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Event

CeFH Genetics Friday: Robyn Wootton "Causal effects of lifetime smoking on risk for depression and schizophrenia: Evidence from a Mendelian randomisation study"

Presentation by Robyn Wootton, University of Bristol

Presentation by Robyn Wootton, University of Bristol


23. Nov | 2018

13:00-14:00
Seminar
Marcus Thranes gate 2, meeting room 2nd floor

About the speaker

Robyn Wootton is a genetic epidemiologist interested in the association between health behaviours and mental health. Her PhD explored the contribution of genetic factors to adolescent subjective wellbeing using: twin modelling, genome-wide association studies, polygenic scores, SNP heritability and Mendelian randomisation. In her postdoctoral research at the University of Bristol she has continued to apply these methods to understanding the association between health behaviours and mental health.  She is currently visiting The Centre for Fertility and Health on a Gro Harlem Brundtland Visiting Scholarship to explore the association between health behaviours, depression and fertility.

“Causal effects of lifetime smoking on risk for depression and schizophrenia: Evidence from a Mendelian randomisation study”

Smoking prevalence is higher amongst individuals with schizophrenia and depression, compared to the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS). We conducted a GWAS of lifetime smoking behaviour (capturing smoking duration, heaviness and cessation) in a sample of 463,003 individuals from the UK Biobank, and validated the findings via MR analyses of positive control outcomes (e.g., lung cancer). Further MR analyses provided evidence that smoking is a causal risk factor for both schizophrenia and depression. We also found some evidence that genetic liability for both depression and schizophrenia cause increased lifetime smoking. These findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking. The genetic variants we identify for lifetime smoking have the potential to be used in further MR studies.