Type 1 diabetes mellitus is an autoimmune disease that is characterized by the destruction of insulin-producing beta cells in the pancreatic islets. Although it is not yet known what initiates the autoimmune process, it is likely that both genetic background and environmental factors contribute to the disease process. Dietary factors have been implicated in the etiology of type 1 diabetes as well as in initiating the autoimmune process that leads to clinical disease. A case-control study from Norway¹ reported that children with diabetes were less likely to have been given cod liver oil during infancy than children without diabetes. Given that cod liver oil contains both vitamin D and the marine omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), it was not clear whether the protective factor in cod liver oil was the vitamin D, the marine fatty acids, or both. Although 2 studies reported that children with diabetes were less likely to have taken vitamin D supplements in infancy than children without diabetes,^2,3 similar investigations focusing on the intake of marine omega-3 fatty acids have not been conducted to resolve this important question.

Type 1 diabetes mellitus (T1DM) is increasing worldwide, with the most rapid increase among children younger than 5 years of age.^1-6 Perinatal factors, such as birth delivery type, birth weight, infant growth, neonatal jaundice, and maternal age have been associated with T1DM and islet autoimmunity (IA), the preclinical stage of T1DM.^7-15

Background Cow's milk intake has been inconsistently associated with islet autoimmunity (IA) and type 1 diabetes (T1D) development. Genetic and environmental factors may modify the effect of cow's milk on IA and T1D risk. Methods The Diabetes Autoimmunity Study in the Young (DAISY) follows children at increased T1D risk of IA (presence of autoantibodies to insulin, GAD65, or IA‐2 twice in succession) and T1D development. We examined 1835 DAISY children with data on cow's milk intake: 143 developed IA, 40 subsequently developed T1D. Cow's milk protein and lactose intake were calculated from prospectively collected parent‐ and self‐reported food frequency questionnaires (FFQ). High risk HLA‐DR genotype: HLA‐DR3/4,DQB1*0302; low/moderate risk: all other genotypes. We examined interactions between cow's milk intake, age at cow's milk introduction, and HLA‐DR genotype in IA and T1D development. Interaction models contained the base terms (e.g., cow's milk protein and HLA‐DR genotype) and an interaction term (e.g., cow's milk protein*HLA‐DR genotype). Results In survival models adjusted for total calories, FFQ type, T1D family history, and ethnicity, greater cow's milk protein intake was associated with increased IA risk in children with low/moderate risk HLA‐DR genotypes [hazard ratio (HR): 1.41, 95% confidence interval (CI): 1.08–1.84], but not in children with high risk HLA‐DR genotypes. Cow's milk protein intake was associated with progression to T1D (HR: 1.59, CI: 1.13–2.25) in children with IA. Conclusions Greater cow's milk intake may increase risk of IA and progression to T1D. Early in the T1D disease process, cow's milk intake may be more influential in children with low/moderate genetic T1D risk.