title: Fatty fish consumption and risk of latent autoimmune diabetes in adults.
abstract: OBJECTIVE
  It has been suggested that intake of fatty fish may protect against both type 1 and type 2 diabetes. Hypotheses rest on the high marine omega-3 fatty acid eicosapentaenoic acid+docosahexaenoic acid (EPA+DHA) and vitamin D contents, with possible beneficial effects on immune function and glucose metabolism. Our aim was to investigate, for the first time, fatty fish consumption in relation to the risk of latent autoimmune diabetes in adults (LADA).
  
  
  METHODS
  Analyses were based on data from a Swedish case-control study with incident cases of LADA (n=89) and type 2 diabetes (n=462) and randomly selected diabetes-free controls (n=1007). Diabetes classification was based on the onset of age (⩾35), glutamic acid decarboxylase autoantibodies, and C-peptide. A validated food frequency questionnaire was used to derive information on previous intake of fish, polyunsaturated long-chain omega-3 fatty acids (n-3 PUFA) and supplementation of fish oil and vitamin D. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using logistic regression, adjusted for age, gender, body mass index (BMI), family history of diabetes, physical activity, smoking, education, and consumption of alcohol, fruit, vegetables and red meat.
  
  
  RESULTS
  Weekly fatty fish consumption (⩾1 vs <1 serving per week), was associated with a reduced risk of LADA but not type 2 diabetes (OR 0.51, 95% CI 0.30-0.87, and 1.01, 95% CI 0.74-1.39, respectively). Similar associations were seen for estimated intake of n-3 PUFA (⩾0.3 g per day; LADA: OR 0.60, 95% CI 0.35-1.03, type 2 diabetes: OR 1.14, 95% CI 0.79-1.58) and fish oil supplementation (LADA: OR 0.47, 95% CI 0.19-1.12, type 2 diabetes: OR 1.58, 95% CI 1.08-2.31).
  
  
  CONCLUSIONS
  Our findings suggest that fatty fish consumption may reduce the risk of LADA, possibly through effects of marine-originated omega-3 fatty acids.
authors.affiliation: Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: J E
authors.initials: JE
authors.lastname: Löfvenborg
authors.affiliation: 1] Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden [2] Center for Occupational and Environmental Medicine, Stockholm County Council, Stockholm, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Andersson
authors.affiliation: Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: P-O
authors.initials: PO
authors.lastname: Carlsson
authors.affiliation: Department of Clinical Sciences, Lund University, Malmö, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Dorkhan
authors.affiliation: Department of Clinical Sciences, Lund University, Malmö, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Groop
authors.affiliation: Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Martinell
authors.affiliation: Division of Endocrinology, Department of Medicine, Helsinki University Central Hospital; Research Program for Diabetes and Obesity, University of Helsinki and Folkhalsan Research Center, Helsinki, Finland.
authors.forename: T
authors.initials: T
authors.lastname: Tuomi
authors.affiliation: Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Wolk
authors.affiliation: Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: S
authors.initials: S
authors.lastname: Carlsson