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J Child Psychol Psychiatry. Author manuscript; available in PMC 2018 June 01.
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Published in final edited form as:

J Child Psychol Psychiatry. 2018 June ; 59(6): 618–627. doi:10.1111/jcpp.12783.

Research Review: What Have We Learned About Adolescent

Substance Use?
Kevin M. Gray, M.D. and Lindsay M. Squeglia, Ph.D.
Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina,
Charleston, South Carolina
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Abstract
Background—Adolescence is a critical biological, psychological, and social developmental
stage involving heightened risk for substance use and associated adverse consequences. This
review, synthesizing emerging findings on this complex topic, is intended to inform research and
clinical care focused on adolescents.

Methods—Literature searches were conducted using PubMed, yielding a cross-section of

observational and interventional studies focused on adolescent substance use. Findings were
organized and categorized to cover key areas of epidemiology, neurobiology, prevention, and
treatment.

Findings—Adolescent substance-related attitudes and use patterns have evolved over time,
informed by adult and peer behaviors, public policy, media messaging, substance availability, and
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other variables. A number of risk and resiliency factors contribute to individual differences in
substance use and related consequences. Advances in observational techniques have provided
enhanced understanding of adolescent brain development, and its implications for substance use.
Prevention efforts have yielded mixed results, and while a number of adolescent-targeted
evidence-based treatments for substance use disorders have been developed, effect sizes are
generally modest, indicating the need for further research to enhance prevention and treatment
outcomes.

Conclusions—Substance use in adolescence is heterogeneous, ranging from normative to

pathological, and can lead to significant acute and long-term morbidity and mortality.
Understanding risk and resiliency factors, underlying neurobiology, and optimal developmentally-
sensitive interventions is critical in addressing substance-associated problems in adolescence.
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Keywords
adolescence; development; substance use; addiction; neurobiology; prevention; treatment

Correspondence to: Kevin M. Gray, M.D., Medical University of South Carolina, Department of Psychiatry and Behavioral Sciences,
67 President Street, MSC861, Charleston, SC USA 29425, Phone: (843) 792-6330, FAX: (843) 792-8206, [email protected].
Dr. Squeglia reports no competing interests.
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Introduction
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Adolescence is a critical developmental phase involving significant physical, cognitive,

emotional, social, and behavioral changes. The neurobiological alterations underlying these
complex developmental processes may predispose adolescents to initiate substance use, to
develop substance use disorders, and to experience potentially serious and long-lasting
substance-related adverse consequences. Given the high prevalence of problematic substance
use in this age range, and given the unique biopsychosocial context, research has
increasingly focused on characterizing adolescent substance use disorders, with particular
focus on optimizing and disseminating evidence-based prevention, assessment, and
treatment interventions. The present review was conducted to provide an overview of recent
clinically relevant advances in the field.

Methods
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Literature searches were conducted via PubMed, and information was compiled to yield an
overview of clinically relevant advances in knowledge regarding adolescent substance use,
spanning epidemiology, neurobiology, assessment, and interventions.

Results
Epidemiology
Prevalence of Use—Substance use is typically initiated during adolescence. Alcohol is
the most commonly used substance among adolescents, with 64% of 18 year olds endorsing
lifetime alcohol use, followed by marijuana (45%) and cigarette use (31%) (Johnston et al.,
2017). Overall, rates of adolescent substance use have remained relatively stable over the
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past several years, with a few notable exceptions. Cigarette use has declined dramatically
over the past several decades, while e-cigarette use has become more prevalent in recent
years. Thirteen percent of teens report using e-cigarettes in the past month, compared to 3%
reporting cigarette use, with a concerning increase in the number of never-smoking youth
reporting e-cigarette use (Bunnell et al., 2015). Another recent trend includes increased
frequency of marijuana use, with 6% of 18 year olds reporting using marijuana daily
(Johnston et al., 2017). Attitudes about marijuana use continue to move toward greater
acceptance; the perception of risk about using marijuana is at the lowest point ever recorded,
with a third of 18 year olds reporting that regular marijuana use is harmful. While overall
rates of marijuana use have remained relatively stable over the past several years, decreased
perception of harm typically corresponds with increased use. Other drug use is relatively
uncommon, with less than 6% of adolescents reporting past month use of other illicit drugs
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(Johnston et al., 2017). A brief summary of rates of current substance use, by substance and
by grade level, among adolescents in the United States is presented in Table 1 (Johnston et
al., 2017).

Prevalence of Substance Use Disorders—Adolescent substance use is

heterogeneous, ranging from normative early experimentation with substance use to heavier
and higher-risk patterns of use. Most youth who use substances do not become addicted;
however, the prevalence of substance use disorders is still quite high, with 15% of youth

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meeting diagnostic criteria for alcohol abuse and 16% for drug abuse by age 18 (Swendsen
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et al. 2012). Tobacco, alcohol, and marijuana are typically the first addictive substances that
youth try. The likelihood of developing a substance use disorder increases significantly when
individuals initiate alcohol and drug use during adolescence. Youth who begin drinking
before age 15 have four to six times the rate of lifetime alcohol dependence than those who
remain abstinent from alcohol use until age 21 (Grant & Dawson, 1997; SAMHSA, 2014).
The majority of adults who have a substance use disorder started using before age 18 and
develop their disorder by age 20, highlighting the need to delay initiation of substance use
for as long as possible (Dennis et al., 2002).

Neurobiology
The brain undergoes significant neurodevelopment between childhood and young adulthood,
with maturation continuing until around age 25 (Pfefferbaum et al., 1994; Giedd 2004).
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Brain gray matter, which includes mostly nerve cell bodies and dendrites, tends to decrease
during adolescence via synaptic pruning and changes in the extracellular matrix (Gogtay et
al., 2004; Paus, 2005; Petjanek et al., 2011; Raznahan et al., 2014; Sowell et al., 1999; Stiles
& Jernigan, 2010). Concurrently, white-matter volume and white matter integrity increases
over this time, which allows for more efficient and rapid communication between brain
regions (Giedd, 2004; Lebel et al., 2011; 2012). Brain regions have time-varying
developmental trajectories, with lower-order sensorimotor regions maturing first, and
regions associated with higher-order cognitive functioning (e.g., frontal and subcortical brain
regions) developing later in adolescence and young adulthood (Sowell et al., 1999, 2004;
Shaw et al., 2008; Giedd and Rapoport, 2010; Stiles & Jernigan, 2010). Healthy brain
development throughout adolescence is imperative, with even minor changes in
neurodevelopmental trajectories affecting a range of cognitive, emotional, and social
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functioning (Nagy et al., 2004; Casey et al., 2008). Altered brain development due to
exposure of neurotoxins during adolescence, particularly alcohol and other drug use, could
set the stage for cognitive problems into adulthood, conferring functional consequences
throughout life.

Adolescents are known to be particularly vulnerable, compared to children and adults, to

initiation of substance use and progression to problematic use. Dopaminergic systems are
significantly reorganized in the adolescent brain, with decreases in dopamine in striatal
structures such as the nucleus accumbens, in the context of limited inhibitory control,
potentially precipitating high-risk behaviors to compensate for dopaminergic void
(Chambers et al., 2003; Spear, 2002). Theories have suggested an “imbalance” in brain
development underlying a propensity for risk behavior, including substance use, during
adolescence, with emotion and reward systems (e.g., amygdala, nucleus accumbens)
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developing before cognitive control systems (e.g., prefrontal cortex) (Casey et al., 2008;
Somerville et al., 2010). Within the window of this imbalance, adolescents’ decisions may
be based on brain processes favoring immediate reward over consideration of longer-term
consequences (Casey & Jones, 2010). This theoretical model has been supported by a
number of recent experimental studies (Baker et al., 2015; Mills et al., 2014; van
Duijvenvoorde et al., 2016).

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In the past 10 years, there has been a proliferation of neuroimaging and neurocognitive
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studies that have attempted to understand neural risk factors that predate adolescent
substance use, as well as determine the effect of substance use on the developing brain.
Because alcohol and marijuana are the two most commonly used substances, most existing
research has focused on these substances. Several large-scale, multisite longitudinal studies
are currently underway to help further understand the consequences of alcohol and
marijuana use on cognitive functioning, as well as determine the effects of tobacco and other
less frequently used drugs on adolescent brain development. These studies include the
National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) which
is following >800 youth across 5 different sites in the US for at least 10 years (Brown et al.,
2015); the IMAGEN study which has followed 2,000 youth from England, Ireland,
Germany, and France for the past 8 years (https://imagen-europe.com/); and the recently
launched Adolescent Brain Cognitive Development (ABCD; http://abcdstudy.org/), which
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will follow 11,500 youth across 21 US sites for at least 10 years. Existing studies have
relatively small, homogeneous samples; therefore, these large scale studies will allow for a
more complex understanding how demographic, social, genetic, and environmental factors
play a role in the impact of substance use on brain development.

Several neurocognitive features have been identified as risk factors for initiation of alcohol
and other drug use during adolescence (Squeglia & Gray, 2016; Squeglia & Cservenka,
2017). Findings suggest poorer performance on tasks of inhibition and working memory
(Heitzeg et al., 2015; Khurana et al., 2013; López-Caneda et al., 2014; Squeglia et al.,
2014a, 2017), smaller brain volumes in reward and cognitive control regions (Cheetham et
al., 2012, 2014; Squeglia et al., 2014a; Urošević et al., 2015; Weiland et al., 2014; Whelan et
al., 2014), less brain activation during executive functioning tasks, and heightened reward
responsivity are important predictors of adolescent substance use (Dager et al., 2014;
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Heitzeg et al., 2014; Mahmood et al., 2013; Norman et al., 2011; Ramage et al., 2015;
Squeglia et al., 2012, 2017; Wetherill et al., 2013a; Whelan et al., 2014).

Alcohol and marijuana use during adolescence has been associated with poorer performance
on a range of cognitive domains. In a sample of 234 healthy adolescents, greater alcohol and
marijuana use between approximately ages 13 to 17 was associated with poorer verbal
memory, visuospatial functioning, and psychomotor speed (Nguyen-Louie et al., 2015).
Gender specific effects have also been found, with heavy-drinking girls showing worsening
performance on tests of visuospatial functioning compared to non-using girls, and alcohol-
using boys showing poorer attention compared to alcohol-naïve boys (Squeglia et al., 2009).
In a 10-year longitudinal study, treatment-seeking youth who continued to use alcohol and
other substances showed poorer verbal learning and memory, visuospatial functioning, and
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working memory and attention by age 25 (Hanson et al., 2011a, 2011b). A dose-dependent
relationship was found, with heavier use patterns and greater hangover and withdrawal
symptoms relating to poorer cognitive functioning. Youth who were in remission from
alcohol and drug use performed similarly to those who continued to meet criteria for a
substance use disorder, suggesting substance use during adolescence could have persisting
effects into adulthood (Hanson et al., 2011b).

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There is some suggestion that cognitive domains are differentially impacted by marijuana
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use in adolescence, with attention, declarative memory, and cognitive control particularly
affected (Randolph et al., 2013). In a longitudinal study of marijuana and alcohol-using
youth, substance use was related to worsening performance on several cognitive domains
when compared to non-using youth, including worse performance on tests of complex
attention, memory, processing speed, and visuospatial functioning, with early use (before
age 16) relating to worse performance (Jacobus et al., 2015). A large longitudinal birth
cohort study from New Zealand (N=1,037) found that persistent adolescent-onset marijuana
use was associated with an IQ decline of more than 5 points in the most persistent
marijuana-use group, with deficits persisting into adulthood (Meier et al., 2012). However, a
recent longitudinal twin study found that IQ deficits observed in marijuana users may be
attributable to confounding factors like familial and environmental influences rather than the
direct neurotoxic effect of marijuana (Jackson et al., 2016). The follow-up assessment
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periods for these studies differed, with the Meier study ending at age 38 and the Jackson
study following youth until age ~20; regular use over a prolonged period may result in more
deleterious effects.

Adolescent alcohol and marijuana use has also been associated with a range of structural and
functional brain changes. In the largest prospective study to date on this topic (N=134),
alcohol-using adolescents showed abnormal neurodevelopmental trajectories when
compared to continuously non-using controls, including accelerated decreases in gray matter
volume (particularly in frontal and temporal regions) and attenuated increases in white
matter volume over the ~5 year follow-up (Squeglia et al., 2015), replicating earlier studies
with smaller sample sizes (Luciana et al., 2013; Squeglia et al., 2014b). These findings
suggest potentially non-beneficial pruning or, alternatively, premature cortical gray matter
decline in alcohol-using youth. In a study examining white matter development, adolescents
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with extensive marijuana- and alcohol-use histories showed worsening white matter integrity
over an 18 month (Baba et al., 2013) and 3-year follow-up (Jacobus et al., 2013a, 2013b) in
a number of important white matter tracts when compared to non-using youth, as well as
poorer performance on tests of neurocognitive functioning. In conjunction with structural
changes, adolescent alcohol and marijuana use appears to also affect brain functioning. On
several functional MRI studies, youth who initiated heavy alcohol use during adolescence
have shown increasing brain activation over time on tests of visual working memory
(Squeglia et al., 2012) and inhibition (Wetherill et al., 2013a, 2013b), when compared to
non-using peers.

Risk Factors—Several factors increase the likelihood of an individual developing a

substance use problem, including familial, social, and individual risk factors (Whitesell et
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al., 2013). Vulnerability for developing substance-related problems is especially heightened

among individuals with a family history of substance use disorder (Cservenka, 2016). A
recent meta-analysis of twin and adoption studies found that alcohol use disorder is
approximately 50% heritable (Verhulst, Neale, & Kendler, 2015); however, identifying
specific genes has been challenging, highlighting the complexity and heterogeneity of the
disorder (Hart & Kranzler, 2015; Tawa, Hall, & Lohoff, 2016). Findings suggest there are a
number of genes, each with relatively small effects, that interact with each other and with the

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environment (Enoch, 2012) to make an individual more or less susceptible to having a

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substance use disorder (Meyers & Dick, 2010). While specific genes have not been
consistently identified, youth with a family history of alcohol use disorder are 3–5 times
more likely to develop an alcohol use disorder than youth without a family history of
alcoholism (Cotton, 1979).

Males tend to have higher rates of substance use than females (SAMSHA, 2014). Other
important risk factors for adolescent substance use include environmental factors such as
early exposure to traumatic life events (Dube et al., 2006), prenatal exposure to alcohol and
other drugs (Enoch et al., 2011), lack of parental supervision and monitoring (Nash et al.,
2005), sleep problems (Shibely et al., 2008), being involved in romantic relationships
(Squeglia et al., 2017; Whelan et al., 2014), and peer substance use (Leung et al., 2014). Co-
occurring psychopathology, including ADHD and depression have been shown to
significantly increase the risk of adolescent alcohol use (Charach et al, 2011; Lee et al.,
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2011; Libby et al., 2005; Rao et al., 1999; Taylor, 2011; Wu et al., 2008). Additionally,
childhood depression and conduct disorder symptoms predict persistence of substance
dependence in adulthood (Meier et al., 2016). Other research suggests that externalizing, but
not internalizing, mental health problems in childhood predict later substance use in males
and females, while among females adolescent substance use predicts internalizing disorders
in adulthood (Miettunen et al., 2014).

Prevention
Prevention science is grounded in the premise that modulation of risk and protective factors
may affect the probability of later problems (Coie et al., 1993). Applied to adolescent
substance use, this has been implemented across a number of modalities and settings, with
the goal of reducing modifiable risk factors and enhancing/reinforcing modifiable protective
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factors (Harrop & Catalano, 2016). Most commonly, programs have been developed and
evaluated in school, family, and community settings. Evidence is mixed amid heterogeneity
of methodology and outcomes between studies, but there is some support for parenting-
focused (Allen et al., 2016), school-based teacher-led (Lize et al., 2017), and peer-led
prevention programs (MacArthur et al., 2016).

Screening and Assessment

Despite the serious implications of adolescent substance use, many clinical providers do not
conduct routine screening, and most that do fail to utilize a validated screening method
(Harris et al., 2012). In light of this, considerable recent effort has focused on developing
and disseminating efficient and reliable screening methods for adolescent substance use
(Levy et al., 2016). Screening tools can potentially be used across a number of settings
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where adolescents are present, though to date most research in this area has focused on
primary care practice. The ideal tool would be both sensitive and specific to substance use
and related problems, and would guide subsequent in-depth assessment and intervention
when appropriate. This must be balanced with the need for time efficiency amid busy
clinical practice in which a wide variety of health screening assessments are indicated.

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Two brief screeners have strong evidence of achieving the balance of the aforementioned
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goals, and can be delivered via interview or electronic administration. The Screening to
Brief Intervention (S2BI), which queries the adolescent regarding frequency of using 8 types
of drugs in the past year, yields high sensitivity and specificity for identifying use and
substance use disorders (Levy et al., 2014). Similarly, the Brief Screener for Tobacco,
Alcohol, and Other Drugs (BSTAD) queries frequency of use in the past year, with optimal
cutoff points for identifying substance use disorders as ≥6 days of tobacco use, ≥2 days of
alcohol use, and ≥2 days of marijuana use (Kelly et al., 2014). Both screeners can be
delivered electronically, which is a preferred method for adolescents. In practice, adolescent
patients can complete the screener via mobile electronic device in the waiting area, and the
results can be delivered to the provider in anticipation of the visit and interview.

Initial screeners such as the S2BI and BSTAD can be complemented with subsequent brief
assessments to evaluate level of substance involvement and severity of substance-related
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problems. These assessments can help determine the level and modality of treatment that
may be needed, spanning from psychoeducation and/or brief intervention in the primary care
office to more intensive service referrals. The CRAFFT (Car, Relax, Alone, Friends/Family,
Forget, Trouble), ASSIST (Alcohol, Smoking and Substance Involvement Screening Test)
and GAIN (Global Appraisal of Individual Needs) are all validated for this purpose. The
CRAFFT and ASSIST serve as adolescent-validated analogues to the adult screener CAGE,
the latter of which is not developmentally appropriate for adolescents (Gryczynski et al.,
2015; Knight et al., 1999). The GAIN assesses for both substance use disorders and
potentially associated mental health disorders, including four subscales assessing substance
use, internalizing disorders, externalizing disorders, and crime/violence (Dennis et al.,
2006).
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When more thorough and formal evaluation is indicated (i.e., when brief screening is highly
suggestive of substance-related problems requiring intervention), diagnostic evaluation via
the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), may be
undertaken (American Psychiatric Association, 2013). Within this framework, problematic
substance use may be diagnostically categorized as a substance use disorder (e.g., Cannabis
Use Disorder), with severity of mild, moderate, or severe, depending on the number of
substance use disorder symptoms endorsed for a given substance. Diagnostic evaluation
should be complemented by functional behavioral analysis, in which substance use is
evaluated as a problem behavior with antecedents and consequences which may be unique to
a given adolescent’s substance use. The functional analysis framework is used to determine
what antecedents and consequences are potentially modifiable to reduce the likelihood of
ongoing problem behavior (Randall et al., 2001).
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Laboratory testing, most commonly urine drug testing, is often used to complement self-
report when evaluating adolescent substance use; it is, however, not generally supported as a
standalone screening or assessment for substance use (Hadland & Levy, 2016). Particularly
in situations when trust has been eroded within a family and the veracity of an adolescent’s
self-report is in doubt, urine testing may serve as a useful, though imperfect, method for
objective assessment. With some exceptions, most studies have shown reasonable agreement
between adolescent self-report and urine drug test results (Gignac et al., 2005). Parental

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report is comparatively less consistent with urine testing, reflecting that parents may not
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often be aware of the adolescent’s day-to-day substance use patterns. Variations in detection
times due to substance, dose, chronicity of use, cutoff used, and metabolism of user, should
be noted as potential limits of urine testing. Additionally, some “designer” and synthetic
substances may not be included among commonly available urine drug testing panels. Home
drug testing kits are widely available, but often lack informational guidance to inform
parents/guardians of empirically supported strategies to incorporate them as a part of
treatment and monitoring, indicating that clear guidance by the provider is critical when
considering drug testing at home rather than in clinic (Washio et al., 2014).

Treatment
Treatment development for adolescent substance use disorders has focused primarily on
psychosocial interventions, spanning individual, group, and family modalities. The intensity
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and duration of investigated treatments has varied from brief (even single-session)
interventions to extended multimodal strategies. The majority of studies have evaluated
office-based outpatient interventions, many of which were developmentally adapted from
established adult-targeted treatments.

Despite the considerable appeal of brief interventions as part of the Screening, Brief
Intervention, and Referral to Treatment (SBIRT) model, standalone brief interventions have
demonstrated very limited effects when provided to adolescents with substance use disorders
(Young et al., 2014). This is similarly the case with brief school-based interventions (Carney
et al., 2016) and brief standalone motivational interviewing approaches (Li et al., 2016).
These strategies appear more useful when provided as a component of multimodal
intervention with increased overall intensity and duration.
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A recent comprehensive review indicated that the most well established efficacious
treatments include ecological family-based treatment, group cognitive-behavioral therapy
(CBT), and individual CBT, while fair evidence supports behavioral family therapy and
motivational enhancement therapy (MET) (Hogue et al., 2014). Substantial evidence
supports combined treatment approaches, incorporating elements from the aforementioned
modalities and others to enhance outcomes. Given that adolescent substance use disorders
are heterogeneous and multidetermined, treatment approaches that address multiple
biopsychosocial targets are often indicated. Among combined treatments, strong evidence
supports combined MET and CBT, as well as combined MET, CBT, and behavioral family-
based treatment (Hogue et al., 2014). Outcomes are further enhanced by complementing the
aforementioned treatments with contingency management (CM), a behavioral treatment
based on operant conditioning principles, in which tangible rewards are provided for
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objectively confirmed desired behaviors (e.g., token provided for negative urine drug test)
(Stanger et al., 2015, 2016). In general, evaluated treatments in large-scale trials have
demonstrated short-term substance reduction and/or cessation, but adolescents with
substance use disorders, even with the best evidence-based care, rarely achieve long-term
abstinence (Dennis et al., 2004; Hogue et al., 2014; Waldron & Turner, 2008).

Pharmacotherapy is an established complement to psychosocial treatment for adults with

substance use disorders, with several medications receiving United States Food and Drug

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Administration (FDA) approval for treatment of alcohol, tobacco, and opioid use disorders.
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While the neuropathology of adolescent substance use disorders is increasingly recognized,

relatively little work has focused on developing pharmacotherapies for this age group. To
date, only buprenorphine-naloxone possesses FDA approval for opioid use disorder in youth
ages 16 and older. Other medications have been studied at least preliminarily for youth
alcohol, tobacco, cannabis, and opioid use disorders, yielding mixed results (Hammond &
Gray, 2016). Findings from randomized controlled trials, though not yet exhaustive, indicate
that select pharmacotherapies may be considered as adjunctive treatments to psychosocial
interventions: buprenorphine-naloxone maintenance to improve treatment retention and
outcomes for opioid use disorder (Marsch et al., 2005; Woody et al., 2008), N-
acetylycysteine as an adjunct to cessation counseling and contingency management for
cannabis use disorder (Gray et al., 2012), and nicotine patch or bupropion SR to improve
tobacco cessation rates (Gray et al., 2011, Moolchan et al., 2005; Muramoto et al., 2007).
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Given the ubiquity of mobile technology among adolescents, and the considerable logistical
barriers to office-based care (e.g., transportation, accessibility), recent research has focused
on translating evidence-based care for delivery via electronic platforms. A meta-analysis
revealed a small positive effect size for text messaging interventions for youth with
substance use problems (Mason et al., 2015), and a pilot study demonstrated the feasibility
of using smartphones to provide recovery support for adolescents after discharge from
residential treatment (Dennis et al., 2015). Ongoing work is focused on combining
ecological momentary assessment and smartphone application intervention in adolescents
with substance use and co-occurring psychiatric disorders (Benarous et al., 2016).

Limitations
This review provides a general overview of a broad, complex topic area, with multiple lines
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of ongoing research. The methodology of the review was by design not structured or meta-
analytic, but rather a general cross-section of recent advances and findings. Additionally, the
review focused largely, but not exclusively, on data derived from United States samples. As
such, caution should be taken in interpreting findings, acknowledging the potential for
limitations in generalizability across populations, policies, and cultural and environmental
factors.

Conclusions
Recent research has significantly advanced the understanding of substance use in
adolescence. Survey-based epidemiological studies have identified trends in substance-
related attitudes and rates of use of various substances, while emerging longitudinal
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neuroimaging studies have elucidated the neurobiology underlying adolescents’ propensity

for substance initiation and progression to substance use disorders, with potentially lasting
substance-related adverse consequences. A variety of prevention programs have been
implemented across settings with varying degrees of success. Novel screening and
assessment instruments have been developed to efficiently identify youth with particular risk
for serious substance-related problems, and a number of evidence-based treatment
approaches have been shown to be effective in reducing substance use and substance-related

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problems. Unfortunately, adolescents with substance use disorders rarely achieve long-term
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abstinence even with the most robust evidence-based treatments, indicating that further work
is needed to optimize methods to understand and address this important public health issue.

Acknowledgments
Dr. Gray has received research support (medication only) from Pfizer.

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Key Points
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▪ Adolescents, amid rapid biopsychosocial development, are more prone than

children or adults to initiating substance use and suffering lasting substance-
related adverse consequences

▪ Recent research has elucidated the neurobiological processes underlying

substance use risk in adolescents, as well as substance-related
neuropathology among adolescents with substance use disorders

▪ Advances in prevention, screening, assessment, and treatment research have

yielded evidence-based interventions to address adolescent substance use
disorders

▪ Further research is needed to enhance outcomes and reduce the considerable

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public health burden of adolescent substance use disorders

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J Child Psychol Psychiatry. Author manuscript; available in PMC 2018 June 01.
 Gray and Squeglia Page 18

Table 1

Rates (%) of current (30-day) substance use among adolescents in the United States, by substance and grade
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level (Johnston et al., 2017).

8th Grade 10th Grade 12th Grade

Alcohol (any) 7.3 19.9 33.2

Alcohol (been drunk) 1.8 9.0 20.4

Marijuana 5.4 14.0 22.5

E-cigarettes 6.2 11.0 12.5

Cigarettes 2.6 4.9 10.5

Smokeless Tobacco 2.5 3.5 6.6

Inhalants 1.8 1.0 0.8

Hallucinogens 0.6 0.9 1.4

Ecstasy (MDMA) 0.3 0.5 0.9

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Cocaine 0.3 0.4 0.9

Heroin 0.2 0.2 0.2

Narcotics other than Heroin NR NR 1.7

Amphetamines 1.7 2.7 3.0

Methamphetamine 0.3 0.2 0.3

Tranquilizers 0.8 1.5 1.9

Any Prescription Drug NR NR 5.4

NR=Not Reported
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J Child Psychol Psychiatry. Author manuscript; available in PMC 2018 June 01.