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Reward Deficiency Syndrome (RDS) Surprisingly Is Evolutionary and Found Everywhere: Is It "Blowin' in the Wind"?奖赏缺乏综合征(RDS)令人惊讶地具有进化性且随处可见:它是“在风中飘荡”吗?
J Pers Med. 2022 Feb 21;12(2):321. doi: 10.3390/jpm12020321.
2
Time of onset and/or diagnosis of ADHD in European children: a systematic review.欧洲儿童注意缺陷多动障碍发病时间和/或诊断时间的系统评价。
BMC Psychiatry. 2021 Nov 16;21(1):575. doi: 10.1186/s12888-021-03547-x.
3
Epigenetic Repair of Terrifying Lucid Dreams by Enhanced Brain Reward Functional Connectivity and Induction of Dopaminergic Homeostatic Signaling.通过增强脑奖赏功能连接和诱导多巴胺能稳态信号对可怕的清醒梦进行表观遗传修复。
Curr Psychopharmacol. 2021 Feb 15;10. doi: 10.2174/2211556010666210215153513.
4
Biotechnical development of genetic addiction risk score (GARS) and selective evidence for inclusion of polymorphic allelic risk in substance use disorder (SUD).遗传成瘾风险评分(GARS)的生物技术发展以及物质使用障碍(SUD)中纳入多态性等位基因风险的选择性证据。
J Syst Integr Neurosci. 2020 Aug;6(2). doi: 10.15761/JSIN.1000221. Epub 2019 Dec 19.
5
Psychostimulant use disorder emphasizing methamphetamine and the opioid -dopamine connection: Digging out of a hypodopaminergic ditch.强调甲基苯丙胺和阿片类药物-多巴胺联系的精神兴奋剂使用障碍:从多巴胺能减退的困境中摆脱出来。
J Neurol Sci. 2021 Jan 15;420:117252. doi: 10.1016/j.jns.2020.117252. Epub 2020 Nov 28.
6
Network and pathway enrichment analysis of Attention Deficit/Hyperactivity Disorder candidate genes.注意缺陷多动障碍候选基因的网络和通路富集分析
Indian J Psychiatry. 2020 Jul-Aug;62(4):400-406. doi: 10.4103/psychiatry.IndianJPsychiatry_105_17. Epub 2020 Jul 27.
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Genetic Influence on Efficacy of Pharmacotherapy for Pediatric Attention-Deficit/Hyperactivity Disorder: Overview and Current Status of Research.遗传因素对儿童注意力缺陷/多动障碍药物治疗疗效的影响:研究概述与现状
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A literature review and meta-analysis on the effects of ADHD medications on functional outcomes.一篇关于注意力缺陷多动障碍(ADHD)药物对功能结局影响的文献综述与荟萃分析。
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Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder.发现首个与注意缺陷多动障碍全基因组显著相关的风险位点。
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Attention-Deficit/Hyperactivity Disorder and Nicotine Dependence in Adults.成人注意缺陷多动障碍与尼古丁依赖
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儿童使用精神兴奋剂:我们用药过量还是不足?

Psychostimulants for Children: Are We Over or Under Dosing?

作者信息

Blum Kenneth, Dennen Catherine, Carney Paul R, Gilley Elizabeth, Thanos Panayotis K, Braverman Eric R, Baron David, Hanna Colin, Modestino Edward J, Gold Mark S, Elman Igor, Badgaiyan Rajendra D

机构信息

Division of Addiction Research & Education, Center for Sports, Exercise & Mental Health, Western University Health Sciences, Pomona, CA, USA.

The Kenneth Blum Institute of Neurogenetics & Behavior, LLC., Austin, TX, USA.

出版信息

J Addict Psychiatry. 2023;7(1):1-4. Epub 2023 Apr 22.

PMID:37560458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10411151/
Abstract

An estimated 3% to 10% of school children meet the DSM-V criteria for ADHD (Attention-Deficit/Hyperactivity Disorder), however, to be over-diagnosed, the rate of children inappropriately diagnosed with ADHD (false positives) would have to be larger than the number of children with ADHD who are under-identified and not diagnosed (false negatives). Accordingly, a number of investigators take the position that under-treatment with psychostimulants, especially in children and adolescence, will result in continued ADHD symptomatology including future Substance Use Disorder (SUD). However, other researchers and clinicians believe otherwise and espouse laudable arguments for caution and prolonged methamphetamine treatment. While there is ongoing controversy of the role of genetics and epigenetics linked to ADHD, it seems clear that a number of dopaminergic genes and their risk polymorphisms act as DNA antecedents impacted by epigenetic induced methylation. Our hypothesis and literature review suggest that one possible solution is to embrace non addictive interventions to induce global dopamine homeostasis.

摘要

据估计,3%至10%的学童符合精神疾病诊断与统计手册第五版(DSM-V)中注意力缺陷多动障碍(ADHD)的标准。然而,要存在过度诊断的情况,被不恰当地诊断为ADHD(假阳性)的儿童比例必须高于未被识别和诊断的ADHD儿童数量(假阴性)。因此,一些研究人员认为,精神兴奋剂治疗不足,尤其是在儿童和青少年中,会导致ADHD症状持续存在,包括未来的物质使用障碍(SUD)。然而,其他研究人员和临床医生则持不同观点,并主张谨慎和延长甲基苯丙胺治疗时间,这一观点值得称赞。虽然关于与ADHD相关的遗传学和表观遗传学作用仍存在争议,但似乎很明显,一些多巴胺能基因及其风险多态性作为受表观遗传诱导甲基化影响的DNA前体。我们的假设和文献综述表明,一种可能的解决方案是采用非成瘾性干预措施来诱导整体多巴胺稳态。