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Cannabis and mental illness: it’s complicated!

By Suzi Gage @soozaphone

This blog originally appeared on the Mental Elf site on 11th May 2016.

The use of recreational drugs is seen at much higher rates in populations with mental health problems than in the general population, and this is true for both legal substances such as alcohol and tobacco, as well as prohibited substances like cannabis.

But understanding what these associations mean is problematic:

  • Do the substances cause psychiatric problems?
  • Do people use recreational drugs to self-medicate?
  • Or, is there some other factor earlier in life that can lead to both risk of substance use and mental health problems?

The impact of cannabis (Hamilton, 2016) on mental health (Kennedy, 2015) is of particular interest in the USA, where cannabis is now legal in some states, and decriminalized in a number of others. There is a fear that cannabis use will increase, and therefore there is a pressing need to understand the nature of its association with psychiatric problems.

Blanco and colleagues state that this is their particular motivation for undertaking the research they have just published, to try and understand whether cannabis use predicts later substance use disorders, and also mood and anxiety disorders.

Methods

This study used a very large sample of adults in the USA, measured at 2 time-points, 3 years apart. Cannabis use in the past year was assessed at wave one, and a variety of outcomes were assessed at wave 2. These were cannabis use disorder, alcohol use disorder, nicotine dependence, other drug use disorder, mood disorder (including depressive disorder, bipolar I or II and dysthymia), and anxiety disorder (including panic disorder, social anxiety disorder, specific phobia, and generalized anxiety disorder). These were all assessed using the Alcohol Use Disorder and Associated Disabilities Interview Schedule DSM-IV.

Regression analyses were used to look at the associations between cannabis and these disorders, before and after adjustment for a variety of other factors that might influence both cannabis use and mental health, and therefore could be confounding the relationship. These were socio-demographic characteristics, family history of substance use disorder, disturbed family environment, childhood parental loss, low self-esteem, social deviance, education, recent trauma, past and present psychiatric disorder, past substance use disorder and history of divorce.

The authors also used propensity score matching to try and further account for these confounders. This is a technique where cannabis users and non-users are matched by their values for the confounding variables, then compared. If confounding is the same between cannabis users and non-users, it cannot therefore drive the associations seen, meaning they’re more likely to be causal, rather than due to other factors (although confounding has to have been known about and measured for this to be the case). The sample size is a lot smaller for these analyses, with 1,254 people in each group.

Cannabis is now legal in some US states, so evidence about it's potential risks is now even more in demand.

Cannabis is now legal in some US states, so evidence about it’s potential risks is even more in demand.

Results

Of the 34,653 participants in the study, only 1,279 (roughly 3.5%) reported having used cannabis in the past 12 months at wave one. Before taking confounders in to consideration, cannabis use at wave one was associated with substance use disorders and mood and anxiety disorders. However, this changed after accounting for the factors the authors believed might confound the relationships.

Across the regressions and the propensity matched analyses, adjustment for confounders attenuated the associations between cannabis use and later mood and anxiety disorders, suggesting that these might be due to confounding. Conversely, associations remained between cannabis use and later substance abuse and dependence. This was particularly strong for cannabis abuse, as might be expected.

  • Cannabis use at wave one was associated with around a 7x increased risk of cannabis abuse or dependence at wave 2
  • Cannabis users also had 2-3x increased risk of alcohol use disorder or any other drug use disorder
  • Cannabis users also had around 1.5x increased risk of nicotine dependence.
Cannabis use was found to increase the risk of various substance use disorders.

Cannabis use was found to increase the risk of various substance use disorders.

Conclusions

The study found evidence that cannabis use predicts substance use disorder, even after adjustment for confounding. However, they also found that associations between cannabis use and later mood and anxiety disorders seemed to be due to confounding, rather than there being a causal association.

The authors concluded:

These adverse psychiatric outcomes [substance use disorders] should be taken under careful consideration in clinical care and policy planning.

After confounders had been taken into account, cannabis use was not found to increase the risk of mood or anxiety problems.

After confounders had been taken into account, cannabis use was not found to increase the risk of mood or anxiety problems.

Strengths and limitations

A strength of this study is the use of a nationwide sample, assessed at two different time points, and that they had a really big sample size. The authors also took steps to try and keep the sample representative, even after drop-out between wave one and wave two. The consideration of confounders is also a strength, although of course causation cannot be ascertained from observational data; a limitation that the authors themselves acknowledge.

When studies are very large, as this one is, it can be hard to get really accurate measures, because of the amount of time it takes to interview 35,000 people! It is particularly impressive that the outcome measures are all according to DSM-IV criteria. However, as all these measures were taken from an Alcohol Use Disorder interview, the measures of mood and anxiety may be less good (the interview has weaker test-retest reliability for mood and anxiety disorders than for substance use disorders).

The rate of cannabis use in this study (roughly 3.5%) seems very low; the UN’s World Drug Report in 2011 (UNODC, 2011) put previous-year cannabis use in the USA at 13.7%. The data used in the Blanco study were collected in 2001, so perhaps cannabis rates have increased since then. It is notoriously hard to monitor rates of illicit drug use as people may not be keen to honestly report their use; indeed, this may be a problem in this study too, meaning people might be misclassified.

The use of other substances at wave one isn’t necessarily adequately controlled for; pre-existing substance use disorders are controlled for, but less extreme use of a substance isn’t. So these participants that are using cannabis might also be smoking cigarettes, drinking alcohol, or using other illicit drugs. There’s no way to know from this study which came first, and this makes it difficult to know whether cannabis is causing the associations seen, or whether it could be another substance, for example.

While the use of propensity score matching is perhaps a stronger method to assess causation than simply adjusting for confounders, the technique cannot take in to account confounders that vary over time, as these could vary differently between cannabis users and non-users, and still be confounding the association despite being the same at one time point.

Although the authors rightly highlight that associations of cannabis use with later substance use disorders are robust to confounding, their conclusions don’t highlight that adjustment actually reduced the association between cannabis use and later mood and anxiety disorders to the null. I think this is a really interesting finding, and maybe should have been made more of.

Why did the authors not make more of their finding that cannabis use does not increase the risk of depression or anxiety?

Why did the authors not make more of their finding that cannabis use does not increase the risk of depression or anxiety?

Summary

This is a well designed study on a really large sample, and provides useful information about associations between cannabis use and later substance use disorders, as well as suggesting that perhaps associations between cannabis use and mood and anxiety disorders might be due to other factors, rather than due to cannabis causing these outcomes. It still doesn’t really tell us why cannabis use might increase the risk of substance use disorders, and doesn’t tell us that cannabis is causing this increase of risk.

Links

Primary paper

Blanco C, Hasin DS, Wall MM, et al. (2016) Cannabis Use and Risk of Psychiatric Disorders: Prospective Evidence From a US National Longitudinal Study. JAMA Psychiatry.Published online February 17, 2016. doi:10.1001/jamapsychiatry.2015.3229. [PubMed abstract]

Other references

Hamilton I. (2016) Cannabis: what do we know and what do we need to know? The Mental Elf, 17 Mar 2016.

Kennedy E. (2015) High potency cannabis and the risk of psychosis. The Mental Elf, 24 Mar 2015.

UNODC (United Nations Office on Drugs and Crime) (2011) UN World Drug report 2011. United Nations.

Photo credits

– See more at: http://www.nationalelfservice.net/mental-health/substance-misuse/cannabis-and-mental-illness-its-complicated/#sthash.U9604663.dpuf

Does tobacco cause psychosis?

by Marcus Munafo @MarcusMunafo

This blog originally appeared on the Mental Elf site on 30th July 2015.

Hot on the heels of a recent study suggesting a dose-response relationship between tobacco smoking and subsequent risk of psychosis, a systematic review and meta-analysis (including the data from that prospective study) has now been published, again suggesting that we should be considering the possibility that smoking is a causal risk factor for schizophrenia.

As I outlined in my earlier post, smoking and psychotic illness (e.g., schizophrenia) are highly comorbid, and smoking accounts for much of the reduced life expectancy of people with a diagnosis of schizophrenia. For the most part, it has been assumed that smoking is a form of self-medication, to either alleviate symptoms or help with the side effects of antipsychotic medication.

It's widely thought that people with psychosis or schizophrenia use smoking as a way to self-medicate and relieve their symptoms.

Methods

This new study reports the results of a systematic review and meta-analysis of prospective, case-control and cross-sectional studies. The authors hoped to test four hypotheses:

  1. That an excess of tobacco use is already present in people presenting with their first episode of psychosis
  1. That daily tobacco use is associated with an increased risk of subsequent psychotic disorder
  1. That daily tobacco use is associated with an earlier age at onset of psychotic illness
  1. That an earlier age at initiation of smoking is associated with an increased risk of psychotic disorder

The authors followed MOOSE and PRISMA guidelines for the conduct and reporting of systematic reviews and meta-analyses, and searched Embase, Medline and PsycINFO for relevant studies. They included studies that used ICD or DSM criteria for psychotic disorders (including schizophrenia, schizophreniform disorder, schizoaffective disorder, delusional disorder, non-affective psychotic disorder, atypical psychosis, psychotic depression, and bipolar mania with psychotic features).

To test the first hypothesis, studies with a control group were used to calculate an odds ratio. To test the second, prospective studies in which rates of smoking were reported for patients who developed psychotic disorders compared to controls were included, so risk ratios could be calculated. To test the third and fourth, prospective and case-control studies were included, and for the onset of psychosis, cross-sectional studies were also included.

Effect size estimates (weighted mean difference for continuous data, and odds ratios for cross-sectional data or relative risks for prospective data) were combined in a random-effects meta-analysis.

Results

A total of 61 studies comprising 72 independent samples were analysed. The overall sample included 14,555 tobacco users and 273,162 non-users.

  1. The overall prevalence of smoking in people presenting with their first episode of psychosis was higher than controls (12 case-control samples, odds ratio 3.22, 95% CI 1.63 to 6.33, P = 0.001). This supports hypothesis 1.
  2. Compared with non-smokers, the incidence of new psychotic disorders was higher overall (6 longitudinal prospective samples, risk ratio 2.18, 95% CI 1.23 to 3.85, P = 0.007). This supports hypothesis 2.
  3. Daily smokers developed psychotic illness at an earlier age compared with non-smokers (26 samples, weighted mean difference -1.04 years, 95% CI -1.82 to -0.26, P = 0.009). This supports hypothesis 3.
  4. Age at initiation of smoking cigarettes did not differ between patients with psychosis and controls (15 samples, weighted mean difference -0.44 years, 95% CI 1-.21 to 0.34, P = 0.270). This does not support hypothesis 4.

Daily tobacco use is associated with an increased risk of psychosis and an earlier age at onset of psychotic illness.

Conclusion

The authors conclude that the results of their systematic review and meta-analysis show that daily tobacco use is associated with an increased risk of psychotic disorder and an earlier age at onset of psychotic illness, although the magnitude of the association is relatively small.

Interestingly, the authors interpret their results in the context of the Bradford Hill criteria for inferring causality (which consider the strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy of an association). They argue that, where these criteria can be applied (the specificity criterion cannot be applied because smoking affects so many disease processes, while the experiment criterion is not met because animal models of psychotic illness that capture important features such as delusions are impossible), they do appear to be met by the evidence available.

Limitations

There are a number of important limitations to this study, which the authors themselves acknowledge:

  • The first is that all analyses relied on observational data, which makes strong causal inference impossible. Longitudinal prospective studies help somewhat in this respect, but only a small number were available for inclusion in the analysis of risk of developing psychosis between smokers and non-smokers. Moreover, even these studies cannot exclude the possibility that symptoms present before a first full episode of psychosis may have led to smoking initiation (i.e., self medication).
  • Another important limitation is that very few studies measured or adjusted for use of other substances (most importantly, perhaps, cannabis, which has been widely discussed as a potential risk factor for schizophrenia). This is a potentially very important source of bias.

Nevertheless, this is a well-conducted systematic review and meta-analysis that brings together a reasonably large literature. The results appear robust, although given the observational nature of the data, and the fact that only data that were comparable across studies could be meta-analysed, any conclusions regarding causality need to be very tentative.

Very few studies in this review, measured or adjusted for use of other substances such as cannabis.

Summary

It seems that we should seriously consider the possibility that smoking is a causal risk factor for schizophrenia. Of course, the data available to date aren’t definitive, and we need to be very cautious about inferring causality from observational data, but this does feel like an area where there is growing, converging evidence from multiple studies using multiple methods.

It’s also worth bearing in mind that even if smoking is a causal risk factor, this does not preclude the possibility that smoking is also used as a form of self-medication. There are several thousand constituents of tobacco smoke; it is possible that some of these alleviate symptoms, while others exacerbate them. For this reason, we shouldn’t assume that nicotine is necessarily the culprit if smoking is indeed a causal risk factor; it may be (and Gurillo and colleagues discuss the biological plausibility of nicotine in this context), but that will need to be tested.

This last point is particularly important in the content of ongoing debate regarding the potential harms and benefits of electronic cigarettes. If smoking does turn out to be a causal risk factor for schizophrenia, then whether nicotine or something else in tobacco smoke is identified as the culprit will have an important bearing on this debate, and attitudes towards these products.

There are several thousands constituents of tobacco smoke; it is possible that some of these alleviate symptoms, while others exacerbate them

Links

Primary paper

Gurillo P, Jauhar S, Murray RM, MacCabe J. (2015) Does tobacco use cause psychosis? Systematic review and meta-analysis. Lancet Psychiatry 2015. doi: 10.1016/S2215-0366(15)00152-2 (Open access paper: features audio interview with authors)

Munafo M. Smoking and risk of schizophrenia: new study finds a dose-response relationship. The Mental Elf, 1 Jul 2015.

– See more at: http://www.nationalelfservice.net/mental-health/psychosis/does-tobacco-use-cause-psychosis/#sthash.sxUwJPIF.dpuf

Smoking and risk of schizophrenia: new study finds a dose-response relationship

by Marcus Munafo @MarcusMunafo

This blog originally appeared on the Mental Elf site on 1st July 2015.

Almost exactly a year ago, a landmark study identified 108 genetic loci associated with schizophrenia (Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). In a Mental Elf post on that study I wrote: “Genetic studies also don’t rule out an important role for the environment – [genome-wide association studies] might even help identify other causes of disease, by identifying loci associated with, for example, tobacco use.”

I mentioned this because one of the loci identified is strongly associated with heaviness of smoking. There are two possible explanations for this: either this locus influences both smoking and schizophrenia, or smoking causes schizophrenia.

Smoking and schizophrenia are highly co-morbid; the prevalence of smoking among people with a diagnosis of schizophrenia is much higher than in the general population. It is widely believed that this is because smoking helps to alleviate some of the symptoms of schizophrenia, or the side-effects of antipsychotic medication.

The possibility that smoking itself may be a risk factor for schizophrenia has generally not been widely considered. Now, however, intriguing evidence has emerged that it may be, from a large study of data from Swedish birth and conscript registries (Kendler et al, 2015).

The leading causes of premature mortality in people with schizophrenia are ischaemic heart disease and cancer, both heavily related to smoking.

Methods

The authors linked nationwide Swedish registers via the unique 10-digit identification number assigned at birth or immigration to all Swedish residents. Data on smoking habits were collected from the Swedish Birth Register (for women) and the Military Conscription Register (for men). The date of onset of illness was defined as the first hospital discharge diagnosis for schizophrenia or non-affective psychosis.

Cox proportional hazard regressions were used to investigate the associations between smoking and time to schizophrenia diagnosis. To evaluate the possibility that smoking began during a prodromal period (where symptoms of schizophrenia may emerge prior to a full diagnosis), buffer periods of 1, 3 and 5 years were included in the models. In the female sample, data from relatives (siblings and cousins) were also used to control for familial confounding (genetic and environmental).

Results

Smoking status information was available for 1,413,849 women, and 233,879 men.

There was an association between smoking at baseline and a subsequent diagnosis of schizophrenia for:

  • Women
    • Light smoking: hazard ratio 2.21, (95% CI 1.90 to 2.56)
    • Heavy smoking: hazard ratio 3.45 (95% CI 2.95 to 4.03)
  • Men
    • Light smoking: hazard ratio 2.15 (95% CI 1.25 to 3.44)
    • Heavy smoking: hazard ratio 3.80 (95% CI 1.19 to 6.60)

Adjustment for socioeconomic status and prior drug abuse (i.e., confounding) weakened these associations slightly.

Taking into account the possibility of smoking onset during a prodromal period also did not weaken these associations substantially, irrespective of whether the buffer period (from smoking assessment to the date at which a first schizophrenia diagnosis would be counted) was 1-, 3- or 5-years. Theoretically, if prodromal symptoms of schizophrenia lead to smoking onset (i.e., reverse causality) the smoking-schizophrenia association should weaken with longer buffer periods.

Finally, the co-relative analyses compared the association between smoking and schizophrenia in the female sample, within pairs of relatives of increasing genetic relatedness who had been selected on the basis of discordance for smoking (i.e., one smoked and one did not). If the smoking-schizophrenia association arises from shared familiar risk factors (genetic or environmental) the association should weaken with increasing familial relatedness. Instead, only modest decreases were observed.

As a validation check on the accuracy of their measure of smoking behaviour, the authors confirmed that heavy smoking was more strongly associated with both lung cancer and chronic obstructive pulmonary disease, two diseases known to be caused by smoking.

These results show a dose-response relationship between smoking and risk of schizophrenia, i.e. the more you smoke, the stronger the association. 

Conclusion

This study provides clear evidence of a prospective association between cigarette smoking and a subsequent diagnosis of schizophrenia. However, observational associations are notoriously problematic, because these associations may arise because of confounding (measured and unmeasured), or reverse causality. Since these analyses were conducted on observational data, these limitations should be borne in mind and we cannot say with certainty that smoking is a causal risk factor for schizophrenia.

Nevertheless, the authors conducted a number of analyses to attempt to rule out different possibilities. First, the associations were weakened only slightly when adjusted for socioeconomic status and prior drug abuse, so the impact of measured confounders appears to be modest (although other confounding could still be occurring). Second, the inclusion of a buffer period to account for smoking onset during a prodromal period also weakened the associations only slightly, which is not consistent with a reverse causality interpretation. Finally, the co-relative analysis did not indicate that the association differed strongly across levels of familial relatedness, suggesting that the impact of unmeasured familial confounders (both genetic and environmental) is relatively modest.

This study provides clear evidence of a prospective association between cigarette smoking and a subsequent diagnosis of schizophrenia.

Limitations

There are some limitations to the study that are worth bearing in mind:

  1. First, there were no data on lifetime smoking, although the authors validated their measure of smoking against outcomes known to be caused by smoking.
  2. Second, the authors used clinical diagnoses, and included both schizophrenia and non-affective psychosis, so the specificity of the findings to these outcomes is uncertain.
  3. Third, because of the small number of schizophrenia diagnoses the co-relative analyses used non-affective psychosis only.

This study is not enough to say with certainty that smoking is a causal risk factor for schizophrenia.

Summary

There are three main ways in which the association between smoking and schizophrenia might arise:

  1. Schizophrenia causes smoking,
  2. Smoking causes schizophrenia, and
  3. The association arises from risk factors common to both.

This study suggests that the first mechanism cannot fully account for the association; if anything there was more support for the third mechanism, including stronger evidence for a role for familial factors than for socioeconomic status and drug abuse. However, critically, this study also finds support for the second mechanism, including a dose-response relationship between smoking and risk of schizophrenia.

Despite this study’s strengths, and the care taken by the authors to explore the three possible mechanisms that could account for the association between smoking and schizophrenia, no single study is definitive. However, evidence is emerging from other studies that support the possibility that smoking may be a causal risk factor for schizophrenia.

Recently, McGrath and colleagues have reported that earlier age of onset of smoking is prospectively associated with increased risk of non-affective psychosis (McGrath et al, 2015).

In addition, Wium-Andersen and colleagues report that tobacco smoking is causally associated with antipsychotic medication use (but not antidepressant use), in a Mendelian randomisation analysis that uses genetic variants as unconfounded proxies for heaviness of smoking (Wium-Andersen et al, 2015).

Identifying potentially modifiable causes of diseases such as schizophrenia is a crucial part of public health efforts. There is also often reluctance among health care professionals to encourage patients with mental health problems (including schizophrenia) to attempt to stop smoking. If smoking is shown to play a causal role in the development of schizophrenia, there may be more willingness to encourage cessation. Since the majority of the mortality associated with schizophrenia is due to tobacco use (Brown et al, 2000), helping people with schizophrenia to stop is vital to their long-term health.

There is now mounting evidence that supports the possibility that smoking may be a causal risk factor for schizophrenia.

Links

Primary paper

Kendler, K.S., Lonn, S.L., Sundquist, J & Sundquist, K. (2015). Smoking and schizophrenia in population cohorts of Swedish women and men: a prospective co-relative control study. American Journal of Psychiatry. doi: 10.1176/appi.ajp.2015.15010126 [Abstract]

Other references

Schizophrenia Working Group of the Psychiatric Genomics Consortium (2014). Biological insights from 108 schizophrenia-associated genetic loci. Nature, 511, 421-427. doi: 10.1038/nature13595

McGrath, J.J., Alati, R., Clavarino, A., Williams, G.M., Bor, W., Najman, J.M., Connell, M. & Scott, J.G. (2015). Age at first tobacco use and risk of subsequent psychosis-related outcomes: a birth cohort study. Australian and New Zealand Journal of Psychiatry. [PubMed abstract]

Wium-Andersen, M.K., Orsted, D.D. & Nordestgaard, B.G. (2015). Tobacco smoking is causally associated with antipsychotic medication use and schizophrenia, but not with antidepressant medication use or depression. International Journal of Epidemiology, 44, 566-577. [Abstract]

Brown S, Inskip H, Barraclough B. (2000) Causes of the excess mortality of schizophrenia. Br J Psychiatry. 2000 Sep;177:212-7.

– See more at: http://www.nationalelfservice.net/mental-health/schizophrenia/smoking-and-risk-of-schizophrenia-new-study-finds-a-dose-response-relationship/#sthash.u3UiDOlG.dpuf

Promoting smoking cessation in people with schizophrenia

by Meg Fluharty @MegEliz_

This blog originally appeared on the Mental Elf site on 14th May 2015.

shutterstock_276469196People with schizophrenia have a considerable reduction in life expectancy compared to the general population (Osborn et al 2007; Lawrence et al 2013). A number of factors lead to cardiovascular disease (Osborn et al 2007; Lawrence et al 2013; Nielsen et al, 2010) one of which is smoking.People with schizophrenia smoke at much higher rates and more heavily than the general population (Ruther et al 2014, Hartz et al 2014).Stubbs et al (2015) carried out a review to assess the current cessation interventions available for individuals with serious mental illnesses and establish if any disparities currently lie in the delivery of these interventions.60% of premature deaths in people with schizophrenia are due to medical conditions including heart and lung disease and infectious illness caused by modifiable risk factors such as smoking, alcohol consumption and intravenous drug use.

Methods

The authors searched several electronic databases (Embase, PubMed, and CINAHL) using the following keywords: “smoking cessation”, “smoking”, “mental illness”, “serious mental illness” and “schizophrenia.”

Studies were eligible if they included individuals with a DSM or ICD-10 diagnosis of schizophrenia and reported a cessation intervention.

The authors included both observational and intervention studies as well as systematic-reviews and meta-analyses.

This paper is a clinical overview (not a systematic review) of a wide range of different studies relevant to smoking cessation in schizophrenia and other severe mental illnesses.

Results

Pharmacological interventions

 Non-pharmacological interventions

  • The evidence for E-cigarettes was inconsistent, with the authors concluding more evidence was needed before clinicians consider e-cigarettes within mental health settings. Additionally, e-cigarette use in people with schizophrenia should have side effects monitored closely.
  • There was little research on exercise in schizophrenia, but one study found a reduction in tobacco consumption.

Behavioural approaches

  • Behavioural approaches such as offering smoking cessation advice alongside pharmacotherapy have been found successful with no harmful side effects.

Disparities in smoking cessation interventions

  • An investigation of GP practices found individuals with schizophrenia did not receive smoking cessation interventions proportional to their needs.

Support while quitting

  • People with serious mental illnesses experience more severe withdrawal symptoms compared to the general population, and therefore should be given extra support during cessation attempts (Ruther et al 2014).
  • Psychiatrists should re-evaluate choice and the dose of antipsychotic medicine being given after abstinence from smoking is achieved. This is because of nicotine’s metabolic influence on antipsychotic medicine.
  • Alongside smoking cessation, exercise should be promoted among people with schizophrenia to combat weight gain and the increased metabolic risk.

People with serious mental illness are likely to need more support when quitting smoking, because they generally suffer more severe withdrawal symptoms.

Discussion

In light of the findings, the authors suggest several steps for clinicians to help people with schizophrenia quit smoking:

  • Patients’ current smoking status, nicotine dependency, and previous quit attempts should be assessed. Assessing nicotine dependency will help predict the level of withdrawal symptoms the patient is likely to experience upon quitting.
  • Cessation attempts are best timed when the patient is stable. Patients should be thoroughly advised on the process needed to give them the best chance of quitting smoking, Thus, allowing the patient to formulate their quit plan and take ownership of their own quit attempt.
  • Cessation counselling should be provided, particularly what to expect with withdrawal symptoms (e.g. depression and restlessness) and how to cope.
  • Pharmacological support should be provided (Bupropion recommended) when there is even mild tobacco dependence.
  • Clinicians should carefully monitor patients’ medication and fluxions in weight for a minimum of 6 months after quitting smoking, and when needed recommended exercise to combat weight gain.

The authors provide a well laid out summary of their findings, alongside some excellent suggestions for clinicians to consider on how to best promote cessation in practice.

However, it should be stressed that Stubbs et al (2015) only searched for high qualities studies and provided an overview of them –  this is not a systematic review or meta-analysis. They included several types of studies, set little inclusion criteria and listed no exclusion criteria. This is quite different from a systematic review with a meta-analysis, which would set stricter predefined search and eligibility criteria, which identify a set of studies all tackling the same question, thus allowing for the statistical pooling and comparison of these studies.

This is not a systematic review, but it does offer some very useful practical advice for clinicians who are trying to promote smoking cessation.

Links

Primary paper

Stubbs B, Vancampfort D, Bobes J, De Hert M, Mitchell AJ. How can we promote smoking cessation in people with schizophrenia in practice? A clinical overview. Acta Psychiatrica Scandinavica. 2015: 1-9. 
[PubMed abstract]

Other references

Osborn DPJ, Levy G, Nazareth I, Petersen I, Islam A, King MB. Relative risk of cardiovascular and cancer mortality in people with severe mental illness from the United Kingdom’s General Practice Research Database. Arch Gen Psychiatry 2007;64:242–249.

Lawrence D, Hancock KJ, Kisely S. The gap in life expectancy from preventable physical illness in psychi- atric patients in Western Australia: retrospective analysis of population based registers. BMJ 2013;346: f2539-f.

Nielsen RE, Uggerby AS, Jensen SOW, McGrath JJ. Increasing mortality gap for patients diagnosed with schizophrenia over the last three decades – a Danish nationwide study from 1980 to 2010. Schizophr Res 2013;146:22–27.  
[PubMed abstract]

Ruther T, Bobes J, de Hert M et al. EPA guidance on tobacco dependence and strategies for smoking cessation in people with mental illness. Eur Psychiatry 2014;29:65– 82. 
[PubMed abstract]

Hartz SM, Pato CN, Medeiros H et al. Comorbidity of severe psychotic disorders with measures of substance use. JAMA Psychiatry 2014;71:248–254.