2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Pro-Dopamine Regulator (KB220) A Fifty Year Sojourn to Combat Reward Deficiency Syndrome (RDS): Evidence Based Bibliography (Annotated)

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          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.

          Bibliography Presentation

          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.

          Conclusion

          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.

          Summary

          Such phenotypes are precisely characterized using the Genetic Addiction Risk Score (GARS). Dopamine homeostasis may thus be achieved via PAM, the customization of neuro-nutrient supplementation (KB220 variants based on previous research with KB220) tied to the GARS test result, along with a behavioral/ spiritual intervention [ 41, 42].

          Related collections

          Most cited references38

          • Record: found
          • Abstract: found
          • Article: not found

          rsfMRI effects of KB220Z™ on neural pathways in reward circuitry of abstinent genotyped heroin addicts.

          Recently, Willuhn et al. reported that cocaine use and even non-substance-related addictive behavior increases as dopaminergic function is reduced. Chronic cocaine exposure has been associated with decreases in D2/D3 receptors and was also associated with lower activation of cues in occipital cortex and cerebellum, in a recent PET study by Volkow's et al. Therefore, treatment strategies, like dopamine agonist therapy, that might conserve dopamine function may be an interesting approach to relapse prevention in psychoactive drug and behavioral addictions. To this aim, we evaluated the effect of KB220Z™ on reward circuitry of 10 heroin addicts undergoing protracted abstinence (average 16.9 months). In a randomized placebo-controlled crossover study of KB220Z, five subjects completed a triple-blinded experiment in which the subject, the person administering the treatment, and the person evaluating the response to treatment were blinded to the treatment that any particular subject was receiving. In addition, nine subjects were genotyped utilizing the GARSDX™ test. We preliminarily report that KB220Z induced an increase in BOLD activation in caudate-accumbens-dopaminergic pathways compared to placebo following 1-hour acute administration. Furthermore, KB220Z also reduced resting-state activity in the putamen of abstinent heroin addicts. In the second phase of this pilot study of all 10 abstinent heroin-dependent subjects, we observed that three brain regions of interest were significantly activated from resting state by KB220Z compared to placebo (p < 0.05). Increased functional connectivity was observed in a putative network that included the dorsal anterior cingulate, medial frontal gyrus, nucleus accumbens, posterior cingulate, occipital cortical areas, and cerebellum. These results and other quantitative electroencephalogy (qEEG) study results suggest a putative anti-craving/anti-relapse role of KB220Z in addiction by direct or indirect dopaminergic interaction. Due to small sample size, we caution definitive interpretation of these preliminary results, and confirmation with additional research and ongoing rodent and human studies of KB220Z is required.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Overcoming qEEG abnormalities and reward gene deficits during protracted abstinence in male psychostimulant and polydrug abusers utilizing putative dopamine D₂ agonist therapy: part 2.

            It is well established that in both food- and drug-addicted individuals there is "dopamine resistance" associated with the DRD2 gene A1 allele. Based on earlier studies, evidence is emerging wherein the potential of utilizing a natural, nonaddicting, safe, putative D2 agonist may play a significant role in the recovery of individuals with reward deficiency syndrome, including those addicted to psychoactive chemicals.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Enhanced functional connectivity and volume between cognitive and reward centers of naïve rodent brain produced by pro-dopaminergic agent KB220Z

              Dopaminergic reward dysfunction in addictive behaviors is well supported in the literature. There is evidence that alterations in synchronous neural activity between brain regions subserving reward and various cognitive functions may significantly contribute to substance-related disorders. This study presents the first evidence showing that a pro-dopaminergic nutraceutical (KB220Z) significantly enhances, above placebo, functional connectivity between reward and cognitive brain areas in the rat. These include the nucleus accumbens, anterior cingulate gyrus, anterior thalamic nuclei, hippocampus, prelimbic and infralimbic loci. Significant functional connectivity, increased brain connectivity volume recruitment (potentially neuroplasticity), and dopaminergic functionality were found across the brain reward circuitry. Increases in functional connectivity were specific to these regions and were not broadly distributed across the brain. While these initial findings have been observed in drug naïve rodents, this robust, yet selective response implies clinical relevance for addicted individuals at risk for relapse, who show reductions in functional connectivity after protracted withdrawal. Future studies will evaluate KB220Z in animal models of addiction.
                Bookmark

                Author and article information

                Journal
                101738637
                48232
                CPQ Neurol Psychol
                CPQ neurology and psychology
                21 December 2018
                4 December 2018
                2018
                04 April 2019
                : 1
                : 2
                : https://www.cientperiodique.com/journal/fulltext/CPQNP/1/2/13
                Affiliations
                [1 ]Western University Health Sciences, Graduate School of Biomedical Sciences, Pomona, CA
                [2 ]Eotvos Loránd University, Institute of Psychology, Budapest, Hungary
                [3 ]Department of Psychiatry, Wright State University Boonshoft School of Medicine and Dayton VA Medical Center, Dayton, OH, USA
                [4 ]Department of Clinical Neurology, Path Foundation NY, New York, USA
                [5 ]Department of Psychiatry, University of Vermont, Burlington, VM, USA
                [6 ]Dominion Diagnostics, LLC., North Kingston, RI, USA
                [7 ]Division of Precision Addiction Management, Geneus Health, LLC., San Antonio, TX, USA
                [8 ]Division of Addiction Therapy Research, Nupathways, Inc., Meadow Ridge Dr. Innsbrook, MO, USA
                [9 ]Division of Neurogenetic Research & Addiction Therapy, The Florida House Experience, Deerfield Beach, FL, USA
                [10. ]Division of Nutrigenomics, Victory Nutrition International. LLC., Lederach, PA
                [11 ]Department of Psychology, Curry College, Milton, MA, USA
                [12 ]Departments of Anatomy & Psychiatry & Behavioral Sciences, Howard University School of Medicine, Washington, DC, USA
                [13 ]Behavioral Neuropharmacology & Neuroimaging Laboratory on Addiction, Research Institute on Addictions, University of Buffalo, Buffalo, NY, USA
                [14 ]Department of Psychiatry, Ichan School of Medicine at Mount Sinai, New York, NY, USA
                Author notes
                [* ]Correspondence to: Dr. Kenneth Blum, Western University Health Sciences, Graduate School of Biomedical Sciences, Pomona, CA, USA.
                Article
                NIHMS1000396
                6448775
                30957097
                5b56bc9b-a55f-4246-a0cd-c7ca350decc0

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Article

                annotated,kb220,restoregen variant,genetic addiction risk score (gars®),precision addiction management (pam®)

                Comments

                Comment on this article