Vitamin B1 is the first vitamin to have been identified, and the one that gave its name to the entire family. It is also the only one whose requirement is not counted per person but per calorie: the more you eat, and especially the more you eat sugar, the more you need. This peculiarity says a lot. Thiamine is the key that allows glucose to become energy; when it is lacking, the brain and heart, two organs that run on sugar almost exclusively, fail first. This is why prolonged deficiency does not cause simple fatigue but a disease with a name, beriberi, and why its acute form, Gayet-Wernicke encephalopathy, is treated in emergency care.
This guide covers the question comprehensively: what thiamine is and why it is inseparable from glucose, what it does, how much you need based on your diet and energy expenditure, where to find it and how not to destroy it during cooking, what a deficiency looks like, why alcohol is its leading cause and why B1 and B6 are systematically combined during withdrawal, what happens after bariatric surgery, what benfotiamine is worth in diabetic neuropathy and the promises about sleep, energy or mosquitoes, and how to choose a supplement. It extends our file on B vitamins and completes our guides to vitamin B6, to vitamin B12 and tofolic acid.
Vitamin B1 never works alone: it produces energy with B2 and B3, and becomes active through magnesium. Our complex brings together all eight B vitamins in active forms, including 10 mg of thiamine, in a daily vegetable capsule made in France.
Vitamin B1 (thiamine) becomes thiamine diphosphate in cells, a coenzyme of three enzymes that transform glucose into energy. The requirement is proportional to calories consumed, 0.1 mg per 100 kcal, or 1.1 to 1.3 mg per day for an adult and more for an athlete. It is found in yeast, wheat germ, pork, legumes and whole grains; refining, cooking water and sulfites destroy it. The body's reserves last only two to three weeks, which explains how quickly deficiencies develop. These take the form of dry beriberi (nerves) or wet beriberi (heart), and acutely, Gayet-Wernicke encephalopathy, a neurological emergency whose leading cause is alcohol, ahead of bariatric surgery and hyperemesis gravidarum. This is why all alcohol withdrawal begins with thiamine, before any sugar, combined with B6 and magnesium without which it does not activate. Outside these situations, deficiency is rare in France, no safety limit exists, and a B complex at nutritional dose is more than sufficient.
- Thiamine, TDP: the glucose vitamin
- What is vitamin B1 for? The claims recognized by EFSA
- How much vitamin B1 per day? A requirement proportional to calories
- Foods rich in vitamin B1 (and what destroys it)
- Deficiency and beriberi: the two faces of lack
- Alcohol, bariatric surgery, vomiting: who is really at risk
- Why vitamin B1 and B6 in alcohol withdrawal?
- Heart, diuretics and heart failure
- Benfotiamine and diabetic neuropathy
- Sleep, mood, energy: what's true and what isn't
- The myths: mosquitoes, weight loss, megadoses
- Forms, blood dosage and interactions
- Choosing well: B1 alone or B complex?
- Frequently asked questions
1. Thiamine, TDP: the glucose vitamin
The story of vitamin B1 begins with a colonial puzzle. In the 19th century, Asia sees an explosion of a disease that paralyzes and causes death from heart failure: beriberi. beriberiIn 1897, a Dutch military physician in Java, Christiaan Eijkman, notices that his chickens fed white rice develop a paralysis that heals as soon as they're given whole grain rice again. The cause was not a microbe, as everyone thought, but the absence of something. This "something," isolated in 1926 and named thiamine, became the first identified vitamin and earned Eijkman the Nobel Prize in 1929. This discovery gave birth to the very concept of vitamins and to the numbering that logically begins with B1.
In the body, thiamine doesn't work as-is: it is phosphorylated into thiamine diphosphate (TDP, also called thiamine pyrophosphate), its active form, a reaction that requires magnesium. This apparently technical detail has major clinical consequences that we will encounter in section 7. TDP then serves as a coenzyme for three central enzymes:
- pyruvate dehydrogenase, which allows the glucose digestion product to enter the cell's energy center; if it blocks, pyruvate transforms into lactate, hence the lactic acidosis of severe deficiencies;
- alpha-ketoglutaratedehydrogenase, a step in the Krebs cycle, the loop that produces most of our energy;
- transcetolase , which fuels the pentose phosphate pathway, supplier of DNA building blocks and antioxidant power in cells. The activity of this enzyme in red blood cells is historically used to measure B1 status.Two practical consequences flow from this biochemistry. First, thiamine is the
sugar vitamin : the more the body burns carbohydrates, the more it consumes. Second, the tissues most dependent on glucose are the most vulnerable: the brain, which consumes one-fifth of everything we absorb, peripheral nerves, and heart muscle. This explains why deficiency produces a neurological and cardiac picture, not, for example, a skin one. This also explains a phenomenon that has cost patients their lives: infusing glucose to a deficient person before giving them thiamine consumes their last reserves at once and can trigger acute encephalopathy. The order matters. 2. What is vitamin B1 for? The claims recognized by EFSA
Key takeaways
European Regulation No. 432/2012 authorizes four claims for thiamine, provided the product contains at least 15% of the NRV (0.165 mg) per serving. Vitamin B1 contributes to:
- normal energy metabolism ;
- normal functioning of the nervous system ;
- normal psychological functions ;
- normal heart function.
The last one deserves special attention, because it is unique. No other B vitamin carries a cardiac claim, and very few nutrients in general. EFSA granted it on the basis of a simple reasoning: thiamine deficiency causes documented cardiac insufficiency for more than a century, wet beriberi, reversible with treatment. The heart muscle beats continuously and derives most of its fuel from glucose and fatty acids; when pyruvate dehydrogenase is blocked, it finds itself in permanent energy deficit, blood vessels dilate, blood flow increases to compensate, and the heart eventually fails. We detail this mechanism and its modern implications in section 8.
It does not provide energy to those who are not deficient in it: "contributing to energy metabolism" means enabling fuel transformation, not supplying it. Taking B1 without deficiency does not increase endurance, no trial in non-deficient athletes has shown performance gains. It does not repel mosquitoes (section 11). It does not cause weight loss nor does it "burn sugars": it transforms them, which is the opposite of eliminating them. It does not treat anxiety or depression in a person with normal status, even if deficiency causes them.
3. How much vitamin B1 per day? A requirement proportional to calories
| Profile | Reference (mg per day) | Source |
|---|---|---|
| Children 1 to 3 years old | 0.5 | EFSA (0.1 mg / 100 kcal) |
| Children 4 to 10 years old | 0.7 to 0.9 | EFSA |
| Adolescents | 1.0 to 1.3 | EFSA |
| Adult men | 1.3 | ANSES (RNP), EFSA |
| Adult women | 1.1 | ANSES (RNP), EFSA |
| Pregnant and breastfeeding women | 1.4 to 1.5 | ANSES, EFSA |
| Athlete or manual laborer (3,000 kcal) | ≈ 3.0 (proportional calculation) | Application of EFSA rule |
| Labeling reference value | 1.1 | EU Regulation No. 1169/2011 |
| Upper safety limit | Not established | EFSA |
This proportionality to calories has a consequence that few people realize: a diet high in simple sugars and refined products increases the need for thiamine while providing little vitamin, since refining has removed it. A high-calorie diet based on sodas, white bread, and processed foods is, in theory, the worst possible intake-to-requirement ratio. Conversely, an athlete who eats a lot but varied foods naturally meets their increased needs, because the whole foods they consume in large quantities provide it proportionally. This is also why alcoholics combine all the risk factors: alcohol provides empty calories that increase the requirement, while blocking the absorption of the vitamin. Like biotin,
no upper safety limit has been set for oral intake: intestinal absorption is saturable beyond approximately 5 mg per dose, the remainder is simply not absorbed, and what does pass is eliminated in the urine. Medical doses of 100 to 500 mg per day, or even more by injection in Gayet-Wernicke encephalopathy, are well tolerated, with very rare allergic reactions to the injectable form. This safety profile explains an emergency medicine principle: when in doubt, treat first. 4. Foods rich in vitamin B1 (and what destroys it)
Key takeaways
| Content (mg per 100 g) | Reference | Nutritional yeast, brewer's yeast |
|---|---|---|
| 5 to 12 | One tablespoon covers several days' worth | Wheat germ |
| 1.7 to 2.0 | Two tablespoons: approximately 0.4 mg | Sunflower and sesame seeds |
| 1.4 to 1.5 | A handful of 30 g: approximately 0.4 mg | Pork (tenderloin, chop, ham) |
| 0.7 to 1.0 | By far the richest meat, five to ten times more than beef | De loin la viande la plus riche, cinq à dix fois plus que le bœuf |
| Legumes (lentils, chickpeas, dried beans) | 0.2 to 0.5 (cooked) | A 200 g serving: 0.4 to 1.0 mg |
| Nuts, hazelnuts, pistachios | 0.3 to 0.9 | Pistachios are the richest of all tree nuts |
| Whole grains (rice, pasta, bread) | 0.15 to 0.4 | Compared to 0.02 to 0.05 for their refined versions |
| Potatoes cooked in their skin | 0.1 | Major source in France based on consumption quantities |
| Eggs, fish, organ meats | 0.05 to 0.2 | Modest but regular contributions |
Orders of magnitude based on composition tables (Ciqual, USDA); contents vary according to variety, refinement and cooking method.
Thiamine is the most fragile of the B vitamins, and four enemies lie in wait for it. First, refinement : hulling rice or bolting flour removes the germ and bran, where it concentrates, with losses of 70 to 80%. This is exactly what triggered beriberi epidemics in Asia when rice polishing machines spread, and this is why many countries now enrich flour. Then heat and water : thiamine is water-soluble and heat-sensitive, losses reach 25 to 50% when boiling in water, much less with steaming or if you reuse the cooking liquid. And baking soda, sometimes added to soften legumes or preserve the color of vegetables, destroys it almost completely in an alkaline environment.
And finally, antithiamines , the least known. The thiaminases from raw fish and shellfish break down the vitamin; deficiencies have been described in heavy consumers of raw fish, and especially in farmed cats and foxes fed this way, which helped understand the mechanism. Cooking destroys them, so the occasional sushi poses no problem. The sulfites, used as preservatives in wine, light dried fruits and certain industrial preparations, also break down the molecule. Tea and coffee in large quantities, betel leaves and certain plants contain polyphenols that oxidize it. None of these factors pose a problem on their own in a varied diet; they matter when they add up to already low intakes.
5. Deficiency and beriberi: the two faces of insufficiency
Korsakoff syndrome is a chronic amnesia resulting from unrecognized or inadequately treated Gayet-Wernicke encephalopathy, caused by thiamine deficiency. Clinical presentation includes loss of appetite, dizziness, accelerated pulse and urinary retention, as well as the confusion that is part of the classic triad. Severe infections, including sepsis of unknown origin, are frequent during the Wernicke phase and may be harbingers. Encephalopathy is most often alcohol-related, but also occurs after bariatric surgery, with uncontrollable vomiting in pregnancy, or mental anorexia. Patients with hypomagnesemia may not respond to thiamine.
Wijnia JW. J Clin Med 2022;11(22):6755. DOI: 10.3390/jcm11226755
Before these established presentations, early deficiency manifests through signs that no one links to a vitamin: fatigue, irritability, loss of appetite, concentration and working memory problems, heavy legs, cramps, sometimes nausea and constipation. This is what French authors call marginal deficiency, which they acknowledge has poorly established clinical consequences (Guilland, Rev Prat, 2013). This ambiguity explains part of the marketing around B1: these symptoms are so common they can be attributed to anything.
Should we be concerned in France? Available data suggest not for the general population. A Japanese study of 270 independent adults aged 25 to 97 years found no cases of deficiency or even borderline values, with no age-related differences, whereas the reported prevalence is 2 to 6% in Europe and the United States (Uchida, Cureus, 2023). Risk is concentrated in specific situations, detailed in the following section.
6. Alcohol, bariatric surgery, vomiting: who is really at risk
The particularity of thiamine is that the body stores almost none: approximately 25 to 30 mg total, essentially in muscle, liver, heart and brain, or two to three weeks of consumption. This is the shortest reserve of all B vitamins, compared to the three to five year reserves of vitamin B12. An interruption in intake of just a few weeks is therefore enough to create true deficiency, which explains the rapid onset of severe presentations.
Alcohol is the leading cause in wealthy countries, and it works through multiple mechanisms simultaneously: alcoholic beverages provide calories without vitamins, increasing the need; alcohol blocks the intestinal transporter of thiamine; it reduces its conversion to active form in the liver and its storage; and it is often accompanied by unbalanced nutrition. A systematic review of homeless people with heavy alcohol consumption found B1 deficiency prevalence rates up to 51% depending on studies, the most frequently deficient vitamin of all those measured (Ijaz, Int J Equity Health, 2017).
Among 118 cases of Gayet-Wernicke encephalopathy occurring after obesity surgery, the majority involved gastric bypasses but also more recent techniques like sleeve gastrectomy. Patients were younger (median age 33 years) than in other medical causes, and presented with vomiting in 87.3% of cases, balance disorders in 84.7%, mental status changes in 76.3%, and eye movement abnormalities in 73.7%. Treatment was often insufficient, particularly due to lack of awareness of low thiamine levels with parenteral administration.
Oudman E, Wijnia JW, van Dam M, Biter LU, Postma A. Obes Surg 2018;28(7):2060-2068. DOI : 10.1007/s11695-018-3262-4
The message of this series is essential for a population that has nothing to do with the stereotypical image of vitamin deficiency: young women and men, often otherwise in good health, who vomit after their surgery and to whom no one thinks to give thiamine. The typical timeframe is one to three months after the procedure. The rule, in France as elsewhere, is systematic vitamin supplementation after bariatric surgery, for life, and absolute vigilance in the face of any vomiting that lasts more than a few days. The same logic applies to severe vomiting in pregnancy (hyperemesis gravidarum), a classic cause of encephalopathy in young women, and to eating disorders with malnutrition, where too-rapid refeeding (refeeding syndrome) can trigger it.
Other situations deserve to be recognized: long-term diuretic treatment for heart failure, which increases urinary thiamine losses (section 8); dialysis ; chronic vomiting regardless of its cause;prolonged hospitalization, where status deteriorates even in patients who are eating, as demonstrated by a Japanese study of 471 hospitalized elderly people, of whom 84% saw their thiamine drop in one week; and infants breastfed by a thiamine-deficient mother, still a cause of infant mortality in Southeast Asia. Non-bariatric digestive surgery , cancers and pancreatitis complete the list (Kohnke et Meek, Ann Clin Biochem, 2020).
7. Why vitamin B1 and B6 in alcohol withdrawal?
"Why B1 and B6 in withdrawal" is one of the most frequently asked questions about this vitamin, and the answer comes in three parts.
B1 because withdrawal can kill neurons. A chronic drinker enters withdrawal with thiamine reserves nearly empty. However, stopping alcohol, resuming food intake, and glucose infusions suddenly ramp up sugar metabolism, thus thiamine consumption. If reserves are empty, pyruvate dehydrogenase becomes blocked where glucose is most abundant, in specific brain regions (mammillary bodies, thalamus, around the third ventricle), and Gayet-Wernicke encephalopathy is triggered, sometimes within hours. Hence the absolute rule in emergency medicine: thiamine before glucose, never the reverse, and in high doses by parenteral route, without waiting to confirm the diagnosis, since the vitamin is harmless and delay, meanwhile, leaves permanent amnesia (Mateos-Díaz, Med Clin, 2022).
B6 because the deficit is present here too, and the brain needs it to calm down. Alcohol lowers vitamin B6 through a documented mechanism: acetaldehyde, its breakdown product, displaces the active form from its carrier proteins and accelerates its destruction. However, pyridoxal-5-phosphate is essential for the manufacture of GABA, the main inhibitory neurotransmitter, precisely the one whose system is dysregulated during withdrawal: alcohol stimulated it artificially, its cessation leaves a hyperexcitable brain, hence anxiety, tremors and seizure risk. Correcting B6 does not replace withdrawal medications, but is part of restoring the body's equilibrium. Our vitamin B6 guide details its role and reminds that, unlike B1, it has a safety ceiling not to be exceeded.
Magnesium, the forgotten piece. The transformation of thiamine into its active form requires magnesium, and chronic drinkers are almost always deficient in it. This is a point that clinicians regularly highlight: a patient who does not respond to thiamine may simply be suffering from hypomagnesemia, a situation worsened by the frequent association of proton pump inhibitors and diuretics (Wijnia, 2022). In hospital practice, magnesium, thiamine, B6 and vitamin PP form the quartet of withdrawal management. In daily practice, this reminds us of one simple thing: B vitamin supplementation makes little sense if magnesium status is low. Our Magnesium+ combines a microencapsulated bisglycinate, malate and taurine with 2 mg of vitamin B6.
A word about "B1-B6 vitamin therapy", which is highly sought after: under this name circulate pharmaceutical products combining the two vitamins, prescribed for neuropathies, pain and withdrawal support. These are medications, with doses far exceeding supplements and, for B6, a safety limit to respect since prolonged high-dose supplementation can itself cause neuropathy. A dietary supplement of B vitamins at nutritional doses does not operate in this category and does not claim to replace it.
B1, B2 and B3 produce energy together, B6 and B9 manage homocysteine, B12 completes the set: the B Complex Vitamins provides all eight B group vitamins in active forms, including 10 mg of thiamine, in one daily vegetable capsule with no allergens, manufactured in France.
Discover B Complex Vitamins →Thiamine needs magnesium to activate: pair it with our Magnesium+ (bisglycinate, malate, taurine).
8. Heart, diuretics and heart failure
The heart muscle beats one hundred thousand times a day without interruption, making it one of the most energy-hungry tissues in the body. When thiamine is lacking, energy production from glucose is blocked, heart cells become exhausted and peripheral vessels dilate; the heart compensates by increasing its output, until it can no longer. This mechanism, described for a century as wet beriberi, manifests as shortness of breath, edema and a rapid pulse, and it regresses within days on thiamine, making it one of the rare reversible heart failures.
The topic returned through an unexpected door: loop diuretics (furosemide, bumetanide), the cornerstone of heart failure treatment, increase the urinary elimination of thiamine. Research has found low levels in a notable proportion of heart failure patients on long-term treatment, who often also have advanced age, decreased appetite and a salt-restricted diet that is sometimes monotonous. Several small supplementation trials showed improvement in ejection fraction, but they involved only dozens of patients, with heterogeneous methodologies and inconsistent results. Cardiology guidelines have not adopted systematic supplementation, while recommending considering it when heart failure worsens without explanation in a malnourished patient or one on high doses of diuretics.
A word about sepsis, where thiamine made headlines. A protocol combining vitamin C, thiamine and hydrocortisone had sparked enormous hope following spectacular preliminary results. The confirmatory randomized trial dampened that enthusiasm.
In ICU patients with sepsis and respiratory or cardiovascular failure, intravenous administration of vitamin C, thiamine and hydrocortisone every six hours did not significantly increase the number of days without ventilation or vasopressors at thirty days compared to placebo: median 25 days versus 26, median difference of less than one day. Thirty-day mortality was 22% in the treated group and 24% in the placebo group.
Sevransky JE, Rothman RE, Hager DN, et al. JAMA 2021;325(8):742-750. DOI: 10.1001/jama.2020.24505
The lesson extends beyond intensive care: a vitamin whose deficiency causes a disease is not necessarily a treatment for that disease when deficiency is not the cause. This is true for the heart, sepsis, and most of the promises surrounding B vitamins.
9. Benfotiamine and diabetic neuropathy
Ordinary thiamine is absorbed by a saturable intestinal transporter: beyond a few milligrams per dose, the excess simply doesn't enter. The benfotiamine circumvents this limit. This fat-soluble derivative, synthesized in Japan in the 1950s, crosses the intestinal wall by diffusion, is then converted to thiamine in the body, and raises blood and tissue concentrations far more than the water-soluble form at equal dose. It's not a "better" vitamin, it's a vitamin better delivered.
The interest focused on diabetes, for a mechanistic reason. Chronic excess glucose overwhelms the sugar degradation pathways and produces compounds toxic to nerves and blood vessels, including the famous advanced glycation end products. Now transketolase, the thiamine-dependent enzyme, diverts this surplus toward a harmless exit pathway. By stimulating this enzyme, benfotiamine would reduce the formation of deleterious compounds. Moreover, diabetics frequently have reduced thiamine status due to increased urinary loss.
The management of diabetic peripheral neuropathy rests on three pillars: causal treatment, pharmacotherapy targeting disease mechanisms, and symptomatic pain relief. Among treatments aimed at pathophysiology, efficacy and excellent safety have been demonstrated in several meta-analyses for alpha-lipoic acid and in randomized clinical trials for benfotiamine, actovegin, and epalrestat. These compounds are currently approved for the treatment of diabetic neuropathy in several countries.
Ziegler D. Diabetes Res Clin Pract 2023;206 Suppl 1:110764. DOI : 10.1016/j.diabres.2023.110764
Two nuances are warranted. On one hand, the positive trials are modest in size and short in duration, focusing mainly on symptoms (pain, tingling) rather than on the progression of nerve damage; the authors themselves call for longer-term trials to confirm. On the other hand, benfotiamine is in Europe a medication in certain countries and not a dietary supplement, at doses of 150 to 600 mg per day: it falls under medical prescription, not self-medication. To cover a nutritional need, thiamine hydrochloride or thiamine mononitrate, at a few milligrams, do exactly the same job for a fraction of the price.
10. Sleep, mood, energy: what is true and what is not
"Vitamin B1 and sleep" is a frequent search query, and the association is not absurd: thiamine carries the claim "contributes to normal psychological functions," its deficiency causes irritability, anxiety, concentration problems and fragmented sleep, and it appears in most market "relaxation" or "anti-stress" formulas. But two very different claims must be distinguished. Correcting a deficiency improves these symptoms : this is established, and it is even one of the ways deficiency was historically described. Adding B1 to someone who is not deficient improves their sleep : this is not shown by any trial.
A few older studies on small samples reported improved mood and alertness in supplemented young women, without these results being reproduced on a large scale. Recent literature on thiamine and sleep is limited to deficient or hospitalized populations. If your sleep is deteriorating, the levers with documented efficacy are elsewhere: schedule regularity, morning light, screens and evening light, caffeine after 2 PM, alcohol in the evening (which fragments sleep and, incidentally, depletes thiamine), and for the nutritional aspect, magnesium, which several trials support for its effect on stress and sleep quality in people with low status. Our chronic fatigue guide details the nutrients that actually have data, and our Optimal Sleep relies on other active ingredients than B vitamins.
The same reasoning applies toenergy and sports performance. Thiamine enables glucose to be burned, so an athlete deficient in it sees performance drop; but in an athlete with normal status, B vitamin supplementation trials have not shown gains in endurance or power. What is true, however, is that the requirement increases with energy expenditure (section 3): an athlete at 4,000 kcal needs about 4 mg of thiamine per day, which abundant and varied food naturally provides, but which a high-calorie diet based on refined products may not cover. It is there, and only there, that additional supplementation makes sense.
11. The myths: mosquitoes, weight loss, megadoses
| Claim | What the data say | Verdict |
|---|---|---|
| B1 repels mosquitoes | Born from an isolated observation in the 1940s, the idea was tested several times: trials where supplemented volunteers exposed their skin to mosquitoes found no reduction in bites, and analysis of compounds emitted by skin and exhaled air showed no change. Health authorities and medical entomology reviews consider the subject closed. Only recognized skin repellents work. | False, refuted |
| B1 causes weight loss or burns sugars | It allows glucose to enter energy production, which is the opposite of eliminating it. No trial has demonstrated weight loss under supplementation. The confusion stems from the vocabulary of "energy metabolism." | False |
| Oral megadoses are more effective | Intestinal absorption occurs through a saturable transporter; beyond approximately 5 mg per dose, the excess is not absorbed. It is precisely to overcome this limitation that benfotiamine (fat-soluble) and injectable administration exist for emergency situations. | Pointless orally |
| B1 is toxic at high doses | No documented oral toxicity, no safety limit established by EFSA. Rare allergic reactions have been described with the injectable form in medical settings. This is the exact opposite of vitamin B6, whose excess is neurotoxic. | False |
| Everyone is deficient in B1 today | Common marketing argument. A study involving 270 independent adults found no deficiency or threshold values; the estimated prevalence is 2 to 6% in Europe and the United States, concentrated in identified populations (section 6). | Exaggerated |
12. Forms, blood dosage, and interactions
| Form | Characteristics | Use |
|---|---|---|
| Thiamine hydrochloride | Most common water-soluble form, stable, inexpensive, saturable absorption | Supplements and medications, routine nutritional intake |
| Thiamine mononitrate | More stable to heat and humidity than hydrochloride, same efficacy | Flour and cereal enrichment, tablets |
| Benfotiamine | Fat-soluble derivative, absorption by diffusion, significantly higher tissue concentrations | Medication in several countries (diabetic neuropathy), by prescription |
| Sulbutiamine | Synthetic derivative that crosses the blood-brain barrier, studied in asthenia | Medication, prescription; does not fall under dietary supplement |
| Injectable thiamine | Bypasses intestinal absorption, doses of several hundred milligrams | Emergencies: Gayet-Wernicke encephalopathy, withdrawal, beriberi |
How is status measured? Two methods coexist: measurement of thiamine diphosphate in whole blood by chromatography, and the activity of red blood cell transketolase before and after thiamine addition, with the gap reflecting the deficiency. A recent study conducted in Laos on over 500 children compared these markers to actual clinical response to thiamine: both distinguish populations well, but their distributions overlap so much that neither reliably predicts whether a given child will respond to treatment (Hess, Curr Dev Nutr, 2024). Practical conclusion, also valid in adult medicine: faced with serious clinical suspicion, treat first and discuss later, since thiamine costs almost nothing and presents no risk.
Loop diuretics (furosemide, bumetanide): increase urinary thiamine elimination; monitor during prolonged treatment, especially in elderly or malnourished individuals.
Alcohol : blocks intestinal absorption and hepatic storage. This is the most important interaction of all.
Magnesium : essential for thiamine activation. A magnesium deficiency can cause B1 supplementation to fail.
Sulfites, tea and coffee in large quantities, raw fish regularly : degrade or inactivate the vitamin in food or the intestine; without consequence in a varied diet.
Pregnancy, breastfeeding, children : thiamine at nutritional doses is necessary and safe; however, severe pregnancy vomiting is a at-risk situation that requires medical attention. Dietary supplements do not replace a varied and balanced diet or a healthy lifestyle, and should be kept out of reach of young children.
13. Choosing well: B1 alone or B complex?
Vitamin B1 is a case where common sense and science say the same thing: there is almost no reason to take it in isolation. It intervenes in a chain where B2 and B3 ensure the following steps, it needs magnesium to become active, and situations that create B1 deficiency (alcohol, surgery, malnutrition) also create deficiencies in other B vitamins. A few guidelines for choosing:
- The dose : 1 to 10 mg per day cover all nutritional intake scenarios, including athletes. Beyond that, absorption plateaus; doses of 100 mg and above are medication doses.
- The form : thiamine hydrochloride or mononitrate, both are equivalent. Benfotiamine requires a prescription and specific indication, not for routine use.
- The entire B group : verify that B2 and B3 are present, as they are the direct partners of B1 in energy production.
- Magnesium : adequate status determines thiamine effectiveness, and it is often low in stressed, athletic, or alcohol-consuming individuals.
- The promises : "immediate energy," "mosquito repellent," "sugar burner" are unfounded claims. The only authorized claims are energy metabolism, nervous system, psychological functions, and cardiac function.
Thiamine, riboflavin, niacin, pantothenic acid, pyridoxal-5-phosphate, biotin, Quatrefolic® and methylcobalamine: the B Complex Vitamins Covers all eight B vitamins at nutritional doses, free from allergens and titanium dioxide. One capsule per day with breakfast.
Discover B Complex Vitamins →Also discover our vitamins and minerals and our selection for fatigue.
Choose the situation that best matches yours: the answer appears right below.
Your thiamine requirement follows your calorie intake: at 3,000 or 4,000 kcal, it rises to 3 or 4 mg per day, three times the reference for a sedentary adult. An abundant and varied diet (whole rice and bread, legumes, pork, seeds, wheat germ) naturally covers it; it's when volume comes from refined and sugary products that the gap widens. A B Complex Vitamins is a reasonable safety net during heavy training periods, with Magnesium+ which athletes often lack and without which thiamine cannot activate. Don't expect direct performance gains: B1 doesn't make you run faster, it prevents deficiency from slowing you down.
This is the most unfavorable configuration for this vitamin: sugars and refined products increase the need (0.1 mg per 100 kcal) while providing little thiamine, since refining removes 70 to 80% of it. The main lever is dietary: gradually switch to whole bread and rice, add legumes two to three times per week, a spoonful of wheat germ or nutritional yeast on your dishes, a handful of seeds. A B Complex Vitamins or our Multivitamins bridge the gap in the meantime, without replacing dietary changes.
Alcohol is the leading cause of vitamin B1 deficiency: it provides calories that increase the need, blocks intestinal absorption, and reduces storage. Among heavy consumers in precarious situations, up to one in two people is deficient. The risk is not theoretical: an abrupt stop, hospitalization, or a glucose infusion can trigger Gayet-Wernicke encephalopathy, which leaves permanent damage if not treated as a medical emergency. Supplementation must be decided and dosed medically, combined with vitamin B6 and magnesium. If stopping is being considered, it must be prepared with a doctor or addiction center, never alone.
Your thiamine reserves only last two to three weeks, and vomiting depletes them even faster. After bariatric surgery, vitamin supplementation is systematic and lifelong; any vomiting lasting more than a few days requires prompt medical attention, with thiamine before any glucose infusion. The same rule applies to severe pregnancy vomiting. If confusion, double vision, balance problems, or leg weakness appear, these are emergencies: call 911. Do not attempt to manage this situation with a dietary supplement.
This test provides guidance; it does not replace a blood test or medical professional advice.
Frequently asked questions about vitamin B1
What is vitamin B1 for?
Vitamin B1, or thiamine, is the glucose vitamin: in its active form, thiamine diphosphate, it allows three key enzymes to convert sugars into usable energy. Since the brain and nerves function almost exclusively on glucose, they are the first to suffer when it's lacking. According to claims authorized by EFSA, it contributes to normal energy metabolism, normal functioning of the nervous system, normal psychological functions, and normal heart function—this last claim being unique to B1 among B vitamins.
How much vitamin B1 per day?
The vitamin B1 requirement is proportional to calories consumed: EFSA sets it at 0.1 milligram per 100 kilocalories, which gives 1.3 milligrams per day for a man and 1.1 milligrams for a woman, and more for an athlete or person with high energy expenditure. The reference nutritional value on labels is 1.1 milligrams. No upper safety limit has been set: excess is eliminated in urine and no toxicity has been documented by oral intake.
Which foods are rich in vitamin B1?
The best sources are nutritional yeast, wheat germ, sunflower seeds, pork (significantly richer than other meats), legumes, whole grains, nuts, potatoes, and eggs. Refining cereals removes most of the thiamine: white rice contains ten times less than brown rice, which caused beriberi epidemics in Asia in the 19th century. Cooking in water and sulfites used as preservatives destroy some of it.
What are the symptoms of vitamin B1 deficiency?
The first signs are nonspecific: fatigue, irritability, loss of appetite, concentration problems, muscle pain. Established deficiency takes two forms. Dry beriberi affects the nerves: tingling, burning feet, leg weakness, difficulty climbing stairs. Wet beriberi affects the heart: shortness of breath, leg swelling, accelerated heart rate, heart failure. The acute neurological form, Gayet-Wernicke encephalopathy, combines confusion, balance problems, and abnormal eye movements: this is a medical emergency.
Why is vitamin B1 and B6 given during alcohol withdrawal?
Alcohol causes vitamin B1 deficiency through three mechanisms: poor food intake, blocked intestinal absorption, and reduced liver storage. During withdrawal, by abruptly boosting glucose metabolism, the little remaining thiamine is consumed and can trigger Gayet-Wernicke encephalopathy, a neurological emergency that leaves permanent damage if untreated. Vitamin B1 is therefore administered as a priority, before any sugar intake. Vitamin B6 is given alongside it because its deficiency is also common in heavy drinkers and because it participates in GABA synthesis, the calming neurotransmitter that withdrawal disrupts. These protocols are medical, at high doses and often by injection.
What is beriberi?
Beriberi is the disease of vitamin B1 deficiency. There are two forms: dry beriberi, neurological, with tingling, weakness, and muscle wasting of the legs; and wet beriberi, cardiac, with shortness of breath, swelling, and high-output heart failure. It severely struck Asia in the 19th century after the introduction of rice-husking machines, which remove the bran rich in thiamine. It remains present today in infants of deficient mothers in certain regions of the world, and in wealthy countries among heavy drinkers, bariatric surgery patients, and malnourished persons.
Do you need vitamin B1 after bariatric surgery?
Yes, it is a systematic supplementation and a major monitoring point. Thiamine reserves cover only two to three weeks, and surgery combines reduced intake, vomiting, and decreased absorption. A review of 118 cases of Gayet-Wernicke encephalopathy after bariatric surgery found a median age of 33 years, vomiting in 87% of patients, balance problems in 85%, and often insufficient treatment. Any prolonged vomiting after such surgery requires prompt medical consultation and thiamine before any glucose infusion.
Does vitamin B1 help you sleep better?
There is no trial showing that vitamin B1 intake improves sleep in someone with normal intake. The link comes from elsewhere: thiamine deficiency causes irritability, anxiety, and disrupted sleep, and correcting them improves these symptoms. B1 is also found in many relaxation formulas alongside magnesium, which has its own evidence for stress. If your sleep deteriorates, look to magnesium, evening light, caffeine, and alcohol before turning to B1.
Does vitamin B1 repel mosquitoes?
No. This is one of the most persistent myths about this vitamin, born from an isolated observation in the 1940s. Controlled studies, including trials where supplemented volunteers exposed their arm to mosquitoes, found no reduction in bites, and analysis of exhaled air and skin showed no change in compounds that attract insects. Recognized skin repellents remain the only effective measure.
What is benfotiamine and is it more effective?
Benfotiamine is a fat-soluble derivative of thiamine, better absorbed than the standard form and raising tissue concentrations more. It is studied in diabetic neuropathy, where several randomized trials have shown symptom improvement, earning it authorization as a medication in some European countries. For simple nutritional intake, it offers no proven advantage over thiamine hydrochloride or mononitrate, which are more than sufficient and less expensive.
Who is at risk of vitamin B1 deficiency?
First and foremost, excessive alcohol consumers, in whom deficiency can affect up to half of those in precarious situations. Then bariatric surgery patients, women suffering from severe pregnancy vomiting, malnourished persons or those with eating disorders, patients on long-term diuretics for heart failure, dialysis patients, hospitalized elderly persons, and those whose diet relies on refined and sugary products. Since need is proportional to calories, a diet very high in sugars and poor in whole foods increases need while providing little thiamine.
How do you know if you're deficient in vitamin B1?
Testing is done on whole blood, by measuring thiamine diphosphate by chromatography, or by measuring the activity of an enzyme, red blood cell transketolase. These markers are reliable for evaluating a population but imperfect at the individual level: recent work shows that children who respond spectacularly to thiamine may have values that overlap with those of children who don't respond. In practice, faced with serious suspicion, the doctor treats without waiting for the result, because thiamine is safe and delay leaves permanent damage.
Vitamin B1 alone or B complex: which to choose?
For daily intake, B vitamin complex makes more sense: B1 works with B2 and B3 in energy production, with magnesium for its activation, and isolated B1 deficiency is rare outside at-risk situations. High-dose B1 alone falls under medical prescription (alcohol withdrawal, bariatric surgery aftermath, neuropathy). Check that the product indicates the dose in milligrams and the form used, and remember that thiamine needs magnesium to become active: well-absorbed magnesium is often the most useful supplement to pair with it.
- Thiamine (vitamin B1)
- The first identified vitamin, water-soluble, essential for transforming glucose into energy. Body reserves limited to two or three weeks.
- Thiamine diphosphate (TDP)
- Active form of vitamin B1, obtained by adding two phosphates, a reaction requiring magnesium. Coenzyme of pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase.
- Transketolase
- Red blood cell enzyme dependent on TDP, whose activity historically serves to measure vitamin B1 status.
- Beriberi
- Disease of thiamine deficiency, in its dry (neurological) or wet (cardiac) form. Historically linked to polished rice, today to alcohol and malnutrition in wealthy countries.
- Gayet-Wernicke encephalopathy
- Acute form of deficiency: confusion, balance problems, and abnormal eye movements. Medical emergency treated with injectable thiamine, before any glucose intake.
- Korsakoff syndrome
- Consequence of untreated Gayet-Wernicke encephalopathy: chronic amnesia with inability to form new memories and confabulation.
- Benfotiamine
- Fat-soluble derivative of thiamine, better absorbed, used as medication for diabetic neuropathy in several countries.
- Thiaminases
- Enzymes present in certain raw fish and shellfish that break down and inactivate thiamine; destroyed by cooking.
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