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.
ME/CFS and depression are discriminated from each other by increased PICs in ME/CFS and differences in the immune cell communication networks.
Psychotherapy and Psychosomatics