Mitochondrial Dysfunction

Mitochondria in our cells are responsible for producing energy (called ATP). High-energy demand organs (including the heart, muscles, and brain) require more mitochondria to produce sufficient energy.

Mitochondrial disease occurs when mitochondria don’t produce the necessary energy for the body to function properly. Mitochondrial disease occurs in one in 5,000 individuals and is not a genetically inherited trait.

Mitochondrial dysfunction has been described as a hallmark of aging because, over time, mitochondria become less able to provide cellular energy.

Mitochondrial Dysfunction and Aging

Mitochondria house a complicated quality control system that functions to minimize damage by either generating new or removing damaged mitochondria in a process that forms the basis of aging.

Somatic mutation in mitochondrial DNA (mtDNA) specifically has been linked to the onset and progression of human cancer. As mammals age, somatic mitochondrial DNA (mtDNA) accumulates. Somatic mutations interrupt the function of the electron transport chain (ETC), a mitochondrial pathway key to the production of ATP.

Studies on mtDNA in mice have demonstrated that high levels of somatic mtDNA mutations induce aging factors, including osteoporosis, hair loss, greying of the hair, weight reduction, and decreased fertility. Age-associated mitochondrial disorder is also linked to increased cell loss.

Symptoms

Chronic fatigue is considered a hallmark symptom of mitochondrial dysfunction.

The degradation of mitochondrial function and oxidant production is linked to the typical processes of aging and the development of age-related disease. These include cardiac and neurodegenerative diseases, muscle atrophy, sarcopenia, cardiac and immune system disorders, hepatic dysfunction, kidney failure, and cancer.

Other conditions include diabetes, fibromyalgia, and mental disorders, including schizophrenia and bipolar disease.

Treatment

Treatment is mostly geared toward relieving symptoms and maintaining optimal health. This includes a regimen of vitamins, preventive measures to reduce or minimize symptom worsening, and avoiding toxins.

Regular exercise is also recommended to “preserve the energetic properties of skeletal muscle” and stave off its decline.

Supplements

Clinical trials suggest that oral replacement supplements, including l-carnitine, alpha-lipoic acid, coenzyme Q10, reduced nicotinamide adenine dinucleotide (NADH), and membrane phospholipids can improve cell function.

These supplements can be combined to naturally restore mitochondrial function and significantly reduce chronic symptoms such as fatigue.