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B is for bones (B vitamins that is)

May 25, 2011
By Mary Lou Williams, M. Ed.

In last week's article I wrote about two 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 in May 2004 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 found 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 study of 161 postmenopausal women published in the December 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.

Next week's article will be on the relationship of B6 and B12 to osteoporosis.

Mary Lou Williams, M. Ed., is a writer and lecturer in the field of nutrition. She welcomes inquiries. She can be reached at 267-6480.



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