Rastmanesh Reza
Clinical Nutrition and Dietetics, National Nutrition and Food Sciences Technology Research Institute, Shahid Beheshti University of Medical Sciences, Arghavane Gharbi, Shahrake Gharb, Tehran, Iran.
Atten Defic Hyperact Disord. 2010 Nov;2(3):149-57. doi: 10.1007/s12402-010-0033-z. Epub 2010 Sep 14.
Abnormal dopamine (DA) transporter functioning has long been suspected to be involved in attention-deficit hyperactivity disorder (ADHD). My extensive search on theories concerning ADHD included: CENTRAL, MEDLINE, EMBASE, CINAHL, ERIC, PsycINFO, Complementary and Alternative Medicine-specific databases, Informit, JST, plus grey literature and trial registries from inception to May 2010. A new understanding of ADHD pathophysiology is required. DA-deficit theory of ADHD is insufficient to cover critical aspects of ADHD pathology and medication. The dominance of this theory discourages the human and financial investments needed to explore alternative theories and has caused an evident bias in health and drug policies. A combined theory of altered DA and serotonin (5HT), deficit DA, and weakened prefrontal cortex (PFC) circuits may serve as a good alternate to DA-theory alone. This combined theory may influence the future of drug polices, pharmaceutical investments, treatment options, and drug developments.
长期以来，人们一直怀疑多巴胺（DA）转运体功能异常与注意力缺陷多动障碍（ADHD）有关。我对有关ADHD的理论进行了广泛搜索，包括：CENTRAL、MEDLINE、EMBASE、CINAHL、ERIC、PsycINFO、补充和替代医学专用数据库、Informit、JST，以及从创刊到2010年5月的灰色文献和试验注册库。需要对ADHD的病理生理学有新的认识。ADHD的多巴胺缺乏理论不足以涵盖ADHD病理和药物治疗的关键方面。该理论的主导地位阻碍了探索替代理论所需的人力和财力投入，并在健康和药物政策方面造成了明显的偏见。多巴胺（DA）和5-羟色胺（5HT）改变、多巴胺缺乏以及前额叶皮质（PFC）回路减弱的联合理论可能是仅用多巴胺理论的一个很好的替代方案。这种联合理论可能会影响药物政策、制药投资、治疗选择和药物开发的未来。
