The association between age of menopause and type 2 diabetes: a systematic review and meta-analysis.

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS
Mansoureh Yazdkhasti, Kyana Jafarabady, Arman Shafiee, Samira Parvizi Omran, Zohre Mahmoodi, Sara Esmaeilzadeh, Touran Bahrami Babaheidari, Kourosh Kabir, Maral Peisepar, Mahmood Bakhtiyari
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引用次数: 0

Abstract

Background: Type-2 diabetes mellitus (T2DM) is considered one of the chronic diseases that can have a relationship with age of menopause onset. Several studies have revealed that early menopause or late menopause can have a correlation with type-2 diabetes. This systematic review and meta-analysis aimed to investigate the association between the age of menopause onset and type-2 diabetes.

Methods and materials: PubMed, Web of Science, Scopus, Science Direct, Google Scholar, and Cochrane were searched for studies that have evaluated the relationship between T2DM and age of menopause onset. We pooled the effect sizes of the included studies using both adjusted odds ratios (OR) and hazard ratios (HR) of interest outcomes with their 95% confidence interval (CI).

Results: Nineteen papers were included in this study, 8 studies were cohorts, and 11 were cross sectional. Studies revealed a statistically significant association between early menopause age and increased odds of T2DM (OR = 1.24, 95% CI: 1.09-1.40; I2 = 67%; p = 0.001). Late menopause age was also associated with an increased odds of T2DM (OR = 1.14, 95% CI: 1.03-1.26; I2 = 56%; p = 0.01) compared to the reference group with normal menopausal age. As our secondary outcome, the hazard of developing T2DM in individuals with early or late menopausal age was assessed. Pooled analysis demonstrated a significantly higher hazard of T2DM among women with early menopause age (HR = 1.31, 95% CI: 1.05-1.64; I2 = 72%; p = 0.02). Late menopause age did not show a significant association (HR = 0.96, 95% CI: 0.84-1.10; I2 = 68%; p = 0.56).

Conclusion: Early and late menopause can both increase the risk of T2DM. Future research is needed to warrant the certainty of our findings.

绝经年龄与 2 型糖尿病之间的关系:系统回顾与荟萃分析。
背景:2型糖尿病(T2DM)被认为是与绝经年龄有关的慢性疾病之一。多项研究表明,绝经早或绝经晚与 2 型糖尿病有关。本系统综述和荟萃分析旨在研究绝经年龄与 2 型糖尿病之间的关系:我们在 PubMed、Web of Science、Scopus、Science Direct、Google Scholar 和 Cochrane 上搜索了评估 T2DM 与绝经年龄关系的研究。我们使用调整后的相关结果的几率比(OR)和危险比(HR)及其 95% 的置信区间(CI)对纳入研究的效应大小进行了汇总:本研究共纳入 19 篇论文,其中 8 篇为队列研究,11 篇为横断面研究。研究显示,绝经年龄过早与 T2DM 发生几率增加之间存在显著的统计学关联(OR = 1.24,95% CI:1.09-1.40;I2 = 67%;P = 0.001)。与绝经年龄正常的参照组相比,绝经年龄晚也与 T2DM 的几率增加有关(OR = 1.14,95% CI:1.03-1.26;I2 = 56%;P = 0.01)。作为次要结果,我们评估了绝经年龄过早或过晚的人患 T2DM 的风险。汇总分析表明,绝经年龄早的女性患 T2DM 的风险明显更高(HR = 1.31,95% CI:1.05-1.64;I2 = 72%;P = 0.02)。结论:绝经年龄晚的妇女与糖尿病的关系并不明显(HR = 0.96,95% CI:0.84-1.10;I2 = 68%;P = 0.56):结论:绝经早和绝经晚都会增加罹患 T2DM 的风险。结论:更年期过早和过晚都会增加 T2DM 的风险。
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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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