Thiamine (B1)
The B vitamin whose deficiency causes beriberi and Wernicke's encephalopathy. Cheap, unglamorous, and the deficiency is far more common in specific groups than most people assume.
Thiamine (B1) quick facts
| Suggested dose | RDA is ~1.1–1.2 mg. Therapeutic use ranges 100–300 mg. Benfotiamine is the fat-soluble derivative with better tissue penetration. |
| How often | Daily |
| Who it's for | Anyone on long-term loop diuretics, metformin, post-bariatric, or with a history of heavy drinking. |
Deficiency is far more common than people assume, and the causes are ordinary: alcohol impairs both absorption and activation, loop diuretics increase urinary loss, and bariatric surgery removes the absorption site. Untreated it causes Wernicke's encephalopathy, which produces permanent damage and is trivially preventable. Anyone drinking heavily or on long-term furosemide should have this on their list. Water-soluble and very safe.
How Thiamine (B1) actually works
Thiamine pyrophosphate is the coenzyme for pyruvate dehydrogenase, the gateway enzyme converting pyruvate into acetyl-CoA and therefore the entry point from glycolysis into the TCA cycle. It also serves alpha-ketoglutarate dehydrogenase inside the cycle and transketolase in the pentose phosphate pathway. Block that gateway and the cell cannot use glucose aerobically, which is why deficiency hits the brain and heart — the two tissues with the least metabolic slack — first and hardest.
Where to get Thiamine (B1)
Find Thiamine (B1) on iHerb →The evidence for Thiamine (B1)
Graded by what exists behind each claim.
✅ Clinically validated
- Corrects deficiency, which is the main and undisputed use.
- Deficiency is well documented in alcohol use disorder, after bariatric surgery, in heart failure treated with loop diuretics, and with chronic metformin use.
- High-dose thiamine trials for fatigue in IBD and Hashimoto's report benefit in small, mostly uncontrolled studies.
📊 Correlative data
- Among the best-documented deficiency epidemiology in nutrition: beriberi in polished-rice populations, and Wernicke-Korsakoff in chronic alcohol use. Both established the requirement long before the vitamin was isolated.
🧪 Theoretical / extrapolated benefits
- Thiamine pyrophosphate is the cofactor for pyruvate dehydrogenase — without it, glucose cannot enter the Krebs cycle, which is why deficiency presents as an energy and neurological problem simultaneously.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Thiamine (B1) actually does
Thiamine matters because of one chemical trick: an acidic carbon on a thiazolium ring. Deprotonating C2 of the thiazolium gives a carbanion that attacks a carbonyl and stabilizes the resulting negative charge, which is what makes decarboxylation of an alpha-keto acid possible. Thiamine itself does none of this; the cofactor is thiamine diphosphate, made by thiamine pyrophosphokinase using ATP as the donor Mrowicka 2023.
Four enzymes carry the entire load and each failure has a recognizable clinical face. Pyruvate dehydrogenase feeds glycolysis into the citric acid cycle; its failure produces lactate and the cardiac and neurological picture of beriberi. Alpha-ketoglutarate dehydrogenase is a rate-limiting step of the cycle itself. The branched-chain ketoacid dehydrogenase handles leucine, isoleucine and valine. And transketolase moves two-carbon units in the non-oxidative pentose phosphate pathway, generating ribose-5-phosphate for nucleotides and NADPH-linked flux for reductive biosynthesis.
Transketolase is also the historical status test, and it is a clever one. The erythrocyte transketolase activation coefficient measures enzyme activity before and after adding thiamine diphosphate in vitro; a large activation means the enzyme was sitting there empty. That is a functional assay rather than a concentration, which is exactly what the rest of this catalog usually lacks.
The reason deficiency hits the brain and heart first is turnover, not distribution. Total body thiamine is only about 25 to 30 mg with a biological half-life of 9 to 18 days, and tissues with high oxidative flux and no capacity for anaerobic compensation run out soonest. Clinically significant deficiency can develop in 2 to 3 weeks of very low intake, which is why refeeding a starved person without thiamine is dangerous Mrowicka 2023.
There is a fourth phosphate ester with a separate biology. Thiamine triphosphate is present in small amounts, is not a decarboxylase cofactor, and appears to have signaling roles; administration of a lipophilic thiamine derivative raises thiamine triphosphate in rat tissues in a way that ordinary thiamine salts do not Bettendorff 1990. That distinction is the seed of the whole derivative market.
Cell, rodent, human — and where it stops
Cell to human is complete and uncontested for deficiency. The part that fails is the step from a corrected status marker to a clinical result in people who were not deficient.
In enzymology and in animals. Thiamine-deficient rodents reproduce the human lesion distribution, with selective damage to periventricular structures, and the cofactor dependencies of all four enzymes are established chemistry Hrubša 2022.
In deficient humans, replacement is one of the most dramatic interventions in medicine. Wet beriberi's high-output heart failure and Wernicke encephalopathy's ophthalmoplegia and confusion respond to parenteral thiamine within hours to days. Nothing on this page disputes that, and nothing about it is a supplement question.
In diabetes the marker said there was a deficiency and the trials could not turn it into an outcome. People with type 1 and type 2 diabetes have low plasma thiamine, apparently because of increased renal clearance rather than low intake, and high-dose thiamine corrects the plasma number and improves some microvascular markers in small studies Beltramo 2021. Larger clinical endpoints have not followed.
The obstacle to transfer is a transporter, and it is the central fact of this page. Intestinal uptake of water-soluble thiamine runs through the carriers THTR-1 and THTR-2, which saturate at around 5 mg per dose. Above that, absorption is by passive diffusion at a few percent. So a 100 mg tablet and a 300 mg tablet deliver a similar amount to the blood, and raising the oral dose of a thiamine salt cannot raise tissue thiamine diphosphate the way the arithmetic implies Bozic 2023.
That is why the derivative literature exists at all. Lipid-soluble and S-acyl derivatives were developed specifically to get past the transporter ceiling Volvert 2008 Bettendorff 1990, and the interesting clinical question moved with them.
Thiamine (B1) — which form, and does it matter
The two salts on the shelf are interchangeable and neither solves anything. Thiamine hydrochloride and thiamine mononitrate differ in hygroscopicity and shelf stability — the mononitrate is preferred in fortified flour for that reason — and behave identically once dissolved. Both are hydrophilic cations that depend on THTR-1 and THTR-2 to cross a membrane.
The exposure ceiling is the number everything else follows from. Carrier-mediated absorption saturates near 5 mg per dose, and fractional absorption of a 100 mg oral dose is on the order of a few percent. Peak plasma arrives in about 1 to 2 hours; the plasma half-life is short, roughly 1.8 hours for the initial phase, with rapid renal clearance of the excess and its metabolites. There is no cytochrome step and no meaningful first-pass metabolism — the limit is transport, not degradation Bozic 2023.
Splitting doses beats increasing them. Because the constraint is per-dose transporter capacity rather than daily total, 5 mg taken four times outperforms 100 mg taken once for raising whole blood thiamine. Almost nobody doses it that way, and almost every product is built around a single large tablet.
The derivatives are a genuinely different pharmacology and they belong on their own page. Benfotiamine is S-benzoylthiamine monophosphate, absorbed as a neutral lipophilic molecule and dephosphorylated at the brush border before entering the cell; sulbutiamine is a lipophilic disulfide that crosses the blood-brain barrier and raises thiamine triphosphate in tissue Bettendorff 1990. Fursultiamine and the thioester series behave similarly. Evidence for a derivative is not evidence for thiamine hydrochloride and the reverse is equally true.
Thiaminases are a form problem hiding in the diet. Raw freshwater fish and shellfish contain thiaminase I, which cleaves the molecule; horsetail and bracken contain a heat-stable antithiamine factor; and sulfites used as preservatives cleave thiamine at the methylene bridge. A supplement taken alongside any of those is delivering less than the label says.
What would have to be true, and how you would know it was not
1. Whole blood thiamine rises modestly and then refuses to rise further. Predict vitamin B1 (thiamine) measured in whole blood or as thiamine diphosphate rises on 100 mg daily and that tripling the dose to 300 mg produces a much smaller further increase, because the carrier is saturated Bozic 2023. Retest at 4 to 6 weeks.
2. The functional test is the one that answers the question. The erythrocyte transketolase activation coefficient reports whether the enzyme was empty. Predict a high activation coefficient normalizes in a genuinely deficient person within 2 to 4 weeks and does not change at all in a replete one. A page selling thiamine for energy owes the reader that distinction.
3. The prediction that cuts against the product. Predict that in an adult eating a fortified Western diet, 100 mg of thiamine hydrochloride produces no measurable change in fatigue, cognition or exercise capacity at 12 weeks. A randomized trial in replete adults showing benefit would falsify this page Hrubša 2022.
4. Predict that the people who respond are identifiable in advance. Chronic alcohol use, bariatric surgery, prolonged vomiting or parenteral nutrition, diuretic therapy for heart failure, and diabetes with high renal clearance are the settings where a deficiency is plausible Beltramo 2021. Predict a measurable functional response in those groups and none outside them.
5. Predict lactate falls only where pyruvate dehydrogenase was the problem. In a person with unexplained lactic acidosis and a plausible deficiency, predict lactate falls within days of parenteral thiamine. In anybody else, predict it does not move — which is a useful diagnostic test and a poor supplement claim.
What nobody has tested yet
Nobody has established what high-dose oral thiamine does to tissue. The transporter ceiling is documented in the intestine, and there is no human study relating a 300 mg oral dose to muscle or brain thiamine diphosphate. That measurement would tell the field whether high-dose thiamine salts are pharmacology or placebo Bozic 2023.
The diabetes question is stuck at surrogates. High-dose thiamine corrects the plasma deficit and improves some microvascular markers, and no trial has followed patients to nephropathy, retinopathy or neuropathy endpoints Beltramo 2021. That is a feasible multi-year study nobody has funded.
Whether thiamine triphosphate does anything in humans is open. It is measurable, it is raised by lipophilic derivatives Bettendorff 1990, and no function has been demonstrated in a person. If it has one, the derivative products are doing something the salts cannot and the entire comparison changes.
And the heart failure literature has never been settled. Loop diuretics increase urinary thiamine loss and small trials of supplementation have reported ejection fraction changes, with inconsistent replication. A properly powered trial in diuretic-treated heart failure has been called for since the 1990s and does not exist.
Thiamine (B1) — its own safety story, not its category's
Oral thiamine is about as safe as a supplement can be, and the reason is the transporter. There is no tolerable upper intake level for thiamine because no adverse effect has been established from oral intake; the saturable carrier means that most of a large dose is never absorbed and what is absorbed is renally cleared within hours Mrowicka 2023.
The one documented serious reaction belongs to the injection. Anaphylaxis has been reported with parenteral thiamine, rarely and mostly historically. It is not a feature of the oral route.
The dangerous mistake is sequencing, not dosing. Giving glucose to a thiamine-deficient person before giving thiamine can precipitate Wernicke encephalopathy, because the glucose load drives pyruvate into a pathway that has no cofactor. That is the reason thiamine precedes dextrose in emergency protocols, and it is the single most consequential fact about this vitamin.
What depletes it, in order of how often it is missed. Chronic alcohol use, which impairs both absorption and phosphorylation. Loop diuretics, through urinary loss. Bariatric surgery. Prolonged vomiting, including hyperemesis. High-carbohydrate refeeding after starvation. Metformin has been reported to interfere with thiamine transport at the same carrier family Beltramo 2021.
Who needs a clinician rather than a capsule. Anyone with confusion, ataxia or eye movement abnormalities in the setting of alcohol use or malnutrition needs parenteral thiamine and an assessment, not a tablet, because the oral route cannot deliver enough fast enough. Nothing here is medical advice or diagnosis, and these statements have not been evaluated by the Food and Drug Administration.
Sources read for this page
- Mrowicka M. The importance of thiamine (vitamin B1) in humans. Biosci Rep 2023 · PMID 37389565
- Beltramo E. Thiamine and diabetes: back to the future?. Acta Diabetol 2021 · PMID 34091762
- Bozic I. Thiamine and benfotiamine: Focus on their therapeutic potential. Heliyon 2023 · PMID 38034619
- Volvert ML, et al. Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives. BMC Pharmacology 2008 · PMID 18549472
- Hrubša M. Biological Properties of Vitamins of the B-Complex, Part 1: Vitamins B1, B2, B3, and B5. Nutrients 2022 · PMID 35276844
- Bettendorff L, et al. Injection of sulbutiamine induces an increase in thiamine triphosphate in rat tissues. Biochemical Pharmacology 1990 · PMID 2268373
How you would know if it worked
This is a deficiency correction rather than an enhancement, so the read-out is whether you were deficient — and the groups where you genuinely might be are named on the label of your other prescriptions: long-term loop diuretics, chronic metformin, post-bariatric anatomy, and heavy drinking. B12 is on the list because metformin and bariatric surgery deplete it by the same routes, and GGT because it is the marker that says whether alcohol is the reason thiamine is low, which changes what should happen next far more than the capsule does. The RDA is roughly 1.1-1.2 mg and therapeutic use runs 100-300 mg, so a level drawn 12 weeks in tells you the dose landed rather than that it was needed. Note what that costs: a thiamine level sits on one panel here and it is the most expensive one, while the vitamin itself is cheap and water-soluble — so in the at-risk groups above the sensible order is to correct first and test only if the picture does not fit. Suspected Wernicke's is an emergency, treated with injected thiamine before any glucose — not with a supplement.
- Vitamin B1 (Thiamine) — Thiamine 50–100 mg/day, or benfotiamine (fat-soluble, better absorbed) 150–300 mg — which has specific evidence for diabetic neuropathy Retest: 12 weeks after supplementation.
- Vitamin B12 Retest: 8–12 weeks after starting supplementation.
- GGT (Gamma-Glutamyl Transferase) Retest: 6 weeks minimum after any change, because of the 2–3 week half-life. Sooner than that and you are measuring the previous month. Every 6–12 months as routine if you drink, carry visceral fat, or run oral compounds.
The cheapest panel carrying Vitamin B1 (Thiamine) and at least one other of these is Bariatric & Long-Term GLP-1 Nutrition, at $377 — the panel is named for a different question, and the marker is the same marker. That is the whole cost of finding out.
Draw before you start, not after. A result with nothing to compare it to answers nothing.
Thiamine (B1) — safety & side effects
- Very well tolerated; no established upper limit for oral use.
- High-dose thiamine given to a malnourished person can precipitate refeeding syndrome — this is a hospital concern rather than a supplement one, but it is why thiamine repletion in alcohol dependence is done medically.
- Rare allergic reactions to injectable forms; oral is not associated with this.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this against it with a pharmacist or doctor — pharmacists are underused and free.
- When to take it, and what to take it with
- Which form actually absorbs
- Who it's worth it for
- Coach Cam's stacks and notes
- Fasted or with food, and when in the day
- Morning or night, and why that window
- Around training, or deliberately away from it
- What it must not share a window with
Everything above is free and stays free. Skool is where it becomes a plan — Thiamine (B1) in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Thiamine (B1)
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Vitamin D (25-Hydroxy) | The one most often actually low, and the one with a real ceiling |
| Vitamin B12 | Commonly low in older adults, vegetarians and metformin users |
| Folate, Serum | Read alongside B12 — supplementing one can mask the other |
| Homocysteine | The functional read on whether your B vitamins are working |
The Full Micronutrient Screen panel covers these in one order — 11 markers, $363.60 with the discount applied.
Check results you already have → · All 103 markers A–Z
Thiamine (B1) — frequently asked questions
What is Thiamine (B1)?
The B vitamin whose deficiency causes beriberi and Wernicke's encephalopathy. Cheap, unglamorous, and the deficiency is far more common in specific groups than most people assume.
What is the suggested dose of Thiamine (B1)?
RDA is ~1.1–1.2 mg. Therapeutic use ranges 100–300 mg. Benfotiamine is the fat-soluble derivative with better tissue penetration. This is a general reference for education only — statements have not been evaluated by the FDA and this is not medical advice.
Where can I find Thiamine (B1) dosing and the full breakdown?
The suggested dose and the full evidence — clinical, correlative and theoretical — are on this page. What's inside Skool is when to take it, which form actually absorbs, the brand worth buying and Coach Cam's stacks.
Where can I buy Thiamine (B1)?
Coach Cam sources Thiamine (B1) from vetted, top-rated brands on iHerb — use the buy link on this page.
Thiamine (B1) inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Thiamine (B1) is used for
Thiamine (B1) appears under 2 goals in the goal router.
Related Vitamins supplements
Where this goes next
Thiamine (B1) is the alcohol arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.