University of Queensland School of Public Health, Public Health Building, Herston, Queensland, Australia.
University of Queensland School of Medicine, Royal Brisbane and Women's Hospital Site, Herston, Queensland, Australia.
Nicotine Tob Res. 2018 Jun 7;20(7):827-835. doi: 10.1093/ntr/ntx144.
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.
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.
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).
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.
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."
成瘾越来越被定义为一种由神经化学变化引起的“脑部疾病”。虽然尼古丁成瘾在成瘾的脑部疾病模型（BDMA）中历来被排除在外，但它开始被标记为一种慢性脑部疾病。我们调查了澳大利亚吸烟者是否认可吸烟的基于大脑的解释，以及这些信念是否与戒烟自我效能或治疗意向相关。
横断面研究澳大利亚吸烟者（N=1538），他们完成了一项测量他们对吸烟对大脑作用的陈述的同意程度的调查。逻辑回归检验了这些项目与社会人口统计学变量、戒烟自我效能和使用戒烟药物的意图之间的关联。
大多数（57.9%）人同意吸烟改变了大脑化学物质，34.4%的人同意吸烟是一种脑部疾病。年龄较小的参与者和受教育程度较高的参与者更有可能认同吸烟的基于大脑的理解。同意吸烟改变大脑化学物质的参与者更有可能报告使用戒烟药物的意图（OR 1.5，95%CI=1.0-2.2），同意吸烟是一种脑部疾病的参与者也是如此（OR 1.5，95%CI=1.1-2.1）。同意吸烟改变大脑化学物质的人与不同意者的自我效能没有差异。然而，那些同意吸烟是一种脑部疾病的人的自我效能高于不同意者（OR 1.7，95%CI=1.3-2.3）。
吸烟的神经生物学观点并没有主导澳大利亚公众对吸烟的理解。对吸烟的神经生物学解释的认可与增加使用戒烟辅助工具的意图有关，但与自我效能的降低无关。
用神经生物学术语解释烟草依赖不太可能导致与戒烟相关的宿命感。那些认可吸烟的生物医学解释的人可能更愿意使用戒烟药物治疗。用大脑化学物质的改变来描述吸烟可能比将吸烟标记为“脑部疾病”或“脑部障碍”更容易被吸烟者接受。
