Kenneth Blum, Edward Modestino J, Marjorie Gondre Lewis C, David Baron, Bruce Steinberg, Panayotis Thanos K, William Downs B, Davis Siwicki, Lisa Lott, Eric Braverman R, Mark Moran, David Miller, Lyle Fried, Rajendra Badgaiyan D
Western University Health Sciences, Graduate School of Biomedical Sciences, Pomona, CA.
Eotvos Loránd University, Institute of Psychology, Budapest, Hungary.
CPQ Neurol Psychol. 2018;1(2). Epub 2018 Dec 4.
We are facing a significant challenge in combatting the current opioid and drug epidemic worldwide. In the USA, although there has been notable progress, in 2017 alone 72,000 people died from a narcotic overdose. The NIAAA & NIDA continue to struggle with innovation to curb or eliminate this unwanted epidemic. The current FDA list of approved Medication Assistance Treatments (MATS) work by primarily blocking dopamine function and release at the pre-neuron in the nucleus accumbens. We oppose this option in the long term tertiary treatment but agree for short term harm reduction potential.
As an alternative motif, the utilization of a well-researched neuro-nutrient called KB220 has been intensely investigated in at least 38 studies showing evident effects related to everything from AMA rate, attenuation of craving behavior, reward system activation including BOLD dopamine signaling, relapse prevention, as well as reduction in stress, anger, and aggressive behaviors. We are continuing research especially as it relates to genetic risk, including the now patented Genetic Addiction Risk Score (GARS) and the development of "Precision Addiction Management (PAM)" to potentially combat the opioid/psychostimulant epidemic.
Based on animal research and clinical trials as presented herein, the Pro-Dopamine Regulator known as KB220 shows promise in the addiction and pain space. Other neurobiological and genetic studies are required to help understand the mechanism of action of this neuro-nutrient. However, the evidence to date points to induction of "dopamine homeostasis"enabling an asymptotic approach for epigenetic induced "normalization" of brain neurotransmitter signaling and associated improved function in the face of either genetic or epigenetic impairment of the Brain Reward Cascade (BRC).With that said, we are encouraged about these results as published over the last 50 years and look forward to continued advancements related to appropriate nutrigenomic solutions to the millions of victims of all addictions (from drugs to food to smoking to gambling and gaming especially in our next generation) called Reward Surfeit Syndrome (RSS) in adolescents and Reward Deficiency Syndrome (RDS) in adulthood.
在全球抗击当前的阿片类药物和毒品泛滥问题上,我们正面临重大挑战。在美国,尽管已取得显著进展,但仅在2017年就有7.2万人死于麻醉品过量。美国国立酒精滥用与酒精中毒研究所(NIAAA)和美国国立药物滥用研究所(NIDA)仍在努力创新,以遏制或消除这一不良泛滥问题。美国食品药品监督管理局(FDA)目前批准的药物辅助治疗(MAT)清单主要通过阻断伏隔核中神经元前体的多巴胺功能和释放来发挥作用。从长期三级治疗角度我们反对这种方法,但同意其在短期减少伤害方面的潜力。
作为一种替代方案,一种名为KB220的经过充分研究的神经营养素的应用已在至少38项研究中得到深入研究,这些研究显示出与从AMA率、渴望行为的减轻、奖励系统激活(包括BOLD多巴胺信号传导)、预防复发以及压力、愤怒和攻击性行为的减少等各方面相关的明显效果。我们正在继续开展研究,特别是与遗传风险相关的研究,包括现已获得专利的遗传成瘾风险评分(GARS)以及“精准成瘾管理(PAM)”的开发,以潜在地抗击阿片类药物/精神兴奋剂泛滥问题。
基于本文所述的动物研究和临床试验,被称为KB220的促多巴胺调节剂在成瘾和疼痛领域显示出前景。需要进行其他神经生物学和遗传学研究,以帮助理解这种神经营养素的作用机制。然而,迄今为止的证据表明,“多巴胺稳态”的诱导能够实现一种渐近方法,用于面对大脑奖励级联(BRC)的遗传或表观遗传损伤时,对大脑神经递质信号进行表观遗传诱导的“正常化”以及相关功能的改善。话虽如此,我们对过去50年发表的这些结果感到鼓舞,并期待与适当的营养基因组解决方案相关的持续进展,以解决数百万成瘾受害者(从毒品到食物、吸烟、赌博和游戏,尤其是在我们的下一代中)所面临的问题,这些问题在青少年中被称为奖励过剩综合征(RSS),在成年人中被称为奖励缺乏综合征(RDS)。