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Environmental trigger(s) of type 1 diabetes: why so difficult to identify?

Rønningen KS - Biomed Res Int (2015)

Bottom Line: T1D results from poorly defined interactions between susceptibility genes and environmental determinants.In contrast to the rapid progress in finding T1D genes, identification and confirmation of environmental determinants remain a formidable challenge.Considering all the large ongoing prospective studies, new and more conclusive data than that obtained so far should instead come from international collaboration on the ongoing cohort studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatric Research, Division for Women and Children, Oslo University Hospital, Rikshospitalet, 0027 Oslo, Norway.

ABSTRACT
Type 1 diabetes (T1D) is one of the most common chronic diseases with childhood onset, and the disease has increased two- to fivefold over the past half century by as yet unknown means. T1D occurs when the body's immune system turns against itself so that, in a very specific and targeted way, it destroys the pancreatic β-cells. T1D results from poorly defined interactions between susceptibility genes and environmental determinants. In contrast to the rapid progress in finding T1D genes, identification and confirmation of environmental determinants remain a formidable challenge. This review article will focus on factors which have to be evaluated and decision to take before starting a new prospective cohort study. Considering all the large ongoing prospective studies, new and more conclusive data than that obtained so far should instead come from international collaboration on the ongoing cohort studies.

No MeSH data available.


Related in: MedlinePlus

The first box to the left shows total number of children genotyped for the high-risk genotype in MIDIA. Of the 997 children who had parents participating in MIDIA, 908 delivered blood samples more than once for autoantibody testing. The rest of participants delivered stool samples and questionnaires. 706 children had parents who had given a new informed consent in 2008/2009. Abs.: autoantibodies.
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Related In: Results  -  Collection


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fig1: The first box to the left shows total number of children genotyped for the high-risk genotype in MIDIA. Of the 997 children who had parents participating in MIDIA, 908 delivered blood samples more than once for autoantibody testing. The rest of participants delivered stool samples and questionnaires. 706 children had parents who had given a new informed consent in 2008/2009. Abs.: autoantibodies.

Mentions: The MIDIA study had the needed approvals for research studies in Norway (from the Regional Ethic Committee and the Data Inspectorate) before recruitment started in the summer of 2001. Since all recruitment was based on special teaching of Norwegian public health care nurses given by the PI and a study coordinator (a pubic health care nurse working together with the PI), the recruitment started in small scale. Most of the public health care nurses in Norway started after they had got the needed information and education to voluntary recruit to MIDIA as well as being responsible for most of the blood samples taken. From 2006 the recruitment covered the whole country. In June 2007, one of the mothers of a participating baby was, however, interviewed in the biggest newspaper in Norway. She here complained about not having received good enough information about MIDIA before she and her husband had consented to participate [50, 51]. The Directorate for Health and Social Affairs then immediately decided that recruitment to MIDIA had to be stopped. Some days later it was, however, decided that new evaluation of the project had to take place according to the Norwegian Biotechnology Law, which tells that genotyping of children under the age of 18 years can only take place if there are a clear health benefit for a certain disease. During the fall of 2007, the Biotechnology Board, the Ethical Committee for the Norwegian Medical Association, the National Committee for Medical Ethics, and several experts contacted by the Directorate of Social and Health Affairs evaluated the MIDIA project. All these boards had earlier evaluated the MIDIA study (e.g., during the time of recruitment to the study). In addition, the Health Department had clearly told that children who also had developed autoantibodies in MIDIA could get health insurance. The last aspect was based on the Biotechnology Law, which Norway has had since 1994, where it is clearly told that genetic risk for a disease cannot be used by the health insurance companies. The Directorate of Social and Health Affairs found, however, genotyping in MIDIA illegal on December 10, 2007. A few days later, the Norwegian Data Inspectorate said in newspapers that all data already collected from participants in MIDIA had to be thrown away. All ended good by the Norwegian Parliament voting in June 2008. As long as the Medical Regional Committee and the Norwegian Data Inspectorate approved the MIDIA study once more, and all parents of children who already had been identified as high-risk children gave a new informed consent, research in MIDIA could continue. Close to 47,000 babies had been genotyped before December 10, 2007, and 1,047 had been identified with high-risk genotype. The parents of 706 children gave new informed consent starting from the fall of 2008 until early in 2009, Figure 1.


Environmental trigger(s) of type 1 diabetes: why so difficult to identify?

Rønningen KS - Biomed Res Int (2015)

The first box to the left shows total number of children genotyped for the high-risk genotype in MIDIA. Of the 997 children who had parents participating in MIDIA, 908 delivered blood samples more than once for autoantibody testing. The rest of participants delivered stool samples and questionnaires. 706 children had parents who had given a new informed consent in 2008/2009. Abs.: autoantibodies.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4390105&req=5

fig1: The first box to the left shows total number of children genotyped for the high-risk genotype in MIDIA. Of the 997 children who had parents participating in MIDIA, 908 delivered blood samples more than once for autoantibody testing. The rest of participants delivered stool samples and questionnaires. 706 children had parents who had given a new informed consent in 2008/2009. Abs.: autoantibodies.
Mentions: The MIDIA study had the needed approvals for research studies in Norway (from the Regional Ethic Committee and the Data Inspectorate) before recruitment started in the summer of 2001. Since all recruitment was based on special teaching of Norwegian public health care nurses given by the PI and a study coordinator (a pubic health care nurse working together with the PI), the recruitment started in small scale. Most of the public health care nurses in Norway started after they had got the needed information and education to voluntary recruit to MIDIA as well as being responsible for most of the blood samples taken. From 2006 the recruitment covered the whole country. In June 2007, one of the mothers of a participating baby was, however, interviewed in the biggest newspaper in Norway. She here complained about not having received good enough information about MIDIA before she and her husband had consented to participate [50, 51]. The Directorate for Health and Social Affairs then immediately decided that recruitment to MIDIA had to be stopped. Some days later it was, however, decided that new evaluation of the project had to take place according to the Norwegian Biotechnology Law, which tells that genotyping of children under the age of 18 years can only take place if there are a clear health benefit for a certain disease. During the fall of 2007, the Biotechnology Board, the Ethical Committee for the Norwegian Medical Association, the National Committee for Medical Ethics, and several experts contacted by the Directorate of Social and Health Affairs evaluated the MIDIA project. All these boards had earlier evaluated the MIDIA study (e.g., during the time of recruitment to the study). In addition, the Health Department had clearly told that children who also had developed autoantibodies in MIDIA could get health insurance. The last aspect was based on the Biotechnology Law, which Norway has had since 1994, where it is clearly told that genetic risk for a disease cannot be used by the health insurance companies. The Directorate of Social and Health Affairs found, however, genotyping in MIDIA illegal on December 10, 2007. A few days later, the Norwegian Data Inspectorate said in newspapers that all data already collected from participants in MIDIA had to be thrown away. All ended good by the Norwegian Parliament voting in June 2008. As long as the Medical Regional Committee and the Norwegian Data Inspectorate approved the MIDIA study once more, and all parents of children who already had been identified as high-risk children gave a new informed consent, research in MIDIA could continue. Close to 47,000 babies had been genotyped before December 10, 2007, and 1,047 had been identified with high-risk genotype. The parents of 706 children gave new informed consent starting from the fall of 2008 until early in 2009, Figure 1.

Bottom Line: T1D results from poorly defined interactions between susceptibility genes and environmental determinants.In contrast to the rapid progress in finding T1D genes, identification and confirmation of environmental determinants remain a formidable challenge.Considering all the large ongoing prospective studies, new and more conclusive data than that obtained so far should instead come from international collaboration on the ongoing cohort studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatric Research, Division for Women and Children, Oslo University Hospital, Rikshospitalet, 0027 Oslo, Norway.

ABSTRACT
Type 1 diabetes (T1D) is one of the most common chronic diseases with childhood onset, and the disease has increased two- to fivefold over the past half century by as yet unknown means. T1D occurs when the body's immune system turns against itself so that, in a very specific and targeted way, it destroys the pancreatic β-cells. T1D results from poorly defined interactions between susceptibility genes and environmental determinants. In contrast to the rapid progress in finding T1D genes, identification and confirmation of environmental determinants remain a formidable challenge. This review article will focus on factors which have to be evaluated and decision to take before starting a new prospective cohort study. Considering all the large ongoing prospective studies, new and more conclusive data than that obtained so far should instead come from international collaboration on the ongoing cohort studies.

No MeSH data available.


Related in: MedlinePlus