Beriberi is the disease that invented the vitamin. Thiamine was the first one identified, which is why it carries the number one. We put it in the flour supply in the 1940s, watched the deficiency disappear from the wards, and closed the file.
Then we wrote one sentence into every textbook: this happens to alcoholics. That sentence stopped being a description and became a filter. If a patient does not drink, the level does not get sent. And because the level does not get sent, the case does not get counted, and the absence of cases keeps confirming that the file was right to close.
Eighty years later, somebody finally counted.
PRACTICE
Send both assays, draw them fasting, and treat before they come back.
If you decide to work a patient up for thiamine deficiency, three things about the mechanics matter more than they should.
Send plasma and whole blood. They disagree, and the disagreement is informative rather than annoying. In the study below, plasma flagged 26.4% and whole blood flagged 2.7% in the same patients on the same draw. The commercial ranges are 8 to 30 nmol/L for plasma (Quest) and 66.5 to 200 nmol/L for whole blood (LabCorp), both by LC-MS. Plasma low with whole blood normal is the pattern that improved with repletion in this cohort. Both low is straightforward. Both normal with a convincing picture still does not exclude it.
Draw it fasting. The standard criticism of plasma thiamine is that it reflects recent intake. For staging body stores that is a weakness. For us it is a handling instruction: draw it after breakfast and you can wash out a real deficiency. These were early-morning fasting draws. Samples also need careful handling and shipping, so a mishandled specimen is its own false result.
Do not wait for the number. Turnaround was 7 to 10 days, which is longer than the window in which the answer would have changed anything. Replacement is inexpensive and has an excellent safety profile. A missed Wernicke's ends in Korsakoff or death. That asymmetry is the entire argument for treating on suspicion and letting the level confirm you later.
PUBLICATION
Mates EA, Kilgore-Gomez A, Phibbs C. Thiamine Deficiency in Hospitalized Veterans Without Alcohol Use Disorder: Prevalence, Biomarker Assessment, and Clinical Characteristics. Diseases 2026;14(8):275. Open access (doi 10.3390/diseases14080275).
286 hospitalized veterans. Alcohol use disorder excluded by protocol. Anyone already taking a B-complex or thiamine supplement excluded as well, so the cohort could not be padded by people who were already being treated.
26.4% had low plasma thiamine. Of the patients with clinical data, all but one had signs or symptoms. This was not an incidental laboratory abnormality hunting for a story.
The symptom rank order:
Decreased appetite, 88%. Nausea or vomiting, 60%. Constipation, 58%. Mental confusion is sixth, at 48%. Memory loss is seventh. Double vision is 13%.
We were taught to find this disease by its neurology. In these patients it announced itself through the gut, and it did so more often and more loudly than it did through the brain.
It also rarely arrived alone.
GI beriberi in 60%. Two or more concurrent syndromes in 77%. One clean syndrome in 19%. Whatever this is, it is not an organ-specific disease, and the habit of looking for it one system at a time is part of why it stays hidden.
Then there is the figure that should change a reflex.
Of 35 patients meeting criteria for Wernicke's, four had the classic triad. Twenty-two had exactly one finding. Altered mental status was present in 94%, ophthalmoplegia in 29%, ataxia in 26%.
Every one of us was trained to recognize this by a triad that showed up in one patient out of nine.
On repletion, among 32 low-plasma patients who returned: MOCA improved a mean of 1.9 points (p = 0.0093), composite motor strength 2.5 points (p = 0.0417), and 27 of 32 reported feeling better.
Two more things: Total body stores are 25 to 30 mg. Two to three weeks of poor intake empties them, or 72 hours in someone acutely ill, which means a hospital admission is long enough to produce this rather than merely reveal it. The screen we would reach for does not find it, which is a fair description of how a disease stays invisible for eighty years.
The honest ceiling. One VA center. Mean age 70.6, 96% male, 90% white. An underpowered exploratory pilot with no signal on length of stay, readmission, or 90-day mortality. The authors also note that 86.6% of enrollees met clinical criteria for some deficiency syndrome, a number they call implausibly high without biomarker confirmation, and they say plainly that clinical criteria alone overcall it. Their conclusion is not that everyone is deficient. It is that nobody knows, because nobody had looked.
PRODUCT
Better-absorbed B1, for the people already asking.
For a diagnosed deficiency, plain thiamine is the answer and it costs pennies. That is what was used in the study and there is no reason to reach past it.
For daily use the calculus differs, because plain thiamine hydrochloride absorbs less and less efficiently as the dose climbs. Two derivatives do measurably better in human comparisons.
Benfotiamine is an S-acyl derivative. It is frequently described as fat-soluble, which is technically wrong: Volvert's 2008 work found it practically insoluble in water, oil, and organic solvents alike, and the authors said directly that it should not be called lipophilic. Its advantage is absorption, not solubility…technically.
Allithiamine is a disulfide, and the disulfides are the lipid-soluble ones. Both out-absorb thiamine salts in head-to-head human studies.
Buy either from a manufacturer that publishes third-party testing and prints the dose on the label. Neither is a treatment for deficiency, and if you think you have one, the answer is a level and a physician, not a bottle.
PERSON
Michael Donnino, Beth Israel Deaconess.
An emergency physician with thirty-one thiamine papers to his name. He is the one who named gastrointestinal beriberi, in the Annals in 2004, and he has spent the twenty years since running randomized trials on thiamine in septic shock, after cardiac arrest, and in diabetic ketoacidosis. He was still publishing on it this year. I think he follows me on Twitter, too!
This man ran controlled trials on this for two decades while the field treated the question as closed. If you want a single argument that this was dismissed rather than disproven, his bibliography is it.
Rick Pescatore, D.O. is an emergency physician and Editor-in-Chief of Emergency Medicine News. He is the founder of BellyMD, which makes MGB+, a line of gut-brain formulas built around well-absorbed B1 and magnesium.
Can B1 deficiency cause functional dyspepsia? Someone I know, their quality of life is in the trenches cuz they cant eat at all, surviving on bread, plain rice, chai, and random stuff here and there. Some fruits and nuts. I'm wondering if I should tell them to get bloodwork for their B1.
I gotta say, reading about thiamine deficiency and the solibility stuff finally makes studying ochem for the mcat a little rewarding 😆.
I haven't given much thought to what speciality I'd like to pursue if I get into med school, but maybe something where I can help patients with symptoms nobody seems to have an answer for - like the dyspepsia - would be nice.