Taylor Mairin Rose, Carrasco Kelly, Carrasco Andres, Basu Arindam
School of Health Sciences, University of Canterbury, Christchurch, New Zealand.
School of Education, Victoria University of Wellington, Wellington, New Zealand.
Front Neurosci. 2022 Apr 12;16:845646. doi: 10.3389/fnins.2022.845646. eCollection 2022.
Attention-deficit/hyperactivity disorder (ADHD) is a relatively commonly occurring neurodevelopmental disorder affecting approximately 5% of children and young people. The neurobiological mechanisms of ADHD are proposed to particularly center around increased dopamine receptor availability related to associated symptoms of reduced attention regulation and impulsivity. ADHD is also persistent across the lifespan and associated with a raft of impulsive and health-risk behaviors including substance abuse and smoking. Research highlighting the potentially significant levels of monoamine oxidase (MAO) inhibitory properties in tobacco smoke and e-cigarettes may provide a mechanism for increased tobacco smoke dependence among those with ADHD, in addition to the role of nicotine.
This scoping review aimed to establish evidence for the above neurobiological pathway between smoking and ADHD symptom-alleviation or "self-medication" with the inclusion of the mechanism of MAO-inhibitors indirect increasing dopamine in the brain.
Scoping review methodologies were employed in this review selected to synthesize multiple sources of empirical research to identify current gaps in the knowledge base and identify key characteristics of research data related to a phenomenon. Databases searched included OVID MEDLINE(R), Embase, Cochrane, PsycINFO and SCOPUS limited to 2000 onward and empirically validated, peer-reviewed research.
There is support for the role of MAO-inhibition on greater reinforcement of smoking for individuals with ADHD through a greater impact on dopaminergic availability than nicotine; potentially moderating ADHD symptoms.
Greater support for a "self-medication" model of ADHD and smoking includes not only nicotine but also MAO-inhibitors as dopamine agonists contained in cigarettes and e-cigarettes.
注意缺陷多动障碍（ADHD）是一种相对常见的神经发育障碍，影响约5%的儿童和青少年。ADHD的神经生物学机制被认为特别围绕与注意力调节和冲动性降低相关症状有关的多巴胺受体可用性增加。ADHD在整个生命周期中持续存在，并与一系列冲动和健康风险行为相关，包括药物滥用和吸烟。除了尼古丁的作用外，强调烟草烟雾和电子烟中可能具有显著水平的单胺氧化酶（MAO）抑制特性的研究，可能为ADHD患者烟草烟雾依赖性增加提供一种机制。
本范围综述旨在为吸烟与ADHD症状缓解或“自我用药”之间的上述神经生物学途径建立证据，包括MAO抑制剂间接增加大脑中多巴胺的机制。
本综述采用范围综述方法，选择综合多个实证研究来源，以识别知识库中当前的差距，并识别与一种现象相关的研究数据的关键特征。检索的数据库包括OVID MEDLINE(R)、Embase、Cochrane、PsycINFO和SCOPUS，限于2000年以后且经过实证验证、同行评审的研究。
有证据支持MAO抑制对ADHD患者吸烟强化作用更大，这是因为其对多巴胺能可用性的影响大于尼古丁，可能减轻ADHD症状。
对ADHD与吸烟“自我用药”模型的更多支持不仅包括尼古丁，还包括香烟和电子烟中作为多巴胺激动剂的MAO抑制剂。
