What is Myalgic Encephalomyelitis (ME)?

Myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome (CFS), is a complex and debilitating chronic illness characterized by profound fatigue that is not relieved by rest and is accompanied by a range of other symptoms. These symptoms can vary widely among individuals and may include:

  • Severe fatigue: Fatigue that is persistent, overwhelming, and not alleviated by rest.
  • Post-exertional malaise: Exacerbation of symptoms following physical or mental exertion, often lasting for days or weeks.
  • Unrefreshing sleep: Despite spending extended periods in bed, individuals with ME/CFS may wake up feeling unrefreshed and exhausted.
  • Cognitive dysfunction: Often referred to as “”brain fog,”” cognitive symptoms may include difficulties with concentration, memory, and processing information.
  • Muscle and joint pain: Widespread muscle pain, joint pain, and headaches are common symptoms experienced by many individuals with ME/CFS.
  • Orthostatic intolerance: Symptoms worsen upon standing, leading to dizziness, lightheadedness, and palpitations.
  • Sensitivity to light and noise: Individuals with ME/CFS may be hypersensitive to light, noise, and other sensory stimuli.
  • Gastrointestinal symptoms: Digestive issues such as nausea, bloating, and irritable bowel syndrome (IBS) are frequently reported.
  • Immune dysfunction: Some individuals with ME/CFS experience recurrent infections and flu-like symptoms, suggesting underlying immune system abnormalities.
  • Mood disturbances: Depression, anxiety, and other mood disorders are common comorbidities in individuals with ME/CFS.


The exact cause of ME/CFS is not fully understood, and it is likely that multiple factors contribute to its development. Possible triggers or predisposing factors may include viral infections, immune dysfunction, hormonal imbalances, genetic predisposition, environmental factors, and psychological stressors.


What is the relationship between ME/CFS and oxidative stress?

The relationship between myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome (CFS), and oxidative stress is an area of ongoing research, and while the precise mechanisms are not fully understood, there is evidence to suggest that oxidative stress may play a role in the pathophysiology of ME/CFS. Here’s how ME/CFS and oxidative stress are interconnected:


  • Mitochondrial Dysfunction: Mitochondria are the powerhouse of the cell, responsible for generating energy in the form of adenosine triphosphate (ATP). Dysfunction of mitochondria has been implicated in ME/CFS, leading to impaired energy production and increased production of reactive oxygen species (ROS). Mitochondrial dysfunction may result from genetic factors, viral infections, immune dysregulation, or environmental toxins. Increased ROS production contributes to oxidative stress and cellular damage, exacerbating symptoms of fatigue and other symptoms associated with ME/CFS.


  • Immune Activation: Immune dysregulation is a hallmark feature of ME/CFS, with evidence of chronic immune activation and inflammation. Immune cells, such as T cells, B cells, and macrophages, release pro-inflammatory cytokines and chemokines, which can stimulate the production of ROS and reactive nitrogen species (RNS) by activating the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme complex. Chronic immune activation and oxidative stress may perpetuate a vicious cycle of inflammation and cellular damage in ME/CFS.


  • Oxidative Damage: Increased levels of oxidative stress markers, such as lipid peroxidation products, protein carbonyls, and DNA damage, have been observed in individuals with ME/CFS. Oxidative damage to lipids, proteins, and nucleic acids can impair cellular function, disrupt signaling pathways, and contribute to mitochondrial dysfunction, inflammation, and neuroendocrine abnormalities associated with ME/CFS.


  • Antioxidant Defenses: To counteract the harmful effects of oxidative stress, cells have antioxidant defense mechanisms that scavenge ROS and protect against oxidative damage. However, in ME/CFS, the balance between ROS production and antioxidant defenses may be disrupted, leading to oxidative stress overload. Reduced levels of antioxidants, such as glutathione, superoxide dismutase (SOD), catalase, and glutathione peroxidase, have been reported in individuals with ME/CFS, further exacerbating oxidative damage and cellular dysfunction.


  • Symptom Severity: There is evidence to suggest that oxidative stress may correlate with symptom severity and disease progression in ME/CFS. Increased levels of oxidative stress markers have been associated with greater fatigue severity, cognitive dysfunction, pain, and functional impairment in individuals with ME/CFS.


Overall, oxidative stress appears to be involved in the pathophysiology of ME/CFS and may contribute to the development and persistence of symptoms associated with the illness.