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Stress & Autoimmunity


Probably the first mention of linking stress to disease was the Greek physician Hippocrates (460-357 BC), who stated that to prevent an asthma attack ‘the asthmatic should guard himself against his own anger’.

Stress is a psychophysiological reaction, a 'fight' or flight' response to ensure survival.  Acute stress causes the release of catecholamines (eg adrenaline) and glucocorticoids (eg cortisol) from the adrenal glands and activates inflammatory pathways to protect the individual in the short-term.  However, prolonged stress can exacerbate chronic inflammation and risk Autoimmunity especially in genetically susceptible people.  Stressors are generally known as mental and emotional but physical stressors and toxic chemical stressors can also add to a persons stress burden.

There is much evidence linking stress to Autoimmune and inflammatory diseases, particularly in genetically susceptible people.  Epidemiological findings suggest childhood traumatic stress increased the likelihood of hospitalisation with a diagnosed Autoimmune disease decades into adulthood.  Retrospective studies observe most patients suffering from Autoimmune diseases report uncommon emotional stress before disease onset.  Studies on active duty military personnel with PTSD show an elevated risk of a range of Autoimmune diseases. Accumulative life time, length, and frequency of exposure to stress certainly play pivotal roles on the individuals pathophysiology to Autoimmune disease.  A vicious cycle also exists where living with a long term Autoimmune disease may exacerbate stress in patients.  Studies suggest stress management can benefit Autoimmune patients. 


There is a bi-directional communication between the nervous system, the immune system and the endocrine system.  Neuroendocrine hormones triggered during stress may lead to immune dysregulation or to altered or amplified cytokine production.  Research suggests that stress promotes T-helper 2 (Th2) cell differentiation, tipping the TH1/TH2 balance and reducing the number of T-helper 1 (Th1) cells.  This may decrease host defence and increase viral susceptibility.  It is well documented that viruses are implicated as a trigger for Autoimmune diseases.  Latent viral reactivation is certainly linked to stress for example the varicella-zoster virus (shingles). 

Interestingly glucocorticoids (eg cortisol) have been described to dampen the immune response, they weaken inflammation signalling pathways such as NFKB and have immunosuppressive effects.  Therefore stress in normal small doses can be anti-inflammatory.  However, chronic stress can cause stress receptors to stop working and hence these ant-inflammatory pathways are no longer triggered and chronic inflammation can result.   Glucocorticoids are often used to control Autoimmune disorders in the form of steroids such as prednisolone due to their inflammation dampening effects.  

The role of stress on the various aspects of the immune system

'During the stress response, catecholamines and glucocorticoids are released from locus coeruleus and adrenal gland. These biomolecules exert control over various immune cells in the innate and adaptive arms of the immune system, thereby altering the cytokine profile released. The increase of IL-4 promotes T-helper 2 (Th2) cell differentiation, while the decrease in IL-12 and the increased IL-10 production reduce the number of T-helper 1 (Th1) cells'.

Reference: (Kassem Sharif et al., 2018)

Role of stress on Immune system
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