Mitochondrial Shutdown Due To Toxins & Oxidative Stress from Free Radicals
Mitochondria are the cellular powerhouses of cells that function to create energy for the cell in the form of ATP. In many Chronic Fatigue Syndrome (CFS/ME) patients, Dr. Sponaugle reported seeing high oxidative stress and inflammatory mediators as indicated by the OAT Test (Organic Acid Tests) that contribute to mitochondrial dysfunction and loss. A vicious cycle is created in which free radicals overwhelm the delicate mitochondrial membrane producing even more highly reactive free radicals.
Electrons leak out of membranes disrupting the electrochemical gradient necessary to form ATP—a phenomenon called “leaky mitochondria.” Leaky mitochondrial membranes promote progressive functional loss linked to a number of chronic illnesses.
Repair mechanisms such as antioxidant enzymes and transporters are hindered, leaving dilapidated machinery unable to meet the body’s energy demands.
From Leaky Mitochondria to Leaky Brain
The brain utilizes oxygen for ATP production more than any other body tissue. As a result, free radical production is abundant in the brain. This is further complicated by the fact that neural tissue is rich in polyunsaturated fats which are easily oxidized promoting free radical damage.
Brain mitochondria house inferior antioxidant defenses compared to the greater cell, with neural mitochondrial damage 10-100 times more likely than nuclear DNA. Neurodegenerative diseases such as Alzheimer’s, Parkinson’s, dementia, and ALS are now believed to stem from mitochondrial damage of neural tissues.
Neuroinflammation was recently documented in a study using advanced imaging techniques in ME/CFS patients. A substantial difference in an inflammatory marker produced by astrocytes and microglia was found to be 45%–199% higher in ME/CFS patients than in healthy controls.
Those with the greatest neuroinflammation also experienced the worst cognitive symptoms. This small study further suggests that mitochondrial damage of neural tissue perpetuates the illness.
New research in the field of neuroplasticity tells us that neural tissue is dynamic and able to repair from oxidative damage. Brain-derived growth factors and neural stem cells can be stimulated by certain nutrients to help repair damaged neuronal mitochondria and cell membranes.
Curcumin, L-carnitine, and glycerophosphocholine (GP) studies show these three nutrients can stimulate neuroplasticity via growth factor promotion. The lipid phosphatidylserine (PS) is directly linked to mitochondrial support as it is the precursor to phosphatidylethanolamine (PE), the most abundant lipid of the mitochondrial membrane.