Decreasing Inflammation by Improving Mitochondrial Function

Mitochondrial functions are mainly attributed to regulation of cell proliferation, ATP synthesis, cell death, and metabolism. However, recent scientific advances reveal that mitochondria also play a central role in pro inflammatory signaling, serving as a central platform for control of innate immunity and the inflammatory response. Consequently, mitochondrial dysfunctions have been related to severe chronic inflammatory disorders. Mitochondrial dysfunction can be characterized by a loss of efficiency in the electron transport chain and reductions in the synthesis of high-energy molecules, such as adenosine-5'-triphosphate (ATP) seen in aging and chronic diseases. These diseases include neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and Friedreich’s ataxia; diabetes and metabolic syndrome, cardiovascular diseases, such as atherosclerosis and other heart and vascular conditions; gastrointestinal disorders; autoimmune conditions, such as multiple sclerosis, type 1 diabetes, and systemic lupus erythematosus; neurobehavioral and psychiatric diseases, such as autism spectrum disorders, bipolar and mood disorders, and schizophrenia; chronic fatigue syndrome and Gulf War illnesses; musculoskeletal diseases, such as skeletal muscle hypertrophy/atrophy and fibromyalgia; cancer; and chronic infections.