The End of Alzheimer's by Dale Bredesen
Author:Dale Bredesen
Language: eng
Format: epub
Publisher: Penguin Publishing Group
Published: 2017-08-22T04:00:00+00:00
Mitochondrial Function
Like tiny batteries, mitochondria supply the energy that allows our cells to function. They convert the energy locked in your food and the oxygen you breathe into the molecule ATP, which in turn powers your cells. The name mitochondria comes from the Greek for “little granular thread,” and these amazing batteries are actually the descendants of bacteria that invaded our cells over a billion years ago, taking up long-term residence much to our own advantage.
Since many chemicals damage mitochondria, it is helpful to know whether you have been exposed to these, especially in significant amounts or over a long period of time. The list includes antibiotics (which kill bacteria, and thus can be toxic to our mitochondria since they are descendants of bacteria), statins, alcohol, L-DOPA (prescribed to treat Parkinson’s disease), griseofulvin (prescribed for fungal infections), acetaminophen (Tylenol), NSAIDs (aspirin, ibuprofen, and related drugs), cocaine, methamphetamine, or AZT (azidothymidine, used for viral infections including HIV/AIDS). In addition, ApoE4 may be associated with mitochondrial damage.
There is not a simple blood test that assesses mitochondrial function, although there are some indirect tests, such as testing organic acids. Mitochondrial testing currently available is directed more at discovering mitochondrial defects in childhood diseases than in cognitive decline, so improved methods of testing are sorely needed. Until they arrive, the best way to test for the alterations in mitochondrial function that may occur with cognitive decline are with breath tests, nuclear magnetic resonance tests, mitochondrial DNA sequencing, and muscle biopsies. For now, with respect to the identification of potential contributors to cognitive decline, it is helpful to know whether there has been exposure to the mitochondrial-damaging agents listed above.
GOAL: no exposure to mitochondria-damaging agents.
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