Coenzyme Q10 As a Modulator of Mitochondrial Dysfunction and Maladaptive Stress Responses in Chronic Fatigue Syndrome

Myalgic encephalomyelitis/Chronic fatigue syndrome (ME/CFS) is a debilitating and complex disorder. It is characterized by extreme mental and physical fatigue, and it is a controversial illness of unclear medical aetiology making diagnosis and treatment challenging. The condition is often precipitated by psychological or physical strain and stress, including infections. It is believed to be perpetuated by personality/behavioural factors and inappropriate coping mechanisms, but also with a growing realisation that biological mechanisms, like a congenital vulnerability may play an important role in predisposing to the symptoms. This primary psychosocial model for ME/CFS is the medical rationale for treating ME/CFS patients with a combination of cognitive behavioural therapy and graded exercise therapy sometimes in combination with medical treatment, mostly anti-depressant medicine. Recent research results have questioned the validity of the psychosocial model for ME/CFS, and argued that chronic fatigue is mainly a clinical expression of mitochondrial dysfunction, and that diagnostics and treatment consequently should be directed towards targeting mitochondrial pathways.
In this chapter we review the increasing evidence for mitochondrial dysfunction in ME/CFS, and focus on the relationship between the autonomic nervous system and mitochondria. We discuss the known molecular triggers and mechanisms that may cause mitochondrial dysfunction, with special focus on the role that coenzyme Q10 (CoQ10) may play in the acquired mitochondrial dysfunction and in the clinical expression of fatigue and exerciseinduced malaise.