Understanding the Scientific Basis of Post-traumatic Stress Disorder (PTSD): Precision Behavioral Management Overrides Stigmatization

Blum, Kenneth; Gondré–Lewis, Marjorie C.; Modestino, Edward J.; Lott, Lisa; Baron, Dror; Siwicki, David; McLaughlin, Thomas J.; Howeedy, Ahmed; Krengel, Maxine; Oscar‐Berman, Marlene; Thanos, Panayotis K.; Elman, Igor; Hauser, Mary; Fried, Lyle; Bowirrat, Abdalla; Badgaiyan, Rajendra D.

doi:10.1007/s12035-019-1600-8

Cited by 25 publications

(17 citation statements)

References 103 publications

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“…Along with other accumulating evidence, dysregulation of monoaminergic transmission in PTSD pathogenesis has been hypothesized (Abdallah et al, 2019;Blum et al, 2019). In this hypothesis, monoamine dysregulation-based altered function of the dlPFC, amygdala, and striatum (Abdallah et al, 2019) or hypodopaminergia (low dopamine function) (Blum et al, 2019) is a key mediator of PTSD. Assuming the involvement of the altered dopaminergic neural circuit, Elfn1 could be associated with the PTSD pathophysiology through the habenular neural circuit as described above (see ''Dopaminergic System and SST-INs'' section).…”

Section: Ptsdmentioning

confidence: 98%

“…A recent genome-wide association studies meta-analysis showed that PARK2, a dopamine regulation-related gene, is associated with PTSD (Nievergelt et al, 2019). Along with other accumulating evidence, dysregulation of monoaminergic transmission in PTSD pathogenesis has been hypothesized (Abdallah et al, 2019;Blum et al, 2019). In this hypothesis, monoamine dysregulation-based altered function of the dlPFC, amygdala, and striatum (Abdallah et al, 2019) or hypodopaminergia (low dopamine function) (Blum et al, 2019) is a key mediator of PTSD.…”

Section: Ptsdmentioning

confidence: 99%

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Trans-Synaptic Regulation of Metabotropic Glutamate Receptors by Elfn Proteins in Health and Disease

Matsunaga

Aruga

2021

Front. Neural Circuits

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Trans-regulation of G protein-coupled receptors (GPCRs) by leucine-rich repeat (LRR) transmembrane proteins has emerged as a novel type of synaptic molecular interaction in the last decade. Several studies on LRR–GPCR interactions have revealed their critical role in synapse formation and in establishing synaptic properties. Among them, LRR–GPCR interactions between extracellular LRR fibronectin domain-containing family proteins (Elfn1 and Elfn2) and metabotropic glutamate receptors (mGluRs) are particularly interesting as they can affect a broad range of synapses through the modulation of signaling by glutamate, the principal excitatory transmitter in the mammalian central nervous system (CNS). Elfn–mGluR interactions have been investigated in hippocampal, cortical, and retinal synapses. Postsynaptic Elfn1 in the hippocampus and cerebral cortex mediates the tonic regulation of excitatory input onto somatostatin-positive interneurons (INs) through recruitment of presynaptic mGluR7. In the retina, presynaptic Elfn1 binds to mGluR6 and is necessary for synapse formation between rod photoreceptor cells and rod-bipolar cells. The repertoire of binding partners for Elfn1 and Elfn2 includes all group III mGluRs (mGluR4, mGluR6, mGluR7, and mGluR8), and both Elfn1 and Elfn2 can alter mGluR-mediated signaling through trans-interaction. Importantly, both preclinical and clinical studies have provided support for the involvement of the Elfn1–mGluR7 interaction in attention-deficit hyperactivity disorder (ADHD), post-traumatic stress disorder (PTSD), and epilepsy. In fact, Elfn1–mGluR7-associated disorders may reflect the altered function of somatostatin-positive interneuron inhibitory neural circuits, the mesolimbic and nigrostriatal dopaminergic pathway, and habenular circuits, highlighting the need for further investigation into this interaction.

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Section: Ptsdmentioning

confidence: 98%

Section: Ptsdmentioning

confidence: 99%

Trans-Synaptic Regulation of Metabotropic Glutamate Receptors by Elfn Proteins in Health and Disease

Matsunaga

Aruga

2021

Front. Neural Circuits

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“…In an effort to shed some new light on this very important issue, the authors, have gathered information from an array of different backgrounds, pooling experience, academic knowledge, and data, that indicates a paradigm shift called "Precision Behavioral Management" is occurring and has therapeutic potential in the future. [14][15][16][17][18][19][20]…”

Section: Substance Use Disorder and Ethnicitymentioning

confidence: 99%

A Review of DNA Risk Alleles to Determine Epigenetic Repair of mRNA Expression to Prove Therapeutic Effectiveness in Reward Deficiency Syndrome (RDS): Embracing “Precision Behavioral Management”

Blum¹,

Steinberg²,

Gondré–Lewis³

et al. 2021

PRBM

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This is a review of research on “Precision Behavioral Management” of substance use disorder (SUD). America is experiencing a high prevalence of substance use disorder, primarily involving legal and illegal opioid use. A 3000% increase in treatment for substance abuse has occurred between 2000 and 2016. Unfortunately, present day treatment of opioid abuse involves providing replacement therapy with powerful opioids to, at best, induce harm reduction, not prophylaxis. These interventions do not enhance gene expression and restore the balance of the brain reward system’s neurotransmitters. We are proposing a generalized approach called “Precision Behavioral Management”. This approach includes 1) using the Genetic Addiction Risk Severity (GARS, a 10 candidate polymorphic gene panel shown to predict ASI-alcohol and drug severity) to assess early pre-disposition to substance use disorder; 2) using a validated reward deficiency syndrome (RDS) questionnaire; 3) utilization of the Comprehensive Analysis of Reported Drugs (CARD™) to assess treatment compliance and abstinence from illicit drugs during treatment, and, importantly; 4) utilization of a “Pro-dopamine regulator (KB220)” (via IV or oral [KB220Z] delivery systems) to optimize gene expression, restore the balance of the Brain Reward Cascade’s neurotransmitter systems and prevent relapse by induction of dopamine homeostasis, and; 5) utilization of targeted DNA polymorphic reward genes to direct mRNA genetic expression profiling during the treatment process. Incorporation of these events can be applied to not only the under-considered African-American RDS community, but all victims of RDS, as a demonstration of a paradigm shift that uniquely provides a novel putative “standard of care” based on DNA guided precision nutrition therapy to induce “dopamine homeostasis” and rebalance neurotransmitters in the Brain Reward Cascade. We are also developing a Reward Deficiency Syndrome Diagnostic Criteria (RDSDC) to assist in potential tertiary treatment.

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“…Previous studies have considered the role of neurotransmitters in lucid dreams [9][10][11][12]. Also, Blum et al characterized the pathogenesis of PTSD as a severe polygenic disorder triggered by environmental factors [15]. An abundance of polymorphic genes, in particular, the alleles that are the genetic determinants of low dopamine function (hypodopaminergia) associate with a predisposition to PTSD as well as SUD [16].…”

Section: Molecular Neurobiology Of Lucid Dreamsmentioning

confidence: 99%

Epigenetic Repair of Terrifying Lucid Dreams by Enhanced Brain Reward Functional Connectivity and Induction of Dopaminergic Homeo - static Signaling

Blum

McLaughlin²,

Modestino

et al. 2021

CPSP

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: During Lucid Dreams, the dreamer is aware, experiences the dream as if fully awake, and may control the dream content. The dreamer can start, stop, and restart dreaming, depending on the nature and pleasantness of the dream. For patients with Reward Deficiency Syndrome (RDS) behaviors, like Attention Deficit Hyperactivity Disorder (ADHD), Tourette's- Syndrome, and Posttraumatic Stress Disorder (PTSD), the dream content may be pleasant, unpleasant, or terrifying. A sample of psychiatric center patients identified as having RDS reported the effectiveness of a neuronutrient, dopamine agonist, KB200Z, in combating terrifying, lucid dreaming. These reports motivated the study of eight clinical cases with known histories of substance abuse, childhood abuse, and PTSD. The administration of KB200Z, associated with eliminating unpleasant or terrifying lucid dreams in 87.5% of the cases. Subsequently, other published cases have further established the possibility of the long-term elimination of terrifying dreams in PTSD and ADHD patients. Induction of dopamine homeostasis may mitigate the effects of neurogenetic and epigenetic changes in neuroplasticity, identified in the pathogenesis of PTSD and ADHD. The article explores how relief of terrifying lucid dreams may benefit from modulation of dopaminergic signaling activated by the administration of a neuronutrient. Recently precision formulations of the KB220 neuronutrient guided by Genetic Addiction Risk Score (GARS) test results have been used to repair inheritable deficiencies within the brain reward circuitry. The proposition is that improved dopamine transmodulational signaling may stimulate positive cognitive recall and subsequently attenuate the harmful epigenetic insults from trauma.

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Understanding the Scientific Basis of Post-traumatic Stress Disorder (PTSD): Precision Behavioral Management Overrides Stigmatization

Cited by 25 publications

References 103 publications

Trans-Synaptic Regulation of Metabotropic Glutamate Receptors by Elfn Proteins in Health and Disease

Trans-Synaptic Regulation of Metabotropic Glutamate Receptors by Elfn Proteins in Health and Disease

A Review of DNA Risk Alleles to Determine Epigenetic Repair of mRNA Expression to Prove Therapeutic Effectiveness in Reward Deficiency Syndrome (RDS): Embracing “Precision Behavioral Management”

Epigenetic Repair of Terrifying Lucid Dreams by Enhanced Brain Reward Functional Connectivity and Induction of Dopaminergic Homeo - static Signaling

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