Dr. Sheldon Cohen‘s keynote presentation at the 8th International Congress of Behavioral Medicine was published in International Journal of Behavioral Medicine (2005 Vol 12 No 3, 123-131).
Cohen summarized 20 years of research on psychosocial influences on infection susceptibility.
Cohen also debunks these pervasive myths of stress and disease:
- Myth: Infectious disease-causing agents is wholly responsible for causing infectious disease.
- Myth: Stress suppresses the immune system, which makes us susceptible to infections and disease.
- Myth: Stress overstimulates cortisol production, which leads to susceptibility to disease.
According to Cohen’s article, infectious disease-causing agents are not sufficient causative agents for disease. Our immune system’s modulating responses against viruses in our body determine whether we become infected.
We would also assume that health-related behaviors like smoking, alcohol consumption, sleep, exercise, and diet contributed to disease susceptibility. Cohen has observed that these behaviors were independent of susceptibility to the common cold across five different strains of viruses (including 3 rhinovirus types).
Stress “type” matters – and Cohen’s work suggested these stress makes one more susceptible to disease:
- Enduring (1 month or longer) work-related problems (such as under- or unemployment)
- Enduring interpersonal problems with family and friends
If you interpret the first item as “work” and second as “life”, as I did, then you’d see how I came to view this as “work-life imbalance can make us sick.”
In studies of human subjects exposed to high levels of stress, there is evidence that acute stress does increase cortisol levels. However, under conditions of chronic stress, Cohen found that cortisol levels were not correlates of disease susceptibility, and in fact, the group with high levels of stress had actually lower levels of cortisol (I guess that flushes the premise of cortisol-based health supplement claims down the toilet). Our bodies’s feedback mechanisms would downregulate cortisol release when we reach saturation level. On the other hand, interleukin-6 (IL-6) levels were abnormally high in the chronically stressed group.
This increased IL-6 production triggers a proinflammatory response that allows disease-causing agents like viruses to get an edge over our immune response. In a way, disease-causing agents simply “show” that an immune system has become dysregulated, rather than causing immune dysregulation.
What I found most interesting was the correlation of increased social integration and effect on stress. When the group with high levels of stress had strong social integration like being part of a strong social support group, this social support acts as a “stress-buffer” and “protecting people (and monkeys) against potential pathogenic influences of stress.”