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Thiamin
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In one pass Vitamin B1 (thiamin) is a part the body cannot do without when it turns sugar into energy.
Educational content, not medical advice — consult a clinician.
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Chapter 1
A part needed to burn sugar
Vitamin B1 (thiamin) is a part the body cannot do without when it turns sugar into energy. It is not a fuel itself: once inside a cell, it becomes thiamin pyrophosphate (TPP) and sits on several key enzymes as their tool head.
The most important of these is pyruvate dehydrogenase (PDC). Glucose is first split into pyruvate in the cell's cytoplasm, and this enzyme has to convert pyruvate into a form that can enter the mitochondria, where it is burned the rest of the way in the citric acid cycle () to produce most of the energy. Without enough B1 this step jams, and sugar is only half burned.
That is why the brain, the nerves, and the heart, which rely most on burning sugar, run into trouble first. Severe deficiency is an emergency. Confusion, unsteady walking, and abnormal eye movements (Wernicke encephalopathy), or breathlessness and swelling that keep getting worse, mean you need medical care immediately, where a doctor gives B1 into a vein. This is not something a self-bought supplement can fix. The risk is highest in people who drink heavily over the long term and in people who vomit repeatedly after weight-loss surgery.
The most important of these is pyruvate dehydrogenase (PDC). Glucose is first split into pyruvate in the cell's cytoplasm, and this enzyme has to convert pyruvate into a form that can enter the mitochondria, where it is burned the rest of the way in the citric acid cycle () to produce most of the energy. Without enough B1 this step jams, and sugar is only half burned.
That is why the brain, the nerves, and the heart, which rely most on burning sugar, run into trouble first. Severe deficiency is an emergency. Confusion, unsteady walking, and abnormal eye movements (Wernicke encephalopathy), or breathlessness and swelling that keep getting worse, mean you need medical care immediately, where a doctor gives B1 into a vein. This is not something a self-bought supplement can fix. The risk is highest in people who drink heavily over the long term and in people who vomit repeatedly after weight-loss surgery.
Mechanism · Where the stalled sugar goes
TPP sits on three key enzymes:1. Pyruvate dehydrogenase complex (PDC): turns the pyruvate made by glycolysis into acetyl-CoA and feeds it into the citric acid cycle ()
2. Alpha-ketoglutarate dehydrogenase: a step inside the citric acid cycle, which also needs TPP
3. Transketolase: part of the pentose phosphate pathway, involved in making nucleotides and in producing (a coenzyme that carries reducing power in the cell)
Once PDC is inactivated, pyruvate cannot enter the mitochondria and can only be turned into lactate by lactate dehydrogenase (LDH), so blood lactate rises.
That is the chemical reason severe B1 deficiency can cause metabolic acidosis (blood that is too acidic). In the emergency department, unexplained lactic acidosis should prompt a check of thiamin status, especially in people who drink heavily over the long term, people on long-term total parenteral nutrition (TPN, where all nutrition goes in through a vein), and patients after weight-loss surgery.
The clinical order: IV thiamin is usually given before glucose, because glucose further uses up the little TPP that is left and can set off Wernicke encephalopathy. The European Federation of Neurological Societies (EFNS) guideline says thiamin should be given before any carbohydrate. This order rests mainly on case reports and reasoning from the mechanism, not on randomized trials.
Chapter 2
Why nerves go first
The brain is only about 2% of body weight, yet it uses about 20% of the body's energy. Neurons store almost no fuel of their own and depend mainly on glucose from the blood (during starvation they can also use some ketone bodies), and burning glucose all the way needs a working pyruvate dehydrogenase (PDC) and citric acid cycle at every step.
So when B1 falls short, the nerves fail first. The typical emergency is Wernicke encephalopathy, and its textbook triad is ophthalmoplegia (eyes that cannot move properly, causing double vision), ataxia (unsteady walking), and confusion. The damage concentrates in a few brain regions with especially high metabolism (the mammillary bodies and the areas around the third and fourth ventricles), where the energy supply has in effect collapsed. But few patients show all three signs, so the European Federation of Neurological Societies (EFNS) guideline says that in people who drink heavily, any two of four signs (poor diet, eye signs, cerebellar dysfunction, and a change in mental state or mild memory impairment) are enough to treat it as Wernicke.
It is an emergency: get medical care immediately so that B1 can be given into a vein. Untreated, it can progress to Korsakoff syndrome, in which people cannot form new memories and lose old ones, and by that stage the damage is often irreversible.
So when B1 falls short, the nerves fail first. The typical emergency is Wernicke encephalopathy, and its textbook triad is ophthalmoplegia (eyes that cannot move properly, causing double vision), ataxia (unsteady walking), and confusion. The damage concentrates in a few brain regions with especially high metabolism (the mammillary bodies and the areas around the third and fourth ventricles), where the energy supply has in effect collapsed. But few patients show all three signs, so the European Federation of Neurological Societies (EFNS) guideline says that in people who drink heavily, any two of four signs (poor diet, eye signs, cerebellar dysfunction, and a change in mental state or mild memory impairment) are enough to treat it as Wernicke.
It is an emergency: get medical care immediately so that B1 can be given into a vein. Untreated, it can progress to Korsakoff syndrome, in which people cannot form new memories and lose old ones, and by that stage the damage is often irreversible.
Clinical · Why bariatric surgery raises the risk
Besides long-term heavy drinking, weight-loss surgery (bariatric surgery) is the other major source of B1 deficiency today. Many people are already short before the operation: in two observational studies, 15.5–29% of people with obesity preparing for weight-loss surgery were deficient in B1.Several things stack up
Gastric bypass (Roux-en-Y) routes food past the duodenum and the upper jejunum, and the upper small intestine is where most B1 is absorbedSleeve gastrectomy does not bypass the small intestine; its risk comes mainly from vomiting after surgery and eating very littleVomiting after surgery: repeated vomiting keeps B1 from getting in, and it usually comes with eating almost nothingA sharp drop in total energy intake after surgery: less food means less B1 from food
The typical course
It mostly appears in the first few months after surgery, especially after repeated vomitingEarly signs are double vision and unsteady walking, which are easy to mistake for a rough recovery from the operationIt can progress from mild symptoms to irreversible Korsakoff syndrome within daysPersistent vomiting after surgery, being unable to eat, or confusion, unsteady walking, or abnormal eye movements mean you need medical care immediately
Prevention
Before surgery: check vitamin status (B1, B12, iron, vitamin D, folate)After surgery: the EFNS guideline recommends following B1 status for at least 6 months after surgery and giving B1 by injection into a vein or muscle; take a B1-containing multivitamin long term, at a dose set by the surgical teamAny patient with persistent vomiting who cannot eat: usually needs IV B1 right away, without waiting for test results, at a dose the doctor sets
Other groups at risk
People who drink large amounts of sugary soda over a long period and eat a very narrow diet (for example teenagers who live on cola and fast food): case reports existPeople on chemotherapy (especially with severe vomiting) and people on long-term total parenteral nutrition (TPN): B1 is routinely added to TPN solutionsPeople with advanced HIV and chronic diarrheaHyperemesis gravidarum (severe, hard-to-treat vomiting in pregnancy): prolonged vomiting drains B1, and giving glucose-containing IV fluids without B1 at that point can set off Wernicke encephalopathy. That is why adding B1 to emergency IV fluids in pregnancy is routine obstetric practice
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Chapter 3
The heart's energy demand
Heart muscle contracts without a break and demands a great deal of energy from its mitochondria: it makes and uses about 6 kg of a day. When B1 runs short, the nerves and the heart fail in two different ways, together called beriberi. It is a nutritional disease, not an infection.
Dry beriberi: mainly damage to the peripheral nerves, with numbness, tingling, and weakness in the hands and feetWet beriberi: mainly the heart, with cardiomyopathy, high-output heart failure (the heart pumps extra hard and still cannot meet the body's needs), and swelling
Wet beriberi runs like this: blood vessels in the body widen, the heart compensates by pumping more, the heart muscle's energy supply cannot keep up, and it finally fails. There is a fulminant form: Shoshin beriberi is the most acute form, can kill within hours, and needs emergency IV thiamin. Breathlessness and swelling that keep getting worse, especially in someone who drinks heavily, has had weight-loss surgery, or has been unable to eat for a long time, mean you need medical care immediately.
Dry beriberi: mainly damage to the peripheral nerves, with numbness, tingling, and weakness in the hands and feetWet beriberi: mainly the heart, with cardiomyopathy, high-output heart failure (the heart pumps extra hard and still cannot meet the body's needs), and swelling
Wet beriberi runs like this: blood vessels in the body widen, the heart compensates by pumping more, the heart muscle's energy supply cannot keep up, and it finally fails. There is a fulminant form: Shoshin beriberi is the most acute form, can kill within hours, and needs emergency IV thiamin. Breathlessness and swelling that keep getting worse, especially in someone who drinks heavily, has had weight-loss surgery, or has been unable to eat for a long time, mean you need medical care immediately.
Evidence · Should heart-failure patients take B1?
B1 deficiency is not rare among people with heart failure, but the numbers vary widely between studies:Hanninen 2006 (a cross-sectional study of people hospitalized with heart failure, judged by TPP in red blood cells): 33% were deficient in B1People on long-term diuretics: the share with abnormal B1 status varies widely from study to study, which itself shows that the studies did not use the same cut-offs or measurement methods
Why people with heart failure run short
Loop diuretics (furosemide, torsemide, bumetanide) are common heart-failure drugs; they greatly increase urine output, and more B1 leaves with the urineHeart failure itself, plus a poor appetite, also means less B1 comes inThe breathlessness, swelling, and fatigue that low B1 causes look just like heart failure, so they are easily put down to the heart failure itself and missed
Trial evidence: small and mixed
Schoenenberger 2012 (randomized, double-blind, crossover, only n=9, all with chronic heart failure on diuretics; 300 mg/day by mouth for 28 days): left ventricular ejection fraction (LVEF, the share of blood in the ventricle pumped out with each beat) was 3.9% higher in absolute terms than during the placebo periodSmithline 2019 (a randomized pilot in acute heart failure, 100 mg IV on the evenings of the first and second days): of 118 evaluable patients, almost none were deficient to begin with; most measures of breathlessness and all the secondary measures did not improveThe existing trials are all small with inconsistent results, and none used death as an endpoint
What guidelines say (as of 2025)
The heart-failure guidelines of the American Heart Association (AHA) and the European Society of Cardiology (ESC) do not recommend routine B1 testing or supplementation; the evidence here is still exploratorySome experts argue that B1 could be considered for people on long-term high-dose diuretics, with repeated admissions, and with heart failure that has no clear cause and is hard to control
In practice
There is no evidence that every person with heart failure should take extra B1For patients on long-term high-dose diuretics who eat poorly, are older, and whose heart failure is getting worse for no clear reason, some experts argue for a few days of empirical IV B1, because it is cheap and safe. This is expert opinion, not a trial result, and whether to use it is the treating doctor's decisionSome hospitals routinely add B1 for people with severe heart failure admitted to the intensive care unit (ICU), on the same logic as preventing Wernicke encephalopathy
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Chapter 4
Why heavy drinking drains B1
Long-term heavy drinking is the classic high-risk setting for B1 deficiency, because four leaks run at the same time:
1. Less comes in: much of the energy comes from alcohol, and meals are poor
2. Absorption gets worse: alcohol damages the transporters in the lining of the small intestine that actively carry B1 in
3. Less is stored: the liver is the main store for B1, and a damaged liver cannot hold it
4. It cannot be put to work: when the liver is damaged, the step that turns B1 into working TPP is impaired too
Together, the four explain an order in the emergency department: give thiamin before giving these patients glucose. Once glucose enters the metabolic pathway it quickly uses up the little TPP that is left and can directly set off Wernicke encephalopathy. A person who drinks and develops confusion, unsteady walking, or double vision needs medical care immediately.
1. Less comes in: much of the energy comes from alcohol, and meals are poor
2. Absorption gets worse: alcohol damages the transporters in the lining of the small intestine that actively carry B1 in
3. Less is stored: the liver is the main store for B1, and a damaged liver cannot hold it
4. It cannot be put to work: when the liver is damaged, the step that turns B1 into working TPP is impaired too
Together, the four explain an order in the emergency department: give thiamin before giving these patients glucose. Once glucose enters the metabolic pathway it quickly uses up the little TPP that is left and can directly set off Wernicke encephalopathy. A person who drinks and develops confusion, unsteady walking, or double vision needs medical care immediately.
Clinical · What is in the ER banana bag
Banana bag is emergency doctors' informal name for a bag of yellow IV fluid, given mainly to patients suspected of long-term heavy drinking, malnutrition, or an unexplained change in consciousness.The classic recipe
Thiamin 100 mg (B1, the most important ingredient)Folate 1 mg (B9)Multivitamin 10 mL (B vitamins, vitamin C, and some fat-soluble vitamins)Magnesium sulfate (MgSO₄) 2 g (magnesium, a common aid during alcohol withdrawal)All added to 1 liter of saline with 5% glucose; the color of the B vitamins turns it yellow
Why it is done
Acute intoxication, severe malnutrition, and unexplained coma cannot wait for blood test resultsSo key water-soluble vitamins and magnesium are given empirically, straight awayThe risk is very low (the EFNS guideline judges the overall safety of thiamin to be very good) and the benefit is high (preventing Wernicke encephalopathy and helping manage withdrawal)The 100 mg in the bag is a preventive dose. When Wernicke encephalopathy is already suspected, the EFNS guideline recommends a treatment dose of 200 mg three times a day, preferably IV
The order is the key
Thiamin must come first, then glucose: in someone short of B1, glucose entering the PDC pathway uses up the little TPP that is left and speeds up acute Wernicke encephalopathyThis is one of the most emphasized order rules in emergency medicineThe textbook phrasing: Thiamin before glucose in altered mental status
Alcohol withdrawal syndrome (AWS)
With long-term drinking, the brain offsets alcohol's sedating effect by turning down its brake, (the brain's main inhibitory signal), and turning up its accelerator, glutamate (the main excitatory signal). When drinking stops suddenly, the brake is weak and the accelerator strong, which brings tremor, anxiety, sweating, a racing heart, hallucinations, seizures, and at worst delirium tremens (DT)Severe withdrawal can be fatal if it is not treated properly. Shaking, heavy sweating, a racing heart, hallucinations, or seizures after suddenly stopping drinking mean you need medical care immediatelyStandard treatment: benzodiazepine sedatives, plus vitamin support (the banana bag), plus monitoringB1 is the foundation: without it, even when withdrawal has been treated, permanent damage from Wernicke encephalopathy or Korsakoff syndrome may remain
A few honest points for home
Taking B vitamins the day after heavy drinking to ease a hangover has weak scientific supportWhat actually prevents a hangover: drink less, drink water in between, and do not drink on an empty stomachChronic heavy drinking with repeated withdrawal: this is not something supplements can solve; it needs medical and psychological treatment together
Chapter 5
Refined grains lose their B1
B1 is concentrated in the bran and germ on the outside of the grain, so the whiter the grain is milled, the more B1 is lost: milling rice into white rice loses about 70–80% of its B1, and milling wheat into refined white flour loses about 80%. Good sources are whole grains, legumes, pork (see Pork), nuts, and fortified cereals.
Historically, beriberi spread widely across East Asia along with the dietary shift from brown rice to polished white rice (the late 19th to early 20th century). The Japanese navy physician Kanehiro Takaki (1884) changed sailors' rations, and the Dutch physician Eijkman (1897) experimented on chickens; from two directions, both pointed to the same cause: the polished white rice.
Who is at risk today: people whose staple food is almost entirely refined rice and flour, people who eat very little in total (after weight-loss surgery, in anorexia nervosa), and people with kidney disease on dialysis (B1 is lost during dialysis). Most people do not need a B1 supplement; replacing part of their staples with whole grains and legumes does more.
Historically, beriberi spread widely across East Asia along with the dietary shift from brown rice to polished white rice (the late 19th to early 20th century). The Japanese navy physician Kanehiro Takaki (1884) changed sailors' rations, and the Dutch physician Eijkman (1897) experimented on chickens; from two directions, both pointed to the same cause: the polished white rice.
Who is at risk today: people whose staple food is almost entirely refined rice and flour, people who eat very little in total (after weight-loss surgery, in anorexia nervosa), and people with kidney disease on dialysis (B1 is lost during dialysis). Most people do not need a B1 supplement; replacing part of their staples with whole grains and legumes does more.
Background · How polished rice caused beriberi
Beriberi swept East Asia in the 1880s and 90s: industrial rice milling made white rice the staple food in cities, and milling stripped away 70–80% of the grain's B1, which was the real cause. At the time many people thought it was an infectious disease. The best-known moment in its history is Eijkman (1897): he found that hospital chickens fed white rice developed a beriberi-like nerve paralysis and recovered quickly when switched to brown rice, and concluded that rice bran held something that prevented the disease (later shown to be B1). The work earned him the 1929 Nobel Prize.What this history leaves us today is the mechanism, not the story: refined staples systematically strip out B1. In many countries, fortification plus a varied diet has made beriberi almost invisible. But mild B1 deficiency, short of causing disease, is still real among people who drink heavily over the long term, people after weight-loss surgery, and people on long-term dialysis, and some studies have reported low B1 in people with diabetes.
References · 5
- National Institutes of Health, Office of Dietary Supplements. (2021). Thiamin — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Thiamin-HealthProfessional
- Bettendorff, L. (2014). Thiamine. In: Zempleni, J., et al. (Eds.), Handbook of Vitamins, 5th ed. (pp. 267-324). CRC Press. 10.1201/b15413
- Galvin, R., Bråthen, G., Ivashynka, A., Hillbom, M., Tanasescu, R., & Leone, M. A. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology, 17(12), 1408-1418. EFNS recommendations: in alcoholics, clinical diagnosis requires two of four signs - dietary deficiencies, eye signs, cerebellar dysfunction, and an altered mental state or mild memory impairment (Level B); thiamine 200 mg three times daily, preferably intravenously, before any carbohydrate (Level C); after bariatric surgery, follow thiamine status for at least 6 months (Level B) and give parenteral thiamine (good practice point); parenteral thiamine for all at-risk patients admitted to the emergency room (good practice point) (abstract, PMID 20642790). 10.1111/j.1468-1331.2010.03153.x
- Whitfield, K. C., Bourassa, M. W., Adamolekun, B., et al. (2018). Thiamine deficiency disorders: diagnosis, prevalence, and a roadmap for global control programs. Annals of the New York Academy of Sciences, 1430(1), 3-43. 10.1111/nyas.13919
- DiNicolantonio, J. J., Liu, J., & O'Keefe, J. H. (2018). Thiamine and cardiovascular disease: a literature review. Progress in Cardiovascular Diseases, 61(1), 27-32. 10.1016/j.pcad.2018.01.009