Lyme Disease

What is Lyme Disease?

Lyme disease is caused by a spirochete—a corkscrew-shaped bacterium called Borrelia burgdorferi. The primary way we become infected is by the bite of an infected tick. These insects are typically found in wooded and grassy areas. Although people may think of Lyme disease as most common on the East Coast, it is found throughout the United States, as well as in more than sixty other countries.

Lyme disease is called “The Great Imitator,” because its symptoms may mimic the symptoms of many other diseases. It can affect any organ of the body, including the brain and nervous system, muscles and joints, and the heart. Patients with Lyme disease are frequently misdiagnosed with other diseases leading to an unfortunate  delay in treatment.

Early stage symptoms include:

  • Bull’s-eye rash (erythema migrans)
  • Fatigue
  • Fever
  • Chills

Later stage symptoms include:

  • Rash in other parts of the body
  • Chronic fatigue
  • Joint pain
  • Numbness
  • Weakness
  • Irregular heartbeat
  • Liver inflammation

How is Lyme Disease linked to Mitochondrial Dysfunction?

The hallmark of a mitochondrial dysfunction disease is the combination of severe fatigue with other symptoms that affect multiple other organ systems (nervous system, circulatory system, musculoskeletal system, etc.). Long term, chronic infections can produce mitochondrial dysfunction due to the stress they place on multiple organ systems including the immune system and the specific organs targeted by the infectious organisms.

Given that Lyme disease is a chronic infection that frequently causes severe fatigue, as well as abnormalities in multiple additional organ systems, it is highly likely that mitochondrial stress eventually leading to mitochondrial dysfunction, is an important aspect of Lyme disease to address.

A 2015 study published in Redox Biology demonstrated that the white blood cells of Lyme disease patients contain increased levels of the mitochondrial enzyme superoxide. This finding provides evidence of a state of elevated oxidative stress. The authors also reported depolarization of the mitochondrial membrane, disruption of intracellular communication, and a release of pro-inflammatory cytokines in Lyme patients. The cumulative effect of these findings Provides evidence for a generalized state of mitochondrial dysfunction present in Lyme disease patients [1].

References: [1] Sies, H. (2015). Oxidative stress: A concept in redox biology and medicine. Redox Biology, 4, 180–183.

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