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An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways.

  [ 5 votes ]   [ 1 Comment ] • August 7, 2014

There is a significant 'comorbidity' between depression and myalgic encephalomyelitis/chronic fatigue syndrome (
ME/CFS). Depressive symptoms frequently occur during the course of ME/CFS. Fatigue and somatic symptoms (F&S), like pain, muscle tension, and a flu-like malaise, are key components of depression. At the same time, depression and ME/CFS show major clinical differences, which allow to discriminate them with a 100% accuracy.

This paper aims to review the shared pathways that underpin both disorders and the pathways that discriminate them. Numerous studies have shown that depression and 
ME/CFS are characterized by shared aberrations in inflammatory, oxidative and nitrosative (IO&NS) pathways, like systemic inflammation and its long-term sequels, including O&NS-induced damage to fatty acids, proteins and DNA; dysfunctional mitochondria; lowered antioxidant levels, like zinc and coenzyme Q10; autoimmune responses to neoepitopes formed by O&NS; lowered omega-3 polyunsaturated fatty acid levels; and increased translocation of gram-negative bacteria. Some IO&NS-related pathways, like the induction of indoleamine 2-3-dioxygenase, neurodegeneration and decreased neurogenesis, are more specific to depression, whereas other pathways, like the 2'-5' oligoadenylate synthetase/RNase L pathway, are specific to ME/CFS.

Most current animal models of depression, e.g. those induced by cytokines, are not reminiscent of human depression but reflect a mixture of depressive and F&S symptoms. The latter symptoms, sometimes called sickness behavior, differ from depression and 
ME/CFS because the former is a (sub)acute response to infection-induced pro-inflammatory cytokines that aims to enhance recovery, whereas the latter are characterized by long-term sequels in multiple IO&NS pathways. Depression and ME/CFS are not 'comorbid' disorders, but should be regarded as 'co-associated disorders' that are clinical manifestations of shared pathways.

Source: PubMed 

Copyright © 2010 Elsevier Inc. All rights reserved.

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Article Comments Post a Comment

Enlightened Research Abstract
Posted by: lacste
Aug 7, 2014
It seems the tide is moving in the right direction in regard to the tone and content of research pertaining to illnesses previously considered (and all too often still considered) somotoform disorders.

Research is pushing practitioners more and more in the direction that an integrative approach is necessary to deal with illnesses that affect both the central nervous system and the peripheral nervous system (including the large network of nerves throughout the digestive system). Especially, since as Dr. Julia Newton at Newcastle University points out the abnormalities may first begin in the peripheral nervous system.

This research abstract points out overlap between depression and ME/CFS that demonstrate inflammation in common pathways - suggesting why so many patients seem afflicted with both illnesses. However, the article points out that substantial research is able to clearly differentiate the two illnesses.
It is quite interesting to see both overlap and distinctions in the inflammatory pathways in the two illnesses.

Also, this is the first article I have seen to distinguish the inflammatory abnormalities between sickness behavior, on the one hand, and depression and ME/CFS on the other. Although I have seen a line of research to investigate the extent that sickness behavior (i.e. the lethargy one feels when fighting off an infection) is involved in ME/CFS, this is the first one I have found to distinguish the two.

I hope the research methodology is strong to back up this enlightened research abstract.
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