Mitochondrial Dysfunction

ME/CFS has been identified as having issues with energy production, which have mainly been associated with problems in the mitochondria. These little organelles are in charge of creating the majority of the body’s energy through the production of adenosine triphosphate, also known as ATP.
The mitochondria are known as the powerhouse of the cell, responsible for generating the energy needed for cellular function. In CFS patients, these energy-producing organelles are not functioning at their optimal level, leading to an inadequate supply of energy for the body’s daily activities. This disturbance in the mitochondria’s function can have a profound impact on the body’s overall health and well-being.

Mitochondrial dysfunction is not a direct cause of CFS but rather a consequence of the condition. The exact mechanism behind this disruption is not fully understood, but studies have shown that it could be linked to viral infections, toxins, and chronic stress.

Oxidative stress, a process in which the body produces an excess of free radicals that can damage cells and tissues is amplified in CFS due to the impaired function of the mitochondria, leading to a vicious cycle of depletion of energy and increased oxidative stress.

The consequences of mitochondrial dysfunction in CFS can be seen in various systems of the body. One of the most affected systems is the immune system. Mitochondria play a crucial role in regulating the immune response, and their dysfunction can lead to an imbalanced and overreactive immune system, which is often observed in CFS patients.

Moreover, the brain and nervous system are heavily reliant on energy production from mitochondria. In CFS patients, the reduced energy supply to these vital organs can result in cognitive impairment and neurological symptoms such as brain fog, memory loss, and difficulty concentrating.

The muscular system is also significantly impacted by mitochondrial dysfunction in CFS. As energy production is compromised, muscles are unable to function at their optimal capacity, leading to fatigue, weakness, and pain.

It was evident that mitochondrial dysfunction plays a crucial role in the development and maintenance of CFS symptoms.

Despite extensive research, no faulty genes or mutations have been found in the mitochondria of most individuals with ME/CFS, suggesting it is not a typical mitochondrial disease.

Studies on mitochondrial function in ME/CFS have yielded conflicting results, with some showing increased activity, some showing reduced activity, and others finding no differences compared to healthy individuals. Recent research suggests that the problem lies “upstream” of the mitochondria, affecting their ability to function properly. This indicates that the issue is not with the mitochondria themselves. Further research is needed to identify this upstream factor, but there are already a few theories.

For example, a lack of oxygen supply to tissues, reduced blood volume and circulation, deficiency of L-carnitine (which is important for oxygen metabolism), problems with calcium ion channels, and impaired red blood cell function have all been proposed as potential factors impacting energy production in ME/CFS. Additionally, difficulties in taking in enough glucose, the fuel source for mitochondria, could also contribute to reduced energy production. The protein known as ‘AMPK’ gets activated, prompting the cell to absorb more glucose, which is necessary for mitochondrial respiration. However, the research discovered that ME/CFS patients have a hindered activation of AMPK.

Targeting mitochondrial dysfunction could potentially improve the symptoms of CFS. Several treatment approaches, such as supplementation with mitochondrial nutrients and improving lifestyle factors like diet and exercise, have shown promising results in managing the condition.

Mitochondrial Support:

Coenzyme Q10 (CoQ10) and nicotinamide adenine dinucleotide (NAD+) are essential for mitochondrial function. Supplementation with these compounds may enhance cellular energy production.
Additionally, dietary adjustments, such as increasing intake of antioxidants and essential nutrients, can support mitochondrial health.

AMPK Activation:Lifestyle modifications, including regular exercise and maintaining a healthy weight, can activate AMPK and improve cellular energy balance.

Certain medications, such as metformin, commonly used in diabetes treatment, may also activate AMPK and have been explored as potential therapies for CFS.

Anti-inflammatory Approaches:

Targeting inflammation through anti-inflammatory medications, such as corticosteroids or non-steroidal anti-inflammatory drugs (NSAIDs), may help alleviate symptoms associated with CFS.
Lifestyle interventions, including stress management and a well-balanced diet, can also contribute to reducing inflammation. Natural alternatives to drugs are available as well.

Immunomodulatory Therapies:

Given the immune system’s involvement in CFS, immunomodulatory therapies, such as low-dose naltrexone or intravenous immunoglobulin (IVIG), are being investigated for their potential to alleviate symptoms and improve cellular function.
There is a range of natural adaptogens as alternative.

Mitochondrial Support Summary

Impaired Mitochondria Symptoms:

  • Fatigue
  • Muscle weakness
  • Pain
  • Memory and cognitive difficulties
  • Gastrointestinal problems
  • Headaches

Top Support:

  • CoQ10
  • Pyrroloquinoline quinone (PQQ)
  • L-carnitine
  • Vitamin B complex
  • Alpha-lipoic acid
  • N-acetyl cysteine (NAC)
  • Nicotinamide adenine dinucleotide (NAD+)
  • Magnesium
  • Selenium
  • Stress reduction
  • Sleep