Kylie Morphett1,2, Adrian Carter3,4, Wayne Hall3,5, Jayne Lucke1,6, Brad Partridge7,8, Coral Gartner1,3. 1. University of Queensland School of Public Health, Public Health Building, Herston, Queensland, Australia. 2. University of Queensland School of Medicine, Royal Brisbane and Women's Hospital Site, Herston, Queensland, Australia. 3. University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital Site, Herston, Queensland, Australia. 4. School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash University, Clayton, Victoria, Australia. 5. University of Queensland Centre for Youth Substance Abuse, Floor K, Mental Health Centre, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia. 6. LaTrobe University, Australian Research Centre in Sex, Health and Society, Melbourne, Australia. 7. Research Development Unit, Caboolture Hospital, Metro North Hospital and Health Service (MNHHS), Caboolture, Queensland, Australia. 8. The University of Queensland, Prince Charles Hospital Northside Clinical Unit, School of Clinical Medicine, Herston, Australia.
Abstract
Introduction: Addiction is increasingly defined as a "brain disease" caused by changes to neurochemistry. While nicotine addiction has historically been excluded in the brain disease model of addiction (BDMA), it is beginning to be labeled a chronic brain disease. We investigated whether Australian smokers endorse brain-based explanations of smoking, and whether these beliefs are associated with quitting self-efficacy or treatment intentions. Method: Cross-sectional study of Australian smokers (N = 1538) who completed a survey measuring their agreement with statements on the brain's role in smoking. Logistic regressions tested associations between these items and socio-demographic variables, quitting self-efficacy and intention to use cessation medications. Results: The majority (57.9%) agreed that smoking changed brain chemistry and 34.4% agreed that smoking was a brain disease. Younger participants and those with more education were more likely to endorse brain-based understandings of smoking. Participants who agreed smoking changed brain chemistry were more likely to report an intention to use cessation medicines (OR 1.5, 95% CI = 1.0-2.2) as were those who agreed that smoking was a brain disease (OR 1.5, 95% CI = 1.1-2.1). Self-efficacy did not differ between those who agreed and disagreed that smoking changed brain chemistry. However, those who agreed that smoking was a brain disease had higher self-efficacy than those who disagreed (OR 1.7, 95% CI = 1.3-2.3). Conclusion: A neurobiological view of smoking does not dominate public understandings of smoking in Australia. Endorsement of neurobiological explanations of smoking were associated with increased intention to use cessation aids, but were not associated with reduced self-efficacy. Implications: Explaining tobacco dependence in neurobiological terms is unlikely to induce feelings of fatalism in relation to smoking cessation. Those who endorse biomedical explanations of smoking may be more open to using cessation pharmacotherapies. Describing smoking in terms of alterations in brain chemistry may be more acceptable to smokers than labeling smoking a "brain disease" or "brain disorder."
Introduction: Addiction is increasingly defined as a "brain disease" caused by changes to neurochemistry. While nicotine addiction has historically been excluded in the brain disease model of addiction (BDMA), it is beginning to be labeled a chronic brain disease. We investigated whether Australian smokers endorse brain-based explanations of smoking, and whether these beliefs are associated with quitting self-efficacy or treatment intentions. Method: Cross-sectional study of Australian smokers (N = 1538) who completed a survey measuring their agreement with statements on the brain's role in smoking. Logistic regressions tested associations between these items and socio-demographic variables, quitting self-efficacy and intention to use cessation medications. Results: The majority (57.9%) agreed that smoking changed brain chemistry and 34.4% agreed that smoking was a brain disease. Younger participants and those with more education were more likely to endorse brain-based understandings of smoking. Participants who agreed smoking changed brain chemistry were more likely to report an intention to use cessation medicines (OR 1.5, 95% CI = 1.0-2.2) as were those who agreed that smoking was a brain disease (OR 1.5, 95% CI = 1.1-2.1). Self-efficacy did not differ between those who agreed and disagreed that smoking changed brain chemistry. However, those who agreed that smoking was a brain disease had higher self-efficacy than those who disagreed (OR 1.7, 95% CI = 1.3-2.3). Conclusion: A neurobiological view of smoking does not dominate public understandings of smoking in Australia. Endorsement of neurobiological explanations of smoking were associated with increased intention to use cessation aids, but were not associated with reduced self-efficacy. Implications: Explaining tobacco dependence in neurobiological terms is unlikely to induce feelings of fatalism in relation to smoking cessation. Those who endorse biomedical explanations of smoking may be more open to using cessation pharmacotherapies. Describing smoking in terms of alterations in brain chemistry may be more acceptable to smokers than labeling smoking a "brain disease" or "brain disorder."