Vitamin B12: Benefits, Dosage, Contraindications
There is an interaction between the metabolism of vitamin B9 and vitamin B12 due to their role in methylation processes, particularly in the remethylation of homocysteine.
Vitamin B12 is present in lamb liver, sardines, oysters, egg yolk, fish, beef, kidneys, cheese, and milk. Between 10% and 50% is lost during cooking.
The bioavailability of vitamin B12 significantly decreases with increased intake, as it is estimated that the intestinal absorption system mediated by intrinsic factors is saturated at about 1.5-2.0 μg/meal for healthy adults with normal gastrointestinal function. The bioavailability of vitamin B12 from different sources is variable: fish (42%), lamb (56-89%), chicken (61-66%), and eggs (<9%).
It is possible to obtain B12 from certain non-animal sources, for example, after consuming Nori (seaweed). Five different biologically active vitamin B12 compounds have been identified in Nori: cyanocobalamin, hydroxycobalamin, sulfitocobalamin, adenosylcobalamin, and methylcobalamin; the source of B12 appears to be a bacterium.
Vitamin B12 deficiencies manifest mainly in hematological and neurological disorders. Older people are particularly at risk, as vitamin B12 deficiency affects 10 to 15% of those over 60 years old.
Vitamin B12 contributes to the normal energy metabolism, the normal functioning of the nervous system, the normal metabolism of homocysteine, normal mental functions, the formation of red blood cells, reduction of fatigue, normal functioning of the immune system, and cell division.
Other name(s)
Cobalamin
Scientific name(s)
Cyanocobalamin, Hydroxocobalamin, Methylcobalamin
Family or group:
Vitamins
Indications
Rating methodology
EFSA approval.
Vitamin B12 Deficiency ✪✪✪✪✪
Vitamin B12 deficiency can take months, or even years, to become symptomatic due to the large reserve capacity of the body. Deficiencies may result from inadequate dietary intake in adults, particularly in those on a vegan diet, very low in dairy products and meats, or secondary to absorption issues.
A vitamin B12 deficiency leads to megaloblastic anemia, gastrointestinal lesions, and neurological lesions that can range from an inability to produce myelin to degeneration of the axon and nerve head. Neurological symptoms caused by vitamin B12 deficiency can include neuropsychiatric disorders such as depression, paresthesia, ataxia, memory loss, weakness, and changes in personality and mood.
The treatment of B12 deficiencies typically relies on the parenteral administration of this vitamin, in the form of cyanocobalamin, less commonly hydroxocobalamin. The recommended regimen involves the injection of 1000 μg of vitamin B12 daily intramuscularly for one week, then 1000 μg weekly for a month, followed by a monthly injection of the same dose, usually for life, particularly in Biermer's disease (a disease due to vitamin B12 malabsorption).
Oral administration of cyanocobalamin has also been shown to be effective in the context of the syndrome of non-dissociation of vitamin B12 from its carrier proteins (this syndrome is characterized by an inability to release vitamin B12 from dietary and/or intestinal transport proteins, particularly in cases of hypochlorhydria, whereas the absorption of ‘unbound’ vitamin B12 is normal) and in Biermer's disease. The attack dose is 500 to 1000 μg/day orally (1000 μg/day if Biermer's disease), for one month. The maintenance dose is 125 to 500 μg/day until the cause is corrected, or 1000 μg/day for life in case of Biermer’s disease.
Posologie
Oral
4 - 1000 μg
cyanocobalamin
Effective treatment of cobalamin deficiency with oral cobalamin.
Normalization of low vitamin B12 serum levels in older people by oral treatment.
Oral or parenteral therapy for B12 deficiency
Vitamin B12 deficiencies in adults: causes, clinical manifestations and treatment
Emotional balance ✪✪✪✪✪
Vitamin B12 contributes to the normal functioning of the nervous system and to normal mental functions. A deficiency in vitamin B12 leads to psychological disorders: memory disturbances, irritability, depression, personality disorder, dementia, delirium, and psychosis.
Posologie
Orally
4 µg
Fatigue ✪✪✪✪✪
Vitamin B12 plays a key role in energy production, DNA synthesis, and the functioning of the nervous system. Its deficiency can cause megaloblastic anemia and neurological disorders, contributing to fatigue and cognitive impairment. By supporting DNA synthesis for cellular repair and red blood cell formation, as well as the metabolism of fats and carbohydrates, B12 is essential for maintaining optimal energy. In 2012, European health authorities (EFSA, European Food Safety Authority and the European Commission) assessed that foods and dietary supplements containing vitamin B12 can claim to contribute to reducing fatigue. Clinically, there is evidence that intramuscular injections of vitamin B12 in the form of hydroxocobalamin, at a dosage of 5 mg twice a week, could improve the general well-being of patients complaining of fatigue.
Posologie
Orally
4 - 5000 µg
hydroxocobalamin
Canker sores ✪✪✪✪✪
In the case of oral aphthosis, clinical research shows that applying a topical ointment containing 500 µg of vitamin B12 for 2 days reduces pain by 80% compared to a control ointment containing no vitamin B12. Other clinical research shows that taking 1000 µg of vitamin B12 sublingually per day for 6 months significantly reduces the duration of canker sore outbreaks, the number of ulcerations, and pain intensity, compared to placebo, in patients with normal vitamin B12 levels.
Posologie
Topically, orally
500 µg
2 - days
ointment
Hyperhomocysteinemia ✪✪✪✪✪
Hyperhomocysteinemia is known as a risk factor for cardiovascular diseases. Oral intake of vitamin B12 in combination with folic acid, and sometimes with pyridoxine (vitamin B6), can reduce serum homocysteine concentrations. Taking folic acid at a dose of 0.5 to 5 mg per day lowers fasting homocysteine levels by an average of 25%. The combination of 0.5 mg of vitamin B12 per day results in an additional reduction in homocysteine levels by an average of 7%, although this effect is likely only observed in individuals with vitamin B12 deficiency. Vitamin B12 in combination with folic acid and other vitamins also appears to significantly reduce homocysteine levels in patients with end-stage renal disease. A dose of 400 to 500 mcg of vitamin B12, in combination with 0.4 to 5 mg of folic acid and 16.5 mg of pyridoxine (vitamin B6), has been used.
Posologie
Orally
400 - 500 µg
cyanocobalamin
Synergies
Vitamin supplements and cardiovascular risk: review of the randomized trials of homocysteine-lowering vitamin supplements.
Vitamin supplementation reduces blood homocysteine levels: a controlled trial in patients with venous thrombosis and healthy volunteers.
Preventive health care, 2000 update: screening and management of hyperhomocysteinemia for the prevention of coronary artery disease events. The Canadian Task Force on Preventive Health Care.
Dose-dependent effects of folic acid on blood concentrations of homocysteine: a meta-analysis of the randomized trials.
Treatment of hyperhomocysteinemia in hemodialysis patients and renal transplant recipients.
Diagnosis and treatment of hyperhomocysteinemia.
Homocysteine lowering effect of different multivitamin preparations in patients with end-stage renal disease.
Treatment of mild hyperhomocysteinemia in renal transplant recipients versus hemodialysis patients.
Lowering blood homocysteine with folic acid based supplements: meta-analysis of randomised trials. Homocysteine Lowering Trialists' Collaboration.
AMD ✪✪✪✪✪
A large-scale clinical study shows that taking 50 mg of pyridoxine per day in combination with 1 mg of cyanocobalamin and 2.5 mg of folic acid, for an average of 7.3 years, significantly reduces, compared to a placebo, the risk of developing AMD (age-related macular degeneration) in women aged 40 years with a history of cardiovascular disease or having risk factors for cardiovascular disease.
Posologie
Orally
1000 µg
7 - years
cyanocobalamin
Synergies
Diabetic neuropathy ✪✪✪✪✪
Clinical evidence shows that taking vitamin B12 in the form of methylcobalamin or cyanocobalamin, in combination with benfotiamine (a natural form of vitamin B1) and pyridoxine (vitamin B6), for 9 to 12 weeks can improve some symptoms of diabetic neuropathy. Furthermore, taking methylcobalamin orally for up to 4 months seems to improve pain associated with diabetic peripheral neuropathy, but may not improve nerve conduction. The daily intake was 1500 mcg of methylcobalamin for 3 to 4 months.
Posologie
Orally
1500 µg
4 - months
methylcobalamin
Synergies
The effect of prostaglandin E1.alpha CD on vibratory threshold determined with the SMV-5 vibrometer in patients with diabetic neuropathy.
Effect of mecobalamin on diabetic neuropathies. Beijing Methycobal Clinical Trial Collaborative Group
A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy.
Therapeutic efficacy of "Milgamma" in patients with painful diabetic neuropathy.
Alzheimer's Disease ✪✪✪✪✪
Research shows that a high intake of vitamin B12 is not associated with a decreased risk of developing Alzheimer's disease. However, clinical research shows that taking 0.5 mg of vitamin B12, 20 mg of vitamin B6, and 0.8 mg of folic acid per day for 24 months slows cerebral atrophy in patients with Alzheimer's disease.
Posologie
Orally
500 µg
24 - months
cyanocobalamin
Synergies
Depression ✪✪✪✪✪
Elevated homocysteine and low levels of vitamin B12 and folate are frequently observed in depression. Observational studies have shown that 30% of patients hospitalized for depression experienced a vitamin B12 deficiency. An epidemiological study revealed that a daily dietary intake of vitamin B12 of at least 4.79 mcg is associated with a 58% lower risk of depression compared to a daily intake below 3.16 mcg in older men.
Posologie
Orally
4 µg
Risk of depression in pregnant women with low-normal serum Vitamin B12
Treatment of depression: time to consider folic acid and vitamin B12
Vitamin B(12) deficiency and depression in physically disabled older women: epidemiologic evidence from the Women's Health and Aging Study
Hepatitis ✪✪✪✪✪
Preliminary clinical research conducted on patients with chronic hepatitis C infection shows that administering vitamin B12 in the form of cyanocobalamin at a dose of 5000 mcg intramuscularly every 4 weeks, combined with standard treatment, significantly improves the viral response compared to standard treatment alone.
Posologie
Oral route
5000 µg
cyanocobalamin
Properties
Essential
Vitamin B12 is involved in DNA synthesis, as well as in the development, myelination, and function of the nervous system. Within the cell, vitamin B12 is involved in two essential metabolic functions:
- In the mitochondria, adenosyl-cobalamin serves as a cofactor for methyl-malonyl-CoA mutase, enabling the production of succinyl-CoA from methylmalonyl-CoA. Succinyl-CoA plays an essential role in fatty acid oxidation and ketogenesis.
- In the cytoplasm, methyl-B12 serves as a cofactor for methionine synthase, which produces methionine from homocysteine. This represents a way to metabolize potentially toxic homocysteine, to make methionine essential for protein synthesis, and to provide the cell with methyl radical donors.
European health authorities (EFSA, European Food Safety Authority, and the European Commission) have determined that dietary supplements containing vitamin B12 (cobalamin) contribute to normal energy metabolism, normal functioning of the nervous system, normal homocysteine metabolism, normal mental functions, formation of red blood cells, reduction of fatigue, normal functioning of the immune system, and cell division.
Usages associés
Neurological
Methylcobalamin, a form of vitamin B12, seems to improve alertness and reduce sleep time in subjects with normal sleep, potentially by acting on melatonin.
Furthermore, some research suggests that high serum homocysteine levels and low folate and vitamin B12 levels may be associated with cognitive decline and dementia.
Some researchers believe that vitamin B12 supplementation may enhance the symptoms of chronic fatigue syndrome by correcting red blood cell abnormalities and improving oxygen delivery to tissues.
Usages associés
Cardiovascular
Vitamin B12 is necessary for one of the pathways of homocysteine metabolism. The remethylation of homocysteine into methionine requires the use of folate and vitamin B12 in the form of methylcobalamin as a cofactor. Consequently, oral intake of vitamin B12 in combination with folic acid and sometimes with pyridoxine (vitamin B6) can reduce serum homocysteine concentrations.
Some studies suggest that elevated homocysteine levels can cause damage to vascular endothelial cells, endothelium-dependent vasodilation, increased oxidation, and arterial deposition of low-density lipoproteins (LDL), increased platelet adhesion, and activation of the coagulation cascade.
Usages associés
Anticancer
Vitamin B12 is believed to have anticancer properties, and vitamin B12 supplementation may play a role in the prevention of cervical cancer. However, high serum vitamin B12 levels have been associated with an increased risk of prostate cancer. Additionally, research in subjects with hepatocellular carcinoma suggests that the presence of tumor markers along with a high serum vitamin B12 level is a poor prognosis.
Hepatoprotective
A deficiency in vitamin B12 leads to decreased activity of serine dehydratase (SDH) (an enzyme involved in liver gluconeogenesis) and tyrosine aminotransferase in the rat liver.
On the other hand, vitamin B12 decreased blood levels of aspartate aminotransferase and alanine aminotransferase in mice with dimethylnitrosamine-induced liver damage, suggesting a possible hepatoprotective effect.
Usages associés
Antioxidant
Recent studies have shown that vitamin B12 and its cobalamin-based derivatives have an antioxidant effect at pharmacological concentrations.
Safety dosage
Pregnant woman from 18 years: 4.5 µg
Breastfeeding woman from 18 years: 5 µg
Infant from 7 to 11 months: 1.5 µg
Adult from 18 years: 4 µg
Child from 1 to 6 years: 1.5 µg
Child from 7 to 10 years: 2.5 µg
Child from 11 to 14 years: 3.5 µg
Child from 15 to 17 years: 4 µg
Interactions
Médicaments
Chloramphenicol: strong interaction
In some individuals, chloramphenicol (antibiotic) may inhibit or delay the reticulocyte crisis response to vitamin B12 supplementation. If unavoidable, close monitoring of reticulocyte levels should be performed.
Colchicine: moderate interaction
Colchicine, at doses of 1.9 to 3.9 mg per day, may disrupt the normal functioning of the intestinal mucosa, leading to malabsorption of several nutrients, including vitamin B12.
H2 antihistamines: moderate interaction
Reduced gastric acid and pepsin secretion by H2 antihistamines can reduce the absorption of vitamin B12 from ingested foods. Consequently, the chances of developing a vitamin B12 deficiency are increased by 25% in individuals taking H2 for 2 years or more. H2 antihistamines include cimetidine (Tagamet), ranitidine (Zantac), nizatidine (Axid), and famotidine (Pepcid).
Metformin: moderate interaction
Metformin, an oral antidiabetic, can lower serum vitamin B12 and folic acid levels. This effect may lead to hyperhomocysteinemia, which can increase the risk of cardiovascular disease in diabetic individuals.
Aspirin: moderate interaction
Clinical research suggests that acetylsalicylic acid (aspirin) increases the risk of vitamin B12 deficiency.
Nitrous oxide: moderate interaction
Nitrous oxide (or nitrous oxide) inactivates the cobalamin form of vitamin B12 through oxidation. Symptoms due to nitrous oxide are invisible in individuals with normal vitamin B12 levels (unless exposure is repeated and prolonged). However, symptoms such as sensory neuropathy, myelopathy, and encephalopathy may be observed in individuals with vitamin B12 deficiency.
Anticonvulsants: moderate interaction
Phenytoin, phenobarbital, and primidone are anticonvulsants that reduce the absorption of vitamin B12 if administered in conjunction with it.
Plantes ou autres actifs
Vitamin B12: moderate interaction
High doses of folic acid can mask a vitamin B12 deficiency. Indeed, folic acid can improve the symptoms of megaloblastic anemia.
Contraindications
Angioplasty: prohibited
The combination of vitamin B12, vitamin B6, and intravenous folic acid is not recommended for a person who has had a coronary stent as part of an angioplasty. Indeed, the combination of these vitamins may increase the risk of restenosis.
Leber's disease: prohibited
Vitamin B12 is contraindicated in the early stages of Leber's disease (which is an hereditary optic nerve atrophy). Vitamin B12 may cause severe and rapid optic atrophy.
