Vitamin B1 (Thiamine)

Turns carbs into energy

The body converts thiamine into thiamine pyrophosphate (TPP), a coenzyme with one specific chemical job. It grabs carbon compounds and helps split off a carbon as CO₂. That reaction sits at the main junctions of fuel metabolism:¹

• Pyruvate dehydrogenase (PDH) is the gate between glycolysis and the mitochondria. Glucose is first split into pyruvate in the cytoplasm, which yields only about 2 ATP. To get the other ~30 ATP, pyruvate has to become acetyl-CoA inside the mitochondria, and PDH, using TPP, is the only route. Without thiamine, pyruvate backs up and becomes lactate.
• α-Ketoglutarate dehydrogenase is a step in the TCA cycle itself, so thiamine is needed again in the middle of the cycle, whatever the fuel.
• Branched-chain keto-acid dehydrogenase breaks down leucine, isoleucine and valine.
• Transketolase is in the pentose phosphate pathway, which makes NADPH for antioxidant defence and the ribose for DNA. Red-cell transketolase activity is the classic lab test for thiamine status.

The body has only about 25–30 mg of thiamine, and its half-life is short, so stores can run out in as little as 2–3 weeks without intake. The demand also scales with carbohydrate. The more glucose flows through PDH, the more TPP is needed. That's the key to why deficiency hits when it does: on diets high in white rice or refined flour (beriberi in Asia), in heavy drinkers (alcohol blocks absorption and supplies calories with no thiamine), and when a starved or malnourished person is suddenly fed carbohydrate.²

Powers the brain

The brain is about 2% of body weight but uses about 20% of resting energy, and runs almost entirely on glucose oxidised through PDH and the TCA cycle. Neurons have little fuel reserve. When thiamine runs short, the brain areas with the highest energy demand fail first. Those include the thalamus, the mammillary bodies, the areas around the third ventricle and the brainstem nuclei that control eye movement. Neurons there build up lactate, lose their ion gradients, release excess glutamate and die.¹

That is Wernicke's encephalopathy, with its classic three signs: confusion, unsteady gait and paralysed eye movements. Untreated, it progresses to Korsakoff syndrome, a permanent loss of the ability to form new memories. It is a medical emergency. Fewer than one in five cases show all three signs, and autopsy studies find it far more often than it's diagnosed in life. Beyond alcoholism, it now shows up after bariatric surgery, with hyperemesis in pregnancy, in cancer, and on long IV feeding.¹

Glucose before thiamine can trigger it. Giving IV glucose to someone who is thiamine-deficient pushes extra glucose into a blocked PDH and can bring on Wernicke's within hours. That's why hospitals give thiamine before glucose to anyone malnourished or alcohol-dependent.¹

Peripheral nerves fail too. Dry beriberi is a symmetrical neuropathy with burning feet, weakness and wasting. Wet beriberi is a high-output heart failure, because blood vessels widen when tissues can't use oxygen properly and the energy-starved heart muscle can't keep up.²

Intake & absorption

The RDA is 1.1 mg/day for women and 1.2 mg/day for men. Absorption in the small intestine uses a high-affinity transporter that saturates at around 5 mg per dose. Above that, extra is absorbed only slowly by passive diffusion, which is why very high oral doses mostly pass through. Fat-soluble forms like benfotiamine get around that limit. Loop diuretics (furosemide) increase thiamine loss in urine, which matters for heart-failure patients.²

Top foods

• Pork loin: about 0.8–1.0 mg in 3 oz, close to a full day's need
• Trout and salmon: about 0.2–0.3 mg in 3 oz
• Black beans and lentils, cooked: about 0.2–0.4 mg per cup
• Sunflower and flax seeds: about 0.4–0.5 mg per oz
• Whole grains: polishing rice or milling flour removes most of it

Deficiency

Early signs are vague: tiredness, irritability, poor appetite and poor memory. More advanced deficiency causes beriberi (neuropathy or heart failure) or Wernicke–Korsakoff syndrome. People most at risk drink heavily, have had weight-loss surgery, have repeated vomiting, take long-term loop diuretics, or are being re-fed after starvation.^1,2 Raw fish and shellfish containing thiaminase, and large amounts of tea or coffee, can break down thiamine in food, but this only matters when intake is already low.