Mitochondrial agents in the treatment of chronic fatigue syndrome: a 20-week, open-label, intervention trial

Chronic fatigue syndrome (CFS) is a prolonged multisystem illness, characterised by very poor stamina, delayed post-exertional fatigue, which adversely affects one’s functioning across numerous physical and mental domains. Current treatments for CFS include pharmacological (e.g. fluoxetine, rintatolimod, galantamine), psychological (e.g. cognitive behaviour therapy (CBT), adaptive pacing therapy), and lifestyle interventions. For many who remain in treatment, they continue to experience significant social, occupational, and functional impairment. Thus new treatment approaches are urgently needed. While significant fatigue remains a common complaint across numerous disorders, it is posited that CFS is related to metabolic dysfunction, mitochondrial dysfunction and impaired biogenesis, in turn related to oxidative stress and systemic inflammation. Mitochondria are structures within cells primarily responsible for energy generation, and are particularly active in oxygen-rich and highly energy dependent tissues, such as the brain. Recent research suggests that patients suffering from CFS may improve with the supplementation of mitochondrial nutrients and antioxidants. This supplementation may be associated with the reduction to mitochondrial membranes, restoring mitochondrial energy production, protecting cellular structures and enzymes from oxidative damage, and decreasing fatigue. Given that CFS is largely a heterogeneous illness associated with a complex and multifactorial aetiology, combined with the present state of available treatments, it is plausible that the introduction of a combination of metabolic therapies may have positive effects on mitochondrial dysfunction and lead to symptom improvement for CFS sufferers.