Public Defence: Linn Rødevand
Cand.Psychol. Linn Rødevand at Institute of Clinical Medicine will be defending the thesis “Cardiovascular disease risk across psychosocial and genetic factors in severe mental disorders” for the degree of PhD (Philosophiae Doctor).
Photo: Kirsten Sjøwall
An electronic copy of the thesis may be ordered from the faculty up to 2 days prior to the public defence. Inquiries regarding the thesis after the public defence must be addressed to the candidate..
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Professor Jeanette Westman, Karolinska Institutet
- Second opponent: Adjunct Professor Giovanni De Girolamo, Catholic University, Milan
- Third member and chair of the evaluation committee: Professor Soili Marianne Lehto, University of Oslo
Chair of the Defence
Professor Emeritus Stein E. Opjordsmoen Ilner, University of Oslo
Professor Ole Andreassen, University of Oslo
The aim of the thesis was to increase knowledge about cardiovascular disease (CVD) in severe mental disorders (SMDs). First, we examined whether the level of CVD risk factors has changed during the past decade in patients with schizophrenia and bipolar disorder, and compared with healthy controls and the general population. Second, we assessed whether loneliness shares a genetic basis with SMDs (schizophrenia, bipolar disorder and major depression) and CVD. Third, we investigated genetic overlap between bipolar disorder and CVD. We used the statistical tool MiXeR to estimate the overall amount of genetic overlap, and conjunctional false discovery rate (conjFDR) to pinpoint specific shared genetic loci.
The level of CVD risk factors remained higher in patients with schizophrenia and bipolar disorder compared to controls and the general population. There was no reduction in CVD risk factors in schizophrenia during the past decade, and only modest improvements in bipolar disorder.
A substantial part of the genetic architecture of loneliness appears to influence SMDs and CVD. We discovered several shared genetic loci between loneliness and SMDs and CVD risk with concordant effect directions, supported by positive genetic correlations.
There was polygenic overlap between bipolar disorder and CVD risk. The shared loci had mixed allelic effect directions, resulting in non-significant genetic correlations.
The results indicate that CVD risk has remained high in schizophrenia with moderate improvements in bipolar disorder during the past decade. Further, the results suggest that a genetic propensity to loneliness increases the risk of SMDs and CVD, and there is overlapping genetic factors in bipolar disorder and CVD, indicating subgroups of bipolar disorder that are more susceptible to CVD. These discoveries provide novel insights into the potential mechanisms related to comorbid CVD in SMDs, and link to loneliness.
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