Koivusaari Katariina, Syrjälä Essi, Niinistö Sari, Takkinen Hanna-Mari, Ahonen Suvi, Åkerlund Mari, Korhonen Tuuli E, Toppari Jorma, Ilonen Jorma, Peltonen Jaakko, Nevalainen Jaakko, Knip Mikael, Alatossava Tapani, Veijola Riitta, Virtanen Suvi M
Department of Public Health Solutions, Finnish Institute for Health and Welfare, FI-00271Helsinki, Finland.
Department of Food and Nutrition, University of Helsinki, FI-00014Helsinki, Finland.
Br J Nutr. 2020 Jul 28;124(2):173-180. doi: 10.1017/S0007114520000744. Epub 2020 Feb 27.
Several prospective studies have shown an association between cows' milk consumption and the risk of islet autoimmunity and/or type 1 diabetes. We wanted to study whether processing of milk plays a role. A population-based birth cohort of 6081 children with HLA-DQB1-conferred risk to type 1 diabetes was followed until the age of 15 years. We included 5545 children in the analyses. Food records were completed at the ages of 3 and 6 months and 1, 2, 3, 4 and 6 years, and diabetes-associated autoantibodies were measured at 3-12-month intervals. For milk products in the food composition database, we used conventional and processing-based classifications. We analysed the data using a joint model for longitudinal and time-to-event data. By the age of 6 years, islet autoimmunity developed in 246 children. Consumption of all cows' milk products together (energy-adjusted hazard ratio 1·06; 95 % CI 1·02, 1·11; = 0·003), non-fermented milk products (1·06; 95 % CI 1·01, 1·10; = 0·011) and fermented milk products (1·35; 95 % CI 1·10, 1·67; = 0·005) was associated with an increased risk of islet autoimmunity. The early milk consumption was not associated with the risk beyond 6 years. We observed no clear differences based on milk homogenisation and heat treatment. Our results are consistent with the previous studies, which indicate that high milk consumption may cause islet autoimmunity in children at increased genetic risk. The study did not identify any specific type of milk processing that would clearly stand out as a sole risk factor apart from other milk products.
多项前瞻性研究表明，食用牛奶与胰岛自身免疫和/或1型糖尿病风险之间存在关联。我们想研究牛奶加工过程是否起作用。对一个基于人群的出生队列进行了研究，该队列中有6081名携带HLA - DQB1基因、有1型糖尿病风险的儿童，随访至15岁。我们将5545名儿童纳入分析。在3个月、6个月、1岁（12个月）、2岁、3岁、4岁和6岁时完成食物记录，并每隔3 - 12个月测量一次与糖尿病相关的自身抗体。对于食物成分数据库中的奶制品，我们采用了传统分类和基于加工方式的分类。我们使用纵向数据和事件发生时间数据的联合模型对数据进行分析。到6岁时，246名儿童出现了胰岛自身免疫。食用所有奶制品（能量调整后的风险比1.06；95%置信区间1.02，1.11；P = 0.003）、非发酵奶制品（1.06；95%置信区间1.01，1.10；P = 0.011）和发酵奶制品（1.35；95%置信区间1.10，1.67；P = 0.005）均与胰岛自身免疫风险增加有关。早期食用牛奶与6岁以后的风险无关。我们没有观察到基于牛奶均质化和热处理的明显差异。我们的结果与之前的研究一致，即高牛奶摄入量可能会使遗传风险增加的儿童出现胰岛自身免疫。该研究未发现任何一种特定的牛奶加工方式能明显区别于其他奶制品而成为唯一的风险因素。
