Change in mental health after smoking cessation: systematic review and meta-analysis
BMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g1151 (Published 13 February 2014) Cite this as: BMJ 2014;348:g1151All rapid responses
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On the subject of causation, I would like to point out that there are multiple plausible and relevant factors which are easily overlooked when interpreting the results of a study pertaining to such an emotinally laden topic. Some of them might in fact be overlooked simply because they seem too obvious.
For example, metacognitive abilities and personality traits like delayed gratification or neuroticism are well known to affect both addictive behavior and the development of mood disorders. A person adversely affected by such background factors would seem less likely to both recover from adverse life events and to cease smoking, even controlling for anxiety, etc, at the beginning of a study.
Or from another angle, even if cessation really does causally affect mood, it still matters whether the causation is direct or mediated by an intermediate variable. One obvious such candidate variable is freely disposable income: a pack a day is nowadays rather an expensive habit. Unlike in the case of exercise as the mediator, in this case the most effective intervention would also not seem to be medical, but rather fiscal.
Competing interests: 2+ packs of Camel per diem.
We included four studies which examined change in mental health outcomes in people with psychiatric illnesses. Diagnoses included: past major depression, current depressive disorders and people with post-traumatic stress disorder. In a further two studies the participants were diagnosed with chronic physical and/or psychiatric conditions including, depression, anxiety, and schizophrenia, bipolar and other emotional difficulties. The direction of the association in these studies did not differ in comparison to the general populations.
There is evidence to suggest that, at the very least; cessation is not associated with harm to the mental health of those with severe psychiatric illness. Banham and Gilbody (Banham & Gilbody 2010) reviewed eight randomised trials of cessation interventions versus no intervention in people with psychotic disorders. Six of the eight trials reported no difference in psychological outcomes after cessation and two showed better function in the cessation support arm. This paper did not report outcomes by cessation status so it is not possible to examine whether achievement of cessation is associated with improved psychological outcome. However the trial design strengthens the argument on causality and excludes the possibility that supporting cessation leads to substantial psychological harm.
References
Banham, L. & Gilbody, S. 2010, "Smoking cessation in severe mental illness: what works?", Addiction, vol. 105, no. 7, pp. 1176-1189.
Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: GT has received grants and personal fees from a National Coordinating Centre for Research Capacity Development scholarship, during the conduct of the study; and personal fees from UK Centre for Tobacco and Alcohol Studies, outside the submitted work. AMcN has received grants from UK Centre for Tobacco and Alcohol Studies, outside the submitted work. AF has received grants from National Prevention Research Initiative, during the conduct of the study; and sat on the professional development group for NICE guidance on stopping smoking in secondary care. NL-H has received personal fees from manufacturers of smoking cessation aids, outside the submitted work; and manages an NIHR HTA funded trial of nicotine patch preloading. The nicotine patches for the trial are provided free of charge by GlaxoSmithKline (GSK). GSK have no other involvement in the trial. PA has received personal fees from Pfizer, grants and personal fees from McNeil, outside the submitted work.
We reported that there was a moderate to strong association between quitting smoking and improvements in mental health compared with continuing to smoke. We favoured the explanation that quitting improved mental health. Dr Searle and Professor Sanderson and colleagues wonder whether the association between quitting smoking and improvements in mental health could be more plausibly caused by improved mental health leading to a greater ability to quit or a common factor causing both improved mental health and increasing the likelihood of cessation.
There is very limited scope for reverse causation. It seems entirely plausible that people try to quit smoking when their mood improves and this could explain the association in some of the population cohorts we examined. However, more than half the studies were smoking cessation trials where all enrollees had mood assessed at baseline and then all attempted to quit more or less immediately so improved mood cannot have caused the decision to quit smoking here. The effect size in these studies was the same as in the population cohorts, suggesting reverse causation was an unlikely causal factor even in the population cohorts.
While improved mood cannot explain the decision to quit, could some third factor explain both the success of attempts to stop and the improvement in mood seen? None of our correspondents were able to hypothesise what such factor might be. It must have occurred after the quit attempt started, because if it was operating prior to cessation it would have been reflected in the pre-cessation mood measure and not reflect in the change score we used for the analysis. Furthermore, our studies assessed mood anywhere between 6 weeks and 9 years after cessation with no evidence of change in effect size over time. We know of no evidence that, for example, positive life events enable people to sustain a quit attempt. Furthermore such events must be common enough to be occurring in a sufficient number of people who quit smoking to influence the mean mood ratings at six weeks after, but not prior to, cessation starting and that such events are still influencing mood to the same extent nine years later. We cannot rule out such an explanation, but it feels much less plausible than the explanation that stopping smoking improves mood.
Sanderson and colleagues propose that changes in behaviours other than smoking may influence mood in those who stop smoking and not in those who continue. We agree this is plausible. It could be that people who stop smoking take-up exercise while continuing smokers do not and exercise may improve mood. This, however, is an example of the causal effect of cessation on mood improvement, albeit by an indirect route.
Whatever the true explanation for the cause, the implications for clinicians and patients remain unchanged. People who either do not stop smoking or try and fail have on average the same mood at follow-up as they did at baseline. People who stop smoking and succeed have a more positive mood state. The reason why mood improves matters much less to people than that it has. Whatever the reason, we can say that people who stop smoking have improved mental health.
Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: GT has received grants and personal fees from a National Coordinating Centre for Research Capacity Development scholarship, during the conduct of the study; and personal fees from UK Centre for Tobacco and Alcohol Studies, outside the submitted work. AMcN has received grants from UK Centre for Tobacco and Alcohol Studies, outside the submitted work. AF has received grants from National Prevention Research Initiative, during the conduct of the study; and sat on the professional development group for NICE guidance on stopping smoking in secondary care. NL-H has received personal fees from manufacturers of smoking cessation aids, outside the submitted work; and manages an NIHR HTA funded trial of nicotine patch preloading. The nicotine patches for the trial are provided free of charge by GlaxoSmithKline (GSK). GSK have no other involvement in the trial. PA has received personal fees from Pfizer, grants and personal fees from McNeil, outside the submitted work.
This is strong evidence for an association between better mental health outcomes & smoking cessation, but are we at risk of making the error of assuming causation - and most especially in the direction - stopping smoking improves mental health rather than improving mental health makes smoking cessation more likely?
Competing interests: No competing interests
Dear Editor
We read with interest the paper by Taylor et al. (BMJ, 12 Feb 2014) in which they showed a clear association between smoking cessation and improved mental health, with quitters reporting more favourable mental health outcomes than continuing smokers. We agree that physicians and others may perhaps find this helpful in reassuring patients that quitting smoking need not necessarily have a lasting adverse effect on their mental health, and that if anything the opposite may be true. Nevertheless, while the authors were careful in their use of causal language in the BMJ article, readers of the subsequent press release and media coverage could be forgiven for believing that the study provided evidence of a causal effect of smoking cessation leading to improved mental health, which it did not.
Taylor et al. state that their hypothesis was that smokers who gave up would experience a resulting improvement in mental health because they would no longer experience multiple episodes of negative affect induced by withdrawal. However, their study design clearly could not support or refute the second half of this hypothesis. The authors reasonably present three possible explanations of their findings: 1) that smoking cessation causes the improvement in mental health; 2) that improving mental health causes cessation; or, 3) that a common factor explains both improved mental health and cessation. We see little in their findings to support the authors’ apparent endorsement of the first over the second and third of these explanations in subsequent media coverage.
Causal inference from observational data is problematic, due to well known problems of confounding and reverse causality. The use of within individual changes in mental health measures may be less subject to confounding than between group comparisons but, given the clustering of health behaviours (1), it is not implausible that there will be changes in other lifestyle factors in addition to smoking cessation which may also influence mental health. In addition, while these data may not suggest that mental health affects likelihood of making quit attempts, reverse causality could still be an explanation if change in mental health influences ability to successfully sustain abstinence following a quit attempt.
For similar reasons, we feel that comparisons of the magnitude of the association between smoking cessation and mental health measures obtained from this systematic review, which is largely based on observational data, with effect sizes obtained from randomised controlled trials of anti-depressants, should be treated with caution. Observational studies are generally more prone to bias, and hence effect size estimates may well be inflated (2, 3). Thus, even if the observed association is causal, any true effect of smoking cessation will not necessarily be of the same magnitude. While we recognize that the term ‘effect size’ is a statistical one, we suggest that care is required when comparing effect sizes obtained from observational data to those from experimental data.
We agree with the authors’ suggestion that additional methodologies will shed light on whether smoking cessation does causally affect mental health. Such methodologies may include the use of instrumental variable analyses including Mendelian randomisation (4).
Saskia Sanderson
Amy Taylor
Marcus Munafò
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Competing interests: No competing interests
This meta-analysis does seem to show that the benefits of smoking cessation on mood are significant, and relatively long-lasting. The authors have looked at 26 studies that assessed levels of anxiety, depression and stress in several groups of patients, before and after quitting, and have found similar positive results across the board. What would be interesting to know, is what the range of psychiatric disorders included were. Was this limited to mood disorders, or were other groups included, such as patients with schizophrenia, who have notoriously high smoking rates, or psychotic illnesses? Also, was the severity of psychiatric illness graded and did this have any bearing on the results?
Whilst it’s clear that smoking cessation should be advocated to all patients where practical, the issue of clinician reluctance in patients with severe mental health illnesses does not entirely seem to have been addressed. Additionally, in order the stop smoking, a degree of motivation is required, and the chaotic lifestyle of certain patient groups would make this harder, which one can imagine might bias the population characteristics of those that quit and those that did not.
Stopping smoking, along with exercise, may be shown to have good efficacy in treating mild or moderate mood disorders. I’m not yet convinced that the results would be so positive in those requiring depot antipsychotics or electroconvulsive therapy however.
Competing interests: No competing interests
In commenting on such a thorough and balanced analysis, I hesitate to quibble. But I cannot resist the temptation to point out that as far as I can tell the review is concerned only with cigarette smoking. Pipe and cigar smoking is far less prevalent. But I wonder if the effect on mental health is generalizable to those, or if there no known association.
Competing interests: Pipe Smoker
Re: Change in mental health after smoking cessation: systematic review and meta-analysis
To the editor:
Smoking cessation should be promoted both for general people and psychiatric patients from a public health perspective and in this sense the study by Taylor et al. (1) is crucially relevant. There are however a couple of points that are worthy of consideration in order for their findings to be generalised to psychiatric patients, a special population.
First, while the data were from 26 studies of which 14 reflected general population only six at most were inclusive of chronic psychiatric conditions. As is clearly seen in Table 8 for instance, estimates were much less reliable in psychiatric conditions compared with general population, well because of lower availability of the studies for such patients (and hence fewer number of subjects studied).
Second, psychiatric patients not infrequently smoke in a manner that appears even compulsive, which plausibly results in heavy smoking. This may notoriously contribute to premature mortality (2). The average number of cigarette smoking was 20 a day in this study, which is not surprisingly large. Less compulsive, or in essence, less amount of smoking may still be meaningful in terms of not only physically but also mentally among psychiatric patients who smoke quite a lot. Further a possible association between less smoking and resultant better mood (or vise versa) would be a topic worthy of investigation, even when complete abstinence is not feasible.
Finally it is important to note that smoking peripherally affects pharmacokinetics of psychotropic medications in part by interfering with cytochrome CYP 450 system for instance (3). It centrally affects central neurotransmitters such as dopamine as well (4). In this context the net effect of smoking under psychotropic medications in the central nervous system is challenging to accurately and dynamically appreciate in a variety of psychiatric disorders for which psychotropic medications are clinically indicated.
References
1. Taylor G, McNeill A, Girling A, Farley A, Lindson-Hawley N, Aveyard P. Change in mental health after smoking cessation: systematic review and meta-analysis. BMJ. 2014 Feb 13;348:g1151. doi: 10.1136/bmj.g1151.
2. Banham L, Gilbody S. Smoking cessation in severe mental illness: what works? Addiction. 2010 Jul;105(7):1176-89. doi: 10.1111/j.1360-0443.2010.02946.x.
3. Sugahara H, Maebara C, Ohtani H, Handa M, Ando K, Mine K, Kubo C, Ieiri I, Sawada Y. Effect of smoking and CYP2D6 polymorphisms on the extent of fluvoxamine-alprazolam interaction in patients with psychosomatic disease. Eur J Clin Pharmacol. 2009 Jul;65(7):699-704. doi: 10.1007/s00228-009-0629-4.
4. Le Foll B, Guranda M, Wilson AA, Houle S, Rusjan PM, Wing VC, Zawertailo L, Busto U, Selby P, Brody AL, George TP, Boileau I. Elevation of dopamine induced by cigarette smoking: novel insights from a [(11)C]-(+)-PHNO PET study in humans. Neuropsychopharmacology. 2014 Jan;39(2):415-24. doi: 10.1038/npp.2013.209.
Competing interests: No competing interests