饮食来源的抗氧化剂与骨质疏松症：一项孟德尔随机化研究。
Diet-derived antioxidants and osteoporosis: A Mendelian randomization study.
机构信息
Department of Orthopeadics, The China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.
Department of Hepatobiliary and Pancreatic Surgery, General Surgery Center, The First Affiliated Hospital of Jilin University, Changchun, Jilin, China.
出版信息
PLoS One. 2023 Nov 29;18(11):e0293145. doi: 10.1371/journal.pone.0293145. eCollection 2023.
BACKGROUND
Antioxidants can prevent osteoporosis, but the association between serum antioxidants and the cause of osteoporosis remains unknown. We aimed to utilize Mendelian randomization (MR) to determine whether genetically predicted serum levels of diet-derived antioxidants can affect the risk of osteoporosis, to determine the effect of dietary supplementation of antioxidants.
METHODS
Genetic variants associated with diet-derived antioxidants were selected from the genome-wide association studies. A total of 12,946 osteoporosis cases and 506,624 healthy controls were obtained from UK Biobank (UKB) and Genetic Factors of Osteoporosis (GEFOS) consortia. We implemented a two-sample MR design and performed several sensitivity analyses to evaluate the causal relationship.
RESULTS
In UKB, the genetically predicted higher β-carotene (OR = 0.863, p = 7.37 × 10-6, power = 100%) and γ-tocopherol (OR = 0.701, p = 0.021, power = 5%) had an inverse relationship with osteoporosis. However, only the association of serum β-carotene passed FDR correction. In GEFOS, there were no significant diet-derived antioxidants. The direction of the association of β-carotene with osteoporosis (OR = 0.844, p = 0.106, power = 87%) was consistent with that in the UKB dataset. A fixed-effects meta-analysis confirmed that β-carotene (OR = 0.862, p = 2.21 × 10-6) and γ-tocopherol (OR = 0.701, p = 2.31 × 10-2) could decrease the risk of osteoporosis. To reduce exclusion limit bias, we used total body bone mineral density, lumbar spine bone mineral density and femoral neck bone mineral density as surrogates and found that the genetically elevated circulating β-carotene level could increase total body BMD (beta = 0.043, p-value = 8.26 x 10-5, power = 100%), lumbar spine BMD (beta = 0.226, p-value = 0.001, power = 100%) and femoral neck BMD(beta = 0.118, p-value = 0.016, power = 100%).
CONCLUSIONS
We observed that genetically predicted serum β-carotene could elevate BMD and prevent osteoporosis.
背景
抗氧化剂可以预防骨质疏松症，但血清抗氧化剂与骨质疏松症病因之间的关系尚不清楚。我们旨在利用孟德尔随机化（MR）来确定遗传预测的血清饮食源性抗氧化剂水平是否会影响骨质疏松症的风险，以确定抗氧化剂饮食补充的效果。
方法
从全基因组关联研究中选择与饮食相关的抗氧化剂相关的遗传变异。从英国生物库（UKB）和骨质疏松症遗传因素（GEFOS）联盟中获得了 12946 例骨质疏松症病例和 506624 例健康对照。我们实施了两样本 MR 设计，并进行了几项敏感性分析来评估因果关系。
结果
在 UKB 中，遗传预测的较高β-胡萝卜素（OR=0.863，p=7.37×10-6，功率=100%）和γ-生育酚（OR=0.701，p=0.021，功率=5%）与骨质疏松症呈负相关。然而，只有血清β-胡萝卜素的关联通过 FDR 校正。在 GEFOS 中，没有发现明显的饮食来源的抗氧化剂。β-胡萝卜素与骨质疏松症的关联方向（OR=0.844，p=0.106，功率=87%）与 UKB 数据集一致。固定效应荟萃分析证实β-胡萝卜素（OR=0.862，p=2.21×10-6）和γ-生育酚（OR=0.701，p=2.31×10-2）可以降低骨质疏松症的风险。为了减少排除限制偏差，我们使用全身骨矿物质密度、腰椎骨矿物质密度和股骨颈骨矿物质密度作为替代物，发现循环β-胡萝卜素水平升高可增加全身 BMD（beta=0.043，p 值=8.26 x 10-5，功率=100%）、腰椎 BMD（beta=0.226，p 值=0.001，功率=100%）和股骨颈 BMD（beta=0.118，p 值=0.016，功率=100%）。
结论
我们观察到，遗传预测的血清β-胡萝卜素可以升高 BMD 并预防骨质疏松症。
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