PDF(Pubmed)
Abstract：
Reward Deficiency Syndrome (RDS) is defined as a breakdown of reward neurotransmission that results in a wide range of addictive, compulsive, and impulsive behaviors. RDS is caused by a combination of environmental (epigenetic) influences and DNA-based (genetic) neurotransmission deficits that interfere with the normal satisfaction of human physiological drives (i.e., food, water, and sex). An essential feature of RDS is the lack of integration between perception, cognition, and emotions that occurs because of (1) significant dopaminergic surges in motivation, reward, and learning centers causing neuroplasticity in the striato-thalamic-frontal cortical loop; (2) hypo-functionality of the excitatory glutamatergic afferents from the amygdala-hippocampus complex. A large volume of literature regarding the known neurogenetic and psychological underpinnings of RDS has revealed a significant risk of dopaminergic gene polymorphic allele overlap between cohorts of depression and subsets of schizophrenia. The suggestion is that instead of alcohol, opioids, gambling disorders, etc. being endophenotypes, the true phenotype is RDS. Additionally, reward deficiency can result from depleted or hereditary hypodopaminergia, which can manifest as a variety of personality traits and mental/medical disorders that have been linked to genetic studies with dopamine-depleting alleles. The carrying of known DNA antecedents, including epigenetic insults, results in a life-long vulnerability to RDS conditions and addictive behaviors. Epigenetic repair of hypodopaminergia, the causative basis of addictive behaviors, may involve precision DNA-guided therapy achieved by combining the Genetic Addiction Risk Severity (GARS) test with a researched neutraceutical having a number of variant names, including KB220Z. This nutraceutical formulation with pro-dopamine regulatory capabilities has been studied and published in peer-reviewed journals, mostly from our laboratory. Finally, it is our opinion that RDS should be given an ICD code and deserves to be included in the DSM-VI because while the DSM features symptomology, it is equally important to feature etiological roots as portrayed in the RDS model.
摘要：
奖励缺乏综合症（RDS）被定义为奖励神经传递的崩溃，导致广泛的成瘾，强迫性,和冲动的行为。RDS是由环境（表观遗传）影响和基于DNA的（遗传）神经传递缺陷的组合引起的，这些缺陷会干扰人体生理驱动的正常满足（即，食物,水,和性别）。RDS的一个基本特征是感知之间缺乏整合，认知，以及由于（1）动机中多巴胺能的显着激增而发生的情绪，奖励,和学习中心在纹状体-丘脑-额叶皮质回路中引起神经可塑性；（2）杏仁核-海马复合体的兴奋性谷氨酸能传入的功能低下。有关RDS已知的神经遗传学和心理基础的大量文献表明，抑郁症和精神分裂症亚群之间存在多巴胺能基因多态性等位基因重叠的显着风险。建议是代替酒精，阿片类药物,赌博障碍,等。作为内表型，真正的表型是RDS。此外,奖赏缺乏可能是由耗尽或遗传性多巴胺减少引起的，这可以表现为各种人格特质和精神/医学障碍，这些障碍与多巴胺消耗等位基因的遗传研究有关。携带已知的DNA前身，包括表观遗传侮辱，导致对RDS疾病和成瘾行为的终身脆弱性。低多巴胺血症的表观遗传修复，成瘾行为的因果基础，可能涉及通过将遗传成瘾风险严重程度（GARS）测试与具有许多变体名称的研究营养品相结合来实现的精确DNA指导治疗，包括KB220Z。这种具有促多巴胺调节能力的营养制剂已被研究并发表在同行评审的期刊上，主要来自我们的实验室。最后,我们认为RDS应该被赋予ICD代码，并且应该被包括在DSM-VI中，因为虽然DSM具有症状学，同样重要的是,如RDS模型中所描绘的,以病因学根源为特征.
