Will Stress Lead to Autoimmune Disease?
There appears to be a correlation between stress and later developments.
Posted Jun 26, 2018
A worrisome report from a group of Icelandic scientists linking stress to autoimmune disorders appeared in a recent edition of JAMA. The media alerted us to their findings in terms that were, well, stressful: If, or more realistically when, we experience severe stress, we will be increasing the likelihood of developing diseases ranging from thyroid to hair-loss disorders. This report resonated with me, as I did develop an autoimmune skin disorder at an age when it was rare to show the first symptoms.
My physician asked whether I had been stressed earlier in the year. The answer was yes. My stress was due to worry and sorrow over a close friend’s diagnosis of a terminal disease. Would I have been “immune” from this autoimmune skin problem if the year had been less stressful? The media description of the results of the study would have you believe it to be so. An acquaintance told me about her son who is working an impossible number of hours as a first-year associate in a large law firm. “He is so stressed,” she told me, “that I am worried he will develop some awful disease.” And she quoted from a news release about the study to me:
The study looked through medical records of more than 100,000 Swedish adults who had been diagnosed with stress-related psychiatric disorders, the medical records of 126,652 siblings of these patients and 1.1 million unrelated individuals. The two latter groups had no stress-related disorders. Forty percent of those with stress-related psychiatric disorders were male and their average age, 41.
What is striking about their results is that over a 10-year follow-up period, a significantly larger number of individuals who had a stress-related psychiatric disorder were diagnosed with an autoimmune disease compared to the other two groups. Some of the diseases included Addison’s disease, rheumatoid arthritis, psoriasis, multiple sclerosis (M.S.), Crohn’s and celiac disease. Also, the risk for developing a particular disease differed. For example, there was a higher risk for celiac disease than rheumatoid arthritis.
Does this mean that a stress-filled year or short-lived acute stress will lead to a lifetime struggle with an autoimmune disease such as M.S.? The answer is no. To begin with, the stress is not simply stress; it is a diagnosed psychiatric disorder. Post-traumatic stress disorder, acute stress reaction, and adjustment disorders are listed by the authors as associated with increased risk for subsequent autoimmune disease. Being stuck in a two-hour traffic jam on the way home from work is very stressful but unlikely to cause the development of the skin lesions associated with psoriasis.
Moreover, as the authors point out (despite the hype in the media), “The relatively modest differences in the incidence rates of autoimmune disease between the exposed and unexposed,” (i.e. stressed and non-stress disordered individuals) “...should not lead to special monitoring of people who have been diagnosed with a stress disorder.”
But this conclusion still leaves the question as to why there should be a connection, even a weak one, between PTSD and M.S. or thyroid disease. Changes in cortisol levels, changes in pro-inflammatory cytokine levels, or an overly active inflammatory response/immune system are put forth to attempt to understand the process leading to the disease. But no workable answer is available yet.
What is so sad about the study results, however, is that those who have a stress-related disorder, such as PTSD, which in itself significantly affects quality of life, might then have to endure many decades of another disease that compounds the diminished quality of life. However, the report found that antidepressant treatment for PTSD reduced the risk of an autoimmune disease. Thus treating the stress disorder may be the answer to preventing another lifetime disorder from developing.
“Association of Stress-Related Disorders With Subsequent Autoimmune Disease,” Song, H., Fang, F., Tomasson, G., et al, JAMA 2018; 319:2388-2319