Calcium intake and risk of fracture: systematic review.
Calcium intake and risk of fracture: systematic review.
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DOI：
10.1136/bmj.h4580
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发表时间：
2015-09-29
期刊：
影响因子：
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通讯作者：
Reid IR
中科院分区：
文献类型：
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作者：
Bolland MJ;Leung W;Tai V;Bastin S;Gamble GD;Grey A;Reid IR
目的 研究支持通过膳食来源或钙补充剂增加钙摄入量以预防骨折的建议的证据。设计 对以骨折为终点的钙摄入量的随机对照试验和观察性研究进行系统评价。将试验结果与随机效应荟萃分析进行汇总。数据来源 Ovid Medline、Embase、PubMed 以及相关系统评价的参考文献。初步检索于 2013 年 7 月进行，并于 2014 年 9 月更新。 选择研究的资格标准 以骨折为结果的膳食钙、牛奶或乳制品摄入量或钙补充剂（含或不含维生素 D）的随机对照试验或队列研究，参与者年龄 > 50 岁。结果 只有两项合格的膳食钙来源随机对照试验 (n=262)，但 44 项队列研究中有 50 份报告涉及膳食钙 (n=37)、牛奶 (n=14) 或乳制品摄入量 (n=8) 与骨折结果之间的关系。对于膳食钙，大多数研究报告钙摄入量与骨折之间没有关联（总钙摄入量为 14/22，髋部骨折为 17/21，脊椎骨折为 7/8，前臂骨折为 5/7）。对于牛奶（25/28）和乳制品摄入量（11/13），大多数研究也报告没有关联。在 26 项随机对照试验中，钙补充剂可降低完全骨折的风险（20 项研究，n=58 573；相对风险 0.89，95% 置信区间 0.81 至 0.96）和脊椎骨折（12 项研究，n=48 967。0.86，0.74 至 1.00），但不能降低髋部骨折（13 项研究， n=56 648；0.95、0.76 至 1.18）或前臂骨折（八项研究，n=51 775；0.96、0.85 至 1.09）。漏斗图检查和艾格回归表明已发表的数据对钙补充剂存在偏见。在偏倚风险最低的随机对照试验中（四项研究，n=44 505），对任何部位的骨折风险都没有影响。钙单一疗法以及钙和维生素 D 联合治疗的试验结果相似。只有一项针对住院护理中体弱老年女性、膳食钙摄入量和维生素 D 浓度较低的试验显示，骨折风险显着降低。结论 膳食钙摄入量与骨折风险无关，并且没有临床试验证据表明增加膳食来源的钙摄入量可以预防骨折。钙补充剂预防骨折的证据薄弱且不一致。
Objective To examine the evidence underpinning recommendations to increase calcium intake through dietary sources or calcium supplements to prevent fractures. Design Systematic review of randomised controlled trials and observational studies of calcium intake with fracture as an endpoint. Results from trials were pooled with random effects meta-analyses. Data sources Ovid Medline, Embase, PubMed, and references from relevant systematic reviews. Initial searches undertaken in July 2013 and updated in September 2014. Eligibility criteria for selecting studies Randomised controlled trials or cohort studies of dietary calcium, milk or dairy intake, or calcium supplements (with or without vitamin D) with fracture as an outcome and participants aged >50. Results There were only two eligible randomised controlled trials of dietary sources of calcium (n=262), but 50 reports from 44 cohort studies of relations between dietary calcium (n=37), milk (n=14), or dairy intake (n=8) and fracture outcomes. For dietary calcium, most studies reported no association between calcium intake and fracture (14/22 for total, 17/21 for hip, 7/8 for vertebral, and 5/7 for forearm fracture). For milk (25/28) and dairy intake (11/13), most studies also reported no associations. In 26 randomised controlled trials, calcium supplements reduced the risk of total fracture (20 studies, n=58 573; relative risk 0.89, 95% confidence interval 0.81 to 0.96) and vertebral fracture (12 studies, n=48 967. 0.86, 0.74 to 1.00) but not hip (13 studies, n=56 648; 0.95, 0.76 to 1.18) or forearm fracture (eight studies, n=51 775; 0.96, 0.85 to 1.09). Funnel plot inspection and Egger’s regression suggested bias toward calcium supplements in the published data. In randomised controlled trials at lowest risk of bias (four studies, n=44 505), there was no effect on risk of fracture at any site. Results were similar for trials of calcium monotherapy and co-administered calcium and vitamin D. Only one trial in frail elderly women in residential care with low dietary calcium intake and vitamin D concentrations showed significant reductions in risk of fracture. Conclusions Dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures. Evidence that calcium supplements prevent fractures is weak and inconsistent.