Stress, depression and fibromyalgia – linked by IL-8

Fibromyalgia Stress Depression - Unhappy Face Image

Increased IL-8 production in response to stress increases the risk of disease

Dysregulation of the inflammatory response system that results in excess pro-inflammatory cytokine production, especially of IL-8, may contribute to the onset of fibromyalgia.

The study briefly summarized below is of interest because:

  • They identify a problem of the “innate inflammatory pathway” (aka the “inflammatory response system”) as the most likely explanation for the observed association between stress and a higher incidence of disease.
  • They specifically observed that an increase in IL-8 in response to stress increased the chance of disease.
  • They most interestingly observed that, with perceived social support, IL-8 did not increase in response to stress, or that such an increase was diminished.
  • The relationship between stress, risk of disease and cytokine elevation was not observed for IL-1, IL-6 or TNF.
  • IL-8 elevation was further associated with symptoms of depression.
  • The study suggests an increased risk for inflammatory conditions. While fibromyalgia may not be associated with gross inflammation, an elevation in pro-inflammatory cytokines is associated with inflammation. Indeed, the suggestion that such an increase in pro-inflammatory cytokines increases the risk of overt inflammatory disease is of particular interest, as it provides a possible explanation for the frequent association of fibromyalgia (a supposedly non-inflammatory condition) with conditions that are obviously inflammatory, such as rheumatoid arthritis and lupus.

February, 2007

Stimulated production of interleukin-8 covaries with psychosocial risk factors for inflammatory disease among middle-aged community volunteers.

Summary of the Abstract

Psychosocial factors such as chronic stress are increasingly associated with greater vulnerability to inflammatory disease, but the mechanism of this effect remains unclear.

One possibility is that these psychosocial characteristics are associated with activation of innate inflammatory pathways.

The relationship between psychosocial risk factors and the pro-inflammatory cytokines IL-1, IL-6, TNF, and IL-8 was explored.

A positive relationship was observed between the level of IL-8 production, symptoms of depression and perceived stress. However, with perceived social support, IL-8 levels decreased, or did not increase as much.

No significant associations between psychosocial factors and IL-1, IL-6 or TNF were observed.

These findings suggest that those at greatest risk for developing inflammatory disease are those whose IL-8 production increases most substantially in response to psychosocial factors such as stress.


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