Your doctor needs to look at this because TNF is referred to, what the magical drug etanercept was supposed to fix.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=126459&CultureCode=en
A new study published in the current issue of Psychotherapy and
Psychosomatics has examined the role of inflammation in chronic fatigue
syndrome, a disorder that affects many people and does not seem to have
an explanation that is likely to yield satisfactory treatment.
Depression is an inflammatory disorder while many authors declare
myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) to be a
functional disorder. The aim of the present study was to compare
inflammatory and cell-mediated immune (CMI) responses between depression
and ME/CFS. The investigators measured two proinflammatory cytokines
(PICs) in plasma, interleukin-1 (IL-1) and tumor necrosis factor-α
(TNF-α), with enzyme-linked immunosorbent assays, and serum neopterin
with a radioimmunoassay in controls, ME/CFS and depressive patients.
Plasma PICs were significantly higher in ME/CFS than in depression and
higher in both patient groups than in controls. Increased PIC levels in
depression were attributable to the presence of fatigue and
physio-somatic symptoms. Serum neopterin did not differ significantly
between depression and ME/CFS but was higher in both patient groups than
in controls.
The significant positive correlations between neopterin and either
IL-1 or TNF-α were significantly greater in depression than in ME/CFS.
Since PICs cause depression-like behaviors and fatigue/malaise, the
investigators suggest that inflammation may play a role in the
pathophysiology of ME/CFS and depression. Increased neopterin also seems
to contribute to the pathophysiology of both disorders. This study has
detected a shared ‘pathway phenotype’, i.e. disorders in inflammatory
and CMI pathways, which underpins both ME/CFS and depression and,
therefore, may explain the co-occurrence of both disorders.
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