DOCSLIB.ORG

QEEG and MEDICATION OUTLINE of PRESENTATION

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
QEEG and MEDICATION OUTLINE of PRESENTATION QEEG and MEDICATION OUTLINE OF PRESENTATION Jack Johnstone, Ph.D. [email protected] Q-Metrx, Inc. July 20, 2007 I. Introduction A. Disclosure B. Scope of Presentation II. Background A. First, Do No Harm B. Use of Antipsychotic Medications in Children III. Powerful and Practical Applications of QEEG technology A. Optimizing Clinical Outcome by Individualized Selection of Medications B. Reduction of Side Effects IV. Drug Effects on EEG: Principles A. Quantity of medication in the patient influences the EEG. This quantity varies according to dose, volume of distribution, and rate of metabolism. B. Combinations of medications (polypharmacy) may produce unpredictable effects V. Pharmaco-EEG A. Long history of study of effects of medications on EEG, as early as Hans Berger’s studies of effects of cocaine of beta frequency activity (Replicated in Herning et al. 1985.) see Herrmann, Itil, Fink, Saletu, Wauquier, others B. Effects have now been studied in detail for many commonly used medications: SEE: Saletu, B., Anderer, P., and G.M. Saletu-Zyhlarz, “EEG Topography and Tomography (LORETA) in the Classification and Evaluation of the Pharmacodynamics of Psychotropic Drugs” Clinical EEG and Neuroscience, April 2006, 66-80. Chlorpromazine Haldol Imipramine Citalopram Clobazam Lorazepam d-Amphetamine Methylphenidate Pyritinol C. General Effects of Medication on EEG 1. Psychostimulants (Ritalin, Dexedrine, Adderall, Concerta): Decreases slow activity (delta and theta frequencies) and increases fast activity (beta frequencies) 2. Benzodiazepines (Xanax, Valium, Ativan): Increases 14-25 Hz. Have anticonvulsant properties 3. Barbiturates (Phenobarbital): Increases delta activity and increases18-35 Hz beta spindles High dosage produces “burst-suppression” 4. Tricyclic Antidepressants: (Elavil, Tofanil, Norpramin, Sinequan, Pamelor) Increases both slow and fast activity and decreases alpha frequency activity (sedating) 5. SSRIs: (Prozac, Zoloft, Luvox, Paxil, Lexipro, Celexa) Produces less delta, decreases alpha, and increase beta (less sedating) 6. OTHER: NRIs (Wellbutrin- lowers seizure threshold); SNRIs (Cymbalta, Effexor); MAO Inhibitors (Nardil, Parnate), Increases 14-20 Hz beta (non-sedating) 7. Antipsychotics: 1) Tranquilizers (Thorazine, Haldol) Decreases fast activity, increases slow activity; 2) Atypical (Zyprexa, Risperdal, Seroquel, Clozaril) Increases delta, theta, increases beta. 8. Mood Stabilizers/Anticyclics: (Lithium, Tegretol) Increased theta frequency activity. Overdose produces marked slowing and triphasic discharges. D. “Recreational” Drugs 1. Marijuana / Hashish / THC: Increased frontal alpha, increased interhemispheric alpha coherence. 2. Cocaine: Increased beta, EEG desynchronization, potentiates seizure activity 3. LSD: Decreased amplitude, suppression of slow activity, increases dominant frequency. VI. Event-Related Potentials (ERPs) A. Generally involves “signal averaging” of brief segments of EEG following sensory stimulation. 1. Visual, auditory, and somatrosensory stimuli are used to test afferent conduction through the central nervous system 2. “Cognitive” components can be identified that reflect psychological processes such as anticipation of stimuli or target detection of specific types of stimuli 3. The “P300” ERP is named because a POSITIVE potential following target stimulus can be identified peaking at 300 milliseconds post target stimulus. 4. The timing (latency) of the P300 appears to shift with age and is significantly delayed in dementing illness. 5. The latency of the P300 (and EEG spectra) can be normalized with the long-term use of anticholinesterase inhibitor such as Aricept (donezepil) VII. The STAR*D Trial: “Sequenced Treatment Alternatives to Relieve Depression” A. Largest and longest study ever done to evaluate treatment of depression 1. Over 4,000 patients enrolled in a “naturalistic” design 2. Four “levels” of treatment were studied (See attached START*D Treatment Flowchart) B. About half of the participants became symptom-free after the first two treatment levels. After that, rates at which participants showed remission of symptoms slowed. C. Over the course of ALL FOUR LEVELS, about 70 percent of those who did not withdraw from the study became symptom-free. VIII. Using qEEG to PREDICT medication response A. Suffin and Emory (1995) studies two groups of patients, one with affective disorder without attentional disturbance and one with attentional disorder without affective disturbance. 1. EEG Markers for response to stimulant medication were seen in each of the two patient groups (elevated frontal theta power) 2. EEG Markers for response to antidepressant medication were seen in each of the two patient groups (elevated frontal alpha) B. R.J. Chabot et al., 1996, 1999 refined this work, examining effects of methylphenidate and Dexedrine. 1. Excess theta activity predicted response to Methylphenidate 2. Excess slow frequency alpha activity predicted response to Dexedrine. C. Leuchter and Cook at UCLA developed a metric of the amount of relative power in the EEG in a given frequency range as a percentage of absolute power in the same frequency range termed “CORDANCE”. 1. Cordance in the theta frequency range showed changes with antidepressant medication. Changes were also seen placebo. 2. “This study demonstrates that although the symptomatic improvement resulting from placebo and medication treatment may be similar, the two treatments are not physiologically equivalent.” IX. The BRITE-MD clinical trial (“STAR*D with qEEG”) A. Following four independent pilot studies at UCLA, Cedars- Sinai Medical Center, and Mass General, Aspect Medical Systems initiated a large scale clinical trial at 10 sites. B. A total of 375 patients with major depression were studies over a 13 week period. (See attached BRITE-MD protocol for details of study design) C. A marker (frontal EEG) measured at one week following initiation of antidepressant medication (Lexipro) predicted clinical outcome at 7 weeks. Clinician prediction was at chance level. D. If the change was NOT seen at one week it did not help to continue on Lexipro or augment Lexipro with Wellbutrin. Clinical outcome was improved by SWITCHING medication to Wellbutrin alone and discontinuing Lexipro (see attached poster). X. EEG Phenotypes A. Johnstone, et al. (2005) suggest that various EEG profiles might be considered as “intermediate phenotypes” falling between genetics and behavior. B. EEG phenotypes may be considered as vulnerability factors and guide intervention for medications and neurofeedback. C. Reprint available on request (contact [email protected]) XI. SUMMARY AND CONCLUSIONS A. Numerous studies document the effects of various medications on EEG B. Recent studies indicate that qEEG predicts medication response better than behavioral symptoms. C. New technologies offer the promise of increased sensitivity and specificity. Treatment Choices Throughout STAR*D LEVEL1 – All participants were treated with citalopram (Celexa) Those who went into remission (e.g., they became well) Went into follow-up Those who did not get well, went on to Level 2 LEVEL 2 – Switching treatments or adding to citalopram (Celexa) Those who chose to switch treatments were randomized to: Those who became • sertraline (Zoloft), well went into follow-up • bupropion-SR (Wellbutrin), • venlafaxine-ZR (Effexor), or • cognitive behavioral therapy (CBT) Those who chose to add treatment were randomized to: Those who became well went into follow-up • bupropion-SR (Wellbutrin), • buspirone (BuSpar), or • cognitive behavioral therapy (CBT) Those who did not get well went on to Level 3 LEVEL 3 – Switching treatments or adding to existing medication Those who chose to switch treatments were randomized Those who became well to: went into follow-up • mirtazapine (Remeron) or • nortriptyline (Aventyl or Pamelor) Those who chose to add treatment were randomized to: Those who became well • lithium or went into follow-up • triiodthyronine (T3) Those who did not get well went on to Level 4 LEVEL 4 – Switching treatments Participants were taken off all other medications and randomized to: • tranylcypromine, an MAOI (Parnate) or • venlafaxine XR (Effexor XR) + mirtazapine (Remeron) Can EEG-guided Antidepressant Selection Improve Response Rates? Insights from the BRITE-MD Trial Andrew F. Leuchter, M.D.1, Ian A. Cook, M.D.1, William S. Gilmer, M.D.2, Scott D. Greenwald, Ph.D.3, Robert H. Howland, M.D.4, Madhukar H. Trivedi, M.D.5 1UCLA Laboratory of Brain, Behavior, and Pharmacology, Semel Institute, Los Angeles, CA, 2Psychiatry, Northwestern University, Chicago, IL,3Neuroscience, Aspect Medical Systems, Norwood, MA, 4Western Psychiatric Institute and Clinic, University of Pittsburgh, Pittsburgh, PA, 5Psychiatry, University of Texas Southwestern Medical School, Dallas, TX ABSTRACT METHODS (Continued) RESULTS (Continued) Objective: The BRITE-MD study (www.BRITE-MD.org) was designed to assess ESC Group (n=40): 90% the accuracy of a frontal quantitative electroencephalographic (fqEEG) biomarker Continue escitalopram (10mg/day) 73% in predicting response to escitalopram (ESC) treatment. This analysis compares the 68% 70% 65% response rate between subjects who received treatment consistent with the 57% 52% biomarker prediction vs. other subjects. 51% 50% 41% Method: 111 subjects (age: 42 ± 14 ; 59% female) meeting DSM-IV criteria for BUP Group (n=35): 36% 35% MDD began treatment with escitalopram (ESC; 10 mg/day) and were randomly Switch to bupropion XL All subjects (300 mg/day) 30% assigned after
Load more

Recommended publications
  • (19) United States (12) Patent Application Publication (10) Pub
    US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 9,005,660 B2 Tygesen Et Al
    USOO9005660B2 (12) United States Patent (10) Patent No.: US 9,005,660 B2 Tygesen et al. (45) Date of Patent: Apr. 14, 2015 (54) IMMEDIATE RELEASE COMPOSITION 4,873,080 A 10, 1989 Bricklet al. RESISTANT TO ABUSEBY INTAKE OF 4,892,742 A 1, 1990 Shah 4,898,733. A 2f1990 DePrince et al. ALCOHOL 5,019,396 A 5/1991 Ayer et al. 5,068,112 A 11/1991 Samejima et al. (75) Inventors: Peter Holm Tygesen, Smoerum (DK); 5,082,655 A 1/1992 Snipes et al. Jan Martin Oevergaard, Frederikssund 5,102,668 A 4, 1992 Eichel et al. 5,213,808 A 5/1993 Bar Shalom et al. (DK); Joakim Oestman, Lomma (SE) 5,266,331 A 11/1993 Oshlack et al. 5,281,420 A 1/1994 Kelmet al. (73) Assignee: Egalet Ltd., London (GB) 5,352.455 A 10, 1994 Robertson 5,411,745 A 5/1995 Oshlack et al. (*) Notice: Subject to any disclaimer, the term of this 5,419,917 A 5/1995 Chen et al. patent is extended or adjusted under 35 5,422,123 A 6/1995 Conte et al. U.S.C. 154(b) by 473 days. 5,460,826 A 10, 1995 Merrill et al. 5,478,577 A 12/1995 Sackler et al. 5,508,042 A 4/1996 OShlack et al. (21) Appl. No.: 12/701.248 5,520,931 A 5/1996 Persson et al. 5,529,787 A 6/1996 Merrill et al. (22) Filed: Feb. 5, 2010 5,549,912 A 8, 1996 OShlack et al.
    [Show full text]
  • Ehealth DSI [Ehdsi V2.2.2-OR] Ehealth DSI – Master Value Set
    MTC eHealth DSI [eHDSI v2.2.2-OR] eHealth DSI – Master Value Set Catalogue Responsible : eHDSI Solution Provider PublishDate : Wed Nov 08 16:16:10 CET 2017 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 1 of 490 MTC Table of Contents epSOSActiveIngredient 4 epSOSAdministrativeGender 148 epSOSAdverseEventType 149 epSOSAllergenNoDrugs 150 epSOSBloodGroup 155 epSOSBloodPressure 156 epSOSCodeNoMedication 157 epSOSCodeProb 158 epSOSConfidentiality 159 epSOSCountry 160 epSOSDisplayLabel 167 epSOSDocumentCode 170 epSOSDoseForm 171 epSOSHealthcareProfessionalRoles 184 epSOSIllnessesandDisorders 186 epSOSLanguage 448 epSOSMedicalDevices 458 epSOSNullFavor 461 epSOSPackage 462 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 2 of 490 MTC epSOSPersonalRelationship 464 epSOSPregnancyInformation 466 epSOSProcedures 467 epSOSReactionAllergy 470 epSOSResolutionOutcome 472 epSOSRoleClass 473 epSOSRouteofAdministration 474 epSOSSections 477 epSOSSeverity 478 epSOSSocialHistory 479 epSOSStatusCode 480 epSOSSubstitutionCode 481 epSOSTelecomAddress 482 epSOSTimingEvent 483 epSOSUnits 484 epSOSUnknownInformation 487 epSOSVaccine 488 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 3 of 490 MTC epSOSActiveIngredient epSOSActiveIngredient Value Set ID 1.3.6.1.4.1.12559.11.10.1.3.1.42.24 TRANSLATIONS Code System ID Code System Version Concept Code Description (FSN) 2.16.840.1.113883.6.73 2017-01 A ALIMENTARY TRACT AND METABOLISM 2.16.840.1.113883.6.73 2017-01
    [Show full text]
  • Cognitive Enhancing Agents: Current Status in the Treatment of Alzheimer's Disease
    LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES REVIEW ARTICLE Cognitive Enhancing Agents: Current Status in the Treatment of Alzheimer's Disease Cheryl Waters ABSTRACT: Extensive recent literature on drugs used to enhance cognitive functioning, reflects the growing social problem of dementia. Many clinical trials have been undertaken with variable success. In most cases the disorder stud­ ied has been Alzheimer's disease. The pharmacological approach has been designed to rectify the presumed patho­ physiological processes characteristic of the condition. Agents tested include cerebral vasodilators, cerebral metabolic enhancers, nootropics, psychostimulants, neuropeptides and neurotransmitters with a special emphasis on drugs used to enhance cholinergic function. Ethical and practical issues concerning clinical drug trials in dementia will be discussed. RESUME: Stimulation cognitive medicamenteuse: etat de la question dans le traitement de la maladie d'Alzheimer La multiplicity des publications recentes sur les medicaments utilises pour stimuler le fonctionnement cognitif est le reflet du probl&me social sans cesse croissant de la d6mence. Plusieurs essais cliniques ont ete tentes avec des resultats variables. Dans la plupart des cas, la maladie etudiee etait la maladie d'Alzheimer. L'approche pharmacologique a ete con^ue pour corriger les processus physiopathologiques caracteristiques de la maladie. Les agents etudies incluent des vasodilatateurs cerebraux, des stimulants metaboliques cerebraux, des agents nootropes, des agents neurotropes,
    [Show full text]
  • Marrakesh Agreement Establishing the World Trade Organization
    No. 31874 Multilateral Marrakesh Agreement establishing the World Trade Organ ization (with final act, annexes and protocol). Concluded at Marrakesh on 15 April 1994 Authentic texts: English, French and Spanish. Registered by the Director-General of the World Trade Organization, acting on behalf of the Parties, on 1 June 1995. Multilat ral Accord de Marrakech instituant l©Organisation mondiale du commerce (avec acte final, annexes et protocole). Conclu Marrakech le 15 avril 1994 Textes authentiques : anglais, français et espagnol. Enregistré par le Directeur général de l'Organisation mondiale du com merce, agissant au nom des Parties, le 1er juin 1995. Vol. 1867, 1-31874 4_________United Nations — Treaty Series • Nations Unies — Recueil des Traités 1995 Table of contents Table des matières Indice [Volume 1867] FINAL ACT EMBODYING THE RESULTS OF THE URUGUAY ROUND OF MULTILATERAL TRADE NEGOTIATIONS ACTE FINAL REPRENANT LES RESULTATS DES NEGOCIATIONS COMMERCIALES MULTILATERALES DU CYCLE D©URUGUAY ACTA FINAL EN QUE SE INCORPOR N LOS RESULTADOS DE LA RONDA URUGUAY DE NEGOCIACIONES COMERCIALES MULTILATERALES SIGNATURES - SIGNATURES - FIRMAS MINISTERIAL DECISIONS, DECLARATIONS AND UNDERSTANDING DECISIONS, DECLARATIONS ET MEMORANDUM D©ACCORD MINISTERIELS DECISIONES, DECLARACIONES Y ENTEND MIENTO MINISTERIALES MARRAKESH AGREEMENT ESTABLISHING THE WORLD TRADE ORGANIZATION ACCORD DE MARRAKECH INSTITUANT L©ORGANISATION MONDIALE DU COMMERCE ACUERDO DE MARRAKECH POR EL QUE SE ESTABLECE LA ORGANIZACI N MUND1AL DEL COMERCIO ANNEX 1 ANNEXE 1 ANEXO 1 ANNEX
    [Show full text]
  • Cognitive Enhancers
    Cognitive enhancers Memory enhancers are often referred to as "smart drugs", "study drugs",[1] "smart nutrients", "cognitive enhancers", "brain enhancers" or in the scientific literature as nootropics.[2] They are drugs that are purported to improve human cognitive abilities.[3][4] The term covers a broad range of substances including drugs, nutrients and herbs with purported cognitive enhancing effects. The word nootropic was coined in 1964 by Dr. Corneliu E. Giurgea, derived from the Greek words noos, or "mind," and tropein meaning "to bend/turn". Typically, nootropics are thought to work by altering the availability of the brain's supply of neurochemicals (neurotransmitters, enzymes, and hormones), by improving the brain's oxygen supply, or by stimulating nerve growth. However the efficacy of nootropic substances in most cases has not been conclusively determined. This is complicated by the difficulty of defining and quantifying cognition and intelligence. Contents 1 Availability 2 Examples 2.1 Stimulants 2.2 Replenishing and increasing neurotransmitters 2.2.1 Cholinergics 2.2.1.1 Piracetam 2.2.1.2 Aniracetam 2.2.1.3 Other cholinergics 2.2.1.4 Acetylcholinesterase inhibitors 2.2.2 Dopaminergics 2.2.3 Serotonergics 2.3 Anti-depression, adaptogenic (antistress), and mood stabilization 2.4 Brain function and improved oxygen supply 2.5 Purported memory enhancement and learning improvement 2.6 Nerve growth stimulation and brain cell protection 2.7 Recreational drugs with purported nootropic effects 2.8 Dietary nootropics 2.9 Other nootropics 2.9.1 Contentious or possibly unsafe nootropics 3 See also 3.1 Brain and neurology 3.2 Thought and thinking (what nootropics are used for) 3.3 Health 4 References 5 External links Availability Currently there are several drugs on the market that improve memory, concentration, planning and reduce impulsive behavior.
    [Show full text]
  • Study Protocol and Statistical Analysis Plan
    Multicenter double-blind placebo-controlled randomized parallel-group clinical study of efficacy and safety of MMH-MAP in the treatment of mild cognitive impairment in subjects in early rehabilitation period of ischemic stroke Phase III Sponsor OOO «NPF «MATERIA MEDICA HOLDING» Protocol number MMH-MAP-001 Version date: August 29, 2018 ClinicalTrials.gov Id: NCT03815292 Protocol No. MMH-MAP-001 29-Aug-2018 Protocol Summary This document represents the protocol summary for the study on human subjects. The study will be carried out in accordance with ICH GCP, National Standard of the Russian Federation GOST 52379-2005 "Good Clinical Practice", World Medical Association Declaration of Helsinki, relevant requirements of the regulatory authorities as well as the study procedures. Title of Study Multicenter double-blind placebo-controlled randomized parallel-group clinical study of efficacy and safety of MMH-MAP in the treatment of mild cognitive impairment in subjects in early rehabilitation period of ischemic stroke. Phase: III Sponsor: Company «MATERIA MEDICA HOLDING», Moscow, Russia Protocol No. MMH-MAP-001 Objective of the study To evaluate efficacy of MMH-MAP in the treatment of mild cognitive impairment in subjects in early rehabilitation period of ischemic stroke. To evaluate the safety of MMH-MAP in the treatment of mild cognitive impairment in subjects in early rehabilitation period of ischemic stroke. Endpoints Primary endpoint 1. Proportion of subjects with improved cognitive functions (MoCA ≥ +1) after 24-week therapy compared to baseline. Secondary endpoints 1. Change in MoCA scores after 24 weeks of treatment. 2. Percentage of patients with improved performance in activities of daily living (total Barthel Index score + 5 or more) after 24 weeks of treatment.
    [Show full text]
  • Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DIX to the HTSUS—Continued
    20558 Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DEPARMENT OF THE TREASURY Services, U.S. Customs Service, 1301 TABLE 1.ÐPHARMACEUTICAL APPEN- Constitution Avenue NW, Washington, DIX TO THE HTSUSÐContinued Customs Service D.C. 20229 at (202) 927±1060. CAS No. Pharmaceutical [T.D. 95±33] Dated: April 14, 1995. 52±78±8 ..................... NORETHANDROLONE. A. W. Tennant, 52±86±8 ..................... HALOPERIDOL. Pharmaceutical Tables 1 and 3 of the Director, Office of Laboratories and Scientific 52±88±0 ..................... ATROPINE METHONITRATE. HTSUS 52±90±4 ..................... CYSTEINE. Services. 53±03±2 ..................... PREDNISONE. 53±06±5 ..................... CORTISONE. AGENCY: Customs Service, Department TABLE 1.ÐPHARMACEUTICAL 53±10±1 ..................... HYDROXYDIONE SODIUM SUCCI- of the Treasury. NATE. APPENDIX TO THE HTSUS 53±16±7 ..................... ESTRONE. ACTION: Listing of the products found in 53±18±9 ..................... BIETASERPINE. Table 1 and Table 3 of the CAS No. Pharmaceutical 53±19±0 ..................... MITOTANE. 53±31±6 ..................... MEDIBAZINE. Pharmaceutical Appendix to the N/A ............................. ACTAGARDIN. 53±33±8 ..................... PARAMETHASONE. Harmonized Tariff Schedule of the N/A ............................. ARDACIN. 53±34±9 ..................... FLUPREDNISOLONE. N/A ............................. BICIROMAB. 53±39±4 ..................... OXANDROLONE. United States of America in Chemical N/A ............................. CELUCLORAL. 53±43±0
    [Show full text]
  • Lessons Learned
    Prevention and Reversal of Chronic Disease Copyright © 2019 RN Kostoff PREVENTION AND REVERSAL OF CHRONIC DISEASE: LESSONS LEARNED By Ronald N. Kostoff, Ph.D., School of Public Policy, Georgia Institute of Technology 13500 Tallyrand Way, Gainesville, VA, 20155 [email protected] KEYWORDS Chronic disease prevention; chronic disease reversal; chronic kidney disease; Alzheimer’s Disease; peripheral neuropathy; peripheral arterial disease; contributing factors; treatments; biomarkers; literature-based discovery; text mining ABSTRACT For a decade, our research group has been developing protocols to prevent and reverse chronic diseases. The present monograph outlines the lessons we have learned from both conducting the studies and identifying common patterns in the results. The main product of our studies is a five-step treatment protocol to reverse any chronic disease, based on the following systemic medical principle: at the present time, removal of cause is a necessary, but not necessarily sufficient, condition for restorative treatment to be effective. Implementation of the five-step treatment protocol is as follows: FIVE-STEP TREATMENT PROTOCOL TO REVERSE ANY CHRONIC DISEASE Step 1: Obtain a detailed medical and habit/exposure history from the patient. Step 2: Administer written and clinical performance and behavioral tests to assess the severity of symptoms and performance measures. Step 3: Administer laboratory tests (blood, urine, imaging, etc) Step 4: Eliminate ongoing contributing factors to the chronic disease Step 5: Implement treatments for the chronic disease This individually-tailored chronic disease treatment protocol can be implemented with the data available in the biomedical literature now. It is general and applicable to any chronic disease that has an associated substantial research literature (with the possible exceptions of individuals with strong genetic predispositions to the disease in question or who have suffered irreversible damage from the disease).
    [Show full text]
  • Pharmaceuticals (Monocomponent Products) ………………………..………… 31 Pharmaceuticals (Combination and Group Products) ………………….……
    DESA The Department of Economic and Social Affairs of the United Nations Secretariat is a vital interface between global and policies in the economic, social and environmental spheres and national action. The Department works in three main interlinked areas: (i) it compiles, generates and analyses a wide range of economic, social and environmental data and information on which States Members of the United Nations draw to review common problems and to take stock of policy options; (ii) it facilitates the negotiations of Member States in many intergovernmental bodies on joint courses of action to address ongoing or emerging global challenges; and (iii) it advises interested Governments on the ways and means of translating policy frameworks developed in United Nations conferences and summits into programmes at the country level and, through technical assistance, helps build national capacities. Note Symbols of United Nations documents are composed of the capital letters combined with figures. Mention of such a symbol indicates a reference to a United Nations document. Applications for the right to reproduce this work or parts thereof are welcomed and should be sent to the Secretary, United Nations Publications Board, United Nations Headquarters, New York, NY 10017, United States of America. Governments and governmental institutions may reproduce this work or parts thereof without permission, but are requested to inform the United Nations of such reproduction. UNITED NATIONS PUBLICATION Copyright @ United Nations, 2005 All rights reserved TABLE OF CONTENTS Introduction …………………………………………………………..……..……..….. 4 Alphabetical Listing of products ……..………………………………..….….…..….... 8 Classified Listing of products ………………………………………………………… 20 List of codes for countries, territories and areas ………………………...…….……… 30 PART I. REGULATORY INFORMATION Pharmaceuticals (monocomponent products) ………………………..………… 31 Pharmaceuticals (combination and group products) ………………….……........
    [Show full text]
  • Customs Tariff - Schedule
    CUSTOMS TARIFF - SCHEDULE 99 - i Chapter 99 SPECIAL CLASSIFICATION PROVISIONS - COMMERCIAL Notes. 1. The provisions of this Chapter are not subject to the rule of specificity in General Interpretative Rule 3 (a). 2. Goods which may be classified under the provisions of Chapter 99, if also eligible for classification under the provisions of Chapter 98, shall be classified in Chapter 98. 3. Goods may be classified under a tariff item in this Chapter and be entitled to the Most-Favoured-Nation Tariff or a preferential tariff rate of customs duty under this Chapter that applies to those goods according to the tariff treatment applicable to their country of origin only after classification under a tariff item in Chapters 1 to 97 has been determined and the conditions of any Chapter 99 provision and any applicable regulations or orders in relation thereto have been met. 4. The words and expressions used in this Chapter have the same meaning as in Chapters 1 to 97. Issued January 1, 2020 99 - 1 CUSTOMS TARIFF - SCHEDULE Tariff Unit of MFN Applicable SS Description of Goods Item Meas. Tariff Preferential Tariffs 9901.00.00 Articles and materials for use in the manufacture or repair of the Free CCCT, LDCT, GPT, following to be employed in commercial fishing or the commercial UST, MXT, CIAT, CT, harvesting of marine plants: CRT, IT, NT, SLT, PT, COLT, JT, PAT, HNT, Artificial bait; KRT, CEUT, UAT, CPTPT: Free Carapace measures; Cordage, fishing lines (including marlines), rope and twine, of a circumference not exceeding 38 mm; Devices for keeping nets open; Fish hooks; Fishing nets and netting; Jiggers; Line floats; Lobster traps; Lures; Marker buoys of any material excluding wood; Net floats; Scallop drag nets; Spat collectors and collector holders; Swivels.
    [Show full text]
  • Dietary Nutrient Intake, Alcohol Metabolism, and Hangover Severity
    Journal of Clinical Medicine Article Dietary Nutrient Intake, Alcohol Metabolism, and Hangover Severity Joris C. Verster 1,2,3,* , Sterre A. Vermeulen 1, Aurora J. A. E. van de Loo 1,2 , Stephanie Balikji 1, Aletta D. Kraneveld 1,2 , Johan Garssen 1,4 and Andrew Scholey 3 1 Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, 3584CG Utrecht, The Netherlands 2 Institute for Risk Assessment Sciences (IRAS), Utrecht University, 3584CM Utrecht, The Netherlands 3 Centre for Human Psychopharmacology, Swinburne University, Melbourne, VIC 3122, Australia 4 Nutricia Research, 3584CT Utrecht, The Netherlands * Correspondence: [email protected]; Tel.: +31-030-253-6909 Received: 14 July 2019; Accepted: 24 August 2019; Published: 27 August 2019 Abstract: Several dietary components have been shown to influence alcohol metabolism and thereby potentially affect the development of a hangover. From the literature, it is evident that dietary nicotinic acid and zinc play a pivotal role in the oxidation of ethanol into acetaldehyde. The aim of the current study was to associate dietary intake of nicotinic acid and zinc with hangover severity. To this end, data from n = 23 healthy social drinkers who participated in a naturalistic hangover study were analyzed. n = 10 of them reported to be hangover-resistant (the control group), whereas n = 13 reported to have regular hangovers (the hangover-sensitive group). Two 24 h dietary recall records were completed, one for the day of alcohol consumption and another one for an alcohol-free control day. Dietary nutrient intake was averaged and did not significantly differ between hangover-sensitive and hangover-resistant drinkers.
    [Show full text]