**6. Acknowledgement**

352 Type 1 Diabetes – Complications, Pathogenesis, and Alternative Treatments

Denver, Colorado, between January 1994 and November 2006, 1770 children at increased genetic risk were followed. Islet autoimmunity was assessed in association with reported daily intake of polyunsaturated fatty acids. The data strongly indicated that dietary intake of omega-3 fatty acids is associated with reduced risk for autoimmunity in children at increased risk for T1D (Norris et al., 2007). We therefore proposed to conduct a prospective double blinded dietary intervention trial using high dosage of the omega-3 fatty acid DHA or "placebo" (containing the same amount of DHA found in the recommended daily dosage of cod liver oil). The reason for choosing 1,8 g DHA daily was to be able to be included in a multi-centre study since a pilot study in USA already have been performed as a feasibility study using exactly this dosage. But in USA they use plant oil as placebo (Chase et al, 2009). In Norway this cannot be given since mother of babies in Norway get recommended from their public health care nurse to give cod liver oil. But they are told to start with one tea spoon and to increase the daily intake to 5 ml within the child is 6 months. But at this stage babies start spotting. Indeed very few parents continue to give their infant cod liver oil. The Directorate for Health decided, however, that "Nutritional Intervention to Prevent Type 1 Diabetes" was illegal, and could therefore never be started based on the Norwegian

Most recently two big NIH funded studies are going on. In the Type 1 Diabetes Genomics Consortium forces worldwide have been working together. All genotyping has been based on linkage studies (two siblings with Type 1 diabetes and parents without the disease is needed). Getting all who earlier was competing in identifying new T1D susceptibility genes to collaborate gave access to all available multiplex families. All genes that earlier was indicated to be of importance for T1D were confirmed, and 40 genes conferring susceptibility to T1D has now been identified (Barrett et al, 2009). In addition genome wide association studies have been performed by the same group (Welcome Trust Case Control

In TEDDY (The Environmental Determinants for Type 1 Diabetes in the Young), another NIH funded study, centres in Denver, Colorado, Seattle, Washington, parts of Georgia and Florida, parts of Finland, Sweden and Germany have recruited and genotyped 350,000 newborns and inform the parents about the high genetic risk. The protocol is the same everywhere, and all collected samples are sent to the coordinating centre in Florida. The follow-up is more intense than in MIDIA. Here all who participate, both scientists and parents know that it is an observational study where any intervention never can be given.

The first nested case-control study in MIDIA on intestinal virus as triggers for Type 1 Diabetes did not support the hypothesis that faecal shedding of enteroviral RNA is a major predictor of advanced islet autoimmunity. Neither was there any association between human parechovirus and islet autoimmunity. Although also the rodent parechovirus, Ljungan virus, has been proposed as a potential environmental factor for Type 1 Diabetes, the results from the MIDIA study indicate that Ljungan virus is rare in young children since it was not found neither in controls or cases. The two cohort studies performed in MIDIA do, however, show that both maternal weight and self reported lower respiratory tract

Biotechnology Law.

Consortium, 2010).

**5. Conclusions** 

**4.1.3 Need for trans-national studies** 

The children Will be followed-up for 15 years.

The MIDIA study was funded by the Norwegian Research Council (grants 135893/330, 155300/320, 156477/730, 166515/V50), The Norwegian Organisational for Help and Rehabilitation (EkstraStiftelsen), Norwegian Diabetes Association, New Generis (EU Grant Food-CT-2005-016320). The Norwegian Mother and Child Cohort Study Was supported by the Norwegian Ministry of Health, NIH-NIEHS (grant no. N01-ES-85433), NIH-NINDS (grant no. 1 UO1 NS 047537-01), and the Norwegian Research Council/FUGE (grant no. 151918/S10). I am very grateful for all the help I got from Trond Rasmussen in writing this book chapter.
