What is thiamine (vitamin B1)?

What is Thiamine (Vitamin B1)?

Thiamine (vitamin B1) is a water-soluble vitamin essential for cellular energy metabolism, nervous system function, and carbohydrate processing—deficiency can cause irreversible neurological damage within days to weeks, making recognition and treatment critical in clinical practice. 1, 2

Biochemical Role and Mechanism

Thiamine functions primarily as thiamine pyrophosphate (TPP), the biologically active coenzyme form that is indispensable for multiple metabolic pathways 1, 3:

• Carbohydrate metabolism: TPP serves as a cofactor for decarboxylation of pyruvic acid to acetaldehyde and CO₂, preventing toxic accumulation of pyruvate and lactate in blood 1, 2
• Energy production: Essential for the citric acid cycle (Krebs cycle) and cellular respiration in mitochondria, converting nutrients to ATP 2, 4
• Pentose phosphate pathway: Required for synthesis of nucleic acids and pentose sugars critical for DNA/RNA production 2, 5
• Fatty acid oxidation: Participates in oxidation of fatty acids and protein synthesis 2
• Neurotransmitter synthesis: Necessary for proper synthesis of neurotransmitters in the central and peripheral nervous system 2, 6

Absorption, Distribution, and Storage

Thiamine has the smallest body stores of all B vitamins—approximately 25-30 mg total in adults—which can be completely depleted within just 20 days of inadequate intake 7, 1:

• Absorbed in the jejunum and ileum through active, carrier-mediated transport at therapeutic doses, switching to passive diffusion at higher concentrations 7
• Highest tissue concentrations occur in liver, brain, kidney, and heart 1
• Tissue stores increase only 2-3 times maximum even with excess intake 1
• Metabolism is rapid with excess excreted in urine—no established upper toxicity limit 7, 1
• Absorption following intramuscular administration is rapid and complete 1

Clinical Consequences of Deficiency

Neurological Manifestations

Early signs of thiamine deficiency include cognitive decline, loss of appetite, weight loss, reduced walking speed, abnormal gait, and muscle weakness 8:

• Wernicke's encephalopathy: Confusion, ataxia, ophthalmoplegia (nystagmus) requiring immediate 500 mg IV three times daily 7, 2
• Korsakoff syndrome: Confabulation, memory loss, psychosis representing irreversible neuronal damage 2, 3
• Peripheral neuropathy: Loss of vibratory sensation in lower extremities, leading to higher fall incidence 8, 3
• Optic neuropathy: Visual disturbances from nerve damage 2, 6

Cardiovascular and Metabolic Effects

• Beriberi: Cardiac failure, edema, neuritis from severe deficiency 8, 6
• Type B lactic acidosis: Impaired aerobic respiration causes lactate accumulation, reversible with thiamine 100-300 mg IV 7, 4
• Dilated cardiomyopathy: Occurs in 6% of ambulatory heart failure patients, especially those on chronic diuretics 9

Mechanism of Neuronal Damage

Thiamine deficiency causes mitochondrial dysfunction through reduced activity of thiamine-dependent enzymes, resulting in increased reactive oxygen species (ROS) production and inflammatory microglial activation 8:

• Animal studies show moderate-low thiamine intake triggers immune response with 90% neural tissue loss by day 10-11 8
• Neuronal commitment to apoptotic pathways becomes irreversible by day 10-11 of deficiency 8
• Region-specific sensitivity occurs in neuronal tissues despite comparable metabolic profiles 8

High-Risk Populations

Thiamine deficiency occurs in specific clinical scenarios where metabolic demands exceed intake or absorption 7, 3:

• Alcohol use disorder: 30-80% show clinical or biological deficiency due to poor intake, impaired absorption, and increased metabolic demands 7
• Critical illness: Over 90% of critically ill patients are thiamine deficient or depleted 7
• Post-bariatric surgery: Highest risk in first 3-4 months postoperatively, requiring lifelong supplementation 50-100 mg daily 7, 10
• Chronic diuretic therapy: Increases renal thiamine losses, affecting 6% of heart failure patients 7, 9
• Malnutrition/eating disorders: Stores deplete within 20 days of inadequate intake 7, 10
• Refeeding syndrome: Requires 300 mg IV before initiating nutrition therapy 7
• Continuous renal replacement therapy: Significant thiamine losses through dialysis 7

Dietary Sources and Requirements

The adequate intake for healthy adults is 1.1-1.2 mg/day, with recommended dietary allowances of 1.1 mg/day for women and 1.2 mg/day for men 7:

• Food sources: Enriched cereals and breads, lean pork, whole grains, legumes, liver, meat, eggs, green vegetables 8
• Increased requirements: Carbohydrate-rich diets increase thiamine needs for glucose metabolism 1
• Factors reducing bioavailability: Alcohol, sulfites, tannins, o-diphenols (from coffee), and diuretics reduce thiamine content and absorption 8

Critical Clinical Pitfalls

Standard multivitamins contain only 1-3 mg thiamine, which is grossly inadequate for treating or preventing deficiency in high-risk patients 7, 10:

• Never administer glucose-containing IV fluids before thiamine in malnourished or at-risk patients—this can precipitate acute Wernicke's encephalopathy causing irreversible brain damage 7, 10
• Cooking methods, storage, and co-ingestion of certain foods significantly reduce thiamine content 8
• Dietary intake assessments often fail to account for relative deficits induced by refined carbohydrate consumption 8
• Plasma thiamine is unreliable—only red blood cell thiamine diphosphate (RBC-TPP) accurately reflects tissue stores 7, 9