Davis W. Lamson, MS, ND

Aging, Disease, Cancer and the Mitochondria: A Mitochondrial Model of Cellular Degneration


AANP 2002 Convention ~ Salt Lake City, Utah

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The dominant paradigm of "old age" assumes that chronic degenerative diseases are a natural consequence of worn cellular machinery. A new viewpoint of aging, cancer and chronic disease would focus on the mechanism of dysfunction, which causes the degenerative diseases. This would permit a logical biochemical approach to the treatment of these conditions. For example many neurodegenerative diseases once thought a consequence of "old age" such as Parkinson's and Alzheimer's have now been linked to specific dysfunctions in the mitochondria. The mitochondria are responsible for producing the majority of cellular energy in the form of ATP through the election transport chain (ETC). The process of oxidative phosphorylation in the ETC not only produces ATP but reactive oxygen species (ROS). As mitochondrial enzymes in ETC are damaged the production of ROS increases damaging the mitochondrial DNA (mtDNA). Unlike nuclear DNA that has protective histones and introns, mtDNA is relatively unprotected in the inner mitochondrial membrane with limited mechanisms of repair. Increasing evidence of mtDNA mutation and oxidative damage in aging human tissues as well as various forms of cancer supports a mitochondrial model of degeneration. A number of nutrients and antioxidants have been found to be effective in partially restoring mitochondrial function and/or having a beneficial effect on the disease process.

ú Introduction

ú Details of mitochondrial function

ú Mitochondrial dysfunction

ú Disease examples

ú Clinical strategies for mitochondrial dysfunction