Vitamin B-12 is a water-soluble crystalline compound that contains phosphorus, nitrogen, and cobalt. The latter gives it a rich red color. It is heat stable in neutral solutions, but it is destroyed by heat in both acid and alkaline mediums. It is also sensitive to light and is destroyed by heavy metals and strong oxidizing and reducing agents.
Vitamin B-12 is the most complex compound of the vitamins. Its chemical symbol is C63H90CON14O14P. It contains one cobalt atom that is similar in structure to the position of iron in hemoglobin. B12 is the only naturally occurring organic compound that contains cobalt. The commercially available form of Vitamin B-12 is Cyanocobalamin.
It helps activate amino acids during protein formation and in the anaerobic degradation of the amino acid lysine. The coenzyme of cobalamin is a carrier of methyl groups and hydrogen, and is necessary for carbohydrate, protein, and fat metabolism.
Cobalamin also provides important protection of the heart by way of its methyl transfer role. It is active in the synthesis of the amino acid methionine from its precursor, homocysteine. The synthesis occurs by first removing a methyl group from methyl folate, a derivative of the biologically active form of folic acid. This methyl group is then transferred to homocysteine and methionine is formed. It has been recently acknowledged that excess homocysteine in the blood is the cause of heart disease, blood clots, stroke and gangrene. Therefore, the understanding of this complementary action between B-12 and folic acid is a significant addition to our arsenal of weapons for the fight against heart disease. It is important to note that adequate amounts of both vitamin B12 and folic acid are necessary for methionine synthesis to take place. You can say keeping homocysteine levels low is a matter of life and death.
Methionine is essential for choline synthesis; therefore, vitamin B12 plays a secondary role in this lipid pathway. A choline deficiency that causes fatty liver can be prevented by cobalamin or the other methyl donors (betaine, methionine, folic acid).
It has been observed that fatty acid synthesis is impaired when this B vitamin is deficient. A lack of sufficient essential fatty acids results in impairment of brain and nerve tissue. The myelin sheath (the insulation around nerve cells) is malformed in a cobalamin deficiency and contributes to faulty nerve transmission. A prolonged B12 deficiency will ultimately lead to neurological disturbances.
DNA replication is dependent on the function of coenzyme cobalamin as a methyl group carrier. It is this role that explains why a deficiency of B-12 leads to megaloblastic anemia. This disorder is characterized by large immature blood cells and changes in bone marrow. Inadequate DNA translation leading to improper cell replication results in the large blood cells observed in this disorder. These large misshapen red blood cells are unable to transport oxygen. This results in anemia, leukopenia, thrombopenia and fewer, but larger and less mature, blood cells. Poor cell division in the gastrointestinal tract and epithelial tissues produces glossitis and megaloblastosis. Furthermore, general growth and repair are likewise impaired.
The characteristic symptom of a severe deficiency of this B vitamin is pernicious or megaloblastic anemia. This condition is most often caused by either inadequate consumption of B-12 or by a reduced gastric secretion of a mucoprotein called intrinsic factor. This intrinsic factor is necessary for proper vitamin B12 absorption through the intestinal tract. It is produced by the parietal cells of the stomach and binds onto the vitamin to transport it into the small intestine. In the presence of calcium, this transport mechanism attaches to the intestinal wall, facilitating absorption of the vitamin.
Pernicious anemia can also result from several other conditions, including:
Gastrectomy (surgical removal of the stomach)
Surgical removal of the lower ileum (were B vitamins are absorbed)
Developing antibodies to intrinsic factor
Hereditary malabsorption
Strict vegetarianism (absence of animal products in diet)
Homocystinuria (characterized by large amounts of homocysteine in the urine)
We now know that a deficiency of B vitamins (B6, Folic Acid & B-12) is the trigger for heart disease. This occurs when homocysteine levels rise unchecked by sufficient blood levels of these three B vitamins. There is good news in this message. Now, we know how to prevent heart disease and have a longer healthier life.
Too much homocysteine in the blood damages arteries and blood vessels causing the formation of arterial plaques. This results in arteriosclerosis and heart disease.
Other deficiency symptoms include glossitis, degeneration of the spinal cord, loss of appetite, gastrointestinal disturbances, fatigue, pallor, dizziness, hypotension, disorientation, numbness, tingling, ataxia, moodiness, confusion, agitation, dimmed vision, delusions, hallucinations, and eventually, “megaloblastic madness” (psychosis).
A long-term marginal b-12 deficiency has been associated with increased risk of Alzheimer’s disease. It has been found that over 70% of older persons having a B-12 deficiency also have Alzheimer’s. Alzheimer’s patients also exhibit lower blood levels of this B vitamin than patients who suffer from other brain or memory disorders. B-12 status correlates with the severity of cognitive impairment in Alzheimer’s patients. It is presently unknown whether the deficiency is a cause or result of the disease. However, cobalamin functions in numerous metabolic processes that affect nerve tissue. These processes include the synthesis of neurotransmitters and phospholipids which may explain B-12’s possible link with the development and progression of Alzheimer’s disease.
Symptoms of Vitamin B-12 deficiency are most commonly found in people over the age of 40 with increasing occurrences as age increased and is often a result of the reduced secretion of intrinsic factor. This condition is corrected with B-12 injections. Patients suffering form dementia often exhibit a deficiency of this B vitamin and supplementation improves mental functioning in some of these cases.
Vitamin B-12 absorption can be inhibited by many gastrointestinal disorders including, gluten-induced enteropathy, tropical sprue, regional ileitis, malignancies, and granulomatous lesions in the small intestine, tapeworm, bacteria associated with blind loop syndrome, and other disorders that impair the proper intestinal function. The need for B12 intake is increased by hyperthyroidism, parasitism and pregnancy.
The only source of vitamin B-12 in nature is microbial synthesis. Cobalamin is not found in plants, but is produced by bacteria in the digestive tract of animals or by microbial fermentation of foods.
Sources containing more than 10mcg/100 grams are organ meats (liver, kidney, heart), clams, and oysters. Good sources (3 to 10mcg/100 grams) are nonfat dry milk, crab, salmon, sardines, and egg yolk. Moderate amounts (1 to 3 mcg/100 grams) are meat, lobster, scallops, flounder, swordfish, tuna and fermented cheese. Other sources are fermented soybean products, poultry, and liquid milk products.
Because cobalamin is affected by temperatures above 100 degrees Celsius, some or all of this B vitamin is lost when meat is cooked.
The minimum daily requirement for B12 can be exceeded by ten thousand fold with no signs of toxicity. Excesses are excreted in the urine.
Many of the tests available to assess cobalamin deficiency have limitations and can give false results. For example, the MCV test (macrocytosis test) is not a sensitive test. Several conditions such as folacin deficiency, vitamin C supplementation, and antibiotics can result in high or low levels of B-12 being indicated in the essay. The Schilling test can give both false abnormal and false normal readings. Vitamin B-12 deficiency detection requires multiple testing methods and the patient’s symptoms being used in combination to diagnose.
References:
Garrison Jr., R.PH., Robert & Somer, M.A., R.D., Elizabeth, The Nutrition Desk Reference, 3rd ed., New Canaan: Keats Publishing, 1999,
pp 124-128, 431, 434
McCully, M.D., Kilmer S. & McCully, Martha, The Heart Revolution, New York: Harper Perennial, 1999, pp 1-10