Vitamin B12 (Cyanocobalamin)
The long history of Vitamin B12's discovery is strewn with wrong turns, mysterious clues, frustration, and finally scientific heroes who saved thousands of people from an agonizing and ghastly death-a "pernicious" death. Today, this B vitamin is a familiar friend: you may have heard of friends or relatives going to their doctors' offices for B12 injections for a purported energy boost. No one is quite sure why these friends and relatives receive the injections, and they aren't sure either. But there's nothing mysterious about the crucial role this B vitamin plays in human health, not the least of which is to prevent pernicious anemia, the deficiency disease.
The search for B12 led scientists on a not-so-merry chase that began in 1822 when a Scottish doctor reported on the "history of a case of anemia." The name they eventually gave this anemia was on target, considering the devastating neurologic damage it causes. The Scottish doctor felt that the disease was the result of a digestion or absorption problem; he just didn't know what. After his report, scientists began to study pernicious anemia with some vigor, and it was an American doctor who deduced the nutrition connection forty years later.
In between these clues, another B vitamin threw researchers off the scent by causing an anemia resembling pernicious anemia. A deficiency of the B vitamin folate causes a macrocytic anemia in which red blood cells are much larger than normal, similar to pernicious anemia. A breakthrough occurred when researcher Wills reported on a macrocytic anemia in pregnant Hindu women from Bombay. Her team of workers successfully treated the women with a yeast extract and later reproduced what they thought was the same anemia in monkeys. They cured the monkeys' anemia with a crude liver extract and named its magic ingredient "the Wills Factor." They found that when they purified the crude extract, it could still cure the monkeys, who actually had B12 deficiency, but not the women, who had a folate deficiency. Although Wills and her team couldn't quite put the last pieces in the puzzle, their work paved the way for the next two sleuths of science.
In 1926, Minot and Murphy tied up some loose ends and developed an oral liver therapy which proved to be an effective treatment for pernicious anemia, work for which they later won the Nobel Prize. The vitamin yielded its secrets in the late 1940s when two independent groups isolated it in crystalline form, and the tangle between folate and B12 began to make sense.
It's not surprising that B12's discovery was long and arduous. This vitamin has the most complex chemical structure of all the vitamins. If you need any more proof of B12's complicated nature after reading about its history, just think about this-it took more than 100 scientists in nineteen countries spanning a decade to understand it! Its chemical name, cyanocobalamin, arises from the presence of the mineral cobalt in the vitamin, and it has a characteristic deep red hue. Interestingly, the other part of its name comes from cyanide used in the synthetic process, not the naturally occurring form.
To understand Biz's role in the body, you have to factor in folate or folic acid. It's not surprising that those earlier researchers and physicians got them mixed up for so many years, because the vitamins are tightly entwined in the body's metabolism. The vitamins team up to make DNA in the following way: BB1212 acts as a coenzyme with an inactive form of folate to help convert one amino acid into another. In the process, folate becomes activated so that it's able to participate in DNA synthesis. Without B12, folate remains inactive and unable to do its job. It's biggest task is DNA synthesis so folate deficiency brings this process to a crawl, and one of the consequences is that new red blood cells aren't able to divide and mature. The anemia shows up as those large and immature red blood cells. It's in this way thata B12 deficiency causes a lack of folate.
This explains the similarity in symptoms of B12 and folate deficiency. It also explains why folate had not been available as a single vitamin supplement until recently. If a person has B12 deficiency, taking a folate supplement will make the red blood cells normal again, lulling the person or their doctor into thinking the problem is resolved. But folate only masks the symptoms of B12 deficiency, and the disease continues to ravage the nervous system until the damage is irreversible and soon causes death.
B12 also does some important things on its own. One important function is to maintain the sheath that surrounds nerve fibers and promotes their growth. This role in nerve function accounts for the neurologic damage when there is a deficiency. B12 also appears to play a role in the activity of bone cells and their metabolism. studies mentioned for B6 also included a role for B12 in lowering homocysteine levels and reducing the risk for heart disease.
How the Body Absorbs B12
The absorption of B12 is almost as complicated as its history, chemical structure, and relationship with folate. When you eat food that contains the vitamin, acid and digestive enzymes made by the stomach free it from other compounds. Once loose, a compound made by the stomach called the R-binding protein snatches it up. Meanwhile, another compound the stomach makes, the intrinsic factor, watches this new couple with envy like a secret admirer, wanting a dance with B12 but having to wait its turn. The intrinsic factor is actually B12's soul mate, but doesn't get its chance until the couple reaches the small intestine. In the last few inches of the small intestine, with the end of the dance seconds away, intrinsic factor makes its move, and R-protein backs off. Intrinsic factor claims his prize and escorts the alluring vitamin into the absorbing cells of the small intestine-oh yes, they do live happily ever after.
But the ending isn't always so happy, because some people who have stomach or intestinal problems may not be able to absorb B12. The stomach plays a key role in B12 absorption by making acid, R-protein, and intrinsic factor. Since it's the acid that keeps the R-protein and B12 together in the stomach, people who've had stomach surgery to reduce acid production, most commonly for ulcers, may have a problem. Some people have a condition known as achlorhydria in which the stomach cells don't produce enough acid. This often happens to the elderly, probably due to aging, and chronic gastritis can also cause low acid production. Besides acid, stomach problems or surgery can affect the organ's ability to make both R-protein or intrinsic factor.
Even after clearing the stomach, the small intestine has to be in tip-top shape to do its part in B12 absorption. In the neutral environment of the small intestine, the R-protein lets go and the intrinsic factor complex with B12 is favored. This new complex moves along to the terminal ileum, the last part of the small intestine, where absorption of the vitamin occurs. Problems affecting the terminal ileum, such as Crohn's and celiac disease, will reduce B12 absorption and often cause the deficiency. Since absorption of the vitamin depends on intrinsic factor and the digestive tract for all the steps, a B12 supplement has to be given by injection into the muscle.
People who've had portions of the small intestine removed, especially the terminal ileum, may develop B12deficiency. Another intestinal problem known as blind loop syndrome can cause deficiency. Blind loop develops when a portion of the small intestine is bypassed, either intentionally as in surgery or from inflammation, causing bacteria to grow. The bacteria need B12 too, so they use it up before the person gets a chance to absorb it.
Where Is B12
The new DRI raised the recommendation for the vitamin from 2 micrograms to 2.4. They also inserted a warning phrase: "10 to 30 percent of older adults malabsorb the vitamin, so these people need to insure the recommended level from foods or supplements:' The targets are achievable for people who don't have an absorption problem and who eat animal products. A little further down the food chain, bacteria, fungi, and algae can make their own B12 but yeasts, plants, animals, and humans have to consume sources of the vitamin. Animal products are the main sources of B12, and the bacteria living in your intestine add a bit, too. Plants don't naturally contain B12 but they may become contaminated with microorganisms who make the vitamin, leaving some behind for the animal or person to eat. Sometimes food labels can be a bit misleading when they show plant products containing B12, if it is present, it's in an inactive form the body can't use. However, some plant products, such as soy milk, have vitamins added during processing, which make them a good source for strict vegetarians. The wide availability of the vitamin makes overt deficiency due to poor dietary intake uncommon, with deficiency arising from absorption problems a more likely cause. Some studies show that strict vegetarians who don't eat any animal products, not even dairy foods, may have low blood levels of B12 and are at risk for a deficiency.
Research into the b 12 status of elderly Americans is of current interest. One recent study from the Netherlands reported that blood levels of b 12 were low in 6 percent of healthy elderly and 5 percent of elderly people in hospitals. And researchers have found high levels of the vitamin's metabolites, which accumulate wp'en vitamin status is impaired, in 63 percent of healthy and 82 percent of hospitalized elderly. This led the authors to conclude that many elderly people are at risk for b 12 deficiency and that measurement of the vitamin's metabolites is a more sensitive indicator that could help in early detection of deficiency. Of special concern was a study from 1988 which reported that the elderly may have psychiatric symptoms of b 12 deficiency from nerve damage even before anemia develops. And a recent study from Scotland supports results from earlier studies by showing that the elderly often have low blood levels; tests for B status shouldn't be limited to looking for large red blood cells, or macrocytic anemia.