Red meat intake during pregnancy and childhood and risk of type 1 diabetes: findings from the ABIS birth cohort

Aims/hypothesis The role of red meat in type 1 diabetes risk remains unclear. We examined whether maternal and early-life red meat intake is associated with the development of type 1 diabetes and whether such associations are modified by genetic susceptibility. Methods We analysed data from 15,717 children participating in the All Babies In Southeast Sweden (ABIS) cohort, followed for type 1 diabetes diagnosis via national registers until the age of 24–26 years. Dietary intake was assessed through food frequency questionnaires during pregnancy and at ages 1, 2.5 and 5 years. Cox models estimated adjusted HRs and 95% CIs for type 1 diabetes in relation to red meat, including beef, pork and sausage, analysed as high vs low intake frequency and per serving/week. Analyses were stratified by HLA risk genotype and family history of type 1 diabetes. Results Frequency of red meat intake during pregnancy or at age 1 was not associated with type 1 diabetes risk. The corresponding HRs per serving/week were 0.98 (95% CI 0.90, 1.07) and 0.98 (95% CI 0.88, 1.08), respectively. In type-specific analyses, higher frequency of beef intake at age 5 was associated with an increased risk of type 1 diabetes (HR 1.29 [95% CI 1.05, 1.58]), with a similar tendency for exposure at age 2.5 (HR 1.12 [95% CI 0.93, 1.36]). The association at age 5 was evident among children with high-risk HLA genotypes (HR 1.40 [95% CI 1.11, 1.78]) or a family history of type 1 diabetes (HR 1.56 [95% CI 1.08, 2.26]). In contrast, no statistically significant association was observed among children with low-risk HLA genotypes (HR 0.34 [95% CI 0.10, 1.19]) or without a family history of type 1 diabetes (HR 1.20 [95% CI 0.92, 1.56]). No associations were found for higher frequency of beef consumption during pregnancy or at age 1, nor for pork and sausage at any age. Conclusions/interpretation Childhood beef consumption may contribute to type 1 diabetes development in genetically at-risk individuals. Further research is needed to confirm this finding and clarify underlying mechanisms.