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 alcoholAlcohol abuse: 4%-5% prevalenceAlcohol dependence: 3.8% point prevalence; 12.5%-14% lifetime8.5% of U.S. adults (17.6 million) suffer from AUDs in given year

Higher prevalence of dependence among malesHighest 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 cultureEnd of 20th century: Increased public concerns about heavy alcohol

and drug use, underage drinking, deaths from drunk driving, alcohol-related 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 treatmentFirst to combine religion, medicine, help of sponsorsCriticisms: Spiritual, powerlessness, abstinence, discourages use of medsNow: 100,000 groups; 150 countries; 2 million membersResearch 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 abstinenceMay 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 diagnosisChanges 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 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 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 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” cultures2 axes: (1) engagement with alcohol; (2) serious drinkingTemperance 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 AUDsBy 12th grade, 72% of adolescents report ever drinking; 55% getting

drunk; 25% binge drinking in past 2 weeksCollege 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 diagnosisPhenotypic 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 behaviorWidely 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 alcoholCertain 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 alcoholismImpulsivity/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. Social-environmental: Situational factors paired with drinking (triggers)

2. 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 alcoholMesolimbic 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 releaseAfter 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 endophenotypesNo single gene likely to fully explain genetic liability

Treatment

Treatment: Overview

700,000 alcoholics receive treatment every dayResidential/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 pharmacotherapyMost approaches highly eclectic, have not been evaluated for efficacyMany 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

treatmentFew effective medication options

FDA-approved for alcohol dependence: Disulfiran (Antabuse), acamprosate, vivitrolNaltrexone: 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 psychotherapiesNaltrexone, acamprosate, placeboCombined 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 carriersExample 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 complexityRole of clinical neuroscience and translational science

Role of clinical scientists and practitioners in advancing understanding of mechanisms of alcoholism and other addictive/complex behaviorsMerge understanding of phenomenology of addiction and

psychopathology with neural findings