Epidemiological studies indicate that higher bone mass is associated with moderate alcohol consumption in postmenopausal women. However, the underlying cellular mechanisms responsible for the putative beneficial effects of alcohol on bone are unknown. Excessive bone turnover, combined with an imbalance whereby bone resorption exceeds bone formation, is the principal cause of postmenopausal bone loss. This study investigated the hypothesis that moderate alcohol intake attenuates bone turnover after menopause.
Bone mineral density was determined by dual-energy x-ray absorptiometry in 40 healthy postmenopausal women (mean ± SE age, 56.3 ± 0.5 y) who consumed alcohol at 19 ± 1 g/day. Serum levels of the bone formation marker osteocalcin and the resorption marker C-terminal telopeptide (CTx) were measured by immunoassay at baseline (day 0) and after alcohol withdrawal for 14 days. Participants then consumed alcohol and were assayed on the following morning.
Bone mineral density at the trochanter and total hip were positively correlated to the level of alcohol consumption. Serum osteocalcin and CTx increased after abstinence (4.1 ± 1.6%, P = 0.01 and 5.8 ± 2.6%, P = 0.02 compared with baseline, respectively). Osteocalcin and CTx decreased after alcohol readministration, compared with the previous day (−3.4 ± 1.4%, P = 0.01 and −3.5 ± 2.1%, P = 0.05, respectively), to values that did not differ from baseline (P > 0.05).
Abstinence from alcohol results in increased markers of bone turnover, whereas resumption of alcohol reduces bone turnover markers. These results suggest a cellular mechanism for the increased bone density observed in postmenopausal moderate alcohol consumers. Specifically, the inhibitory effect of alcohol on bone turnover attenuates the detrimental skeletal consequences of excessive bone turnover associated with menopause.
From the 1Nutrition Division, 2Exercise Sciences Division, and 3Biostatistics Division, School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR; and 4Maine Medical Center Research Institute, Scarborough, ME.
Received November 4, 2011; revised and accepted January 11, 2012.
Funding/support: This work was supported by National Institutes of Health grant AA011140 and by the John C. Erkkila, MD, Endowment for Health and Human Performance.
Financial disclosure/conflicts of interest: None reported.
Jill A. Marrone and Gianni F. Maddalozzo contributed equally to this work.
Address correspondence to: Urszula T. Iwaniec, PhD, 108 Milam Hall, Oregon State University, Corvallis, OR 97331. E-mail: firstname.lastname@example.org