
Vitamin B12 deficiency
Vitamin B12 deficiency, also known as cobalamin deficiency, is the medical condition in which the blood and tissue have a lower than normal level of vitamin B12.[5] Symptoms can vary from none to severe.[1] Mild deficiency may have few or absent symptoms.[1] In moderate deficiency, feeling tired, headaches, soreness of the tongue, mouth ulcers, breathlessness, feeling faint, rapid heartbeat, low blood pressure, pallor, hair loss, decreased ability to think and severe joint pain and the beginning of neurological symptoms, including abnormal sensations such as pins and needles, numbness and tinnitus may occur.[1] Severe deficiency may include symptoms of reduced heart function as well as more severe neurological symptoms, including changes in reflexes, poor muscle function, memory problems, blurred vision, irritability, ataxia, decreased smell and taste, decreased level of consciousness, depression, anxiety, guilt and psychosis.[1] If left untreated, some of these changes can become permanent.[1][6] Temporary infertility, reversible with treatment, may occur.[1][7] A late finding type of anemia known as megaloblastic anemia is often but not always present.[2] In exclusively breastfed infants of vegan mothers, undetected and untreated deficiency can lead to poor growth, poor development, and difficulties with movement.[2]
Vitamin B12 deficiency
Hypocobalaminemia, cobalamin deficiency
Decreased ability to think, feeling tired, depression, irritability, abnormal sensations, changes in reflexes[1]
Megaloblastic anemia, irreversible damage to the brain and nervous system[2]
Poor absorption, decreased intake, increased requirements[1]
Blood levels below 148–185 pmol/L (200–250 pg/mL) in adults[2]
Supplementation in those at high risk[2]
Supplementation by mouth or injection[3]
6% (< 60 years old), 20% (> 60 years old)[4]
Causes are usually related to conditions that give rise to malabsorption of vitamin B12 particularly autoimmune gastritis in pernicious anemia.[8]
Other conditions giving rise to malabsorption include surgical removal of the stomach, chronic inflammation of the pancreas, intestinal parasites, certain medications such as long-term use of proton pump inhibitors, H2-receptor blockers, and metformin, and some genetic disorders.[1][9] Deficiency can also be caused by inadequate dietary intake such as with the diets of vegetarians, and vegans, and in the malnourished.[1][10] Deficiency may be caused by increased needs of the body for example in those with HIV/AIDS, and shortened red blood cell lifespan.[1] Diagnosis is typically based on blood levels of vitamin B12 below 148–185 pmol/L (200 to 250 pg/mL) in adults.[2] Diagnosis is not always straightforward as serum levels can be falsely high or normal.[11] Elevated methylmalonic acid levels may also indicate a deficiency.[2] Individuals with low or marginal values of vitamin B12 in the range of 148–221 pmol/L (200–300 pg/mL) may not have classic neurological or hematological signs or symptoms.[2]
Treatment is by vitamin B12 supplementation, either by mouth or by injection.[3] Initially in high daily doses, followed by less frequent lower doses, as the condition improves.[3] If a reversible cause is found, that cause should be corrected if possible.[12] If no reversible cause is found, or when found it cannot be eliminated, lifelong vitamin B12 administration is usually recommended.[13] A nasal spray is also available.[2] Vitamin B12 deficiency is preventable with supplements, which are recommended for pregnant vegetarians and vegans, and not harmful in others.[2] Risk of toxicity due to vitamin B12 is low.[2]
Vitamin B12 deficiency in the US and the UK is estimated to occur in about 6 percent of those under the age of 60, and 20 percent of those over the age of 60.[4] In Latin America, about 40 percent are estimated to be affected, and this may be as high as 80 percent in parts of Africa and Asia.[1] Marginal deficiency is much more common and may occur in up to 40% of Western populations.[2]
History[edit]
Between 1849 and 1887, Thomas Addison described a case of pernicious anemia, William Osler and William Gardner first described a case of neuropathy, Hayem described large red cells in the peripheral blood in this condition, which he called "giant blood corpuscles" (now called macrocytes), Paul Ehrlich identified megaloblasts in the bone marrow, and Ludwig Lichtheim described a case of myelopathy.[176] During the 1920s, George Whipple discovered that ingesting large amounts of liver seemed to most rapidly cure the anemia of blood loss in dogs, and hypothesized that eating liver might treat pernicious anemia.[177] Edwin Cohn prepared a liver extract that was 50 to 100 times more potent in treating pernicious anemia than the natural liver products. William Castle demonstrated that gastric juice contained an "intrinsic factor" which when combined with meat ingestion resulted in absorption of the vitamin in this condition.[176] In 1934, George Whipple shared the 1934 Nobel Prize in Physiology or Medicine with William P. Murphy and George Minot for discovery of an effective treatment for pernicious anemia using liver concentrate, later found to contain a large amount of vitamin B12.[176][178]
Other animals[edit]
Ruminants, such as cattle and sheep, absorb B12 synthesized by their gut bacteria.[179] Sufficient amounts of cobalt and copper need to be consumed for this B12 synthesis to occur.[180]
In the early 20th century, during the development for farming of the North Island Volcanic Plateau of New Zealand, cattle had what was termed "bush sickness". It was discovered in 1934 that the volcanic soils lacked the cobalt salts essential for synthesis of vitamin B12 by their gut bacteria.[181][180] The "coast disease" of sheep in the coastal sand dunes of South Australia in the 1930s was found to originate in nutritional deficiencies of the trace elements, cobalt and copper. The cobalt deficiency was overcome by the development of "cobalt bullets", dense pellets of cobalt oxide mixed with clay given orally, which then was retained in the animal's rumen.[180][182]