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Trial Lecture – time and place
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Adjudication committee
- First opponent: Associate Professor Catharina Lavebratt, Karolinska Institutet, Sweden
- Second opponent: Associate Professor Helene Speyer, Copenhagen University Hospital, Denmark
- Third member and chair of the evaluation committee: Researcher Philipp Paul Lobmaier, University of Oslo
Chair of the Defence
Professor Erik Gunnar Jönsson, University of Oslo
Principal Supervisor
Professor Ole A. Andreassen, University of Oslo
Summary
Antipsychotic drugs, which reduce psychotic symptoms, are important pharmacological treatment for patients with severe mental disorders. Unfortunately, antipsychotics are associated with adverse effects, such as weight gain, diabetes, lipid disturbance, hormonal and autonomic adverse effects. These adverse effects affect somatic health of the treated patients and might be one of the contributing factors to the reduced lifespan of patients with severe mental disorders. More knowledge is needed to better understand the adverse effects and their underlying mechanisms. Sex is essential here, because of the physiological differences between males and females. Males are in general overrepresented in clinical studies, which also concerns studies of antipsychotics.
The main aim of the PhD-project was to identify sex differences in adverse effects of antipsychotic drugs and explore the role of hormones in the underlying biological pathways. We used a cross-sectional sample of participants from the ongoing Thematically Organized Psychosis (TOP) study, including patients with severe mental disorders (i.e., schizophrenia and bipolar spectrum). To test the associations between adverse effects, antipsychotic drugs and sex, we applied regression analyses with interactions, and several confounders were adjusted for.
The main findings were sex differences in several adverse effects related to antipsychotics. Males treated with antipsychotics had increased triglyceride and insulin levels, decreased testosterone levels and a higher risk of palpitations/tachycardia compared to females, which indicate a higher vulnerability of certain cardiovascular disease (CVD) risk factors in males. Furthermore, the sex-specific findings were associated with differences in hormone levels (e.g. cortisol, insulin, leptin, thyroid-stimulating hormone (TSH), prolactin). Thus, the biological pathways underlying sex-specific adverse effects may be influenced by hormonal differences between males and females.
Additional information
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