Cyanocobalamin

What it is

Cyanocobalamin is a manufactured form of vitamin B12, a large cobalt-containing molecule. The cobalt atom carries a cyanide group, which the body swaps for a methyl or adenosyl group to make the two active coenzymes. As a medicine it is given by injection into muscle or under the skin, as high-dose tablets, and as a nasal spray. Injectable vials commonly contain benzyl alcohol as a preservative and aluminium as a contaminant. It is the same molecule sold as a supplement, but the doses used as a drug are hundreds to thousands of times the amount in food.

What the research says

B12 is needed to make DNA, red blood cells and the myelin sheath around nerves. Replacing it corrects the anaemia and, if given early enough, halts the nerve damage of deficiency; B12 deficiency left untreated for more than three months can cause permanent spinal cord damage. Where it has repeatedly failed is in people who are not deficient: Cochrane found no effect of B12 on cognition in people with dementia and low B12, and in two large trials high-dose B vitamins including 1 mg or 0.4 mg B12 made things worse, speeding loss of kidney function in diabetic nephropathy and raising cancer and all-cause death in Norwegian heart patients. Injections can cause anaphylaxis and death, and in early Leber's disease they caused rapid optic atrophy.

Evidence grade: Disputed.

How it works

Drug class: Cobalamin (vitamin B12) replacement; haematopoietic vitamin. Cyanocobalamin is the synthetic form carrying a cyanide group on the cobalt atom

B12 is a cofactor for two reactions the body cannot run without it. One recycles homocysteine into methionine, which the body needs to make DNA and to keep cell division going, so without it red blood cells come out large and immature and the marrow fails. The other converts methylmalonyl-CoA in the mitochondria, and its failure is what damages the myelin sheath around nerves and the spinal cord. That is why deficiency shows up as anaemia and as numbness, unsteadiness and, eventually, irreversible cord damage. (Source 1)

What it is used for

• This is what the injection is licensed for and the effect is not in doubt: replacement corrects the anaemia and, given promptly by injection, stops nerve damage progressing. Pernicious anaemia needs treatment for life. Evidence: established. (Source 1)
• Cochrane found three small randomised trials, 153 people in total. Oral 1000 mcg a day normalised blood B12 as well as injections and cost less, but the evidence was low quality because of imprecision, and no trial measured symptoms or quality of life. The injection label still calls the oral route undependable in malabsorption. Evidence: limited. (Source 2)
• The label lists this, but it is largely historical; blood and metabolite tests have replaced it. Evidence: established. (Source 3)
• Two randomised trials found harm, not benefit. In DIVINe, B vitamins including 1 mg B12 daily accelerated the fall in kidney function and doubled vascular events. In the combined Norwegian trials, folic acid plus 0.4 mg B12 raised cancer incidence, cancer death and all-cause death. Evidence: not-supported. (Source 4)
• A Cochrane review found only two acceptable trials, in people with dementia and low serum B12, and no statistically significant effect on cognitive function. No trial had been done in people without dementia. Evidence: not-supported. (Source 5)

Interactions

• Alcohol (heavy intake for more than two weeks) (label): Sustained heavy drinking can stop B12 being absorbed from the gut, which both causes deficiency and undermines oral treatment for it. Limit: The label prints this list without a comma after the first drug - "Colchicine para-aminosalicylic acid and heavy alcohol intake" - so it reads as one item. These are three separate things: colchicine, para-aminosalicylic acid, and heavy alcohol intake. (Source 6)
• Folic acid supplements above 0.1 mg per day (label): This is the most dangerous B12 interaction in the supplement aisle. Folic acid can fix the anaemia of B12 deficiency, which removes the clue that leads to diagnosis, while the nerve and spinal cord damage carries on and eventually becomes permanent. (Source 7)
• Metformin (clinical trial): Long-term metformin lowers B12. In the Diabetes Prevention Program Outcomes Study, low B12 was about twice as common on metformin as on placebo at 5 years, each extra year of metformin use carried a 13 per cent higher odds of B12 deficiency, and the authors said routine testing of B12 should be considered in people on metformin. (Source 8)
• Nitrous oxide (dental or medical anaesthesia, and recreational use) (case reports): Nitrous oxide chemically inactivates B12 in the body, producing deficiency with a normal or near-normal blood B12 level. A review of 257 publications covering 1,809 patients found neuropathy in 1,753 of them, plus thrombosis, psychosis and skin changes, and found nerve and MRI abnormalities even when the blood count and serum B12 were normal. (Source 9)
• Colchicine and para-aminosalicylic acid (label): Both can stop B12 being absorbed from the gut if taken for more than a couple of weeks. Limit: The label prints this list without a comma after the first drug - "Colchicine para-aminosalicylic acid and heavy alcohol intake" - so it reads as one item. These are three separate things: colchicine, para-aminosalicylic acid, and heavy alcohol intake. (Source 6)
• Vitamin C (ascorbic acid) in the same solution (pharmacokinetic study): Ascorbic acid destroys cyanocobalamin in water, fastest around pH 5, converting it to hydroxocobalamin and then to broken-up corrin ring products. This is a laboratory finding about liquid mixtures, most relevant to combined liquid preparations, not a demonstrated problem with taking a vitamin C tablet. (Source 10)
• Most antibiotics, methotrexate and pyrimethamine (label): These do not change B12 in the body but they make the blood test unreliable, so a level taken while on them cannot be trusted. (Source 6)
• A diet with no animal products at all (label): B12 comes only from animal foods, so a fully plant-based diet supplies none. The label notes deficiency has been found in breastfed infants of vegetarian mothers who had no symptoms themselves. (Source 11)

Stopping it

• For pernicious anaemia, stopping is not an option: the underlying failure to absorb B12 does not go away, so the injections are for life. The label states this plainly and tells patients they will need monthly injections for the rest of their lives. (Source 12)
• The cost of stopping, or of not starting in time, is measured in months rather than days: deficiency allowed to run for more than three months can leave permanent spinal cord damage. Where the cause was reversible, such as a tapeworm, an operable gut problem or a drug causing malabsorption, treating that cause removes the need for long-term B12. (Source 7)
• There is no withdrawal syndrome and no dependence. High-dose B vitamin regimens given to people who were not deficient are a different matter: two randomised trials found net harm from continuing them, so stopping those was a benefit rather than a loss. (Source 13)

What goes wrong

High-dose B vitamins including 1 mg cyanocobalamin daily accelerated kidney function loss and doubled vascular events in diabetic nephropathy. (Source 14)

• Randomized trial, Moderate certainty.
• Size: 238 participants at 5 Canadian university centres.
• Who: adults with type 1 or type 2 diabetes and a clinical diagnosis of diabetic nephropathy.
• How long: mean follow-up 31.9 months, outcome at 36 months.
• Result: Radionuclide GFR fell by 16.5 mL/min/1.73 m2 on B vitamins versus 10.7 on placebo, mean difference -5.8 (95% CI -10.6 to -1.1), P = 0.02. The composite of myocardial infarction, stroke, revascularisation and all-cause death occurred more often on B vitamins, hazard ratio 2.0 (95% CI 1.0-4.0), P = 0.04. Homocysteine fell as intended, so the harm was not a failure to lower it.
• Funding: not stated (academic multicentre trial)

Limit of this finding: This trial is evidence of harm, not benefit. The B-vitamin tablet did what it was meant to do biochemically: homocysteine fell by 4.8 micromol/L more than on placebo (P < .001, in favour of B vitamins). Kidney function still declined faster and heart attacks, strokes, revascularisations and deaths were twice as common on the vitamins. The vascular result is borderline (hazard ratio 2.0, 95% CI 1.0 to 4.0) and this was one trial of 238 people with diabetic kidney disease on high doses, so it does not describe ordinary B12 replacement in someone who is deficient.

The composite outcome occurred more often in the B-vitamin group (HR, 2.0; 95% CI, 1.0-4.0; P = .04).

Folic acid plus 0.4 mg cyanocobalamin daily increased cancer, cancer death and all-cause death in Norwegian heart patients. (Source 15)

• Randomized trial, Moderate certainty.
• Size: 6,837 patients across two randomised placebo-controlled trials.
• Who: patients with ischaemic heart disease in Norway, a country with no folic acid fortification of food.
• How long: median 39 months of treatment plus 38 months further observation.
• Result: Cancer in 341/3,411 (10.0 per cent) on folic acid plus B12 versus 288 (8.4 per cent) not given it, hazard ratio 1.21 (95% CI 1.03-1.41), P = 0.02, an absolute excess of about 1.6 percentage points. Cancer death 4.0 versus 2.9 per cent, HR 1.38 (1.07-1.79). All-cause death 16.1 versus 13.8 per cent, HR 1.18 (1.04-1.33). Driven mainly by lung cancer. Vitamin B6 alone had no significant effect.
• Funding: not stated (investigator-initiated Norwegian trials)

Limit of this finding: Read this as a safety signal from a secondary analysis, not a cancer trial. Cancer was not a prespecified primary endpoint of either Norwegian trial; the two trials were combined afterwards and followed for a further 38 months of observation. The participants all had ischaemic heart disease and lived in a country with no folic acid fortification of food, and the excess was driven mainly by lung cancer in a population with high smoking rates. Vitamin B6 alone showed no significant effect. It is also folic acid plus B12 together, so it cannot separate the two.

341 participants (10.0%) who received folic acid plus vitamin B(12) vs 288 participants (8.4%) who did not receive such treatment were diagnosed with cancer (hazard ratio [HR], 1.21; 95% confidence interval [CI], 1.03-1.41; P = .02)

Injected B12 has caused anaphylactic shock and death, and rapid optic atrophy in early Leber's disease. (Source 16)

• Case series, Low certainty.
• Size: not stated.
• Who: patients receiving parenteral vitamin B12; separately, patients with early Leber's hereditary optic neuropathy.
• How long: any time.
• Result: No rates given. The label records severe and swift optic atrophy in early Leber's disease, anaphylactic shock and death after parenteral administration, and hypokalaemia and sudden death when severe megaloblastic anaemia is treated intensely. An intradermal test dose is advised in anyone suspected of being sensitive.
• Funding: manufacturer's label (postmarketing reports)

Patients with early Leber's disease (hereditary optic nerve atrophy) who were treated with cyanocobalamin suffered severe and swift optic atrophy.

Reported adverse reactions to injected B12 include pulmonary oedema, heart failure early in treatment and peripheral vascular thrombosis. (Source 17)

• Case series, Very low certainty.
• Size: not stated.
• Who: patients receiving cyanocobalamin injection.
• How long: early in treatment for the cardiovascular reactions.
• Result: No rates given; reactions listed are anaphylactic shock and death, pulmonary oedema and congestive heart failure early in treatment, peripheral vascular thrombosis, polycythaemia vera, mild transient diarrhoea, itching and transitory exanthema, and a feeling of swelling of the whole body.
• Funding: manufacturer's label (postmarketing reports)

Cardiovascular: Pulmonary edema and congestive heart failure early in treatment; peripheral vascular thrombosis.

Taking folic acid while B12 deficient corrects the anaemia but lets the nerve damage go on to become irreversible. (Source 7)

• Official position, Certainty not rated.
• Size: not stated.
• Who: people with untreated vitamin B12 deficiency taking folic acid above 0.1 mg per day.
• How long: over months.
• Result: No rates given; the label states that folic acid above 0.1 mg/day may produce haematologic remission in B12 deficiency, that neurologic manifestations will not be prevented, and that irreversible damage will result if B12 is not given. Conversely, cyanocobalamin above 10 mcg daily can produce a haematologic response in folate deficiency and mask that diagnosis.
• Funding: manufacturer's label.

Neurologic manifestations will not be prevented with folic acid, and if not treated with vitamin B 12 , irreversible damage will result.

What the evidence supports

Given promptly by injection, B12 stops the neurological damage of deficiency progressing. (Source 1)

• Expert review, not systematic, Low certainty.
• Size: not stated.
• Who: people with intrinsic factor deficiency and pernicious anaemia, which may be associated with subacute combined degeneration of the spinal cord.
• How long: lifelong treatment.
• Result: No trial numbers given; the label states as established pharmacology that prompt parenteral administration prevents progression of neurologic damage, and separately that deficiency left more than 3 months may produce permanent degenerative lesions of the spinal cord.
• Funding: manufacturer's label (expert summary, no stated method)

Prompt parenteral administration of vitamin B 12 prevents progression of neurologic damage.

High-dose oral cyanocobalamin normalised blood B12 as well as injections, on low quality evidence, and cost less. (Source 18)

• Systematic review, Low certainty.
• Size: 3 RCTs, 153 participants (74 oral, 79 intramuscular)
• Who: adults with vitamin B12 deficiency, mean age 38.6 to 72 years.
• How long: 3 to 4 months.
• Result: In two trials using 1000 mcg/day orally, no clinically relevant difference in B12 levels versus injection; in one trial using 2000 mcg/day, a mean difference of 680 pg/mL (95% CI 392.7 to 967.3) favouring oral. Only one trial had low or unclear risk of bias across all domains. No trial reported clinical signs and symptoms, quality of life or acceptability.
• Funding: independent (Cochrane)

Low quality evidence shows oral and IM vitamin B12 having similar effects in terms of normalising serum vitamin B12 levels, but oral treatment costs less.

Oral cyanocobalamin raised the active carrier form of B12 in blood more than the same dose of hydroxocobalamin. (Source 19)

• Blood level study, Low certainty.
• Size: 101 adults (59 with low and 42 with normal cobalamin status)
• Who: adults with low and with normal cobalamin status.
• How long: 2 days of dosing.
• Result: Median change in holotranscobalamin was higher with cyanocobalamin at every dose tested (1.5, 3, 6 and 9 mcg); overall a more than twofold increase versus hydroxocobalamin; no difference between 1.5 and 3 mcg, so absorptive capacity was only reached above 3 mcg.
• Funding: not stated.

Administration of cyanocobalamin resulted in a more than twofold increase in holoTC in comparison with hydroxocobalamin. The absorptive capacity was reached only by doses above 3 µg cobalamin.

What the evidence does not support

B12 supplementation did not improve cognitive function in people with dementia and low B12. (Source 5)

• Systematic review, Very low certainty.
• Size: 2 randomised double-blind trials, small numbers of patients.
• Who: people with dementia (mostly Alzheimer's disease) and low serum vitamin B12 levels.
• How long: not stated.
• Result: No statistically significant treatment effect of B12 versus placebo on cognitive function. The reviewers noted the two acceptable trials were restricted to a small number of patients and that no trials involving people without dementia were found.
• Funding: independent (Cochrane)

Limit of this finding: This is the 2003 version of the review and is more than twenty years old, so it should not be read as the current state of the evidence. It found only two usable trials, both small and both in people who already had dementia and low serum B12. It explicitly found no trials at all in people without dementia, so it says nothing about B12 and memory or thinking in people who are not demented.

From the two included studies (Seal 2002; Fourniere 1997) of people with dementia and low serum vitamin B12 levels, there was no statistically significant evidence of treatment effect, vitamin B12 supplementation compared with placebo, on cognitive function.

Cochrane could not establish that oral B12 is as safe as injected B12; the safety evidence was very low quality. (Source 18)

• Systematic review, Very low certainty.
• Size: 2 of the 3 trials reported adverse events.
• Who: adults with vitamin B12 deficiency.
• How long: 3 to 4 months.
• Result: One trial reported no treatment-related adverse events in either group; in the other, 2 of 30 participants (6.7 per cent) in the oral group left early because of adverse events. Downgraded for performance bias, detection bias and serious imprecision.
• Funding: independent (Cochrane)

We found very low-quality evidence that oral vitamin B12 appears as safe as IM vitamin B12.

Where the research disagrees

Whether cyanocobalamin or hydroxocobalamin is the better form to give

• Cyanocobalamin injection US label, position: Hydroxycobalamin is equally as effective as cyanocobalamin, and they share the cobalamin molecular structure. (Source 20)
• Greibe and colleagues (2018), CobaSorb absorption study, pharmacokinetic study in 101 adults: Administration of cyanocobalamin resulted in a more than twofold increase in holoTC in comparison with hydroxocobalamin. (Source 19)

Whether tablets can replace injections for B12 deficiency

• Cochrane review (2018), systematic-review of 3 RCTs, 153 participants: Low quality evidence shows oral and IM vitamin B12 having similar effects in terms of normalising serum vitamin B12 levels, but oral treatment costs less. (Source 18)
• Cyanocobalamin injection US label, position: Oral absorption is considered too undependable to rely on in patients with pernicious anemia or other conditions resulting in malabsorption of vitamin B 12 . (Source 20)

How much

• Reference intake: Dosing is set by the prescriber. As a position, the injection label's regimen for pernicious anaemia is 100 mcg daily for 6 or 7 days by intramuscular or deep subcutaneous injection, then on alternate days for seven doses, then every 3 to 4 days for 2 to 3 weeks, then 100 mcg monthly for life. The same label cites the Food and Nutrition Board figures of 4 mcg daily in pregnancy and lactation and 0.5 to 3 mcg daily in children as dietary reference amounts, not doses. (Source 12)
• Upper limit: The label sets no maximum dose and states that no overdosage has been reported with the drug. That is an absence of reports, not a demonstration of safety at any dose: the trials that gave 0.4 mg and 1 mg daily with folic acid found harm. (Source 17)
• Studied: DIVINe gave a single tablet containing folic acid 2.5 mg, vitamin B6 25 mg and vitamin B12 1 mg daily, or matching placebo, for up to 36 months. (Source 4)
• Studied: The Norwegian trials gave folic acid 0.8 mg daily plus vitamin B12 0.4 mg daily, with or without vitamin B6 40 mg. (Source 21)
• Studied: The trials in the Cochrane review of oral versus injected B12 used 1000 mcg/day and 2000 mcg/day orally. (Source 2)

A common belief, and what the research shows

The belief: B12 is a harmless vitamin, so extra can only help - it gives you energy, protects your heart and sharpens your memory.

What the research shows: Extra B12 in people who are not deficient has been tested and has not helped, and twice it did harm. For memory, Cochrane reported that in people with dementia and low B12 "there was no statistically significant evidence of treatment effect, vitamin B12 supplementation compared with placebo, on cognitive function". For the heart and kidneys, DIVINe found that "Among patients with diabetic nephropathy, high doses of B vitamins compared with placebo resulted in a greater decrease in GFR and an increase in vascular events." In two Norwegian trials, folic acid plus 0.4 mg B12 was followed by more cancer and more deaths from any cause. The injection itself has caused anaphylaxis and death. What B12 does reliably is treat deficiency, which is a different question from taking more when you have enough.

Questions and answers

What is it?

Cyanocobalamin is the manufactured form of vitamin B12, a large molecule built around a cobalt atom. In this form the cobalt carries a cyanide group, which the body removes and replaces to make the two working versions of the vitamin. It is given as an injection into muscle or under the skin, as high-dose tablets, and as a nasal spray. It is the most widely used form and works as well as the liver-extract factor it replaced. (Source 20)

What does it do in the body?

B12 is needed to build DNA, to make red blood cells and to make the myelin that insulates nerves. Without it the marrow cannot divide cells properly, so red cells come out large and few, and the myelin in the spinal cord degenerates. That is why deficiency shows up both as anaemia and as numbness, pins and needles and unsteadiness on the feet. (Source 1)

Is it good or bad for you?

Both, and the difference is whether you are deficient. If you are, replacement corrects the anaemia and, started early, stops nerve damage getting worse. If you are not, high doses have not helped and have twice caused harm: in people with diabetic kidney disease, high-dose B vitamins including 1 mg B12 daily made kidney function fall faster and doubled heart attacks, strokes and deaths. (Source 13)

How do you get more of it?

From animal foods for ordinary needs, and from tablets, injections or nasal spray when absorption has failed. As a position, the injection label's pernicious anaemia schedule is 100 mcg daily for 6 or 7 days, then alternate days, then every 3 to 4 days, then 100 mcg monthly for life. Trials of tablets used 1000 to 2000 mcg a day, far more than the diet supplies, because only about 1 per cent of a large oral dose crosses the gut by simple diffusion. (Source 12)

If it is harmful, what reduces it?

B12 is water-soluble and the kidneys dump what is not stored, which is why large injections are mostly wasted: within 48 hours of a 100 or 1000 mcg injection, 50 to 98 per cent of the dose can appear in the urine. Giving it into a vein flushes out almost all of it, which is why the label says to avoid that route. In practice, stopping the supplement is what brings levels down. (Source 1)

Why might someone be low in it or missing it?

Absorbing B12 takes a normal stomach, intrinsic factor, and a healthy last part of the small intestine, so anything that breaks that chain causes deficiency: pernicious anaemia, stomach or bowel surgery, coeliac disease, bacterial overgrowth, fish tapeworm. A diet with no animal products supplies none. Long-term metformin lowers it, roughly doubling the rate of low levels at 5 years in the Diabetes Prevention Program Outcomes Study, and nitrous oxide inactivates it directly. (Source 3)

Which whole foods contain it or feed it?

Only animal foods: meat, offal, fish, shellfish, eggs, milk and cheese, plus fortified foods and drinks. Plants contain none, so a diet with no animal products at all supplies no B12 and the label advises regular oral B12 for people eating that way. Nothing you eat feeds or regenerates B12 the way fibre feeds gut bacteria; you either take it in or you do not. (Source 20)

What happens if you do not have it?

First the blood: red cells become large and few, causing tiredness and breathlessness. Then the nervous system: numbness, pins and needles, unsteadiness, and in the spinal cord a pattern called subacute combined degeneration. The timing matters more than most people realise. Deficiency allowed to run for more than three months can leave permanent damage that treatment cannot undo. (Source 7)

How can you test for it?

A serum B12 level is the usual test and it is the weakest link. In a review of 1,809 patients with nitrous-oxide-induced B12 deficiency, serum B12 was abnormal in only about half, while homocysteine was abnormal in 83 to 85 per cent and methylmalonic acid in 68 to 84 per cent; MRI and nerve conduction were often abnormal with a normal blood count and a normal B12. So a normal level does not rule deficiency out, and the metabolite tests are more sensitive. Antibiotics, methotrexate and pyrimethamine make the assay unreliable altogether. (Source 9)

References

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