|June 19, 2014||
Depression, Inflammation and Pain…The Clinical Link to Success
Article presented by Labrix Clinical Services, LLC
In clinical practice we routinely work with patients who are depressed, and also suffering from
inflammation frequently coupled with life altering pain. While an individual patient may present with a
single concern, exploration of their overall chemistry often reveals multiple comorbid variables.
Depression and inflammation are strongly correlated, as demonstrated by a 2013 peerreviewed
report. The clinical findings of this report revealed significantly higher inflammatory index scores (a
composite score including the inflammatory markers tumor necrosis factorα (TNFα), interleukin6 (IL
6), interleukin10 (IL10), and Creactive protein (CRP)) in individuals with major depressive disorder
(MDD) who attempt or complete suicide when compared to both controls and patients with MDD and
lower suicidal ideation.
Often thought of as affecting cognition and mood, depressive symptoms may manifest somatically as
pain in some individuals and, as with suicidal ideation, may be linked to inflammation. A 2013 study
examining participants with metabolic syndrome correlated the increased leptin levels seen in
metabolic syndrome with somatic depressive symptoms but not total or cognitive depressive
symptoms. The conclusion that leptin is independently associated with somatic depressive symptoms
in patients with metabolic syndrome suggests that depression can hurt, independent of the patient’s
state of mind.
As practitioners, we can address the interrelationship among depression, inflammation and pain not
only with our typical hormonal, dietary and lifestyle interventions but also with neurotransmitter
assessment and support. Often thought of as the main moodregulating neurotransmitter, serotonin
support may be key for many patients in this population. Proinflammatory cytokines including IL6 and
IL10, among others, acutely stimulate central serotonin neurotransmission. Of particular note here is
interferon gamma (IFNγ) and its relationship with serotonin. IFN γ reduces serotonin production by
stimulating the enzyme indoleamine 2,3dioxygenase (IDO), which converts tryptophan into
kynurenine. Overstimulation of IDO leads to depletion of tryptophan and, therefore, to reduced
synthesis of serotonin.
In what other ways can supporting neurotransmitter balance benefit our patients with depression,
inflammation and pain? How do neurotransmitter imbalances beyond serotonin affect these patients?
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