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Thiamine (vitamin B1) is a water-soluble vitamin that has important phosphorylated relatives. B1 deficiency is a well known nutritional problem I encounter in patients with chronic alcoholism which can lead to syndromes like Wernicke-Korsakoff syndrome and beriberi. B1 deficiency can also damage the brain’s mammillary bodies, thalamus, hypothalamus, and cerebellar vermis as these areas tend to have relatively high metabolic demands. As an intensivist, I often administer intravenous thiamine supplementation for several days in patients with known alcoholism and/or coming in with altered mentation.

Thiamine (Image: REBELEM)

So what’s the big deal about “thiamine before glucose?”

Thiamine is phosphorylated into thiamine pyrophosphate (TPP), an incredibly important cofactor involved with cellular aerobic respiration and the production of ATP – our energy currency molecule. The first step in aerobic respiration is glycolysis which transforms glucose into pyruvate. At this point, pyruvate has two major options -> proceed into the pyruvate dehydrogenase complex (PDC) en route to the TCA cycle (which requires TPP) or get fermented into lactate. In thiamine deficiency, low amounts of TPP force much of the pyruvate down the lactate pathway which can ultimately lead to acidosis. If we start administering glucose, we generate and force MORE pyruvate down the lactic acid pathway only perpetuating the problem. Thiamine supplementation restores TPP and promotes the formation of more ATP via aerobic respiration.

Furthermore, TPP is required in the pentose phosphate pathway – a series of biochemical reactions that produces NADPH which, in turn, keeps glutathione reduced to help mitigate oxidative damage. No thiamine -> no TPP -> more oxidative damage.

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