Summary: The link between smoking, depression, and schizophrenia is due, in part, to a causal effect of tobacco use. Findings reveal that smoking increased the risk of schizophrenia and depression. Additionally, depression and schizophrenia increased the likelihood of a person becoming nicotine dependent.

Source: University of Bristol

It is well-known that smoking is much more common amongst people with mental illness – especially depression and schizophrenia. However, most studies that have looked at this association have not been able to disentangle whether this is a cause-and-effect relationship, and if so in which direction. Does mental illness increase the likelihood of smoking, or is smoking itself a risk factor for mental illness?

Researchers from the University’s Tobacco and Alcohol Research Group (TARG) with support from Bristol’s MRC Integrative Epidemiology Unit (IEU) and the NIHR Bristol Biomedical Research Centre (BRC), used UK Biobank data from 462,690 individuals of European ancestry, comprising eight percent current smokers and 22 percent former smokers.

The team applied an analytic approach called Mendelian randomisation, which uses genetic variants associated with an exposure (e.g. smoking) to support stronger conclusions about cause-and-effect relationships. They found evidence that tobacco smoking increased risk of depression and schizophrenia, but also that depression and schizophrenia increase the likelihood of smoking (although the evidence was weaker in this direction for schizophrenia).

The study adds to a growing body of work suggesting that smoking can have adverse effects on mental health. The same group published a similar study in British Journal of Psychiatry earlier this year in collaboration with the University of Amsterdam, showing evidence that tobacco smoking increases the risk of bipolar disorder.

The UK government’s mental health task force made the recommendation in their 2016 review that psychiatric hospitals should be smoke free by 2018. This new evidence adds further weight to support the implementation of smoke-free policies. Not only is there evidence that smoking can be detrimental for mental health, but much of the excess mortality associated with mental illness is due to smoking.

Dr Robyn Wootton, Senior Research Associate in the School of Psychological Science and the study’s lead author, said: “Individuals with mental illness are often overlooked in our efforts to reduce smoking prevalence, leading to health inequalities. Our work shows that we should be making every effort to prevent smoking initiation and encourage smoking cessation because of the consequences to mental health as well as physical health.”

Marcus Munafò, Professor of Biological Psychology in Bristol’s School of Psychological Science and senior author on the study, added: “The increasing availability of genetic data in large studies, together with the identification of genetic variants associated with a range of behaviours and health outcomes, is transforming our ability to use techniques such as Mendelian randomisation to understand causal pathways. What this shows is that genetic studies can tell us as much about environmental influences – in this case the effects of smoking on mental health – as about underlying biology.”

About this neuroscience research article

Source:

University of Bristol

Media Contacts:

Press Office – University of Bristol

Image Source:

The image is adapted from the University of Bristol news release.

Original Research: Open access

“Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study”. Robyn Wotton, Marcus Munafò et al.

Psychological Medicine doi:10.1017/S0033291719002678.

Abstract

Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study

Background

Smoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).

Methods

We conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.



Results

There was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.

Conclusions

These findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

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