Adams Sally
Department of Psychology, University of Bath, 10 West, Bath, BA2 7AY UK.
UK Centre for Tobacco and Alcohol Studies, Bath, UK.
Curr Addict Rep. 2017;4(1):25-34. doi: 10.1007/s40429-017-0129-z. Epub 2017 Feb 18.
Comorbidity of alcohol and tobacco use is highly prevalent and may exacerbate the health effects of either substance alone. However, the mechanisms underlying this comorbidity are not well understood. This review will examine the evidence for shared neurobiological mechanisms of alcohol and nicotine comorbidity and experimental studies of the behavioural consequences of these interactions.
Studies examining the shared neurobiology of alcohol and nicotine have identified two main mechanisms of comorbidity: (1) cross-reinforcement via the mesolimbic dopamine pathway and (2) cross-tolerance via shared genetic and nAChR interaction. Animal and human psychopharmacological studies demonstrate support for these two mechanisms of comorbidity.
Human behavioural studies indicate that (1) alcohol and tobacco potentiate each other's rewarding effects and (2) nicotine reduces the sedative and intoxication effects of alcohol. Together, these findings provide a strong evidence base to support the role of the cross-reinforcement and cross-tolerance as mechanisms underlying the comorbidity of alcohol and tobacco use. Methodological concerns in the literature and recommendations for future studies are discussed alongside implications for treatment of comorbid alcohol and tobacco use.
酒精和烟草使用的共病现象极为普遍,可能会加剧单一物质对健康的影响。然而,这种共病现象背后的机制尚未得到充分理解。本综述将审视酒精和尼古丁共病的共享神经生物学机制的证据,以及这些相互作用行为后果的实验研究。
研究酒精和尼古丁共享神经生物学的研究已经确定了共病的两个主要机制:(1)通过中脑边缘多巴胺途径的交叉强化,以及(2)通过共享基因和nAChR相互作用的交叉耐受。动物和人类精神药理学研究为这两种共病机制提供了支持。
人类行为研究表明,(1)酒精和烟草会增强彼此的奖赏效应,(2)尼古丁会降低酒精的镇静和中毒效应。这些发现共同提供了强有力的证据基础,以支持交叉强化和交叉耐受作为酒精和烟草使用共病潜在机制的作用。文中还讨论了文献中的方法学问题以及对未来研究的建议,同时探讨了对酒精和烟草共病使用治疗的影响。