Lab result explainedVitamins and mineralsLast updated November 11, 2026

Methylmalonic acid (MMA) test: what a high level means for vitamin B12

Methylmalonic acid (MMA) · Stand-alone test; ordered with vitamin B12, homocysteine and a CBC when B12 deficiency is suspected · reported in µmol/L (micromoles per liter) or nmol/L for serum; 1 µmol/L = 1,000 nmol/L. Urine: mmol per mol creatinine or µg per mg creatinine

Methylmalonic acid (MMA) is a small molecule that builds up in blood and urine when your cells do not have enough usable vitamin B12. One of the two enzymes that depend on B12 converts methylmalonyl-CoA into succinyl-CoA; without B12 the reaction stalls, the backlog is released as methylmalonic acid, and the level rises before anemia or nerve symptoms appear. For that reason an MMA test is the most specific way to tell whether a borderline B12 result (roughly 150 to 300 pg/mL) reflects a real deficiency inside the cells. Normal serum MMA is below about 0.40 µmol/L (400 nmol/L); some labs set the cut-off at 0.27 or 0.38, and many report in nmol/L.

A high MMA most often means B12 deficiency, whether from pernicious anemia, a vegan or near-vegan diet, stomach or small bowel surgery, long-term metformin or acid-suppressing medicines, celiac or Crohn's disease, or simply reduced absorption with age. The second most common reason is reduced kidney function, which slows MMA clearance and raises the level modestly (typically to 0.4 to 1.0 µmol/L) even when B12 is adequate, so MMA is always read alongside creatinine or eGFR. Dehydration, bacterial overgrowth in the small intestine, hypothyroidism and advanced age push it up a little, and recreational nitrous oxide inactivates B12 and can send it very high within weeks.

The companion test is homocysteine, which rises in both B12 and folate deficiency, whereas MMA rises only with B12 deficiency; the two together separate the deficiencies. A urine MMA, reported per gram or mole of creatinine, is less affected by kidney function and is used in children, in people who cannot easily have blood drawn, and in some newborn screening programs. Once B12 replacement starts, MMA falls within days and is usually normal in one to two weeks, which makes it a useful check that treatment is working.

MMA at a glance

  • What it is: a metabolite that accumulates when the B12-dependent enzyme methylmalonyl-CoA mutase cannot work; a functional marker of B12 status inside cells.
  • Normal (serum): below about 0.40 µmol/L, which is the same as 400 nmol/L; some labs use 0.27–0.38 µmol/L. Urine: below about 3.6 mmol per mol of creatinine in adults (labs differ).
  • High MMA (above 0.40 µmol/L) with low or borderline B12 means tissue B12 deficiency, even if the B12 level looks acceptable; above 0.75 µmol/L is convincing in almost any setting.
  • Other reasons MMA is high: reduced kidney function (the commonest non-B12 cause), dehydration, older age, small intestinal bacterial overgrowth, hypothyroidism, pregnancy, nitrous oxide use and, very rarely, an inherited methylmalonic acidemia (values hundreds of times normal).
  • Low MMA has no clinical significance.
  • Next step: check B12, homocysteine, a CBC with MCV, creatinine and folate; if deficient, replace B12 and expect MMA to normalize within 1 to 2 weeks, then find the cause of the deficiency.

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What MMA measures

Vitamin B12 works in two reactions. As methylcobalamin it helps convert homocysteine to methionine; as adenosylcobalamin it helps methylmalonyl-CoA mutase convert methylmalonyl-CoA, a product of odd-chain fatty acid and amino acid breakdown, into succinyl-CoA, which feeds the energy cycle. When cellular B12 runs short, methylmalonyl-CoA accumulates, is hydrolyzed to methylmalonic acid, and leaks into blood and urine. Folate plays no part in this second reaction, which is why MMA is specific to B12 while homocysteine is not. MMA also rises before the serum B12 falls below the usual cut-off and before the MCV increases, which is why it is called a functional or early marker.

The lab measures MMA by gas or liquid chromatography coupled to mass spectrometry, a specialized method that is why the test costs more and takes longer than a B12 level. Serum or plasma results are reported in µmol/L (micromoles per liter) or nmol/L; 1 µmol/L equals 1,000 nmol/L, so a result of 350 nmol/L is 0.35 µmol/L. Urine MMA is normalized to creatinine and reported as mmol per mol or µg per mg of creatinine to correct for how dilute the sample is.

Fasting is not strictly required but many labs prefer it, and the result is affected by things that have nothing to do with B12: MMA is cleared by the kidneys, so it rises as eGFR falls; it is concentrated by dehydration; it increases with age, so that 15 to 25 percent of apparently healthy people over 65 exceed 0.27 µmol/L; and bacteria in the small intestine produce propionate, a precursor, so bacterial overgrowth or recent antibiotics can shift it. A high MMA should therefore be interpreted with creatinine or eGFR on the same sample, and a repeat after B12 treatment is the cleanest way to confirm that B12 was the cause: if it falls to normal, it was.

Normal range for MMA

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

GroupTypical range (µmol/L (micromoles per liter) or nmol/L for serum; 1 µmol/L = 1,000 nmol/L. Urine: mmol per mol creatinine or µg per mg creatinine)Notes
Serum MMA, normal (adults)Below about 0.40 µmol/L (400 nmol/L)Printed cut-offs range from 0.27 to 0.40 µmol/L (some labs 70–270 nmol/L). Use the one on your report.
Serum MMA, borderline0.27–0.40 µmol/L (270–400 nmol/L)A gray zone, especially in people over 65 or with an eGFR under 60; weigh against the B12, homocysteine and symptoms, or repeat after a trial of B12.
Serum MMA, raised0.40–0.75 µmol/L (400–750 nmol/L)Consistent with B12 deficiency when B12 is low or borderline; also the typical range produced by moderate kidney impairment alone.
Serum MMA, clearly raisedAbove 0.75 µmol/L (750 nmol/L)Strongly suggests tissue B12 deficiency whatever the kidney function; values of 1 to 10 µmol/L occur in pernicious anemia and after nitrous oxide exposure.
Inherited methylmalonic acidemiaUsually above 100 µmol/L, often in the thousandsA rare inborn error presenting in infancy with vomiting, lethargy and acidosis; picked up by newborn screening in all US states.
Urine MMA, normal (adults)Below about 3.6 mmol per mol creatinine (some labs under 2.0–3.8)Less affected by kidney function than serum MMA. Children's reference values are higher in the first years of life.
Expected response to B12 treatmentFalls by more than half within a week and into the normal range within 1 to 2 weeksA persistently high MMA after adequate B12 replacement points to kidney function, bacterial overgrowth or an inherited defect rather than ongoing deficiency.

High methylmalonic acid

A high MMA with a low or low-normal B12 means your cells are short of B12, however the B12 number itself looks. Serum B12 is an imperfect test: it counts B12 bound to a carrier protein that cells cannot use, it has a wide gray zone between about 150 and 300 pg/mL, and it can be falsely normal in liver disease and falsely low in pregnancy or on the pill. MMA cuts through that because it reflects what is happening inside cells. In the classic series of people with proven B12 deficiency, MMA was raised in more than 98 percent, and a raised MMA that normalizes with B12 treatment is as good a confirmation of deficiency as exists. The level correlates loosely with severity: values of 0.4 to 0.75 µmol/L are typical of early or mild deficiency, and values in the several µmol/L range go with pernicious anemia, nitrous oxide toxicity and established nerve damage.

The main confounder is the kidneys. MMA is filtered and excreted, so as eGFR drops below about 60 mL/min the level drifts up, and in advanced kidney disease values of 0.5 to 1.0 µmol/L are common with normal B12 stores. A high MMA in someone with kidney impairment is therefore ambiguous unless it is well above 0.75, homocysteine and B12 point the same way, or a trial of B12 brings it down. Dehydration concentrates it, age raises it, and small intestinal bacterial overgrowth adds propionate from gut bacteria, so a modestly raised MMA with a normal B12 and a normal homocysteine in an older person with reduced kidney function is often not B12 deficiency at all.

A very high MMA has two further explanations. Recreational or repeated medical nitrous oxide oxidizes the cobalt in B12 and inactivates it; MMA and homocysteine climb within weeks, serum B12 may remain normal, and the result is a B12-deficiency neuropathy and spinal cord damage in otherwise healthy young people. And inherited methylmalonic acidemias, defects in the mutase enzyme or in the processing of B12 into its active form, produce values hundreds to thousands of times normal and present in infancy; they are on every US newborn screening panel, and mild variants are occasionally diagnosed later in childhood or adulthood.

Common causes

  1. Pernicious anemia

    Autoimmune destruction of stomach parietal cells removes intrinsic factor, which B12 needs for absorption. The commonest cause of severe deficiency in older adults; MMA is usually above 1 µmol/L, B12 under 200 pg/mL, and intrinsic factor antibodies are positive in about half to two thirds.

  2. Low intake: vegan, vegetarian and low-animal-food diets

    B12 comes only from animal foods and fortified products. Unsupplemented vegans develop raised MMA within a few years (liver stores last 2 to 5 years); breastfed infants of deficient mothers can be affected within months.

  3. Metformin

    Long-term metformin reduces B12 absorption and lowers B12 by about 10 to 20 percent; after 4 or more years, 10 to 30 percent of users have biochemical deficiency with raised MMA. The American Diabetes Association recommends periodic B12 checks in metformin users.

  4. Acid-suppressing medicines

    Proton pump inhibitors and H2 blockers for 2 years or more reduce the acid needed to free B12 from food protein and raise the risk of deficiency by roughly 60 percent in population studies.

  5. Stomach and intestinal surgery, and gut disease

    Gastric bypass, sleeve gastrectomy, gastrectomy, resection of the terminal ileum, Crohn's disease, celiac disease and chronic pancreatitis all impair absorption; after bypass 20 to 30 percent of people become deficient without supplements.

  6. Small intestinal bacterial overgrowth and parasites

    Bacteria consume B12 and also produce propionate, which raises MMA directly; fish tapeworm is a rare cause. MMA may stay somewhat elevated after B12 treatment until the overgrowth is treated.

  7. Reduced kidney function

    MMA clearance falls with eGFR; levels of 0.4 to 1.0 µmol/L are common in chronic kidney disease with normal B12 stores. The commonest reason for a raised MMA that is not B12 deficiency.

  8. Nitrous oxide exposure

    Recreational whippets or repeated anesthetic exposure inactivate B12; MMA and homocysteine rise sharply within weeks and a neuropathy or spinal cord syndrome can follow, often with a normal serum B12.

  9. Older age, dehydration and hypothyroidism

    Each raises MMA modestly; 15 to 25 percent of healthy people over 65 exceed 0.27 µmol/L. Pregnancy raises it slightly in the third trimester.

  10. Inherited methylmalonic acidemia and cobalamin processing defects

    Rare autosomal recessive disorders (mutase deficiency, cblA, cblB, cblC and others) with MMA hundreds of times normal, metabolic acidosis and developmental problems; identified by newborn screening and treated by metabolic specialists.

Symptoms that can go with it

  • Often none in early deficiency; MMA rises before symptoms appear
  • Fatigue, breathlessness and pallor from anemia with large red cells (high MCV)
  • Numbness, tingling or burning in the feet and hands, starting symmetrically
  • Unsteady walking, poor balance in the dark, and weakness or stiffness in the legs from spinal cord involvement
  • Memory problems, low mood, irritability or, in severe cases, confusion and psychosis
  • A sore, smooth, red tongue and mouth ulcers
  • Loss of appetite, weight loss, and in infants poor growth and developmental slowing
  • In inherited methylmalonic acidemia: vomiting, lethargy, poor feeding and rapid breathing in a newborn

Low methylmalonic acid

There is no lower limit of concern for MMA. A low or undetectable value simply means the B12-dependent mutase reaction is running normally and B12 stores inside cells are adequate. It is the expected result in anyone with a healthy B12 status, in people who have recently been treated with B12 injections or high-dose tablets, and in people who have recently taken antibiotics, which reduce the gut bacteria that make the MMA precursor propionate.

A normal MMA is also reassuring when the serum B12 is low. Serum B12 between 150 and 300 pg/mL with a normal MMA and a normal homocysteine most often reflects a low carrier-protein level or an assay quirk rather than true deficiency, and in that situation many guidelines advise either a repeat in a few months or a short trial of oral B12 rather than lifelong injections. The exception is the person with clear neurological symptoms, who is treated regardless of the MMA.

Common causes

  1. Adequate B12 status

    The normal state; MMA is low in people eating animal foods or taking a supplement and with normal absorption.

  2. Recent B12 treatment

    Injections or oral doses of 1,000 µg or more bring MMA into the normal range within 1 to 2 weeks, so a test taken after treatment started cannot diagnose the prior deficiency.

  3. Recent antibiotics

    Suppressing gut bacteria reduces propionate production and lowers MMA slightly for a week or two.

  4. Well-hydrated, younger adults with good kidney function

    Values at the low end of the range are typical; MMA climbs with age and falling eGFR.

Symptoms that can go with it

  • None; a low MMA does not cause symptoms
  • If you have neuropathy or anemia despite a normal MMA, another cause (diabetes, alcohol, thyroid disease, copper deficiency, folate deficiency) needs looking for

Read it alongside

  • Vitamin B12 — the primary test; MMA is the tie-breaker when B12 is between about 150 and 300 pg/mL, and the two are interpreted together rather than either alone.
  • Homocysteine — raised in both B12 and folate deficiency; high MMA plus high homocysteine means B12 deficiency, normal MMA plus high homocysteine points to folate deficiency (or kidney disease, hypothyroidism or an MTHFR variant).
  • Folate — checked at the same time, because the two deficiencies coexist and treating folate alone can worsen B12-related nerve damage.
  • CBC with MCV and RDW — a high MCV with a high RDW supports deficiency, but up to a third of people with B12 deficiency and nerve symptoms have a normal MCV, so a normal count does not rule it out.
  • Creatinine and eGFR — essential for interpreting MMA, since kidney impairment raises it; a value under 0.75 µmol/L with an eGFR under 60 is ambiguous.
  • Intrinsic factor and parietal cell antibodies — ordered once deficiency is confirmed, to diagnose pernicious anemia, which needs lifelong treatment.
  • Reticulocyte count and LDH — severe B12 deficiency destroys red cell precursors in the marrow, giving a very high LDH and low haptoglobin that mimic hemolysis.
  • TSH — hypothyroidism raises MMA slightly and often coexists with pernicious anemia as part of autoimmune clustering.

What usually happens next

  1. If MMA is high and B12 is low or borderline, expect B12 replacement to start without further delay; the route (injections, or oral or sublingual doses of 1,000 to 2,000 µg a day) depends on the cause and the severity of symptoms, and both routes correct MMA in trials.
  2. Expect a repeat MMA (with B12, homocysteine and a CBC) around 2 to 3 months after starting treatment; normalization confirms that B12 was the cause, and a persistently high value prompts a look at kidney function, bacterial overgrowth or adherence.
  3. Once deficiency is confirmed, the question becomes why: ask about diet, metformin, acid suppressants, stomach or bowel surgery, gut symptoms and nitrous oxide use, and expect intrinsic factor antibodies and sometimes celiac serology; pernicious anemia and surgical causes need lifelong replacement.
  4. If MMA is mildly raised (under 0.75 µmol/L) with a normal B12, normal homocysteine and reduced eGFR or age over 65, a sensible plan is a repeat in 3 to 6 months or a short trial of oral B12 with a recheck, rather than committing to injections.
  5. If you have numbness, balance problems or memory change, treatment should not wait for the repeat test; nerve recovery depends on how long the deficiency has gone on, and improvement can take 6 to 12 months.

Diet, lifestyle and natural levers with evidence

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

Oral or sublingual vitamin B12 at 1,000–2,000 µg a day

Strong evidence

About 1 percent of an oral dose is absorbed by passive diffusion even without intrinsic factor, so high doses work in pernicious anemia and after gastric surgery. In the randomized trial that established this, 2,000 µg a day by mouth lowered MMA from a mean of about 3.85 to 0.17 µmol/L over 4 months, at least as well as a standard injection schedule, and a dose-finding trial in older adults with mild deficiency found that 500 to 1,000 µg a day was needed to normalize MMA, with lower doses (as in most multivitamins) producing only partial falls. Sublingual and oral forms perform similarly in head-to-head trials; cyanocobalamin and methylcobalamin both correct MMA.

People with neurological symptoms, severe anemia or doubtful adherence are usually started on injections; high-dose folic acid alone can mask B12 deficiency while nerve damage progresses.

B12-containing foods and fortified products if you eat little or no animal food

Moderate evidence

Meat, fish, eggs and dairy supply 2 to 6 µg of B12 a day in a typical omnivorous diet against a requirement of 2.4 µg; unsupplemented vegans show rising MMA within 1 to 3 years and raised MMA in roughly half of long-term adherents in cross-sectional studies. Fortified cereals, plant milks and nutritional yeast supplying 2 to 6 µg a day, or a supplement of at least 25 to 100 µg daily or 1,000 µg twice a week, keep MMA normal in trials of vegetarians. Seaweed, spirulina and fermented foods contain mostly inactive B12 analogs and do not reliably lower MMA.

Review metformin and acid-suppressing medicines with your prescriber

Moderate evidence

Metformin lowers B12 and raises MMA in a dose- and duration-dependent way; in the Diabetes Prevention Program follow-up, 13 years of metformin roughly doubled the rate of low B12, and randomized trials show 1,000 µg a day of oral B12 or calcium supplementation partly reverses the effect. Long-term proton pump inhibitor use raises the risk of deficiency by about 60 percent. Neither drug needs to be stopped on this basis; the usual approach is periodic B12 and MMA checks and a B12 supplement.

Avoid recreational nitrous oxide

Strong evidence

Case series and a systematic review of more than 100 cases show that regular nitrous oxide use inactivates B12 within weeks, raising MMA and homocysteine and causing a neuropathy and spinal cord syndrome that is reversible only partly and only if use stops and B12 is given. Serum B12 can be normal, so MMA is the test that reveals it. There is no safe pattern of heavy use; occasional medical anesthetic exposure is a risk mainly in people who are already deficient.

Treat small intestinal bacterial overgrowth and gut disease that impair absorption

Preliminary evidence

Bacterial overgrowth both consumes B12 and produces propionate that raises MMA independently; small studies show MMA falling after antibiotic treatment of overgrowth, and untreated celiac disease or Crohn's disease of the terminal ileum keeps absorption poor regardless of intake. A gluten-free diet in celiac disease restores B12 absorption over 6 to 12 months. Probiotic supplements have not been shown to lower MMA.

When to see a clinician promptly

  • High MMA with numbness or tingling that is spreading, unsteady walking, falls, leg weakness or problems with bladder control: possible spinal cord involvement, which can become permanent and is treated urgently with B12.
  • High MMA with confusion, marked memory loss, personality change or psychosis, especially in an older person or a nitrous oxide user.
  • Severe anemia symptoms: breathlessness at rest, chest pain, palpitations or fainting, which with a hemoglobin under about 7 g/dL may need urgent treatment.
  • A high MMA in an infant or child with vomiting, lethargy, poor feeding or rapid breathing: possible inherited methylmalonic acidemia, an emergency.
  • A high MMA that has not come down 2 to 3 months after starting B12 treatment, to review the dose, the route, kidney function and absorption.
  • Any B12 deficiency without an obvious dietary cause, to be tested for pernicious anemia and gut disease rather than simply supplemented.

Frequently asked questions

What is a normal methylmalonic acid level?

Most laboratories consider serum MMA below about 0.40 µmol/L normal, which is the same as 400 nmol/L; some use a tighter cut-off of 0.27 or 0.38 µmol/L, and reference values rise with age and with falling kidney function. Urine MMA is reported against creatinine, with normal adult values below roughly 3.6 mmol per mol of creatinine. Check the cut-off printed on your own report, and note whether your result is in µmol/L or nmol/L: 350 nmol/L is 0.35 µmol/L and normal, while 3.5 µmol/L is markedly high.

What does high methylmalonic acid mean?

Most often that your cells are short of usable vitamin B12, even if the B12 blood level looks borderline or acceptable. The common causes are pernicious anemia, a diet with little animal food, long-term metformin or acid-suppressing medicines, stomach or bowel surgery, and celiac or Crohn's disease. The second most common cause is reduced kidney function, which slows MMA clearance; dehydration, age, bacterial overgrowth, hypothyroidism and nitrous oxide use also raise it. The usual response is to check B12, homocysteine, folate, a blood count and kidney function, treat with B12 if deficiency is likely, and recheck.

Why test MMA if my B12 was normal?

Because serum B12 misses a meaningful share of real deficiency. It measures B12 attached to carrier proteins, most of which cells cannot use, it has a wide gray zone between about 150 and 300 pg/mL, and it can be normal despite deficiency in liver disease, with some supplements, and after nitrous oxide. MMA reflects whether the B12-dependent reaction inside cells is actually running. A high MMA with a normal B12 is called functional B12 deficiency and is treated the same way; a normal MMA with a low B12 suggests the low number is not causing harm.

Does kidney disease raise methylmalonic acid?

Yes, and it is the most common reason for a raised MMA that is not B12 deficiency. MMA is cleared by the kidneys, so as eGFR falls below about 60 the level drifts up, and in advanced kidney disease values of 0.5 to 1.0 µmol/L are common with perfectly adequate B12. In someone with kidney impairment, an MMA under 0.75 is ambiguous; clinicians look at B12 and homocysteine together, consider a urine MMA, or simply treat with B12 and see whether the level falls.

What is the difference between MMA and homocysteine?

Both rise when B12 is short, but homocysteine also rises with folate deficiency, vitamin B6 deficiency, kidney disease, hypothyroidism, smoking and certain gene variants, so it is sensitive but not specific. MMA rises only with B12 deficiency (plus the kidney and gut effects described above). Read together: high MMA and high homocysteine means B12 deficiency; normal MMA with high homocysteine points to folate deficiency or another cause; both normal makes B12 and folate deficiency unlikely.

What is a urine methylmalonic acid test?

The same molecule measured in urine and corrected for creatinine so that concentration does not depend on how dilute the sample is. It is less affected by kidney function than the blood test, needs no needle, and is used in infants and children, in newborn screening programs for inherited methylmalonic acidemia, and as an alternative in adults. Normal adult values are below about 3.6 mmol per mol of creatinine; a first-morning or random sample is usually adequate.

How quickly does MMA come down after starting B12?

Fast. Once B12 reaches the cells the mutase enzyme restarts and MMA falls by more than half within a week and into the normal range within one to two weeks, whether B12 is given by injection or in high oral doses. Clinicians usually recheck at 2 to 3 months, along with B12, homocysteine and a blood count. Symptoms lag behind: energy and blood counts improve over weeks, while numbness and balance can take 6 to 12 months to recover and may not fully resolve if the deficiency was long-standing.

Can MMA be high in a vegan or vegetarian with no symptoms?

Yes, and it is common. Liver stores of B12 last 2 to 5 years, so MMA creeps up well before anemia or nerve symptoms, and cross-sectional studies find raised MMA in roughly half of long-term vegans who do not supplement, along with a fifth to a third of vegetarians. Because nerve damage can begin without anemia, a raised MMA is the signal to start a reliable supplement (at least 25 to 100 µg a day or 1,000 µg a few times a week) or fortified foods and recheck in a few months; seaweed and spirulina are not reliable sources.

References

  1. Methylmalonic acid (MMA) test. MedlinePlus, US National Library of Medicine (2023)View source
  2. Stabler SP. Vitamin B12 deficiency. New England Journal of Medicine (2013)
  3. Green R, Allen LH, Bjørke-Monsen AL, et al.. Vitamin B12 deficiency. Nature Reviews Disease Primers (2017)
  4. 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)
  5. National Institute for Health and Care Excellence. Vitamin B12 deficiency in over 16s: diagnosis and management (NICE guideline NG239). NICE (2024)
  6. Savage DG, Lindenbaum J, Stabler SP, Allen RH. Sensitivity of serum methylmalonic acid and total homocysteine determinations for diagnosing cobalamin and folate deficiencies. American Journal of Medicine (1994)
  7. Kuzminski AM, Del Giacco EJ, Allen RH, Stabler SP, Lindenbaum J. Effective treatment of cobalamin deficiency with oral cobalamin. Blood (1998)
  8. Eussen SJ, de Groot LC, Clarke R, et al.. Oral cyanocobalamin supplementation in older people with vitamin B12 deficiency: a dose-finding trial. Archives of Internal Medicine (2005)
  9. Mineva EM, Sternberg MR, Zhang M, et al.. Age-specific reference ranges are needed to interpret serum methylmalonic acid concentrations in the US population. American Journal of Clinical Nutrition (2019)
  10. 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)
  11. Oussalah A, Julien M, Levy J, et al.. Global burden related to nitrous oxide exposure in medical and recreational settings: a systematic review and individual patient data meta-analysis. Journal of Clinical Medicine (2019)
  12. Vitamin B12: fact sheet for health professionals. National Institutes of Health, Office of Dietary Supplements (2024)View source

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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.