Vitamin B12, known also as cobalamin, is a water-soluble vitamin, meaning that it dissolves in water, so is not easily stored and is excreted via your urine. Chemically, vitamin B12 comprises a cobalt element surrounded by five nitrogen atoms, forming a structure called a corrin ring. Humans are incapable of synthesising this corrin ring, so are dependent on getting vitamin B12 in their diets.
Vitamin B12 is primarily sourced from foods of animal origin, including red meat, shellfish, eggs and dairy foods. Once consumed, vitamin B12 is manufactured via pepsin combining with hydrochloric acid in the stomach to break down the animal protein. The cobalamin that is released later binds to intrinsic factor (IF), which allows vitamin B12 to be absorbed by the intestine and into the bloodstream. Vitamin B12 blood concentrations are directly linked to intake; a reduced intake will invariably result in deficiency.
Discovery and deficiency
Pernicious anaemia (PA) was first chronicled in 1821 and was known to be fatal. It wasn’t until 1926 that research teams in both the United Kingdom and the United States determined that PA could be treated by giving humans liver to consume. This illusive “liver factor†was further studied and, by 1948, the “anti-pernicious anaemia factor†was isolated and determined to be, in fact, vitamin B12.
Ways an individual can become vitamin B12-deficient
- Pernicious anaemia (PA) is a type of megaloblastic (larger then normal red blood cells) anaemia and occurs as a result of vitamin B12 malabsorption due to IF deficiency. This is considered an autoimmune condition as the body’s own antibodies attack the stomach cells that produce IF.
- Insufficient dietary intake by vegetarians, vegans, lacto-ovo vegetarians and those with a limited meat intake.
- A reduced or absent production of hydrochloric acid, leading to less cobalamin being extracted from food.
Vitamin B12 has a range of actions, so signs and symptoms of deficiency are varied and include non-specific tiredness, a loss of co-ordination, poor reflexes, loss of memory, dementia and mood disturbances. Left untreated, a vitamin B12 deficiency could lead to irreversible nervous system damage and mental impairment.
People considered at risk of a vitamin B12 deficiency are far-ranging and include people with gastrointestinal disorders and vegetarians. Importantly, 16 per cent of older Australians (65 and older) are vitamin B12-deficient and, of these, 2 per cent can be classified as having a moderate to severe deficiency.
If a vitamin B12 deficiency is suspected medical practitioners will assess blood concentrations of methylmalonic acid (MMA) and homocysteine (Hcy). Both MMA and Hcy levels increase early in cases of vitamin B12 deficiency. These markers are therefore also used to monitor the response to vitamin B12 supplementation.
Vitamin B12 as medicine
Pernicious anaemia
In the Western world, about 90 per cent of cases of megaloblastic anaemia are from vitamin B12 deficiency. Signs and symptoms of PA include weakness, heart palpitations, fatigue, lightheadedness, shortness of breath and jaundice. Research suggests that 1000µg (micrograms) per day of vitamin B12 over 30 days improves biochemical markers in megaloblastic anaemia.
Nervous system
Research has determined that neurological problems such as loss of sensation in the arms and legs, memory loss and dementia are present in about 75–90 per cent of people with vitamin B12 deficiency. One of the chemical markers for vi-tamin B12 deficiency, methylmalonic acid (MMA), is increased in elderly patients who have problems with understanding and verbal expression.
High levels of homocysteine, probably indicating low levels of vitamin B12, have also been linked to an increased risk of Alzheimer’s disease, dementia and cognitive decline.
Cardiovascular system
Homocysteine has a significant impact on cardiovascular health as it causes free radical damage to blood vessels. Research has also identified that a higher intake of vitamin B12 is related to a lowering of risk for stroke.
Infant and children’s health
While vitamin B9 (folic acid) is well-known for its association with neural tube defects (NTD) such as spina bifida in infants, vitamin B12 deficiency in the mother is also highly correlated with developing NTD. Canadian research teams have revealed there is possibly a tripled risk for an infant to develop an NTD if the mother is deficient in vitamin B12.
Dietary vitamin B12 is primarily sourced from animal products, so strict vegetarians and their children are at risk of deficiency. Some studies indicate that children on a macrobiotic diet (cereals, pulses, vegetables, seaweed, nuts, seeds and seasonal fruit) have noticeably lower vitamin B12 levels, with lowered muscle reactivity compared with that of children on no such diet. Due to possible deficiencies, vegans and vegetarians should eat vitamin B12-fortified foods such as cereals and some soy products.
Taking vitamin B12
Sublingual (placed under the tongue) and oral vitamin B12 tablets are effective at ameliorating vitamin B12 deficiency (within 12–14 days). As well as being convenient, sublingual and oral tablets are preferred methods of administration of vitamin B12 over intramuscular injection, which can be painful, problematic in patients who bleed excessively or are underweight, and costly if given by health professionals.
Ideally, individuals should drink a glass of water (to avoid possible dryness of the mouth) and hold the vitamin B12 sublingual tablet under the tongue until it is fully dissolved. Dosages of 1000μg–2000μg are considered safe.
