As covered in the upcoming issue of the CFIDS Chronicle
(Vol. 19 Issue 3, Summer 2006)

Research evidence indicates that diminished mitochondrial function caused by oxidation occurs during aging and in fatiguing illnesses. When mitochondrial function is impaired, the net energy available to cells is limited. There are a number of conditions and substances that can weaken the mitochondria, but oxidation and damage of mitochondrial membrane lipids can lead to a loss of electron transport function.

A report in the Spring 2006 edition of the Journal of Chronic Fatigue Syndrome described clinical studies where lipid replacement therapy (LRT) combined with antioxidants appeared to reduce fatigue levels and improve mitochondrial function by protecting the membranes and replacing damaged lipids.

Concentrations of orally ingested lipids, such as in the products NTFactor and Propax, diffuse through the gut, are transported via the blood and deposited onto specific cell membrane receptors, where they are taken into the cells.

In clinical studies, subjects using dietary LRT and antioxidants experienced a 40 percent reduction in fatigue scores after eight weeks. Researchers also observed a correlation between reductions in fatigue and gains in mitochondrial function.

Though these studies are preliminary, the report suggests that people with CSF may benefit from exploring LRT and antioxidant consumption as one part of their overall treatment strategy.

[Editor’s note: This is one of several studies covered in the “Research Briefs” section of the Summer 2006 CFIDS Chronicle. Other stories in this issue address how people with CFS are using the Internet to reduce isolation, problems with long-term disability insurance and implications of recent brain studies of CFS patients. To learn more about the CFIDS Chronicle visit http://www.cfids.org/support/membership.asp.]