{"title":"母乳喂养、遗传易感性和后代晚年2型糖尿病的关系。","authors":"Ying Hu, Hao Ma, Xuan Wang, Shuqi Zhu, Danqing Chen, Zhaoxia Liang","doi":"10.1002/oby.24344","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Our objective was to assess the prospective association between breastfeeding and the risk of type 2 diabetes (T2D) in offspring and to investigate the joint effects of breastfeeding and genetic susceptibility on T2D risk.</p><p><strong>Methods: </strong>We included 364,562 participants free from prevalent T2D from the UK Biobank. Cox proportional hazards models were employed to evaluate the association between breastfeeding and incident T2D.</p><p><strong>Results: </strong>Over a median follow-up of 12 years, 12,795 cases of incident T2D were recorded. Ever breastfeeding was associated with a significantly lower risk of T2D compared with never breastfeeding (hazard ratio = 0.94, 95% CI: 0.89-0.99). Additionally, significant interaction effects on T2D risk were observed between breastfeeding and T2D genetic risk score (T2D-GRS), both multiplicatively and additively. The association between T2D-GRS and risk of T2D was stronger in participants who were never breastfed compared with those who were breastfed (p for multiplicative interaction = 0.040). The risk of T2D associated with never breastfeeding combined with a high T2D-GRS was greater than the sum of the risks associated with each individual factor (p for additive interaction = 0.007).</p><p><strong>Conclusions: </strong>Breastfeeding is associated with a lower risk of incident T2D in offspring, showing both multiplicative and additive interactions with T2D-GRS.</p>","PeriodicalId":94163,"journal":{"name":"Obesity (Silver Spring, Md.)","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Breastfeeding, genetic susceptibility, and type 2 diabetes in offspring in later life.\",\"authors\":\"Ying Hu, Hao Ma, Xuan Wang, Shuqi Zhu, Danqing Chen, Zhaoxia Liang\",\"doi\":\"10.1002/oby.24344\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Our objective was to assess the prospective association between breastfeeding and the risk of type 2 diabetes (T2D) in offspring and to investigate the joint effects of breastfeeding and genetic susceptibility on T2D risk.</p><p><strong>Methods: </strong>We included 364,562 participants free from prevalent T2D from the UK Biobank. Cox proportional hazards models were employed to evaluate the association between breastfeeding and incident T2D.</p><p><strong>Results: </strong>Over a median follow-up of 12 years, 12,795 cases of incident T2D were recorded. Ever breastfeeding was associated with a significantly lower risk of T2D compared with never breastfeeding (hazard ratio = 0.94, 95% CI: 0.89-0.99). Additionally, significant interaction effects on T2D risk were observed between breastfeeding and T2D genetic risk score (T2D-GRS), both multiplicatively and additively. The association between T2D-GRS and risk of T2D was stronger in participants who were never breastfed compared with those who were breastfed (p for multiplicative interaction = 0.040). The risk of T2D associated with never breastfeeding combined with a high T2D-GRS was greater than the sum of the risks associated with each individual factor (p for additive interaction = 0.007).</p><p><strong>Conclusions: </strong>Breastfeeding is associated with a lower risk of incident T2D in offspring, showing both multiplicative and additive interactions with T2D-GRS.</p>\",\"PeriodicalId\":94163,\"journal\":{\"name\":\"Obesity (Silver Spring, Md.)\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-07-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Obesity (Silver Spring, Md.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/oby.24344\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Obesity (Silver Spring, Md.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/oby.24344","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Breastfeeding, genetic susceptibility, and type 2 diabetes in offspring in later life.
Objective: Our objective was to assess the prospective association between breastfeeding and the risk of type 2 diabetes (T2D) in offspring and to investigate the joint effects of breastfeeding and genetic susceptibility on T2D risk.
Methods: We included 364,562 participants free from prevalent T2D from the UK Biobank. Cox proportional hazards models were employed to evaluate the association between breastfeeding and incident T2D.
Results: Over a median follow-up of 12 years, 12,795 cases of incident T2D were recorded. Ever breastfeeding was associated with a significantly lower risk of T2D compared with never breastfeeding (hazard ratio = 0.94, 95% CI: 0.89-0.99). Additionally, significant interaction effects on T2D risk were observed between breastfeeding and T2D genetic risk score (T2D-GRS), both multiplicatively and additively. The association between T2D-GRS and risk of T2D was stronger in participants who were never breastfed compared with those who were breastfed (p for multiplicative interaction = 0.040). The risk of T2D associated with never breastfeeding combined with a high T2D-GRS was greater than the sum of the risks associated with each individual factor (p for additive interaction = 0.007).
Conclusions: Breastfeeding is associated with a lower risk of incident T2D in offspring, showing both multiplicative and additive interactions with T2D-GRS.
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