Subtropical Island
Senior Member (Voting Rights)
investigated which aspects of depression may predict changes in tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 over 4 weeks.
Methods
Forty-one patients with major depression diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), and 45 healthy controls were enrolled. Serum measurements of TNF-alpha and IL-6 were conducted at baseline and 4 weeks later. Psychometric measures included the assessment of cognitive-affective depressive symptoms and somatic symptoms during the last 7 days as well as somatic symptoms during the last 2 years.
Conclusion
The present study demonstrated that a history of somatoform symptoms may be important for predicting future changes in TNF-alpha in women with major depression.
Depression itself is considered to be a heterogeneous disorder. Current findings suggest that “cognitive” and “somatic” symptom dimensions are related in different ways to immune function and cardiovascular outcomes. Somatic symptoms have been shown to be better predictors of cardiovascular mortality and cardiac events in post-myocardial infarction patients and in patients with chronic heart failure (CHF).6–10Additionally, somatic but not cognitive-affective depressive symptoms have been related to cardiovascular risk factors such as decreased heart rate variability and reduced baroreflex sensitivity.11,12 Somatic symptoms (especially sleeping disorders) predict further depressive episodes better than cognitive-affective symptoms.13 Regarding immunological measures, Duivis et al demonstrated that somatic symptoms of depression and anxiety but not cognitive symptoms are associated with higher inflammatory levels of C-reactive protein (CRP), IL-6, and TNF-alpha in a population-based sample.14 In patients with major depression, increased levels of soluble interleukin-2 receptors (sIL-2R) were associated with higher severity ratings of somatic symptoms but not with cognitive-affective depressive symptoms.15
Trying to understand where depression usefully features here. Given the repeated statements that somatic (but not cognitive nor affective) symptoms are associated with things like cardiac events and higher levels of CRP, IL-6 and TNF-alpha, it seems more reasonable to identify the specific somatic symptoms which predict poor health outcomes and to ensure that a diagnosis of depression not prevent people (patients and researchers) from doing something about it.
But maybe I’m not reading it well?
Looks like a lot of evidence cited to demonstrate (or at least indicate) that cognitive-affective symptoms don’t mean much?
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