I came across this study while researching something else and thought it was fascinating. They theorize that thiamine deficiency is the cause of the fatigue from inflammatory bowel disease and after 20 days of oral thiamine supplements, 10 out of 12 patients’ fatigue was gone. Amazing!
J Altern Complement Med. 2013 Feb 4.
Thiamine and Fatigue in Inflammatory Bowel Diseases: An Open-label Pilot Study.
Costantini A, Pala MI.
1 Department of Neurological Rehabilitation, Villa Immacolata , Viterbo, Italy .
Abstract Objectives: To demonstrate that fatigue and other disorders related to ulcerative colitis and Crohn’s disease are the manifestation of an intracellular mild thiamine deficiency and not due to malabsorbtion, augmented requirements, or nutritional factors, and that this dysfunction is curable with high doses of thiamine administered orally or parenterally. Design: In this pilot study, we treated fatigue in eight patients with ulcerative colitis and four patients affected by Crohn’s disease from January to April 2011. The patients were recruited through general practitioners’ surveys and among personnel and affiliated personnel of the clinic Villa Immacolata. Fatigue was measured using the chronic fatigue syndrome scale, and the determination of thiamine and thiamine pyrophosphate levels in the blood was carried out through blood tests. The levels of thiamine and thiamine pyrophosphate in the blood were normal. All patients were assigned to receive high doses of thiamine orally. Depending upon the body weight of each patient, dosage ranged from 600?mg/day (60?kg) to 1,500?mg/day (90?kg). The chronic fatigue syndrome scale as well as thiamine and thiamine pyrophosphate levels in the blood were measured 20 days after the beginning of the therapy. Results: Ten patients out of twelve showed complete regression of fatigue, while the remaining two patients showed nearly complete regression of fatigue compared to the chronic fatigue syndrome scale scores before therapy. Conclusions: The absence of blood thiamine deficiency and the efficacy of high-dose thiamine in our patients suggest that fatigue is the manifestation of a thiamine deficiency, likely due to a dysfunction of the active transport of thiamine inside the cells, or due to structural enzymatic abnormalities. The administration of large quantities of thiamine increases the concentration in the blood to levels in which the passive transport restores the normal glucose metabolism in all cells and leads to a complete regression of fatigue.