Benfotiamine is a man-made form of vitamin B1 (thiamine), sold as "the fat-soluble B1" that gets into the body far better than ordinary thiamine. In Germany it is a licensed, pharmacy-only medicine (Milgamma mono 300) for vitamin B1 deficiency, including nerve and heart problems caused by that deficiency, and Switzerland authorized it in 2023 through a simplified review based on the German license. Those approvals are not the same as proof that it works for nerve symptoms in general; in the US it is a dietary supplement. Most of the interest comes from research on nerve symptoms in people with diabetes.
The short answer: benfotiamine really does raise blood thiamine much more than plain thiamine, but it is not actually fat-soluble, and the nerve evidence fades as trials get longer and more rigorous. Short trials, at least one co-authored by an executive of the German drug maker Wörwag Pharma, reported better symptom scores; two longer placebo-controlled trials found no benefit on nerve function. This guide walks through what it is, how it is absorbed, what each line of research found, and what it costs compared with plain B1.
The short version
- It is not really fat-soluble. A 2008 laboratory study found benfotiamine "practically insoluble in water, organic solvents or oil." It is absorbed after gut enzymes trim off a phosphate group. The truly fat-soluble B1 forms are allithiamine, fursultiamine and sulbutiamine.
- It does raise blood thiamine more. In one study, plasma thiamine exposure (the amount in the liquid part of the blood over several hours) was about 11 times that from thiamine hydrochloride, but the active form inside red blood cells was only about twice as high; an older review put the plasma advantage at about 3.6 times.
- Nerve results weaken with longer trials. A 6-week trial found better symptom scores only in its per-protocol analysis (counting only people who followed the study plan); trials of 12 and 24 months found no difference from placebo on nerve function.
- Other claims did not hold up. Placebo-controlled trials found no effect on kidney markers, blood sugar or blood vessel function, and a 12-month memory trial missed its main goal.
- It costs more. A typical 300 mg dose costs about $0.23 to $0.32, against about 6 cents for a 100 mg tablet of plain thiamine.
- Side effects looked similar to placebo at 300 to 600 mg a day in trials of up to a year, and a 2-year trial reported normal safety lab results. Numbness, tingling or burning feet need a doctor's evaluation (including a B12 check if you take metformin). Trial data in pregnancy and kidney failure are lacking, and confusion or unsteady walking in a heavy drinker is an emergency.
What benfotiamine is
Thiamine is the B vitamin the body uses to turn carbohydrate into energy, and nerves depend on it heavily. The adult RDA is only 1.2 mg a day for men and 1.1 mg for women, and most people get that from whole grains, pork, legumes and fortified foods. Severe deficiency causes beriberi, whose main features include nerve damage and wasting, and Wernicke-Korsakoff syndrome, most common in people who drink heavily. NIH lists heavy drinkers, older adults, people with diabetes and people who have had weight-loss surgery among those more likely to run low.
Benfotiamine (S-benzoylthiamine O-monophosphate) was first described by researchers in Japan in 1961 as a way to deliver more thiamine. By our arithmetic from its molecular weight, 300 mg of benfotiamine contains the equivalent of about 171 mg of thiamine, more than 100 times the RDA. It is often mentioned in the same breath as the disulfide forms of B1 (allithiamine, fursultiamine and sulbutiamine), but it is chemically different.
The fat-soluble myth and how it is absorbed
Many product labels, and even several trial papers, call benfotiamine "fat-soluble" or "lipid-soluble." When Belgian researchers tested it directly in 2008, they found it "practically insoluble in water, organic solvents or oil," could not dissolve it in octanol or oils, and wrote that it "should not be classified as a lipophilic compound as many authors still do." NIH's fact sheet avoids the fat-soluble label, describing benfotiamine only as "not water soluble" and "converted to thiamin in the body"; the same lab study found it dissolves well in water only under alkaline conditions.
The proposed route is this: enzymes on the gut lining strip off the phosphate group, the resulting S-benzoylthiamine passes into the blood, and red blood cells and the liver convert it to thiamine. The benzoyl part leaves the body as hippuric acid. In a mouse study, benfotiamine raised thiamine in blood and liver but not in the brain, unlike sulbutiamine, although the same paper notes an earlier rat study that found a rise in brain thiamine after 6 months of benfotiamine in the diet.
Whatever the route, the blood levels are real. In a 2014 study in healthy Chinese volunteers, plasma thiamine exposure after benfotiamine was about 11 times that after thiamine hydrochloride (results varied widely from person to person), while the active coenzyme inside red blood cells, thiamine diphosphate, was about twice as high. An older German review put the advantage at up to about 3.6 times. Plain thiamine's active absorption route saturates at fairly low doses (US nutrition experts cite a rapid drop in absorption at intakes above 5 mg), which is part of why a better-absorbed form seemed attractive. Blood levels still rise at higher doses, though: in a 2012 study, single oral doses of 100 to 1,500 mg of thiamine hydrochloride raised blood thiamine quickly through passive absorption.
The evidence at a glance
| The question | Best evidence | What it found | Our read |
|---|---|---|---|
| Does it raise blood thiamine? | Absorption (pharmacokinetic) studies; long trials | Plasma thiamine about 3.6 to 11 times higher than plain B1; red-cell coenzyme about 2 times | Yes |
| Nerve symptom scores, short term | 3- to 12-week trials, at least one with a manufacturer co-author | Better scores in some; the largest was significant per protocol only | Weak and inconsistent |
| Nerve function, 12 to 24 months | Two placebo-controlled trials (67 and 57 people) | No difference from placebo on nerve conduction, nerve fibers or symptom scales | No benefit shown |
| Kidney markers, blood sugar, blood vessels | Placebo-controlled trials and a meta-analysis | No effect | No benefit shown |
| Memory and thinking | 12-month trial in 70 older adults | Missed its main goal; a larger trial is under way | Unproven |
| Safety | Phase 1 study; trials up to 12 months, plus safety labs from a 24-month trial | Side effects similar to placebo at 300 to 600 mg a day | Well tolerated so far |
These summaries describe research. They are not claims about what a supplement does. Numbness, tingling or burning in the feet can have several causes and should be evaluated by a clinician.
The nerve trials
The appeal of benfotiamine for nerves comes from animal work. In a 2003 study in diabetic rats, it activated an enzyme called transketolase, which helps cells process glucose, and blocked several pathways by which high blood sugar damages tissue, preventing early eye damage in the animals. Human trials then tested whether it helps people with diabetes who have nerve symptoms.
Short trials. In a 3-week pilot trial (BEDIP, 2005) of 40 hospital patients, 400 mg a day improved a neuropathy score and pain compared with placebo, though a vibration test did not change. The largest short trial, BENDIP (2008), randomized 165 adults to 300 mg, 600 mg or placebo for 6 weeks. Its main symptom score was significantly better on benfotiamine in the per-protocol analysis (p = 0.033), but not in the larger intention-to-treat analysis, which kept people who did not follow the plan exactly (133 of the 165; p = 0.055), and a total symptom score did not differ. One of its authors is identified in a 2010 trial paper as head of medical affairs at Wörwag Pharma, which holds the German license for the benfotiamine medicine Milgamma mono 300. A 1996 trial in 24 people found better nerve conduction in one nerve, but it used benfotiamine combined with vitamins B6 and B12, so its effect cannot be credited to benfotiamine alone.
Long trials. In a 24-month trial (2012) of 67 Norwegians with long-standing type 1 diabetes, 300 mg a day raised blood thiamine markedly but produced no difference from placebo in nerve function or inflammation markers. The authors themselves noted that most participants had no nerve symptoms, and a published critique argued that few had confirmed nerve damage, which left little room to show improvement. That objection does not apply to BOND (2026), a 12-month trial of 57 people with type 2 diabetes and mild to moderate symptomatic nerve damage, given 600 mg a day. It found no difference from placebo on its main measure (nerve fibers in the cornea) or on skin biopsies, 13 nerve conduction measures, sensory and autonomic tests, symptom scales or quality of life. Only one symptom score trended better (p = 0.098). BOND was sponsored by Wörwag Pharma, and three authors were employees. The paper states the funder had no role in design, analysis or interpretation, and the trial still came out negative. A third 12-month pilot was stopped early.
A 2026 meta-analysis of 13 trials of B vitamins for nerve symptoms in diabetes described the benfotiamine results as "mixed." Pooled across all B vitamins, not benfotiamine alone, an examination score improved statistically but fell short of a clinically meaningful difference, and the authors judged combination B vitamin regimens more promising than single agents. We found no meta-analysis of benfotiamine alone. Put simply, no trial lasting 12 months or longer has shown that benfotiamine improves nerve function.
Does B1 status explain the mixed results?
There is a plausible reason benfotiamine might help some people and not others. In a 2007 UK study, plasma thiamine was about 75 percent lower in people with type 1 or type 2 diabetes than in healthy controls, apparently because the kidneys cleared thiamine 16 to 24 times faster. Yet a standard red blood cell test did not flag them as deficient.
In BOND, most participants had normal thiamine levels at the start, and the authors suggested this "may have contributed to the negative outcome." We found no trial that selected people with diabetes because their thiamine was low, so whether benfotiamine helps that group specifically is an open question.
Kidneys, blood vessels, memory and alcohol
Kidneys. In a 12-week placebo-controlled trial (2010) of 82 people with type 2 diabetes and early kidney damage, 900 mg a day improved thiamine status but did not lower urine albumin or a kidney injury marker, and a follow-up analysis found no change in blood or urine AGEs (advanced glycation end products, compounds formed when sugar binds to proteins) or inflammation markers. NIH's thiamin fact sheet (updated February 2023) says studies found benfotiamine "lowered urinary albumin excretion," but the three references attached to that sentence are a benfotiamine symptom trial that did not measure albumin, a plain-thiamine trial and an article on the history of thiamin. This looks like a referencing error, and the fact sheet's next sentence correctly reports that the benfotiamine kidney trial found no effect. A small plain-thiamine trial did report lower urine albumin.
Blood sugar. A 2022 meta-analysis of 6 trials of thiamine or benfotiamine found no effect on blood sugar measures.
Blood vessels. A German group found that 3 days of high-dose benfotiamine blunted the drop in artery widening after a high-AGE meal (13 people) or a cigarette (20 smokers), but neither study had a placebo group. In its only placebo-controlled test, 6 weeks at 900 mg a day in 31 people, there was no meal-related drop for benfotiamine to prevent.
Memory. In a 12-month trial (2020) of 70 older adults with mild cognitive impairment or mild dementia due to Alzheimer's disease, 600 mg a day did not significantly slow decline on the main memory and thinking test compared with placebo (p = 0.162 in the intention-to-treat analysis; the p = 0.125 in the paper's abstract is the per-protocol figure). Some secondary measures favored benfotiamine, but the authors noted these could be due to chance, and there were 2 strokes in the benfotiamine group and none on placebo, judged unrelated by the authors. A larger 406-person trial testing 600 and 1,200 mg a day for 72 weeks is due to finish around the end of 2027.
Alcohol. In a 24-week trial of 120 actively drinking adults with alcohol dependence, drinking fell in both the benfotiamine and placebo groups. A difference appeared only in a subgroup of 21 women, too small to rely on. Separately, an 8-week placebo-controlled trial (1998) reported better vibration sense and motor function with benfotiamine in people with nerve damage from alcohol, based on the 84 who completed it, and a 21-day trial of 303 such patients found no clinically relevant difference between benfotiamine plus B6 and plain thiamine plus B6. People who drink heavily are at real risk of thiamine deficiency, and that calls for medical care rather than self-treatment with a supplement.
Benfotiamine vs plain thiamine: cost
Here is what common products cost on November 1, 2026, from Vitacost listings. Prices change.
| Product | Form | Pack and price | Price per 300 mg |
|---|---|---|---|
| NOW B-1 100 mg | Thiamine hydrochloride | 100 tablets for $6.00 | $0.18 (3 tablets) |
| Life Extension Mega Benfotiamine 250 mg | Benfotiamine plus 10 mg thiamine | 120 capsules for $23.25 | About $0.23 |
| Doctor's Best Benfotiamine 150 mg | Benfotiamine | 360 capsules for $44.28 | $0.25 (2 capsules) |
| Doctor's Best Benfotiamine 300 mg | Benfotiamine | 60 capsules for $18.99 | $0.32 |
Prices from Vitacost listings, read November 1, 2026. Price per 300 mg is our arithmetic.
Most people taking thiamine for general use need far less than 300 mg; a single 100 mg tablet of plain thiamine costs about 6 cents. At 600 mg a day, the dose in BOND and several other trials, benfotiamine costs about $14 to $19 a month.
Is it worth trying?
If you have numbness, tingling or burning in your feet, start with a clinician. These symptoms have many causes, including low vitamin B12, which long-term metformin use can cause, and getting blood sugar under control is the foundation of care for nerve symptoms in diabetes. Our nerve pain supplements guide covers the broader evidence.
If you are low in thiamine, plain thiamine is cheap and corrects low levels; benfotiamine raises blood levels higher but has not been shown to work better on symptoms. Heavy drinkers and people who have had weight-loss surgery should get medical guidance, because severe B1 deficiency is a medical emergency treated with injected thiamine.
If you and your clinician decide to try it anyway, it was well tolerated at the doses studied (300 to 600 mg a day), and the short trials leave room for a modest change in symptom scores in some people. No trial has shown nerve repair. Do not stop or delay prescribed treatment.
Safety
- See a clinician for nerve symptoms. Numbness, tingling, burning or weakness can signal diabetes complications, B12 deficiency or other conditions that need diagnosis.
- Taking metformin? Long-term metformin use can lower vitamin B12, which itself causes numbness and tingling. Ask about a B12 test.
- Check combination "nerve" formulas for vitamin B6. Many pair benfotiamine with B6, and long-term B6 above 100 mg a day can itself cause nerve symptoms.
- Doses studied. Trials used 300 to 600 mg a day for up to two years. Side effect rates were similar to placebo in trials lasting up to a year, and the 2-year trial reported that safety lab results stayed normal. Single doses up to 1,200 mg were tolerated in healthy volunteers. No official upper limit has been set for thiamine, but that decision concerns thiamine itself, not benfotiamine, and long-term data beyond two years are lacking.
- Reported side effects. Mostly mild; in one trial at 900 mg a day, one person withdrew because of hives and one because of dizziness.
- Other trial events. A 12-month memory trial recorded 2 strokes on benfotiamine and none on placebo; the authors judged them unrelated. We found no drug interaction studies, so tell your prescriber you take it.
- Pregnancy and kidney disease. We found no trial data in pregnancy or kidney failure; ask your clinician.
- Severe B1 deficiency is an emergency. Confusion, unsteady walking or eye movement problems in someone who drinks heavily need urgent medical care.
Frequently asked questions
What is benfotiamine?
Benfotiamine is a man-made form of vitamin B1 (thiamine) first described in Japan in 1961. The body converts it to thiamine, and it raises blood thiamine much more than ordinary thiamine supplements. It is sold as a dietary supplement in the US; in Germany it is a licensed medicine for vitamin B1 deficiency.
Is benfotiamine fat-soluble?
No, despite the common claim. A 2008 laboratory study found it practically insoluble in water, organic solvents and oil, and it dissolves well in water only under alkaline conditions. It appears to be absorbed after gut enzymes remove its phosphate group. The truly fat-soluble forms of B1 are allithiamine, fursultiamine and sulbutiamine.
Does benfotiamine help diabetic nerve pain?
The evidence is weak. In a 6-week trial of 165 people, a nerve symptom score improved only in the per-protocol analysis (counting only people who followed the study plan), and a total symptom score did not differ from placebo. Trials of 12 and 24 months found no difference from placebo on nerve function, including a 2026 trial sponsored by benfotiamine maker Wörwag Pharma. Nerve symptoms should be evaluated by a clinician.
Is benfotiamine better than regular thiamine?
It raises blood thiamine more: in one study plasma thiamine exposure was about 11 times higher, though the active form in red blood cells was only about twice as high. But no trial has shown it works better than plain thiamine for symptoms, and plain thiamine costs less, especially at the low doses most people need.
How much benfotiamine do studies use?
Most trials used 300 to 600 mg a day, for periods from 3 weeks to 2 years. By our arithmetic, 300 mg of benfotiamine contains the equivalent of about 171 mg of thiamine, far above the adult RDA of 1.1 to 1.2 mg. Short blood vessel and kidney studies used 900 to 1,050 mg a day.
Is benfotiamine safe?
In trials of 300 to 600 mg a day lasting up to a year, side effects were similar to placebo, a 2-year trial reported normal safety lab results, and healthy volunteers tolerated single doses up to 1,200 mg. One person withdrew for hives and one for dizziness in a 900 mg trial. Long-term data beyond two years, and data in pregnancy or kidney failure, are lacking.
The bottom line
Benfotiamine is a well-absorbed form of vitamin B1 that raises blood thiamine much more than plain thiamine, though it is not actually fat-soluble. The hope that it protects nerves in diabetes rests mainly on short trials, at least one co-authored by a Wörwag Pharma executive, with modest and inconsistent symptom results. The two longest placebo-controlled trials, one sponsored by Wörwag, found no benefit on nerve function, and placebo-controlled trials on kidneys, blood sugar, blood vessels and memory found no clear benefit.
It was well tolerated at studied doses, so trying it alongside proper medical care is a personal choice to make with a clinician, but it is not a proven nerve treatment. Plain thiamine is far cheaper for correcting low B1, and nerve symptoms deserve a clinician's evaluation first.