Two closely-linked processes achieve the production of energy within the mitochondria: 1) the citric acid cycle, also referred to as the Krebs cycle, and 2) oxidative phosphorylation (OXPHOS). The citric acid cycle converts dietary fats and carbohydrates into small amounts of adenosine triphosphate (ATP), the molecular currency of intracellular energy. Through multiple steps of a complex chemical process, OXPHOS—oxidative phosphorylation, the main energy-producing process of all breathing organisms—generates about 10 times more ATP compared to the citric acid cycle, accounting for over 80% of the body’s total ATP production.

During youth, mitochondria adapt to increased energy requirements by rapidly replicating themselves, resulting in increased numbers of mitochondria producing higher levels of ATP. As the body ages, various chemical processes degrade and component structures of the mitochondria dysfunction, reducing the efficiency of their replication. This leads to a decrease in the number of mitochondria and a corresponding decrease in energy production. A vicious cycle ensues as free radical attacks contribute to mitochondrial energy depletion, which in turn leads to increased free radical pathology. A growing amount of evidence indicates that age-related mitochondrial dysfunction is a principal cause of many age-related diseases, including Alzheimer’s disease, Parkinson’s disease, fatigue syndromes, cancer, and cardiovascular diseases.

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Further, when mitochondrial energy levels fall below a certain minimum metabolic capacity, they lack the energy to carry out apoptosis, the organized cell death and removal process necessary in the normal life-cycle of all cells. If apoptosis doesn’t occur in an orderly fashion, abnormal cells can become cancerous, or die on site while failing to be removed, thereby contributing to the inflammatory process.

The decrease in mitochondrial energy production is the result of several factors, including free radical damage, as mentioned. Interestingly Denham Harman, M.D., Ph.D., who first proposed the Free Radical Theory of Aging in 1956, was first to propose mitochondrial dysfunction as a principal cause of aging and age-related diseases some 15 years later. It is free radical damage, Harman suggests, which is primarily responsible for age-related mitochondrial degradation.

DNA, or deoxyribonucleic acid, is the material containing the genetic code—or blueprint—for the proper development, functioning, and duplication of cells that is held within each cell’s nucleus. Mitochondria are unique in that they contain their own uniquely-structured DNA. Unlike nuclear DNA (nDNA), which is contained in cells other than mitochondria, mitochondrial DNA (mtDNA) lack certain structural protections and repair mechanisms, rendering them significantly more vulnerable to attacks by free radicals.

Mitochondrial DNA is located close to the inner mitochondrial membrane where both cellular energy and free radicals are produced. Therefore, mtDNA is particularly susceptible to the damaging effects of superoxide, hydroxyl, and perhydroxyl radicals, resulting in more than 10 times the damage in comparison to nuclear DNA.1 Free radical-induced damage to mtDNA leads to mitochondrial dysfunction including loss of cellular energy, accelerated cellular aging, and onset of the age-related diseases previously mentioned.

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