Blum Kenneth, Mclaughlin Thomas, Gold Mark S, Gondre-Lewis Marjorie C, Thanos Panayotis K, Elman Igor, Baron David, Bowirrat Abdalla, Barh Debamyla, Khalsa Jag, Hanna Colin, Jafari Nicole, Zeine Foojan, Braverman Eric R, Dennen Catherine, Makale Milan T, Makale Miles, Sunder Keerthy, Murphy Kevin T, Badgaiyan Rajendra D
The Kenneth Blum Behavioral and Neurogenetic Institute, LLC., Austin, TX, USA.
Center for Sports, Exercise, Psychiatry, Western University Health Sciences, Pomona, CA, USA.
J Addict Psychiatry. 2023;7(1):5-516. Epub 2023 Dec 8.
In the USA alone, opioid use disorder (OUD) affects approximately 27 million people. While the number of prescriptions may be declining due to increased CDC guidance and prescriber education, fatalities due to fentanyl-laced street heroin are still rising. Our laboratory has extended the overall concept of both substance and non-substance addictive behaviors, calling it "Reward Deficiency Syndrome (RDS)." Who are its victims, and how do we get this unwanted disorder? Is RDS caused by genes (Nature), environment (Neuro-epigenetics, Nurture), or both? Recent research identifies resting-state functional connectivity in the brain reward circuitry as a crucial factor. Analogously, it is of importance to acknowledge that the cumulative discharge of dopamine, governed by the nucleus accumbens (NAc) and modulated by an array of additional neurotransmitters, constitutes a cornerstone of an individual's overall well-being. Neuroimaging reveals that high-risk individuals exhibit a blunted response to stimuli, potentially due to DNA polymorphisms or epigenetic alterations. This discovery has given rise to the idea of a diminished 'thrill,' though we must consider whether this 'thrill' may have been absent from birth due to high-risk genetic predispositions for addiction. This article reviews this issue and suggests the general concept of the importance of "induction of dopamine homeostasis." We suggest coupling a validated genetic assessment (e.g., GARS) with pro-dopamine regulation (KB220) as one possible frontline modality in place of prescribing potent addictive opioids for OUD except for short time harm reduction. Could gene editing offer a 'cure' for this undesirable genetic modification at birth, influenced by the environment and carried over generations, leading to impaired dopamine and other neurotransmitter imbalances, as seen in RDS? Through dedicated global scientific exploration, we hope for a future where individuals are liberated from pain and disease, achieving an optimal state of well-being akin to the proverbial 'Garden of Eden'.
仅在美国,阿片类药物使用障碍(OUD)就影响了约2700万人。尽管由于疾病控制与预防中心(CDC)的指导增加以及开处方者教育的加强,处方数量可能在下降,但因掺有芬太尼的街头海洛因导致的死亡人数仍在上升。我们的实验室扩展了物质和非物质成瘾行为的总体概念,将其称为“奖赏缺乏综合征(RDS)”。它的受害者是谁,我们又是如何患上这种不良疾病的呢?RDS是由基因(天性)、环境(神经表观遗传学,后天培养)还是两者共同导致的?最近的研究表明,大脑奖赏回路中的静息态功能连接是一个关键因素。类似地,必须认识到,由伏隔核(NAc)控制并由一系列其他神经递质调节的多巴胺累积释放,是个体整体幸福感的基石。神经影像学显示,高危个体对刺激的反应迟钝,这可能是由于DNA多态性或表观遗传改变所致。这一发现引发了“快感”降低的观点,不过我们必须考虑这种“快感”是否可能由于成瘾的高危遗传易感性而从出生就不存在。本文回顾了这个问题,并提出了“诱导多巴胺稳态”重要性的总体概念。我们建议将经过验证的基因评估(如GARS)与促多巴胺调节(KB220)相结合,作为一种可能的一线治疗方式,以取代除短期减少伤害外为OUD开具强效成瘾性阿片类药物。基因编辑能否治愈这种出生时受环境影响并代代相传的不良基因改变,这种改变会导致多巴胺和其他神经递质失衡,就像在RDS中看到的那样?通过专门的全球科学探索,我们希望有一个未来,个体能从疼痛和疾病中解脱出来,实现类似于“伊甸园”的最佳幸福状态。