Chronic Fatigue
Chronic fatigue syndrome (CFS) is a complex neurological disorder associated with persistent, overwhelming fatigue that affects > 3% of the population in Western countries and is more prevalent in women (
Griffith and Zarrouf, 2008).
Diagnostic criteria include severe, persistent fatigue for at least 6 months, exclusion of other medical disorders, and observation of at least four minor symptoms, including impaired memory, nausea, extreme post-exertion fatigue, headaches, muscle pain, sore throat, and poor sleep (
Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome et al., 2015).
There remains a lack of treatment and diagnostics tools for CFS, although glucocorticoids have been used (
McKenzie et al., 2000).
Bone loss and increased fracture risk have been reported in individuals with CFS, independent of glucocorticoid use. Hoskin et al. found that hip BMD was approximately 7% lower in women with CFS (
Hoskin et al., 2006). A prospective study reported a 1.16-fold increased risk of fracture in the CFS cohort without osteoporosis compared to the non-CFS cohort (
Chen C.-S. et al., 2014).
However, no mechanistic insights were provided in these studies. Other studies have reported that IGF-1 levels are altered in CFS patients (
Buchwald et al., 1996;
Berwaerts et al., 1998;
Cleare et al., 2000;
Nijs et al., 2003). IGF-1 is essential for osteoblast proliferation, thus impaired secretion could lead to bone loss.
Studies are needed to further characterize those CFS patients with low serum IGF-1 to determine if these subgroups have increased fracture risk compared to CFS patients with normal or high levels of IGF-1. High prevalence of mycoplasma infections has also been reported in CFS patients (
Choppa et al., 1998;
Nasralla et al., 1999), which can stimulate macrophage activation and release of pro-inflammatory cytokines that enhance osteoclast activity.
M. fermentans has been shown to produce 2-kDa macrophage-activating lipopeptide (MALP-2), which stimulates macrophages and bone resorption in a dose-dependent manner and is increased with CFS (
Piec et al., 1999). Thus, chronic fatigue may induce bone loss or increase fracture risk through increased inflammation and/or dysregulation of growth factors.
