Vitamin B12 Helps Build Blood and Bone
Elderly people with a B12 deficiency may need
more than 200 times the RDA to get enough
By Hyla Cass, M.D.
Wouldn’t it be nice if scientists decided that we all ought to be eating 200 times as much chocolate as we do? Or if the government admitted that we’ve been paying 200 times as much in taxes as we should? (The refund would help pay for all that chocolate. And by the way, doesn’t a tax refund make you feel great? Until you realize that it was your money to begin with.) It’s not often that we’re told that something we’ve been doing is off by a factor of 200. It gets your attention, doesn’t it?
Of course, how easily you’ll be able to handle a 200-fold change in something will depend on what that something is: whereas 200 times a large number is a huge number, 200 times a tiny number is still a small number. This article is about a tiny number—2.4 mcg (micrograms) per day—which is the FDA’s Recommended Dietary Allowance (RDA) for vitamin B12. That’s by far the smallest amount for any vitamin, because B12 is by far the most biologically active of all the vitamins.
Vitamin B12 is unique in other ways too: it has the largest and most complex molecular structure of any vitamin, and it’s the only vitamin to contain a metal ion (cobalt—which is why cobalt is an essential trace element). It was the last vitamin to be discovered (in 1948), but the possibility of other vitamins yet to be discovered cannot be ruled out. (For more on this odd vitamin, including why it should always be taken together with folic acid, see the first sidebar.)
Good Diet May Not Prevent B12 Deficiency
Except among vegetarians, dietary deficiency of vitamin B12 is rare in American adults, because the RDA of 2.4 mcg/day is easy to obtain through foods of animal origin. That fact, however, obscures a much more important one: physiological B12 deficiency—inadequate B12 in the circulation—is easy to come by as we grow older, regardless of our diet. That’s because B12 from food can become increasingly difficult for the body to absorb—most of it is eliminated as waste. As far back as 1986, Linus Pauling recommended that all adults take 100–200 mcg/day of B12, along with what came to be called “megadoses” of most other vitamins.1
The common symptoms of vitamin B12 deficiency are anemia, neuropathy (any disorder of the nervous system), and neuropsychiatric disorders, including cognitive decline or dementia;* there may also be glossitis (inflammation of the tongue). Anemia is any condition in which there is a deficiency of hemoglobin or red blood cells; there are dozens of causes. Its characteristic symptoms are pallor of the skin and mucous membranes, shortness of breath, heart palpitations, lethargy, and fatigue.
*For more on how vitamin B12 and folic acid may help prevent dementia, see “Fight Alzheimer’s and Heart Disease with B-Vitamins” (December 2001), “Folic Acid to the Rescue!” (September 2002), and “Add Brain Assault to Homocysteine’s Rap Sheet” (February 2006).
Although there are numerous causes of physiological B12 deficiency (including celiac disease, Crohn’s disease, tropical sprue, pancreatic insufficiency, alcoholism, AIDS, and chronic use of antacids), two conditions stand out as the most important: pernicious anemia and food-bound vitamin B12 malabsorption.2
Low levels of vitamin B12 are associated with pernicious anemia, a formerly fatal disease that is now treated with the vitamin. Thus it might appear that a dietary deficiency of B12 causes pernicious anemia—but diet has nothing to do with it. Pernicious anemia is a chronic, progressive, autoimmune disease that arises spontaneously in older adults. It causes a physiological B12 deficiency even if dietary intake is adequate by normal standards. This condition—the B12 deficiency and the anemia it causes—represents the end stage of the disease. The deficiency and anemia can take years to develop, because B12 is stored in the liver, and the average healthy adult liver holds enough of it to last for up to five years.*
*Pernicious anemia acquired its sinister name before the advent of vitamin B12 therapy. Now that it’s treatable in this way, the anemia is no longer considered “pernicious,” but the name has stuck. That may be appropriate, however, because of another, decidedly pernicious, factor: the underlying autoimmune disease causes neurological damage leading to mental illness, which often appears years before the symptoms of anemia do. Also, pernicious anemia is associated with a higher risk for bone fracture (see the sidebar below).
In pernicious anemia, the patient’s own antibodies gradually destroy glands in the stomach lining that produce the acid and digestive enzymes required for releasing B12from the proteins to which the vitamin is chemically bound in our food. And unless the B12 is freed from such “bondage,” it’s useless. The destruction of these glands also leads to decreased secretion of a protein called intrinsic factor, which is required for the next step in the process: absorption of the B12 by facilitating its active transport through the walls of the gut. If the vitamin cannot be absorbed, it will remain in the gastrointestinal (GI) tract and be eliminated as waste.
As the degenerative processes of pernicious anemia unfold in our GI tract, absorption of vitamin B12 declines—and so, therefore, does our production of hemoglobin (see the first sidebar). The result is anemia. Because the vitamin is so poorly absorbed, therapy with an oral B12 supplement must entail very large dosages in order for adequate amounts to get through to the circulation (the maximum absorbable amount in the presence of intrinsic factor is about 3 mcg per meal).
Even in the absence of intrinsic factor, about 1% of a given amount of oral B12 is absorbed by passive diffusion (as opposed to active transport) through the gut, so it would take 100 times the normal amount of B12 to get this amount through that way. (To bypass the GI tract, the vitamin can also be given by intramuscular injection, and it can be taken transmucosally in the form of liposomes.)
Food-bound vitamin B12 malabsorption
Here the disorder is different, but the result is similar. Food-bound vitamin B12malabsorption is thought to result mainly from atrophic gastritis, a chronic inflammation of the stomach lining that leads to the gradual loss (atrophy) of glands that produce digestive acid and enzymes. (Gastritis is strongly associated with infection by Helicobacter pylori, the bacterium that also causes peptic ulcers and stomach cancer.)
In this disorder, however, production of intrinsic factor is not impaired, so free (non-food-bound) vitamin B12, if it were present, could be absorbed. This is a key fact, because one can easily obtain free B12 in the form of supplements. Thus, people with food-bound vitamin B12 malabsorption don’t need increased amounts of B12—they just need their B12 in the form of a supplement rather than from food.2
How Much B12 Do We Need?
An important question is how much oral B12 should be prescribed for patients with a confirmed deficiency of this vitamin. A research group from the Netherlands, England, and Norway has addressed this question by seeking to determine the lowest dose of B12required to normalize certain biological markers for B12 deficiency.3 The primary marker they chose was methylmalonic acid (MMA), whose blood levels increase when B12levels decrease (see the first sidebar). The specific objective was to determine the lowest dose of B12 that would produce 80–90% of the estimated maximal reduction in MMA levels, which would indicate a satisfactory return to healthy B12 levels.
The researchers recruited 120 healthy, elderly Dutch adults (average age 80) who had mild B12 deficiency, as evidenced by B12 levels within a certain below-normal range and MMA levels above a certain value. Over a 16-week period, the volunteers were given vitamin B12 (cyanocobalamin) in a range of doses: 2.5, 100, 250, 500, and 1000 mcg daily. The 2.5-mcg dose represented the Dutch RDA, and the 1000-mcg (1-mg) dose represented the amount used for intramuscular injections (typically monthly) for B12-deficient patients. No adverse events were reported with any dosage.
The patients’ blood was tested at the outset and again at 8 weeks and 16 weeks; the results seen during the first 8 weeks remained stable for the next 8 weeks. The principal result was that the 500-mcg dose was the lowest dose required for the purpose described above; there was little additional benefit in using more than that. The authors summarized their work as follows:3
The results of this trial indicate that the lowest dose of oral cyanocobalamin required to normalize biochemical markers of mild vitamin B12 deficiency in older people with a mild vitamin B12 deficiency is more than 200 times greater than the recommended dietary allowance for vitamin B12 of approximately 3 mcg/day. Clinical trials are currently assessing the effects of high doses of oral cobalamin on markers of cognitive function and depression. If such trials can demonstrate that the reported associations of vitamin B12 deficiency with cognitive impairment or depression are causal and reversible by treatment, the relevance of correction of vitamin B12 deficiency in older people could be substantial. However, the present trial demonstrates that much higher doses of cyanocobalamin are required to normalize vitamin B12 deficiency than were previously believed.
As far as scientists know, the FDA’s RDA value of 2.4 mcg/day for vitamin B12 is appropriate—assuming your digestive tract is in perfect working order. But what if it’s not? You are getting older, aren’t you? The problem is that there may be a yawning gulf between ingesting 2.4 mcg and actually getting 2.4 mcg into your circulation, where it’s needed.
Thus, the older you get, the more likely it is that you will need to take far more B12 than the RDA to obtain this vitamin’s benefits. If you actually have a B12 deficiency (only a lab test can tell for sure), you may need to ingest at least 200 times the RDA: about 500 mcg or more. That’s 0.5 mg—still a very small amount, but getting up there. Now, about the RDA for
Dr. Hyla Cass is a nationally recognized expert in integrative medicine, an assistant clinical professor of psychiatry at the UCLA School of Medicine, and the author or coauthor of several popular books, including Natural Highs: Supplements, Nutrition, and Mind-Body Techniques to Help You Feel Good All the Time and 8 Weeks to Vibrant Health: A Woman’s Take-Charge Program to Correct Imbalances, Reclaim Energy, and Restore Well-Being.
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