Chronic psychological stress is associated with the body losing its ability to regulate the 
inflammatory response, a research team led by Carnegie Mellon University’s Sheldon Cohen has found.
Stress wreaks havoc on the mind and body. Psychological stress is associated with greater risk for depression, heart disease and infectious diseases. But, until now, it has not been clear exactly how stress influences disease and health.
Proceedings of the National Academy of Sciences has published a research that shows for the first time that the effects of psychological stress on the body’s ability to regulate inflammation can promote the development and progression of disease.
Cohen, the Robert E. Doherty Professor of Psychology within CMU’s Dietrich College of Humanities and Social Sciences, says, “Inflammation is partly regulated by the hormone cortisol and when cortisol is not allowed to serve this function, inflammation can get out of control.”
To regulate the inflammatory response, prolonged intensive stress alters the effectiveness of cortisol, Cohen argued, because it decreases tissue sensitivity to the hormone. Specifically, immune cells become insensitive to cortisol’s regulatory effect. Runaway inflammation, in turn, is thought to promote the development and progression of many diseases.
An earlier groundbreaking by Cohen showed that people suffering from psychological stress are more susceptible to developing common colds. He used the common cold as the model for testing his theory.
Symptoms are not caused by the virus during common cold, but they are instead a side effect of the inflammatory response that is triggered as part of the body’s effort to fight infection.
After completing an intensive stress interview, in Cohen’s first study, two hundred and seventy six healthy adults were exposed to a virus that causes the common cold. They were monitored in quarantine for five days for signs of infection and illness.
Those with the inability to regulate the inflammatory response, in turn, were more likely to develop colds when exposed to the virus.
Seventy nine healthy participants were assessed, in the second study, for their ability to regulate the inflammatory response and then exposed to a cold virus and monitored for the production of pro-inflammatory cytokines, the chemical messengers that trigger inflammation.
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