How & Why Alcohol Use Disorders (AUDs) Develop in Adolescents

Alcohol Medical Scholars Program

Hayley Treloar Padovano, Ph.D.

Center for Alcohol Addiction Studies

Brown University

I. Introduction (SLIDE 2)

A. Alcohol use by teens is common

1. Alcohol is most used substance by teens1

a. 80% high school seniors ever drink

b. 30% high schoolers (freshmen through seniors) ever drunk

2. Drinking to drunkenness escalates during adolescence1

a. 10% 8th grade ever drunk

b. 50% 12th grade ever drunk

B. Alcohol use by teens can be harmful (SLIDE 3)

1. Immediate consequences2–4

a. Unintentional injuries

b. Physical or sexual assault

c. Depressive symptoms suicidal ideation

d. Blackouts (periods of memory loss for events while drinking)

e. ↓academic performance

f. Risky sexual behavior

g. Alcohol poisoning death

2. Long-term consequences5,6

a. Heavy drinking in late adolescence persists into adulthood

b. Early problems → later problems & ↑ risk Alcohol Use Disorders (AUDs)

C. This lecture covers (SLIDE 4)

1. Definitions of heavy drinking AUDs

2. How AUDs might develop in general

3. Why adolescents are particularly vulnerable to AUD development

4. Unique challenges solutions for adolescent alcohol research

5. Clinical example

D. Clinical Case (Joanne): Is she at risk for AUDs? [HAVE A PICTURE] (SLIDE 5)

1. We’ll follow her from age 12 to 17

2. A typical child of a well-functioning family

3. At 12 no experience with alcohol

4. Familial history of AUD

II. Definitions (SLIDE 6)

A.  Heavy drinking: many definitions (SLIDE 7)

1. Typically

a. Amount: 5+ drinks

b. Timeframe: “in a row” or “in a sitting”7

2. National Institute on Alcohol Abuse and Alcoholism definition

a. Pattern of drinking alcohol →BAC .08 g/%

b. 4+/5+ drinks for women/men

c. 2-hour period

B.  Alcohol use disorder (SLIDE 8)

1. Recurring problems

2. Affecting multiple life areas

3. DSM-5 (5th diagnostic manual of American Psychiatric Assn)

4. Diagnosis associated with

a. Long-term alcohol problems

b. Earlier death

5. 2+ of 11 symptoms (in same 12 months) (SLIDE 9)

a. Taken in larger amounts or over longer periods than intended

b. Unsuccessful efforts to cut down or control use

c. Much time spent obtaining, using, or recovering

d. Craving or strong desire/urge to use (new)

e. Failure to fulfill major role obligations (e.g. in school or work)

f. Continued use despite negative social consequences (e.g., arguments with parents)

g. Important activities are reduced or given up

h. Use in physically hazardous situations (e.g., driving)

i. Use despite knowledge of physical/psychological problem (e.g., depression)

j. Tolerance defined by either

1’. ↑ amounts needed for same effect

2’. ↓ effect with continued use of same amount

h. Withdrawal manifested by either

1’. Withdrawal syndrome; opposite of acute effects for 4+ days include:

a’. Insomnia, anxiety, ↑ blood pressure, heart rate, etc.

b’. Develops when ↓ BAC

2’. Drinking to relieve/avoid withdrawal

III. How AUDs might develop in general (SLIDE 10)

A. Why do people drink? (Ask audience to participate, list reasons.) (SLIDE 11)

1. Positive expectations/motives8,9 (SLIDE 12)

a. Expectations: If ______; then ______. (Using Joanne (J) as example)

b. Can have expectations for drinking outcomes without ever drinking yourself

c. But expectancies can change with experience with alcohol

d. At 12 J’s expectations might be: (SLIDE 13)

1’. What do I think happens when people drink?

2’. If people drink, they fall down, slur words, act funny.

d. At 17 and after some alcohol experience expectations might be:

1’. What happens when I drink?

2’. Drinking makes me more social.

3’. If I drink, then I have a better time at parties, can relax.

2. Motives: Reasons for drinking: I drink to ______. (Again use J) (SLIDE 14)

a. What do I want to happen when I drink?

b. I drink to feel less anxious around people, to be more social.

c. Motivational = requires that you drink yourself

B. AUD Risk is both genetic environmental (SLIDE 15)

1. Genes explain 50-70% 10

2. But no single gene explaining entire risk

3. Operate through intermediate characteristics, including:

a. How a person responds to alcohol (e.g., their level of response or LR)

b. Impulsivity (e.g., spur of moment acting without thinking of consequences)

C. Example: Low level of response (low LR) to alcohol11–13 (SLIDE 16)

1. Focus on initial alcohol responses

2. Need more alcohol than most to get desired effect

3. Can be seen first time drink: is sensitivity, not tolerance

4. To get desired effect drinks more & spend more time drinking

5. Most friends also drink heavily/spend more time drinking

6. That changes expectations14,15

D. As noted, LR changes expectations (SLIDE 17)

1. JoAnne required more alcohol to get desired effect

2. Drank more heavily and more often

3. Associated with friends who drank more heavily

4. Developed more positive expectations for alcohol’s effects

IV. Adolescent vulnerability to AUDs (SLIDE 18)

A. Adolescent heavy drinking predicts later problems (SLIDE 19)

1. AUDs typical onsets prior to legal drinking age5

2. Not all “mature out”; 1 in 3 persistent problems6

3. At 17, JoAnne may have experienced (SLIDE 20)

a. Blackouts

b. Risky sexual behavior

c. Use in hazardous situations, e.g., driving while drunk

d. Trouble with police, e.g. minor in possession of alcohol

4. In college, JoAnne’s positive expectations & drinking persist despite these experiences

B. Adolescent brain development18 (SLIDE 21)

1. Transform immature brain into a more efficient, mature brain

2. Brains develop back to front

a. Emotional regions before planning regions

b. “Gas pedal before brakes”

c. Forebrain critical for restricting behaviors before targeting rewards

3. Adolescent brains focus on

a. Social interactions and peer affiliations

b. Novelty-seeking and risk-taking behaviors

C. Adolescent sensitivity to alcohol’s effects (SLIDE 22)

1. Primarily preclinical (animal) studies

2. ↓ sensitivity aversive & impairing effects

3. ↑ sensitivity social-facilitation & rewarding effects

D. Adolescence and the development of alcohol expectancies8 (SLIDE 23)

1. Expectancies learned at early ages, prior to direct experience

2. What we think happens when we drink à later problems

3. Expectations of positive outcomes ↑ in adolescence

4. Predict intentions to drink and onset of drinking

E. Summary: Why this matters? (SLIDE 24)

1. Drinking often starts & increases rapidly in adolescence

3. Sensitivity to alcohol’s effects & expectancies related to AUD development

4. Adolescent brains differ from adults

5. Adolescence sets stage for AUD development

V. Unique challenges solutions for adolescent research (SLIDE 25)

A. Human adolescent drinking laboratory studies often prohibited (SLIDE 26)

1. Legal and ethical restrictions

2. Precludes real-time understanding of key components of AUD development

a. Example: What are J’s responses to alcohol in the moment in daily life?

b. Example: What are her motivations to drink at the daily level?

B. Ecological Momentary Assessment (EMA)19: Observations in daily life (SLIDE 27)

1. Repeated collection of real-time data in the real-world environment19,20

a. Evolution of delivery methods

1’. Paper-and-pencil diaries

2’. Repeated online surveys

3’. Interactive voice response

4’. Smartphones

5’. Physiological assessment, e.g., heart rate, breathalyzer

b. Various report formats (SLIDE 28)

1’. User-initiated or device-prompted

2’. Types of reports (Visual scales, check boxes, forced choice, text or # entry)

3’. Schedule (When? Where? How many? How often?)

c. Example data stream from JoAnne (SLIDE 29)

2. Benefits19,21,22 (SLIDE 30)

a. Increased “ecological” validity: study adolescents in their typical drinking settings

b. Avoids retrospective recall bias: “Here and now” rather than “There and then”

c. Not only whether alcohol à effect, but also for whom & under what conditions

VI. Clinical example (SLIDE 31)

A. Summary of JoAnne (SLIDE 32)

1. Typical teenager, well-functioning family, genetic risk for AUD

2. Insensitivity to alcohol, drinks more, associates with heavy drinking peers

3. Expectations and social norms change to be more positive

4. By 17, JoAnne experienced consequences, but positive expectations persist

5. What will her future hold?

a. Likely to drink heavily in college

b. Mature out or persistent AUD?

B. How might we intervene for JoAnne? Brief Motivational Interviewing (SLIDE 33)

1. A particular type of conversation about change well-suited for JoAnne

2. Non-confrontational, collaborative style [SEE EXAMPLE TEXT] (SLIDE 34)

3. Guide JoAnne to strengthen her own motivations/reasons to change drinking

a. Identify her + & − expectations about drinking (SLIDE 35)

b. Understand her reasons for & against drinking

c. Draw out her own motivations and goals for change (SLIDE 36)

d. Explore her ambivalence about changing her drinking (SLIDE 37)

4. JoAnne’s Outcomes (SLIDE 38)

a. J identified goal to ↓ drinking amount & frequency but not abstinence

b. Drank socially in college, but limited amounts & no harms

c. Went on to get law degree & lives with son

C. Lecture covered (SLIDE 39)

1. Definitions of heavy drinking & AUDs

2. How AUDs might develop in general

3. Why adolescents are particularly vulnerable to AUD development

4. Unique challenges & solutions for adolescent alcohol research

5. Clinical example

D. Takeaway points (SLIDE 40)

1. Adolescent drinking is common but not without harms

2. Adolescents are not tiny adults: differences set stage for AUD

3. Research & intervention during adolescence is key

1. Johnston LD, Malley PMO, Miech RA, Bachman JG, Schulenberg JE. Monitoring the Future National Survey Results on Drug Use, 1975-2015: Overview, Key Findings on Adolescent Drug Use. Ann Arbor: Institute for Social Research, The University of Michigan; 2016.

2. U.S. Department of Health and Human Services. The Surgeon General’s Call to Action to Prevent and Reduce Underage Drinking. 2007;1(1):1-93. doi:10.1097/DMP.0b013e3180cac8c7.

3. Substance Abuse and Mental Health Services Administration. Drug Abuse Warning Network (DAWN). Off Appl Stud. 2009.

4. Marshall EJ. Adolescent Alcohol Use: Risks and Consequences. Alcohol Alcohol. 2014;49(2):160-164. doi:10.1093/alcalc/agt180.

5. Hasin DS, Stinson FS, Ogburn E, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry. 2007;64(7):830-842. doi:10.1001/archpsyc.64.7.830.

6. Vergés A, Jackson KM, Bucholz KK, et al. Deconstructing the age-prevalence curve of alcohol dependence: Why “maturing out” is only a small piece of the puzzle. J Abnorm Psychol. 2012;121(2):511-523. doi:10.1037/a0026027.

7. Sher KJ, Grekin ER, Williams N a. The development of alcohol use disorders. Annu Rev Clin Psychol. 2005;1:493-523. doi:10.1146/annurev.clinpsy.1.102803.144107.

8. Treloar H, Pedersen SL, McCarthy DM. The Role of Expectancy in Substance-use Progression. In: Kopetz CE, Lejuez CW, eds. Addictions: A Social Psycholoigcal Perspective. New York, NY: Routledge; 2016:120-147.

9. Cooper ML, Frone MR, Russell M, Mudar P. Drinking to regulate positive and negative emotions. J Pers Soc Psychol. 1995;69(5):990-1005.

10. Agrawal A, Lynskey MT. Are there genetic influences on addiction: Evidence from family, adoption and twin studies. Addiction. 2008;103(7):1069-1081. doi:10.1111/j.1360-0443.2008.02213.x.

11. Schuckit MA. Subjective Responses to Alcohol in Sons of Alcoholics and Control Subjects. Arch Gen Psychiatry. 1984;41(9):879-884. doi:10.1001/archpsyc.1984.01790200061008.

12. Schuckit MA. Low level of response to alcohol as a predictor of future alcoholism. Am J Pscyhiatry. 1994;151:184-189.

13. Schuckit MA, Smith TL. An 8-year follow-up of 450 sons of alcoholic and control subjects. Arch Gen Psychiatry. 1996;53:202-210.

14. Quinn PD, Fromme K. Subjective response to alcohol challenge: A quantitative review. Alcohol Clin Exp Res. 2011;35:1759-1770. doi:10.1111/j.1530-0277.2011.01521.x.

15. Morean ME, Corbin WR. Subjective response to alcohol: A critical review of the literature. Alcohol Clin Exp Res. 2010;34:385-395. doi:10.1111/j.1530-0277.2009.01103.x.

16. Goldman MS, Del Boca FK, Darkes J. Alcohol Expectancy Theory: The Application of Cognitive Neuroscience. In: Leonard KE, Blane HT, eds. Psychological Theories of Drinking and Alcoholism. 2nd ed. New York, NY: Guilford Press; 1999:203-246.

17. Goldman MS, Darkes J, Del Boca FK. Expectancy mediation of biopsychosocial risk for alcohol use and alcoholism. In: Kirsch I, ed. How Expectancies Shape Experience. Washington, DC, US: American Psychological Association; 1999:233-262.

18. Bava S, Tapert SF. Adolescent Brain Development and the Risk for Alcohol and Other Drug Problems. Neuropsychol Rev. 2010;20:398-413. doi:10.1007/s11065-010-9146-6.

19. Shiffman S. Ecological momentary assessment (EMA) in studies of substance use. Psychol Assess. 2009;21(4):486-497. doi:10.1037/a0017074.

20. Shiffman S. Conceptualizing Analyses of Ecological Momentary Assessment Data. Nicotine Tob Res. 2014;16(Suppl 2):S76-S87. doi:10.1093/ntr/ntt195.

21. Piasecki TM, Richardson AE, Smith SM. Self-monitored motives for smoking among college students. Psychol Addict Behav. 2007;21(3):328-337. doi:10.1037/0893-164X.21.3.328.

22. Trull TJ, Ebner-Priemer UW. Using experience sampling methods/ecological momentary assessment (ESM/EMA) in clinical assessment and clinical research: introduction to the special section. Psychol Assess. 2009;21(4):457-462. doi:10.1037/a0017653.

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