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1 From the University of Nebraska Medical Center, Omaha.
See corresponding article on page 1206.
Osteoporosis, the most common type of metabolic bone disease, affects 20 million Americans and leads to 1.3 million fractures/y, including 250000 hip fractures. During the course of their lifetime, 30% of all postmenopausal women eventually sustain osteoporotic fractures; by extreme old age, one-third of all women have a hip fracture (1). Up to 80% of patients with osteoporosis receive no diagnosis and, because no effective therapy is available, the importance of prophylactic therapy and risk factor reduction cannot be emphasized enough.
The relation between alcohol use and osteoporotic bone disease was first reported in 1965 by Saville (2). Like osteoporosis, alcohol use in elderly women is underdiagnosed, but these conditions are not mutually exclusive. Alcohol was shown to have direct effects on bone cells by decreasing osteoblast number, osteoid formation, and osteoblast proliferation as well as indirect effects through its action on mineral regulatory hormones (3). However, there have been conflicting results regarding the relation between alcohol consumption and bone metabolism. Recently, an increase in bone mineral density (BMD) was reported in elderly women with moderate alcohol consumption (4). To the relatively uninitiated, this appears to fly in the face of conventional wisdom, but further proof supporting this relation has now been provided by Rapuri et al (5).
In this issue of the Journal, Rapuri et al (5) present intriguing data on the effects of moderate alcohol consumption on bone metabolism in elderly women. In a well-conceived cross-sectional study, an approximation of alcohol consumption was obtained by a self-administered questionnaire from elderly women (65–77 y) recruited for a multicenter osteoporotic study. The women were divided into 2 groups, drinkers and nondrinkers; the drinkers were further subdivided into 5 categories based on weekly alcohol consumption. Serum and urine indexes, calciotropic hormones, calcium absorption, and BMDs were determined for all subjects. Interestingly, 18% of both alcohol drinkers and nondrinkers had used estrogen for >1 y, but the distribution of use was not significantly different between the various categories of alcohol intake.
After adjustment for significantly correlated covariates (smoking, estrogen use, and diet), the most important finding of this study was a significant positive effect of moderate alcohol consumption on BMD. This effect was observed with an alcohol intake >28.6 but 57.2 g/wk, an intake lower than reported in previous studies (6). A notable aspect of this study was an attempt to explain the mechanism of alcohol's effects on bone metabolism. Moderate alcohol consumption was shown to decrease bone remodeling, as evidenced by a reduction in bone resorption markers (serum osteocalcin and parathyroid hormone and urinary N-telopeptides). After adjustment for age at menopause, a further explanation for the increase in BMD was elevated serum calcitonin and estrogen concentrations, which were stimulated by alcohol.
In summary, Rapuri et al not only showed elegantly that moderate alcohol consumption has positive effects on BMD in elderly women, but also provided evidence that these effects are mediated, at least in part, by a decrease in bone remodeling. However, we remain unable to explain why only moderate doses of alcohol have been shown to have a significant positive effect on bone density. This article should encourage further investigations of the pathogenesis of alcohol-related bone injury; until then it would be premature to recommend alcohol use in the prevention of osteoporotic bone disease.
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