Allt starkare bevis för att rökning kan ge psykisk ohälsa

Det har länge stått klart att rökning (och nikotinberoende) är vanligare bland personer med psykisk ohälsa, men vad som är hönan eller ägget har diskuterats. I en redaktionell kommentar skriver den välrenommerade forskaren Marcus Munafò i tidskriften Nicotine and Tobacco Research följande (fortsättning på engelska):

Growing Evidence for a Causal Role for Smoking in Mental Health

Marcus Munafò Professor. Editorial,  Nicotine and Tobacco Research Volume 24, Issue 5, May 2022, Pages 631–632

It has long been evident that smoking (and nicotine dependence) is more common among those with mental health problems, but the direction of causality has remained controversial. Does chronic tobacco use lead to neurobiological dysregulation that can contribute to the onset of mental health problems? Or do people with mental health problems smoke to alleviate symptoms? Or is it a combination of both?

Historically, the self-medication argument has been preferred, but this narrative was actively encouraged by the tobacco industry, who sought to market their products to this population. One inevitable challenge with research of this kind is the reliance on observational data. Even prospective analyses may be inadequate to infer causality with confidence—smoking may be initiated during a prodromal phase before a clinical diagnosis. Nevertheless, smoking is typically initiated in adolescence, whereas the onset of most mental health problems is generally later—in early adulthood and beyond. A meta-analysis of prospective studies concluded that smoking is indeed a causal risk factor for psychosis, and a sophisticated analysis taking into account the possible role of a prodromal phase, and comparing across genetically related family members, reached a similar conclusion.

To arrive at robust conclusions, we need to triangulate evidence from multiple sources, using multiple (and innovative) methodologies.  George Davey Smith showed that the association between smoking and homicide was as strong as the association between smoking and suicide, and equally robust to adjustment for confounders. While there is a plausible causal pathway to suicide, it is difficult to imagine one for homicide: “Unless the provisional wing of the health education lobby has moved on to a direct action phase, during which they shoot smokers, this association is very unlikely to be causal.”  The use of negative controls such as homicide is one way to probe the likelihood that observed associations are causal.

Another approach is to use genetic proxies for the exposure of interest, a technique known as Mendelian randomization.  This approach has also provided evidence that smoking is a causal risk factor for depression and psychosis, although not suicide. Every approach has its limitations. For example, genetic proxies may be pleiotropic and influence the outcome via pathways other than the exposure that is being proxied—the genetic variants associated with smoking initiation may capture a broad, underlying risk taking phenotype, which would reintroduce confounding into analyses of mental health outcomes. Hence, the need for a considered approach that incorporates multiple lines of evidence, and methodologies with different strengths, weaknesses, and causes of potential bias.

The news that smoking is unhealthy will not surprise any of our readers. But understanding the causal role of smoking in mental health remains important, to counter therapeutic nihilism—it is still common in some settings for health care professionals to enable smoking among their patients—and to reinforce the view that tobacco control measures contribute to psychiatric public health. Given evidence that smoking patterns have changed for the worse during the pandemic, and concerns about the mental health toll of the pandemic, understanding whether reducing smoking may help to reduce the burden of mental health problems as well as physical health problems is critical.