so its going to be sad when some of my vegan friends get sick and/or die...
vitamin b12... ever heard of it? it is a vitamin that ONLY comes from animals...
THIS IS WHAT IT DOES:
also called Cyanocobalamin, a complex water-soluble organic compound that is essential to a number of microorganisms and animals, including humans. Vitamin B12, known as the anti-pernicious-anemia factor, is also known as the extrinsic factor-a substance from outside the body-that aids in the development of red blood cells in higher animals. The vitamin, which is unique in that it contains a
metallic ion, cobalt, has a complex chemical structure. Vitamin B12 occurs in several forms, called cobalamins; cyanocobalamin is the principal one used in vitamin supplements and pharmaceuticals.
In the 1930s the American physician W.B. Castle isolated an “intrinsic factor” in normal gastric secretion that was absent in the stomachs of persons suffering from perniciousanemia, an acute and sometimes fatal disorder of the red blood cells. Castle postulated that an “extrinsic factor” that alleviated or prevented pernicious anemia was to be found in animal liver, because improvement had been noted when diets of these patients included large amounts of liver. In 1948-49 simultaneous studies by the chemists Karl Folkers in the United States and Alexander Todd (later created Baron Todd) in England isolated and identified vitamin B12 as the pure antianemia factor present in liver. The human daily requirement for vitamin B12 is 3 micrograms; good dietary sources are eggs, meat, and dairy products.
So far as is known, vitamin B12 is not present in higher plants. It is required in the diet of all higher animals that have been studied. It is synthesized by bacteria, fungi, and algae, and the ultimate source of the vitamin in liver and other animal materials generally appears to be microorganisms of various kinds. Microorganisms that synthesize vitamin B12 occur in the rumen (the first stomach chamber) of cows and sheep. From the rumen it is transferred to the muscle and other tissues, which humans eat. Several kinds of bacteria unable to make the substance require minute amounts for growth.
Vitamin B12 is involved in cellular metabolism in two active coenzyme forms-methylcobalamin and 5-deoxyadenosylcobalamin. Vitamin B12 cooperates withfolate in the synthesis of DNA. A deficiency of either compound leads to disordered production of DNA and, hence, to the impaired division of red blood cells that is the cause of pernicious anemia (q.v.). Vitamin B12 also has a separate biochemical role, unrelated to folate, in the synthesis of fatty acids in the myelin sheath that surrounds nerve cells.
THIS IS WHAT HAPPENS WHEN YOU DONT GET IT:
a condition in which an organism fails to receive a sufficient quantity of vitamin B12 (cyanocobalamin), a micronutrient that is essential to human and animal digestion and nutritional absorption and which is known to prevent pernicious anemia**. Lack of vitamin B12 occasions defective formation of the papillae (small projections) of the tongue, giving an appearance of abnormal smoothness. A deficiency of vitamin B12 often causes defective function of the intestine, resulting in indigestion and sometimes constipation or diarrhea. A very serious effect is degeneration of certain motor and sensory tracts of the spinal cord: if the degeneration continues for some time, treatment with vitamin B12 may not correct it. Initial numbness and tingling of fingers or toes may, without treatment, progress to great instability of gait or virtual paralysis.
Because vitamin B12 is found in animal but not vegetable foods, complete vegetarianism may lead to deficiency. Deficiency may also result from competition for vitamin B12 by the broad tapeworm or by intestinal bacteria growing in cul-de-sacs or above partial obstructions in the digestive tract. Additional nutritional deficiencies, such as those of folic acid or iron, are likely to develop in such cases, as in primary intestinal diseases such as chronic celiac disease, tropical sprue, or regional ileitis, all of which affect the absorptive capacity of the small bowel.
**a slow-developing disease in which the production of red blood cells is impaired as the result of a defect in the body's ability to absorb vitamin B12. An absence of hydrochloric acid in gastric secretions (achlorhydria) is also characteristic. Pernicious anemia is in most cases associated with an inflammation of the stomach called autoimmune gastritis. Pernicious anemia is one of many types of anemia, a condition marked by a reduction in red blood cells or in the oxygen-carrying hemoglobin found in those cells; anemias are distinguished from one another by cause, symptoms, and cell characteristics.
Vitamin B12 is necessary for red blood cells to mature properly in the bone marrow, and intrinsic factor is a substance responsible for the intestinal absorption of the vitamin. In a healthy person intrinsic factor is produced by the parietal cells of the stomach, the cells that also secrete hydrochloric acid. Intrinsic factor forms a complex with dietary vitamin B12 in the stomach. This complex remains intact, preventing degradation of the vitamin by intestinal juices, until it reaches the ileum of the small intestine, where the vitamin is released and absorbed into the body.
When intrinsic factor is prevented from binding with vitamin B12 or when the parietal cells are unable to produce intrinsic factor, the vitamin is not absorbed and pernicious anemia results. It is believed to stem from an autoimmune reaction in which the malfunctioning immune system produces antibodies against intrinsic factor and against the parietal cells. Without an adequate amount of vitamin B12, the body is unable to synthesize DNA properly. This in turn affects red blood cell production: the cells divide, but their nuclei remain immature. These cells, called megaloblasts, are forthe most part destroyed in the bone marrow and are not released to the circulation. Some megaloblasts mature to become large red blood cells called macrocytes; they reach the circulation but function abnormally. A deficiency of white blood cells (leukopenia) and of platelets (thrombocytopenia) is also seen in the blood.
Pernicious anemia occurs most often in persons older than 35 years, although a juvenile form of the disease does occur, usually in children younger than 3 years of age. The disease shows a familial tendency and is more common in individuals of northern European descent. Symptoms and signs include weakness, waxy pallor, shortness of breath, rapid heart beat, unsteady gait, smooth, shiny tongue, gastrointestinal disturbances, and neurological problems. The anemia may become severe before the disorder is diagnosed, because the vitamin deficiency develops very gradually. A diagnosis can be made with the Schilling test, which measures the body'sability to absorb vitamin B12. Treatment involves a monthly intramuscular injection of vitamin B12 that must be continued for life. Most patients improve quickly, although neurological damage is seldom fully reversible and atrophy of the parietal cells and achlorhydria persist. Before the discovery of treatment in the 1920s, the modifier pernicious, although something of a misnomer today, was sadly appropriate, since the disease was usually fatal.
MAN, isnt encyclopedia britannica FUN!?
THIS IS WHAT IT DOES:
also called Cyanocobalamin, a complex water-soluble organic compound that is essential to a number of microorganisms and animals, including humans. Vitamin B12, known as the anti-pernicious-anemia factor, is also known as the extrinsic factor-a substance from outside the body-that aids in the development of red blood cells in higher animals. The vitamin, which is unique in that it contains a
metallic ion, cobalt, has a complex chemical structure. Vitamin B12 occurs in several forms, called cobalamins; cyanocobalamin is the principal one used in vitamin supplements and pharmaceuticals.
In the 1930s the American physician W.B. Castle isolated an “intrinsic factor” in normal gastric secretion that was absent in the stomachs of persons suffering from perniciousanemia, an acute and sometimes fatal disorder of the red blood cells. Castle postulated that an “extrinsic factor” that alleviated or prevented pernicious anemia was to be found in animal liver, because improvement had been noted when diets of these patients included large amounts of liver. In 1948-49 simultaneous studies by the chemists Karl Folkers in the United States and Alexander Todd (later created Baron Todd) in England isolated and identified vitamin B12 as the pure antianemia factor present in liver. The human daily requirement for vitamin B12 is 3 micrograms; good dietary sources are eggs, meat, and dairy products.
So far as is known, vitamin B12 is not present in higher plants. It is required in the diet of all higher animals that have been studied. It is synthesized by bacteria, fungi, and algae, and the ultimate source of the vitamin in liver and other animal materials generally appears to be microorganisms of various kinds. Microorganisms that synthesize vitamin B12 occur in the rumen (the first stomach chamber) of cows and sheep. From the rumen it is transferred to the muscle and other tissues, which humans eat. Several kinds of bacteria unable to make the substance require minute amounts for growth.
Vitamin B12 is involved in cellular metabolism in two active coenzyme forms-methylcobalamin and 5-deoxyadenosylcobalamin. Vitamin B12 cooperates withfolate in the synthesis of DNA. A deficiency of either compound leads to disordered production of DNA and, hence, to the impaired division of red blood cells that is the cause of pernicious anemia (q.v.). Vitamin B12 also has a separate biochemical role, unrelated to folate, in the synthesis of fatty acids in the myelin sheath that surrounds nerve cells.
THIS IS WHAT HAPPENS WHEN YOU DONT GET IT:
a condition in which an organism fails to receive a sufficient quantity of vitamin B12 (cyanocobalamin), a micronutrient that is essential to human and animal digestion and nutritional absorption and which is known to prevent pernicious anemia**. Lack of vitamin B12 occasions defective formation of the papillae (small projections) of the tongue, giving an appearance of abnormal smoothness. A deficiency of vitamin B12 often causes defective function of the intestine, resulting in indigestion and sometimes constipation or diarrhea. A very serious effect is degeneration of certain motor and sensory tracts of the spinal cord: if the degeneration continues for some time, treatment with vitamin B12 may not correct it. Initial numbness and tingling of fingers or toes may, without treatment, progress to great instability of gait or virtual paralysis.
Because vitamin B12 is found in animal but not vegetable foods, complete vegetarianism may lead to deficiency. Deficiency may also result from competition for vitamin B12 by the broad tapeworm or by intestinal bacteria growing in cul-de-sacs or above partial obstructions in the digestive tract. Additional nutritional deficiencies, such as those of folic acid or iron, are likely to develop in such cases, as in primary intestinal diseases such as chronic celiac disease, tropical sprue, or regional ileitis, all of which affect the absorptive capacity of the small bowel.
**a slow-developing disease in which the production of red blood cells is impaired as the result of a defect in the body's ability to absorb vitamin B12. An absence of hydrochloric acid in gastric secretions (achlorhydria) is also characteristic. Pernicious anemia is in most cases associated with an inflammation of the stomach called autoimmune gastritis. Pernicious anemia is one of many types of anemia, a condition marked by a reduction in red blood cells or in the oxygen-carrying hemoglobin found in those cells; anemias are distinguished from one another by cause, symptoms, and cell characteristics.
Vitamin B12 is necessary for red blood cells to mature properly in the bone marrow, and intrinsic factor is a substance responsible for the intestinal absorption of the vitamin. In a healthy person intrinsic factor is produced by the parietal cells of the stomach, the cells that also secrete hydrochloric acid. Intrinsic factor forms a complex with dietary vitamin B12 in the stomach. This complex remains intact, preventing degradation of the vitamin by intestinal juices, until it reaches the ileum of the small intestine, where the vitamin is released and absorbed into the body.
When intrinsic factor is prevented from binding with vitamin B12 or when the parietal cells are unable to produce intrinsic factor, the vitamin is not absorbed and pernicious anemia results. It is believed to stem from an autoimmune reaction in which the malfunctioning immune system produces antibodies against intrinsic factor and against the parietal cells. Without an adequate amount of vitamin B12, the body is unable to synthesize DNA properly. This in turn affects red blood cell production: the cells divide, but their nuclei remain immature. These cells, called megaloblasts, are forthe most part destroyed in the bone marrow and are not released to the circulation. Some megaloblasts mature to become large red blood cells called macrocytes; they reach the circulation but function abnormally. A deficiency of white blood cells (leukopenia) and of platelets (thrombocytopenia) is also seen in the blood.
Pernicious anemia occurs most often in persons older than 35 years, although a juvenile form of the disease does occur, usually in children younger than 3 years of age. The disease shows a familial tendency and is more common in individuals of northern European descent. Symptoms and signs include weakness, waxy pallor, shortness of breath, rapid heart beat, unsteady gait, smooth, shiny tongue, gastrointestinal disturbances, and neurological problems. The anemia may become severe before the disorder is diagnosed, because the vitamin deficiency develops very gradually. A diagnosis can be made with the Schilling test, which measures the body'sability to absorb vitamin B12. Treatment involves a monthly intramuscular injection of vitamin B12 that must be continued for life. Most patients improve quickly, although neurological damage is seldom fully reversible and atrophy of the parietal cells and achlorhydria persist. Before the discovery of treatment in the 1920s, the modifier pernicious, although something of a misnomer today, was sadly appropriate, since the disease was usually fatal.
MAN, isnt encyclopedia britannica FUN!?