thiamine deficiency book

Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition

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This book by Lonsdale D, and Marrs C, is available on Amazon books. It is published by Elsevier. Written particularly for physicians who are practicing in the field of Integrative Medicine, it would be of interest to the educated public, particularly those affected by chronic disease.

Beriberi, the classical thiamine deficiency disease, long known to have been caused by consumption of white rice, is thought to have been abolished in developed cultures. It is actually widespread in America due to the colossal ingestion of sugar and is usually diagnosed as psychosomatic disease. Because the standard laboratory studies are negative or nonspecific, it is assumed that no organic disease is responsible.

Beginning with a review of the many symptoms of beriberi, it is described as the “great imitator” of a large number of disease conditions, each of which is thought to have its own etiology. It is relevant in all mitochondrial disease, because thiamine sits astride the vital initiation of energy synthesis. Thiamine deficiency interferes with carbohydrate, fat and protein metabolism, but is particularly important in the etiology of diabetes, types I and II and metabolic syndrome. It also has a place in the etiology of Alzheimer disease and may have an important part to play in cancer.

Evidence is provided to show that the relatively new science of epigenetics is crucial to the understanding of the part played by nutrition and lifestyle in genetic function. If the early symptoms of nutritional deficiency are treated symptomatically and high calorie malnutrition continues, the result is an array of chronic brain diseases. When thiamine deficiency was discovered as the cause of beriberi, the early investigators recognized that therapeutic doses of the vitamin involved the administration of 100-300 mg a day for months. The book reviewed here should be in the library of any Integrative Medicine physician.

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The publisher is offering a 30% discount off of the list price and free shipping if the book is ordered from their site. Just click the link below enter the promotional code ATR30 at checkout.

Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

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Derrick Lonsdale M.D., is a Fellow of the American College of Nutrition (FACN), Fellow of the American College for Advancement in Medicine (FACAM). Though now retired, Dr. Lonsdale was a practitioner in pediatrics at the Cleveland Clinic for 20 years and was Head of the Section of Biochemical Genetics at the Clinic. In 1982, Lonsdale joined the Preventive Medicine Group to specialize in nutrient-based therapy. Dr. Lonsdale has written over 100 published papers and the conclusions support the idea that healing comes from the body itself rather than from external medical interventions.


  1. Long standing impaired GI motility, constipation, dusautonomia, SIBO, CFS/fibro, dysbiosis and mast cell/histamine.

    Used 400mg magnesium citrate, 2000 as ascorbic acid, 600mg NAC daily for 3 days prior.

    Single dose of 250mg benfotiamine. After 30 minutes muscle burning and weakness, stood up to walk to bedroom, full body shaking/rigors. Muscles rigid all over. 8g dextrose, no improvement after 10 minutes, 8g more dextrose, no improvement after another 10 minutes, 400mg magnesium, symptoms began to resolve after 20 minutes and were fully resolved after 40 leaving me extremely warm and drowsy and ready to go to sleep.

    4 more days of 250mg benfotiamine per day. This reaction has not recurred although I don’t feel right on it. Healing reaction or go back to the regime that made the biggest improvement before this? (Huperzine/Alpha GPC – AChE inhibitor and choline source to increase ACh)

    I know that Thiamine is responsible for Acetyl-CoA which is what sent me down this route.

    I was not using Huperzine/Alpha GPC within 48 hours of my first dose of Benfotiamine so I don’t think was a cholinergic reaction.

    Any insights please?

  2. Lack of brain energy = lack of metal detox, sure seems possible. Wondering if you ever came across patients you treated with thiamine who also had evidence of heavy metal toxicity say from childhood vaccine’s? Did you ever employ heavy metal 24 hr urine testing in your practice?

    • I frequently saw traces of SH reactive metals in urine. Whether they contributed to symptoms is an open question.

  3. Dr Lonsdale….Does thiamine deficiency play any role in heavy metal toxicity in the brain? As always, thanks for sharing your knowledge with the rest of us.

    • An interesting question. Several animal studies have shown that thiamine does in fact remove lead. Even more interesting, it was shown that the lead was excreted through the bile ducts. Therefore, the excreted lead would be found in the stools, not in the urine. Since lead is an SH reactive metal (a sulfur/hydrogen combination), an important part of the removal mechanism, thiamine could be used to remove the other SH reactive metals, mercury, arsenic and cadmium.

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