Transcript Child and Adolescent Psychopathology

Chapter 15: Alcohol Use
Disorders
Lara A. Ray
Kelly E. Courtney
Guadalupe A. Bacio
Prevalence of Alcohol Use
 Alcohol is third largest risk factor for disability and disease
 90% of U.S. adults report consuming alcohol
 Alcohol abuse: 4%-5% prevalence
 Alcohol dependence: 3.8% point prevalence; 12.5%-14% lifetime
 8.5% of U.S. adults (17.6 million) suffer from AUDs in given year
 Higher prevalence of dependence among males
 Highest prevalence of abuse and dependence in 18-29 age
group
 Highest risk for lifetime alcohol abuse in older cohorts (30-65)
 In past decade, 12 month prevalence of dependence has
declined and prevalence of abuse has increased
 Economic cost of abuse and dependence in 1998 = $184.6
billion
History
Perspectives on Alcohol Use
 Mid-1930s: Alcohol legalized in U.S.
 Societal and political views on alcohol consumption have
varied considerably since then:
 1960s and early 1970s: Drug-friendly culture
 End of 20th century: Increased public concerns about heavy alcohol
and drug use, underage drinking, deaths from drunk driving, alcoholrelated deaths on college campuses
 Two approaches to deal with alcohol use:
1. Conservative with focus on punishment
2. Liberal with focus on reducing harm
 Treatment modalities have also shifted over the years
Self-Help Approaches
 Alcoholics Anonymous (1935): First community-based
approach offering free peer-delivered group treatment
 First to combine religion, medicine, help of sponsors
 Criticisms: Spiritual, powerlessness, abstinence, discourages use of meds
 Now: 100,000 groups; 150 countries; 2 million members
 Research evidence from RCTs
 More rational, humanistic approaches developed, focusing on
cognitive-behavioral principles and self-empowerment
 Rational Recovery (RR), Moderation Management (MM), Self-
Management and Recovery Training (SMART)
 More limited research
 Due to low cost and accessibility, self-help approaches likely to
remain core part of treatment, but more research needed
Treatment Approaches
 Throughout past 20 years, treatments evolved primarily from two
major approaches:
1.
Rehabilitation
(e.g., employee assistance programs, education classes)
• Belief that treatment better alternative to punishment and will increase chances of
returning to baseline of productive functioning
2.
Harm-reduction
• Belief that human beings will continue to engage in behaviors that are potentially
dangerous
• Goal to reduce intake and minimize harm by providing individuals with safer ways
to engage in such risky behaviors (e.g., designated drivers)
• Widely debated, but research support for use in treatment and prevention
Treatment Goals
 Continuing debate between abstinence and moderation as
treatment goals
1. Abstinence: Standard clinical practice in U.S.
2.
Moderation/controlled drinking: Alternative to abstinence
 May be more appropriate for certain cases (e.g., less severe, younger,
no family history, less impaired control over drinking)
 Some evidence for better outcomes when clients choose their
treatment goals
 One study found abstinence goal > conditional abstinence >
controlled drinking
 But, treatment x drinking goal interaction
History of Diagnosis of AUDs
 Personality disorder in DSM-I (“addictive personality”) (1952)
 Then (1976), shift to focusing on impact of substances on
person’s life and functioning
 DSM-III (1980)
 First time specific diagnostic criteria
 Added abuse vs. dependence distinction
 DSM-III-R (1987) and DSM-IV (1994)
 More concrete operational criteria, increased reliability of diagnosis
 Changes to withdrawal and tolerance criterion (DSM-III required one)
 DSM-IV tolerance and withdrawal as sufficient but not necessary
Substance-Related and Addictive
Disorders
 Uses Alcohol Use Disorder (AUD) for prior abuse and
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dependence diagnoses
Adds Gambling Disorder, Cannabis Withdrawal and
Caffeine Withdrawal
Eliminates polysubstance dependence and
physiological subtype
New specifiers indicate if: in a controlled environment
or on maintenance therapy
Early remission is 3 to 12 months; Sustained remission
is more than 12 months ( both without meeting full
criteria but not counting the craving symptom)
DSM-5 Criteria for Alcohol Use
Disorder (AUD)
Mild = 2 to 3 symptoms; Moderate = 4 to 5 symptoms; Severe= 6 to 11 symptoms
(within a 12 month period)
Includes DSM-IV criteria for alcohol abuse
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Recurrent alcohol use resulting in a failure to fulfill major role obligations
Recurrent alcohol use in situations in which it is physically hazardous.
Continued alcohol use despite having persistent or recurrent social or
interpersonal problems caused or exacerbated by the effects of alcohol.
DSM-IV criteria for alcohol dependence
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Tolerance
Withdrawal
Alcohol is often taken in larger amounts and/or over longer periods of time
Persistent desire or unsuccessful efforts to stop or cut down alcohol use.
Increased amount of time is spent consuming, obtaining, or recovering
Important occupational, social, or recreational activities are given up/reduced
Alcohol consumption continues despite the knowledge of having persistent
or recurrent physiological and psychological problems
AUDs Cross-Culturally
 Patterns of alcohol use and misuse vary cross-culturally
 U.S. high-risk subgroups: Whites, Native Americans, males
 Lower risk for immigrants (“immigrant paradox”)
 Observed cross-cultural differences in drinking patterns may be due to
cultural factors (e.g., attitudes toward drinking, role of family, gender roles,
alcohol expectancies)
 Typologies for cultural views towards drinking:
 “Wet” vs. “dry” cultures
 2 axes: (1) engagement with alcohol; (2) serious drinking
 Temperance vs. nontemperance cultures
 Recent directions: Mediators and moderators of relationship
between culture and alcohol use; cultural influence on cognitive
factors (e.g., expectancies); other cultural factors (e.g., role of family)
Developmental Considerations
 Alcohol use typically starts in early adolescence
 Starting to drink before age 15 increases risk for later dependence
 Escalates during late adolescence (ages 16-20)
 Period of highest risk for developing AUDs
 By 12th grade, 72% of adolescents report ever drinking; 55% getting
drunk; 25% binge drinking in past 2 weeks
 College students: 44% binge drinking; 25% AUD in past 12 months
 Gender differences emerge in late adolescence/early adulthood
 Risk factors for drinking in adolescence: Peer (e.g., substance-
using peers) and family contexts (e.g., decrease in parental
monitoring)
 Need to develop prevention programs to delay drinking initiation
Theory
Biopsychosocial Model
 Psychosocial and biological factors interplay in the
development of the complex, heterogeneous phenomenon
known as AUDs
 (Psychosocial: Personality, environmental variables)
 (Biological: Genetics, neurobiology)
 Diverse pathways to diagnosis
 Phenotypic complexity of alcoholism = diverse symptom
presentations
Psychosocial Factors
 Expectancy theory: Information reflecting alcohol’s reinforcement
value stored as memory templates  when templates activated
affective experience triggered  can influence behavior
 Widely studied and empirically supported theory of alcohol misuse
 Tension-reduction theory: Individuals drink alcohol because of
its ability to reduce tension
 Stress-response dampening (SRD) effects of alcohol
 Certain contextual differences moderate effects of alcohol on tension
(e.g., hostility, anxiety sensitivity, heightened stress reactivity)
Psychosocial Factors
 Personality theory: Personality traits account for some of
variance in vulnerability to AUDs, but no support for “alcoholic
personality”
 Proposed clinical subtypes (sets of personality characteristics):
• Type 1 and Type 2 alcoholics
• Type A and Type B alcoholics
 Also, specific personality traits relevant to risk for alcoholism
 Impulsivity/disinhibition (particularly impulsive decision making)
 Starting to integrate this research with behavioral genetics, cognitive
neuroscience, stress and coping, physiological responses to alcohol,
and developmental theories
Psychosocial Factors
 Social learning theory (SLT) focuses on three aspects of behavior:
1.
2.
Social-environmental: Situational factors paired with drinking (triggers)
Coping skills: Ability to cope with stressful events without drinking
• CBT skills building: Refusal skills, coping with urges and negative feelings
3.
Cognitive factors: Self-efficacy and alcohol expectations
 SLT applied to relapse process:
 Lapses from poor coping skills in high-risk situations  low self-efficacy
regarding ability to cope  expectancies that drinking is an effective
coping strategy in future situations
 Dynamic interplay between distal and proximal risk factors in determining
relapse (Marlatt-Witkiewitz model)
• Distal: Less active coping efforts, lower self-efficacy, higher craving, less self-help group
and treatment participation
• Proximal: Personal characteristics and experiences
Biological Factors
 Multiple neurotransmitter systems underlying
pharmacological and behavioral effects of alcohol
 Mesolimbic dopamine activation: Alcohol consumption and cue
exposure increase dopamine activity in the nucleus accumbens
 Psychostimulant theory of addiction: Stimulant effects of
addictive substances produce positive reinforcement
 Individuals who experience greater rewards from alcohol more likely to
develop problems
 Shift to models focusing on incentive salience (i.e., craving)
 Acquisition and sensitization of craving for alcohol produced by
repeated ingestion and associated dopamine release
 After pathways sensitized, craving can be activated by the dopamine
release initiated in response to alcohol cues or priming doses
Biological Factors
 Allostatic model of dependence: Integrates neurobiology of
rewarding effects of alcohol with mechanisms related to
negative reinforcement (e.g., alcohol withdrawal, influence of stress)
 Reward and stress circuits become dysregulated with repeated
alcohol exposure
 Clinical neuroscience of addiction: Insights from neuroscience
are being incorporated into clinical research and practice
 Still need more research to effectively translate these findings to
patients suffering from alcoholism
 Behavior genetics: 50% to 60% heritability (twin and adoption studies)
 Some phenotypes heritable (e.g., alcohol sensitivity, metabolism)
 Recent interest in identifying endophenotypes
 No single gene likely to fully explain genetic liability
Treatment
Treatment: Overview
 700,000 alcoholics receive treatment every day
 Residential/inpatient  intensive outpatient programs
 85% of individuals who meet lifetime criteria for AUD never receive
formal treatment or participate in self-help groups
 Most common modalities: Detoxification, behavioral treatments (e.g., AA),
pharmacotherapy, brief primary care interventions
 Psychosocial intervention more common than pharmacotherapy
 Most approaches highly eclectic, have not been evaluated for efficacy
 Many with empirical support, but none highly successful
 Attempts to identify specific patient characteristics that might predict
response to a particular treatment
 Project MATCH: Only 4/21 variables found to improve outcome (e.g., anger,
social networks)
Psychosocial Treatments
Psychosocial Treatments
Pharmacological Treatments
 Often used to manage withdrawal symptoms
 Few community programs combine meds and psychosocial treatment
 Few effective medication options
 FDA-approved for alcohol dependence:
 Disulfiran (Antabuse), acamprosate, vivitrol
 Naltrexone: Most studied; some evidence reduces drinking days and lower
rates of relapse, but inconsistent
 Ondansetron: 5-HT3 antagonist; reduction of drinking among early-onset
alcoholics; mechanism unknown
 Topiramate: Anticonvulsant; reduced drinking and craving; mechanism unclear
 Quetiapine and olanzapine: Reduce craving by targeting mesolimbic DA
Pharmacological Treatments:
Future Directions
 Identify psychosocial predictors of medication compliance and
efficacy
 Expand knowledge of dosing issues
 Improve the dissemination of research findings to practicing
clinicians
 Examine the combined effects of psychosocial and
pharmacotherapy treatments
 Investigate the role of genetic factors in predicting treatment
response to pharmacotherapies as one way to potentially match
patients to treatments
COMBINE Project
 Looked at different combinations of meds and psychotherapies
 Naltrexone, acamprosate, placebo
 Combined behavioral intervention (CBI) or medication management (MM)
 MM with naltrexone, CBI, or both most effective
 Investigated whether Asn40Asp SNP in the mu opioid receptor gene
predicted clinical response to naltrexone (an opioid antagonist)
 Better response to MM and naltrexone for Asp40 than Asn40/Asn40
carriers
 Consistent with other findings:
 Stronger hedonic response to alcohol in Asp40 carriers
 Naltrexone attenuates rewarding effects of alcohol more strongly among
Asp40 carriers
 Example of pharmacogenetics allowing for more personalized
medicine
Summary and Future
Directions
Summary
 AUDs are multifaceted in their etiology, maintenance, and
relapse processes
 Biopsychosocial model: Alcohol pathology results from interplay
between biological and psychosocial variables
 Increased understanding of biological and psychological factors used
to inform DSM-5 and guide treatment development
 Individuals develop AUDs through multiple pathways, and
different factors may maintain the disorder or lead to relapse
 Various historical, cultural, developmental, diagnostic,
theoretical, and treatment considerations
 Current recovery rates modest
Future Directions
 Future progress hinges on ability to capture the complexity of
AUDs (e.g., multiple pathways)
 Research and clinical work needed to integrate various aspects
of the biopsychosocial model to capture this complexity
 Role of clinical neuroscience and translational science
 Role of clinical scientists and practitioners in advancing
understanding of mechanisms of alcoholism and other
addictive/complex behaviors
 Merge understanding of phenomenology of addiction and
psychopathology with neural findings