Vanadium

What it is

Vanadium is a metallic trace element found in air, soil, water and food, where in living systems it occurs mainly as the vanadyl cation or the vanadate anion. Very little of what is swallowed gets into the body: absorption is under 5 per cent, so most passes out in the stool. No functional role for vanadium in humans has been identified, and typical adult dietary intakes are only a few mcg a day. Supplement forms, usually vanadyl sulfate, have been given at doses roughly a hundred times usual dietary intake.

What the research says

The evidence does not support vanadium supplements for blood sugar control. A systematic review searching 14 databases found no controlled trial that met basic quality criteria, and concluded there is no rigorous evidence that oral vanadium improves glycaemic control in type 2 diabetes. Small uncontrolled studies did lower fasting glucose and HbA1c, but they had no placebo group, and the same doses regularly caused gastrointestinal upset. In animals vanadium mimics insulin, but no human requirement or deficiency state has been demonstrated, and a placebo-controlled trial in weight-training athletes found no effect on body composition.

Evidence grade: Not supported by the research.

What goes wrong

The same systematic review recorded that vanadium treatment frequently causes gastrointestinal side effects. (Source 1)

• Systematic review, Low certainty.
• Size: 5 trials of 30-150 mg/day oral vanadium in diabetic humans.
• Who: adults with diabetes.
• How long: 2 weeks to 10 weeks across the included trials.
• Result: No pooled rate reported; the review states side effects occur often.
• Funding: not stated.

Treatment with vanadium often results in gastrointestinal side-effects.

In the same study the higher vanadyl sulfate doses caused gastrointestinal intolerance and total cholesterol fell together with HDL cholesterol. (Source 2)

• Case series, Very low certainty.
• Size: 16 patients.
• Who: adults with type 2 diabetes.
• How long: 6 weeks.
• Result: Gastrointestinal intolerance at 150 and 300 mg/day; at the highest dose total cholesterol decreased with a decrease in HDL.
• Funding: not stated.

The 150- and 300-mg vanadyl doses caused some gastrointestinal intolerance but did not increase tissue oxidative stress as assessed by thiobarbituric acid-reactive substances (TBARS).

A woman who swallowed ammonium vanadate developed severe acute kidney failure, hypoglycaemia and erosive gastritis, and died the following morning. (Source 3)

• Case report, Certainty not rated.
• Size: 1 patient.
• Who: 24-year-old woman.
• How long: died the morning after admission; the paper's own account of the timing is self-contradictory.
• Result: Estimated glomerular filtration rate 21 ml/min; blood vanadium 6.22 mg/L, which the authors state is about 6000 times the normal concentration in the general population; blood glucose 0.2 g/L (about 11 mg/dL)
• Funding: not stated.

Limit of this finding: Three things in this paper do not hold together. Its own sentence reads "This patient had taken an undetermined amount of ammonium vanadate 12 h after ingesting", which puts the swallowing after itself; the authors almost certainly mean she reached hospital about 12 hours after swallowing it, but the paper as published does not say so. The "6000 times higher than normal" figure is the authors' own multiplier and the paper never states the reference concentration it is measured against. The hypoglycaemia is given as 0.2 g/L with no reference range, a unit style unusual outside France, which is roughly 11 mg/dL. This is also one deliberate poisoning with an industrial vanadium salt and says nothing about vanadium in food or in supplements.

She died next morning in the context of respiratory distress despite intensive care and oxygen therapy.

In a population-based prospective study, higher urinary vanadium was associated with a modestly increased risk of newly impaired kidney function or chronic kidney disease; this is an association, not proof that vanadium caused it. (Source 4)

• Cohort study, Low certainty.
• Size: 1,455 participants developed impaired kidney function or CKD; 123 had rapid eGFR decline.
• Who: general adult population, mean age 51.9 years at baseline.
• How long: mean follow-up 12.5 years.
• Result: Urinary vanadium hazard ratio 1.07 (95% CI 1.03-1.12) for incident impaired kidney function or CKD.
• Funding: not stated.

Limit of this finding: This study measured seven elements at once, and urinary vanadium was one of seven linked to newly impaired kidney function or chronic kidney disease. Vanadium was not among the elements linked to rapid loss of kidney function in the same paper - those were copper, silver, molybdenum and cadmium, and the silver estimate's confidence interval reaches exactly 1, meaning it is compatible with no effect. The hazard ratio of 1.07 is per unit of urinary vanadium as modelled by the authors, not per supplement dose, and an association in a population study cannot show that vanadium damaged anyone's kidneys.

we found that urinary vanadium [hazard ratio (HR) = 1.07, 1.03-1.12], cobalt (HR = 1.69, 1.21-2.37), nickel (HR = 1.19, 1.08-1.3), copper (HR = 1.03, 1.01-1.06), selenium (HR = 1.33, 1.02-1.73), molybdenum (HR = 1.48, 1.2-1.82) and iodine (HR = 1.1, 1.02-1.2) were associated with an increased risk of new incident IKF or CKD cases during the follow-up

What the evidence supports

In an uncontrolled 6-week study, 150 mg/day vanadyl sulfate lowered fasting glucose and HbA1c in 11 people with type 2 diabetes; with no placebo group this cannot be separated from other effects of study participation. (Source 5)

• Case series, Very low certainty.
• Size: 11 patients.
• Who: adults with type 2 diabetes.
• How long: 6 weeks.
• Result: Fasting plasma glucose 194 +/- 16 to 155 +/- 15 mg/dL; HbA1c 8.1 +/- 0.4 to 7.6 +/- 0.4%; fructosamine 348 +/- 26 to 293 +/- 12 micromol/L, all P < 0.01; endogenous glucose production reduced by about 20% (P< 0.01); insulin-mediated glucose disposal 4.3 +/- 0.4 to 5.1 +/- 0.6 mg/kg lean body mass x min (P< 0.03)
• Funding: not stated.

Treatment significantly improved glycemic control: fasting plasma glucose (FPG) decreased from 194 +/- 16 to 155 +/- 15 mg/dL, hemoglobin A(1c) decreased from 8.1 +/- 0.4 to 7.6 +/- 0.4%, and fructosamine decreased from 348 +/- 26 to 293 +/- 12 micromol/L (all P < 0.01) without any change in body weight.

What the evidence does not support

A systematic review of 14 databases found no controlled trial of oral vanadium in type 2 diabetes that met its pre-set quality criteria, and concluded there is no rigorous evidence of benefit. (Source 1)

• Systematic review, Low certainty.
• Size: 151 studies screened; 0 met inclusion criteria; 5 trials of 30-150 mg/day included under relaxed criteria.
• Who: adults with type 2 diabetes.
• How long: trials of at least 2 months were sought.
• Result: No eligible trials; the five studies found under relaxed criteria 'demonstrated significant treatment-effects' but were judged poor quality.
• Funding: not stated.

There is no rigorous evidence that oral vanadium supplementation improves glycaemic control in type 2 diabetes.

A dose-ranging study in 16 people with type 2 diabetes found that at tolerated doses vanadyl sulfate did not dramatically improve insulin sensitivity or glycaemic control. (Source 6)

• Case series, Very low certainty.
• Size: 16 patients across 75, 150 and 300 mg/day.
• Who: adults with type 2 diabetes.
• How long: 6 weeks.
• Result: Glucose metabolism during euglycaemic clamp did not increase at 75 mg/day; improved in 3 of 5 at 150 mg and 4 of 8 at 300 mg; basal hepatic glucose production unchanged at all doses.
• Funding: not stated.

Vanadyl sulfate appears safe at these doses for 6 weeks, but at the tolerated doses, it does not dramatically improve insulin sensitivity or glycemic control.

A 12-week double-blind placebo-controlled trial in weight-training volunteers found vanadyl sulfate ineffective for body composition, and two participants on vanadyl sulfate withdrew because of apparent side effects. (Source 7)

• Randomized trial, Low certainty.
• Size: 31 subjects completed.
• Who: weight-training volunteers.
• How long: 12 weeks.
• Result: No significant treatment effects for anthropometric parameters or body composition; only significant treatment effect a Treatment x Time interaction in 1 RM leg extension (p = .002), attributed to lower baseline in the vanadyl group.
• Funding: not stated.

There were no significant treatment effects for anthropometric parameters and body composition during the trial.

Where the evidence is mixed

A 2025 review of vanadium in the nervous system states its therapeutic use remains controversial because of toxicity concerns and possible links to cognitive disorders. (Source 8)

• Expert review, not systematic, Very low certainty.
• Size: not stated.
• Who: not applicable.
• How long: not applicable.
• Result: No pooled estimate; the review reports unresolved safety and efficacy questions.
• Funding: not stated.

However, its therapeutic use is controversial due to postulated concerns regarding its toxicity and possible involvement in cognitive disorders.

What official bodies say

The Institute of Medicine set a Tolerable Upper Intake Level of 1.8 mg/day of elemental vanadium for adults, derived from kidney damage in rats rather than from human data, and could not set any upper level for children or in pregnancy. (Source 9)

• Official position, Certainty not rated.
• Size: not applicable.
• Who: US and Canadian population, adults 19 years and older.
• How long: not applicable.
• Result: LOAEL 7.7 mg/kg/day in rats divided by an uncertainty factor of 300, giving 1.78 mg/day rounded to 1.8 mg/day.
• Funding: independent (US Institute of Medicine)

The resulting UL for adults is 1.78 mg/day (which was rounded to 1.8 mg/day).

The Institute of Medicine reported that no human requirement for vanadium has been established and no reference intake was set. (Source 10)

• Official position, Certainty not rated.
• Size: not applicable.
• Who: all life stages.
• How long: not applicable.
• Result: No EAR, RDA or AI set for vanadium.
• Funding: independent (US Institute of Medicine)

A biological role of vanadium in humans has not yet been identified. Therefore, neither an Estimated Average Requirement, Recommended Dietary Allowance, nor Adequate Intake was determined for vanadium.

Where the research disagrees

Whether oral vanadium does anything useful for blood sugar in type 2 diabetes

• Smith, Pickering and Lewith (systematic review, QJM 2008), systematic review of 14 databases in which no trial met the inclusion criteria: There is no rigorous evidence that oral vanadium supplementation improves glycaemic control in type 2 diabetes. (Source 1)
• Cusi and colleagues (JCEM 2001), uncontrolled 6-week before-and-after study in 11 patients, no placebo group: We conclude that VOSO(4) at maximal tolerated doses for 6 weeks improves hepatic and muscle insulin sensitivity in T2DM. The glucose-lowering effect of VOSO(4) correlated well with the reduction in EGP, but not with insulin-mediated glucose disposal, suggesting that liver, rather than muscle, is the primary target of VOSO(4) action at therapeutic doses in T2DM. (Source 5)

How much

• Reference intake: No Estimated Average Requirement, Recommended Dietary Allowance or Adequate Intake has been set for vanadium (Institute of Medicine, 2001), because no biological role in humans has been identified. (Source 10)
• Upper limit: Institute of Medicine, 2001: Tolerable Upper Intake Level of 1.8 mg/day of elemental vanadium for adults aged 19 and over, based on kidney lesions in rats; no upper level could be set for infants, children, pregnancy or lactation. (Source 9)
• Studied: Vanadyl sulfate 150 mg/day for 6 weeks in 11 adults with type 2 diabetes. (Source 5)
• Studied: Vanadyl sulfate 75, 150 or 300 mg/day for 6 weeks in 16 adults with type 2 diabetes. (Source 2)
• Studied: Vanadyl sulfate 0.5 mg/kg/day for 12 weeks in weight-training volunteers. (Source 7)
• Studied: The Institute of Medicine records supplement use of vanadyl sulfate at 100 mg/day and sodium metavanadate at 125 mg/day in diabetic patients, about 100 times usual dietary intake. (Source 11)

A common belief, and what the research shows

The belief: Vanadium is an essential trace mineral, so a supplement tops up something the body needs.

What the research shows: No human role has been demonstrated. The Institute of Medicine states that "A biological role of vanadium in humans has not yet been identified. Therefore, neither an Estimated Average Requirement, Recommended Dietary Allowance, nor Adequate Intake was determined for vanadium." Usual dietary intake is in mcg - "The intake of vanadium for adults and the elderly ranged from 6 to 18 μg/day" - while supplement doses used in diabetes research were tens of mg and "greatly exceed the Tolerable Upper Intake Level (UL) for vanadium."

Questions and answers

What is it?

Vanadium is a metallic trace element present in air, soil, water and food. In the body it exists mainly as the vanadyl cation or the vanadate anion. Very little is taken up from the gut, so most of what is swallowed leaves in the stool. Highest tissue concentrations are in liver, kidney and bone. (Source 12)

What does it do in the body?

No function for vanadium in the human body has been identified. In laboratory animals it behaves a little like insulin, lowering blood glucose, and it blocks several enzyme families including phosphatases. Those animal observations are the reason it was tested as a diabetes treatment; they are not evidence of a human role. (Source 10)

Is it good or bad for you?

Vanadium from ordinary food has not been linked to harm. As a supplement at the doses used in diabetes research the picture is unfavourable: a systematic review found no rigorous evidence of benefit, and those doses commonly cause stomach and bowel upset. High intakes also sit far above the official upper limit, which was set on the basis of kidney damage in animals. (Source 1)

How do you get more of it?

Ordinary intake comes from food and drink, and adult diets supply only a few mcg a day. Supplements sold for blood sugar or bodybuilding use vanadyl sulfate or sodium metavanadate; research doses of 100-125 mg of the compound per day are roughly a hundred times usual dietary intake and exceed the official upper limit. (Source 11)

If it is harmful, what reduces it?

We found no validated treatment for chronic vanadium excess in people. What the literature describes is stopping the source: in the reported trials gastrointestinal effects were dose-related and resolved on withdrawal, and in a fatal poisoning case intensive care did not save the patient. Most swallowed vanadium is never absorbed and leaves in the stool. (Source 12)

We searched: Searched Europe PMC for vanadium chelation, vanadium poisoning treatment and vanadium case reports, plus the Institute of Medicine 2001 vanadium chapter; no human trial of any agent to lower body vanadium was found.

Why might someone be low in it or missing it?

The question does not really apply. No vanadium requirement has been set for people and no human deficiency disease has been described, so there is no recognised state of being low in it. Intakes vary with diet because grains, beverages and processed foods carry most of it. (Source 10)

Which whole foods contain it or feed it?

Vanadium is spread thinly through the food supply. Mushrooms, shellfish, black pepper, parsley and dill seed are relatively rich in it, and grains, sweeteners and beverages including beer and wine contribute most of the total in adult diets. Processed foods generally contain more than unprocessed ones. (Source 13)

What happens if you do not have it?

Nothing is known to happen in people. Deprivation experiments in goats raised abortion rates and chicks and rats show changes, but no equivalent human deficiency has ever been documented, which is why no reference intake exists. (Source 10)

How can you test for it?

There is no clinically validated test of vanadium status. Research studies measure vanadium in urine or blood by inductively coupled plasma mass spectrometry, and a forensic case used blood vanadium to confirm poisoning, but no reference range defines adequacy or deficiency because no requirement exists. (Source 4)

We searched: Searched Europe PMC for vanadium status biomarker, urinary vanadium reference values and the Institute of Medicine 2001 chapter; measurement methods exist but no validated status test or cut-off was found.

References

1. QJM: monthly journal of the Association of Physicians. A systematic review of vanadium oral supplements for glycaemic control in type 2 diabetes mellitus. 2008. PMID 18319296, DOI 10.1093/qjmed/hcn003. Read the source
2. Metabolism: Clinical and Experimental. Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. 2000. PMID 10726921, DOI 10.1016/s0026-0495(00)90418-9. Read the source
3. Forensic Science International. Fatal poisoning by vanadium. 2011. PMID 21130588, DOI 10.1016/j.forsciint.2010.10.027. Read the source
4. Clinical Kidney Journal. Association between urinary heavy metal/trace element concentrations and kidney function: a prospective study. 2025. PMID 39950154, DOI 10.1093/ckj/sfae378. Read the source
5. The Journal of Clinical Endocrinology and Metabolism. Vanadyl sulfate improves hepatic and muscle insulin sensitivity in type 2 diabetes. 2001. PMID 11238540, DOI 10.1210/jcem.86.3.7337. Read the source
6. Metabolism: Clinical and Experimental. Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. 2000. PMID 10726921, DOI 10.1016/s0026-0495(00)90418-9. Read the source
7. International Journal of Sport Nutrition. The effect of oral vanadyl sulfate on body composition and performance in weight-training athletes. 1996. PMID 8953340, DOI 10.1123/ijsn.6.4.382. Read the source
8. Toxicology Letters. Vanadium - good or bad - The role of vanadium in the central nervous system disorders, potential therapeutic targets and its toxicity. 2025. PMID 40467016, DOI 10.1016/j.toxlet.2025.06.006. Read the source
9. Institute of Medicine (US), National Academies Press. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - Chapter 13: Arsenic, Boron, Nickel, Silicon, and Vanadium. 2001. DOI 10.17226/10026. Read the source
10. Institute of Medicine (US), National Academies Press. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - Chapter 13: Arsenic, Boron, Nickel, Silicon, and Vanadium. 2001. DOI 10.17226/10026. Read the source
11. Institute of Medicine (US), National Academies Press. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - Chapter 13: Arsenic, Boron, Nickel, Silicon, and Vanadium. 2001. DOI 10.17226/10026. Read the source
12. Institute of Medicine (US), National Academies Press. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - Chapter 13: Arsenic, Boron, Nickel, Silicon, and Vanadium. 2001. DOI 10.17226/10026. Read the source
13. Institute of Medicine (US), National Academies Press. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - Chapter 13: Arsenic, Boron, Nickel, Silicon, and Vanadium. 2001. DOI 10.17226/10026. Read the source