Do Dreams Have Show Repair Of The Brain
Curr Psychopharmacol. Author manuscript; available in PMC 2022 Oct 26.
Published in final edited course as:
PMCID: PMC8547281
NIHMSID: NIHMS1726353
Epigenetic Repair of Terrifying Lucid Dreams by Enhanced Brain Reward Functional Connectivity and Induction of Dopaminergic Homeostatic Signaling
Kenneth Blum
1Western University Health Sciences, Pomona, CA., Us;
2Department Psychiatry, Wright University, Boonshoff School of Medicine, Dayton, OH., USA;
iiiPartitioning of Neuroscience & Addiction Inquiry Therapy, Pathway Healthcare, Birmingham, AL., Us;
4Segmentation of Nutrigenomics, Geneus Genomic Testing Center, Geneus Wellness, LLC., San Antonio, TX., USA;
5Plant of Psychology, ELTE Eötvös Loránd University, Budapest, Hungary;
Thomas McLaughlin
6Center for Psychiatric Medicine, Laurence, MA., USA;
Edward J. Modestino
7Department of Psychology, Back-scratch Higher, Milton. MA., USA,
David Baron
twoDepartment Psychiatry, Wright Academy, Boonshoff School of Medicine, Dayton, OH., United states of america;
Abdalla Bowirrat
8Department of Neuroscience and Genetics, Interdisciplinary Eye Herzliya, Israel;
Raymond Brewer
4Segmentation of Nutrigenomics, Geneus Genomic Testing Center, Geneus Health, LLC., San Antonio, TX., USA;
Bruce Steinberg
sevenDepartment of Psychology, Curry College, Milton. MA., U.s.a.,
A. Kenison Roy
9Department of Psychiatry, School of Medicine, University of Tulane, New Orleans, LA., Usa;
Marcello Febo
10Section of Psychiatry, McKnight Brain Institute, Academy of Florida, School of Medicine, Gainesville, FL.USA;
Rajendra D. Badgaiyan
11Department of Psychiatry, Ichan School of Medicine, Mount Sinai Hospital, New York, NY.& Department of Psychiatry, South Texas Veteran Health Care System, Audie Fifty. Potato Memorial VA Infirmary, San Antonio, TX, Long School of Medicine, Academy of Texas Medical Center, San Antonio, TX, Us;
Marks Southward. Gold
12Department of Psychiatry, Washington University School of Medicine, St. Louis, Mo. U.s.a.
Abstract
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, similar Attention Arrears 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 written report of viii clinical cases with known histories of substance corruption, childhood abuse, and PTSD. The assistants of KB200Z, associated with eliminating unpleasant or terrifying lucid dreams in 87.5% of the cases. Subsequently, other published cases take further established the possibility of the long-term elimination of terrifying dreams in PTSD and ADHD patients. Induction of dopamine homeostasis may mitigate the furnishings 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 Habit Risk Score (Bloke) 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.
Keywords: Lucid dreams, pro-dopamine regulation (KB220), functional connectivity, neuroplasticity, Genetic Addiction Risk Score (Bloke), dopaminergic homeostatic signaling
1. INTRODUCTION
1.i. Background
During Lucid Dreams, the dreamer becomes aware of dreaming within a dream. Equally if fully awake, the dreamer can control the dream content; start, stop, and restart dreaming, depending on the dream'southward nature. The dream content may be pleasant, unpleasant, or terrifying. Lucid dreaming is a symptom of Reward Deficiency Syndrome (RDS) behaviors, similar Attending Deficit Hyperactivity Disorder (ADHD), Tourette's- Syndrome, and Posttraumatic Stress Disorder (PTSD) [1].
Humans take evolved through many adaptations to evolutionary pressures and, many of the genetic polymorphisms that currently exist, represent survival alleles that load onto "Selfishness" [2]. These aboriginal alleles, especially those tied to dopaminergic function, such as the 7R DRD4 gene and others, while previously advantageous for survival, today represent a risk for addictive behaviors. In particular, Opazo et al. [three] reported that according to a phylogenetic tree, the DRD2l and DRD4rs gene lineages would have originated in the ancestor of gnathostomes between 615 and 473 meg (mya) years ago. Conservation of sequences required for dopaminergic neurotransmission and pocket-sized changes in regulatory regions suggest a functional refinement of the dopaminergic pathways during development [4]. Comprehension of the part of dopaminergic part, from so until now, makes possible the epigenetic induction of required homeostatic rest in the brain advantage circuitry of Homo sapiens.
All the same, presently DNA polymorphisms remain in the man genome, which can signify a loftier chance for drug and non-drug RDS behaviors [five]. Research studies have demonstrated that iterations of pro-dopamine regulator KB220 increased functional connectivity in both animal [half-dozen] and human brains [vii] and prolonged neuroplasticity changes [8]. This consequential show of this neuro-plastic result combined with prolonged cessation of terrifying lucid dream after short term use of KB220 heralds a new research surface area involving Lucid Dream therapeutics.
1.two. Evidence for Alleviating Terrifying Lucid Dreams: A Snapshot
A sample of psychiatric center patients identified as having RDS behaviors reported that the neuronutrient dopamine agonist KB200Z could effectively gainsay terrifying, lucid dreaming. These reports motivated the study of eight clinical cases with known histories of substance abuse, babyhood corruption, and PTSD. The administration of KB200Z, associated with the elimination of unpleasant or terrifying lucid dreams in 87.v% of the cases [9]. In two additional cases, like consolation of terrifying lucid dreams in patients with PTSD was reported [10]. In the offset case, a 51-year-old, obese woman diagnosed with PTSD and low had a history of attempted suicide. She complained of terrifying, lucid nightmares, reminiscent of the sexual/concrete abuse she had suffered in her early babyhood from family members, including her alcoholic father. Her vivid, "bad dreams" remained refractory to treatment, despite six months of Dialectical Behavioral Therapy (DBT) and standard pharmaceutical agents, including prazosin and clonidine. Within one calendar month of treatment with KB220, there was a total alleviation of her terrifying, lucid dreams. A like reduction of terrifying lucid dreams occurred in a 39-twelvemonth-quondam female person with PTSD [10].
In four additional cases, dramatic and persistent alleviation of terrifying lucid dreams in patients diagnosed with ADHD, PTSD, and opioid use disorder (OUD) with KB220 could well have been permanent. Although the patients had stopped taking the nutraceutical for between 10 to 12 months, they no longer reported any recollection or recurrence of terrifying lucid dreams. In the first of these cases, the patient was a 47-year-former married male who required continued buprenorphine-naloxone combination treatment, the second a 32-year-old female with the sole diagnosis of ADHD, the third a 38-twelvemonth-old male, diagnosed with ADHD and Substance Employ Disorder (SUD). The fourth case was a l-yr-old female diagnosed with Booze Employ Disorder (AUD), ADHD, and PTSD [11].
The nigh dramatic instance involved C.J., a 38-year-sometime, unmarried female, living with her mother, who had a history of SUD and ADHD, inattentive type. Her SUD and ADHD had been stable on buprenorphine/naloxone combination equally well as dextro-amphetamine mixed salts for many years. When CJ unexpectedly lost her job for oversleeping and not calling into work, she became depressed and unmotivated. After taking the KB200 nutraceutical for four weeks, she noticed a marked improvement in her mental and motivational status. As well, she noted that her previously unreported shopping and hoarding addictions had dramatically decreased. Moreover, KB220 eliminated her life-long history of terrifying lucid dreams. Finally, she felt more than empowered, with her locus of control shifting from an external to a more internal one [12].
One goal of this review is to provide imaging data related to the function of KB220, discuss the neuro-genetics of lucid dreaming every bit a sub-type of RDS, and advocate for the adoption of a pro-dopamine lifestyle to sustain dopamine homeostasis, despite evolutionary genetics.
one.iii. Molecular Neurobiology of Lucid Dreams
While Freud (1899) portrayed dreams as the regal road to the unconscious and a means of "wish fulfillment," nightmares have been regarded by many every bit a psychic means of processing threatening data, which, brought into cognitive consciousness, would increment anxiety [13]. A more contempo explanation of prolonged, intense nightmares is that they might reduce the physiological responses associated with frightening stimuli and reduce anxiety [fourteen].
Previous studies take considered the role of neurotransmitters in lucid dreams [9–12]. Also, Blum et al. characterized the pathogenesis of PTSD every bit a severe polygenic disorder triggered by environmental factors [xv]. 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]. An early study past Comings et al. [17] screened subjects exposed to severe combat conditions in Vietnam for PTSD; 58.3% of the 24 subjects who met the criteria for PTSD carried the D2A1 allele, of eight who did not 12.5% carried the D2A1 allele (p = 0.04). In a replication study of 13 subjects with PTSD, 61.5% carried the D2A1 allele; of the remaining xi, none had a PTSD diagnosis and, zero% carried the D2A1 allele (p = 0.002). In the combined group, 59.5% with PTSD carried the D2A1 allele, vs. 5.3% who did not take PTSD (p = 0.0001) carried the allele. These results propose that a DRD2 variant in linkage disequilibrium with the D2A1 allele confers an increased risk for PTSD, and the absence of the D2A1 variant confers resilience, relative resistance to PTSD.
Despite substantial literature on the neurobiology of dreams currently, we practise non fully empathise the neurological mechanisms involved in nightmares or their part. It is noteworthy that the release of norepinephrine and acetylcholine from the ascending fibers are strongly activated during wakefulness; however during rapid-heart-motility slumber, the neocortical tone is sustained mainly by acetylcholine. Concentrations of acetylcholine, dopamine, and cortisol increment, and serotonin and noradrenaline are absent-minded during Rapid Middle Movement (REM) [paradoxical] sleep. The paradox is that even though activity in the forebrain and midbrain during the REM stage of sleep is intense and consumes large amounts of energy, the muscles are relaxed, and the body remains inactive except for the diaphragm and eye muscles. Cycles of REM often comprise the smallest portion of the sleep, occur several times during slumber, and more than oft towards the morning.
Sil'kis [18] agrees that nightmares involve altered concentrations of acetylcholine, noradrenaline, dopamine, serotonin, and glutamate. These neurotransmitter changes may impair contextual memory through hippocampal interest in dreams during REM sleep [18, nineteen]. Paradoxical slumber occurs due to cholinergic neurons' activation in the pedunculopontine nucleus, disinhibited from the output basal ganglia nuclei. Sil'kis [18, twenty] suggests that improved episodic retentivity and reduced nightmares might occur with the introduction of a neurotransmitter or neuropeptide capable of promoting potentiation in all components of the polysynaptic pathway through the hippocampus, especially at CA1 and CA3 pyramidal cells.
In the absenteeism of signals from the retina, the disinhibition of neurons in the pedunculopontine nucleus and superior colliculus allows the signals to excite neurons in the lateral geniculate body and other thalamic nuclei projecting to the primary and college visual cortical areas, prefrontal cortex, and back into the striatum. Thus, dreams as visual images and motor hallucinations issue from an increment in the activity of groups of thalamic and neocortical neurons. The involvement of dopamine is paramount in that its homeostasis provides synaptic transmission efficacy during the apportionment of signals in closed interconnected loops, each which includes ane of the visual cortical areas, one of the thalamic nuclei, limbic regions, and a region of the basal ganglia.
1.4. Can Pro-dopamine Regulation Induce Neuroplasticity and Attenuate Terrifying Dreams?
Remarkably, in at least three of the original cases mentioned earlier, it seems that this profound elimination of terrifying lucid dreams and conversion to happy dreams continued for ~ 9 months subsequently cessation of KB220z assistants. This prolonged nature of the event of KB220 variation is perplexing.
i.4.ane. Encephalon Office following Traumatic Events and Equally Such PTSD
A review of the existing literature regarding brain part post-obit traumatic events such equally PTSD may inform agreement of the prolonged nature of the KB220 issue. Bowirrat et al. [21] pointed out that early life trauma provokes neurochemical responses to subsequently stressful events. Long term, several biological systems, including mesolimbic brain structures and various neurotransmitters, are affected. These furnishings include the size and duration of the Dopamine /Norepinephrine catecholamine response and the extent of the cortisol response [22].
Many relevant studies revealed profound long-term neurotransmission abnormalities in PTSD. Mueller et al. [23] reported that male person veterans with a positive diagnosis of PTSD compared to negative controls (no PTSD) had a thinner rostral inductive cingulate and insular cortex simply no hippocampal volume loss. Moreover, PTSD was characterized past decreased nodal degree (orbitofrontal, inductive cingulate) and clustering coefficients (thalamus) just increased nodal betweenness (insula, orbitofrontal) and a reduced small-earth index in the whole-brain analysis and by orbitofrontal and insular nodes with an increased nodal degree, clustering coefficient and nodal betweenness in the restricted assay.
Mueller's grouping [24] recently investigated the polygenic hazard score (PRS) for PTSD. They used the latest summary statistics from the well-nigh extensive published genome-wide association study (GWAS) conducted past Psychiatric Genomics Consortium for PTSD (PGC-PTSD). Interestingly, they found the PRS of a cohort comprising veterans of contempo wars (n = 244) explained some variations in PTSD onset (Nagelkerke R2 = 4.68%, P = 0.003) and severity (Nagelkerke R2 = 4.35%, P = 0.0008) except for an African ancestry sub-accomplice. These findings demonstrate the importance of the Genetic Addiction Take chances Score (GARS) exam results that identify polygenic risk for hypodopaminergia.
Moreover, in agreement with the work of Mueller et al. [23, 24], Du et al. [25] revealed in the Wenchuan convulsion survivors that while iii weeks after the disaster, functional connectivity changes involved both frontal-limbic-striatum and default-mode networks (DMN). Only changes in the DMN persisted at the 2-yr follow-up, despite complete recovery from loftier initial anxiety levels. Taken together, this crucial new evidence demonstrates that post-trauma anxiety experienced by survivors alters functional connectivity in the frontal-limbic-striatal network; however, parallel changes in the DMN persist despite the apparent absence of anxiety symptoms [25]. The authors advise that changes in disaster survivor neural networks, involved in cadre aspects of self-processing, cerebral and emotional performance, are long-term, contained of anxiety symptoms, and may also increase subsequent development of PTSD.
Bierer et al. [26], evaluating brain functionality in Gulf War Veterans diagnosed with PTSD reported a significantly lower mean diffusivity (Md) [average molecular motion independent of whatsoever tissue directionality] in the right cingulum packet. Still, no meaning differences in MD or fractional anisotropy (FA) [direction] in the left cingulum parcel, and PTSD symptom severity scores both clinician and cocky-rated were associated significantly with increased FA and reduced MD and in the right cingulum. Forth similar lines, Saar-Ashkenazy et al. [27] establish a reduction in corpus-callosum (CC) white affair volume in PTSD patients compared to controls correlated with lower associative memory performance. Admon et al. [28] establish that Israeli soldiers with diagnosed PTSD compared to non- PTSD soldiers had decreased hippocampal (HC) book, displayed more PTSD-related symptoms mail service-exposure and reduced HC functional connectivity with the ventromedial prefrontal cortex (vmPFC). Chao et al. [29] found a significant reduction of left occipital gray matter compared to the controls and correlated negatively with the severity of PTSD symptoms. Abe et al. [thirty, 31] evaluated victims of the Tokyo subway sarin gas assault with PTSD. They reported that compared to not-PTSD matched controls, the voxel-based analysis revealed that FA increased significantly in the left anterior cingulum and the subjacent left anterior cingulate cortex (ACC) gray thing. Previously, these investigators had found a book decrement in PTSD subjects.
Synaptic plasticity known to occur at glutamate synapses throughout the brain, including the neocortex, has a probable role in neurodevelopment and a wide spectrum of adult neural functions [32]. Thus, prolongation of the KB220 consequence on lucid nightmares may be the issue of neuro-plastic mechanisms that can repair some of these deficits acquired past trauma. From the review of PTSD studies, polygenic risk score (PRS) tin explain variations in onset and severity of PTSD, and functional connectivity changes in the DMN persist despite the credible absence of anxiety symptoms later on three months. Increases in FA and reduced Md in the correct cingulum associate with PTSD symptom severity and decreased HC volume reduced HC functional connectivity and lowered associative retention performance. Also, a reduction of left occipital grey matter book significantly correlates with increased PTSD symptom severity. A voxel-based analysis revealed FA increased significantly in the left anterior cingulum, subjacent to the left anterior cingulate cortex (ACC) gray matter.
Attention Deficit Hyperactivity Disorder (ADHD) is a developmental illness associated with cortical gray matter book deficits that may represent a state of diminished dopamine stimulation that is equally disruptive to healthy synaptic plasticity mechanisms [33–39]. In PTSD, withal, long term potentiation necessary for conditioned fear-extinction is thought to be impaired. Bear witness suggests that genetic polymorphisms related to hypodopaminergic neurotransmission (every bit adamant past the Bloke test) confers vulnerability to PTSD. Thus, "hypodopaminergic" trait and state thwart some of the synaptic plasticity that underlies consolidation and retentivity of fear extinction. Therefore, dopamine--modulated synaptic plasticity is essential, and when disrupted, either precipitates or is symptomatic of neuropsychiatric illness. Novel treatments that can restore balanced synaptic plastic modulation may be preventative equally a therapeutic intervention for Lucid Dreams associated with PTSD and ADHD abnormal behaviors [12].
Also, many of the patients described herein are victims of childhood parental abuse, and there is evidence in this population of deficits in gray and white matter book. The deficits are most prominently in the dorsolateral and vmPFC and hippocampus, amygdala, and corpus callosum (CC) regions of the brain. Diffusion tensor imaging (DTI) studies show evidence of structural interregional connectivity deficits betwixt these areas, suggesting neural network abnormalities [xl].
The function and structure of the lateral and ventromedial frontolimbic brain areas and networks that mediate consequence and behavioral command are too prominent deficits associated with early childhood corruption [41]. These environmental events may also impact the futurity evolution of terrifying lucid dreams [42]. The Prefrontal Cortex (PFC) undergoes significant changes during evolution and may compromise advisable decision making in an adolescent population. The potential for environmental insults to affect mRNA expression of dopaminergic genes, reported in the literature, may serve as a possible therapeutic target for unwanted lucid dreams. Specifically, Wiers et al. [43] showed that peripheral DAT1 promoter methylation might be predictive of striatal DAT availability in adults with ADHD. Moreover, Weder et al. [44] showed that with experiences of maltreatment, epigenetic changes (DNA methylation) in ID3, GRIN1, and TPPP genes, may confer take a chance for depression and adversity in children, which could then lead to nightmares [45]. These studies add to a growing body of literature supporting a role for epigenetic mechanisms in the pathophysiology of stress-related psychiatric disorders.
Although epigenetic changes are ofttimes long-lasting, they are non necessarily permanent, and interventions to reverse the adverse biological and behavioral sequelae associated with child maltreatment and future problems, including nightmares, deserve consideration. Soldiers with a groundwork of violence during childhood or with a familial susceptibility take chances would benefit from being genotyped for high--risk alleles utilizing the GARS exam before combat [22].
Importantly, since hypodopaminergic function in the brain's reward circuitry due to factor polymorphisms associates with substance use disorder (SUD) in individuals with co-occurring PTSD, and administration of dopaminergic agonist to upshot cistron expression (mRNA) and overcome dopamine deficiency might exist prudent. One applied issue is that pre-screening with the Bloke examination to place individuals at risk before combat could be a prophylactic measures. Soldiers with PTSD, as well as recruits adamant by the Gars examination equally at high genetic risk for PTSD, tin be treated with neuronutrient precision pro-dopamine (KB220) regulation to induce "dopamine homeostasis."
Early on genetic testing for hypodopaminergic risk alleles could too offer valuable information that parents, and caregivers may find helpful in early life. They may change parenting styles and enhance attachment affecting dopaminergic role and known bonding substances like oxytocin and vasopressin [33, 46] (Fig. 1).
Is a schematic that represents a treatment model that includes early genetic risk diagnosis, medical monitoring, and nutrigenomic dopamine agonist modalities to gainsay addiction, ADHD, and PTSD, including terrifying lucid dreams [1, 9–12, 47] may brand the lives of our children happier [48].
Neuroimaging studies go along to reflect region-specific differential responses (dopamine surfeit or arrears) to substance and non-substance-addictive behaviors that are impediments, preventing healthy productive lives [49, 50].
2. PTSD A SUBSET OF REWARD DEFICIENCY SYNDROME: NEUROIMAGING EVIDENCE OF FUNCTIONAL CONNECTIVITY & NEUROPLASTICITY
Finally, based on studies that deprived rats of sleep for one month, lack of sleep on a chronic basis can induce fatal indisposition [51]. All the same, despite the impact of restricted sleep on immune and hormonal office, the virtually powerful effect occurs in the brain, especially working retentiveness. Tucker et al. [52] showed that sleep-deprived human subjects had a forty% refuse in working memory compared to non-deprived healthy controls. These studies and many others [53, 54] advise the importance of eliminating PTSD/ ADHD induced Lucid Dreams of a terrifying nature by in the induction of dopamine homeostasis and neuroplasticity as recently observed in abstinent heroin addicts (run into Fig.two) and rat studies (see Figs. 3, iv).
Illustrates one dose of KB220Z (Synaptose Variant) compared to placebo in x abstemious heroin-dependent patients studied. The placebo grouping (due north=v) notices a blue circle showing no Bold activation of Dopamine in Caudate and an overactive Bold activation of dopamine in the cerebellum (pink circle). In contrast, the KB220Z group (n=5) find a BOLD activation (blue circle) in the caudate and an attenuated BOLD activation in the cerebellum (pink circumvolve). Based on this representation, the authors suggested a putative induction of "dopamine Homeostasis." Comparative resting-state fMRI one hour subsequently i dose of placebo or KB220z report abstinent Chines Heroin addicts, with permission [7].
Representative cross-correlation maps show four subjects: placebo compared to KB220Z treated rats Maps represent to resting-state connectivity for the left nucleus accumbens (highlighted in green in the atlas map above the effigy). Annotation the distributed but meaning connectivity between diverse encephalon regions and the nucleus accumbens in the placebo subjects. KB220Z improved connectivity, especially between left-correct accumbens, dorsal striatum, and limbic cortical areas, including the anterior cingulate, prelimbic, and infralimbic regions. Correlation maps for characteristic participants presented at a threshold between 0.35≤ r ≥0.9 (Fisher's z transformed), with permission [half-dozen].
Plots differences in functional connectivity between various ROI and three seed regions. Data presented here as a mean correlation (z transformed) ± standard error. * Significantly dissimilar than placebo t221 > 2.one p < 0.05 (p values FDR corrected at q = 0.05), with permission [six].
To help understand the importance of agonist therapy to treat terrifying dreams, we refer to the work of Willuhn et al. [55], who reported that cocaine apply and even non-substance-related addictive behavior increases every bit dopaminergic part reduces. Chronic cocaine exposure has been associated with decreases in D2/D3 receptors and was besides associated with lower activation of cues in the occipital cortex and cerebellum in a recent PET written report by Volkow et al. [56, 57]. Therefore, handling strategies, like dopamine agonist therapy that might conserve dopamine part, possibly an exciting arroyo to treat RDS behaviors, including abnormal dreams. Blum et al. [7] evaluated the upshot of KB220Z™ on reward circuitry of ten heroin apply disordered (HUD) subjects undergoing protracted forbearance (average 16.nine months). A placebo-controlled, crossover, triple-blinded written report of KB220Z in v subjects found that KB220Z induced increased BOLD activation in caudate-accumbens-dopaminergic pathways and a reduction of resting-state action in the cerebellum compared to placebo 1-hr after acute administration. In the second phase of this pilot study of all ten abstemious HUD subjects, activation increased significantly from resting-land by KB220Z compared to placebo in 3 brain regions of interest (p < 0.05). The increased functional connectivity was observed in a putative network, including the dorsal anterior cingulate, medial frontal gyrus, nucleus accumbens, posterior cingulate, occipital cortical areas, and cerebellum. These results and other Quantitative Electroencephalography (qEEG) report results [58] suggest a putative anti-craving/anti-relapse role of KB220Z in addiction by direct or indirect dopaminergic interaction. These preliminary results may also help explain our previous findings, including the prolonged nature of the KB220 anti-terrifying nightmare effect. Due to the small sample size, nosotros circumspection definitive interpretation of these preliminary results, and confirmation, with boosted research and ongoing rodent and human studies of KB220Z, is required.
The literature supports dopaminergic dysfunction in RDS behaviors. There is evidence that alterations in synchronous neural activeness betwixt brain regions subserving advantage and diverse cognitive functions may significantly contribute to substance-related disorders and other hypodopaminergic disorders, PTSD, and ADHD [59]. The Febo et al. [half dozen] rodent study represents the commencement evidence showing that a pro-dopaminergic nutraceutical (KB220Z) significantly enhances, above placebo, functional connectivity betwixt reward and cognitive brain areas in the rat (encounter Fig. 3 and four). These areas include the nucleus accumbens, anterior cingulate gyrus, anterior thalamic nuclei, hippocampus, prelimbic, and infralimbic loci. Pregnant functional connectivity increased brain connectivity volume recruitment and potential neuroplasticity. See Fig. 4 showing increased neuronal recruitment and dopaminergic functionality across the brain advantage circuitry. Increases in functional connectivity were specific to these regions and not broadly distributed beyond the brain. While these robust initial findings are observed in drug naïve rodents, the selective response implies clinical relevance for individuals at adventure for RDS behaviors, including nightmares, who show reductions in functional connectivity [9–12, 60].
3. A CLINICAL PERSPECTIVE
Equally described by the American Association of Sleep Disorders [2005], Lucid dreams are vivid and life-similar and may exist associated with an awareness that one is dreaming and an ability to control the onset or offset of the dream. The didactics of lucid dreaming is, in fact, a method of overcoming nightmares. Furthermore, at that place is currently some controversy about whether lucid dreaming may represent a brief, wakeful state [61].
In our sample, the dreams reported were uniformly terrifying in their content. Some were PTSD patients, so a distinction must exist fabricated equally to whether "the use of KB220z ameliorated lucid dreams" or the "PTSD dreams" (nightmares)?
Thus, the question posed by these findings is: "Do patients with RDS diagnoses, who report terrifying and unpleasant, lucid dreams have their dreams ameliorated by a trial of KB220z" [9–12]?
Future analyses of lucid terrifying dreams in this population should focus on the symbolic nature of the dream content and its relevance to the PTSD trauma. If the dreamer is terrified past dinosaurs, for case, this content would not be consistent with that of a trauma-induced dream and not hands interpreted as relevant to the PTSD, historical trauma. With these caveats in listen, we, the authors, discuss the nature of dreaming and traumatic dreams and leave aside the question of the origin and part of terrifying, lucid dreams.
Previous papers [9–12] accept discussed the literature related to lucid dreams and provided two cases that showed complete elimination of Lucid dreams with KB220Z [9, 10]. While we do not desire to reiterate the same clarification, the following references volition serve equally a useful resource related to Lucid Dreams and neurotransmitter part [62–73].
iii.ane. Standard Treatment Options for Nightmares
In an attempt to provide medical guidelines to treat unwanted "bad dreams," especially in PTSD patients, Aurora et al. [74] the following treatment options [see Table 1].
Table 1.
Handling option recommendations.
| Treatment Options | Nightmare Types |
|---|---|
| • Prazosin | PTSD-associated nightmares. |
| • Image Rehearsal Therapy (IRT) | Nightmare disorder |
| • Systematic Desensitization and Progressive Deep Muscle Relaxation training | Idiopathic nightmares |
| • Clonidine considered for | PTSD-associated nightmares |
| • Consider the following medications: trazodone, atypical antipsychotic medications, topiramate, low dose cortisol, fluvoxamine, triazolam and nitrazepam, phenelzine, gabapentin, cyproheptadine, and tricyclic antidepressants. | PTSD-associated nightmares, but the data are low course and sparse |
| • Consider the following behavioral therapies ed: Exposure, Relaxation, and Re-scripting Therapy (ERRT); Slumber Dynamic Therapy; Hypnosis; Eye-Motion Desensitization and Reprocessing (EMDR); and the Testimony Method. | PTSD-associated nightmares based on depression-course bear witness |
| • Consider the following behavioral therapies: Lucid Dreaming Therapy and Self-Exposure Therapy. | Nightmare disorder based on low-grade bear witness |
| Clonazepam and private psychotherapy | No recommendation is fabricated based on sparse data |
| Venlafaxine | not suggested for PTSD-associated nightmares |
iv. SUMMARY
Based on the clinical experience of ane of united states (TM) decided to comprise a well-researched putative natural, safe dopamine agonist, known every bit KB220Z [63], in a diagnosed PTSD and RDS patient'south treatment program to determine if this circuitous would provide any beneficial effects to gainsay reoccurring lucid nightmares ("bad dreams"), otherwise refractory to other pharmaceutical agents.
In some published case series [9–12], we describe patients who written report lucid dreams, which are mainly unpleasant or terrifying. Rendering the scientific question even more problematic is that these patients take all suffered some form of psychological trauma and, equally such, epigenetics (untested) was most likely involved in the promotion of terrifying lucid dreams.
FUNDING
The piece of work of RDB was partially supported by the National Institutes of Health grants 1R01NS073884 and 1R21MH073624. MG-Fifty is the recipient of R01 AA021262/AA/NIAAA NIH HHS/U.s.a.. KB and MGL are the recipients of R41 MD012318/NIMHD NIH HHS/U.s.a.. PT is the recipient of R01HD70888-01A1. The work was also supported by the NY Enquiry Foundation funds PT (RIAQ0940) and the NIH (DA035923 and DA035949)
Footnotes
CONFLICT OF Interest
KB is a chairman and CSO of the Geneus Health Board of Directors and CSO. He is the inventor of Bloke and the Pro-dopamine regulator (KB220PBM) and credited with the patents issued and awaiting. Through their company, Igene KB owns stock in Geneus Health RB and KB are members of the GeneUs Wellness LLC Board KB is also the Chairman of the Lath of Directors and Scientific Advisory Board of Geneus Health that includes MGL, EJM, PKT, RDB, and DB. In that location are no other conflicts to report.]
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8547281/
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