Smoking increases risk of depression and schizophrenia


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 study adds to a growing body of work suggesting that smoking can have adverse effects on mental health.

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.”

Schizophrenia spectrum disorders (SSD) are heterogeneous syndromes with well-established risk factors including exposure to childhood adversity, cannabis use during adolescence, a history of obstetric complications, stressful events during adulthood, and low maternal serum folate level (1).

In recent years, there has been a growing interest in tobacco smoking as a risk factor for SSD (23).

Tobacco smoking is known to cause a wide range of physical health problems.

It is the leading cause of preventable death, through increasing the risk of lung and other malignancies, chronic obstructive pulmonary disease (COPD), coronary heart disease, cerebrovascular disease, asthma and diabetes (4).

Two systematic reviews and meta-analyses have examined the association between tobacco smoking and psychotic disorders (23).

In pooling longitudinal studies (n = 5), Gurillo and colleagues reported a 2-fold increase in the risk of incident psychotic disorders in people who were daily tobacco smokers compared to those who were not (RR = 2.18; 95% CI 1.23–3.85).

Similarly, Hunter et al. (3) who pooled data from studies identified using inclusion criteria with the outcome restricted to schizophrenia (N = 5) also reported smoking tobacco was associated with a 2-fold risk of schizophrenia (RR = 1.99; 95% CI 1.10–3.61). Both studies concluded that further research was needed to examine the potential causal role of tobacco smoking in the onset of SSD.

The association between tobacco smoking and SSD is of growing significance. There is evidence that nicotine alters signaling in the dopaminergic, cholinergic, and glutamatergic neurotransmitter systems, particularly in adolescence (5).

Whilst the smoking of tobacco by young people has declined in many high income countries, there has been an increase in exposure to nicotine by this demographic through the availability of e-cigarettes (6).

It is therefore important to critically examine the evidence for a causal relationship between tobacco smoking and SSD.

In this review we aimed to evaluate the relationship between tobacco smoking and SSD which we defined as any non-affective psychotic disorder against causal criteria based on the Bradford Hill Framework (78). The Bradford Hill Framework provides nine criteria for establishing a causal relationship between an exposure and outcome.

This review examined longitudinal studies identified from the two recent systematic reviews of tobacco smoking and incident SSD and other identified studies. The evidence for a causal relationship between tobacco smoking and SSD, alternative explanations for the association and the health implications are discussed.

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.


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