Nutrition Division, School of Biological and Population Health Sciences, Oregon State University, Corvallis, OR 97331, USA.
Menopause. 2012 Sep;19(9):974-9. doi: 10.1097/gme.0b013e31824ac071.
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.
流行病学研究表明,绝经后妇女的骨量与适量饮酒有关。然而,酒精对骨骼的潜在有益作用的潜在细胞机制尚不清楚。骨转换过度,加上骨吸收超过骨形成的不平衡,是绝经后骨丢失的主要原因。本研究旨在探讨适量饮酒是否能减轻绝经后骨转换的假说。
对 40 名健康绝经后妇女(平均年龄 ± SE 为 56.3 ± 0.5 岁)进行双能 X 线吸收法测定骨密度,这些妇女每天饮酒 19 ± 1 克。在基线(第 0 天)和酒精戒断 14 天后,通过免疫测定法测定骨形成标志物骨钙素和骨吸收标志物 C 端肽(CTX)的血清水平。然后,参与者饮酒,并在第二天早上进行测定。
转子间和全髋骨密度与饮酒量呈正相关。血清骨钙素和 CTx 在戒断后增加(分别为 4.1 ± 1.6%,P = 0.01 和 5.8 ± 2.6%,P = 0.02,与基线相比)。与前一天相比,重新饮酒后骨钙素和 CTx 降低(分别为-3.4 ± 1.4%,P = 0.01 和-3.5 ± 2.1%,P = 0.05),与基线值无差异(P > 0.05)。
酒精戒断会导致骨转换标志物增加,而恢复饮酒则会降低骨转换标志物。这些结果表明,绝经后适量饮酒者骨密度增加的细胞机制可能是酒精对骨转换的抑制作用减弱了与绝经相关的骨转换过度对骨骼的不利影响。