Gateway effects: why the cited evidence does not support their existence for low-risk tobacco products (and what evidence would)

It is often claimed that low-risk drugs still create harm because of “gateway effects”, in which they cause the use of a high-risk alternative. Such claims are popular among opponents of tobacco harm reduction, claiming that low-risk tobacco products (e.g.,ecigarettes, smokeless tobacco) cause people to start smoking, sometimes backed by empirical studies that ostensibly support the claim. However, these studies consistently ignore the obvious alternative causal pathways, particularly that observed associations may represent causation in the opposite direction (smoking causes  people to seek low risk alternatives) or confounding (the same individual factors increase the chance of using any tobacco product).

Published: 9 March 2015

Positive: Yes

Link to publication: http://antithrlies.com/2015/03/12/new-phillips-working-paper-on-thr-related-gateway-claims/

Author:

Carl V. Philips (CASAA)


Summary

Abstract

It is often claimed that low-risk drugs still create harm because of “gateway effects”, in which they cause the use of a high-risk alternative. Such claims are popular among opponents of tobacco harm reduction, claiming that low-risk tobacco products (e.g., ecigarettes, smokeless tobacco) cause people to start smoking, sometimes backed by empirical studies that ostensibly support the claim. However, these studies consistently ignore the obvious alternative causal pathways, particularly that observed associations may represent causation in the opposite direction (smoking causes people to seek low risk alternatives) or confounding (the same individual factors increase the chance of using any tobacco product). Due to these complications, any useful analysis must to deal with simultaneity and confounding by common case. In practice, existing analyses provide almost cartoon examples of drawing naïve causal conclusions from observed associations. The present analysis examines what evidence and research strategies would be needed to empirically detect such a gateway effect, if there were one, explaining key methodological concepts including causation and confounding, examining the logic of the claim, identifying potentially useful data, and debunking common fallacies on both side of the argument, as well as presenting an extended example of proper empirical testing. The analysis demonstrates that none of the empirical studies to date that purport to show a gateway effect from tobacco harm reduction products actually does so. The observations and approaches can be generalized to other cases where observed association of individual characteristics in cross-sectional data can result from one or several causal relationships.


Conclusion

Searching for some signal of a gateway effect amidst overwhelming confounding requires more rigorous methods than are typical in public health epidemiology. This generalizes to any attempt to use cross-sectional data to sort out causation in a particular direction from confounding or reverse causation. When seeking epidemiologic associations where confounding is minimal or relatively simple in its causes, the typical methods used in the field are still far from optimal, but the empirical results might still be basically useful. That is not the case in this context. While it might never be possible to convincingly demonstrate a gateway effect given the challenges, and statistical analyses have no hope of detecting a tiny effect, there are clearly better and worse ways to pursue the question.

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Electronic cigarette use among patients with cancer: Characteristics of electronic cigarette users and their smoking cessation outcomes

Given that continued smoking after a cancer diagnosis increases the risk of adverse health outcomes, patients with cancer are strongly advised to quit. Despite a current lack of evidence regarding their safety and effectiveness as a cessation tool, electronic cigarettes (E-cigarettes) are becoming increasingly popular. To guide oncologists’ communication with their patients about E-cigarette use, this article provides what to the authors’ knowledge is the first published clinical data regarding E-cigarette use and cessation outcomes among patients with cancer.

Published: 22 September 2014

Positive: No

Link to publication: http://onlinelibrary.wiley.com/enhanced/doi/10.1002/cncr.28811/

Debunked by Carl Philips: http://antithrlies.com/2015/03/12/what-is-peer-review-really-part-8-the-case-of-borderud-et-al/

Authors:

Sarah P. Borderud
Yuelin Li
Jack E. Burkhalter
Christine E. Sheffer
Jamie S. Ostroff


Summary

METHODS

A total of 1074 participants included smokers (patients with cancer) who recently enrolled in a tobacco treatment program at a comprehensive cancer center. Standard demographic, tobacco use history, and follow-up cessation outcomes were assessed.

RESULTS

A 3-fold increase in E-cigarette use was observed from 2012 to 2013 (10.6% vs 38.5%). E-cigarette users were more nicotine dependent than nonusers, had more prior quit attempts, and were more likely to be diagnosed with thoracic and head or neck cancers. Using a complete case analysis, E-cigarette users were as likely to be smoking at the time of follow-up as nonusers (odds ratio, 1.0; 95% confidence interval, 0.5-1.7). Using an intention-to-treat analysis, E-cigarette users were twice as likely to be smoking at the time of follow-up as nonusers (odds ratio, 2.0; 95% confidence interval, 1.2-3.3).


Conclusions

The high rate of E-cigarette use observed is consistent with recent articles highlighting increased E-cigarette use in the general population. The current longitudinal findings raise doubts concerning the usefulness of E-cigarettes for facilitating smoking cessation among patients with cancer. Further research is needed to evaluate the safety and efficacy of E-cigarettes as a cessation treatment for patients with cancer. Cancer 2014;120:3527–3535. © 2014 American Cancer Society.

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