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Stressing Out Over Stress

The vicious circle of stress and inflammation. Or not.




It has been shown that, in patients with known rheumatoid arthritis (RA), stress can have pro-inflammatory effects by activating the immune system. However, what is not known is if stress levels also promote inflammation during the development of RA in a given patient.
A clinical study, the results of which were recently published in “Arthritis Research & Therapy,” examined whether the psychological stress response was increased in patients with clinically concerning joint pain (and when joint pain is discussed here, it is joint pain without the swelling seen in active RA), and if this joint pain was indeed associated with inflammation at presentation, and eventually with progression to clinical arthritis.
The researchers studied 241 patients with significant joint pain.  Psychological stress was measured by the Mental Health Inventory (MHI-5) and the Perceived Stress Scale (PSS-10) at first presentation and during follow-up visits. Systemic inflammation was measured by a blood test, and joint inflammation was assessed by magnetic resonance imaging (MRI) of wrist, finger, and toe joints.
In some ways, the results were expected and unexpected: Psychological stress was not increased in the phase of joint pain, raised at the time of diagnosis of RA (when you would see joint swelling and warmth), and decreased thereafter. The lack of an association with inflammation in patients with joint pain and this temporal relationship, argue against psychological stress having a significant contribution to progression from “simply” joint pain to an active inflammatory arthritis. 
This temporal relationship, as well as the lack of an association of stress with local or systemic inflammation in those patients dealing with joint pain only (and not concomitant swelling) may suggest that in this very early disease phase, when disease chronicity has not yet been established, stress may have no significant impact on the inflammatory response; this seems to make one conclude that stress does not mediate the progression from simple joint pain to clinical arthritis.
Although further studies on the association of stress and inflammation in pre-RA are required, the vicious circle of stress and inflammation as observed in patients with established RA was not yet observed in these so-called pre-RA patients.
Is this perhaps because individuals who know they have a chronic disease suffer a higher and more persistent burden of stress, which in turn has more of an impact on the body?

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