Came across this thread about Thiamine and Fatigue. so I thought I'd post it.
Thiamine and Fatigue in Inflammatory Bowel Diseases
https://www.liebertpub.com/doi/full/10.1089/acm.2011.0840
Theres more in the link provided.
Enjoy.
Thiamine and Fatigue in Inflammatory Bowel Diseases
https://www.liebertpub.com/doi/full/10.1089/acm.2011.0840
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.
Introduction
Among patients with Inflammatory Bowel Diseases (IBD), fatigue is the most commonly reported symptom and one of the most debilitating. Despite its high prevalence and significant impact, fatigue is still poorly understood and often underemphasized because of its complexity and subjective nature. Fatigue is often observed together with sleep disorders, depression, anxiety, and other disturbances that, in this study, were described in detail by our first patient.
The classic syndrome caused primarily by thiamine deficiency in humans is beriberi, for which the benefit of thiamine in prevention and treatment is uncontested.1,2 In older texts, beriberi has been divided into categories known as “wet,” “dry,” and Wernicke-Korsakoff syndrome. Manifested beriberi and Wernicke-Korsakoff syndrome show evident symptoms, whereas mild forms of thiamine deficiency are less known and the symptoms are often attributed to other pathologies. According to the World Health Organization (1999), “The symptoms of mild thiamine deficiency are vague and can be attributed to other problems, so that diagnosis is often difficult. […]The symptoms of mild thiamine deficiency clinically improve by the administration of thiamine.”2
Characteristic early symptoms include anorexia, weakness, aching, burning sensation in hands and feet, indigestion, irritability, and depression. After 6 to 8 weeks, the only objective signs at rest may be a slight fall in blood pressure and moderate weight loss. After 2 to 3 months, apathy and weakness become extreme, calf muscle tenderness develops, along with loss of recent memory, confusion, ataxia, and sometimes persistent vomiting.2
Neurologists often see, in the outpatient practice, patients with nonspecific symptoms such as fatigue, irritability, difficulties in concentration, and depression. Our team has seen, from June to November 2010, three subjects with definitive diagnoses of ulcerative colitis (UC) who presented these symptoms in a typical fashion.
The first patient, a 51-year-old woman with a definite diagnosis of ulcerative colitis for about 23 years, presented several “extraintestinal” symptoms of variable intensity during both acute phases and periods of relapse. These symptoms included fatigue immediately upon waking, nightmares, sleep disorders, anxiety, depression, mood fragility, memory loss, attention disorders, lack of tolerance to stress, often lack of appetite, episodes of tachycardia and extrasistolia, generalized muscular weakness, muscular cramps, calf and foot sole pain (of the burning type) mostly during the night, intolerance to cold, and dry skin. The fatigue could vary greatly, even during the same day, from a tolerable degree to one that interrupted all activities and required complete rest.
For about 15 years, the patient had laboratory signs of a slight renal insufficiency due to interstitial glomerulopathy. Over the last three years, episodes of migraine appeared almost every weekend, along with nausea and vomiting, which required an anti-migraine therapy.
The patient was under gastroenterologist care and followed therapy with mesalazine and azathioprine. Blood tests, except the renal function, were normal. Brain nuclear magnetic resonance (RM) and cardiology checkup were normal.
Besides the numerous subjective symptoms, an objective examination showed slight muscular hypotone, a stabbing pain when pressing calves and soles of feet, and slight edema in the ankles. Stretching reflections were present and symmetrical. At the time of the checkup, the disease was quiescent and the intestinal disturbances were minimal.
The patient's diet varied, but rice and potatoes (poor in vitamin B1) were strongly represented. Some aspects of the diet (strong consumption of rice), and clinical features such as (1) cardiac symptoms; (2) symptoms related to a predominantly sensitive polyneuropathy; (3) central nervous system symptoms; and (4) symptoms due to multiorganic suffering led the authors to conclude that the patient could be affected by a thiamine deficiency that was secondary to absorption deficiency.1,2
We proposed a therapy comprising 50 mg of thiamine intramuscular (IM) for three days, to be continued if positive in effect, with an oral maintenance dose of 600 mg/day.1,3 The thiamine does not have any known collateral effects even if administrated at high doses for prolonged periods of time.3
A few hours after the first IM administration, the fatigue completely disappeared and, day after day, the related symptoms remitted. Renal laboratory tests showed normalization in a week's time. Within 20 days, the patient regained complete wellness.
In August, one of the co-authors visited a relative, a 50-year-old woman affected by UC for 20 years. The patient showed a symptomatic background similar to the case above, along with constipation. The therapy, comprising 600 mg of oral thiamine per day, led to the disappearance of fatigue and other extraintestinal symptoms within a few days.
The third patient was a 40-year-old woman affected by UC for five years in a relapsing disease phase. The patient had about 10 episodes of diarrhea during the day and 5 at night and was affected by extreme fatigue. The oral therapy of 600 mg of thiamine per day led to disappearance of the fatigue within 48 hours. An unexpected event occurred leading to a dramatic improvement of the intestinal functions. At this point, the authors formulated the hypothesis that fatigue and all extraintestinal symptoms were the expression of thiamine deficiency.
Theres more in the link provided.
Enjoy.
