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
