Search PubMed⌕ Search

Biomedical subjects

Kenneth Blum

Publications and source records attributed to Kenneth Blum.

14 recordsLinked to original sources
PubMed2026

Sequential rTMS for MDD and OCD in a patient with left parietal perinatal ischemic infarct: a case report.

Major depressive disorder (MDD) commonly co-occurs with obsessive-compulsive disorder (OCD), resulting in greater symptom severity, functional impairment, and suboptimal response to standard pharmacologic and psychotherapeutic interventions. These challenges underscore the need for neuromodulation strategies to target distinct neural networks implicated in mood regulation and compulsivity. This report describes outcomes of high-frequency (HF) repetitive transcranial magnetic stimulation (rTMS) of the left dorsolateral prefrontal cortex (DLPFC), and low-frequency (LF) rTMS of the right orbitofrontal cortex (OFC), in a patient with comorbid MDD, OCD, and a left parietal perinatal ischemic infarct. Over the course of treatment, serial psychometric assessments demonstrated progressive reductions in frequency and intensity of depressive symptoms, anxiety, and obsessive-compulsive behaviors, measured via Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder 7-Item Scale (GAD-7), and Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). This case adds to the growing body of literature demonstrating efficacy of DLPFC and OFC stimulation for depression and OCD. Further large-scale, blinded, and randomized trials are warranted to examine the efficacy of sequential DLPFC and OFC stimulation for comorbid MDD and OCD compared with single-site DLPFC stimulation.

dorsolateral prefrontal cortex (DLPFC)↗
PubMed2025

Precision Genomics: A Reality Having Universal Impact in a New Era of Psychiatry - Lessons Learned, Past and Present.

Addiction neuroscience explores the complex interplay between genetic, neurobiological, environmental, and socio-spiritual factors underlying substance and behavioral addictions. Over the past three decades, research in this domain has identified critical molecular and epigenetic mechanisms-particularly those affecting dopaminergic signaling and reward pathways-that contribute to both vulnerability and resilience to addictive behaviors. Central to this understanding is the concept of reward deficiency syndrome (RDS), first introduced by Kenneth Blum, which posits that hypodopaminergic functioning predisposes individuals to seek maladaptive rewards. Advances in neurogenetics, including the identification of key polymorphisms such as the DRD2 A1 allele, have paved the way for precision tools like the genetic addiction risk severity (GARS®) test. This test, alongside pro-dopaminergic nutraceutical interventions like KB220, demonstrates the potential for early detection and individualized treatment of "pre-addiction" risk states. Despite ongoing reliance on opioids for opioid use disorder (OUD), emerging paradigms advocate for dopamine homeostasis through non-addictive, integrative approaches. Furthermore, the integration of whole genome sequencing data can be used for Genome-Wide Association Studies (GWAS), multi-omics, and machine learning into clinical practice holds promise for advancing personalized medicine in addiction treatment. As the field progresses, addressing health equity and improving genomic representation across populations remain critical goals. This evolving framework underscores the importance of leveraging genomic insights to prevent, predict, and personalize interventions for addiction and mental illness at scale.

Disorder↗
PubMed2025

Multi-Locus Pro-Dopaminergic Restoration of Reward Brain Circuitry in Reward Deficiency Rescinds Mono-Pharmaceutical Targeting.

Dopaminergic dysfunction in reward circuitry is well-documented as a contributor to addictive behaviors. Evidence indicates that changes in synchronous neural activity between brain regions mediating reward and cognitive functions may significantly contribute to substance-related disorders. In this commentary we highlight findings showing that the pro-dopaminergic nutraceutical (KB220) enhances functional connectivity between reward and cognitive brain areas in both animal and human studies. Animal studies demonstrate that KB220 activates important brain reward-related regions, including the nucleus accumbens, anterior cingulate gyrus, anterior thalamic nuclei, hippocampus, and prelimbic and infralimbic loci. Kb220 induced significant functional connectivity, enhanced neuroplasticity, and improved dopaminergic functionality within the brain reward circuitry with effects localized to these regions rather than broader distributed across the brain. In abstinent heroin-dependent individuals, acute KB220 administration significantly induced BOLD activation in caudate-accumbens dopaminergic pathways relative to placebo. Furthermore, data from 36 clinical trials and preclinical studies encompassing over 1,000 subjects, demonstrate that KB220 supports "dopamine homeostasis" across various reward deficiency behaviors. Clinical outcomes and quantitative electroencephalogy (qEEG) results underscore KB220's potential anti-craving/anti-relapse effects in addiction and other psychiatric disorders through direct or indirect dopaminergic modulation. Based on a review of the existing knowledge and further intensive investigation, we propose that instead of relying on mono-pharmaceutical approaches, the scientific community should endorse multi-loci dopaminergic restoration of reward brain circuitry as a fundamental paradigm for addressing mental illness.

Alcohol Use Disorder (AUD)↗
PubMed2025

Personalized Repetitive Transcranial Magnetic Stimulation (PrTMS®) Coupled with Transcranial Photobiomodulation (tPBM) For Co-Occurring Traumatic Brain Injury (TBI) and Post-Traumatic Stress Disorder (PTSD).

This study provides further evidence demonstrating the beneficial effects of PrTMS® treatment in co-occurring disorders. Furthermore, this study illustrates the benefit of augmenting PrTMS® with tPBM for superior outcomes. The positive results of this novel case study can be attributed to brain wave neuromodulation and increased neuronal ATP production, resulting in synergistic enhanced neuroplasticity and brain optimization. Further, large-scale, randomized and blinded studies are recommended to validate our promising preliminary observations utilizing multifaceted interventions for co-occurring disorders.

Co-Occurring Disorders↗
PubMed2006

Genotrim, a DNA-customized nutrigenomic product, targets genetic factors of obesity: hypothesizing a dopamine-glucose correlation demonstrating reward deficiency syndrome (RDS).

Obesity is the second largest cause of preventable death in the United States. Historically, obesity was considered a behavioral problem that could be simply addressed with behavioral modifications in diet and exercise. As scientific advancements have demonstrated in other neurological healthcare conditions such as alcoholism, there are important biological and genetic components that limit the efficacy of behavioral adjustments alone. In light of data suggesting frequent co-morbidities to obesity, including diabetes mellitus, atherosclerosis, osteoporosis, and potentially others, we hypothesize that the biologic and genetic factors, synergistically with behavioral modifications, must be addressed to adequately treat this disease. We hypothesize that one such genetic factor that influences behavior and thus obesity is a predisposition to glucose craving and the overall effect of dopaminergic activity in the reward center of the brain. This defect drives individuals to engage in activities of behavioral excess, which will increase brain dopamine function, for which we have created the term reward deficiency syndrome (RDS) to categorize such biological influences on behavior. Consuming large quantities of alcohol or carbohydrates (carbohydrate bingeing) stimulates the brain's production of and utilization of dopamine. So too does the intake of crack/cocaine and the abuse of nicotine. We are proposing that a novel approach to nutritional supplementation may be required to target the RDS role in obesity. In this regard, Genotrim, a DNA based customized nutraceutical has been designed and is currently under investigation in several clinical studies. This is the first hypothesis paper whereby this new paradigm shift in thinking about obesity is presented.

Anti-Obesity Agents↗
PubMed2006

DNA based customized nutraceutical "gene therapy" utilizing a genoscore: a hypothesized paradigm shift of a novel approach to the diagnosis, stratification, prognosis and treatment of inflammatory processes in the human.

We hypothesize that using a multi-variant nutrigenomic index for the purposes of customizing or adjusting the formulation of nutritional supplements will result in an improved and novel approach to the diagnosis, stratification, prognosis, and treatment of inflammatory processes in the human. This multi-variant genetic index, or Genoscore, is derived by analyzing genotype and/or phenotype through measuring multiple genetic mutations of single nucleotide polymorphisms, gene expression, or other forms of genetic and phenotypic measurements. We also propose that manipulation of neurochemical reward circuitry in the mesolimbic brain region providing dopamine release at the nucleus accumbens (NAc), will have both pain and stress relief benefists, which are a cornerstone to the human inflammatory process. This hypothesis, applies to all genes currently discovered or which will be discovered and any nutritional or dietary supplement ingredient currently available or which will become available. For example, if a DNA test was measuring two genes through single nucleotide polymorphisms (Gene A and Gene B), the index scores (Genoscore) that would be reported to the clinician and patient would be based upon the number of mutations. An index score of 0 would mean no mutation. An index score of 1 may mean a mutation in Gene A. An Index Score of 2 may mean a mutation in Gene B. An Index Score of 3 may mean a mutation in Gene A and Gene B, resulting in a simple report, easily understandable to both the clinician and patient that provides insights into disease diagnosis, stratification, prognosis, as well as the metabolism, efficacy and/or toxicity associated with specific vitamins, minerals, herbal supplements, homeopathic ingredients and other ingredients in the nutritional and/or dietary supplement regimen. Furthermore, we have provided support that evidence shows the importance of the dopaminergic connection as an anti-pain and anti-stress molecule, working at the mesocorticolimbic region of the brain, specifically at the NAc. Additionally, we have provided support that clinical evidence demonstrates the effectiveness and safety of natural substances for joint health, such as glucosamine sulfate , chondroitin sulfate, and Ganoderma lucidum.

Dietary Supplements↗
PubMed2005

Neurogenetic interactions and aberrant behavioral co-morbidity of attention deficit hyperactivity disorder (ADHD): dispelling myths.

BACKGROUND: Attention Deficit Hyperactivity Disorder, commonly referred to as ADHD, is a common, complex, predominately genetic but highly treatable disorder, which in its more severe form has such a profound effect on brain function that every aspect of the life of an affected individual may be permanently compromised. Despite the broad base of scientific investigation over the past 50 years supporting this statement, there are still many misconceptions about ADHD. These include believing the disorder does not exist, that all children have symptoms of ADHD, that if it does exist it is grossly over-diagnosed and over-treated, and that the treatment is dangerous and leads to a propensity to drug addiction. Since most misconceptions contain elements of truth, where does the reality lie? RESULTS: We have reviewed the literature to evaluate some of the claims and counter-claims. The evidence suggests that ADHD is primarily a polygenic disorder involving at least 50 genes, including those encoding enzymes of neurotransmitter metabolism, neurotransmitter transporters and receptors. Because of its polygenic nature, ADHD is often accompanied by other behavioral abnormalities. It is present in adults as well as children, but in itself it does not necessarily impair function in adult life; associated disorders, however, may do so. A range of treatment options is reviewed and the mechanisms responsible for the efficacy of standard drug treatments are considered. CONCLUSION: The genes so far implicated in ADHD account for only part of the total picture. Identification of the remaining genes and characterization of their interactions is likely to establish ADHD firmly as a biological disorder and to lead to better methods of diagnosis and treatment.

Attention Deficit Disorder with Hyperactivity↗
PubMed2005

Are dopaminergic genes involved in a predisposition to pathological aggression? Hypothesizing the importance of "super normal controls" in psychiatricgenetic research of complex behavioral disorders.

We hypothesize that pathological aggression, a complex behavioral disorder, in adolescents may in part involve polymorphisms of the dopaminergic system. While a number of neurotransmitter systems must be involved, due to polygenic inheritance, one major pathway should involve the dopaminergic system. Advances in our knowledge of the neurobiology of aggression and violence have given rise to rational pharmacological treatments for these behaviors. The main biological systems that are known to be involved are certain reward neurotransmitters including: serotonin, opioid peptides, gamma-aminobutyric acid, and the catecholamines (dopamine and norepinephrine). It is our notion that pathological aggressive behavior is in part similar mechanistically to other forms of impulsive behaviors such as pathological gambling. By analogy to drug dependence, it has been speculated that the underlying pathology in pathological gambling is a reduction in the sensitivity of the reward system. While studying pathological gamblers and controls during a guessing game using functional Magnetic Resonance Imaging, Reuter et al. observed a reduction of ventral striatal and ventromedial prefrontal activation in the pathological gamblers that were negatively correlated with gambling severity. Subsequently, linking hypo activation of these areas to disease severity. A positive correlation of both the dopamine D2 receptor gene (DRD2) and the dopamine transporter gene (DAT1) polymorphisms were observed with pathological violence in adolescents in a blinded clinical trial. Thus, this and other cited work preliminary suggest a role for both the DRD2 and DAT genes in pathological aggressive behavior. We further hypothesize that follow-up gene research in this area, albeit premature, resulting in confirmation of positive correlations with dopaminergic polymorphisms, and utilizing highly screened controls (eliminating any addictive, compulsive and impulsive behaviors in both proband and family) may have important ramifications in our young population.

Adolescent↗
PubMed2004

Narcotic antagonists in drug dependence: pilot study showing enhancement of compliance with SYN-10, amino-acid precursors and enkephalinase inhibition therapy.

We decided to test the hypothesis that possibly by combining a narcotic antagonist and amino-acid therapy consisting of an enkephalinase inhibitor (D-phenylalanine) and neurotransmitter precursors (L-amino- acids) to promote neuronal dopamine release might enhance compliance in methadone patients rapidly detoxified with the narcotic antagonist Trexan (Dupont, Delaware). In this regard, Thanos et al. [J. Neurochem. 78 (2001) 1094] and associates found increases in the dopamine D2 receptors (DRD2) via adenoviral vector delivery of the DRD2 gene into the nucleus accumbens, significantly reduced both ethanol preference (43%) and alcohol intake (64%) of ethanol preferring rats, which recovered as the DRD2, returned to baseline levels. This DRD2 overexpression similarly produced significant reductions in ethanol non-preferring rats, in both alcohol preference (16%) and alcohol intake (75%). This work further suggests that high levels of DRD2 may be protective against alcohol abuse [JAMA 263 (1990) 2055; Arch, Gen. Psychiatr. 48 (1991) 648]. The DRD2 A1 allele has also been shown to associate with heroin addicts in a number of studies. In addition, other dopaminergic receptor gene polymorphisms have also associated with opioid dependence. For example, Kotler et al. [Mol. Phychiatr. 3 (1997) 251] showed that the 7 repeat allele of the DRD4 receptor is significantly overpresented in the opioid-dependent cohort and confers a relative risk of 2.46. This has been confirmed by Li et al. [Mol. Psychiatry 2 (1997) 413] for both the 5 and 7 repeat alleles in Han Chinese case control sample of heroin addicts. Similarly Duaux et al. [Mol. Psychiatry 3 (1998) 333] in French Heroin addicts, found a significant association with homozygotes alleles of the DRD3-Bal 1. A study from NIAAA, provided evidence which strongly suggests that DRD2 is a susceptibility gene for substance abusers across multiple populations (2003). Moreover, there are a number of studies utilizing amino-acid and enkephalinase inhibition therapy showing reduction of alcohol, opiate, cocaine and sugar craving behavior in human trials (see Table 1). Over the last decade, a new rapid method to detoxify either methadone or heroin addicts utilizing Trexan sparked interest in many treatment centers throughout the United States, Canada, as well as many countries on a worldwide basis. In using the combination of Trexan and amino-acids, results were dramatic in terms of significantly enhancing compliance to continue taking Trexan. The average number of days of compliance calculated on 1000 patients, without amino-acid therapy, using this rapid detoxification method is only 37 days. In contrast, the 12 subjects tested, receiving both the Trexan and amino-acid therapy was relapse-free or reported taking the combination for an average of 262 days (p < 0.0001F). Thus coupling amino-acid therapy and enkephalinase inhibition while blocking the delta-receptors with a pure narcotic antagonist may be quite promising as a novel method to induce rapid detox in chronic methadone patients. This may also have important ramifications in the treatment of both opiate and alcohol-dependent individuals, especially as a relapse prevention tool. It may also be interesting too further test this hypothesis with the sublingual combination of the partial opiate mu receptor agonist buprenorphrine.

Adult↗
PubMed2003

P300 (latency) event-related potential: an accurate predictor of memory impairment.

To determine if P300 latency changes precede and correlate with memory and mental status, patients (N=1506 aged 20-100 years) who received medical and psychiatric diagnoses (from 1997 to 2002), were assessed for P300 (N=1496), WMS-III (N=694), and MMSE (N=456). Patient and control groups included, a) normal WMS-III on all 4 subscales (N=36), b) normal WMS-III and MMSE (N=189) with subjective memory/mental status complaints, and c) medical patients with normal WMS-III and no memory complaints (N=205), and d) P300 control group without medical, psychiatric or memory problems for ROC. Patients with impaired/borderline memory had a prolonged P300 latency (P<0.02) compared to age matched non-impaired controls; in patients with normal WMS-III/MMSE, with subjective mild memory/mental status impairment, P300 latency was prolonged compared to controls (P=0.0004). The P300 latency increased by 0.72ms per year (P=7.9x10(-65)) and voltage decreased by 0.03dV per year (P=6.7x10(-10)), and both parameters were linearly correlated with the age of the subjects. Male subjects had an average voltage of 6.1dV and female 6.8dV (P=0.00009). Statistically, prolonged latency began at age range 41-50 (P=0.0002); reduced P300 voltage began at age range 51-60 (P=0.003). WMS-III memory decline for all measures began in females at age range 61-70 (P value at least=0.02) and for males at age range 61-80 (P=0.02). Prolonged P300 latency (P<0.0001) and memory impairment (at least <0.02) were greater for females than males. MMSE memory decline, male and female, began at age range 81-90 (P value of at least 0.00007). In our logistic regression model P300 latency was more predictive of WMS-III impairment than MMSE > 24. In patients whose WMS-III score is impaired < or = 69, or borderline < or = 79 (P at least=0.004), a P300 latency more prolonged than the norm (> or = 300 + 30 + Age) identifies these patients, whereas a MMSE > 24 failed. With the ROC curve, we confirmed that P300 latency could accurately identify borderline/impaired memory.

Adolescent↗
PubMedDate not supplied

Delayed P300 latency correlates with abnormal Test of Variables of Attention (TOVA) in adults and predicts early cognitive decline in a clinical setting.

Delayed P300 latency identifies dementia better than the Mini-Mental Status Exam and, in some cases, the Wechsler Memory Scale (WMS-III). The purpose of this study was to determine whether the outcome of an objective Test of Variables of Attention (TOVA) correlates with the findings of an electrophysiologic test-P300 latency-in patients 40 y of age or older. Adult attention deficit disorder may be an important premorbid marker of memory dysfunction or dementia. In males, the means for P300 latency and age-adjusted P300 latency were significantly greater for patients classified as SD-BL (significantly deviant or borderline: TOVA<-1.0) than for those categorized as normal (TOVA(3)0) for attention failure (ie, omissions [P<.010] and commissions [P<.005]) but not for response time or for variability. Males with >2 SD-BL quarters had significantly delayed P300 latency and age-adjusted P300 latency compared with males who had 0 SD-BL quarters (P<.020) and 1 SD-BL quarter (P<.005). In females, the means for P300 latency and age-adjusted P300 latency were significantly delayed for those grouped as SD-BL than for those labeled normal for response time (P<.001) and variability (P<.010), but not for omissions or for commissions. Females with >2 SD-BL quarters had significantly delayed P300 latency and age-adjusted P300 latency compared with females who had 0 SD-BL quarters (P<.005) and 1 SD-BL quarter (P<.010). Results suggest that TOVA abnormalities may be an indicator of delayed P300 and attention disorder. Recent research correlates TOVA abnormalities with impaired WMS scores of early dementia. Coupling of TOVA assessment findings with results of P300, Mini-Mental Status Exam, and WMS-III may allow for enhanced accuracy in the diagnosis and evaluation of the complex pathway of failing attention, memory, and cognition that leads to dementia.

Adult↗
PubMedDate not supplied

H-Wave, a nonpharmacologic alternative for the treatment of patients with chronic soft tissue inflammation and neuropathic pain: a preliminary statistical outcome study.

The burden of chronic soft tissue inflammation and neuropathic pain on individuals and society is substantial. This study was conducted to evaluate the H-wave device--an innovative form of treatment for chronic pain and inflammation--in patients with persistent pain associated with injuries or conditions affecting the upper or lower extremities or the back. Patients with at least moderate pain despite conventional therapy were included in a systematic survey after they had been given 2 to 6 wk of treatment with the H-wave device. Measures of improvement involved the proportion of patients with diminished medication requirements, improved function, or pain relief greater than 25%. More than 60% of patients with pain in the lower extremities, upper extremities, or back experienced pain relief exceeding 25%. The proportion of patients whose function improved and who were able to perform a new activity was consistently greater than 50% across the 3 anatomic subgroups. More than 40% of patients in each group were able to reduce or completely eliminate the use of pain medications. These benefits of treatment were independent of the type of pain therapy administered previously. In each anatomic subgroup, the proportion of patients who reported improvement on more than 1 of the 3 endpoints was significantly higher than the expected response to placebo therapy (P<.001). Results suggest that the H-wave device provided important benefits to patients with chronic soft tissue inflammation and neuropathic pain.

Chronic Disease↗
PubMedDate not supplied

The H-Wave small muscle fiber stimulator, a nonpharmacologic alternative for the treatment of chronic soft-tissue injury and neuropathic pain: an extended population observational study.

In a previous study, the H-Wave small-muscle fiber stimulator significantly reduced chronic pain and restored physical function among patients with pain in the lower and upper extremities and spine. In this extended population observational study, a cross-sectional,computer-administered 10-item survey was administered to 6774 patients (3367 men [49.7%], 3406 women [50.3%], and 1 sex not reported [<1%]; mean+/-SD age, 45.28+/-10.08 y; range, 18-65 y) with chronic soft-tissue injury or neuropathic pain to assess their therapeutic response. The mean+/-SE duration of self-administered H-Wave treatment before the survey was completed was 87.35+/-1.39 d. Sixty-five percent of study participants reported a reduced or eliminated need for pain medication; 79% reported improved functional capacity or activity; and 78% reported 25% or greater reduction of pain. This cross-sectional evaluation represents the largest outcome study on the benefits of the H-Wave device in patients with chronic soft-tissue injury or neuropathic pain. The results suggest that this nonpharmacologic approach may provide an important alternative to standard pharmacologic treatment.

Adolescent↗