Text gBeriberi is a serious medical condition caused by a deficiency of thiamine (vitamin B1), an essential nutrient for energy metabolism and nerve function. This deficiency leads to significant impairment of the cardiovascular and nervous systems, producing a range of symptoms depending on the type of beriberi. Although once thought to be a historical disease, beriberi continues to affect populations worldwide, particularly in regions with poor nutrition, chronic alcoholism, or medical conditions that impair thiamine absorption. 

Thiamine is a vital cofactor in carbohydrate metabolism and neural energy supply. When deficient, energy production fails, leading to dysfunction in highly active tissues such as nerves and the heart. Untreated beriberi can cause severe complications, including heart failure, neuropathy, and even death. This article provides a comprehensive overview of beriberi, including its causes, pathophysiology, clinical presentation, diagnosis, treatment, and prevention. oes here.

Beriberi is a nutritional deficiency disorder caused by inadequate levels of thiamine (vitamin B1), a water-soluble vitamin essential for converting food into energy. Thiamine functions as a coenzyme in critical metabolic reactions, including: 

• Pyruvate dehydrogenase complex: Converts pyruvate to acetyl-CoA for energy production. 

• Alpha-ketoglutarate dehydrogenase: Involved in the Krebs cycle for ATP synthesis. 

• Transketolase: Key enzyme in the pentose phosphate pathway for nucleic acid and NADPH production. 

When thiamine is deficient, energy production in cells becomes impaired, leading to lactic acidosis and tissue dysfunction. Beriberi manifests in several forms: 

• Wet beriberi – affects the cardiovascular system, causing edema and heart failure. 

• Dry beriberi – affects the nervous system, leading to peripheral neuropathy. 

• Infantile beriberi – occurs in infants of thiamine-deficient mothers. 
• Wernicke-Korsakoff syndrome – a neuropsychiatric condition associated with chronic thiamine deficiency, particularly in alcohol use disorder. 

Beriberi remains a global health concern in both developing and developed regions. It is most common in: 

• Populations relying on polished rice or processed grains low in thiamine. 

• Individuals with alcohol use disorder, which interferes with thiamine absorption and metabolism. 

• Patients receiving prolonged parenteral nutrition without supplementation. 

• Individuals with malabsorption syndromes or post-bariatric surgery. 

• Groups with increased metabolic demand, such as pregnant or lactating women. 

Although rare in industrialized nations, thiamine deficiency persists in vulnerable populations. In low-resource settings, infantile beriberi remains a leading cause of preventable cardiac failure. 

Beriberi occurs when thiamine intake, absorption, or utilization is insufficient to meet metabolic needs. Common causes include: 

Dietary deficiency 

• Diets based on polished rice or refined grains. 

• Famine or limited food access. 

Alcohol use disorder 

• Impaired intestinal absorption of thiamine. 

• Reduced conversion to its active form, thiamine pyrophosphate (TPP). 

• Coexisting malnutrition. 

Increased physiological demand 

• Pregnancy and lactation. 

• Systemic infections or hyperthyroidism. 

• Fever or sepsis. 

Malabsorption 

• Chronic diarrhea or intestinal inflammation. 

• Post-gastric or bariatric surgery. 

• HIV/AIDS and other chronic illnesses. 

Excessive loss 

• Dialysis or diuretic therapy causing urinary thiamine losses. 

Enzyme defects and antithiamine factors 

• Rare genetic enzyme deficiencies. 

• Consumption of foods with thiaminases (raw freshwater fish, ferns). 

Thiamine is critical for carbohydrate metabolism and energy generation. Deficiency leads to cellular energy failure, particularly in tissues with high metabolic activity such as the brain, nerves, and heart. 

Key mechanisms include: 

• Impaired carbohydrate metabolism: Pyruvate cannot enter the Krebs cycle, leading to lactic acidosis. 

• Neuronal injury: Energy deficit disrupts axonal transport and causes demyelination, resulting in neuropathy. 

• Cardiac dysfunction: Myocardial energy failure leads to vasodilation, fluid retention, and high-output heart failure. 
• Cerebral effects: Deficiency affects neurotransmitter synthesis, causing Wernicke’s encephalopathy and Korsakoff’s psychosis. 

The clinical manifestations depend on the affected organ system and the duration of deficiency. 

1. Wet Beriberi (Cardiovascular) 

• Peripheral edema. 

• Tachycardia and wide pulse pressure. 

• Warm extremities and bounding pulses. 

• Shortness of breath and orthopnea. 

• Elevated jugular venous pressure. 

• Cardiomegaly on imaging. 

Severe cases, known as Shoshin beriberi, present with fulminant cardiac failure and lactic acidosis, which can be fatal if untreated. 

2. Dry Beriberi (Neurological) 

• Symmetrical peripheral neuropathy. 

• Numbness, tingling, and burning sensations in feet. 

• Muscle weakness, especially in lower limbs. 

• Loss of reflexes and difficulty walking. 

• Muscle wasting and paralysis in advanced stages. 

3. Infantile Beriberi 

• Occurs in infants aged 2–6 months breastfed by thiamine-deficient mothers. 

• Restlessness, crying, vomiting, and aphonia. 

• Tachycardia, cyanosis, and heart failure. 

• May lead to sudden death if not promptly treated. 

4. Wernicke-Korsakoff Syndrome 

• Wernicke’s encephalopathy: confusion, ataxia, and eye movement abnormalities. 

• Korsakoff’s psychosis: memory loss, confabulation, and apathy. 

Prompt thiamine administration can prevent irreversible brain damage. 

Clinical diagnosis 

Beriberi is often diagnosed clinically in at-risk patients presenting with characteristic symptoms. Early recognition is essential to prevent complications. 

Laboratory tests 

• Thiamine levels: measured in plasma or whole blood. 

• Erythrocyte transketolase activity: decreased in deficiency. 

• Lactate and pyruvate levels: elevated with increased lactate-to-pyruvate ratio. 

• Electrolyte disturbances: hypokalemia and hypomagnesemia. 

• BNP levels: elevated in cardiac involvement. 

Imaging studies 

• Echocardiography: shows high-output cardiac failure in wet beriberi. 

• Brain MRI: reveals characteristic lesions in Wernicke’s encephalopathy (thalami, mammillary bodies). 

Conditions that may resemble beriberi include: 

• Diabetic neuropathy. 

• Guillain-Barré syndrome. 

• Dilated cardiomyopathy. 

• Vitamin B12 deficiency. 

• Alcoholic neuropathy. 

• Multiple sclerosis. 

• Sepsis with lactic acidosis. 

Careful history-taking and laboratory testing help differentiate beriberi from other metabolic and neurological conditions. 

Thiamine replacement 

Immediate thiamine repletion is the cornerstone of treatment. 

• IV thiamine: 100–500 mg daily for several days. 

• Oral thiamine: 50–100 mg daily for maintenance. 

• Always administer thiamine before glucose to avoid precipitating Wernicke’s encephalopathy. 

Supportive care 

• Manage heart failure with gentle diuresis. 

• Correct electrolyte imbalances. 

• Provide balanced nutrition with adequate calories and other B vitamins. 

Address underlying causes 

• Alcohol cessation programs. 

• Nutritional counseling and food fortification. 

• Manage chronic diseases affecting absorption or metabolism. 

If left untreated, thiamine deficiency can result in: 

• Irreversible neuropathy and paralysis. 

• Memory loss and cognitive decline. 

• Severe cardiac failure or shock. 

• Sudden death (Shoshin beriberi). 

• Developmental delays in infants. 

The prognosis depends on the severity and duration of deficiency and the rapidity of treatment initiation. Most patients show dramatic improvement in cardiac and neurological symptoms within days to weeks of thiamine replacement. However, prolonged deficiency may cause permanent neurological deficits, particularly in Wernicke-Korsakoff syndrome. 

Preventive measures focus on ensuring adequate thiamine intake and addressing risk factors: 

• Consume thiamine-rich foods such as whole grains, legumes, nuts, and pork. 

• Supplement thiamine in high-risk populations (alcohol use disorder, bariatric surgery patients). 

• Enforce food fortification programs in endemic regions. 

• Educate communities about balanced nutrition. 

• Screen and supplement during pregnancy and lactation. 

Most individuals recover completely with prompt treatment. Long-term management focuses on maintaining adequate nutrition, abstaining from alcohol, and addressing any residual neurological symptoms through physical therapy and rehabilitation. Education and dietary awareness are key to preventing recurrence. 

Beriberi is a preventable yet potentially fatal condition that highlights the importance of micronutrient balance in human health. Though largely avoidable, it persists in settings of poverty, malnutrition, and alcohol misuse. Early recognition, rapid thiamine replacement, and sustained nutritional support can fully reverse symptoms in most cases. 

Global health initiatives emphasizing food fortification, public education, and clinician awareness are essential to eradicating beriberi. Continued research into improved diagnostic methods and prevention strategies will further reduce the burden of thiamine deficiency. 

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