Toru Nakamura,1,2
Stephan K. Schwander,3,*
Robert Donnelly,3
Felix Ortega,3
Fumiharu Togo,4
Gordon Broderick,5
Yoshiharu Yamamoto,6
Neil S. Cherniack,1,3,†
David Rapoport,7 and
Benjamin H. Natelson1,
Cytokines across the Night in Chronic Fatigue Syndrome with and without Fibromyalgia
Discussion
A major hypothesis for the cause of CFS is an immune dysfunction characterized by a general upregulation of proinflammatory cytokines.
This hypothesis is based, in part, on clinical reports that administration of proinflammatory cytokines in the treatment of disease in humans produces a flu-like syndrome resembling that of CFS (
26). However, there have been few empirical data supporting this hypothesized link between proinflammatory cytokines and CFS, and our own prior studies in CFS patients did not find any cytokine abnormalities (
15,
38).
The results of this study using nocturnal samples also do not support the hypothesis of an upregulated inflammatory immune system mediated by cytokines in the genesis of CFS. A similar conclusion has been reached in a study of a sample of patients with postinfectious fatigue (
32)...
...In summary, we designed this study to examine two alternative hypotheses: one, that CFS and FM are caused by increases in proinflammatory cytokines, and two, that CFS and FM are caused by disrupted sleep produced by increases in anti-inflammatory cytokines.
Since disparate results have come from studies sampling the blood once during the daytime, we decided to sample blood several times during the nighttime while subjects slept. We reduced variability by studying women with CFS alone or with CFS plus FM, at the same menstrual phase, and after excluding any subjects with current major depression.
Despite using these “pure” patient groups, we found evidence for a rather small elevation of one anti-inflammatory cytokine, IL-10, only in those patients with CFS alone, and in only one of three assays, the one quantifying cytokines in plasma. Obvious limitations of this study are the relatively small sample size and our focus on female patients only.
These data provide additional experimental evidence against the hypothesis that CFS is a manifestation of an upregulated proinflammatory state and leave open the role for anti-inflammatory cytokines in the genesis of CFS.