The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Professor Ilona Koupil, University of Stockholm
- Second opponent: Professor Anne-Marie Nybo Andersen, University of Copenhagen
- Third member and chair of the evaluation committee: Professor Tor Iversen, University of Oslo
Chair of the Defence
Professor Mette Brekke, University of Oslo
Principal Supervisor
Associate professor Øyvind Næss, University of Oslo
Summary
The association between restricted fetal growth and higher risk of cardiovascular disease (CVD) is well documented. The explanatory pathways underlying this association are not clearly established. Transgenerational studies have been used to investigate the likely mechanisms underlying this association. However, it has been difficult to assess the contribution of environmental versus genetic factors on the association as these factors are closely connected in nuclear families.
The overall aims of the thesis were to investigate the significance of both genetic and environmental causal factors, to uncover the underlying mechanisms, and to understand the role of traditional risk factors for transgenerational association between birth weight (BW) and CVD.
In this population-based study, we linked different Norwegian health registries (the Medical Birth Registry, the Cause of Death Registry, the Education Registry) and health surveys (County study, Age 40 Program, CONOR) to study the association between offspring BW and risk of CVD in parents, aunts/uncles and partners of aunts/uncles.
Offspring BW was inversely associated with CVD mortality among parents and among aunts/uncles, with stronger association in mothers compared to fathers and aunts/uncles. There were no differences in the estimates among the four classes of aunts/uncles. We found that established CVD risk factors contributed substantially to the associations among all relationships, and that smoking was the most influential risk factor. We also found that low offspring BW was associated with an unfavorable CVD risk factor profile in all family members. For smoking and higher education, the associations were also reported among partners of aunts/uncles.
The results show that both shared genetic and environmental factors play a role in the transgenerational associations between BW and CVD. Assortative mating and genetic nurturing can also contribute to these associations. A stronger association in mothers indicates the importance of intrauterine factors. Our findings may contribute to early identification of individuals at increased risk of CVD and to develop an effective prevention.
Additional information
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