Lab result explainedVitamins and mineralsLast updated November 8, 2026

Vitamin B12 blood test: what low and high B12 levels mean

Vitamin B12 (cobalamin) (B12) · Vitamin B12 (often ordered with folate, CBC and ferritin) · reported in pg/mL (identical to ng/L; some labs report pmol/L — multiply pg/mL by 0.738)

Vitamin B12 (cobalamin) is a nutrient your body needs to make red blood cells, build the insulation around nerves and copy DNA, and a B12 blood test measures how much of it is circulating in your serum. Most US labs call 200 to 900 pg/mL normal. Below 200 pg/mL is deficient. The band from 200 to 300 pg/mL is a grey zone where a third or more of people turn out to be functionally short of B12 when a second test, methylmalonic acid, is checked.

B12 comes only from animal foods and fortified products, but low intake is not the usual reason for a low result in the US. Most deficiency comes from poor absorption: autoimmune pernicious anemia, the thinning of the stomach lining that is common after 60, long-term metformin, acid-suppressing drugs such as omeprazole, stomach or bowel surgery, and Crohn's or celiac disease. Roughly 6 percent of US adults under 60 and close to 20 percent over 60 have low or borderline B12, and most do not know it.

A low B12 matters because it can damage nerves before it causes anemia, and nerve damage that has been present for more than a few months may not fully reverse. The good news is that it is one of the easiest deficiencies to treat: trials show that a high-dose oral tablet of 1,000 to 2,000 mcg a day corrects blood levels as well as injections do for most people, including many with pernicious anemia.

B12 at a glance

What it is: a water-soluble vitamin needed for red blood cell production, nerve insulation (myelin) and DNA synthesis; stored in the liver for 3 to 5 years.
Normal: about 200–900 pg/mL on most US reports (some labs 180–914 or 232–1,245). Some report pmol/L: multiply pg/mL by 0.738.
Low: below 200 pg/mL is deficient. 200–300 pg/mL is borderline; a methylmalonic acid (MMA) above about 0.4 µmol/L or homocysteine above 15 µmol/L confirms a true deficiency.
High: above 900–1,000 pg/mL is almost always from supplements or injections and is harmless; an unexplained high B12 in someone taking nothing is checked for liver disease, kidney disease or a blood disorder.
Commonest causes of low B12: pernicious anemia, atrophic gastritis of ageing, metformin, proton pump inhibitors and H2 blockers, vegan diets, bariatric surgery, Crohn's and celiac disease.
Next step for a low result: check MMA or homocysteine if borderline, CBC with MCV, folate and intrinsic factor antibodies; then replace B12 (oral 1,000–2,000 mcg daily or injections) and recheck in 2 to 3 months.

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What B12 measures

The serum B12 test measures total cobalamin bound to two carrier proteins. About 70 to 80 percent is bound to haptocorrin and is not available to cells; only the 20 to 30 percent bound to transcobalamin (holotranscobalamin, or active B12) can be taken up by tissues. Because the total figure is dominated by the inactive fraction, serum B12 can look acceptable while cells are starved, which is why the 200 to 300 pg/mL band is unreliable and a second marker is used.

Methylmalonic acid (MMA) and homocysteine are the functional markers. Both build up when B12-dependent enzymes slow down, so an MMA above roughly 0.4 µmol/L (lab cut-offs range 0.27 to 0.4) or a homocysteine above 15 µmol/L alongside a borderline B12 confirms tissue deficiency. MMA is the more specific of the two: homocysteine also rises with folate or B6 deficiency, hypothyroidism and kidney disease, while MMA rises mainly with B12 deficiency and, more modestly, with impaired kidney function.

Absorption is a multistep process that explains most causes of deficiency. Stomach acid and pepsin free B12 from food protein, intrinsic factor made by stomach parietal cells binds it, and the complex is absorbed in the last part of the small bowel (the terminal ileum). Anything that removes acid, intrinsic factor or the ileum lowers B12 over months to years, because liver stores of 2 to 5 mg last a long time. About 1 percent of any oral dose is also absorbed by simple diffusion without intrinsic factor, which is why very large oral doses work even in pernicious anemia. Fasting is not required for the test, but a recent injection or high-dose supplement will raise the result for days to weeks.

Normal range for B12

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (pg/mL (identical to ng/L; some labs report pmol/L — multiply pg/mL by 0.738))	Notes
Deficient	Below 200 pg/mL	Deficiency is likely; treatment is usually started while the cause is investigated. Some labs use 180 or 150 as the cut-off.
Borderline (grey zone)	200–300 pg/mL	Up to a third of people in this band have raised MMA or homocysteine and a true tissue deficiency, especially if they have symptoms, macrocytosis, are over 60, vegan or on metformin or acid suppressants.
Normal	About 300–900 pg/mL	Reference intervals differ by assay: common US ranges are 200–900, 180–914 and 232–1,245 pg/mL. Use the interval printed on your report.
Above the reference interval	Above 900–1,000 pg/mL	Expected on supplements or after injections. Without supplements, prompts a look at liver, kidney and blood counts.
Methylmalonic acid (MMA)	Normal below about 0.27–0.4 µmol/L (lab dependent)	Raised MMA with a borderline B12 confirms deficiency. Also rises modestly with reduced kidney function.
Homocysteine	Normal below about 15 µmol/L	Raised in B12 deficiency, but also in folate or B6 deficiency, hypothyroidism and kidney disease.
Pregnancy	Falls by 20–30 percent, often below 200 pg/mL in the third trimester	Partly a dilution effect and a drop in haptocorrin; MMA or holotranscobalamin is more reliable in pregnancy.
Daily requirement (RDA)	2.4 mcg adults; 2.6 mcg pregnancy; 2.8 mcg breastfeeding	A serving of beef, salmon, fortified cereal or a glass of milk each provides 1 to 3 mcg.

High vitamin B12

A high B12, meaning a result above the lab's upper limit (usually 900 to 1,000 pg/mL), is most often the simple consequence of taking it. A daily multivitamin, a B-complex, an energy drink or a recent injection can push the serum value above 1,000 and sometimes above 2,000 pg/mL. B12 is water-soluble, excess is passed in urine, and no toxic dose has been identified; the Institute of Medicine sets no upper limit for it. In this situation the result needs no action.

In someone who is not taking any B12, an unexpectedly high level is a different signal and deserves a look at the liver, kidneys and blood counts. Liver cells store most of the body's B12 and release it when they are damaged, so hepatitis, alcohol-related liver disease, cirrhosis and liver cancers raise the level. Blood disorders that increase haptocorrin, particularly chronic myeloid leukemia, polycythemia vera and other myeloproliferative conditions, can produce very high values. Reduced kidney clearance in chronic kidney disease raises it more modestly.

Large Danish registry studies have found that people with an unexplained B12 above about 1,100 pg/mL had a higher chance of being diagnosed with a cancer, most often a blood or liver cancer, in the following year. This is an association, not a cause: the cancer raises the B12, not the other way around, and the absolute risk remains small. It is a reason to repeat the test and review symptoms rather than a reason for alarm.

Common causes

Supplements, B-complex, fortified energy drinks and injections
By far the most common cause. Oral doses of 500 to 1,000 mcg typically raise serum B12 to 1,000 to 2,000 pg/mL; a recent intramuscular injection can send it above the assay's measurable range for several weeks.
Liver disease
Hepatitis, alcohol-related liver disease, cirrhosis and liver cancer release stored B12 from damaged liver cells and reduce its uptake, raising the serum level even though tissue supply may be poor.
Myeloproliferative disorders and leukemia
Chronic myeloid leukemia, polycythemia vera, essential thrombocythemia and myelofibrosis increase production of the carrier protein haptocorrin by white cells; B12 values of several thousand pg/mL occur. A CBC usually shows the clue.
Chronic kidney disease
Reduced kidney clearance of B12 and its carrier proteins raises the serum level modestly; the effect is larger at lower eGFR.
Solid cancers
Liver metastases, hepatocellular carcinoma and some lung, pancreatic and kidney cancers are associated with raised B12, usually alongside other abnormal results or symptoms.
Autoimmune and inflammatory conditions
Rheumatoid arthritis, lupus and other inflammatory conditions can raise haptocorrin and B12; this is a minor and inconsistent effect.
A functional deficiency with a high serum value
Rarely, antibodies against transcobalamin, or very high haptocorrin, hold B12 in the blood where cells cannot use it, so a person can have a high serum B12 and a raised MMA at the same time. Suspected when symptoms persist despite a high reading.

Symptoms that can go with it

None; a high B12 from supplements causes no symptoms
Acne-like skin eruptions have been reported with very high-dose supplementation and settle when it is stopped
If liver disease is the cause: fatigue, nausea, right upper abdominal discomfort, dark urine or yellowing of the skin
If a blood disorder is the cause: night sweats, itching after a hot shower, an enlarged spleen felt as left upper abdominal fullness, unexplained weight loss or easy bruising
Unexplained symptoms despite a high B12 (numbness, memory problems) can point to a functional deficiency and need MMA checked

Low vitamin B12

A B12 below 200 pg/mL means your stores are depleted and your bone marrow and nervous system are probably already affected, whether or not you feel it. Two things are checked at the same time: a CBC for the large red cells (MCV above 100 fL) and anemia that B12 deficiency causes, and a folate level, because the two deficiencies look alike and treating with folic acid alone can correct the anemia while nerve damage continues. In practice treatment is started as soon as the diagnosis is made, since delay carries real risk and the treatment carries almost none.

A result between 200 and 300 pg/mL is a grey zone rather than a clean normal. Serum B12 is an insensitive test: it misses a substantial share of people with tissue deficiency, and in this band an MMA or homocysteine is the deciding test. If either is raised, you are treated as deficient. If both are normal and you have no symptoms, the level is simply rechecked in 6 to 12 months. People over 60, vegans and vegetarians, anyone on metformin or acid suppressants, and anyone with numbness, tingling, memory change or a raised MCV should have the functional test rather than being reassured by a value of 250.

Finding the cause matters because it decides how long treatment lasts. Pernicious anemia and surgical loss of the stomach or ileum are permanent and need lifelong replacement. Metformin- and acid-suppressant-related deficiency responds to supplementation while the drug continues. Dietary deficiency in vegans is corrected with fortified foods or a modest supplement. Intrinsic factor antibodies (positive in about half of people with pernicious anemia and very specific when positive), a gastrin level and sometimes an endoscopy are used to sort this out.

Common causes

Pernicious anemia
An autoimmune attack on the stomach's parietal cells and on intrinsic factor removes the carrier needed to absorb B12. The most common cause of severe deficiency in the US and Europe, more frequent after 60 and in people with autoimmune thyroid disease, type 1 diabetes or vitiligo. Needs lifelong replacement.
Atrophic gastritis of ageing and Helicobacter pylori
Thinning of the stomach lining reduces acid and pepsin, so B12 cannot be released from food protein even though intrinsic factor is adequate. Affects 10 to 30 percent of people over 60 and is why the Institute of Medicine advises adults over 50 to get most B12 from fortified foods or supplements, which do not need acid.
Metformin
Metformin interferes with calcium-dependent B12 uptake in the ileum and lowers serum B12 by 10 to 30 percent; in the Diabetes Prevention Program, 13 years of metformin roughly doubled the risk of deficiency. The American Diabetes Association recommends periodic B12 checks for people on metformin, especially with anemia or neuropathy.
Proton pump inhibitors and H2 blockers
Omeprazole, pantoprazole, lansoprazole, famotidine and similar drugs suppress the acid needed to free B12 from food. Two or more years of use raised the odds of deficiency by about 65 percent in a large case-control study, with a dose-response relationship.
Vegan or largely vegetarian diet
B12 occurs naturally only in animal foods. Without fortified foods or a supplement, vegans deplete their stores over 2 to 5 years; vegetarians who eat little dairy or egg run lower levels too. Breastfed infants of deficient mothers can become deficient within months.
Gastric bypass, sleeve gastrectomy and stomach surgery
Removing or bypassing the acid- and intrinsic-factor-producing part of the stomach causes deficiency in a large proportion of patients within a few years; lifelong supplementation is standard after bariatric surgery.
Crohn's disease, celiac disease and ileal resection
B12 is absorbed only in the terminal ileum, so inflammation, celiac damage or surgical removal of that segment blocks absorption. Small intestinal bacterial overgrowth also consumes B12 before it can be absorbed.
Nitrous oxide
Nitrous oxide (dental or surgical anesthesia, or recreational 'whippets') permanently inactivates the B12 in your body. Repeated recreational use can cause severe nerve damage within weeks even with a normal diet, sometimes with a serum B12 that is still in range.
Alcohol use disorder and chronic pancreatitis
Alcohol damages the stomach lining, reduces intake and impairs liver storage; pancreatic enzymes are needed to transfer B12 from haptocorrin to intrinsic factor, so pancreatic insufficiency also lowers absorption.
Other medications and rare causes
Long-term colchicine, some anticonvulsants and high-dose vitamin C with meals reduce absorption; HIV, fish tapeworm, Imerslund-Grasbeck syndrome and transcobalamin deficiency are rare inherited or infectious causes.

Symptoms that can go with it

Fatigue, weakness and breathlessness on exertion from anemia
Numbness, tingling or pins and needles in the feet and hands, often symmetrical and starting in the feet
Unsteadiness when walking, particularly in the dark or with eyes closed, from damage to the spinal cord's position-sense tracts
A sore, smooth, red tongue (glossitis), mouth ulcers and loss of taste
Memory problems, difficulty concentrating, low mood, irritability and, in older people, a picture that can mimic dementia
Pale or slightly yellow-tinged skin from the breakdown of fragile red cells
Blurred vision from optic nerve involvement, heart palpitations, and in severe cases confusion or psychosis
No symptoms at all: many people with a B12 under 200 feel well and are picked up on a routine CBC showing a raised MCV

Read it alongside

MCV and MCH — B12 deficiency enlarges red cells (MCV often above 100 fL); a normal MCV does not exclude it, especially with coexisting iron deficiency or thalassemia trait.
Hemoglobin and reticulocyte count — show whether the deficiency has produced anemia and, after treatment starts, whether the marrow is responding (reticulocytes rise within 5 to 7 days).
Folate — the other cause of megaloblastic anemia; always checked together, because folic acid given alone can mask B12 deficiency while nerve damage progresses.
Methylmalonic acid — the confirmatory test for a B12 of 200 to 300 pg/mL; raised MMA means true deficiency.
Homocysteine — rises in B12 and folate deficiency; also a cardiovascular risk marker and a check on treatment response.
Intrinsic factor antibodies and parietal cell antibodies — identify pernicious anemia; intrinsic factor antibody is highly specific when positive but misses about half of cases.
Ferritin — iron deficiency often coexists (atrophic gastritis, celiac disease, bariatric surgery) and can hide the raised MCV.
TSH — autoimmune thyroid disease clusters with pernicious anemia and causes overlapping fatigue and mild macrocytosis.

What usually happens next

Below 200 pg/mL: expect a CBC with MCV, folate, ferritin and intrinsic factor antibodies, a review of your medicines (metformin, acid suppressants) and diet, and treatment to start promptly, before all results are back if you have neurological symptoms.
200 to 300 pg/mL: ask for a methylmalonic acid (or homocysteine) level; if raised, you are treated as deficient. If normal and you feel well, recheck B12 in 6 to 12 months.
Replacement: oral cyanocobalamin or methylcobalamin 1,000 to 2,000 mcg daily is as effective as injections for most causes, including many cases of pernicious anemia; injections (1,000 mcg several times a week for 1 to 2 weeks, then monthly) are preferred for severe neurological symptoms, very low levels, or when adherence or absorption is in doubt.
Recheck B12, CBC and, if it was raised, MMA 2 to 3 months after starting; hemoglobin normalises within about 8 weeks, MCV within 2 to 3 months, and nerve symptoms improve over 6 to 12 months but may not fully reverse.
If pernicious anemia is confirmed, replacement is lifelong and a one-off endoscopy is often advised because atrophic gastritis carries a small increase in stomach cancer and carcinoid risk.
Ask whether a persistently high result without supplements warrants liver tests, kidney function and a CBC to look for the causes above.

Diet, lifestyle and natural levers with evidence

What can move B12 once the cause is known. Nothing here replaces finding the cause.

High-dose oral B12 (1,000–2,000 mcg a day)

Strong evidence

About 1 percent of an oral dose is absorbed by passive diffusion without intrinsic factor, so 1,000 mcg delivers around 10 mcg, four times the daily requirement, even in pernicious anemia. In a randomised trial, 2,000 mcg orally each day produced higher serum B12 at 4 months than 1,000 mcg by monthly injection and normalised MMA and homocysteine at least as well; a Cochrane review of the trials concluded oral and intramuscular routes are similarly effective at correcting levels. Cyanocobalamin and methylcobalamin both work; sublingual tablets perform the same as swallowed ones.

Not a substitute for injections in someone with severe or rapidly progressing neurological symptoms, where injections are usually used first. Treating with folic acid alone when B12 is low can worsen nerve damage, so B12 is checked before high-dose folic acid is started.

Fortified foods and modest supplements for vegans, vegetarians and adults over 50

Strong evidence

The Institute of Medicine advises that adults over 50 meet most of their 2.4 mcg daily requirement from fortified foods or supplements, because the crystalline B12 in those products does not need stomach acid to be absorbed. Fortified breakfast cereals, plant milks and nutritional yeast typically supply 1 to 6 mcg a serving. For vegans, a daily supplement of 25 to 100 mcg or a weekly 1,000 mcg dose maintains normal levels in trials; intake from unfortified plant foods, seaweed or spirulina does not, and spirulina contains analogues that can block true B12.

Animal foods rich in B12

Strong evidence

Clams (about 17 mcg per 3 oz), beef liver (70 mcg per 3 oz), salmon, trout, tuna and sardines (2.5 to 5 mcg), beef (1.5 to 2.5 mcg), milk and yogurt (1 to 1.5 mcg a cup) and eggs (0.5 mcg each) are the main dietary sources. Dairy B12 is particularly well absorbed. Diet alone cannot correct deficiency caused by malabsorption, but it prevents dietary deficiency and shortens recovery time once absorption problems are treated.

Review of metformin and acid-suppressing medicines

Moderate evidence

Metformin lowers B12 by 10 to 30 percent and long-term use roughly doubles deficiency risk, so the American Diabetes Association advises periodic B12 testing on metformin; supplementing with B12 restores levels without stopping the drug, and calcium supplements partly reverse metformin's effect on absorption in a small trial. For proton pump inhibitors, the lowest effective dose, intermittent use or a switch to an H2 blocker when appropriate reduces the risk, which rises with dose and duration beyond two years.

Do not stop metformin or a prescribed acid suppressant on your own; the deficiency is corrected with B12 while the medicine is reviewed with your clinician.

Treating Helicobacter pylori

Preliminary evidence

H. pylori infection contributes to atrophic gastritis and food-bound B12 malabsorption. In a trial of 138 people with B12 deficiency and H. pylori, eradication therapy alone corrected anemia and B12 levels in about 40 percent, and smaller studies show similar improvements in serum B12 after eradication. Testing is reasonable when a low B12 comes with dyspepsia, iron deficiency or a family history of stomach cancer.

Limiting alcohol

Preliminary evidence

Heavy drinking lowers B12 absorption by damaging the stomach lining, displaces B12-containing foods and impairs liver storage; it also raises MCV independently, muddying the picture. Observational studies show B12 and folate status improve within weeks of stopping heavy drinking, though controlled trials of alcohol reduction on B12 specifically are lacking.

When to see a clinician promptly

Numbness, tingling, unsteadiness, weakness or visual change with a low or borderline B12: nerve damage from B12 deficiency can become permanent and treatment should not wait for further results.
New confusion, memory loss, severe low mood or psychotic symptoms in anyone with a low B12, particularly an older adult.
Severe anemia (hemoglobin below about 8 g/dL) with breathlessness, chest pain, palpitations or fainting: same-day assessment, since rapid correction can also disturb potassium levels.
A B12 below 200 pg/mL in someone with no dietary explanation, to be tested for pernicious anemia, celiac disease and other absorption problems.
A high B12 (above about 1,000 pg/mL) in someone taking no supplements, particularly with night sweats, weight loss, itching, abdominal fullness or abnormal liver tests or blood counts.
Recreational nitrous oxide use with any tingling or unsteadiness, which needs urgent B12 treatment regardless of the blood level.

Frequently asked questions

What is a normal vitamin B12 level?

Most US labs consider roughly 200 to 900 pg/mL normal, though reference intervals vary (180–914 and 232–1,245 pg/mL are also common). Below 200 pg/mL is deficient. Many clinicians regard 200 to 300 pg/mL as borderline and confirm it with a methylmalonic acid or homocysteine test. If your lab uses pmol/L, multiply pg/mL by 0.738 to convert: 200 pg/mL is about 148 pmol/L.

Is a B12 level of 200 low?

A B12 of 200 pg/mL sits right at the cut-off and should not be treated as a clean normal. Up to a third of people in the 200 to 300 band have a raised methylmalonic acid, which means their tissues are short of B12 even though the serum figure is technically in range. If you have symptoms such as tingling, fatigue or memory change, a raised MCV, are over 60, vegan, or take metformin or acid suppressants, ask for MMA; many clinicians will simply treat a level of 200 and recheck.

What are the symptoms of B12 deficiency?

Fatigue, breathlessness and pallor from anemia; numbness and tingling in the feet and hands; unsteadiness when walking; a sore, smooth tongue; memory and concentration problems; low mood or irritability; and blurred vision. The nerve symptoms can appear before the anemia and without it. Many people with a low level have no symptoms and are found through a routine blood count showing large red cells.

What causes high B12 levels?

Taking B12 is by far the most common reason: multivitamins, B-complex, energy drinks or injections easily push the level above 1,000 pg/mL, and this is harmless. If you take no supplements, a high B12 can come from liver disease, chronic kidney disease, or a blood disorder such as chronic myeloid leukemia or polycythemia vera, and registry studies link unexplained very high levels to a modestly increased chance of a cancer diagnosis in the following year. A repeat test, liver and kidney tests and a CBC are the usual next step.

Can you have too much B12?

No toxic level has been identified and the Institute of Medicine sets no upper intake limit, because excess water-soluble B12 is excreted in urine. Doses of 1,000 to 2,000 mcg a day are used safely for years to treat deficiency. Very high doses occasionally cause acne-like rashes, which settle when the dose is cut.

Are B12 tablets as good as injections?

For most people, yes. About 1 percent of an oral dose is absorbed without intrinsic factor, so 1,000 to 2,000 mcg a day delivers more than the body needs even in pernicious anemia. A randomised trial found 2,000 mcg orally produced higher B12 levels at 4 months than monthly injections, and a Cochrane review found the two routes similarly effective. Injections are still preferred when neurological symptoms are severe, the level is very low, or absorption or adherence is uncertain.

Does metformin cause B12 deficiency?

Yes. Metformin lowers B12 absorption in the ileum, reducing serum B12 by 10 to 30 percent on average, and long-term use (more than 4 to 5 years, or higher doses) roughly doubles the risk of deficiency. The American Diabetes Association recommends periodic B12 checks for people on metformin, especially anyone with anemia or neuropathy, since diabetic neuropathy and B12 neuropathy can be confused. The fix is to take B12, not to stop a useful drug.

How long does it take to raise B12 levels?

Serum B12 rises within days of starting tablets or injections. Reticulocytes (new red cells) increase within a week, hemoglobin normalises in about 8 weeks and the MCV in 2 to 3 months. Nerve symptoms improve more slowly, over 6 to 12 months, and symptoms that have been present for over 6 months may not fully resolve, which is why treatment should start promptly.

References

Vitamin B12 level. MedlinePlus, US National Library of Medicine (2023)View source
Vitamin B12: fact sheet for health professionals. National Institutes of Health, Office of Dietary Supplements (2024)View source
Stabler SP. Vitamin B12 deficiency. New England Journal of Medicine (2013)
Green R, Allen LH, Bjørke-Monsen AL, et al.. Vitamin B12 deficiency. Nature Reviews Disease Primers (2017)
Langan RC, Goodbred AJ. Vitamin B12 deficiency: recognition and management. American Family Physician (2017)
Devalia V, Hamilton MS, Molloy AM; British Committee for Standards in Haematology. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. British Journal of Haematology (2014)
Kuzminski AM, Del Giacco EJ, Allen RH, Stabler SP, Lindenbaum J. Effective treatment of cobalamin deficiency with oral cobalamin. Blood (1998)
Wang H, Li L, Qin LL, Song Y, Vidal-Alaball J, Liu TH. Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency. Cochrane Database of Systematic Reviews (2018)
Aroda VR, Edelstein SL, Goldberg RB, et al.. Long-term metformin use and vitamin B12 deficiency in the Diabetes Prevention Program Outcomes Study. Journal of Clinical Endocrinology and Metabolism (2016)
Lam JR, Schneider JL, Zhao W, Corley DA. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA (2013)
Arendt JF, Pedersen L, Nexo E, Sørensen HT. Elevated plasma vitamin B12 levels as a marker for cancer: a population-based cohort study. Journal of the National Cancer Institute (2013)
Allen LH. How common is vitamin B-12 deficiency?. American Journal of Clinical Nutrition (2009)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.