Myalgic Encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), and Chronic Fatigue (CF) are distinguished accurately: Results of supervised learning techniques applied on clinical and inflammatory data

Increased nuclear factor-κB and loss of p53 are key mechanisms in Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS)

“…Other more liberal criteria require the presence of idiopathic chronic fatigue [2,3]. Maes et al [4] found that Fukuda's criteria may be adequate to differentiate people with CFS from those with idiopathic chronic fatigue. However, the terms CFS and even chronic fatigue have been used to describe people with Myalgic Encephalomyelitis (ME).…”

“…However, the terms CFS and even chronic fatigue have been used to describe people with Myalgic Encephalomyelitis (ME). The diagnosis of CFS according to Fukuda's criteria [1] defines a heterogeneous population of individuals with chronic fatigue, of whom individuals with ME are a subset [4,5]. In fact, patients with ME/CFS according to Fukuda's criteria should be divided into those with post-exertional malaise (PEM; termed ME) and without PEM (termed CFS) [4].…”

“…The diagnosis of CFS according to Fukuda's criteria [1] defines a heterogeneous population of individuals with chronic fatigue, of whom individuals with ME are a subset [4,5]. In fact, patients with ME/CFS according to Fukuda's criteria should be divided into those with post-exertional malaise (PEM; termed ME) and without PEM (termed CFS) [4]. Thus, the use of the much wider criteria created by Sharpe et al [3] and Reeves et al [2], coupled with the mandatory exclusion of neurological signs and symptoms, produce heterogeneous study cohorts or cohorts where only few if any patients actually suffer from ME [6].…”

“…ME/CFS is an acquired neuro-immune disease [4,8,9] involving malfunctioning of the central nervous (CNS) [10][11][12] and immune system [4,[13][14][15][16]; pathologically dysfunctional impairments in cellular energy metabolism and ion transport mechanisms [17][18][19]; and abnormalities of the autonomic nervous and cardiovascular system [20][21][22]. Other findings indicate that ME may share basic immune pathophysiology with CFS but with additional PEM and significantly more immune disorders [4]. Marked cognitive and or physical fatigability following mental and physical activities are symptoms that typically occur in ME [8,9].…”

“…Previously, we have explained that activation of immunoinflammatory pathways, including increased levels of pro-inflammatory cytokines and cyclo-oxygenase 2, oxidative and nitrosative stress (O&NS) pathways and mitochondrial aberrations may explain ME/CFS symptoms, such as fatigue, malaise, sleep disorders, hyperalgesia and neurocognitive disorders [4,8,24]. Here we hypothesize that the symptoms of ME/CFS, such as fatigue and fatigability, and ME, such as PEM following mental and physical activities, may be caused by an interplay between intracellular signal molecules and mitochondrial dysfunction.…”