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Marijuana and Madness
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Details

  • 14 b/w illus. 10 tables
  • Page extent: 236 pages
  • Size: 247 x 174 mm
  • Weight: 0.63 kg

Library of Congress

  • Dewey number: 615/.7827
  • Dewey version: 22
  • LC Classification: RC568.C2 M375 2004
  • LC Subject headings:
    • Marijuana--Physiological effect
    • Marijuana--Psychological aspects
    • Marijuana abuse--Complications
    • Psychoses--Etiology
    • Schizophrenia--Etiology

Library of Congress Record

Hardback

 (ISBN-13: 9780521819404 | ISBN-10: 0521819407)




Index




Numbers in italics indicate tables, figures and boxes.

N-acylphosphatidylethanolamine (NAPE) 9–10

Addiction Severity Index (ASI) 189

adenylate cyclase 7

affect regulation model of substance use 171

alcohol

   Drinking Motives Questionnaire 173, 174, 176, 177

   exacerbation of psychotic symptoms 169

   motivational models for use see motivational models of substance use

   see also reasons for substance use in psychosis

Alzheimer’s disease 134

AM-251 12

AM-281 12

AM-404 12

ambivalence 193

‘amotivational syndrome’

   components 49

   debate about 48, 50

   laboratory study 50

   observational studies 48–50

   and personality type 50

   similarity with negative dimension of psychosis 80

‘amfetamine psychosis’ 90

anandamide

   appetite stimulation 29

   bioassay 8

   biosynthesis 9–10, 130

   chemical structure 19–20

   CSF levels in schizophrenia 96, 132–3

   distribution in brain 130

   half-life 132

   inactivation 10–11, 130

   isolation 7–8

   role in sleep–waking cycle 28

   synthetic analogues 12

   transport 130–1

animal studies of cannabinoids

   memory effects 26–7

   psychomotor effects 24–5

   rewarding effects 31–2

   self-administration 32, 33

   withdrawal syndrome 32–3

   see also CB1 receptor knockout mice

antianxiety effects of cannabidiol 6, 46

anticonvulsant effects of cannabidiol 5

antidepressant effects of Δ9-THC 45

antipsychotic drug metabolism and cannabis 124

antipsychotic effects of cannabidiol 6

anxiety

   effects of cannabidiol 6, 46

   effects of cannabis 45–6, 149–50, 149, 150

   effects of CB1 antagonists 46

appetite effects of cannabinoids 29

2-arachidonoylglycerol (2-AG)

   biosynthesis 10, 130

   chemical structure 19–20

   CNS concentrations 130

   entourage effect 8

   inactivation 10–11, 130

   isolation 8

assessment of cannabis use in psychosis

   aspects for consideration 188, 188

   importance of therapeutic relationship 190

   readiness to change 190

   reasons for use 189–90

   summarized 191

   tools 189–90

association of cause and disease 103

attentional effects of cannabis 47

Australian National Survey of Mental Health and Wellbeing 104

Berkson’s bias 57

bhang 93

bias

   comorbidity studies 57

   studies of long-term cannabis use 199–200

binocular depth inversion 131

bipolar disorder and cannabis use 56

brain

   CB1 receptor changes in schizophrenia 133–5

   CB1 receptor distribution 20–1, 22, 25, 28, 128, 128, 129

brain, effects of cannabinoids 19–40

   appetite control 29

   inhibition of neurotransmitter release 21–2, 25, 134–5

   intoxication see cannabis intoxication

   memory

      deficits 26, 48

      hippocampal involvement 26–8

      recall studies 150–2

   neocortical effects 28–9

   psychomotor function

      animals 24–5

      humans 25, 47

      interactions with other signalling systems 26

      mechanisms 25–6

   retrograde synaptic signalling 22–4

   tolerance 32

Brief Psychiatric Rating Scale (BPRS) 83

Buschke’s Selective Reminding Test, alternative versions 201, 202

cannabidiol (CBD) 5–6, 46

cannabinoid chemistry 3–13

   active constituent, isolation of 3

   cannabidiol 5–6

   current research 12–13

   endogenous cannabinoids 6–7

      biosynthesis and inactivation 9–11

      new types 8–9

      see also 2-arachidonoylglycerol (2AG); anandamide

cannabinoid ‘model’ psychosis 155

   see also cannabis and psychosis, exogenous hypothesis: possible mechanisms

cannabinoid receptor agonists 12, 19, 46

cannabinoid receptor antagonists 12, 19–20, 21, 46

cannabinoid receptors

   CB1 see CB1 receptors

   CB1A 127–8, 130

   CB2 7, 19

   discovery 6–7

   non-CB1 in CNS 12, 128, 130

cannabinoid/opioid synergism 31–2

cannabinoids, synthetic 11–12

cannabinol 3

cannabis

   early therapeutic use 2–3

   as gateway to harder drugs 111

   and mental illness, historical overview 1–3

   trends in use (USA) 115, 115

   withdrawal 32–3, 198–9

Cannabis Amount Used and Symptom Evaluation (CAUSE) 189

cannabis intoxication

   actions on emotional behaviour 31

   correlation with regional cerebral blood flow 30–1

   dopamine release 31

   mediation via CB1 receptors 30

   rewarding effects in animals 31–2

   subjective experience see psychomimetic effects of cannabis

‘cannabis psychosis’ 89–100

   biological plausibility 96

   case reports 91–2

   controlled clinical studies 92

      ‘cannabis psychosis’/schizophrenia patients 92–3

      psychosis in cannabis users/non-users 93–4

   debate over existence 96–7

   epidemiological studies 91

      drug use and psychotic experiences 95

      limitation of 95

      prevalence of symptoms in drug users 95

      time trends in schizophrenia 95–6

   ethically acceptable studies 90

   evidence needed to infer cause 89–90

   hypothesis 89

   rarity of 97

cannabis and psychosis, exogenous hypothesis 142

   hypothesis outlined 142

   pharmacological study of Δ9-THC

      study conditions 144–5

      data analysis 145

      effects on distractibility and vigilance 152–3, 153

      effects on recall 150–2, 151, 152

      effects on verbal fluency 152, 153

      induction of anxiety and panic 149, 150, 149–50

      induction of negative symptoms and euphoria 148, 149, 148–9

      induction of perceptual alterations 147, 148, 147–8

      induction of positive symptoms 145–7, 146

      study participation effects 153–4

      summary of findings 154

      interpretation of findings 154–5

   possible mechanisms 156

      dopaminergic 156–9

      GABAergic 158, 159–60

      glutamatergic 159

   review of published studies

      laboratory-based pharmacological studies 143–4

      limitations of naturalistic studies 143

Cannabis sativa, variations in Δ9-THC content 41

cannabis use and depression 54–74

   antidepressant effects of cannabis 45

   cannabis as cause of depression 55

   lack of clinical attention 54

   limitations of the research 65–6

      measurement of cannabis use 66

      measurement of depression 66–7

   reasons for the association 57–60

      cannabis causes depression 60, 68

      depression causes cannabis use 60–1

      shared risk factors 61, 68

   review of evidence

      cross-sectional surveys 62

      effects of cannabis on mood 61

   review of evidence, longitudinal studies 62

      cannabis use and later depression 62–4, 65–6

      depression and later cannabis use 64–5

   study designs 67

      genetically informative 67–8

      longitudinal 67

   study samples

      clinical 55–6, 57

      convenience 56–7, 67

      general population 57–9, 67, 68

Cannabis Use Effect Survey (CUES) 189

caudate putamen (C-P)

   CB1 density 134

   dopamine transporter levels 135

causation

   concept defined 101

   defining criteria 103

   necessary and sufficient causes

      causal pie model 102, 101–2

      illustrative example 102

   strengths of component causes 113

CB1 receptor knockout mice

   absence of DSI 23

   cannabinoid/opioid interaction studies 33–4

   hippocampal function studies 28

   impaired extinction of aversive memories 28

   locomotor activity 25–6

   schizophrenia symptoms 96

CB1 receptors

   in Alzheimer’s disease 134

   changes in schizophrenia 133–5

   distribution in brain 20–1, 22, 25, 28, 128, 128, 129

   gene polymorphisms in schizophrenia 137

      1359A/G polymorphism 136–7

      triplet repeat 136

   in Huntington’s disease 133, 134

   inhibition of neurotransmitter release 134–5

   mediation of cognitive effects of cannabinoids 159–60

   molecular biology 127–8

   mRNA distribution 128–30

CB1A receptors 127–8, 130

CB2 receptors 7, 19

change, readiness to 190

charas 2

cholecystokinin 27, 28

clinical bias 57

cognitive deficits, conditions causing 145–7

cognitive effects of cannabis 29, 48, 158–60

   see also residual cognitive effects of long-term cannabis

cognitive motivational model 171–2, 174, 179, 181

Community Assessment of Psychic Experiences (CAPE) 77, 79

comorbidity

   artefactual 57

   defined 55

   true 57

conditioned place preference paradigm 31

confounding 103

Cooper’s DMQ see Drinking Motives Questionnaire (DMQ)

CP-55940 20, 22

cultural divergence

   of cannabis users 201

   Navajo American study 202, 201–2

cytokine suppression by cannabidiol 5

DA see specific dopamine entries

dagga 6

dependence on cannabis

   attitude change regarding 32

   and opiate dependence 33–4

   self-administration in animals 32, 33

   withdrawal syndrome studies 32–3, 198–9

depolarization-induced suppression of excitation (DSE) 23–4

depolarization-induced suppression of inhibition (DSI) 22–3, 24

direction and causation 103

distractibility, effects of Δ9-THC 153, 152–3

Donovan, M. 2

dopamine D2 signalling in schizophrenia 133

dopamine (DA)–cannabinoid interactions 156

   cognitive effects 158–60

   dopamine transporter (DAT) levels 135

   effects of D2 receptor antagonists 44, 157, 158

   facilitation of DA neurotransmission 31, 135–6, 156–7

   inhibition of DA neurotransmission 157–8

   summarized

dorsolateral prefrontal cortex (DLPFC), CB1 density in schizophrenia 134

dose–response relationships of Δ9-THC 43–4, 143

Drinking Motives Questionnaire (DMQ) 173, 174, 176, 177

driving, effects of cannabis 47

dronabinol see Δ9-tetrahydrocannabinol (Δ9-THC)

DSE (depolarization-induced suppression of excitation) 23–4

DSI (depolarization-induced suppression of inhibition) 22–3, 24

Dunedin Multidisciplinary Health and Development Study 107, 108–9, 110, 110, 111, 114

Edinburgh High Risk Study 113

EEG activity, effects of cannabis 28

endogenous cannabinoid system

   components 127

   in time estimation 47

   see also specific components

endogenous cannabinoid system in schizophrenia 131–8

   CB1 receptor gene polymorphism studies 137

      1359A/G polymorphism 136–7

      triplet repeat 136

   endogenous hypothesis 142

   FAAH gene polymorphism study 137

   human CSF studies 132–3

   perceptual disturbance studies 131–2

   postmortem human brain studies

      CB1 receptor changes 133–5

      dopamine transporter levels 135

endogenous cannabinoids

   biosynthesis and inactivation 9–11

   discovery of receptors 6–7

   new types 8–9

   non-neuronal sources 133

   retrograde synaptic signalling 22–4

   see also 2-arachidonoylglycerol (2AG); anandamide

entourage effect 8, 155

euphoriant effects of cannabis 42, 44–5, 149

exogenous hypothesis of cannabis and psychosis see cannabis and psychosis, exogenous hypothesis

Experience Sampling Method (ESM) studies 81–2

experiences of cannabis use see psychomimetic effects of cannabis

fatty acid amide hydrolase (FAAH)

   activity 10–11

   gene polymorphism study 137

fatty acid amide hydrolase (FAAH) inhibitors 46

GABA–cannabinoid interactions 25, 27, 158, 159–60

gelastic epilepsy 45

genetically informative research designs 67–8

glutamate 159

haloperidol pretreatment and Δ9-THC effects 44, 157, 158

harm reduction strategies 193

hashish intoxication, Moreau’s experiments 1–2

hibernation 12

hippocampus

   CB1 receptors 27

      effects of knockout/antagonists on function 27–8

      mediation of cognitive effects of cannabinoids 159–60

   synaptic plasticity and cannabinoids 27, 159

HU-210 11

HU-211 12

HU-308 12

Huntington’s disease 133, 134

immunohistochemical mapping of CB1 receptors 20

Indian hemp 2

JWH-133 12

laughter and cannabis 42, 44–5

learning effects of Δ9-THC 150, 151

2-linoleoylglycerol (2-Lino-G) 8

long-term depression (LTD) 25, 27, 159

long-term potentiation (LTP) 27, 28, 159

Ludlow, F. H. 42

mania and cannabis use 55

Marshall, C. R. 42

Maudesley Addiction Profile (MAP) 189

mediation motivational model 180–1, 181

memory, cannabinoid effects

   deficits 26, 48

   hippocampal involvement 26–8

   recall studies 150–2, 151, 152

metanandamide 12

‘model’ psychoses

   cannabinoid 155

   limitations 155–6

   uses 155

   see also cannabis and psychosis, exogenous hypothesis: possible mechanisms

monkeys, Δ9-THC effects 3–4

Moreau, J. J. 1–2

morphine 3

motivational interviewing (MI) 193

motivational models of substance use 167, 171

   cognitive 171–2, 174, 181

   supporting studies 172–4

   two-dimensional (Cooper) 173–4

motivational models of substance use in psychosis

   cognitive 179, 181

   mediational 180–1, 181

   motives as predictors of use/problems 179–80

   supporting studies 175–80, 177, 178

   see also reasons for substance use in psychosis

mRNA

   CB1 receptor 128–30

   CB1A receptor 130

naloxone 33

Navajo American study 201–2, 202

neocortical effects of cannabinoids 28–9

Netherlands Mental Health Survey and Incidence Study (NEMESIS) 107, 108, 114

neurotransmitters, modulation of release 21–2, 25, 134–5

noladin ether 8, 12

nucleus accumbens (NAc), Δ9-THC and DA release in 156

oleamide 13

opiate dependence, links with cannabinoid dependence 33–4

opioid/cannabinoid synergism 31–2

oral ingestion of cannabis 41

O’Shaughnessy, W. B. 2

Oxford–Liverpool Inventory of Feelings and Experiences 77

palmitoylethanolamide (PEA) 13, 132

2-palmitoylglycerol (2-Palm-G) 8

panic attacks 46, 150, 150

perceptual effects of cannabis 28–9, 131–2, 147–8, 147, 148

   see also time perception and cannabis use

personality and cannabis use 50, 182

Peters et al. Delusion Inventory (PDI-21) 77

peyote 201

population attributable fraction (PAF) 115

prefrontal cortex (PFC), cannabinoid effects 158–9

psychomimetic effects of cannabis 41–53

   ‘amotivational syndrome’ see ‘amotivational syndrome’

   anxiety 45–6, 149–50, 149, 150

   cognitive see cognitive effects of cannabis

   effects summarized 42, 44

   euphoria and laughter 42, 44–5

   experience of ‘high’ 30

   factors affecting experience 41

   historical accounts 42

   human experiments

      dose–response relationships 43–4, 143

      early observational study 43

      effects of CB1 blockade 44

      role of DA 44, 157, 158

   memory see memory, cannabinoid effects

   psychomotor effects 47

      see also brain, effects of cannabinoids: psychomotor function

   surveys of individuals’ experiences 42–3

   time perception 29, 42, 47–8

   see also cannabis intoxication

psychomotor function see brain, effects of cannabinoids: psychomotor function

psychoses

   amfetamine 90

   cannabis see ‘cannabis psychosis’

   controlled studies in cannabis users/non-users 93–4

   difficulties in adaptation to symptoms 181

   model see model psychoses

   self-medication see self-medication hypothesis: psychoses

   symptom exacerbation by substance use 169

   vulnerability to 83

   see also cannabis and psychosis, exogenous hypothesis; motivational models for substance use in psychosis; reasons for substance use in psychosis; specific schizophrenia entries

psychosis proneness in cannabis users 75–88

   cannabis as risk factor 75, 82, 85

   cross-sectional studies

      dimensions of psychosis proneness 76–8

      implications of findings 80

      main limitation 80

      methodological considerations 79–80

      positive psychosis proneness 76

   defined 75–6

   direction of causality 80

   further research 85

   pre-existing psychosis vulnerability 82

      defined 83

      implications of findings 84

      long-term effects of cannabis 83–4

      short-term effects of cannabis 82–3

   prospective studies

      antiemetic trials 81

      Experience Sampling Method studies 81–2

   see also ‘cannabis psychosis’

R-(+)-WIN55212 128, 129

reasons for substance use in psychosis

   affect regulation model 171

   assessment in individuals 189–90

   dysfunctional beliefs 182

   factors for consideration 166

   importance of understanding of 166

   investigations

      forced-choice methods 167–8

      hypotheses generated 170

      open-ended questions 168–70

   personality 50, 182

   self-medication see self-medication hypothesis: psychoses

   social affiliation 171

   summarized 183

   see also motivational models of substance use

recall see memory, cannabinoid effects

receptors, cannabinoid see cannabinoid receptors

referral bias 57

regional cerebral blood flow (rCBF) in cannabis intoxication 30–1

relapse prevention (RP) 193

residual cognitive effects of long-term cannabis 198–210

   and age of onset of use 206, 207

   and lifetime duration of use 205–6, 207

   long-term effects 199

      current knowledge 204–5

   problems with naturalistic studies 199

      confounding variables 200

      cultural divergence 201–2

      selection/information bias 199–200

   residual effects defined 198

   short-term effects

      current knowledge 149, 151

      duration 143

      withdrawal effects 143

retrograde synaptic signalling 22–4

Reynolds, Russell 2

rimonabant (SR-141716A)

   activity 19

   anxiogenicity 46

   appetite suppression 29

   chemical structure 21

   induction of cannabis withdrawal 32–3

   locomotor stimulation in mice 25

routes of administration and bioavailability 41

schizophrenia

   anandamide levels 96, 132–3

   cognitive deficits 119

   compared with ‘cannabis psychosis’ 92–3

   dimensions 119

   effect of cannabidiol 6

   endogenous cannabinoid system in see endogenous cannabinoid system in schizophrenia

   epidemiological trends and cannabis use 95–6

   hebephrenic 136

   positive psychotic symptoms on cannabis use 96

   self-medication with cannabis 123–4, 136

   symptoms in CB1 knockout mice 96

   see also cannabis and psychosis, exogenous hypothesis; treatment of cannabis use in psychosis

schizophrenia, cannabis as causal factor 101–18

   component cause 112

   evidence for association 103–4

      local surveys 105

      national surveys 104–5

   evidence for temporal priority/direction, retrospective studies 105–6

   evidence for temporal priority/direction, prospective studies 106

      alternative explanations of results 111–12

      Dunedin birth cohort 107, 108–9, 110, 110, 111, 114

      Dutch NEMESIS sample 107, 108

      methodological issues 110–11

      summarized 107, 112, 114

      Swedish conscript cohort 106–8, 107, 114

   high-risk studies 113

   necessary or sufficient cause 112

   strength of causal effect 113–16

schizophrenia, cannabis effects on course 119–26

   biological explanation 124

   cross-sectional and retrospective studies 120

   future studies 124

   long-term prospective studies 122–3

   short-term prospective studies 121, 122

      effects on symptom dimensions 121–2

      follow-up study 122

      psychotic relapses 121, 123

   vulnerability to stress 124

Schizotypal Personality Questionnaire (SPQ) 76

Schizotypy-A scale (STA) 76

screening for cannabis use in psychosis

   basic procedure 187

   clinical correlates 187–8

   collateral information 187

   combined approach 187

   importance 186

   reasons for underdetection 186–7

   summarized 188, 188

   tools 187

   urinalysis 187

self-administration of Δ9-THC in animals 32, 33

self-medication hypothesis

   depression 60–1, 65–6

   psychoses 80, 82–3, 170–1, 182

      schizophrenia 123–4, 136

service delivery models

   integrated 191–2

   parallel 191

   sequential 191

   summarized 191

smoked cannabis 4, 41

social adjustment and cannabis use 59, 80

SPECT study, cannabis-induced DA changes 135–6

SR-141716A see rimonabant (SR-141716A)

SR-144528 12

Stage of Change Readiness and Treatment Eagerness Scale (SOCRATES) 190

stearoyl ethanolamide 13

stereoselectivity of cannabinoids 6–7

subjective experiences of cannabis use see psychomimetic effects of cannabis

substance use, reasons for see reasons for substance use in psychosis

Substance Use Scale for Psychosis (SUSP) 189–90

suicidality and cannabis use 55, 56, 63

Swedish conscript cohort studies 107, 106–8, 114

synthetic cannabinoids 11–12

temporal priority of cause over disease 103

Δ8-tetrahydrocannabinol (Δ8-THC) 3

Δ9-tetrahydrocannabinol (Δ9-THC)

   antidepressant properties 45

   appetite effects 29

   chemical structure 19–20

   comparison in humans and monkeys 3–4

   content of Cannabis sativa 41

   distractibility and vigilance effects 152–3, 153

   dose estimation difficulties 143

   effects on DA 31, 135

   effects on endogenous enkephalins 33

   euphoriant effects 45

   identification as cannabis active constituent 3

   induction of anxiety and panic 149–50, 149, 150

   induction of perceptual alterations 147, 148, 147–8

   inhibition of neurotransmitter release 21–2

   recall effects 151, 152, 150–2

   rewarding effects in animals 31–2

   route of administration and bioavailability 41

   verbal fluency effects 152, 153

   see also cannabinoid chemistry; specific cannabis entries

Δ8-THC 3

Δ9-THC see Δ9-tetrahydrocannabinol (Δ9-THC)

time perception and cannabis use 29, 42, 47–8

tolerance to cannabis 32

trans-theoretical model of change 190

treatment of cannabis use in psychosis

   approaches 192

      12-step 192

      combined 192–3

      harm reduction 193

      motivational interviewing 193

      relapse prevention 193

   programmes 193–5

   see also assessment of cannabis use in psychosis; screening for cannabis use in psychosis; service delivery models

twin studies, cannabis use and depression 67

two-dimensional motivational model (Cooper) 173–4

tyrosine hydroxylase (TH) 135

UK National Psychiatric Morbidity Survey 104

US National Epidemiological Catchment Area study 104

verbal fluency, Δ9-THC effects 152, 153

vigilance, Δ9-THC effects 152–3

virodhamine 8

VR1 receptors 8

WIN55 212-2, chemical structure 19–20

withdrawal syndrome 32–3, 198–9



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