Issue 36 / 21 September 2015

THE use of anti-inflammatories to treat depression, comorbidity of non-communicable diseases, stress as a trigger for diabetes, omega-3 fatty acid supplementation for heart disease, the role of physical activity in preventing telomere shortening — what do all these have in common?
Is it possible to link all these disparate findings together in a single narrative?
Twenty years ago, a model was proposed with the potential to integrate these diverse observations. The allostatic load model provides a useful narrative to understand how non-communicable diseases like diabetes, depression and stroke develop, and how they may best be treated.
At the heart of the allostatic load model is the notion of stress.
It’s helpful to think of three broad types of stress:
  • Background stress, arising from general life circumstances, such as having a subordinate job with little personal autonomy or experiencing poverty
  • Specific life events, such as separation and divorce, relationship problems, changing jobs or homes
  • Physical stresses from exposure to viruses and bacteria, environmental toxins and injuries.
We can quantify background stress using measures of socioeconomic status, such as income, education or postcode. Life stresses are often measured using inventories such as the Holmes–Rahe scale, which allocate points for stressors, with a maximum of 100 (death of a spouse) and a minimum of 11 (minor law violations, eg, jay walking). Even good events can be stressful — holidays score 12 points and an outstanding personal achievement 28.
Physical stresses can be quantified by common clinical measures — opportunistic infections, white blood cell counts, the presence of viruses.
The body reacts to stress via the systemic inflammatory response, where immune cells and agents are released, fats and sugars are released into the bloodstream, heart rate increases, blood pressure rises, clotting agents are elevated to prevent potential blood loss and stress hormones make us hypervigilant.
In the short run, the stress response is adaptive. However, chronic stress or poor recovery from intermittent stressors can lead to chronic low-grade inflammation, and this can be very harmful.
Chronic stress is often measured using levels of inflammatory agents such as C-reactive protein or interleukin-6.
Stress, perhaps via inflammation, is associated with a shortening of telomeres. Over time, telomeres get shorter and when they become too short, chromosomes become “frayed” and errors occur when they are reproduced. Telomere length has proved to be a good marker of biological age — older people tend to have shorter telomeres.
Chronic low-grade stress will increase the body’s allostatic load, which includes risk factors for non-communicable diseases such as blood lipids, waist circumference and blood sugar levels. High allostatic load will eventually translate into overt disease — persistently high blood sugar leads to diabetes; persistently high blood pressure affects the heart; high blood fats lead to atherosclerotic plaques; high levels of clotting agents increase the risk of stroke.
Chronic low-grade inflammation is also associated, through mechanisms which are not yet entirely clear, with depression, asthma and perhaps even osteoporosis and oral disease.
The good news is that lifestyle behaviours such as physical activity, sleep, diet and social interactions can buffer or exacerbate the effects of stress, and increase individual resilience. Physical activity, 7‒8 hours sleep a night and certain dietary patterns dampen the inflammatory response and preserve telomere length. However, excessive sitting, too little or too much sleep, and diets high in refined foods are pro-inflammatory.
While an obvious response is to try to minimise stress (eg, through more equal societies, greater autonomy in employment, minimising stressful life events, reducing exposure to pathogens), this may not always be the optimal route. Physical activity, for example, is a stressor which produces an inflammatory response.
Clearly, lifestyle behaviours which dampen inflammatory responses are important. This should all be familiar advice: eat lots of fruit, vegetables and whole grains, and minimise refined and fatty foods; get at least 30 minutes of physical activity five times a week; get enough sleep; and minimise sitting within reason. One felicitous finding is that wine and coffee are good for diabetes: it’s not all self-denial.
There are also encouraging findings for studies using anti-inflammatory drugs for treating depression and diabetes.
The allostatic load theory is not a done deal, but studies have been supportive. At the very least, the lessons from an allostatic load model of treatment will certainly do no harm. And who could argue against a cup of coffee, a glass of wine and a good sleep?
Professor Tim Olds is a professor of behavioural epidemiology at the School of Health Sciences, University of South Australia.

One thought on “Tim Olds: Stress effects

  1. Catherine Treece says:

    Nice article. With regard to physical activity as stressor, there is actually some interesting nuance on this which is good news.  Besides such obvious differences as between moderate vs extreme exertion or between exertion relative to fitness  level, there is some evidence that otherwise proinflamatory cytokines like IL-6 when produced by working muscle functions differently and is anti-inflammatory.  Needless to same the same goes for increases in stress hormones in the short  term vs the longterm in the context of intentional exertion/exercise.  

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