Vitamin B12 is an essential water-soluble vitamin, member of the vitamin B complex. It contains cobalt, and so is also known as cobalamin. It is exclusively synthesised by bacteria and is found primarily in meat, eggs and dairy products. B12 is the most chemically complex of all the vitamins.

There has been considerable research into proposed plant sources of vitamin B12. Fermented soya products, seaweeds, and algae such as spirulina have all been suggested as containing significant B12. However, the present consensus is that any B12 present in plant foods is likely to be unavailable to humans and so these foods should not be relied upon as safe sources. Many vegan foods are supplemented with B12. Vitamin B12 is necessary for the synthesis of red blood cells, the maintenance of the nervous system, and growth and development in children. Deficiency can cause anemia. Vitamin B12 neuropathy, involving the degeneration of nerve fibers and irreversible neurological damage, can also occur.

Vitamin B12 is bound to the protein in food. Hydrochloric acid in the stomach releases vitamin B12 from proteins in foods during digestion. Once released, vitamin B12 combines with a substance called intrinsic factor. This complex can then be absorbed by the intestinal tract.

The human body stores several years’ worth of vitamin B12, so nutritional deficiency of this vitamin is extremely rare. Elderly are the most at risk. However, deficiency can result from being unable to use vitamin B12. Inability to absorb vitamin B12 from the intestinal tract can be caused by a disease known as pernicious anemia. Additionally, strict vegetarians or vegans who are not taking in proper amounts of B12 are also prone to a deficiency state.

Synonyms and Terminology

  • B-12, B Complex, B Complex Vitamin, bedumil, cobalamin, cobalamins, cobamin, cyanocobalamin, cyanocobalaminum, cycobemin, hydroxocobalamin, hydroxocobalaminum, hydroxocobemine, idrossocobalamina, methylcobalamin, vitadurin, vitamin B-12.

Selected name brands

  • Alphamin®, Anacobin®, Bedoz®, Cobex®, Cobolin-M®, Crystamine®, Cryst®, Cyanoject®, Cyomin®, Hydrobexan®, Hydro-Cobex®, Hydro-Crysti®, Hydroxy-Cobal®, LA-12®, Neuroforte-R®, Nascobal®, Primabalt®, Rubramin PC®, Shovite®, Vibal®, Vibal LA®, Vitabee®.

Functions of Vitamin B12

Vitamin B12’s primary functions are in the formation of red blood cells and the maintenance of a healthy nervous system. B12 is necessary for the rapid synthesis of DNA during cell division. This is especially important in tissues where cells are dividing rapidly, particularly the bone marrow tissues responsible for red blood cell formation. If B12 deficiency occurs, DNA production is disrupted and abnormal cells called megaloblasts occur. This results in anemia. Symptoms include excessive tiredness, breathlessness, listlessness, pallor, and poor resistance to infection. Other symptoms can include a smooth, sore tongue and menstrual disorders. Anemia may also be due to folic acid deficiency, folic acid also being necessary for DNA synthesis.
B12 is also important in maintaining the nervous system. Nerves are surrounded by an insulating fatty sheath comprised of a complex protein called myelin. B12 plays a vital role in the metabolism of fatty acids essential for the maintainence of myelin. Prolonged B12 deficiency can lead to nerve degeneration and irreversible neurological damage.

When deficiency occurs, it is more commonly linked to a failure to effectively absorb B12 from the intestine rather than a dietary deficiency. Absorption of B12 requires the secretion from the cells lining the stomach of a glycoprotein, known as intrinsic factor. The B12-intrinsic factor complex is then absorbed in the ileum (part of the small intestine) in the presence of calcium. Certain people are unable to produce intrinsic factor and the subsequent pernicious anaemia is treated with injections of B12.

Storage and reabsortion of vitamin B12

Vitamin B12 can be stored in small amounts by the body. Total body store is 2-5mg in adults. Around 80% of this is stored in the liver.

Vitamin B12 is excreted in the bile and is effectively reabsorbed. This is known as enterohepatic circulation. The amount of B12 excreted in the bile can vary from 1 to 10ug (micrograms) a day. People on diets low in B12, including vegans and some vegetarians, may be obtaining more B12 from re absorption than from dietary sources. Reabsorption is the reason it can take over 20 years for deficiency disease to develop in people changing to diets absent in B12. In comparison, if B12 deficiency is due to a failure in absorption it can take only 3 years for deficiency disease to occur.

Dietary Sources

The only reliable unfortified sources of vitamin B12 are meat, dairy products and eggs. There has been considerable research into possible plant food sources of B12. Fermented soya products, seaweeds and algae have all been proposed as possible sources of B12. However, analysis of fermented soya products, including tempeh, miso, shoyu and tamari, found no significant B12.
Spirulina, an algae available as a dietary supplement in tablet form, and nori, a seaweed, have both appeared to contain significant amounts of B12 after analysis. However, it is thought that this is due to the presence of compounds structurally similar to B12, known as B12 analogues. These cannot be utilized to satisfy dietary needs. Assay methods used to detect B12 are unable to differentiate between B12 and it’s analogues, Analysis of possible B12 sources may give false positive results due to the presence of these analogues.

Researchers have suggested that supposed B12 supplements such as spirulina may in fact increase the risk of B12 deficiency disease, as the B12 analogues can compete with B12 and inhibit metabolism.

The current nutritional consensus is that no plant foods can be relied on as a safe source of vitamin B12.

Bacteria present in the large intestine are able to synthesize B12. In the past, it has been thought that the B12 produced by these colonic bacteria could be absorbed and utilized by humans. However, the bacteria produce B12 too far down the intestine for absorption to occur, B12 not being absorbed through the colon lining.

Human faeces can contain significant B12. A study has shown that a group of Iranian vegans obtained adequate B12 from unwashed vegetables which had been fertilized with human manure. Faecal contamination of vegetables and other plant foods can make a significant contribution to dietary needs, particularly in areas where hygiene standards may be low. This may be responsible for the lack of anemia due to B12 deficiency in vegan communities in developing countries.

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Good sources of vitamin B12 for vegetarians are dairy products or free-range eggs. ½ pint of milk (full fat or semi skimmed) contains 1.2 µg. A slice of vegetarian cheddar cheese (40g) contains 0.5 µg. A boiled egg contains 0.7 µg. Fermentation in the manufacture of yoghurt destroys much of the B12 present. Boiling milk can also destroy much of the B12.

Vegans are recommended to ensure their diet includes foods fortified with vitamin B12. A range of B12 fortified foods are available. These include yeast extracts, Vecon vegetable stock, veggie burger mixes, textured vegetable protein, soya milks, vegetable and sunflower margarines, and breakfast cereals.

The table below lists a variety of food sources of vitamin B12.

Food Micrograms (µg)
per serving
Percent
DV*
Mollusks, clam, mixed species, cooked, 3 ounces 84.1 1400
Liver, beef, braised, 1 slice 47.9 780
Fortified breakfast cereals, (100%) fortified), ¾ cup 6.0 100
Trout, rainbow, wild, cooked, 3 ounces 5.4 90
Salmon, sockeye, cooked, 3 ounces 4.9 80
Trout, rainbow, farmed, cooked, 3 ounces 4.2 50
Beef, top sirloin, lean, choice, broiled, 3 ounces 2.4 40
Fast Food, Cheeseburger, regular, double patty & bun, 1 sandwich 1.9 30
Fast Food, Taco, 1 large 1.6 25
Fortified breakfast cereals (25% fortified), ¾ cup 1.5 25
Yogurt, plain, skim, with 13 grams protein per cup, 1 cup 1.4 25
Haddock, cooked, 3 ounces 1.2 20
Clams, breaded & fried, ¾ cup 1.1 20
Tuna, white, canned in water, drained solids, 3 ounces 1.0 15
Milk, 1 cup 0.9 15
Pork, cured, ham, lean only, canned, roasted, 3 ounces 0.6 10
Egg, whole, hard boiled, 1 0.6 10
American pasteurized cheese food, 1 ounces 0.3 6
Chicken, breast, meat only, roasted, ½ breast 0.3 6

DV = Daily Value. DVs are reference numbers developed by the Food and Drug Administration (FDA) to help consumers determine if a food contains a lot or a little of a specific nutrient. The DV for vitamin B12 is 6.0 micrograms (µg). Most food labels do not list a food’s vitamin B12 content. The percent DV (%DV) listed on the table indicates the percentage of the DV provided in one serving. A food providing 5% of the DV or less is a low source while a food that provides 10% to 19% of the DV is a good source. A food that provides 20% or more of the DV is high in that nutrient. It is important to remember that foods that provide lower percentages of the DV also contribute to a healthful diet. For foods not listed in this table, please refer to the US Department of Agriculture’s Nutrient Database Web site: http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl.

Required Intakes of Vitamin B12

The old Recommended Daily Amounts (RDA’s) have now been replaced by the term Reference Nutrient intake (RNI). The RNI is the amount of nutrient which is enough for at least 97% of the population.

Reference Nutrient Intakes for Vitamin B12, µg/day. (1000 µg = 1mg)

(tabla vegsoc)

Symptoms and damage from deficiency

B12 deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system.

The first deficiency symptom that was discovered was anemia characterized by enlarged blood corpuscles, so called megaloblastic anemia.

The anemia is thought to be due to problems in DNA synthesis, specifically in the synthesis of thymine, which is dependent on products of the MTR reaction . Other cell lines such as white blood cells and platelets are often also low. Bone marrow examination may show megaloblastic hemopoiesis. The anemia is easy to cure with vitamin B12.

Far more serious is the damage to the nervous system that may occur due to deficiency.

Early and even fairly pronounced deficiency does not always cause distinct or specific symptoms. Common early symptoms are tiredness or a decreased mental work capacity. Decreased concentration and decreased memory. Irritability and depression.

Sleep disturbances may occur, because B12 is important for the regulation of the sleep wake cycle by the pineal gland (through melatonin) . Treatment with B12 normalizes the melatonin level, and thereby the sleep disturbance. Seasonal Affective Disorder (SAD), with severe seasonal depressions has a know connection with disturbed pineal (melatonin) functioning including disturbed sleep-wake rytm. The concentration of melatonin in SAD patients was on average 2.4 times as high as in the control group according to one study.

Neurological signs of B12 deficiency, which can occur without anemia, include sensory disturbances due to damage to peripheral nerves caused by demyelination and irreversible nerve cell death. Symptoms include numbness, tingling of the extremities, disturbed coordination and, if not treated in time, an ataxic gait, a syndrome known as Subacute combined degeneration of spinal cord.

Recent studies have reported a close connection between B12 deficiency and Alzheimers dementia. This is thought to be caused by accumulation of the neurotoxic amino acid Homocystein, which needs B12 and also vitamin B6 and folic acid for its decomposition.

The American Psychiatric Association’s American Journal of Psychiatry has published studies showing a relationship between Clinical depression levels and deficient B12 blood levels in elderly people in 2000 and 2002.

Causes of deficiency

Recent research indicates that B12 deficiency is far more widespread than formerly believed. A large study in the US found that 39 percent had low values. This study at Tufts university used the B12 concentration 258 picomoles per liter (pmol/l) as a criterion of “low level”. However, recent research has found that B12 deficiency may occur at a much higher B12 concentration (500-550 pmol/l). This gives reasons to suspect that a major part of the american population may have B12 deficiency.

B12 is mostly absorbed in the terminal ileum, the lower part of the small intestine. The production of intrinsic factor in the parietal cells of the stomach is vital to absorption of this vitamin in terminal ileum. Vitamin B12 deficiency can result from inadequate intake of B12, inadequate production of intrinsic factor (pernicious anemia), disorders of the terminal ileum resulting in malabsorption, or by competition for available B12 (such as fish tapeworms or bacteria present in blind loop syndrome).

Absorption decreases with age so older people are under significant risk to be deficient. In one study 40% of people above 65 were deficient in vitamin B12.
Recent research has found that B12 deficiency is common among vegetarians – as much as 30% may be deficient. In vegans who don’t supplement with B12 the risk is very high because virtually none of their natural food sources contain B12.

The popular stomach acid reducing drugs like Omeprazol, Pariet, Rifun, Zantac, Cimitidin, Tagamet, decrease the B12 uptake to a large extent. For example in one study Omeprzol decreased the B12-uptake with 80 percent. So they are an increasingly common cause of vitamin B12 deficiency.

The diabetes medication, metformin, can cause vitamin B12 deficiency, according to a retrospective study. The mechanism may include inhibition of calcium-dependent ileal absorption of the B12-intrinsic factor complex. Primary care health professionals should consider vitamin B12 deficiency in the differential diagnosis of diabetic patients with neuropathic symptoms while taking metformin.

Another common cause is Helicobacter Pylori infection which is a major cause of gastritis.

B12 deficiency has been severely underdiagnosed. This is because it was believed that its primary manifestation is so called megaloblastic (large erythrocyte) anemia. Consequently the diagnostic and laboratory criteria of deficiency were set on the basis of anemia.

But recently it has been realized that considerably deficiency in the nervous system can be there, including damage to the peripheral and central nervous system (Alzheimers dementis), although no conspicuous anemia is present. Regrettably, in many countries, the laboratories are still applying the outdated deficiency criteria.

Serum homocysteine and methylmalonic acid levels are high in B12 deficiency and can be helpful if the diagnosis is unclear.

Routine monitoring of methylmalonic acid levels in urine is an option for people who may not be eating enough B12, as a rise in methylmalonic acid levels is an early indication of deficiency.

Diagnosis of Vitamin B12 deficiency

Serum B12 levels are often low in B12 deficiency, but there does not exist a robust assay, and if other features of B12 deficiency are present then the diagnosis must not be discounted. One possible explanation for normal B12 levels in B12 deficiency is antibody interference in people with high titres of intrinsic factor antibody.

Recent research indicates that the reference values for vitamin B12 have been wrong, accepting far to low levels as normal. This is because the reference values were set using the presence or absence of megaloblastic anemia as a criterion of deficiency. But now that it has been realized that even severe nervous system damage may occur without anemia, the levels are being changed. In Japan where it has been well researched, the lowest acceptable level for vitamin B12 in blood has been raised from about 200 picograms/litre (pg/l) = 145 picomol/litre (pm/l) to 550 pg/l = 400 pm/l. Unfortunately, in most countries the labs have been slow in adopting these new norms, so many people with B12 deficiency are erroneously diagnosed as normal.’

Serum Homocysteine and Methylmalonic acid levels are considered more reliable indicators of B12 deficiency than the concentration of B12 in blood. Recent research indicates that also the normal acceptable lower limit for homocystein has been too high, about 14-15 micromol/l (reference added later). But recent research indicates that it should not be higher than 6,3 micromol/l (0,85 mg/ml). Unfortunately most laboratiories have been slow in adapting to the new findings and still apply the old values.

Because of this, B12 deficiency is very often underdiagnosed in most countries.

Bone marrow aspiration may be helpful if there are doubts about the nature of the anemia. If nervous system damage is suspected, B12 analysis in cerebrospinal fluid can also be helpful.

Treatment of B12 deficiency

Traditionally, treatment for B12 deficiency was through intramuscular injections of cyanocobalamin. However, allergy against B12 may sometimes be triggered by injections.

Also, it has been questioned whether cyanocobalamin should be used as it is an artificial molecule that is transformed to B12 after release of highly toxic cyanide. The amounts of cyanide are very small with normal dosage, but may not be insignificant at high dose treatment which occurs in deficiency conditions. Because of its artificial nature, it is not easily transformed into physiological vitamin B12, and may therefore not allways be well assimilated.

Actually, research indicates that cyanocobalamin is not easily assimilated into the brain (reference will be added later). For this reason some researchers advocate the use of methylcobalamin, which is well assimilated and has no harmful effects even at very high dosage (ref will be added). An advantage is that methylcobalamin is available as sublingual tablets, that is absorbed effectively. The same goes for intranazal spray administration. The vitamin is directly absorbed into the blood stream through the mucous membranes. This evades the problem with oral intake, see next paragraph.

It has been appreciated since the 1960s that deficiency can sometimes be treated with oral B12 supplements when given in sufficient doses. When given in oral doses ranging from 0.1–2 mg daily, B12 can be absorbed in a pathway that does not require an intact ileum or intrinsic factor. However, with the advent of sublingual and intranazal adminstration, tablet usage is becoming outdated. Oral absorption is limited so regular intramuscular injections or sublingual/intranazal administration of a cobalamin (preferably methyl- or hydroxycobalamin) is necessary to restore systemic stores to physiological levels. Recent research indicates that sublingual administration eliminates a deficiency as well as injections (reference will be added) with the advantage of evading the allergy risk.

The Schilling test can determine whether symptoms of B12 deficiency are caused by lack of intrinsic factor, though this is being performed less often due to the lack of availability of reagent for the test.

Side effects, contraindications, and warnings of B12

  • Cardiovascular: Caution should be used in patients undergoing angioplasty since an intravenous loading dose of folic acid, vitamin B6 and vitamin B12 followed by oral administration of folic acid 1.2mg plus vitamin B6 48mg and vitamin B12 60mcg taken daily after coronary stenting might actually increase restenosis rates[citation needed]. Due to the potential for harm this combination of vitamins should not be recommended for patients receiving coronary stents.
    *Dermatologic: Itching, rash, transitory exanthema, and urticaria have been reported. Vitamin B12 (20 micrograms/day) and pyridoxine (80mg/day) has been associated with cases of rosacea fulminans, characterized by intense erythema with nodules, papules, and pustules. Symptoms may persist for up to 4 months after the supplement is stopped, and may require treatment with systemic corticosteroids and topical therapy.
  • Gastrointestinal: Diarrhea has been reported.
  • Hematologic: Peripheral vascular thrombosis has been reported. Treatment of vitamin B12 deficiency can unmask polycythemia vera, which is characterized by an increase in blood volume and the number of red blood cells. The correction of megaloblastic anemia with vitamin B12 can result in fatal hypokalemia and gout in susceptible individuals, and it can obscure folate deficiency in megaloblastic anemia. Caution is warranted.
  • Leber’s disease: Vitamin B12 in the form of cyanocobalamin is contraindicated in early Leber’s disease, which is hereditary optic nerve atrophy. Vitamin B12 can cause severe and swift optic atrophy.

Interactions with drugs

  • Alcohol (ethanol): Excessive alcohol intake lasting longer than two weeks can decrease vitamin B12 absorption from the gastrointestinal tract.
  • Aminosalicylic acid (para-aminosalicylic acid, PAS, Paser): Aminosalicylic acid can reduce oral vitamin B12 absorption, possibly by as much as 55%, as part of a general malabsorption syndrome. Megaloblastic changes, and occasional cases of symptomatic anemia have occurred, usually after doses of 8 to 12 grams/day for several months. Vitamin B12 levels should be monitored in people taking aminosalicylic acid for more than one month.
  • Antibiotics: An increased bacterial load can bind significant amounts of vitamin B12 in the gut, preventing its absorption. In people with bacterial overgrowth of the small bowel, antibiotics such as metronidazole (Flagyl®) can actually improve vitamin B12 status. The effects of most antibiotics on gastrointestinal bacteria are unlikely to have clinically significant effects on vitamin B12 levels.
  • Birth control pills: The data regarding the effects of oral contraceptives on vitamin B12 serum levels are conflicting. Some studies have found reduced serum levels in oral contraceptive users, but others have found no effect despite use of oral contraceptives for up to 6 months. When oral contraceptive use is stopped, normalization of vitamin B12 levels usually occurs. Lower vitamin B12 serum levels seen with oral contraceptives probably are not clinically significant.
  • Chloramphenicol (Chloromycetin®): Limited case reports suggest that chloramphenicol can delay or interrupt the reticulocyte response to supplemental vitamin B12 in some patients. Blood counts should be monitored closely if this combination cannot be avoided.
    *Cobalt irradiation: Cobalt irradiation of the small bowel can decrease gastrointestinal (GI) absorption of vitamin B12.
  • Colchicine: Colchicine in doses of 1.9 to 3.9mg/day can disrupt normal intestinal mucosal function, leading to malabsorption of several nutrients, including vitamin B12. Lower doses do not seem to have a significant effect on vitamin B12 absorption after 3 years of colchicine therapy. The significance of this interaction is unclear. Vitamin B12 levels should be monitored in people taking large doses of colchicine for prolonged periods.
  • Colestipol (Colestid®), Cholestyramine (Questran®): These resins used for sequestering bile acids in order to decrease cholesterol, can decrease gastrointestinal (GI) absorption of vitamin B12. It is unlikely that this interaction will deplete body stores of vitamin B12 unless there are other factors contributing to deficiency. In a group of children treated with cholestyramine for up to 2.5 years there was not any change in serum vitamin B12 levels. Routine supplements are not necessary.
  • H2-receptor antagonists: include cimetidine (Tagamet®), famotidine (Pepcid®), nizatidine (Axid®), and ranitidine (Zantac®). Reduced secretion of gastric acid and pepsin produced by H2 blockers can reduce absorption of protein-bound (dietary) vitamin B12, but not of supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Clinically significant vitamin B12 deficiency and megaloblastic anemia are unlikely, unless H2 blocker therapy is prolonged (2 years or more), or the person’s diet is poor. It is also more likely if the person is rendered achlorhydric (with complete absence of gastric acid secretion), which occurs more frequently with proton pump inhibitors than H2 blockers. Vitamin B12 levels should be monitored in people taking high doses of H2 blockers for prolonged periods.
  • Metformin (Glucophage®): Metformin may reduce serum folic acid and vitamin B12 levels. These changes can lead to hyperhomocysteinemia, adding to the risk of cardiovascular disease in people with diabetes. There are also rare reports of megaloblastic anemia in people who have taken metformin for 5 years or more. Reduced serum levels of vitamin B12 occur in up to 30% of people taking metformin chronically. However, clinically significant deficiency is not likely to develop if dietary intake of vitamin B12 is adequate. Deficiency can be corrected with vitamin B12 supplements even if metformin is continued. The metformin-induced malabsorption of vitamin B12 is reversible by oral calcium supplementation. The general clinical significance of metformin upon B12 levels is as yet unknown.
  • Neomycin: Absorption of vitamin B12 can be reduced by neomycin, but prolonged use of large doses is needed to induce pernicious anemia. Supplements are not usually needed with normal doses.
  • Nicotine: Nicotine can reduce serum vitamin B12 levels. The need for vitamin B12 supplementation has not been adequately studied.
  • Nitrous oxide: Nitrous oxide inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy, and encephalopathy, can occur within days or weeks of exposure to nitrous oxide anesthesia in people with subclinical vitamin B12 deficiency. Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete. People with normal vitamin B12 levels have sufficient vitamin B12 stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (such as recreational use). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anesthesia.
  • Phenytoin (Dilantin®), phenobarbital, primidone (Mysoline®): These anticonvulsants have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluid levels in some patients. This may contribute to the megaloblastic anemia, primarily caused by folate deficiency, associated with these drugs. It’s also suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs. Patients should be encouraged to maintain adequate dietary vitamin B12 intake. Folate and vitamin B12 status should be checked if symptoms of anemia develop.
  • Proton pump inhibitors (PPIs): The PPIs include omeprazole (Prilosec®, Losec®), lansoprazole (Prevacid®), rabeprazole (Aciphex®), pantoprazole (Protonix®, Pantoloc®), and esomeprazole (Nexium®). The reduced secretion of gastric acid and pepsin produced by PPIs can reduce absorption of protein-bound (dietary) vitamin B12, but not supplemental vitamin B12. Gastric acid is needed to release vitamin B12 from protein for absorption. Reduced vitamin B12 levels may be more common with PPIs than with H2-blockers, because they are more likely to produce achlorhydria (complete absence of gastric acid secretion). However, clinically significant vitamin B12 deficiency is unlikely, unless PPI therapy is prolonged (2 years or more) or dietary vitamin intake is low. Vitamin B12 levels should be monitored in people taking high doses of PPIs for prolonged periods.
  • Zidovudine (AZT, Combivir®, Retrovir®): Reduced serum vitamin B12 levels may occur when zidovudine therapy is started. This adds to other factors that cause low vitamin B12 levels in people with HIV, and might contribute to the hematological toxicity associated with zidovudine. However, data suggests vitamin B12 supplements are not helpful for people taking zidovudine.

Sources: Vegetarian society, wikipedia, NIH

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