Vitamin B1

What is vitamin B1 (thiamin), and what does it do?

Thiamin is a water-soluble vitamin made up of a thiazole and a pyrimidine ring. In human tissues it is mostly present in phosphorylated form, as thiamin diphosphate (TDP, thiamin pyrophosphate); TDP is a coenzyme in carbohydrate and branched-chain amino acid metabolism and in energy-producing reactions. In the body it is found mainly in skeletal muscle, heart, brain, liver, and kidneys. More than 80% of the thiamin in blood is in erythrocytes. ^[2]

More than 95% of thiamin is absorbed at usual intakes; however, absorption occurs through a saturable transport system. As reported by the SCF, absorption decreases at intakes above 5 mg per day and the excess absorbed amount is excreted in urine. Alcohol and some phenolic compounds, sulfites, and thiaminases (thiamin-degrading enzymes found in some raw and fermented fish and in ferns) can reduce bioavailability. ^[2]

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How much B1 is needed daily?

The NIH reports the adult RDA values as 1.2 mg for men and 1.1 mg for women; the value is 1.4 mg in pregnancy and breastfeeding. ^[1]

EFSA ties the reference values for thiamin to energy intake: the average requirement (AR) is 0.072 mg/MJ (0.3 mg/1,000 kcal), and the population reference intake (PRI) is 0.1 mg/MJ (0.4 mg/1,000 kcal) for all adults. The same mg/MJ values also apply to infants (7–11 months), children aged 1–18, and to pregnancy and breastfeeding. By EFSA’s own conversion, the PRI is about 0.8 mg for an adult consuming 2,000 kcal per day and about 1.0 mg for 2,500 kcal (calculated). ^[2]

Intake in Türkiye

In the analysis of TÜBER (Türkiye Dietary Guidelines) 2022 based on TBSA 2017 data, the proportion of individuals aged 15 and over with B1 intake below the estimated average requirement (EAR) was found to be 1.6% (0.9% in men, 2.4% in women). TÜBER notes that the frequency of inadequate intake in women increases with age: 6.5% in women aged 65 and over and 9.5% in women aged 75 and over. This intake distribution is not a blood level measurement and cannot be read as the frequency of deficiency. ^[8]

Which foods contain B1?

The NIH lists whole grains, meat, and fish as food sources. In the US, bread, cereals, and infant formulas are fortified, and the most common sources are cereals and bread; pork is also an important source. Dairy products and most fruits contain little thiamin. Heating can reduce thiamin content. ^[1] For Türkiye, the TÜBER 2022 serving table gives the following values (cooked serving, rounded to one decimal):

The table is taken from TÜBER for Türkiye; the NIH statements above, on the other hand, are based on US data and fortification practice. TÜBER also notes that deficiency of some micronutrients, including thiamin (B1), can be seen in elimination diets that exclude gluten or grains. ^[8]

What B1 deficiency means: beriberi and Wernicke encephalopathy

According to the NIH, in the early stage of thiamin deficiency, weight loss and loss of appetite, confusion, short-term memory loss, muscle weakness, and heart-related symptoms (such as an enlarged heart) can be seen. The most common picture is beriberi, characterized mainly by peripheral neuropathy and muscle wasting; rarely it leads to congestive heart failure with edema and sometimes to death. Beriberi is rare in developed countries but is seen from time to time; the NIH reports that supplemental thiamin, often given intravenously, rapidly cures beriberi. ^[1]

EFSA distinguishes the forms as follows: dry beriberi is a neurologic picture mainly with sensory and motor peripheral neuropathy; in wet beriberi, cardiovascular findings such as heart failure, an enlarged heart, and tachycardia are added; its rapidly developing form (Shoshin beriberi) is acute and severe; infantile beriberi can be seen in 2–6-month-old infants breastfed by mothers with thiamin deficiency. Impairment of metabolic functions in the brain can lead to Wernicke encephalopathy (eye findings, ataxia, and impaired consciousness) and Korsakoff syndrome (amnesia, disorientation, often confabulation). ^[2]

Detailed guideB1 deficiency symptoms: why are beriberi and Wernicke encephalopathy an emergency?→

Who is at risk of thiamin deficiency?

The NIH lists the risk groups as follows: people with alcohol dependence (in developed countries, chronic alcohol use disorder appears to be the most common cause of thiamin deficiency; up to 80% of those with chronic alcoholism develop deficiency), people with HIV/AIDS, people with diabetes, older adults, and those who have had bariatric surgery. ^[1] EFSA states that in Western countries deficiency is associated with alcoholism and substance use; it can also be seen in people with bariatric surgery, gastrectomy, and chronic digestive and liver diseases. ^[2]

The EFNS 2010 guideline states that Wernicke encephalopathy should be considered in non-alcoholic people as well, in any situation that can lead to thiamin deficiency; it recommends monitoring thiamin status for at least 6 months after bariatric surgery and parenteral thiamin support. ^[3]

Thiamin in hyperemesis gravidarum

The 2023 systematic review by Fiorentini and colleagues examined 82 cases (case reports and case series from 66 publications) of Wernicke encephalopathy developing because of hyperemesis gravidarum (prolonged, severe vomiting in pregnancy). Hospitalization occurred at a mean of 14.6 weeks of gestation, after a mean of 6.6 weeks of vomiting; encephalopathy appeared at a mean of 16.5 weeks; eye findings were present in 93.9% of cases, ataxia in 74.4%, and confusion in 76.8%. Thiamin treatment was given in almost all cases; data on clinical course and birth outcomes were often missing. Case reports do not show the frequency of this complication in hyperemesis gravidarum; they only describe the picture that emerges. ^[7]

Drug interactions with thiamin

The NIH reports that thiamin has no known drug interactions, but that some medications can adversely affect thiamin levels. The loop diuretic furosemide has been associated with low or even deficient levels because of urinary thiamin loss; whether thiamin supplementation prevents deficiency in people using loop diuretics must be determined by clinical trials. Cases of beriberi or Wernicke encephalopathy have been reported with 5-fluorouracil, used in colorectal and other solid cancers; it is thought that the drug may increase thiamin metabolism and prevent formation of the active form TDP. ^[1]

How is thiamin deficiency measured?

According to EFSA, erythrocyte transketolase activity (ETKA) is a functional test of a TDP-dependent enzyme; a transketolase activity coefficient (αETK, “TDP effect”) below 1.15 is generally accepted as reflecting adequate thiamin status. The NIH reports that the TDP effect is generally 0–15% in healthy people, 15–25% in borderline deficiency, and above 25% in deficiency. Total thiamin in blood (whole blood, serum, erythrocytes) and erythrocyte TDP levels have also been examined; EFSA states that there are no established cutoff values for these measurements. It does not consider 24-hour urinary thiamin alone to be a reliable indicator. ^{[2] [1]}

The EFNS guideline recommends that total thiamin measurement from blood be done immediately before thiamin is given (a good practice point). For this reason, if there is suspicion, treatment can be started without waiting for the test result; the guideline bases the diagnosis on clinical findings. ^[3]

Does B1 supplementation have a benefit?

Thiamin’s role in metabolism does not mean that extra supplementation will improve energy, performance, or disease outcomes in a person without deficiency. Evidence is limited for claims other than beriberi treatment.

Benfotiamine and diabetic neuropathy

The NIH reports that benfotiamine is a synthetic derivative that is insoluble in water and has been examined in diabetic neuropathy in only a few small randomized trials: in three trials benfotiamine (alone or with other B vitamins) reduced the severity of neuropathy symptoms and urinary albumin excretion, a marker of early kidney damage, compared with placebo; in another trial no effect was found on urinary albumin and a marker of kidney damage. The NIH states that larger, longer, well-designed trials are needed. ^[1] In the BENDIP trial, 165 people with symmetric distal diabetic polyneuropathy were randomized to receive two different doses of benfotiamine or placebo; at the end of 6 weeks of treatment, the primary outcome, the neuropathy symptom score (NSS), differed significantly between groups in the per-protocol analysis (p=0.033) and was just above significance in the intention-to-treat analysis (p=0.055); the total symptom score (TSS) did not differ. Treatment was well tolerated. ^[4] A single short RCT and small trials are not sufficient for a definitive result; the decision on benfotiamine treatment is left to the physician.

Heart failure

The NIH reports that poor thiamin status in heart failure patients has been reported in studies at between 21% and 98%; causes listed include advanced age, comorbid diseases, inadequate intake, diuretic therapy, and frequent hospitalizations. ^[1] The 2023 meta-analysis by Syed and colleagues pooled 6 randomized trials with 298 participants with symptomatic heart failure (158 thiamin, 140 placebo); there was no significant difference in left ventricular ejection fraction (EF), NT-proBNP, walking test, death, hospitalization, and shortness of breath; only heart rate differed significantly (p=0.04). ^[5] In a smaller crossover pilot study (9 patients using diuretics with EF below 40%), EF showed a 3.9% absolute increase compared with placebo after 28 days of thiamin (32.8% and 28.8%; p=0.024). The result of this very small sample has not been confirmed in the meta-analysis. ^[6]

B1 excess and the upper limit

EFSA reports that the SCF stated that data on the adverse effects of oral thiamin intake in humans are limited and that there are no dose-response studies; because a LOAEL or NOAEL could not be determined, a UL could not be set either. This is not an “it is safe” ruling but a finding that “there are not enough data to set a limit.” ^[2]

Detailed guideB1 deficiency symptoms: who gets it, how is it measured?→

Pregnancy, breastfeeding, and other B vitamins

In pregnancy and breastfeeding, the NIH RDA value is 1.4 mg; EFSA considers the same mg/MJ value (0.1 mg/MJ) valid for pregnancy and breastfeeding, because it assumes that thiamin requirement is proportional to energy requirement. ^{[1] [2]} The main clinical problem related to thiamin in pregnancy is the prolonged vomiting described above; this topic and follow-up are under physician management.

Thiamin is found in B-complex and multivitamin products together with other B vitamins such as B6 and B12; the reference values, upper limits, and evidence for these vitamins are given in their separate guides. Total intake is calculated from the labels of products. The vitamin B6 and vitamin B12 guides are on separate pages; combination products are covered in the B-complex guide.

Common misunderstandings about B1

• “Beriberi is an old disease and is no longer seen.” The NIH reports that beriberi is rare in developed countries such as the US but is seen from time to time. ^[1]
• “Because it is a water-soluble vitamin, excess is harmless.” EFSA could not set a UL because of insufficient data; the safety limit is not known. ^[2]
• “Wernicke occurs only in alcoholics.” The EFNS states that the disease should be considered in non-alcoholic people as well, in any situation that can lead to thiamin deficiency. ^[3]
• “Benfotiamine is better.” In BENDIP, benfotiamine was compared with placebo; no direct comparison with thiamin was made. ^[4]

This guide does not recommend a personal dose.