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Mitochondrial Derailment

Dr. Michael R. Eades says, “As the high-energy electrons are passed along down the inner mitochondrial membrane they occasionally break free. When they break free, they become free radicals. These rogue free radicals can then attack other molecules and damage them. Because these free radicals are loosed within the mitochondria, the closest molecules for them to attack are the fats in the mitochondrial membranes. If enough of these fats are damaged, the membrane ceases to work properly. If enough of the membrane doesn’t work, the entire mitochodrium is compromised and ceases functioning. If enough mitochondria bite the dust, the cell doesn’t work and undergo apoptosis, a kind of cellular suicide. This chronic damage and loss of cells is the basic definition of aging.” (Note that Dr. Johanna Budwig’s Diet basic principle is to injest the best fats to heal these membranes.)

Mitochondria work by generating an electrical
potential and a pH gradient across that inner membrane.

The mitochondrion is different from other organelles because it has its own DNA and reproduces independently of the cell in which it is found; an apparent case of endosymbiosis.[1] They really are not quite us in the sense that their genetic pool is outside of our own DNA that make us uniquely us. Unlike nuclear DNA, mitochondrial DNA doesn’t get shuffled every generation, so it is presumed to change at a slower rate.

Multiple Sclerosis is the most common inflammatory demyelinating disease of the central nervous system and is the leading cause of non-traumatic neurological disability in young adults. Researchers believe that mitochondria play a key role in chronic axonal loss in this disease. The mitochondria present within the chronically demyelinated axons will be functioning at full capacity for many years but eventually, despite antioxidant defenses, free radical damage will accumulate and mitochondrial function will become compromised. ATP concentration within the axon will decrease and the effect on axonal function will be profound.[2]

Tissue damage in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis is accompanied by the arrest of mitochondrial respiration, loss of mitochondrial DNA, and the expression of nuclear-encoded mitochondrial proteins. Selenium effectively protects colon mitochondria prevented inflammatory and necrotic changes. Selenium in a high dose is therefore a potential therapeutic agent in inflammatory bowel disease.[3]

Our mitochondria are where the majority of free radicals are generated, so when high amounts of free radicals overpowers antioxidant defenses the battle for life is lost as dysfunctions in mitochondria accumulate, become overwhelmingly destructive. Excessive free radicals overwhelm the body’s ability to neutralize them. We produce a natural antioxidant compound known as glutathione that works to minimize damage done by free radicals, but optimal levels tend to be lacking because the basic ingredients like magnesium, selenium and sulfur are deficient.  Elevated pollution levels in urban environments create oxidative stress that adversely affects DNA and cellular health, while altering lipids and proteins within the mitochondria.

The mitochondria are extremely sensitive to heavy metals and general chemical insults. If the mitochondria are denied the basic nutrition they need to function, they cease to function normally.

Many avoid a simple fact—at the heart of Alzheimer’s is mitochondrial dysfunction. This makes logical sense when we consider that our mitochondria are instrumental in producing the energy currency in our body, and without energy, nothing will work properly, especially the brain, which needs a lot of this energy. The only organ that has similar needs is the heart, which has its own order of intelligence and sensitivity to each second of life, which is represented in our heart rate variability (HRV).

“Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer’s disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson’s disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis.

[1] The endosymbiotic theory concerns the origins of mitochondria and plastids (e.g. chloroplasts), which are organelles of eukaryotic cells. According to this theory, these organelles originated as separate prokaryotic organisms which were taken inside the cell as endosymbionts. Mitochondria developed from proteobacteria (in particular, Rickettsiales or close relatives) and chloroplasts from cyanobacteria.

[2] Mitochondrial dysfunction plays a key role in progressive axonal loss in Multiple Sclerosis. Medical Hypotheses, Volume 64, Issue 4, Pages 669-677 H.Andrews, P.Nichols, D.Bates, D.Turnbull

[3]  High selenium diet protects against tnbs-induced acute inflammation, mitochondrial dysfunction, and secondary necrosis in rat colon. TIROSH Oren ; LEVY Eran; REIFEN Ram; Hebrew University of Jerusalem. ISSN 0899-9007  2007, vol. 23, no11-12, pp. 878-886