Public Defence: Gunn-Helen Øiseth Moen - Genetic Epidemiology
M.Sc. Gunn-Helen Øiseth Moen at Institute of Clinical Medicine will be defending the thesis “Genetic and environmental etiology of glucose metabolism and cardiometabolic traits during pregnancy and in later life” for the degree of PhD (Philosophiae Doctor).
Trial Lecture - time and place
See Trial Lecture.
- First opponent: Professor Markku Laakso, Institute of Clinical Medicine, Internal Medicine, University of Eastern Finland and Kuopio University Hospital, Finland
- Second opponent: Researcher Bettina Kulle Andreassen, Cancer registry of Norway, Oslo
- Third member and chair of the evaluation committee: Professor Stine M. Ulven, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor Emeritus Kristian Folkvord Hanssen, Faculty of Medicine, University of Oslo
Chief Physician Elisabeth Qvigstad, Oslo University Hospital
The prevalence of overweight, obesity and type 2 diabetes are increasing world-wide, and research findings suggest that the intrauterine life is important for subsequent health. Associations with type 2 diabetes and coronary heart disease are found for both low and high birth weight, but the physiological mechanisms behind these associations are not fully understood.
In the Norwegian STORK study, over one thousand pregnant women underwent two oral glucose tolerance tests. A genome-wide-association study (GWAS) of the women was summarized in genetic risk scores, and findings suggest that the impact of genetic on fasting glucose (FG) in pregnant and non-pregnant individuals is similar. This was less apparent in the case of 2-hour glucose values. This indicates a potential difference in the post prandial glucose metabolism during pregnancy compared to non-pregnant individuals.
In the second part of the thesis we developed and made public available a statistical tool called The “Maternal and Fetal Genetic Effects Power Calculator” (MFGPC). This is a freely available online web utility that can be used to estimate statistical power to detect maternal and fetal effects in genetic association studies.
In article III, we used Mendelian Randomization (MR) to examine whether vitamin B12 (vB12) is likely to causally affect risk of cardiometabolic disease. No evidence was found for causal relations between serum levels of vB12 and most of the cardiometabolic traits under study. This is contrary to previous observational studies, but in line with the current MR literature on the subject. However, a potential causal effect of vB12 on FG and HOMA-β was found.
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