Abstract and Introduction
Abstract
Objective: 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.
Methods: 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.
Results: 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).
Conclusions: 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.
Introduction
Postmenopausal women comprise 80% of patients with osteoporosis. Postmenopausal bone loss occurs because of elevated and unbalanced bone turnover, in which bone resorption predominates over bone formation. Although osteoporosis is characterized by low bone mass and deterioration of bone microarchitecture, the elevated turnover after menopause is an independent risk factor for osteoporotic bone fractures.
Pharmacological interventions that reduce bone turnover are commonly used for the treatment of postmenopausal bone loss. However, high cost and the significant potential for adverse effects contraindicate universal preventive drug therapy. It is therefore important to identify modifiable lifestyle factors that influence the risk of osteoporosis.
Alcohol consumption is a lifestyle factor that has context-dependent effects on the skeleton. Chronic alcohol abuse is associated with reductions in bone mineral density (BMD), osteoblast number, and osteoblast function. In contrast, moderate alcohol intake (0.5-2 standard drinks/d) is associated with increased BMD. It is uncertain, however, whether the difference in BMD in moderate alcohol consumers is caused by alcohol intake or potential confounding variables.
Carefully controlled animal studies suggest that moderate alcohol consumption decreases bone turnover while maintaining the balance between bone formation and bone resorption. The purpose of the present study was to assess the effects of regular moderate alcohol consumption on bone turnover in healthy early postmenopausal women. An intervention trial conducted for a 15-day period evaluated the effects of alcohol withdrawal and readministration on biochemical markers of bone formation and bone resorption. The working hypothesis was that alcohol withdrawal would result in increased bone turnover markers and that subsequent return to normal alcohol consumption would decrease the turnover markers.