Thiamine Deficiency (Beriberi): Wet Beriberi (Heart)

Table of Contents

1. What Wet Beriberi Feels Like
2. The Mechanism: Why a Missing Vitamin Floods the Body
3. Shoshin Beriberi: the Fulminant Emergency
4. Honesty: Swelling and Breathlessness Have Many Causes
5. Clues That Point to Wet Beriberi
6. What Causes the Deficiency
7. Getting Diagnosed
8. Correcting It: the Thiamine Trial
9. When to Seek Care / Red Flags
10. Key Research Papers
11. Connections
12. Featured Videos

What Wet Beriberi Feels Like

Wet beriberi tends to announce itself through the plumbing of the body — the way fluid moves, pools, and overflows — rather than through the numbness and burning of its “dry” cousin (dry beriberi). The classic picture builds over days to a few weeks and includes:

• Swollen legs and ankles (edema) — the “wet” in the name. Press a thumb into the shin and the dent stays for a moment (pitting edema). In advanced cases the swelling climbs to the thighs, the genitals, the abdomen, and even the face.
• Breathlessness — first on exertion (climbing stairs, walking uphill), then at rest. Many people find they can't breathe comfortably lying flat and have to prop themselves up on pillows to sleep (orthopnea), or wake at night gasping for air.
• A racing or pounding heart — the pulse is often fast even at rest, and people may feel their heart thudding or fluttering. The hands and feet may feel oddly warm, because blood vessels are dilated wide open.
• A bloated, heavy abdomen — fluid can collect in the belly (ascites) and the liver can become congested and tender as blood backs up behind a struggling heart.
• Fatigue out of proportion to effort — a deep, draining tiredness, often layered on top of the early fatigue and appetite loss that precede full beriberi.

To a doctor, the combination of warm extremities, a bounding fast pulse, low blood pressure that doesn't quite explain how unwell the person is, and worsening edema is a recognizable — if uncommon — pattern. It looks like heart failure, but the hands are warm rather than cold and clammy, which is a quiet hint that this is not the usual kind of failing heart.

Back to Table of Contents

The Mechanism: Why a Missing Vitamin Floods the Body

To understand wet beriberi you have to understand what thiamine actually does. Thiamine, as its active form thiamine pyrophosphate, is an essential helper (a cofactor) for a small set of enzymes that sit at the very center of how cells turn food into usable energy — chiefly pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, the gatekeepers that feed sugar into the mitochondria, plus transketolase. Without thiamine, cells cannot fully burn glucose for energy. They are forced to stop short, and instead of completing the process they pile up lactic acid.

Now apply that to the circulation. Two things happen at once, and together they explain the “high-output” paradox:

1. The blood vessels throw open their gates. The smooth muscle lining small arteries and arterioles depends on a steady energy supply to stay partly constricted (this background tone is what keeps blood pressure up). Starved of energy and bathed in lactic acid — which is itself a powerful vasodilator — these vessels relax and widen dramatically. Resistance to blood flow collapses. The body responds the way it would to a major internal “short circuit” in the plumbing: the heart speeds up and pumps more blood per minute to fill all that newly opened space and keep pressure from falling. This is why the output is high.
2. The kidneys hold on to salt and water. Even though the heart is pumping a large volume, the wide-open vessels mean blood pressure and the “effective” circulation the kidneys sense can stay low. The kidneys interpret this as the body being under-filled and switch on the salt-and-water-retaining hormone systems (the renin-angiotensin-aldosterone axis). They clamp down and retain fluid. With nowhere useful to go, that retained fluid leaks out of the over-stretched circulation into the tissues — producing the leg swelling, the abdominal fluid, and the lung congestion. That overflow is the wet in wet beriberi.

An analogy. Picture the circulation as a household water system with a powerful pump. In wet beriberi, someone has opened every tap and faucet in the house at once (the dilated vessels). The pump (the heart) responds by working harder and pushing out far more water than usual — but the pressure at any single tap still sags because so many are open. The water company (the kidneys), reading low pressure, sends even more water into the system to compensate. The result is a house that is simultaneously moving huge volumes of water and overflowing onto the floor. Restore the missing part — close the taps by giving back thiamine — and the vessels tighten, the pressure recovers, the kidneys stop hoarding fluid, and the flood drains away. Crucially, the heart muscle itself was rarely the original problem; it was responding correctly to an impossible plumbing situation.

Over a longer time the overworked heart can genuinely weaken and dilate, producing a true cardiomyopathy — but the defining and reversible feature of wet beriberi is the high-output, vasodilated state described above.

Back to Table of Contents

Shoshin Beriberi: the Fulminant Emergency

There is a sudden, life-threatening version of wet beriberi with its own name: shoshin beriberi (from a Japanese term meaning “acute heart damage”). Instead of building over weeks, it explodes over hours to a day or two, and it is a true medical emergency.

In shoshin beriberi the vasodilation and lactic acid accumulation become so severe that blood pressure collapses despite a racing heart. People become acutely breathless, develop a blue tinge to the lips (cyanosis), and may slip into cardiogenic shock — a state where the circulation can no longer deliver enough oxygen to the organs. Blood tests show a striking lactic acidosis (the blood turns acidic from all the unburned-fuel lactic acid). Left untreated, shoshin beriberi is rapidly fatal.

What makes it one of the most dramatic conditions in medicine is the reversal. Because the heart muscle is often intact and the whole crisis is being driven by a single missing molecule, intravenous thiamine can reverse cardiogenic shock within hours — blood pressure climbs, the lactic acid clears, the breathing eases, and a patient who looked moments from death recovers. Case series and reviews of shoshin beriberi repeatedly describe this near-miraculous response. The catch is that the diagnosis has to be suspected: a person in shock who is given fluids and standard heart-failure drugs but not thiamine can deteriorate, because those treatments don't touch the root cause. This is exactly why thiamine is given empirically whenever the picture might fit.

Back to Table of Contents

Honesty: Swelling and Breathlessness Have Many Causes

It is important to be candid: swollen legs and breathlessness are extremely common, and in wealthy countries they are almost never caused by thiamine deficiency. Wet beriberi is rare. For a person with puffy ankles and shortness of breath, the overwhelming odds are that the cause is something else entirely, and a missing vitamin is an unlikely explanation. The far more frequent explanations include:

• Ordinary (left- or right-sided) heart failure — usually the low-output kind, from a heart weakened by coronary disease, prior heart attack, or long-standing high blood pressure. Here the hands tend to be cold, not warm.
• Kidney disease — failing kidneys or heavy protein loss in the urine cause salt and water retention and widespread swelling.
• Liver disease — cirrhosis lowers blood protein and raises pressure in the abdominal veins, causing leg edema and ascites.
• Venous problems — varicose veins and chronic venous insufficiency cause leg swelling without any heart or vitamin involvement; a blood clot (deep vein thrombosis) causes one-sided swelling.
• Medications — certain blood-pressure drugs (calcium-channel blockers), anti-inflammatories, and some diabetes medicines cause fluid retention.
• Thyroid disease, severe anemia, and pregnancy — each can cause edema, and severe anemia, like beriberi, can itself produce a high-output state.

A symptom of swelling is therefore not evidence of thiamine deficiency on its own. Wet beriberi earns consideration only when the clinical setting fits (see the next two sections) — and even then it is confirmed by the response to treatment as much as by any single test.

Back to Table of Contents

Clues That Point to Wet Beriberi

Several features shift suspicion toward thiamine deficiency as the cause of heart failure and swelling, especially in combination:

• A high-output picture. Warm hands and feet, a bounding fast pulse, and a wide pulse pressure — the opposite of the cold, clamped-down picture of ordinary low-output failure. When tests (an echocardiogram or other measures) show the heart is pumping a large volume yet the person is still in failure, the differential narrows sharply toward causes like beriberi, severe anemia, and overactive thyroid.
• Unexplained lactic acidosis. A high blood lactate with no obvious reason (no sepsis, no shock from blood loss) in someone with heart failure is a classic flag — it is the biochemical fingerprint of cells unable to finish burning fuel.
• A risk context for poor thiamine intake. Heavy alcohol use, prolonged poor nutrition, bariatric (weight-loss) surgery, persistent vomiting, dialysis, or long-term high-dose heart-failure diuretic therapy (see Causes below). Wet beriberi rarely appears in someone eating a normal varied diet with none of these risks.
• Heart failure that doesn't add up. A relatively young person, or someone with no coronary disease and no obvious reason to be in failure, who nonetheless develops rapid edema and breathlessness — particularly alongside the nerve or brain features of dry beriberi or Wernicke encephalopathy (confusion, eye-movement problems, unsteadiness). Wet and dry beriberi can coexist in the same patient.
• The thiamine response. The single most convincing clue of all is a rapid improvement after intravenous thiamine — the diuresis (suddenly passing large amounts of urine), falling heart rate, and clearing breathlessness that follow a dose. This is treated as a diagnostic test in its own right.

Back to Table of Contents

What Causes the Deficiency

The body stores only a small amount of thiamine — enough for roughly two to three weeks — so deficiency develops faster than for most vitamins once intake drops or losses rise. The situations that produce wet beriberi are the same ones that produce thiamine deficiency generally:

• Chronic heavy alcohol use — the leading cause in wealthy countries. Alcohol reduces thiamine intake (calories from drink displace food), impairs its absorption in the gut, and blocks its conversion to the active form. Alcohol-related beriberi often blends heart, nerve, and brain features.
• Loop-diuretic therapy for heart failure — a genuine and somewhat ironic problem. The strong “water pills” (such as furosemide) used to treat heart failure flush thiamine out in the urine along with the fluid. Earlier studies reported thiamine deficiency in as many as 50% of heart-failure outpatients and as many as 96% of heart-failure patients in hospital, raising the concern that the treatment for one kind of failure can quietly contribute to another. The results have been inconsistent: a 2016 study of 30 stable heart-failure outpatients at the Mayo Clinic, all on standard loop diuretics, put the share with deficiency below 11.6% and found no link between diuretic dose and thiamine levels; its authors called the prevalence very low, while noting that earlier work found heart-function gains with high-dose thiamine regardless of blood levels.
• Poor or unbalanced nutrition — severe dieting, eating disorders, homelessness, or a diet built around polished (white) rice and refined carbohydrate with little whole grain, meat, or legumes. Historically, beriberi swept through populations that switched to milled white rice, which strips away the thiamine-rich outer layers.
• Babies of thiamine-deficient mothers — beriberi is not only history. A 2021 review describes infantile beriberi, which can be fatal, as still a cause of infant deaths in parts of South and Southeast Asia where white rice is the staple. Breastfed babies become deficient because their mothers are deficient and the breast milk carries too little thiamine; poor dietary variety, food preparation and cooking practices, and traditional food restrictions after childbirth likely play a role. The signs overlap with other illnesses, so it is often missed.
• Increased needs or losses — pregnancy with severe vomiting (hyperemesis), prolonged vomiting from any cause, kidney dialysis, and refeeding after starvation (giving carbohydrate rapidly burns through thiamine and can precipitate acute deficiency).
• Bariatric and other gastrointestinal surgery — operations that reduce stomach size or bypass parts of the intestine can sharply cut thiamine absorption, sometimes producing deficiency within weeks to months.
• High intake of glucose without thiamine — giving intravenous glucose-containing fluids to a depleted person before replacing thiamine can tip them into acute deficiency, because metabolizing the sugar consumes the little thiamine that remains. This is why thiamine is given first or alongside glucose in at-risk patients.

Back to Table of Contents

Getting Diagnosed

Diagnosing wet beriberi is more about recognizing the pattern and confirming the response to treatment than about waiting on a single number. Blood tests for thiamine exist but are not available quickly everywhere, and a depleted person can be dangerously ill before any result returns — so when the picture fits, treatment is started without waiting for confirmation. Still, several tests build the case:

• Thiamine status testing. The most reliable laboratory measure is erythrocyte transketolase activity (and how much it increases when thiamine is added — the “TPP effect”), or a direct measurement of thiamine and its phosphate esters in whole blood. These confirm deficiency but often come back after treatment has already begun.
• Blood lactate. A raised lactate with no other explanation supports the diagnosis and tends to fall dramatically as thiamine takes effect.
• An echocardiogram. This ultrasound of the heart can show the high-output, hyperdynamic state and rule in or out other causes of heart failure (a weak, scarred, or valve-damaged heart).
• An electrocardiogram and basic blood panel. A routine metabolic panel checks kidney and liver function and electrolytes — including magnesium, which is needed for thiamine to be converted to its active form and is often low in the same patients. An electrocardiogram (ECG) looks for rhythm changes and helps exclude other cardiac problems (arrhythmia).

The practical bottom line: in the right clinical setting, a clinician will give thiamine first, draw confirmatory tests if available, and let the dramatic improvement help close the loop on the diagnosis.

Back to Table of Contents

Correcting It: the Thiamine Trial

Treatment is, on the surface, almost startlingly simple — give back the missing vitamin — but the way it is given matters, and a few cautions are vital.

• Intravenous thiamine, promptly. For wet beriberi and especially for shoshin beriberi, thiamine is given by injection (intravenous or intramuscular), not by mouth, because a sick gut may not absorb it reliably and because the situation can be too urgent to wait. Doses used in serious cases are far higher than the dietary requirement — tens to hundreds of milligrams, repeated — and depend on the severity. For suspected or confirmed Wernicke encephalopathy (the brain form), the 2010 European Federation of Neurological Societies (EFNS) guideline gives 200 mg three times a day, preferably intravenously, before any carbohydrate, and rates the overall safety of thiamine as very good. The same guideline calls for injected thiamine for every at-risk person admitted to the emergency room, and for follow-up of thiamine status for at least 6 months after bariatric surgery. The improvement in the high-output, vasodilated state can begin within hours.
• Thiamine before glucose. A critical rule: in anyone who may be thiamine-deficient, thiamine is given before (or at least together with) any glucose-containing intravenous (IV) fluids, because a sugar load can otherwise consume the last reserves and precipitate or worsen the crisis (the same principle that protects against Wernicke encephalopathy).
• Magnesium alongside. Because magnesium is a cofactor for the enzyme that activates thiamine, a coexisting magnesium deficiency can blunt the response. It is checked and corrected alongside.
• Supportive care alongside thiamine. Standard heart-failure measures — oxygen, careful fluid management, monitoring — are used as supportive care, but they do not fix the underlying problem. The thiamine is the cure; everything else buys time.
• Then food and the cause. Once stable, the person transitions to oral thiamine and a thiamine-adequate diet (whole grains, legumes, pork, and fortified foods), and the underlying driver — alcohol use, malnutrition, diuretic therapy, post-surgical malabsorption — is addressed so the deficiency does not simply return. People on long-term high-dose loop diuretics for heart failure are sometimes given supplemental thiamine for this reason.

The contrast with ordinary heart failure is striking: most heart failure is managed, not cured, over a lifetime. Wet beriberi, caught in time, can be reversed — which is exactly why it is worth recognizing.

Thiamine in ordinary heart failure. Reversing beriberi is not the same as helping every failing heart. A 2024 meta-analysis of 7 randomized, double-blind trials (274 people with chronic heart failure) found that thiamine did not improve the heart's pumping strength (ejection fraction, +1.65%, not statistically significant), heart size, the 6-minute walking distance, the heart-strain blood marker NT-proBNP, or symptom class. It did correct thiamine deficiency where present. The authors concluded that thiamine has no direct treatment effect in chronic heart failure beyond correcting a deficiency.

Back to Table of Contents

When to Seek Care / Red Flags

New or worsening swelling and breathlessness usually do not mean beriberi, but the more common causes (heart, kidney, liver, and lung disease, or a blood clot) are themselves serious. The following are signs that hospitals treat as urgent — a matter for emergency services rather than a routine appointment:

• Severe or rapidly worsening breathlessness, breathlessness at rest, or being unable to lie flat without gasping.
• Chest pain, a blue tinge to the lips or fingers (cyanosis), or fainting.
• A very fast, pounding, or irregular heartbeat — especially with light-headedness (see arrhythmia).
• Rapidly spreading swelling reaching the abdomen or face, particularly with breathlessness.
• Confusion, double vision, or sudden unsteadiness on the feet — in a person at risk (heavy alcohol use, malnutrition), this can signal Wernicke encephalopathy, a neurological emergency that needs immediate thiamine.
• Signs of shock — cold sweats with collapse, or a known at-risk person becoming acutely, severely ill: this is the shoshin-beriberi pattern, which is fatal without rapid thiamine.

In a person with a known risk for thiamine deficiency (heavy alcohol use, recent weight-loss surgery, severe malnutrition or vomiting, or long-term diuretic use for heart failure) who develops heart-failure symptoms, that risk is the key clue — mentioning it can prompt the one treatment that turns this condition around.

Back to Table of Contents

Key Research Papers

1. Levy WC, Soine LA, Huth MM, Fishbein DP (1992). Thiamine deficiency in congestive heart failure. The American Journal of Medicine;93(6):705-706. — DOI: 10.1016/0002-9343(92)90212-t. — doi:10.1016/0002-9343(92)90212-t
2. DiNicolantonio JJ, Niazi AK, Lavie CJ, et al. (2013). Thiamine Supplementation for the Treatment of Heart Failure: A Review of the Literature. Congestive Heart Failure;19(4):214-222. — DOI: 10.1111/chf.12037. — doi:10.1111/chf.12037
3. Sica DA (2007). Loop Diuretic Therapy, Thiamine Balance, and Heart Failure. Congestive Heart Failure;13(4):244-247. — DOI: 10.1111/j.1527-5299.2007.06260.x. — doi:10.1111/j.1527-5299.2007.06260.x
4. Teigen LM, Twernbold DD, Miller WL (2016). Prevalence of thiamine deficiency in a stable heart failure outpatient cohort on standard loop diuretic therapy. Clinical Nutrition;35(6):1323-1327. — DOI: 10.1016/j.clnu.2016.02.011. — doi:10.1016/j.clnu.2016.02.011
5. Meulders Q, Laterrc PF, Sergant M, Corbeel L (1988). Shoshin Beriberi: A Fulminant Beriberi Heart Disease. Acta Clinica Belgica;43(2):115-119. — DOI: 10.1080/17843286.1988.11717918. — doi:10.1080/17843286.1988.11717918
6. Amiya E, Morita H (2024). Characteristics of Shoshin Beriberi, a Fulminant Cardiovascular Type of Beriberi. International Heart Journal;65(2):171-172. — DOI: 10.1536/ihj.24-034. — doi:10.1536/ihj.24-034
7. Schreiber SS (1984). Shoshin Beriberi-Cardiomyopathy and Thiamine Deficiency. Alcoholism: Clinical and Experimental Research;8(4):425. — DOI: 10.1111/j.1530-0277.1984.tb05692.x. — doi:10.1111/j.1530-0277.1984.tb05692.x
8. Maramattom BV (2025; online 2024). Dry and Wet at the Same Time. Acute Polyneuritic Beriberi Complicated by Heart Failure (Shoshin Beriberi). Neurology India;73(1):173-176. — DOI: 10.4103/neuroindia.ni_431_19. — doi:10.4103/neuroindia.ni_431_19
9. Cui R, et al. (2014). Thiamine Deficiency (Beriberi) Induced Polyneuropathy and Cardiomyopathy: Case Report and Review of the Literature. Journal of Medical Cases;5(8). — DOI: 10.14740/jmc1780w. — doi:10.14740/jmc1780w
10. Galvin R, Bråthen G, Ivashynka A, et al. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology;17(12):1408-1418. — DOI: 10.1111/j.1468-1331.2010.03153.x. — doi:10.1111/j.1468-1331.2010.03153.x
11. Smith TJ, Hess SY (2021). Infantile thiamine deficiency in South and Southeast Asia: An age-old problem needing new solutions. Nutrition Bulletin;46(1):12-25. — DOI: 10.1111/nbu.12481. — PubMed PMID: 33776582
12. He S, Wang S, Xu T, Wang S, Qi M, Chen Q, Lin L, Wu H, Gan P (2024). Role of Thiamine Supplementation in the Treatment of Chronic Heart Failure: An Updated Meta-Analysis of Randomized Controlled Trials. Clinical Cardiology;47(7):e24309. — DOI: 10.1002/clc.24309. — PubMed PMID: 38940395

PubMed Topic Searches

1. PubMed: Wet beriberi and high-output heart failure
2. PubMed: Shoshin beriberi, cardiogenic shock, and thiamine
3. PubMed: Thiamine deficiency, loop diuretics, and heart failure
4. PubMed: Thiamine, lactic acidosis, and vasodilation
5. PubMed: Thiamine supplementation and left ventricular function
6. PubMed: Thiamine deficiency, wet beriberi, and high-output heart failure

Back to Table of Contents

Connections

• All Vitamins
• Thiamine Deficiency (Beriberi) Hub
• Dry Beriberi (Nerves)
• Wernicke-Korsakoff Syndrome
• Fatigue & Appetite Loss
• Vitamin B1 Overview
• Thiamine and Beriberi
• Thiamine and Brain Health
• Heart Failure
• Arrhythmia
• Kidney Disease
• Magnesium
• Comprehensive Metabolic Panel

Back to Table of Contents

×

Featured Videos