OR WAIT 15 SECS
Adolescents evolve from child to young adult without the maturity of adulthood to help them navigate the transition, particularly when it comes to the perils of substance use and addiction. Pediatricians who care for transitional-aged youth with substance use disorders have new paradigms that have shown promise for treating addiction and its accompanying comorbidities and for sustaining recovery over time.
The special issues related to adolescents who are transitioning into adulthood have become an area of increasing interest for clinicians. In particular, the age range of 16 to 26 years is referred to as transitional-aged youth (TAY). These transition years span the potentially perilous developmental years of growing out of childhood and into adulthood, often not yet having mastered the maturity of adulthood. Critical developmental steps occur during this transition encompassing neurobiology, separation and individuation, and the emergence or sequelae of mental health and/or substance use issues. Pediatricians are increasingly asked to provide care for youth as they evolve through these developmental transitions. This article focuses on a major area of concern in TAY, namely, the emergence, risk, recognition, and management of the misuse and abuse of substances.
Trying to reach the addicted adolescent or young adult in denial about his or her problem? Listen to our podcast interview with Timothy Wilens, MD, Director of Substance Abuse Services and Pediatric Psychopharmacology and Director of the Center for Addiction Medicine at Massachusetts General Hospital in Boston, who provides tips from Mass General's ARMS program on how to make the connection that spurs these patients into the addiction treatment process-and how, surprisingly, parents can often be key gatekeepers to that engagement.
Substance use disorders (SUD) including drug and alcohol abuse or dependence are now conceptualized as having their developmental roots in childhood with the vast majority beginning during adolescence or young adulthood.1-5 Recent epidemiologic data report that 20% of youths experiment with substances before completing the 8th grade, and over 20% of high school seniors have used illicit drugs or have been drunk in the past month, with other data indicating that 1 in 10 adolescents has a SUD.5,6 Researchers have shown that in adolescents with a drug use disorder, over half had the onset of the disorder before their 18th birthdays. Roughly 80% experienced onset before age 25 years.4
Many theories have been formulated regarding the etiologies of SUD. Neurobiologically, numerous brain regions are involved in the genesis and maintenance of addiction, often referred to as the mesolimbic circuits. Neurochemical abnormalities including dopamine, norepinephrine, glutamate, and others in specific brain regions have been linked with the various substances of abuse.7
Core to addiction, disruption in the normal circuitry in the reward and inhibition centers of the brain appear operant. Disruption in signaling between the executive centers (frontal lobes, inhibition based) and emotional/motivation centers (hippocampal formation, amygdala; reward based) are seen with addiction, and may even predate some of the addictive changes.8-10 For instance, disruption in frontal activity dampens inhibitions as well as a number of executive functions (planning, organization, motivation) that are critical in TAY functioning. Similarly, limbic regions such as the hippocampus and amygdala are involved in reward, emotion, and risk taking.10 It may be that many of these regions, which are vulnerable in producing addiction, are affected by or have a delay in maturation associated with specific psychiatric disorders known to predispose to later SUD (eg, attention-deficit/hyperactivity disorder [ADHD]).8,11
Moreover, research in developmental neurobiology has given insights into understanding some limitations in decision making, impulsivity, and risk taking that may be related to the developing brain.10 Comprehensive reviews highlight that in adolescence the limbic areas emerge early and govern reward-based issues.8,10 In contrast, areas of the frontal lobes that are related to processing, inhibiting, decision making, and cognitive flexibility develop through the second decade of life.10 Researchers have articulated that the dissymmetry between the maturity of the limbic and executive operations may result in excess emotionality, reward seeking, poor judgment, and risk for SUD.8,9
The effects of substance use on the developing brain are also a concern. Alcohol has been shown to diminish executive, visuospatial, and memory functions.12,13 Drugs of abuse such as marijuana have been speculated to affect the proper formation of dopamine tracts that predisposes to a higher risk for psychosis and schizophrenia.14 The use of designer drugs such as synthetic marijuana has anecdotally been reported to be linked to dysfunction based in both physiologic (pulmonary, cardiac) and central nervous systems (strokes, seizures, delirium). Alcohol has been shown to have more neuropsychologic effects on attention, executive functioning, and memory than presumably believed to be linked to underlying changes in brain substance.12,13
It is estimated that approximately half of addiction is genetically related, although it appears that many genes interact alone and in combination with one another and the environment to manifest addictive behaviors.15 Moreover, half of addiction is environmentally mediated and may be related to earlier trauma, poverty, life stressors, community values, peers, self esteem, direct exposure to a parent’s using substances, and the self-medication of overt (anxiety, panic) and covert issues (past unbearable traumas).15-17 Hence, biologic deficits may heighten environmental vulnerabilities and vice versa.
Psychiatric disorders are common in TAY with SUD. One robust risk factor for SUD is delinquency in childhood, or conduct disorder.18 Conduct disorder may be a result of a difficult upbringing and may be genetically determined. Either alone or in combination with other psychiatric disorders, conduct disorder incrementally increases the risk for cigarette smoking and SUD as well as onset of SUD as early as age 10 to 12 years. For instance, in our pediatric studies the presence of conduct disorder increased the risk for early-onset SUD by 4- to 6-fold along with a more pernicious SUD.19
One of the best-studied disorders in early-onset SUD is ADHD. The onset of ADHD occurs in early childhood and affects 6% to 9% of children and adolescents.5,20 Childhood ADHD persists into adolescence in 75% of cases and into adulthood in approximately half of cases.20 Follow-up studies of children with ADHD report that their risk for SUD is almost twice that of those without ADHD, with children with concurrent conduct disorder (delinquency) at highest risk.19 The major age of risk for SUD in individuals with ADHD starts around the time of separation from the family, or at 18 years of age.
Increasingly recognized as important for long-term optimal outcome in ADHD is the use of medication treatment including stimulants.20 Longitudinal data suggest that in adolescents and young adults (eg, college-aged students), pharmacotherapy may reduce the risk for cigarette smoking and SUD. The reduction in SUD risk with treatment is lost in later adulthood, however, perhaps related to discontinuation of treatment or severity of SUD in ADHD.
Longstanding interest in mood disorders in early-onset and TAY SUD exists. High rates of low-level longstanding (dysthymia) and more-severe episodic depressions (major depressive disorder) are found in TAY with SUD. Longitudinal data indicate that having a depressive disorder in childhood increases the likelihood for later SUD, although SUD does not appear to be the cause of a new mood disorder.21
Similarly, frank manic behavior, poor judgment, severe mood swings, and dysregulation indicative of bipolar disorder in youth are also highly linked with SUD. Pediatric-onset bipolar disorder occurs in 3% of youth and is a high risk for cigarette smoking and SUD.5 For example, a third of young adolescents with bipolar disorder have SUD compared with 4% of controls, with the SUD rate climbing to over 50% in college-aged students with bipolar disorder.22
As with depression, the ability of TAY to manage their own emotions may be an important factor within the context of youth with SUD and comorbid bipolar disorder.23 Not surprisingly, deficits in self-monitoring and regulation of mood and anxiety in TAY are related to the continuation of SUD.24 Substance use may serve as a coping mechanism for negative affect, avoidance of depression, or substance withdrawal, whereas excessive affect such as mania or agitation may drive SUD.
Anxiety disorders such as posttraumatic stress disorder (PTSD) are increasingly recognized as comorbid with SUD. Anxiety in early to mid-adolescence has been shown to be linked to the initiation and maintenance of SUD, particularly in the context of mood dysfunction.21,25 Interestingly, SUD typically does not create the new onset of an anxiety disorder. Posttraumatic stress disorder in children is an increasingly studied disorder associated with substantial distress and morbidity occurring in approximately 5% of youth.5 Rates of SUD and other psychiatric issues are substantially higher in youths who had a diagnosis of PTSD before age 18 years compared with youths who had never experienced a trauma, and somewhat higher than youths who had experienced a trauma but did not develop PTSD.
Over the past decade, there has been an increase in the nonmedical use of medications by TAY.6,26 The aggregate data suggest that the most commonly misused medications in TAY
include painkillers (opioids), sedative/hypnotics (benzodiazepines), and stimulants. For instance, up to 20% of high school students have misused prescriptions, and from 5% to 35% of college students have misused stimulants.27 Approximately 75% of prescription drugs are from friends, family, and their own supplies. A higher risk for medication misuse exists in those with mental health disorders.26 Of concern, an equal number of TAY now initiate drug experimentation with prescription medications and marijuana. This group does not appear to view prescription drug abuse as problematic (Table 1).
Parents and practitioners should be suspicious of TAY who present with “pinpoint” (constricted) pupils, slurred speech, flushing, sweating, and/or appetite changes. These youth may also have prominent emotionality, personality changes, sleep changes, and forgetfulness. Those who misuse or abuse prescription medication may isolate and withdraw from their family and friends, become more secretive, socialize with a new group of friends, develop money issues, start skipping classes, and fail academically.
Practitioners and parents should communicate with TAY about the medical, psychologic, addictive, and legal issues of prescription drug abuse. These young people should be advised to take their medications as prescribed and not give or sell their medications to others. Parents should be instructed to safeguard their own medications, properly disposing of unused or old medications and monitoring any active controlled prescriptions.
Similar to other age groups dealing with addiction, the chronic management of recovery from substances is paramount. Unfortunately, traditional treatment appears to be less than effective for TAY. According to national survey findings, only a minority of TAY enter treatment per year, with a vast majority of treatment seekers either dropping out or being terminated from treatment before completion.28
They experience increasing autonomy to make decisions independent of authority figures and enjoy increased legal responsibility for themselves and increased access to financial means. Diminished dependence on adults results in lower social control by others, lowered environmental pressure, and fewer negative consequences to limit substance use.29 Alcohol and drug use is sanctioned by their peer group and the substances are easily available.
Certainly the aim of treatment is to achieve abstinence or sobriety and to sustain the recovery over time. A number of treatment modalities have shown promise in providing treatment that benefits young people. Skills-based cognitive-behavioral therapy (CBT) combined with motivational enhancement therapy (MET) has been shown to be effective in younger adolescents and is promising for TAY.30,31 Another promising strategy is contingency management (CM), in which youth are able to earn desired tokens (money, objects) for treatment attendance and clean toxicology screens.32
One more useful treatment model is the community reinforcement approach (CRA), an evidence-based approach for both youth and adults designed to increase the positive reinforcing value of activities and relationships while decreasing the reinforcing value of substance use. Recent work with this model for young adults, known as the adolescent community reinforcement approach (A-CRA), suggested that although TAY reduce substance use while in treatment, it is difficult for them to maintain the gains after treatment.29 In addition, recent data clearly suggest that attending meetings of Alcoholics Anonymous and Narcotics Anonymous has a strong positive effect on substance use outcomes.33
Although not fully examined, it appears that TAY SUD may respond more favorably to a “harm reduction” model-less substance use is better than more and some degree of substance use can be tolerated for the short term. However preferable, abstinence is much more difficult to obtain, and if required for ongoing treatment will exclude a number of TAY who would ultimately benefit from treatment.
Transitional-aged youth may also benefit from additional services given that they have not become fully independent and continue to have psychologic and financial reliance on family (parents). In particular, the loss of social control, that is, reduced influence and oversight from parents and school settings, increases the risk for ongoing SUD issues in TAY.29 The treatment of TAY with SUD involves an extended collaborative process to increase motivation, teach skilled living in recovery, and address a range of psychiatric and social needs. Parental support and coaching is another cornerstone of the treatment. Parents should be able to receive services either in conjunction with their child or separately if their child is not yet willing to engage. A key point is that parent work is for all age groups within TAY.
Utilizing the previously described conceptual considerations in treatment, we developed a program at Massachusetts General Hospital for TAY addiction: the Addiction Recovery Management Service (ARMS). The core of the ARMS program for TAY is a set of services provided by recovery coaches who receive formal feedback about response every 3 months (Table 2). The main areas of focus for the ARMS recovery coach include consultation/evaluation, TAY treatment, family support, and care management. The evaluation process includes substance use, mental health, legal, medical, and psychosocial appraisal. Because of the chronic waxing and waning course of addiction in TAY, reducing the likelihood of relapse (relapse prevention) and developing a plan if there is a relapse (relapse intervention) is essential. Regular contact occurs either in person or by electronic media.
Within the ARMS program, parental involvement is critical with several parent-specific interventions (Table 2). Education, support, and directed coaching and problem solving are components of parent care.
Medication may be directed to reduce the core symptoms of addiction such as urges or craving (naltrexone, acamprosate, topiramate), opioid replacement (buprenorphine/naloxone), or for co-occurring psychiatric disorders.34 For instance, studies of selective serotonin reuptake inhibitors in combination with CBT in substance-abusing TAY with depression resulted variably in some improvement in depression but not in SUD directly related to the medication versus placebo.34,35 Conversely, pharmacotherapy of underlying bipolar disorder through SUD results in improved substance use and functionality.34 Data suggest that the treatment of current substance-abusing patients with ADHD with stimulants is not particularly helpful for either ADHD or SUD. If the SUD is somewhat stabilized, however, atomoxetine may be useful for both disorders.
Transitional-aged youth is a critical developmental period during which individuals experience the onset of substance use and more fulminant addictions. Mental health issues frequently co-occur with addiction. Addressing SUD in TAY necessitates a thorough evaluation and multimodal interventions for both the individual and his or her family. New treatment paradigms that are flexible and adaptable to this population’s developmental needs are resulting in improved engagement in treatment and better overall long-term outcomes.
1. Kandel D, Faust R. Sequence and stages in patterns of adolescent drug use. Arch Gen Psychiatry. 1975;32(7):923-932.
2. Kandel DB, Logan JA. Patterns of drug use from adolescence to young adulthood: I. Periods of risk for initiation, continued use, and discontinuation. Am J Public Health. 1984;74(7):660-666.
3. Kessler RC, Crum RM, Warner LA, et al. Lifetime co-occurrence of DSM-III-R alcohol abuse and dependence with other psychiatric disorders in the National Comorbidity Survey. Arch Gen Psychiatry. 1997;54(4):313-321.
4. Compton WM, Thomas YF, Stinson FS, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry. 2007;64(5):566-576.
5. Merikangas KR, He JP, Burstein M, et al. Lifetime prevalence of mental disorders in U.S. adolescents: results from the National Comorbidity Survey Replication-Adolescent Supplement (NCS-A). J Am Acad Child Adolesc Psychiatry. 2010;49(10):980-989.
6. Johnston LD, O'Malley PM, Bachman JG, Schulenberg JE. Monitoring the future. National results on adolescent drug use: overview of key findings, 2011. Ann Arbor, MI: Institute for Social Research, University of Michigan; 2012.
7. Urban NB, Martinez D. Neurobiology of addiction: insight from neurochemical imaging. Psychiatr Clin North Am. 2012;35(2):521-541.
8. Casey BJ, Getz S, Galvan A. The adolescent brain. Dev Rev. 2008;28(1):62-77.
9. Casey BJ, Jones RM. Neurobiology of the adolescent brain and behavior: implications for substance use disorders. J Am Acad Child Adolesc Psychiatry. 2010;49(12):1189-1201.
10. Giedd JN. The teen brain: insights from neuroimaging. J Adolesc Health. 2008;42(4):335-343.
11. Toga AW, Thompson PM, Sowell ER. Mapping brain maturation. Trends Neurosci. 2006;29(3):148-159.
12. Hanson KL, Medina KL, Padula CB, et al. Impact of adolescent alcohol and drug use on neuropsychological functioning in young adulthood: 10-year outcomes. J Child Adolesc Subst Abuse. 2011;20(2):135-154.
13. Mahmood OM, Jacobus J, Bava S, et al. Learning and memory performances in adolescent users of alcohol and marijuana: interactive effects. J Stud Alcohol Drugs. 2010;71(6):885-894.
14. Myles N, Newall H, Nielssen O, Large M. The association between cannabis use and earlier age at onset of schizophrenia and other psychoses: meta-analysis of possible confounding factors. Curr Pharm Des. 2012;18(32):5055-5069.
15. Kendler KS, Sundquist K, Ohlsson H, et al. Genetic and familial environmental influences on the risk for drug abuse: a national Swedish adoption study. Arch Gen Psychiatry. 2012;69(7):690-697.
16. Yule AM, Wilens TE, Martelon MK, et al. Does exposure to parental substance use disorders increase substance use disorder risk in offspring? A five-year follow-up study. Am J Addict. 2013;22(5):460-465.
17. Khantzian EJ. Reflections on treating addictive disorders: a psychodynamic perspective. Am J Addict. 2012;21(3):274-279.
18. Robins LN. Deviant children grown up; a sociological and psychiatric study of sociopathic personality. Baltimore, MD: Williams and Wilkins; 1966.
19. Wilens TE, Martelon M, Joshi G, et al. Does ADHD predict substance-use disorders? A 10-year follow-up study of young adults with ADHD. J Am Acad Child Adolesc Psychiatry. 2011;50(6):543-553.
20. Wilens TE, Spencer TJ. Understanding attention-deficit/hyperactivity disorder from childhood to adulthood. Postgrad Med. 2010;122(5):97-109.
21. Wolitzky-Taylor K, Bobova L, Zinbarg RE, et al. Longitudinal investigation of the impact of anxiety and mood disorders in adolescence on subsequent substance use disorder onset and vice versa. Addict Behav. 2012;37(8):982-985.
22. Wilens TE, Biederman J, Adamson JJ, et al. Further evidence of an association between adolescent bipolar disorder with smoking and substance use disorders: a controlled study. Drug Alcohol Depend. 2008;95(3):188-198.
23. Lorberg B, Wilens TE, Martelon M, et al. Reasons for substance use among adolescents with bipolar disorder. Am J Addict. 2010;19(6):474-480.
24. Cheetham A, Allen NB, YÅ±cel M, Lubman DI. The role of affective dysregulation in drug addiction. Clin Psychol Rev. 2010;30(6):621-634.
25. Fröjd S, Ranta K, Kaltiala-Heino R, Marttunen M. Associations of social phobia and general anxiety with alcohol and drug use in a community sample of adolescents. Alcohol Alcohol. 2011;46(2):192-199.
26. McCabe SE, West BT, Cranford JA, et al. Medical misuse of controlled medications among adolescents. Arch Pediatr Adolesc Med. 2011;165(8):729-735.
27. Wilens TE, Adler LA, Adams J, et al. Misuse and diversion of stimulants prescribed for ADHD: a systematic review of the literature. J Am Acad Child Adolesc Psychiatry. 2008;47(1):21-31.
28. Godley MD, Kahn JH, Dennis ML, et al. The stability and impact of environmental factors on substance use and problems after adolescent outpatient treatment for cannabis abuse or dependence. Psychol Addict Behav. 2005;19(1):62-70.
29. Smith DC, Godley SH, Godley MD, Dennis ML. Adolescent Community Reinforcement Approach outcomes differ among emerging adults and adolescents. J Subst Abuse Treat. 2011;41(4):422-430.
30. Dennis M, Godley SH, Diamond G, et al. The Cannabis Youth Treatment (CYT) Study: main findings from two randomized trials. J Subst Abuse Treat. 2004;27(3):197-213.
31. Cornelius JR, Douaihy A, Bukstein OG, et al. Evaluation of cognitive behavioral therapy/motivational enhancement therapy (CBT/MET) in a treatment trial of comorbid MDD/AUD adolescents. Addict Behav. 2011;36(8):843-848.
32. Dutra L, Stathopoulou G, Basden SL, et al. A meta-analytic review of psychosocial interventions for substance use disorders. Am J Psychiatry. 2008;165(2):179-187.
33. Kelly JF, Dow SJ, Yeterian JD, Myers M. How safe are adolescents at Alcoholics Anonymous and Narcotics Anonymous meetings? A prospective investigation with outpatient youth. J Subst Abuse Treat. 2011;40(4):419-425.
34. Gignac M, Waxmonsky JG, Wilens T. Psychopharmacology and substance use disorders: a pediatric approach. In: Martin A, Scahill L, Kratochvil C, eds. Pediatric Psychopharmacology, Principles and Practice. 2nd ed. New York: Oxford; 2010:587-599.
35. Riggs PD, Mikulich-Gilbertson SK, Davies RD, et al. A randomized controlled trial of fluoxetine and cognitive behavioral therapy in adolescents with major depression, behavior problems, and substance use disorders. Arch Pediatr Adolesc Med. 2007;161(11):1026-1034.
DR WILENS is director, Center for Addiction Medicine, Massachusetts General Hospital, Boston. He has received grant support from the National Institute on Drug Abuse at the National Institutes of Health and Shire; has been a consultant for Euthymics Bioscience and Shire; and serves as consultant for Bay Cove Human Services, National Football League/ERM Associates, and Major/Minor League Baseball. DR MCKOWEN is staff psychologist, Child CBT Program, Child Psychiatry Service, Massachusetts General Hospital, Boston, and instructor of psychology, Department of Psychiatry, Harvard Medical School, Boston. DR KANE is clinical director, West End Clinic Addiction Services, Department of Psychiatry, Massachusetts General Hospital, Boston. The co-authors have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article.