ganelle that produces the ATP needed for cellular functions by the process of oxidative phosphory- lation. This organelle is separated from the interior of the cell by a double membrane (inner and outer membranes) barrier, and it has its own unique DNA (mtDNA). The electron transport machinery that generates the ATP from oxygen and fats re- sides in the inner mitochondrial membrane, and it is completely dependent on the maintenance of a chemical-electrical potential across the inner mi- tochondrial membrane.
The inner mitochondrial membrane is also one of the most sensitive membranes of the cell to oxida- tive damage. This is because of its unique mem- brane structure and the presence of a very oxida- tion-sensitive phospholipid, cardiolipin. Cardiolipin is functionally required for the electron transport system, and it is synthesized inside the mitochon- dria from two phosphatidylglyerol molecules, one of the 5 types of phosphatidyl phospholipids that make up biological membranes. When mitochon- drial cardiolipin and to a lesser degree other phos- phatidyl phospholipids are damaged by oxidation, the chemical/electrical potential across the inner mitochondrial membrane is altered due to an in- creasingly “leaky” membrane that allows protons and ions to move across the membrane. This oc- curs because the oxidized membrane phospholip- ids no longer form a tight ionic/electrical “seal” or barrier. The loss of this ionic/electrical barrier has significant effects on a number of cellular proper- ties, such as loss of electron transport and cellular energy, altered metabolism and even initiation of cell death.
At the level of the organism the loss of mitochon- drial function is perceived as loss of overall energy or fatigue. Although fatigue is a complex phenom- enon with a number of elements, these elements all depend on mitochondrial energy generation. In experiments that link mitochondrial function with fatigue we have found that mitochondrial function is impaired during injury, disease, inflammation and aging. When fatigue persists for some time, usually at least 6 months, and can’t be refreshed by sleep, it is called chronic fatigue.
In the last few years we have been examining the 10 Focus August 2012
role that mitochondria play in chronic fatigue and in various chronic illnesses. There are a number of chronic illnesses that are characterized by exces- sive fatigue, such as the fatiguing illnesses, and these illnesses (chronic fatigue syndrome, myal- gic encephalomyelitis, fibromyalgia syndrome, Gulf War illnesses, chronic Lyme disease, among others) all show loss of mitochondrial function. Indeed, essentially all chronic illnesses have as- sociated with them various degrees of fatigue as a major symptom. However, one doesn’t have to have a chronic illness to be affected by fatigue. In fact, it is the most common complaint of all patients seeking general medical care, and it is a natural consequence of aging. It is also present as an important symptom in neurodegenerative, neurobehavioral, metabolic, autoimmune, inflam- matory and other diseases.
Fortunately our bodies have a marvelous system to replace the damaged membrane components, especially the oxidation-sensitive membrane phospholipids that contribute to loss of mito- chondrial function, fatigue and other alterations of membrane and cellular functions. This system depends on the ingestion and transport of un- damaged membrane phospholipids and their pre- cursors to each of our cells via specialized carrier complexes that protect the phospholipids from oxidative damage. Once inside the cell, the un- damaged phospholipids and other components of membranes can replace the damaged membrane components. Then the damaged components are degraded and removed from our cells or reutilized after their repair. The problem is that we often do not have good sources of undamaged membrane phospholipids in our diets or even our dietary supplements. Almost all of our dietary and sup- plement sources of membrane phospholipids also contain oxidized phospholipids that cannot repair mitochondrial damage and restore function.
This is where Lipid Replacement Therapy (LRT®) comes in. This is a natural medicine approach or more specifically a dietary source of undamaged membrane phospholipids, especially the 5 most important phosphatidyl phospholipids that make up biological membranes and provide precursors for specialized phospholipids like cardiolipin.
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