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David Nutt - Addiction

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Part of the Oxford Psychiatry Library series, this pocketbook is a clear and comprehensive overview of the brain science underpinning addiction and how this helps explain the current and future therapeutics for the range of addictions, using full colour images to enhance understanding. Substance Abuse focuses on the nature of addiction as a brain disorder that includes a range of different behavioural traits such as impulsivity and reward dependence, and discusses the critical role of kinetic and pharmacological factors. The text explains how the primary pharmacological targets of drugs of abuse are now understood, the relation to the variable nature of addiction to different substances, and how this may lead to new approaches to treatment

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OPL
OXFORD PSYCHIATRY LIBRARY

Addiction OPL OXFORD PSYCHIATRY LIBRARY Addiction Professor David - photo 1

Addiction

OPL
OXFORD PSYCHIATRY LIBRARY

Addiction Professor David J Nutt The Edmond J Safra Chair in - photo 2

Addiction

Professor David J. Nutt

The Edmond J Safra Chair in Neuropsychopharmacology,
Centre for Neuropsychopharmacology,
Division of Brain Sciences,
Department of Medicine,
Imperial College London
United Kingdom

Dr Liam J. Nestor

Centre for Neuropsychopharmacology,
Division of Brain Sciences,
Department of Medicine,
Imperial College London
United Kingdom

Addiction - image 3

Addiction - image 4

Great Clarendon Street, Oxford, OX2 6DP,
United Kingdom

Oxford University Press is a department of the University of Oxford.
It furthers the Universitys objective of excellence in research, scholarship,
and education by publishing worldwide. Oxford is a registered trade mark of
Oxford University Press in the UK and in certain other countries

Oxford University Press 2013

The moral rights of the authors have been asserted

First Edition published in 2013

Impression: 1

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by licence or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above

You must not circulate this work in any other form and you must impose this same condition on any acquirer

Published in the United States of America by Oxford University Press 198 Madison Avenue, New York, NY 10016, United States of America

British Library Cataloguing in Publication Data

Data available

Library of Congress Control Number: 2013937072

ISBN 9780199685707

Printed in the UK
by Bell & Bain Ltd, Glasgow

Oxford University Press makes no representation, express or implied, that the
drug dosages in this book are correct. Readers must therefore always check
the product information and clinical procedures with the most up-to-date
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and the most recent codes of conduct and safety regulations. The authors and
the publishers do not accept responsibility or legal liability for any errors in the
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Contents

Substance addiction is conceived to involve a loss of self-control. Despite their best efforts and expressed preferences to remain abstinent, substance addiction populations often appear incapable of exerting sufficient control over their substance urges, their substance-seeking and substance-taking behaviours. The origins of substance addiction appear to be related to the long-term pharmacological effects of substances on an already, potentially genetically compromised set of neural circuits in the brain. There are credible theories regarding the initiation of substance abuse (e.g. a reward deficiency syndrome, impulsivity/impaired cognitive control, stress) whose antecedents likely involve interactions between several neurotransmitter systems (e.g. dopamine, endorphins, GABA, glutamate) in the brain. This appears to be supported, to some degree, by the potential efficacy of some pharmacotherapies (e.g. agonists/antagonists at dopamine, endorphin, GABA, and glutamate receptors) that have been shown to increase the likelihood of substance abstinence and prevent relapse. Further research is required, however, in an attempt to fully define the neurochemistry of important behavioural components of substance addiction (e.g. craving, impulsivity) that feature prominently in substance use disorders, particularly with respect to substance relapse after significant periods of protracted abstinence.

The following volume will attempt to inform clinicians and other healthcare professionals about some of the more fundamental psychological, neurobiological, and pharmacological concepts that are applicable to the treatment of substance abuse and addiction. The following volume will place particular emphasis on reporting and discussing the seminal findings of human neuroscience research in substance addiction and clinical trials in different substance addiction populations.

David J. Nutt
Liam J. Nestor

approximately

beta

%

percent

equal to or less than

5-HT

5-hydroxytryptomine

A118G

arginine (A) to glycine (G) substitution at position 118 of exon 1

A&E

Accident and Emergency

ACG

anterior cingulate gyrus

ADHD

attention deficit hyperactive disorder

AMPA

-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid

Amyg

amygdala

ARS

Alcohol Rating Scale

ATP

adenosine triphosphate

AUD

alcohol-use disorder

BPND

parametric binding potential

BrAC

breath alcohol concentration

C-11

carbon 11

Ca2+

calcium

cAMP

cyclic adenosine monophosphate

CB1

cannabinoid 1 receptor

CEQ

Cocaine Effects Questionnaire

CI

confidence interval

Cl

chloride

CIWA-Ar

Clinical Institute Withdrawal Assessment for Alcohol-revised

DA

dopamine

DALY

disability-adjusted life-year

DAT

dopamine transporter

DCS

D-cycloserine

DIAZ

diazepam

DLPFC

dorsolateral prefrontal cortex

dOR

delta opioid receptor

D1R

dopamine 1 receptor

D2R

dopamine 2 receptor

DS

dorsal striatum

DXM

dextromethorphan

fMRI

functional magnetic resonance imaging

g

gram

GABA

gamma-aminobutyric acid

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