Our analysis demonstrates a J-shaped relationship between alcohol consumption and hip fracture risk, with persons consuming up to 1 drink per day having the lowest risk of hip fracture. In contrast, most data on alcohol consumption and bone density suggest a linear association between greater alcohol consumption and both higher bone density and lower bone density loss over time. Studies evaluating hip fracture risk included subjects with greater alcohol consumption than studies evaluating bone density, which may explain why the association between alcohol consumption and hip fracture was J-shaped rather than linear. Because studies of alcohol consumption and bone density included few heavier drinkers, current evidence is insufficient to determine a precise amount of alcohol consumption that is associated with higher bone density.
Compared with abstainers, moderate drinkers had lower hip fracture risk and heavier drinkers had higher hip fracture risk. However, important biases may have influenced these results. It is likely that falls contributed to the observed increase in hip fracture risk among heavier drinkers. Further, most categories of nondrinkers included both lifetime abstainers and former drinkers. If former drinkers stopped for health reasons, this may partially explain the higher hip fracture risk among nondrinkers.
In contrast with the J-shaped association between alcohol consumption and hip fracture risk, pooled data suggest a linear relationship between alcohol consumption and bone density. These data were derived from studies mainly of individuals consuming less than 2 drinks per day. Because these studies may have been underpowered to demonstrate changes in bone density at greater alcohol consumption levels, the observed linear association may not fully describe this relationship. In addition, the increase in bone density associated with each additional drink per day was small in magnitude and of uncertain clinical significance.
The exact mechanism by which alcohol influences bone density is not clear. Putative biological mechanisms for a beneficial effect of alcohol on bone density include increases in the concentration of serum estradiol57,58
and liver estrogen receptors.59
However, as has been suggested regarding other beneficial effects of moderate alcohol consumption, the observed benefit may reflect confounding by unmeasured healthy behaviors.60,61
An important limitation of the existing literature, and the reason most studies were rated “fair,” is that few studies sufficiently adjusted for major potential confounders, and none included markers of socioeconomic status. Although our finding that alcohol consumption augments the benefits of estrogen therapy is based on a small number of studies, it is consistent with research suggesting that alcohol ingestion leads to elevations in circulating estradiol levels in women taking estrogen replacement therapy.62-64
Because of this association, studies that did not control for estrogen exposure may be particularly vulnerable to bias.
Most studies of bone density loss in women demonstrated an inverse linear relationship between alcohol consumption and bone density loss over time, whereas most studies in men reported a J-shaped relationship. Although sex differences in the effect of alcohol consumption on bone density have been suggested,65
observed differences might be explained by differences in alcohol exposure. Studies of bone density loss over time frequently combined moderate and heavy drinkers in a single category, making the greatest drinking category heterogeneous. For example, if the population of women categorized as consuming more than 1.4 drinks per day consumed less alcohol than men in the same drinking category, data from men and women would suggest different patterns of association between alcohol consumption and bone density due partly to misclassification. Further research is needed to characterize sex differences in the effect of alcohol on bone density loss over time.
Data from experimental studies indicate that osteocalcin increases after abstinence and decreases after alcohol administration. These results suggest a reversible suppression of bone formation when administered rapidly or in large doses, and are consistent with prior research.66,67
The effect of long-term alcohol consumption on bone remodeling likely involves a complex uncoupling of formation and resorption.68
Heavy alcohol consumption may have a direct acute negative effect on osteoblasts, but positive effects of alcohol on bone density may be due to indirect long-term hormonal effects.69
The precise effects of moderate alcohol consumption on bone metabolism are still unknown.
A key limitation of many original studies in this review was the method and timing of alcohol consumption measurement, a weakness that has been noted by other reviews and meta-analyses of alcohol consumption.29,70,71
Studies that measured alcohol consumption only at baseline are vulnerable to misclassification if exposure to alcohol changed before the outcome was measured. In addition, collecting data on alcohol consumption by self-report using simple surveys may lead to underreporting, particularly among heavy drinkers.72,73
Despite this potential reporting bias, the rank order of alcohol consumption reported by individual studies is unlikely to be affected.
Because most included studies were observational, these results must be interpreted with caution. Although many benefits, including decreased mortality,74
have been attributed to moderate alcohol consumption, the appropriateness of using nondrinkers as a reference group has been questioned.75,76
To expand our understanding of the effects of alcohol on bone density, rigorous prospective studies are needed that carefully measure potential confounders. Because bone density reflects the cumulative effects of numerous factors on bone metabolism over long periods of time, future studies should adjust for baseline bone density.