Dataset from Nutritional Intervention to Prevent Diabetes

Type 1 Diabetes (T1D) is an autoimmune disease. This means that the immune system (the part
of the body which helps fight infections) mistakenly attacks and destroys the cells that
produce insulin (islet cells found in the pancreas). As these cells are destroyed, the body's
ability to produce insulin decreases.

The autoimmune process is thought to be initiated by a gene-environment interaction. The
genetics involved in the development of T1D are fairly well understood. There is a higher
risk of developing T1D with the presence of the human leukocyte antigen (HLA) DR3 or DR4. It
is also known that not everyone with these genes actually develops T1D. Therefore, one or
more environmental factors are thought to contribute to the process of developing T1D.

The consumption of the anti-inflammatory fatty acids, the omega-3 fatty acids, has decreased
significantly in the past 100 years. At the same time a rise in the incidence of T1D,
especially in young children has occurred. Because of the warnings to eliminate fish during
pregnancy, pregnant women are consuming even less omega-3 fatty acids during fetal
development.

Observations have been made that children who have received omega-3 fatty acid
supplementation have a lower risk of T1D. Omega-3 fatty acids could have a protective effect
that may occur during pregnancy, infancy, or both. The mechanism of this protection may be
due to the DHA mediated suppression of the inflammatory response.

Patients at higher risk for T1D have an increased pro-inflammatory environment. We
hypothesize that DHA supplementation during pregnancy and early childhood will block the
initial pro-inflammatory events and prevent development of islet cell autoimmunity in
children at higher risk for T1D.

This study is a feasibility study to determine if a full-scale DHA supplementation study will
be implemented. If a full study is implemented, the primary outcome will be to determine if
nutritional supplementation with omega-3 fatty acids during the last trimester of a mother's
pregnancy and/or the first three years of life for children who are at higher risk of T1D
will prevent the development of islet autoimmunity.

1型糖尿病（Type 1 Diabetes, T1D）是一种自身免疫性疾病，即机体免疫系统——负责抵御感染的身体组分——会错误地攻击并破坏产生胰岛素的细胞（胰腺内的胰岛细胞）。随着这类细胞被破坏，机体合成胰岛素的能力逐渐下降。

目前认为，自身免疫过程由基因-环境交互作用触发。学界对T1D发病相关的遗传学机制已有较为充分的认知。携带人类白细胞抗原（human leukocyte antigen, HLA）DR3或DR4基因型的个体，罹患T1D的风险更高；但并非所有携带此类基因的人群都会发病，因此推测存在一种或多种环境因素参与了T1D的发病进程。

过去百年间，抗炎脂肪酸ω-3脂肪酸（omega-3 fatty acids）的摄入量出现显著下降。与此同时，T1D的发病率持续攀升，尤以幼儿群体为甚。由于孕期规避鱼类摄入的健康警示，孕妇在胎儿发育阶段摄入的ω-3脂肪酸进一步减少。

已有观察研究表明，补充ω-3脂肪酸的儿童罹患T1D的风险更低。ω-3脂肪酸或可在孕期、婴幼儿期或二者兼具的阶段发挥保护作用，其保护机制可能有赖于二十二碳六烯酸（DHA）介导的炎症反应抑制。

T1D高风险人群体内促炎环境水平升高。本研究提出假说：在孕期及幼儿早期补充DHA，可阻断初始促炎事件，从而预防T1D高风险儿童发生胰岛细胞自身免疫。

本研究为可行性研究，旨在评估是否可开展大规模DHA补充试验。若启动大规模研究，其主要结局指标为：针对T1D高风险儿童，在母亲妊娠晚期及/或儿童出生后的前三年通过膳食补充ω-3脂肪酸，能否预防其发生胰岛自身免疫。