Abstract The full article is behind a paywall. Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune…
CFS individuals analyzed in this study show no differences in B-cell compartment, skewed NK cells and poorly responsive T cells.
The observed immunological defaults do not provide any causative link to the illness, but could explain some of the symptoms and in particular the poor control of viral infections reported in these individuals. Some of these biomarkers may be useful for the characterization of CFS. (But you have to distinguiesh between ME, CFS ,or both).
Abstract Myalgic encephalomyelitis (ME, also called Chronic Fatigue Syndrome), a common disease with chronic fatigability, cognitive dysfunction and myalgia of unknown etiology, often starts with an infection. The chaperonin human heat shock protein 60 (HSP60) occurs in mitochondria and in bacteria, is highly conserved, antigenic and a major autoantigen. The anti-HSP60 humoral (IgG and IgM)…
43 Patients and 36 controls from Belgium and Norway were included in the study. Gut flora composition differed between people from different geographical origins. Significant alterations of gut microbiota composition were observed in patients.
This is relevant because 70% of all immune cells are located in the gastro-intestinal tract. Increased intestinal permeability may explain the systemic inflammatory situation in CFS.
Excess d-lactic acid production could contribute to mitochondrial dysfunction, but also to neurocognitive impairments in patients, since d-lactic acidosis is known to affect CNS function.
The predominance of women among patients, the fact that disease symptoms change upon e.g. puberty, pregnancy and menopause, has long suggested an involvement of hormones in ME/CFS. ER β, the preferred receptor of equol, is down-regulated in patients.
Disruption of estrogen signaling is consistent with some dysfunctions observed in ME/CFS. It could be related, for instance, with immune dysregulation since isoflavones, and more specifically equol, induce expression of antioxidant enzymes, and exert an anti-inflammatory action. Another potentially relevant aspect of phytoestrogens and their metabolites is their capacity to regulate vitamin D receptor activity, and vitamin D synthesis. The vitamin D system is critical for maintenance of gut mucosal immunity.Vitamin D has also been shown to modulate some processes that are critical for prevention of mucosal inflammation. One of the things not known yet is if the altered gut microbiota are cause or result of CFS.
Very long and technical article. 22 patients and 30 healthy controls were tested for certain cells that are part of the immune system. They found an unaffected B-cell compartment, a biased NK-cell phenotype and a poorly responsive T-cell compartment as the main immune features of ME/CFS affected individuals. The striking down modulation of T cell mediated immunity may help to understand intercurrent viral infections in CFS.
Researchers found that both CFS/fibromyalgia patients have low Coenzyme Q10 levels and low ATP levels, and increased levels of lipid peroxidation (which is an indicator for damage caused by oxidative stress).
In addition fibromyalgia patients had low levels of two mitochondrial enzymes and a mitochondrial protein, and reduced levels of mitochondrial DNA content, while all of those were normal in CFS patients. Therefor mitochondrial dysfunction-dependent events could be a biomarker to distinguish between FM and CFS.
Positive autoimmune reactions against serotonin were significantly higher in CFIDS patients than controls.
Patients with serotonin( 5-HT ) autoimmune activity displayed higher TNFα, IL-1 and neopterin and increased IgA responses against LPS of commensal bacteria than those without 5-HT autoimmune activity. Anti-5-HT antibody positivity was significantly associated with increased scores on hyperalgesia, fatigue, neurocognitive and autonomic symptoms, sadness and a flu-like malaise.
Researchers found evidence of altered sympathetic-neural and sympathetic adrenomedulla reactivity in CFS.
Exercise stress revealed a subtle catecholaminergic hyporeactivity in CFS patients.
Researchers were able to differentiate patients with FM from those with osteoarthritis (OA) and rheumatoid arthritis (RA), and to identify molecular species associated with the spectral patterns.
They demonstrated the ability of IRMS to achieve reliable resolution of unique spectral patterns specific to FM.
Metabolomic analysis revealed that RA and OA groups were metabolically similar, whereas biochemical differences were identified in the FM that were quite distinctive from those found in the other two groups.
Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we use the more general term “neuromuscular strain.”
Neuromuscular restrictions are common in CFS, and many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination.
In this paper we submit that neuromuscular strain is a previously unappreciated peripheral source of sensitizing input to the nervous system, and that it contributes to the pathogenesis of CFS symptoms, including cognitive dysfunction.