B is for bones (B vitamins that is)
In last week’s article I wrote about two new studies in the May 2004, New England Journal of Medicine supporting the homocysteine theory of osteoporosis.
This is the theory that homocysteine, a common amino acid that is a by-product of protein metabolism, can cause osteoporosis. This theory grew out of the observation of the damage homocysteine can do in the genetic disease of homocystinuria, an inherited disorder in which homocysteine builds up to unusually high levels. Children with this disease often develop osteoporosis before the age of twenty.
Even small elevated amounts, however, can do damage. And the theory is that small elevated amounts over the course of decades can lead to osteoporosis later in life among people who do not have the genetic disease but for various reasons have elevated homocysteine levels.
Among the various reasons is a lack of one or more of three B vitamins: folic acid, B6, or B12.
Other Studies in Support of the Homocysteine Theory
Besides the two studies published this May in support of the theory, other studies have been done that corroborate their results.
The first of these was done in 1985 and published in the journal Metabolism. It raised the question – could homocysteine be implicated in the sharp rise in the risk of osteoporosis after menopause? This study, done in Sweden, found that fasting plasma homocysteine levels were significantly higher in normal postmenopausal women. The difference in homocysteine metabolizing capacity was shown to be even more pronounced after a methionine loading test, which measures the rise in plasma homocysteine after ingesting a meal high in methionine, an essential amino acid found in protein. After methionine loading, homocysteine concentrations in the postmenopausal women rose markedly and were considerably higher than in premenopausal women.
Folic Acid
Since folic acid is one of the vitamins involved in homocysteine metabolism, the authors investigated whether supplementing with folic acid would prevent the rise in plasma homocysteine fou7nd in postmenopausal women. Each group was supplemented with folic acid daily for four weeks. The result of the study was that in postmenopausal women folic acid therapy resulted in significant reduction in homocysteine levels both before methionine loading and after. The authors speculated that moderately elevated homocysteine levels might contribute to postmenopausal osteoporosis. They concluded that should such a connection prove to be the case, folic acid therapy might have a preventive effect.
Such a preventive effect of folic acid was suggested by a recent study of 161 postmenopausal women published in the Dec ember 2003 issue of Bone. The study showed a major association between folic acid and bone mineralization. Folic acid was lower in osteoporotic women than in normal women. Bone mineral density was lowest in women whose folic acid levels were the lowest. Bone mineral density was the highest in women whose folic acid levels were the highest.
Methotrexate is an anticancer drug that is also used to treat rheumatoid arthritis and psoriasis among other diseases. In 1998 a case study was done of a patient on methotrexate therapy for scleroderma. The patient developed four stress fractures within a period of 13 months. She was not on steroid therapy and had no risk factors for osteoporosis. The authors of the study reviewed the literature and found 13 cases of stress fractures in other patients under methotrexate therapy. The significance of this study for the effect of folic acid on bone health is that methotrexate interferes with folic acid absorption or function.
Vitamin B6
B6 also plays a role in homocysteine metabolism. Studies have been done showing a relationship between vitamin KB6 deficiency and osteoporosis. One such study done in 1972 and published in the journal Biochemical Medicine showed that rats receiving a B6 deficient diet developed osteoporosis.
Vitamin B12
A 1992 study on human subjects published in Clinical Science found a relationship between pernicious anemia and osteoporosis in 21 postmenopausal women wi th pernicious anemia. In the women with pernicious anemia, the bone mineral density of the lumbar spine was decrease by 16 percent compared to 24 normal postmenopausal women. Pernicious anemia is caused by B12 deficiency, and B12 is also a coenzyme in homocysteine metabolism.
Two more recent studies support the role of vitamin B12 in bone density. One appeared in the March 2003 issue of the Journal of Nutrition. In this study, osteoporosis occurred more often among women whose vitamin B12 status was considered marginal or deficient than in women with normal status. The authors concluded that vitamin B12 status is associated with bone health in elderly women.
A study done a year later in the March 2004 Journal of Clinical Endocrinology and Metabolism found the same association.
The purpose of the study was to test whether low serum vitamin B12 levels at or below 280 (the lowest category of serum B12 levels in which the women were grouped) had a greater annual loss in total hip bone mineral density compared to women with vitamin B12 levels above 280. They concluded that low serum vitamin KB12 levels are associated with increased rates of hip bone loss in older women.
Finally, a study published in The New England Journal of Medicine in 1988 found that sufficient availability of vitamin KB12 may be critical to osteopath activity and osteocalcin production, which are both involved in bone mineral building.
How To Protect Yourself
Folic acid is present in a wide variety of foods, but the most concentrated source is fresh vegetables, especially green leafy vegetables. Vitamin B6 is also widely concentrated in foods. But both of these vitamins are easily destroyed by processing and overcooking. Vitamin B12 is found only in foods of animal origin. Eating a well balanced diet of fresh, unprocessed foods, especially fresh fruits and vegetables, is the best way to get all of these vitamins.
However, in the case of a vitamin B12 deficiency, the cause is rarely a dietary deficiency. More than 95% of the cases of vitamin B12 deficiency seen in the United States are due to inadequate absorption of the vitamin. Although it is popular to inject vitamin B12 in the treatment of B12 deficiency, injections are not required, since the oral administration of an appropriate dosage has been shown to produce results as good as those of injectable preparations.
Vitamin B12 is necessary in only very small quantities. The RDA is 2 micrograms. However, in the treatment of vitamin B12 deficiency with oral preparation, the recommended dosage is a daily intake of 1,000 micrograms. Such large amounts are necessary because only one percent to a tenth of one percent will be absorbed.
Mary Lou Williams, M. Ed., is a lecturer and writer in the field of nutrition. She welcomes inquiries. She can be reached at (239) 267-6480.