LifeGen Inc

San Diego, CA, United States

LifeGen Inc

San Diego, CA, United States

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Blum K.,University of Florida | Blum K.,LifeGen Inc | Blum K.,Path Research and Medical Foundation | Blum K.,G and listic Treatment Center | And 11 more authors.
Medical Hypotheses | Year: 2010

Using fMRI, Menon and Levitin [9] clearly found for the first time that listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing including the nucleus accumbens (NAc) and the ventral tegmental area (VTA), as well as the hypothalamus, and insula, which are thought to be involved in regulating autonomic and physiological responses to rewarding and emotional stimuli. Importantly, responses in the NAc and VTA were strongly correlated pointing to an association between dopamine release and NAc response to music. Listing to pleasant music induced a strong response and significant activation of the VTA-mediated interaction of the NAc with the hypothalamus, insula, and orbitofrontal cortex. Blum et al. [10] provided the first evidence that the dopamine D2 receptor gene (DRD2) Taq 1 A1 allele significantly associated with severe alcoholism whereby the author's suggested that they found the first "reward gene" located in the mesolimbic system. The enhanced functional and effective connectivity between brain regions mediating reward, autonomic, and cognitive processing provides insight into understanding why listening to music is one of the most rewarding and pleasurable human experiences. However, little is known about why some people have a more or less powerful mesolimbic experience when they are listening to music. It is well-known that music may induce an endorphinergic response that is blocked by naloxone, a known opioid antagonist (Goldstein [19]). Opioid transmission in the NAc is associated with dopamine release in the VTA. Moreover, dopamine release in the VTA is linked to polymorphisms of the DRD2 gene and even attention-deficit hyperactivity disorder (ADHD), whereby carriers of the DRD2 A1 allele show a reduced NAc release of dopamine (DA). Thus it is conjectured that similar mechanisms in terms of adequate dopamine release and subsequent activation of reward circuitry by listening to music might also be affected by an individual's D2 density in the VTA mediated interaction of the NAc. It is therefore hypothesized that carriers of DRD2 A1 allele may respond significantly differently to carriers of the DRD2 A2 genotype. In this regard, carriers of the D2 A1 allele have a blunted response to glucose and monetary rewards. In contrast powerful D2 agonists like bromocryptine show a heightened activation of the reward circuitry only in DRD2 A1 allele carriers. If music causes a powerful activation in spite of the DRD2 A1 allele due to a strong DA neuronal release which subsequently impinges on existing D2 receptors, then it is reasonable to assume that music is a strong indirect D2 agonist (by virtue of DA neuronal release in the NAc) and may have important therapeutic applicability in Reward Deficiency Syndrome (RDS) related behaviors including Substance Use Disorder (SUD). Ross et al. [18] found that music therapy appears to be a novel motivational tool in a severely impaired inpatient sample of patients with co-occurring mental illness and addiction. © 2009 Elsevier Ltd.

Miller D.K.,LifeStream Solutions Inc | Miller D.K.,Bridging the Gaps Treatment Center | Miller D.K.,LifeGen Inc | Bowirrat A.,Ziv Government Medical Center | And 15 more authors.
Postgraduate Medicine | Year: 2010

It is well established that in both food- and drug-addicted individuals, there is dopamine resistance due to an association with the DRD2 gene A1 allele. Evidence is emerging whereby the potential of utilizing a natural, nonaddicting, safe, putative D2 agonist may find its place in recovery from reward deficiency syndrome (RDS) in patients addicted to psychoactive chemicals. Utilizing quantitative electroencephalography (qEEG) as an imaging tool, we show the impact of Synaptamine Complex Variant KB220™ as a putative activator of the mesolimbic system. We demonstrate for the first time that its intravenous administration reduces or "normalizes" aberrant electrophysiological parameters of the reward circuitry site. For this pilot study, we report that the qEEGs of an alcoholic and a heroin abuser with existing abnormalities (ie, widespread theta and widespread alpha activity, respectively) during protracted abstinence are significantly normalized by the administration of 1 intravenous dose of Synaptamine Complex Variant KB220™. Both patients were genotyped for a number of neurotransmitter reward genes to determine to what extent they carry putative dopaminergic risk alleles that may predispose them for alcohol or heroin dependence, respectively. The genes tested included the dopamine transporter (DAT1, locus symbol SLC6A3), dopamine D4 receptor exon 3 VNTR (DRD4), DRD2 TaqIA (rs1800497), COMT val158 met SNP (rs4680), monoamine oxidase A upstream VNTR (MAOA-uVNTR), and serotonin transporter-linked polymorphic region (5HTTLPR, locus symbol SLC6A4). We emphasize that these are case studies, and it would be unlikely for all individuals to carry all putative risk alleles. Based on previous research and our qEEG studies (parts 1 and 2 of this study), we cautiously suggest that long-term activation of dopaminergic receptors (ie, DRD2 receptors) will result in their proliferation and lead to enhanced "dopamine sensitivity" and an increased sense of happiness, particularly in carriers of the DRD2 A1 allele. This is supported by a clinical trial on Synaptamine Complex Variant KB220™ using intravenous administration in. 600 alcoholic patients, resulting in significant reductions in RDS behaviors. It is also confirmed by the expanded oral study on Synaptose Complex KB220Z™, published as part 2 of this study. Future studies must await both functional magnetic resonance imaging and positron emission tomography scanning to determine the acute and chronic effects of oral KB220™ on numbers of D2 receptors and direct interaction at the nucleus accumbens. Confirmation of these results in large, population-based, case-controlled experiments is necessary. These studies would provide important information that could ultimately lead to significant improvement in recovery for those with RDS and dopamine deficiency as a result of a multiple neurotransmitter signal transduction breakdown in the brain reward cascade. © Postgraduate Medicine.

Chen T.J.H.,Chang Jung Christian University | Blum K.,University of Florida | Blum K.,LifeGen Inc. | Blum K.,Holistic Addiction Treatment Center | And 14 more authors.
Journal of Psychoactive Drugs | Year: 2011

This document presents evidence supporting the role of the KB220/KB220Z neuroadaptagens consisting of amino-acid neurotransmitter precursors and enkephalinase-catecholamine-methyl- transferase (COMT) inhibition therapy called Neuroadaptagen Amino Acid Therapy (NAAT) in brain reward function. It is becoming increasingly clear that this novel formulation is the first neuroadaptagen known to activate the brain reward circuitry. Ongoing research repeatedly confirms the numerous clinical effects that ultimately result in significant benefits for victims having genetic antecedents for all addictive, compulsive and impulsive behaviors. These behaviors are correctly classified under the rubric of "Reward Deficiency Syndrome" (RDS). We are proposing a novel addiction candidate gene map. We present preliminary findings in the United States using qEGG and in China using Functional Magnetic Resonance Imaging (fMRI) regarding the effects of oral NAAT on the activation of brain reward circuitry in victims of SUD. In unpublished data utilizing an fMRI 2X2 design at resting state, NAAT in comparison to placebo shows activation of the caudate brain region and potentially a smoothing out of heroin-induced putamen (a site for emotionality) abnormal connectivity. Although awaiting final analysis, if confirmed by ongoing studies in China coupled with published qEEG results in America, showing an increase in alpha and low beta, NAAT may be shown to impact treatment outcomes. Copyright © Taylor & Francis Group, LLC.

Westcott W.,Quincy College | Varghese J.,Quincy Medical Center | DiNubile N.,University of Pennsylvania | Moynihan N.,Quincy Medical Center | And 9 more authors.
Journal of Exercise Physiology Online | Year: 2011

This study examined the effects of exercise alone and exercise and nutritional supplementation on lumbar spine bone mineral density, lean weight, and resting blood pressure. The subjects (N = 52) were placed into a Control Group [no exercise or nutritional supplements], an Exercise Group [strength training and aerobic activity; no nutritional supplementation]; and an Exercise and Nutrition Group [strength training and aerobic activity; supplementary protein, calcium, and vitamin D]. Changes in lumbar spine bone mineral density did not attain significance. Lean weight increased significantly in the Exercise and Nutrition Group. Resting SBP and DBP decreased significantly in the Exercise and Nutrition Group. These findings indicate that strength training, aerobic exercise, and nutritional supplements may be more effective than just exercise for increasing lean weight and for reducing resting blood pressure.

Westcott W.,Quincy College | Han D.,University of Texas at San Antonio | DiNubile N.,University of Pennsylvania | Neric F.,National Strength and Conditioning Association | And 5 more authors.
Journal of Exercise Physiology Online | Year: 2013

The aim of this study was to determine the effects of electrical stimulation using the Marc ProTM Device (MPD) during the recovery period on calf muscle strength and fatigue in two separate studies (n = 43, Mean age = 61.3 yrs; n = 62, Mean age = 61.7 yrs). The subjects performed the calf press exercise twice a week for 10 wks with or without electrical stimulation (M = 4 hr·wk-1) between training sessions. Subjects who received electrical stimulation (n = 54) in both studies attained a significant (P<0.05) increase in calf strength versus subjects who did not receive electrical stimulation (n = 51). Only the exercise plus electrical stimulation group in both studies showed a significant (P = 0.05) reduction in feelings of calf fatigue. The results indicate that using MPD electrical stimulation during recovery enhances the effects of resistance exercise by increasing muscle strength while decreasing the feelings of muscle fatigue.

Blum K.,Florida College | Blum K.,National Institute of Holistic Studies | Blum K.,G and listic Addiction Treatment Center | Blum K.,LifeGen Inc | And 18 more authors.
Postgraduate Medicine | Year: 2010

Background: 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. Findings: Positive outcomes demonstrated by quantitative electroencephalographic (qEEG) imaging in a randomized, triple-blind, placebo-controlled, crossover study involving oral Synaptose Complex KB220Z™ showed an increase of alpha waves and low beta wave activity in the parietal brain region. Using t statistics, significant differences observed between placebo and Synaptose Complex KB220Z™ consistently occurred in the frontal regions after week 1 and then again after week 2 of analyses (P = 0.03). This is the first report to demonstrate involvement of the prefrontal cortex in the qEEG response to a natural putative D2 agonist (Synaptose Complex KB220Z™), especially evident in dopamine D2 A1 allele subjects. Independently, we have further supported this finding with an additional study of 3 serious polydrug abusers undergoing protracted abstinence who carried the DRD2 A1 allele. Significant qEEG differences were found between those who received 1 dose of placebo compared with those who were administered Synaptose Complex KB220Z™. Synaptose Complex KB220Z™ induced positive regulation of the dysregulated electrical activity of the brain in these addicts. The results are indicative of a phase change from low amplitude or low power in the brain to a more regulated state by increasing an average of 6.169 mV2 across the prefrontal cortical region. In the first experiment we found that while 50% of the subjects carried the DRD2 A1 allele, 100% carried ≥ 1 risk allele. Specifically, based on the proposed addiction risk score for these 14 subjects, 72% had moderate-to-severe addiction risk. Similar findings were obtained by repeating the experiment in 3 additional currently abstinent polydrug abusers carrying the DRD2 A1 allele. Conclusion: This seminal work will provide important information that may ultimately lead to significant improvement in the recovery of individuals with psychostimulant and polydrug abuse problems, specifically those with genetically induced dopamine deficiency. Based on this small sample size, we are proposing that with necessary large populations supporting these initial results, and possibly even additional candidate genes and single nucleotide polymorphisms, we may eventually have the clinical ability to classify severity according to genotype and possession of risk alleles, along with offering a safe, nonaddicting, natural dopaminergic receptor agonist that potentially upregulates instead of downregulates dopaminergic receptors, preferably the D2 subtype. © Postgraduate Medicine.

Chen A.L.C.,Chang Jung Christian University | Blum K.,University of Florida | Blum K.,G and listic Addiction Treatment Center | Blum K.,LifeGen Inc. | And 10 more authors.
Food and Function | Year: 2012

While there is a considerable body of literature correlating the role of dopaminergic genes and obesity, body mass index, body type, overeating, carbohydrate binging, energy expenditure and low dopamine D2 receptor (D2R) receptor density, there is a paucity of research concerning the dopamine D2 receptor gene (DRD2) variants and percent body fat. We report here the potential association of DRD2 genotypes and the percent fat phenotype. In this study we genotyped 122 obese/overweight (O/OW) Caucasian subjects and 30 non-obese Caucasian controls, screened to exclude substance abuse. The subjects were assessed for weight, body mass index (BMI; kg m -2) and percent body fat using dual energy X-ray absorptiometry (DEXA). The sample was separated into two independent groups; those with the Taq1 A1 allele (A1/A1 or A1/A2) and those without the A1 allele (A2/A2). The controls had a normal range of body fat (25-31% for females and 18-25% for males). The O/OW subjects had a percent body fat value of over 32% for females and over 25% for males. For the O/OW subjects, the mean BMI was 29.3 ± 6.25 kg m -2, mean body fat was 42.1 ± 7.5% and mean weight was 82.7 ± 21.7 kg. The DRD2 Taq1 A1 allele was present in 67% of the O/OW subjects compared to 3.3% of super controls (A group), 33.3% of screened (for drug abuse and obesity) controls (B group) and unscreened literature controls 29.4% (P ≤ 0.001). Comparing all cases with more than 34% body fat, utilizing logistic regression analysis, the DRD2 A1 allele accounts for 45.9% of the variance, which is statistically significant (χ 2 = 43.47, degrees of freedom (df) = 1, P < 0.0001). These results are consistent with a role for the DRD2 gene in obesity, as measured by percent body fat as well as by weight and BMI. © 2012 The Royal Society of Chemistry.

LifeGen Inc. | Date: 2012-02-28

Dietary supplements; and ingredients for use as integral components of dietary supplements.

LifeGen Inc. | Date: 2010-03-10

Nutritional additives for medical purposes for use in foods and dietary supplements for human consumption.

PubMed | LifeGen Inc.
Type: Journal Article | Journal: Journal of genetic syndromes & gene therapy | Year: 2013

This article co-authored by a number of scientists, ASAM physicians, clinicians, treatment center owners, geneticists, neurobiologists, psychologists, social workers, criminologists, nurses, nutritionist, and students, is dedicated to all the people who have lost loved ones in substance-abuse and reward deficiency syndrome related tragedies. Why are we failing at reducing the incidence of Bad Behaviors? Are we aiming at the wrong treatment targets for behavioral disorders? We are proposing a paradigm shift and calling it

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