beta-Alanine and gamma-aminobutyric acid in chronic fatigue syndrome. Clin Chim Acta. 2006 Jul 14; [Epub ahead of print] Ulf Hannestad [a,*], Elvar Theodorsson [a] and Birgitta Evengård [b] Affiliations: [a] Faculty of Health Science, Division of Clinical Chemistry, Linköping University, SE-581 85 Linköping, Sweden [b] Department of Laboratory Medicine, Karolinska Institutet at Karolinska University Hospital, Huddinge, SE-141 86 Stockholm, Sweden [*] Corresponding author: Tel.: +46 13 223246; fax: +46 13 223240; E-Mail: Received 7 June 2006; revised 7 July 2006; Available online 14 July 2006. NLM Citation: PMID: 16934791 BACKGROUND: Due to the occurrence of sleep disturbances and fatigue in chronic fatigue syndrome (CFS), an investigation was performed to examine if there is an abnormal excretion of gamma-aminobutyric acid (GABA) and/or its structural analogue beta-alanine in the urine from CFS patients. Both GABA and beta-alanine are inhibitory neurotransmitters in the mammalian central nervous system. METHODS: The 24 h urine excretion of GABA and beta-alanine was determined by isotope dilution gas chromatography mass spectrometry in 33 CFS patients and 43 healthy controls. The degree of symptoms in both patients and controls was measured by grading of three typical CFS symptoms using a Visual Analogue Scale. RESULTS: Men had a significantly higher excretion of both beta-alanine and GABA than women. Comparing CFS patients with healthy controls showed no significant difference in excretion of neither beta-alanine nor GABA. No correlation was found between the excretion of beta-alanine or GABA and any of the three characteristic CFS symptoms measured. However, two female and two male CFS patients excreted considerably higher amounts of beta-alanine in their 24 h urine samples than control subjects. CONCLUSIONS: Increased excretion of beta-alanine was found in a subgroup of CFS patients, indicating that there may be a link between CFS and beta-alanine in some CFS patients. Keywords: Chronic fatigue syndrome; ß-Alanine; ?-Aminobutyric acid; Polyamines; Ornithine decarboxylase; Immunosuppression