Skeletal response to alcohol.

This review briefly assesses the well-established effects of alcohol consumption on bone and mineral metabolism and addresses areas of controversy that need additional research. Alcohol consumption is a risk factor for osteoporosis based on the frequent finding of a low bone mass, decreased bone formation rate, and increased fracture incidence in alcoholics. Alcohol also has been shown to reduce bone formation in healthy humans and animals and to decrease proliferation of cultured osteoblastic cells. On the other hand, it has been difficult to demonstrate alcohol-induced bone loss and increased fracture rate in population-based studies. Indeed, most population-based studies have shown a positive association between alcohol and bone mass and no change or a decrease in fracture risk. Overall, the evidence generally supports a detrimental effect of chronic alcohol abuse on the skeleton of men and a neutral or generally beneficial effect of light to moderate alcohol consumption, especially in older women. This latter putative beneficial effect may be due to a reduction in the age-related increase in bone remodeling associated with postmenopausal bone loss. Specific areas of research are recommended to clarify the dose and sex effects of alcohol consumption and to determine cellular and molecular mechanisms of action. The goals of this proposed research emphasis are to determine the degree of risk for the range of alcohol consumption, to set guidelines of consumption compatible with maintaining bone health, and to develop appropriate countermeasures to prevent or reverse the detrimental skeletal effects of alcohol abuse.