Several past studies have found a correlation between the presence of PTSD and the risk of multiple autoimmune diseases including rheumatoid arthritis, autoimmune thyroiditis, inflammatory bowel disease, multiple sclerosis, and psoriasis. There has also been suggestion that PTSD was associated with a significantly elevated risk of systemic lupus erythematosus (SLE).
PTSD is the result of severe and sustained stress which imbalances several internal functions in the body. It makes the ideal model to study the relationship between stress and autoimmunity. In a study of more than 50,000 women over 24 years, those with PTSD had a 184% increased risk of developing SLE.(1) Those who had sustained a significant and sustained psychological trauma had a similar increased risk even if they did not meet the diagnostic criteria of PTSD.
The mechanisms behind how stress may trigger autoimmunity are beginning to be defined. Humans do not actually have an inherent “stress mechanism” but rather have a danger response. When confronted with danger the fight or flight response is activated. It involves expression of large amounts of the stress hormone cortisol and activation of the sympathetic nervous system which raises blood pressure, heart rate and other functions to ready for either fight or flight. This served humans well in the early hostile world but has become injurious for modern humans.
Danger typically is short term. You fight and escape or out run the danger in a short period of time. At that point the body quickly resets operating in “rest, repair and digest” by lowering cortisol and activating the parasympathetic nervous system. Psychological stress tends to be chronic over long periods of time from a bad job, a bad relationship, chronic sickness of a loved one and other common life circumstances. The body activates the same danger response, but it then becomes ongoing.
The result of this chronic shift is thought to work on 2 mechanisms which are risk factors for autoimmune activation, inflammation and gut barrier breakdown/leaky gut. The high expression of the stress hormone cortisol increases the activity of T cells, immune cells that can cause inflammation.
Immune cells also have the task of cleaning up our old/dead cells. Fragments of those, however, should not cause antibody production against our cell components. With inflammation, immune cells are more active and more prone to making a mistake such as assuming self-tissue fragments are foreign causing antibody production.
The second mechanism by which stress increases the risk of immune reaction against self-tissue is that stress causes the gut barrier to weaken and let inflammatory bacterial toxins from the gut enter the system causing yet more inflammation.(2) The parasympathetic nervous system or that which activates “rest, digest and repair” maintains the integrity of the gut barrier structure. Dominance of the sympathetic nervous system which drives “fight or flight” over parasympathetic activity gradually lets the gut barrier breakdown.
Fortunately there are many good treatment modalities that help reset the body following stress. These include vagus nerve stimulation, photobiomodulation and heart rate variability biofeedback. The vagus nerve is the main parasympathetic communication between the body and the brain and electrical stimulation has been shown to increase vagal activation decreasing inflammation.
Unfortunately, life is associated with periods of very high stress. In some cases that is sustained over long periods increasing the risk of activation of autoimmunity. Humans have a tendency to underestimate the negative impact of psychosocial stress. Searching the PubMed database of biomedical research brings up over 28,000 studies concerning the negative health effects of stress including hypertension, heart disease, cancer and many more. Stress is not benign!