Vitamin B1

Scientific studies (review articles) on the relationship between vitamin B1 and disease prevention:
One swallow does not make a summer. A famous Dutch saying that could not be any more obvious. Just because one single scientific study about a certain topic makes certain claims, it does not necessarily mean it is true. On the other hand, a review article (a collection of scientific studies on a certain topic) of randomized, placebo-controlled double blind clinical trials (RCTs) will answer the following question:
"Do taking dietary supplements make sense?" Yes for a positive conclusion and no for a negative conclusion.

One swallow does not make a summer. A famous Dutch saying that could not be any more obvious. Just because one single scientific study about a certain topic makes certain claims, it does not necessarily mean it is true. On the other hand, a review article (a collection of scientific studies on a certain topic) of cohort studies or case-control studies will answer the following question:
"Should I change my diet?".

1. Vitamin B1 supplementation reduces ICU delirium in critically ill patients
2. Vitamin B1 + vitamin C supplementation does not reduce mortality in patients with sepsis or septic shock
3. Peripheral neuropathy is associated with lowered plasma vitamin B12 levels
4. Vitamin B1 deficiency increases systolic heart failure risk
5. Oral vitamin B supplementation does not prevent cognitive decline in cognitively unimpaired individuals

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• Vitamin B1 (thiamin(e)) is a water-soluble vitamin.
• Thiamine (as thiamin pyrophosphate (TPP)) functions as a coenzyme in more than 24 enzymes, most importantly pyruvate dehydrogenase (for energy production in the Krebs cycle), transketolase (for lipid and glucose metabolism, production of branched chain amino acids and production and maintenance of myelin sheath) and 2-oxo-glucarate dehydrogenase (for synthesis of acetylcholine, GABA and glutamate).
• Because the thiamin requirement depends on energy intake, the suggested RDA is 0.5 mg/1000 kcal.
• Thiamine is present in lean pork and other meats, wheat germ, liver and other organ meats, poultry, eggs, fish, beans and peas, nuts and whole grains.
  Dairy products, fruit and vegetables are not good sources of vitamin B1.
• Thiamine deficiency results in dry beriberi, a peripheral neuropathy, wet beriberi, a cardiomyopathy with edema and lactic acidosis and Wernicke–Korsakoff syndrome, whose manifestations consist of nystagmus, ophthalmoplegia and ataxia evolving into confusion, retrograde amnesia, cognitive impairment and confabulation.
  Thiamin deficiency is also involved in foetal alcohol syndrome, characterized by growth retardation, psychomotor abnormalities and congenital malformations, in the offspring of alcoholic mothers.
• Alcohol can impair the uptake and utilization of thiamin and these effects may contribute to the prevalence of thiamin deficiency in alcoholics.
  Alcohol also reduces cellular thiamin diphosphokinase activity.
• Thiamine is rapidly absorbed in the jejunum and ileum by an active, carrier-mediated and rate-limited process, but at higher concentrations, the uptake is by passive diffusion.
• Thiamine occurs in the human body as free thiamine and as various phosphorylated forms: thiamine monophosphate, thiamine triphosphate and thiamine pyrophosphate, which is also known as thiamine diphosphate.
  Thiamine pyrophosphate is the active form of thiamine and it serves as a cofactor for several enzymes involved in energy metabolism.
  All known thiamine pyrophosphate-dependent enzymes also require a divalent cation, commonly magnesium (Mg²⁺).
• The total body pool size is approximately 25-30 mg of thiamine, mainly in skeletal muscle, heart, brain, liver and kidneys.
  Liver contains the highest concentration of thiamin.
• The biological half-life of thiamin is approximately 10-20 days.
  In a deficient state, body stores can be depleted in 2-3 weeks.
• An excess intake of thiamin does not cause toxicity in humans.