1999 Clinical and Scientific Meeting

by Alex Young

ME/CFS Society of Queensland Inc.

Hypercitricemia in Chronic Fatigue Syndrome

Chronic fatigue syndrome or CFS is known to be closely associated with excessive levels of citric acid excreted in the urine. This is usually thought to be merely a symptom of CFS.

What if elevated citric acid is not just a symptom of a dysfunctional Krebs cycle? This paper explores this question by starting with a presumption of severely elevated citric acid, and explores the biochemical consequences. The prediction is that hypercitricemia initiates a cascade of abnormally elevated or suppressed biochemical pathways and feedback effects that result in chronic tissue hypoxia.

Severe hypercitricemia is shown to cause abnormalities in levels of most amino acids (especially glycine) and problems with insulin, adenosine, uric acid and homocysteine metabolism. Post-arachidonic acid eicosanoids and nitric oxide synthesis are upregulated, causing further problems in the disorder. Disruption to cell membranes is expected. The theory also predicts that hypercitricemia is accompanied by mild hemopathic hemolytic anemia.

Treatment of hypercitricemia promises to be simple and effective if the inherent contraindications from the affected metabolic pathways can be overcome.

Keywords: chronic fatigue syndrome, hypercitricemia, citric acid cycle, glycolysis, phosphofructokinase, 2,3 bisphosphoglycerate, glycogen storage disorder, adaption to hypoxia, hemopathic hemolytic anemia, glycine, homocysteine, alanine, adenosine, uric acid, eicosanoids, nitric oxide.

 

Alison Hunter Memorial Foundation
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