Restoring mitochondrial function

Garth L. Nicolson, Ph.D. and Rita Ellithorpe, M.D.
The Institute for Molecular Medicine, Huntington Beach, California, USA, Journal of Chronic Fatigue Syndrome 2006; 13(1): 57-68.

When mitochondrial function is impaired, such as during moderate to severe fatigue, the net energy available to cells is limited to the Krebs Cycle and anaerobic metabolism.

Mitochondrial function appears to be directly related to fatigue, and when patients experience moderate to severe fatigue their mitochondrial function is inevitably impaired. Fatigue is a complex phenomenon determined by several factors, including psychological health [22,23], but at the biochemical level fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial electron transport.

Thus the integrity of mitochondrial membranes is critical to cell function and energy metabolism.

When mitochondrial membrane lipids are damaged by oxidation, they must be repaired or replaced in order to maintain the production of cellular energy to alleviate fatigue. During aging and in many diseases, including fatiguing illnesses, ROS/RNS-mediated accumulation of oxidized mitochondrial lipid occurs.

The failure to repair or replace these damaged molecules at a rate that exceeds their damage results in impaired mitochondrial function.

The results indicate that in moderately to severely fatigued subjects dietary LRT can significantly improve and even restore mitochondrial function and significantly improve fatigue. Using the Piper Fatigue Scale our unpublished data on a small number of CFS (and/or Fibromyalgia Syndrome) patients indicates that LRT plus antioxidants (NTFactor®) for 8 weeks reduces moderate to severe fatigue by 43.1%.