Facts, Articles, Research

What the science says (1990–2026): Vitamin B12

These citations support correction of deficiency, specified forms, and elemental amounts — the same logic used in MD's Choice formulas. They are not claims that a supplement treats disease.

Stabler 2013 NEJM; Green 2017; 2023–2025 geriatric reviews. B12 deficiency causes anemia and irreversible nerve injury if missed. Older adults and people with low stomach acid often need a reliable form, not just 'more food.'

These products are not intended to diagnose, treat, cure, or prevent disease. Historic monograph text below is kept for the original library.

Vitamin B12

I. Structure

Vitamin B₁₂ is a generic term for a group of compounds called corrinoids because of their corrin nucleus
Corrin is a macrocyclic ring of four reduced pyrrole rings linked together with Co at its center to which is attached a nucleotide, 5, 6-dimethylbenzimidazole. (Figure 9.33)
Also attached is one of the following:
1. CN..............................Cyanocobalamin
2. OH..............................Hydroxocobalamin
3. H₂0.............................Aquocobalamin
4. NO₂............................Nitrocobalamin
5. 5'- deoxyadenosyl......5'- deoxyadenosylcobalamin
6. CH₃............................Methylcobalamin
Only 5'- deoxyadenosylcobalamin and methylcobalamin are active as coenzymes

II. Functions

Conversion of homocysteine into methionine
1. Requires methylcobalamin
2. Necessary for converting inactive methyl folate to the active form, THF
  1. Cobalamin, bound to homocysteine methyl transferase apoenzyme, picks up CH₃ group from N⁵ methyl THF and transfers it to homocysteine
  2. Methionine and free THF are produced
  3. THF can then be converted into any of its coenzyme forms
  4. This reaction largely explains the synergism between folate and vitamin B₁₂
Conversion of methylmalonyl CoA a metabolite of propionyl CoA to succinyl CoA, the Krebs cycle intermediate
1. This reaction is inhibited in cobalt deficient ruminants.
2. Reaction requires adenosylcolbalamin for methylmalonyl CoA mutase
3. When vitamin B₁₂ is deficient, mutase activity is impaired and methylmalonic acid accumulates in body fluids
Isomerization of L-leucine and beta-leucine
1. The enzyme leucine aminomutase requires adenosylcobalamin
2. Beta-leucine generated by intestinal bacteria may be converted to L-leucine within the body
3. L-leucine may be converted to beta leucine which can be transaminated in a vitamin B₆(PLP) -dependent reaction and provide an alternative pathway for leucine catabolism

III. Sources

All naturally occurring vitamin B₁₂ is produced by microorganisms
Dietary sources for humans are animal products which derived their cobalamins from microorganisms
Any vitamin B₁₂ in plant foods could probably be traced to microorganisms
1. Contamination with manure
2. Presence of nitrogen fixing bacteria in legume root nodules
3. Contaminated hands taking food to mouth
Food sources of cobalamins
1. Adenosyl - and hydroxocobalamin
  1. Meat and meat products
  2. Poultry, fish, shellfish (clams, oysters)
  3. Eggs (especially yolk)
2. Methyl and hydroxocobalamin
  1. Milk and milk products (cheese, yogurt)
3. Cyonocobalaman
  1. Tobacco
  2. Commercially available vitamins (along with hydroxocobalamin)
  3. Within the body, cyonocobalamin is converted to aquo- or hydrocobalamin

IV. Metabolism

Absorption and transport
1. Ingested cobalamins are released from polypeptides in foods by the gastric proteolytic enzyme pepsin
2. Once released from foods, vitamin B₁₂ absorption involves 2 proteins
  1. Intrinsic factor (IF), a glycoprotein synthesized by gastric parietal cells
  2. R proteins which have a high affinity for cobalamins are found in body fluids
3. Free cobalamin complexes with R protein
  1. Complex moves into the small intestine
  2. Pancreatic proteases in the duodenum hydrolyze R protein and release cobalamin
  3. R proteins may protect vitamin B₁₂
4. In the proximal small intestine, IF binds cobalamin released from R protein
  1. Cobalamin-IF complex travels to ileum where receptor sites for vitamin B₁₂ are present
  2. Peak levels in blood not reached before 8-12 hr after ingestion
  3. With pharmacologic doses of vitamin B₁₂, passive diffusion accounts for much of the absorption (thus effectiveness of high vitamin B₁₂levels in treatment of pernicious anemia)
  4. Much of cobalamin in bile and other intestinal secretions can be reabsorbed
  5. Following absorption, cobalamins bind to transcobalamins (TC) which carry them to tissues
  6. TCII also assists uptake of cobalamin by tissues which have receptors for TCII
  7. Cobalamins with TC are taken up by endocytosis
  8. Within the lysosome, TCII is degraded and hydroxycobalamin is released
  9. Hydroxycobalamin is converted to the active coenzyme forms, methylcobalamin and adenosylcobalamin
  10. Vitamin B₁₂ is stored in the liver for up to years (other water soluble vitamins are not stored)
Excretion
1. Most of cobalamin excretion occurs in feces via bile but 65-75% of that secreted into the gastrointestinal tract is reabsorbed.
2. Little urinary excretion occurs.
3. Whole body turnover of vitamin B₁₂ is approximately 0.1% per day.

V. Requirements

Recommended allowances
1. Human = 2 micrograms per day
2. Poultry = 2-4 micrograms per pound of diet
3. Swine = 5-10 micrograms per pound of diet
Factors increasing requirement
1. Vitamin C in doses of 500 mg or more with meals or up to 1 hr after a meal may diminish vitamin B₁₂ availability or destroy it
2. Pancreatic insufficiency could interfere with release of cobalamin from R protein
3. Deficiency of intrinsic factor (pernicious anemia)

VI. Deficiency

Human- pernicious anemia
1. Macrocytic anemia
2. Megaloblastic bone marrow
3. 3Achlorohydria
4. Glossitis
5. Neurological manifestations
  1. Peripherial neuritis
  2. Degenerative lesions of spinal cord
  3. Paresthesia (abnormal skin sensation)
Chicks
1. No anemia
2. Reduced growth
3. Reduced hatchability
4. Chicks from deficient eggs have muscle and leg abnormalities (perosis)
Swine
1. No anemia
2. Reduced growth, rough hair coat, dermatitis
3. Nervous and irritable
Sheep and cattle
1. B₁₂ normally synthesized in rumen
2. Lack of cobalt
  1. Anemia
  2. Loss of appetite
  3. Emaciation
  4. Urinary excretion of methylmalonic acid

VII. Toxicity

No clear toxicity from massive doses of vitamin B₁₂ has been reported

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Vitamin B12 (cobalamin) formula C₆₃H₈₈CoN₁₄O₁₄P

Vitamin B12 (cobalamin) — C₆₃H₈₈CoN₁₄O₁₄P

A large molecule with a cobalt atom in the center (the only vitamin that is built around a metal). It helps make blood cells and keep nerves working. Animals foods and good supplements supply it; plants do not, unless fortified.

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Vitamin A	Vitamin B1 (Thiamin)	Vitamin B2 (Riboflavin)	Vitamin B3 (Niacin)
Vitamin B5 (Pantothenic Acid)	Vitamin B6	Vitamin B12	Vitamin C
Vitamin D	Vitamin E	Vitamin K	Biotin
Folic Acid

Calcium	Magnesium	Phosphorus	Sodium, Potassium, Chloride
Sulfur (Sulfer)

Boron	Chromium	Cobalt	Copper
Fluorine	Iodine	Iron	Manganese
Molybdenum	Nickel (Nickle)	Selenium	Silicon
Tin	Vanadium	Zinc	Ultra Trace

Aluminum	Arsenic	Cadmium	Lead
Mercury

What the science says (1990–2026): Vitamin B12

Vitamin B12

Vitamins, Major Elements, Trace Elements, Toxic Elements

Vitamins

Major Elements

Trace Elements

Toxic Elements

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