. There are also behavioural implications of raised stress hormones, such as greater levels of violence and risk-taking.

There is now an enormous body of work from scientists suggesting that early life experience, low social status and lack of friends are the three main psychosocial risk factors leading to ill-health and premature death. All seem to be mediated through higher levels of the stress hormone cortisol. “Together these three things tell us about the stress associated with the quality of the social environment,” says Richard Wilkinson, the professor of social epidemiology at the University of Nottingham medical school.

Since we now have epidemic levels of cardiovascular disease and diabetes, does this indicate that we live in a much more stressful world? The answer is a resounding no. If anything, we live much less stressful lives than our forebears. “It’s a privilege to die from stress-related diseases,” says Sapolsky, explaining that it is the elimination of other causes of death such as infectious disease that is responsible for pushing lifestyle diseases to the top of the agenda.

It is the need to protect the body from adverse effects of chronic stress that drives the work at Bristol. “Removing the cause of stress is one solution,” says Lightman, but of course that isn’t always possible. “Understanding the pathways in stress responses means that you can design drug therapies to block their effect.”

Given that stress is causing so much disease, has it outlived its purpose? Is a stress response designed for sabre-tooth tigers over the top when running for a bus? Again, the answer is a resounding no. We have modern equivalents of bears and tigers in road accidents and bombs on the Tube. Our stress response continues to keep us safe in emergency. But we need to find ways of preventing its harmful effect. Hopefully, the work at Bristol and elsewhere will give us clues how to tame it in the future.

Stressed Out will be broadcast on Radio 4, September 7, at 9pm

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