75 Thiamine Facts 1. Thiamine was discovered by Christiaan Eijkman in 1897, isolated in 1926 by Barend Jansen and Willem Donath, and first synthesized by Robert Williams in 1936. 2. Thiamine was the first B vitamin ever discovered. It was initially thought to be a "vital amine", but was later found not to be an amine at all. Still, the spelling with the "e" remains most common. 3. The active form of thiamine is thiamine pyrophosphate (TPP). This is the coenzyme involved in breakdown of sugar and amino acids. 4. “Beriberi” is the classical manifestation of chronic thiamine deficiency. It was a major health problem in East Asian countries, where polished rice (a sign of wealth) was the staple food. The removal of the husk left the rice totally devoid of thiamine. 5. In 1882, Japanese naval vessel Ryūjō sailed for 272 days. On its return, 169/376 of the crew developed beriberi, and 25 died. Two years later, another ship was sent on the same voyage, but this time with dried milk and meat. Only 14 members developed beriberi, and none died. 6. Thiamine has a short half-life ranging from 1 to 12 hours. 7. About 30 mg of thiamine is stored in tissues with high metabolic needs such as skeletal muscle, the heart, brain, liver, and kidneys. Excess free thiamine and TMP are excreted in urine. 8. Without regular consumption, thiamine storage is depleted within 2–3 weeks. With acute illness, thiamine deficiency may set in within 72 hours. 9. Potent forms of thiamine include benfotiamine, allithiamine, sulbutiamine, prosultiamine, and fursultiamine (TTFD). These forms have a bioavailability of 50-90% compared to thiamine HCl’s 3-10%. Besides benfotiamine and TTFD, there is limited research, so caution is warranted. 10. Vitamin B1 analogues such as benfotiamine, fursultiamine, and sulbutiamine are synthetic. These were developed in Japan in the ’50s and ’60s as higher potency forms of B1 meant to have more clinical application. 11. Synthetic B1 analogues are approved for use in some countries as a drug or non-prescription dietary supplement for treatment of diabetic neuropathy or other health conditions. 12. Most research on potent forms of thiamine, such as TTFD, comes out of Japan from Takeda Pharmaceutical Company. 13. “Beriberi”, the textbook disease of thiamine deficiency, comes from the Sinhalese phrase meaning “weak, weak”, or “I can’t, I can’t”. 14. Thiamine lowers serum lactate. 15. Without thiamine, there is no oxidative metabolism. 16. Thiamine and magnesium act as essential cofactors for a family of 3 mitochondrial dehydrogenases: PDH, αKGDH, and BCKDH. These orchestrate efficient mitochondrial aerobic ATP production. 17. Thiamine can trigger apoptosis in cancer cells by stimulating pyruvate dehydrogenase (PDH). 18. Thiamine HCl and TTFD were shown to be very protective in the heavy metal toxicity-induced oxidative stress and mitochondrial dysfunction seen in autism. 19. Thiamine reduces hypoxia. 20. Thiamine is a carbonic anhydrase inhibitor, meaning it improves retention of CO2 and thus the CO2/lactate ratio, oxygenating the tissue via the Bohr effect. 21. Thiamine is comparably potent to acetazolamide, a carbonic anhydrase inhibitor given to people suffering from mountain sickness and edema. 22. 24 schizophrenic patients were successfully treated with the addition of acetazolamide and thiamine in addition to their unchanged existing therapies in a double-blind, placebo-controlled crossover study. 23. High dose thiamine produces a growth-inhibitory effect in cancer. 24. In one study, chemotherapy caused a patient to go completely blind in both eyes. After just 5 days of thiamine, administered by IV, their vision returned rapidly. 25. When plants are stressed, they up-regulate thiamine production as a defense mechanism. 26. 50 Parkinson’s sufferers were treated with 100 mg of intramuscular thiamine 2x/week. They saw a significant improvement in motor and non-motor symptoms. Some with milder cases saw complete regression, and recovery was stable in all patients. 27. Many strange, polysymptomatic chronic illnesses can be attributed to impaired oxidative metabolism. This can manifest as any number of illnesses stemming from dysautonomia. In many cases, dietary thiamine deficiency or functional thiamine deficiency is a major factor. 28. Thiamine deficiency affects brain serotonin turnover, potentially leading to an inflammatory excess. 29. High doses of thiamine administered to patients in the early stages of COVID-19 have the potential to reduce hypoxia and hospitalization. 30. Thiamine deficiency is likely a cause of encephalopathy in severe COVID-19 patients and treatment with thiamine may be a safe and low-risk way to reduce the neurological burden. 31. Thiamine deficiency is implicated in beriberi, Wernicke-Korsakoff syndrome, IBD, ulcerative colitis, Crohn’s, SIBO, gastritis, POTS, CFS, MS, sleep apnea, Parkinson’s, Alzheimer’s, ADD, autism, schizophrenia, fibromyalgia, diabetes, dysautonomia, cancer, and more. 32. Thiamine does its work inside the cell, and serum thiamine tests only indicate recent intake. The only accurate test of thiamine status is a pair of tests known as the ETKA/TPPE (erythrocyte transketolase activity/thiamine pyrophosphate effect). 33. When testing for thiamine status via the ETKA/TPPE method, (generally) the higher the thiamine pyrophosphate effect (TPPE), the greater the deficiency. 34. In the ETKA/TPPE thiamine test, a normal range for TPPE is allowed up to 18%, but ideally should be 0%, indicating total cofactor enzyme saturation. 35. Regardless of the best available tests for thiamine status, many patients have tested within acceptable ranges yet still saw improvements from thiamine therapy. 36. Because thiamine is vital to cellular energy, its deficiency first affects the most active oxygen-using tissues: the brain, nervous system and heart. 37. Sleep apnea is essentially a hypothyroid state of CO2 deficiency. This means thiamine can help. 38. Thiamine is dopaminergic. 39. A significant association has been demonstrated between Parkinson’s disease and low levels of serum thiamine. 40. Thiamine supplements have beneficial clinical effects against Parkinson’s disease. 41. Fursultiamine’s chemical name is “thiamine tetrahydrofurfuryl disulfide” or simply “TTFD”. 42. TTFD brand names include Alinamin, Benlipoid, Bevitol, Lipophil, Judolor, and Lipothiamine. 43. Alcohol destroys thiamine and can reduce body stores over time. 44. Tea and coffee contain tannins which inactivate thiamine in the gut. 45. Nicotine inhibits thiamine availability via antagonism of a thiamine transporter in the pancreatic acinar cells by >40% and possibly in other tissues as well. 46. Thiamine can be depleted in chronic illness, intense physical exercise, and infection. 47. LD50 of TTFD for a 70 kg (154 lb) human is 2.5 grams if administered via IV and 12.5 grams if taken orally. 48. In 1970, Dr. Otto Warburg and his colleagues demonstrated they could induce cancer in normal cells specifically by depriving them of thiamine. 49. Intake of an appropriate amount of thiamine can prevent HPV infection. 50. HPV vaccine, Gardasil, is known to induce POTS, a syndrome of dysautonomia which can be treated with thiamine. 51. Thiamine deficiency dysautonomia, a condition of inefficient oxidative metabolism, can lead to widely variable brachial blood pressures in each arm. 52. Thiamine deficiency can lead to a reduced immune response to oral antigens. 53. The gastrointestinal (GI) tract is one of the main systems affected by a deficiency of thiamine. Clinically, this is recognized as “gastrointestinal beriberi”. 54. Symptoms of gastrointestinal beriberi may include GERD, gastroparesis, abdominal pain, bloating, and gas. People with this condition often see negligible benefits from probiotics or antimicrobials, and have a dependence on betaine HCL, digestive enzymes, and/or laxatives. 55. Thiamine-deficiency beriberi is considered the “great imitator” because of how many different symptoms can manifest from the resulting dysautonomia. 56. Shoshin beriberi, a sudden and severe variant of beriberi, often presents with lactic acidosis and cardiac shock. Due to the sparsity of this condition, delays in diagnosis can be fatal. However, rapid reversal can be easily achieved through IV thiamine replacement. 57. Dr. Derrick Lonsdale successfully treated patients with sleep apnea by giving them 150 mg TTFD, on the basis that automatic breathing is controlled in the brain stem where function is easily damaged by thiamine deficiency. 58. Thiamine is central to the production of acetylcholine. 59. Thiamine deficiency inhibits the release of hydrochloric acid from gastric cells and leads to hypochlorhydria (low stomach acid). 60. Despite being widely discussed throughout medical school as one of the most common syndromes attributed to thiamine deficiency, Wernicke’s encephalopathy is missed 80% of the time in clinical settings. 61. The thiamine and niacin deficiency diseases known as beriberi and pellagra, respectively, were the most devastating vitamin deficiency diseases in the history of the United States. 62. Nutrients likely to be put under stress by high doses of B1 are B2, B3, B5, B7, B12, CoQ10, sodium, potassium, glutathione, molybdenum, and copper. 63. Despite being the more poorly absorbed form of B1, thiamine hydrochloride can passively diffuse through the intestine when taken in a high enough dose, meaning it can bypass transporters and be absorbed at a much higher rate than when taken in a lower dose. 64. Low thiamine status means poor glucose tolerance. 65. Bacteroidetes and Fusobacteria are the most common two bacterial phyla that are able to synthesize thiamine pyrophosphate (TPP). 66. Some intestinal microbiota can produce vitamin B1, such as Bacteroides fragilis, Prevotella, Fusobacterium varium, Actinobacteria, and Clostridium. 67. In the ICU, “banana bags” (yellow due to their riboflavin content, hence, “banana”) are administered intravenously to help those with TBI, sepsis, diabetic ketoacidosis, and alcohol-induced thiamine deficiency. The bags contain thiamine, folic acid, magnesium, and a multivitamin. 68. Metabolizing carbohydrates, regardless of quality, diminishes thiamine stores. This is not a negative but a biological reality. 69. Both in vitro and in vivo studies demonstrate B1 supplementation reduces or reverses metabolic patterns and clinical manifestations of hyperglycemia, hypertension, dyslipidemia and other related symptoms via the upregulation of TKT, PDC and other thiamine dependent enzymes. 70. Benfotiamine was shown to improve spatial memory, amyloid precursor protein/presenilin-1, reduce amyloid plaques and tau levels dose-dependently after 8 weeks of treatment in a mouse model. 71. A total of 150 mg thiamine/day significantly reduced blood glucose within a month in a randomized, placebo control trial of 24 type 2 diabetics. 72. After 45 days of benfotiamine and vitamin B6 supplementation, 19/22 patients saw statistically significant reductions in pain, symptom scores, neurophysiological and biological markers of diabetic neuropathy. 73. A total of 100 mg thiamine/day significantly corrected lipid profiles and creatinine levels in a 6 month randomized trial of 60 type 2 diabetics with medication-controlled blood sugar and 26 age and BMI-matched controls. 74. A total of 300 mg/day oral thiamine improved left ventricular ejection fraction (LVEF) significantly in heart failure patients on diuretics. 75. In cell cultures, metformin has been shown to inhibit ThTR-2, a high-affinity transporter for thiamine uptake.