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Impulsivities and addictions: A multidimensional integrative framework informing assessment and interventions for substance use disorders



Impulse control is becoming a critical survival skill for the twenty-first century. Impulsivity is implicated in virtually all externalizing behaviours and disorders, and figures prominently in the aetiology and long-term sequelae of substance use disorders (SUDs). Despite its robust clinical and predictive validity, the study of impulsivity is complicated by its multidimensional nature, characterized by a variety of trait-like personality dimensions, as well as by more state-dependent neurocognitive dimensions, with variable convergence across measures. This review provides a hierarchical framework for linking self-report and neurocognitive measures to latent constructs of impulsivity and, in turn, to different psychopathology vulnerabilities, including substance-specific addictions and comorbidities. Impulsivity dimensions are presented as novel behavioural targets for prevention and intervention. Novel treatment approaches addressing domains of impulsivity are reviewed and recommendations for future directions in research and clinical interventions for SUDs are offered. This article is part of the theme issue ‘Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications’.
Cite this article: Vassileva J, Conrod PJ. 2019
Impulsivities and addictions:
a multidimensional integrative framework
informing assessment and interventions for
substance use disorders. Phil. Trans. R. Soc. B
374: 20180137.
Accepted: 15 November 2018
One contribution of 14 to a theme issue ‘Risk
taking and impulsive behaviour: fundamental
discoveries, theoretical perspectives and clinical
Subject Areas:
behaviour, cognition, neuroscience
addiction, substance use disorders, personality,
impulsivity, treatment and prevention
Author for correspondence:
Patricia J. Conrod
Impulsivities and addictions:
a multidimensional integrative framework
informing assessment and interventions
for substance use disorders
Jasmin Vassileva1,2 and Patricia J. Conrod3,4
Institute for Drug and Alcohol Studies, and
Department of Psychiatry, Virginia Commonwealth University,
Richmond, VA, USA
Department of Psychiatry, University of Montreal, Montreal, Canada
Centre de Recherche, CHU Ste Justine, Montreal, Canada
JV, 0000-0003-2397-2657; PJC, 0000-0002-5570-481X
Impulse control is becoming a critical survival skill for the twenty-first cen-
tury. Impulsivity is implicated in virtually all externalizing behaviours and
disorders, and figures prominently in the aetiology and long-term sequelae
of substance use disorders (SUDs). Despite its robust clinical and predictive
validity, the study of impulsivity is complicated by its multidimensional nature,
characterized by a variety of trait-like personality dimensions, as well as by more
state-dependent neurocognitive dimensions, with variable convergence across
measures. This review provides a hierarchical framework for linking self-report
and neurocognitive measures to latent constructs of impulsivity and, in turn,
to different psychopathology vulnerabilities, including substance-specific
addictions and comorbidities. Impulsivity dimensions are presented as novel be-
havioural targets for prevention and intervention. Novel treatment approaches
addressing domains of impulsivity are reviewed and recommendations for
future directions in research and clinical interventions for SUDs are offered.
This article is part of the theme issue ‘Risk taking and impulsive behaviour:
fundamental discoveries, theoretical perspectives and clinical implications’.
1. Introduction
Impulsivity is implicated in virtually all substance-related and addictive disorders
and many other forms of psychopathology, which has caused an explosion of
research in this area over the last two decades. This research has revealed that
the construct is highly multidimensional and complex in its measurement, despite
having robust and repeatable predictive validity. However, the translation of this
knowledge to clinical practice has been strikingly slow. The novelty of this review
relative to previous reviews on this topic is the integration of multiple comp-
lementary models of addiction in which impulsivity and its different
dimensions and measurement modalities figure prominently. Furthermore, this
review will attempt to demonstrate empirical evidence in support of the link
between the multidimensional structure of impulsivity and its neurocognitive cor-
relates with contemporary views on the structure of psychopathology and risk for
different types of substance use disorders (SUDs). Finally, this multidimensional,
integrative framework will serve to highlight promising intervention strategies for
the treatment and prevention of addictive behaviours focusing on management of
dimensions of impulsivity.
2. Impulsivity in the twenty-first century
The term impulsivity has existed in human language for more than five centuries
and has been recognized as playing a key role in psychiatric conditions since the
&2019 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution
License, which permits unrestricted use, provided the original
author and source are credited.
birth of the fields of neurology and psychiatry [1]. Impulsivity
is defined by the International Society for Research on Impul-
sivity as behaviour without adequate thought, the tendency
to act with less forethought than do most individuals of
equal ability and knowledge, or a predisposition toward
rapid, unplanned reactions to internal or external stimuli with-
out regard to the negative consequences of these reactions’.
Impulse control has become recognized as a crucial survival
skill and enhancing impulse control is viewed as a key societal
goal for the twenty-first century, as for the first time in human
history we live in a society where food is readily available,
addictive substances and technology are easily accessible,
and immediate gratification is the modus operandi of popular
culture. As eloquently argued by Terry Moffitt, impulse control
is more necessary now than ever before in human history in
order to prevent addiction, stay healthy, resist spending, and
save for retirement [2].
3. Impulsivity and drug addiction
With regards to SUDs in particular, impulsivity has been
shown to be both an antecedent risk factor considered a
vulnerability marker for SUDs [3] and a consequence of
chronic substance use associated with structural and func-
tional neurobiological changes [4]. The definition of
impulsivity maps closely to current conceptualizations of
addiction, considered to be a chronic relapsing brain dis-
ease characterized by ‘uncontrollable, compulsive drug
craving, seeking and use, even in the face of negative
health and social consequences [5]. Indeed, contemporary
theories of addiction [6 10] conceptualize the disorder
primarily as a syndrome of impaired impulse control, pro-
posed to be the core mechanism underlying the compulsive
pattern of drug seeking and use, which, in combination
with individual differences in other neurobiological
domains such as compulsivity or negative emotionality,
are crucial to understanding the heterogeneity of addictive
disorders [9,11].
Despite the notable advances in the study of impulsivity
in addictive disorders, the lack of clinical translation of these
advances has been striking. One source of variability in
linking impulsivity to addiction vulnerability is the attempt
by researchers to study the role of impulsivity in single
disorders, by statistically covarying other forms of psycho-
pathology, or other forms of substance use. This artificial
simulation of unitary conditions is not supported by research
on the structure of psychopathology (e.g. [12,13]), where
impulsivity also appears to be a central common vulnerability
to many externalizing conditions [12], and potentially all
psychiatric conditions [13,14]. What is lacking in the literature
is an integrative model that incorporates a multimodal
approach to the measurement of impulsivity and its different
dimensions, which attempts to explore their specificity with
respect to different types of addictions and co-occurring
mental disorders.
4. Impulsivity versus impulsivities: integrative
multimodal framework
Trait dimensions of impulsivity are measured with self-report
instruments that are based on self-evaluation of how people
view themselves relative to others. In contrast, state dimen-
sions are measured by performance on neurocognitive tasks
tapping much more narrowly defined cognitive and affective
processes, in which individuals are generally required to
choose between short-term and long-term gains and losses,
or to inhibit a response to a pre-potent urge, a valued
reward, or a delay cue [16–18]. While it is recognized
that such measures can also be used to identify trait-level
individual differences [19], they have the potential to tap
more within- person variability. In this respect, self-report
measures could reveal who is at general risk, whereas neuro-
cognitive measures, may more accurately predict who is at
immediate risk [16]. Combining the two approaches may
lead to better identification of individuals who are at parti-
cularly high risk and increase our understanding of the
relationship between multiple putative addiction phenotypes,
which may help redefine them as multi-level combination
of traits and states [20] that could be targeted by tailored
personality and neurocognitive interventions.
(a) Trait impulsivity—personality dimensions
Most models of personality propose that behaviour is gov-
erned by at least two independent systems, considered to
be heritable biological traits. One is associated with avoid-
ance behaviour, broadly reflecting the personality trait of
anxiety, and the other with approach behaviour, reflecting
impulsivity [21]. Eysenck and his biologically-based trait
theory of personality [22] inspired other similar omnibus
theories, such as those of Cloninger [23] and Zuckerman
[24], which incorporate variously named constructs related
to impulsivity (e.g. impulsiveness, venturesomeness, novelty
seeking, sensation seeking) and emphasize their importance
in relation to specific subtypes of substance abuse. Barratt
and colleagues [25,26] propose a more multifaceted conceptu-
alization of trait impulsivity, delineating attentional, motor,
and non-planning sub-components. Similarly, others
[2729] have used the Five Factor Model of Personality [30]
to emphasize the hierarchical and context-dependent nature
of self-report impulsivity, identifying five lower-order trait
impulsivity facets: (lack of) premeditation, (lack of) persever-
ance, sensation seeking, negative urgency (tendency to act
impulsively under negative affect), and positive urgency (ten-
dency to act impulsively under positive affect). Valiant
attempts have been made to impose structure across these
various trait measures to come to some agreement on the
true nature of trait impulsivity and its dimensions, with hier-
archical factor analyses agreeing on at least two broad
dissociable trait dimensions that account for a significant por-
tion of the variance across most self-report impulsivity
measures: Impulsiveness (Unprepared/Spontaneous) and
Sensation Seeking (in [31]). Importantly, these traits were
shown to be hierarchically organized and their common var-
iance captured by a higher-order Impulsivity construct.
Within this hierarchical structure, each domain was shown
to subdivide into two additional lower order facets: Impul-
siveness into traits of preparedness and spontaneous; and
Sensation Seeking into thrill and adventure seeking and
impatient pleasure seeking. As noted by Woicik et al. [32],
many personality scales were developed when impulsivity
was considered a unitary construct and therefore fail to
fully differentiate between these facets. Sensation Seeking
[24] has items that tap impulsiveness and thrill and Phil. Trans. R. Soc. B 374: 20180137
adventure seeking, despite its name, which causes further
confusion in the field. In figure 1, we attempt to provide
some clarification of how the most widely used impulsivity
scales map onto four empirically derived subfacets of impulsiv-
ity, as suggested in [31]. Another widely used multidimensional
scale, the UPPS/UPPS-P [27] measures three dissociable traits,
despite its numerous subscales, Negative/Positive Urgency,
(lack of) Premeditation/perseverance, and Sensation Seeking,
as revealed in meta-analysis of studies investigating the
discriminative validity of this scale [27].
Self-report measures of trait impulsivity tend to have high
predictive value with respect to substance use and misuse,
psychopathology and other health risk behaviours [2,33,34].
Numerous studies using these personality scales have
found a consistent relationship between measures of impul-
sivity, sensation seeking and drug addiction [35– 40].
Importantly, evidence from prospective studies indicates
that impulsivity measured as a childhood temperament is
linked to the later development of SUDs [41,42]. Research
indicates that trait impulsivity is a drug-vulnerability pheno-
type that exists prior to the development of SUDs, which is
also elevated in biological siblings of chronic drug users,
supporting its role as a behavioural endophenotype for
SUDs [43].
Increasingly, research has noted the need to consider
specific facets of trait impulsivity when exploring different sub-
stance misuse profiles, defined along clinical, substance-related,
and motivational dimensions [44,45]. The emotion-based
(negative and positive urgency), conscientiousness-based
(lack of premeditation and lack of perseverance), and sensation
seeking-based facets have been associated with different
patterns of substance misuse that likely reflect different
aetiological mechanisms with differential implications for treat-
ment [38,46]. Some facets, such as sensation seeking, appear to
be more adaptive because despite their associations with early
onset and heavy drinking [13,33,34,47], individuals scoring
high on this trait show greater ability to maintain some control
over drug intake and have fewer co-occurring symptoms of
psychopathology [12,38,48]. In contrast, Impulsiveness (Unpre-
pared/Spontaneous) is associated with problem drug and
alcohol use (in [45]), with some studies suggesting that the
link between this facet of impulsivity and SUD is indirect
and mediated through general tendency towards rule breaking
and misconduct (e.g. [49]). Whereas the majority of the
evidence supporting the personality model of addiction
vulnerability is based on alcohol, recent studies provide evi-
dence for the role of facets of trait impulsivity as prospective
risk factors for heavy alcohol and cannabis misuse [50,51]
and for sensation seeking as a risk factor for early initiation
of both alcohol and cannabis use [51]. Impulsivity and
sensation seeking are increasingly being recognized as separate
[52,53], genetically distinct constructs [54] implicated in risk for
substance misuse. Dissociating between them when consider-
ing the role of impulsivity in substance-related behaviours
may increase their diagnostic and prognostic utility.
Despite a widely accepted notion of personality traits
reflecting lasting and consistent individual differences, there
is unequivocal evidence that personality traits tend to
change across the lifespan [55], with some traits (e.g. con-
scientiousness, extraversion) being more stable than others
(e.g. neuroticism) [56]. For the most part, the measurement
of personality traits involves central tendency variables, is
often limited to a single assessment, and rarely involves
methods that capture within-person variability.
Figure 1. Schemata for linking different impulsivity measures and facets to patterns of substance use and comorbid psychopathology through latent constructsof
impulsivity and psychopathology. Self report trait measures in dark green, neurocognitive and computational parameters in lighter green, latent neurocognitive
impulsivity constructs in orange, latent hierarchical psychopathology dimensions in light blue and observed DSM disorder in dark blue. Thick dark blue arrows
from internalising symptoms and externalising symptoms reflect indirect relationship between latent psychopathology construct and specific substance use outcomes
through externalizing and externalizing symptoms. Pfactor represents variance common to all psychiatric symptoms. Adapted from Castellanos-Ryan et al. [12] and
Conrod & Nikolaou [11].
3 Phil. Trans. R. Soc. B 374: 20180137
(b) State impulsivity—neurocognitive dimensions
Although impulsivity is often thought of as a personality trait
or predisposition, many of its contemporary conceptualiz-
ations involve distinct performance-based neurobehavioural
manifestations, reflecting individual differences in valuation
and decision-making that could be more sensitive to fluctuat-
ing momentary lapses in impulse control, influenced by
environmental context and the current state of the individual.
Neurocognitive manifestations of impulsivity fall into two
broad domains, dissociable at both neuroanatomical and
neuropharmacological levels [21,52]. The first is impulsive
action [57], also known as motor impulsivity, involving
response inhibition [1,58] and manifested as difficulty inhibit-
ing or stopping prepotent or ongoing responses. Common
tasks of impulsive action include stop signal tasks [59,60],
which require cancellation of an already initiated response
[61], and go/no-go type of tasks [6264], which require inhi-
bition of prepotent responses to external or internal signals.
The second neurocognitive domain is impulsive choice’ [65],
also known as cognitive impulsivity or reward-based impulsivity,
which refers to the compromised ability to make decisions in
line with long-term goals. It is related to: (i) sensitivity of
choices to delay and preference for ‘smaller-sooner over
larger-later’ rewards, measured with delay discounting para-
digms [66]; and (ii) sensitivity of choices to risk and reward,
measured with reward-based decision-making tasks such as
the Iowa Gambling Task [67] or the Cambridge Gambling
Task [68], or with risk-taking tasks such as the Balloon Ana-
logue Risk Task [69]. These neurocognitive distinctions do
show specificity with respect to relationships to facets of
self-report impulsivity when investigated in a multivariate
framework: Impulsiveness correlates with measures of
response inhibition (action impulsivity), sensation seeking cor-
relates with reward sensitivity measures on learning and
passive avoidance tasks, and self-report measures of impatient
pleasure seeking (a sub-facet of sensation seeking) most
robustly correlate with delay discounting [31].
Neuroimaging and neuropsychological studies assessing
the relationship between facets of impulsivity and risk for
SUDs suggest that self-report and neurocognitive measures
of impulsivity are implicated as both causes and consequences
of early onset substance misuse [4]. Castellanos-Ryan et al. [34]
demonstrated that neurocognitive measures of reward sensi-
tivity and action impulsivity independently mediated the
longitudinal relationships between self-report sensation seek-
ing and impulsiveness respectively, and adolescence
substance misuse. Whelan et al. [70] showed that stopping be-
haviour, a form of impulsive action involving action
cancellation, and its correlated neural network involving the
inferior frontal gyrus, was implicated specifically in frequency
of drug use, whereas other networks involved in stopping be-
haviour were related to drug use vulnerability, but not to
frequency or severity of use. More recently, Morin et al. [71]
analysed data from a longitudinal study of 4000 adolescents
who were assessed annually on a number of impulsivity and
executive cognitive functions over the course of adolescence
(from 12 to 17 years). This analysis showed that neurocogni-
tive measures of working memory and response inhibition
(impulsive action) were associated with vulnerability to sub-
stance use in adolescence, but multi-level modelling of
within-person variability on these neurocognitive measures
also showed that onset and frequency of substance use,
particularly cannabis use, were associated with, and longi-
tudinally predicted, further changes in working memory
and response inhibition (impulsive action), suggesting
action inhibition is both causal and consequential to
substance misuse.
A more recent analysis examining the role of different
measures of impulsivity in adolescent substance use beha-
viours using this same longitudinal cohort and multi-level
framework tested the independent contribution of self-
report trait impulsivity and errors of commission on a go/
no-go task (impulsive action) on adolescent drinking, binge
drinking and drug use [72]. When age-related changes in
impulsivity were modelled over a 4 year period at the
between- and within-person level, both self-report and neuro-
cognitive measures significantly contributed to the prediction
of vulnerability to drug-related behaviours. However,
between-group differences (mean level over the 4 year
period) on both on self-report trait measures and on response
inhibition/impulsive action measures were related to riskier
patterns of alcohol and drug use, whereas within- person
changes in trait impulsivity were related to within-person
variability in frequency of alcohol consumption. Two
machine-learning analyses involving large longitudinal
cohorts of European [73], Canadian and Australian [74] ado-
lescents further confirm the independent and predictive role
of trait impulsivity and sensation seeking in risk for alcohol
misuse, and suggest that neurocognitive measures of impul-
sivity do not add to model prediction of ‘who’ is at risk
when self-report traits are included. However, consistent
with [72] there is emerging evidence that more complex pre-
dictive models that account for the multi-level and variable
nature of impulsivities and substance use and that involve
multimodal measures of impulsivity might prove to be
additionally useful in determining when risk is most
likely to be expressed, rather than who is at risk. This
notion is being further investigated using more complex
computational models of task-based neurocognitive measures.
(c) State impulsivity—computational dimensions
Neurocognitive tasks of impulsivity are often deliberately
designed to be complex, in order to be ecologically valid
and capture important aspects of real-life decision-making.
Although this increases their ecological validity, it also
leads to significant heterogeneity and implies that neurocog-
nitive performance is an interaction and synthesis of several
different underlying motivational, learning, and choice pro-
cesses [75]. Therefore, failure to perform well on such tasks
may have many different causes. For example, poor perform-
ance on the Iowa Gambling Task [76] of impulsive action,
arguably the most commonly used decision-making task in
the addiction literature, may be due to increased sensitivity
to reward, to decreased sensitivity to loss, to poor learning
and retention of task contingencies, or to an erratic and
inconsistent response style. Computational models of
such complex tasks break down performance into under-
lying components and use the parameters associated
with these components to understand the mechanisms of
the neurocognitive deficits displayed by different clinical
populations [77,78].
Computational ideas permeate many areas of science, but
have had surprisingly little impact on the way psychiatric dis-
orders are phenotyped [79]. Recently, there has been an
4 Phil. Trans. R. Soc. B 374: 20180137
increased interest in the utility of computational modelling as a
novel phenotyping tool in psychiatry and a novel paradigm for
understanding psychopathology [80,81]. Computational mod-
elling has proven valuable for uncovering important
differences in neurocognitive decision processes in various
clinical populations [78]. Notably, computational parameters
have been shown to be more sensitive to substance-specific
and disorder-specific neurocognitive deficits than standard
neurobehavioural performance indices [82– 84]. For example,
computational parameters robustly discriminate between
opiate and stimulant users in protracted abstinence even
within the context of no group differences in neurobehavioural
performance [83]. Moreover, dynamic changes in specific com-
putational parameters of decision-making, such as ambiguity
tolerance, have been shown to predict imminent relapse in
abstinent opioid-dependent individuals, who were followed
up for the first seven months of treatment and retested up to
15 times with a decision-making/impulsive choice task [85].
This suggests that computational parameters may have not
only diagnostic, but also prognostic utility when used in
repeated measures designs, which can inform not only with
whom to intervene, but also when to intervene. Overall, compu-
tational parameters can serve as novel prognostic and
diagnostic state-dependent markers of addiction that can be
used to track the trajectory of various neurocognitive dimen-
sions of impulsivity and their associations with critical risk
behaviours across different stages of the addiction cycle.
There is an unexplored potential of using computational
approaches to refine neurocognitive phenotyping of addic-
tions, identify neurocognitive mediators of response to
treatment, and increase the precision of treatment inter-
ventions for addictions. While between-group differences in
self-report impulsivity and sensation seeking are robustly
predictive of risk for substance use (e.g. [74]) and hold promise
as diagnostic markers, new research designs incorporating
within-subject repeated measures, using multilevel modelling
or ecological momentary assessment along with neurocogni-
tive and computational modelling of measures of impulsive
action and impulsive choice will help to better understand
when an individual is more likely to take up use or relapse
back to problematic use.
5. Dimensions of impulsivity and risk for
Impulsivity is proposed to be a prime transdiagnostic marker
for a wide range of psychiatric disorders [80,86] and is one of
the most frequent diagnostic criteria in the new edition of the
Diagnostic and statistical manual of mental disorders (DSM-5;
[87]). It figures most prominently in externalizing spectrum
disorders, such as attention deficit hyperactivity disorder
(ADHD), conduct disorder, and antisocial personality dis-
order (ASPD), which are commonly comorbid with SUDs
[18]. A common characteristic of these disorders is that they
originate in childhood, have a pervasive pattern, and are
frequently lifelong. Developmentally, there is a strong associ-
ation between such disorders and subsequent drug use
Personality disorders in particular, such as ASPD, are
thought of as trait-like dysfunctional patterns in cognitive,
affective, interpersonal, and impulsivity domains [90] and
are highly comorbid with SUDs [91], which has led some to
question whether antisocial behaviours should be viewed as
independent of SUDs [92]. A potentially more informative
alternative to the somewhat over-inclusive diagnosis of ASPD
is psychopathy [93], an extreme variant of ASPD, consisting
of a constellation of affective, interpersonal and behavioural
characteristics. Theories of psychopathy distinguish between
primary (callous/unemotional) and secondary (antisocial/
impulsive) subtypes [94], both of which share common traits
such as hostility and aggression. However, primary psycho-
paths are characterized by grandiosity, superficiality, lack of
empathy and remorse, and low to moderate levels of anxiety,
whereas secondary types are more impulsive, anxious, with
high levels of negative affectivity and emotional disturbances
[95,96]. Trait impulsivity has been shown to be the best predic-
tor of both psychopathy and conduct disorder/ASPD [33,97].
Psychopathy, particularly secondary psychopathy, is associ-
ated with SUDs [95,98–100] but tends to be more strongly
related to illicit drug use than to alcohol use [100].
Research reveals differential relationships between exter-
nalizing disorders and neurocognitive dimensions of
impulsive choice and impulsive action. ADHD has been
associated more strongly with motor/action impulsivity
[101,102], evidenced by studies with children and adults
with ADHD, which indicate that the disorder is related
more strongly to performance-based deficits on simpler
tasks of impulsive action that involve response inhibition
[101], than on tasks of impulsive choice that involve reward
and punishment contingencies (reviewed in [102]). In contrast,
studies with individuals with psychopathic traits indicate that
psychopathy is primarily related to performance-based deficits
on more complex tasks of impulsive choice involving various
reward and punishment contingencies or delays [103–107].
A number of theorists have suggested that SUDs and
externalizing disorders represent common syndromes of disin-
hibition [108,109]. The phenotypic association between trait
impulsivity and externalizing disorders has been traced to
common aetiological factors between these phenotypes [109],
which share a common genetic basis [54], which suggests
that impulsivity could be the common underlying mechanism
linking externalizing disorders and SUDs. Longitudinal studies
that have attempted to study the intra-individual coevolution
of these two sets of problems suggest that substance misuse
tends to be secondary to the onset of conduct problems in
impulsive adolescents [33,34,49,110]. By contrast, other dimen-
sions of externalizing personality, such as sensation seeking,
have been shown to be more directly linked to early
onset alcohol misuse, with conduct problems arising after the
onset of binge drinking [110].
Recognizing that impulsivity and its facets exist along a
continuum in the general population, the IMAGEN Research
Consortium designed a longitudinal study to assess the role
of different facets of impulsivity and reward-related beha-
viours in the emergence of psychopathological symptoms
in a large sample of European adolescents (n¼2200).
Among the numerous studies from this consortium, three
studies directly test how facets of impulsivity are implicated
in different psychiatric outcomes [12,13,70]. Importantly,
these studies first represented psychiatric symptoms and
their comorbidity by deriving transdiagnostic latent dimen-
sions (represented in figure 1) using structural equation
modelling, which confirmed results from other similar studies
on the structure of psychopathology [14]. The IMAGEN
studies then showed that self-report, neurocognitive and
5 Phil. Trans. R. Soc. B 374: 20180137
functional neuroimaging measures of impulsivity and its
facets naturally dissociated along these dimensions of psycho-
pathology: variance common to all externalizing symptoms
(including substance use) was related to self-report impulsivity
and delay discounting. Variance specific to ADHD and Con-
duct Disorder symptoms was related to behavioural and
functional brain imaging measures of stopping behaviour on
go/no-go tasks of motor/action impulsivity, and variance
specific to early onset alcohol misuse was specifically related
to trait thrill seeking (SURPS-SS) and brain functional activity
during reward anticipation [12,13]. This study demonstrated
that neurocognitive and functional neuroimaging measures
provide additional specificity with respect to dissociating
latent dimensions of psychopathology that could not be fully
dissociated using self-report measures. In line with the emer-
ging evidence reviewed in figure 1, we place neurocognitive
facets as intermediary variables between self-report measures
and latent dimensions of psychopathology to demonstrate
where diagnostic specificity might be achieved.
6. Impulsivities and substance-specific addiction
Mounting evidence from the voluminous research on impul-
sivity over the past 20 years reveals that the multidimensional
conceptualization of impulsivity is relevant to prediction and
diagnosis of important addiction profiles that differ not only
on patterns of comorbid psychopathology, but also with
respect to specific class of substance of abuse.
Numerous studies show that in addition to general
liability to SUDs, substance-specific liability accounts for a
significant portion of the variance in substance-related beha-
viours and problems [12,13,111]. Merikangas and colleagues
[112] reveal substantial drug specificity in the type of drugs
abused by individuals with dependence on a range of illicit
drugs and the type of drugs abused by their relatives, with
opiates exhibiting the highest degree of specificity relative
to cocaine, cannabis, and alcohol. Similarly, there are key
differences between different classes of drugs with regards
to common versus drug-specific genetic variance, indicating
that, despite evidence for shared vulnerability factor that
underlies the misuse of marijuana, sedatives, stimulants,
heroin/opiates, and psychedelics, there are marked differ-
ences in the extent to which different classes of drugs are
influenced by shared vulnerability [113]. For instance,
heroin has larger genetic influences unique to itself than
any other drug, whereas most of the genetic influences on
marijuana, stimulants, and sedative abuse are shared across
drugs. Shared and specific environmental influences likely
cause further dissociation in patterns of drug use.
When investigating the substance-specificity of different
dimensions of impulsivity, it would be important to control
for the general liability towards substance use (and potentially
the role of impulsivity in that overall liability), and examine
whether specific dimensions of impulsivity predict more
specific behaviours and drug preferences. After accounting
for the general drug use vulnerability, personality traits can
predict which substances an individual is most likely to use
more regularly or problematically in the context of polysub-
stance use. Analyses on adult substance users, heavy
substance using college students, and high school students
all indicate that self-report measures of trait impulsivity and
sensation seeking discriminate between substance users who
are prone to stimulant versus alcohol misuse, respectively
[32,33,38,114]. Trait impulsiveness has been associated with
deficits in response inhibition/impulsive action, which predict
a pattern of substance misuse that co-occurs with other exter-
nalizing symptoms more generally, and with conduct disorder
symptoms specifically [34]. In contrast, trait sensation seeking
has been associated with reward response bias/impulsive
choice, which uniquely predicted binge drinking [34].
Interestingly, these two facets of trait impulsivity also predict
self-report motives for substance use that map onto these
different neurocognitive patterns: sensation seeking youth
reported using alcohol for enhancement reasons, while impul-
sive youth reported a motivationally-undefined pattern of use
and drinking, but were particularly at risk of misusing stimu-
lants [32]. These findings on different self-report drinking
motives have been replicated in college students and in adult
inpatient polysubstance users [38,115].
Similarly, a recent study with a community sample of
mono-dependent opiate and stimulant users who were in pro-
tracted abstinence revealed that only externalizing traits such
as impulsivity and sensation seeking discriminate between
substance-dependent individuals and non-dependent controls,
whereas internalizing traits such as hopelessness and anxiety
sensitivity do not [116]. Another study investigating the role
of personality traits in differentiating patterns of substance
misuse showed that among opioid-dependent individuals
receiving opioid substitution therapy, self-report personality
factors predicted who is likely to report illicit drug misuse
during such treatment and what type of substance they are
likely to misuse: sensation seeking predicted cannabis use,
hopelessness predicted prescription opioid misuse, anxiety
sensitivity predicted prescription sedative misuse and impul-
sivity predicted injection drug use [117]. According to the
framework presented in figure 1, some studies suggest that
opioid dependence is predicted by the callous/unemotional
factor of psychopathy (psychopathy 2) and internalizing
traits such as depression and anxiety [38,118], whereas stimu-
lant dependence is predicted by externalizing traits,
particularly impulsiveness [32] and disinhibited/impatient
sensation seeking [118], which, according to [31], likely reflects
delay discounting/impatient sensation seeking.
With regards to neurocognitive measures of impulsivity,
some neurocognitive deficits are associated with a general
tendency towards substance misuse [68]. Indeed, reliable
impairments have been documented on both impulsive
choice [66,107,119122] and impulsive action tasks
[123128] across a number of different drug classes. Yet,
because specific drugs of abuse also differentially affect
specific cognitive and motivational brain systems, many
have hypothesized that specific neurocognitive profiles
should be linked to misuse of specific classes of substances
of abuse with distinct pharmacological properties [11], for
which there is empirical support from animal studies (e.g.
[129,130]). Studies that have accounted for overall patterns
of substance use and then examined the relationship between
specific facets of impulsivity and specific patterns of sub-
stance use demonstrate substance-specific relationships
[32,117,131], reflected in figure 1, with all substances of
abuse loading on a general Pfactor (strongly related to
delay discounting [31]) and then personality-specific neuro-
cognitively-mediated trajectories that are either primarily
associated with specific substance use or secondarily
6 Phil. Trans. R. Soc. B 374: 20180137
associated through other psychopathological symptoms
(thick blue arrows).
Research designs that have attempted to more closely
examine this question have used adolescent cohort designs to
observe the role of personality in predicting drug-specific pat-
terns of use before the onset of substance dependence. Such
studies similarly show that trait impulsivity but not trait sen-
sation seeking predict stimulant prescription drug misuse,
while other more internalizing traits predict misuse of prescrip-
tion drugs with more sedative andanalgesic properties [32,49],
secondarily through psychiatric symptoms.
Using a functional neuroimaging approach to the study of
impulsivity and its multifaceted nature, Whelan and colleagues
[70] used data from the IMAGEN cohort of 2200 14-year-olds to
link facets of action impulsivity, represented by distinct brain
activation patterns during stopping, failed inhibition, and
response to feedback, to different drug use patterns. General
resilience to drug use was related to greater activation patterns
in bilateral frontal regions during stopping, while frequent
polysubstance use was associated with greater activity in the
supplementary motor area and reduced activity in a right
frontal region during stopping. Using this same dataset, Castel-
lanos-Ryan et al. [13] examined the extent to which different
substance use profiles were concurrently and longitudinally
predicted by these same functional activity patterns during
the stop task along with functional activity patterns on a
reward anticipation task of reward sensitivity and a number
of relevant neurocognitive measures. Cortical and subcortical
brain activity patterns during stopping behaviour predicted
general susceptibility to drug use and other externalizing psy-
chopathology, whereas activity patterns during reward
anticipation predicted substance-specific behaviours, particu-
larly alcohol-related behaviours. Delay discounting related to
general substance use vulnerability, whereas reduced prefron-
tal cortical activity during failed stopping behaviour and errors
of commission on a go/no-go task of impulsive action pre-
dicted conduct problems and ADHD. Other multi-site studies
involving brain and behavioural measures during neurocogni-
tive tasks of impulsivity suggest not only that impulsivity
dimensions predict future risk for substance misuse, but also
that early onset substance misuse further impacts the develop-
ment of these neurocognitive domains during adolescence and
that there might be important substance-specific effects on
certain neurocognitive functions [71,74].
A recent multi-site study investigated this question in adults
at the level of brain structure by mega-pooling structural
neuroimaging studies comparing participants with current
dependenceon at least one of five substances (alcohol,nicotine,
cocaine, methamphetamine, or cannabis) to age-, sex- and site-
matched controls [132]. This study revealed lower volume or
thickness across many brain regions in substance-dependent
individuals relative to non-dependent participants. Some of
these differences were general and affected by all substances,
whereas others were substance-specific. Structures related to
substance dependence in general, regardless of drug class,
included the insula and the medial orbitofrontal cortex,
associated with disadvantageous choices on reward- based
decision-making tasks of impulsive choice [76]. Alcohol
was associated with the most pervasive, yet specific effects,
which were particularly robust in subcortical regions, such
as the hippocampus, amygdala, and nucleus accumbens,
a region centrally implicated in reward processing.
Surprisingly, nicotine, cannabis, and methamphetamine
dependence did not have any substance-specific relation-
ships to brain volume, but that is not to say that other
imaging modalities such as task-based functional MRI might
not be more sensitive to subtle functional differences that are
not detectable at a structurallevel. Notably, opioid dependence
was not investigated, which is in line with a general trend in the
literature that has provided considerably less research attention
to opioid addiction relative to other drugs [133].
A few more recent studies have begun to compare the neu-
robehavioural performance of stimulant users with that of
opiate users on performance-based measures of impulsive
choice and impulsive action. Results generally indicate that
stimulant users show higher neurocognitive impulsivity than
opiate users [66,68,122,134–136]. However, virtually all of
these studies have been based on polysubstance users, which
significantly complicates the study of drug-specific effects
and represents one of the most formidable methodological
challenges for the study of the unique effectsof different classes
of drugs in humans. Polysubstance use may explain some key
inconsistencies between clinical and preclinical studies on
addiction, as the majority of clinical studies are based on poly-
substance using patterns, whereas the preclinical literature is
largely based on single drug administration.
An interesting research design that helps elucidate the
unique effects of specific classes of drugs while circumventing
the problem of polysubstance use in human studies involves
comparisons between unique populations of ‘pure’ substance
users who are mono-dependent on different classes of drugs
(e.g. [83,106,107,118,137– 139]). Such studies have revealed
that mono-dependent heroin and amphetamine users display
opposite relationships between trait and neurocognitive dimen-
sions of impulsivity. Specifically, in amphetamine users high
composite score on trait impulsivity (derived by factor analysis
and likely reflecting the higher-order construct) was associated
with poor response inhibition (motor/action impulsivity),
whereas in heroin users high trait impulsivity was associated
with intact response inhibition [137]. Further, a computational
modelling study of impulsive choice in ‘pure’ heroin and
amphetamine users using the Iowa Gambling Task revealed
that decision-making deficits in opiate and stimulant users are
driven by different underlying mechanisms, namely by
reduced loss aversion in opiate users versus increased reward
sensitivity in stimulant users [83]. A more recent study [118]
used machine-learning approaches to examine the predictive
utility of 54 personality, psychiatric, and neurocognitive indices
of impulsivity and related constructs to differentiate heroin and
amphetamine dependence. The study identified distinct sub-
stance-specific multivariate risk profiles that classified heroin
and amphetamine dependence in new samples with high
degree of accuracy (heroin AUC (area under the receiver-
operating characteristic (ROC) curve) 0.87, amphetamine
AUC 0.74). Amphetamine dependence was (uniquely) pre-
dicted by higher impulsive sensation seeking (disinhibition
and excitement seeking) and higher hostility, whereas heroin
dependence was uniquely predicted by lower sensation seek-
ing, lower trait motor impulsivity, higher negative urgency,
higher callous/unemotional levels of psychopathy, and
higher depression and trait anxiety. From the neurocognitive
measures of impulsivity, higher delay discounting and longer
decision-making deliberation time predicted amphetamine
dependence. In contrast, heroin dependence was predicted by
higher delay aversion, lower risk-taking, and impaired
decision-making on choice impulsivity tasks. Out of 54
7 Phil. Trans. R. Soc. B 374: 20180137
predictors, the antisocial/impulsive facet of psychopathy was
the only common predictor of both heroin and amphetamine
dependence. A parallel study [140] used a similar machine-
learning approach to predict current cocaine dependence and
found analogous findings, which classified out-of-sample
cocaine dependence with even higher degree of accuracy
(AUC 0.91). These findings suggest that quick, economical,
and easy to administer behavioural measures of impulsiv-
ity can serve as objective behavioural markers of distinct
addiction risk profiles, which may facilitate the develop-
ment of reliable and cost-effective risk assessment
batteries and targeted interventions.
Recognizing the highly heritable nature of addiction
vulnerability, many studies have investigated the extent to
which personality and neurocognitive dimensions of impul-
sivity might represent putative endophenotypes for
addiction. From the multiple neurocognitive dimensions of
impulsivity, delay discounting has received the strongest
support as a candidate endophenotype for SUDs [120,141],
though it is also a candidate marker for a number of exter-
nalizing disorders [80,120] and general psychopathology
[12]. The first genome-wide association study (GWAS) of
delay discounting [142] revealed that the most significant
association was with a gene implicated in the internalization
of the serotonin transporter. Recent GWAS studies of trait
impulsivity and sensation seeking [54,143] revealed that
these traits are genetically distinct, which further supports
their conceptual separation. These findings are consistent
with twin and sibling-pairs design studies reporting evi-
dence for potential substance-specificity of different trait
and state markers. For example, trait impulsiveness
(measured with the Barratt Impulsiveness Scale-11 [26])
appears to be a putative endophenotype for stimulant
dependence, as indicated by significant correlations
between sibling-pairs of stimulant-dependent individuals
and their biological non-dependent siblings [43,144]. In con-
trast, sensation seeking (measured with the Sensation
Seeking Scale—Form V [24]) was specific for sibling-pairs
discordant for heroin dependence [144]. ADHD [145] and
anxiety sensitivity [146] were specific to sibling-pairs discor-
dant for amphetamine dependence, whereas hopelessness
(measured with the Substance Use Risk Profile Scale [32])
was specific to sibling-pairs discordant for heroin depen-
dence [144], suggesting that these traits are specifically
implicated as endophenotypes, and not consequences, of
drug use. Finally, neurocognitive indices of impulsive
choice were common to both opiate and stimulant sib-
pairs (general risk), whereas an index of impulsive action,
go/no-go commission errors, was specific to amphetamine
sibling-pairs (substance-specific risk linked to ADHD) [144].
These substance-specific phenotypic associations suggest that
certain endophenotypic markers may be common across
addictions, whereas others may be specific to risk for
dependence on specific classes of drugs.
7. Impulsivities as novel diagnostic and
prognostic tools for addictions
One of the key problems in addictive disorders is their aetio-
logical and functional heterogeneity, which is not well
captured by the current psychiatric nosology, despite revolu-
tionary advances in understanding the neurobiology of
addiction. Integrating neuroscience and computationally-
based assessments with self-report trait assessments may
transform the diagnosis and classification of addictive dis-
orders and lead to better targeted and more effective
prevention and intervention approaches. To address the futi-
lity of DSM criteria to address the heterogeneity of DSM
diagnostic categories, the US National Institute of Mental
Health (NIMH) launched the Research Domain Criteria
(RDoC) [147] as an attempt to determine if a novel way of
classifying mental illness based on neurobiology, observable
behaviour, and context will be useful for diagnosing mental
disorders. The recently proposed heuristic framework for
neuroclinical assessment of addictions (Addictions Neurocli-
nical Assessment, ANA) [9] is a modified version of the
RDoC criteria adapted specifically for the assessment of
addictions. The ANA framework posits that in order to
better understand the different aetiological mechanisms
implicated in various forms of addictions, their assessment
should be multidimensional and combine clinical, personal-
ity, neurocognitive, neuroimaging and genetic approaches
that focus on three key neurofunctional domains associated
with impulsivity and compulsivity: executive function, incen-
tive salience, and negative emotionality. Another recent
conceptual framework that derived from the European con-
text focuses on variance that is unique to SUDs (chronic
and elevated patterns of consumption) in an attempt to
steer clear of psychopathological constructs and potentially
stigmatizing terms when addressing harm from substances,
but recommends a similar framework when referring to risk
for SUDs [148].
tric conceptualizations of addition (e.g. [149]), all of which
recommend more refined approaches to phenotyping, to
accurately and efficiently capture the hierarchical and
multidimensional nature of addiction vulnerability, par-
ticularly around brain processes linked to impulsivity,
compulsivity, and positive and negative emotionality
[9,149]. Consistent with other reviews, we recommend
incorporating self-report trait measures, as well as neuro-
cognitive state measures that include both the standard
neurobehavioural performance indices as well as compu-
tational indices that hold promise as novel phenotyping
tools. Unlike these other reviews, we also suggest that
such a multidimensional framework will further inform
patterns of comorbidity and specific patterns of substance
misuse vulnerability. Despite its complexity relative to the
very simple task of assessing severity of substance use (e.g.
the World Health Organisation’s Alcohol Use Disorder
Identification Test [150]), assessment time and burden
could be reduced significantly through adaptive design
optimization [75,151], which may facilitate the develop-
ment of ‘smart’ assessment batteries, composed of brief,
targeted, and accurate multivariate assessment modules
that may improve the precision around underlying
motivational processes driving the behaviour and
personalized treatment options.
Within this context, motor/action impulsivity and cogni-
tive/choice impulsivity, best captured by a combination of
self-report, neurocognitive, and computational measures,
seem to provide important discriminant and predictive val-
idity with respect to predicting or explaining dissociable
substance misuse and concurrent psychiatric symptom
dimensions. Measures of motor/action impulsivity appear
8 Phil. Trans. R. Soc. B 374: 20180137
to be useful in differentiating between individuals who might
be prone to a primary disorder of ADHD and Conduct Dis-
order (including ASPD) as well as stimulant dependence,
whereas differential responses to reward-based impulsive
choice tasks might help identify individuals who are differen-
tially susceptible to alcohol (risk sensitivity), or opiate
dependence (loss insensitivity). Other reviews focus more
attention on the progression of addiction and the impact of
substances of abuse on these brain processes (see [149]).
This distinction might further explain why reward sensitivity
is not predictive of risk for stimulant drug use but seems to
characterize stimulant drug users with a history of dependence
(e.g. [83,118,140]).
Conceptualizing individuals prone to high levels of
comorbidity across substance use and psychiatric disorders
as having transdiagnostic impairments on specific trait or
state dimensions of impulsivity might save clinicians time
in pursuing diagnostic specificity, which often delays treat-
ment and contributes to the revolving door between
addiction and mental health services for such patients. One
important outstanding question is whether treatment plan-
ning in accordance with this framework will lead to better
outcomes for individuals with SUDs. New evidence indicates
this is a promising approach.
8. Impulsivities: novel behavioural targets for
prevention and treatment of substance use
Researchers in the field have begun to address the question
about the extent to which different dimensions of impulsiv-
ity are modifiable by various psychosocial, pharmacological
and neurocognitive interventions. A number of psycho-
social interventions could now be considered helpful tools
in the management of impulsivity. For example, contin-
gency management is used to reduce delay discounting
around abstinence, cognitive-behavioural interventions are
used to help patients better manage positive and negative
urgency states in high-risk situations (e.g. relapse preven-
tion), and mindfulness-based approaches are hypothesized
to reduce negative urgency by reducing stress and rebalan-
cing fronto-striatal connectivity [152]. However, few
interventions directly arise from current research on impul-
sivity and even fewer targeted interventions have been
shown to reduce impulsivity [153].
One such personality-targeted cognitive-behavioural
approach involves modifying traditional cognitive-behaviour
therapy (CBT) strategies to target individual differences in
trait impulsivity. This programme, known as the Preventure
Programme (see [154]), uses the CBT framework to help
high-risk youth understand how individual differences in
trait impulsivity and response inhibition affect behavioural
and emotional control and decision making. Cognitive-
behavioural interventions are adapted to help impulsive
youth become better ‘stoppers’ by helping them to identify
high-risk situations and the interoceptive cues that precede
an impulsive action. They are also given cognitive strategies
to help them be more cognizant of the ‘stopping’ process
and the cognitive processes required for better stopping
(e.g. attentiveness, self-talk, goal-orientation). When deliv-
ered to adolescents with elevated scores on self-report
measures of impulsiveness, measured with the Substance
Use Risk Profile Scale (SURPS) [32], the intervention is
shown to produce long-term changes in theoretically pre-
dicted ways: substance use onset is delayed [114,155],
conduct symptoms are reduced and/or prevented [156],
and reductions in self-report levels of impulsivity specifically
mediate long-term changes in these behaviours [157]. The
Preventure Programme also includes a second intervention
targeting sensation seeking by using a different set of cogni-
tive strategies focused on managing reward sensitivity and
reward-driven behaviours. This second intervention has
been shown to produce robust effects on binge drinking
[154] and cannabis use outcomes [51], without having a sig-
nificant impact on conduct problems, aggressive behaviours
or impulsivity, suggesting some treatment specificity in per-
sonality-targeted CBT interventions. It remains to be
determined if these interventions produce changes in neuro-
cognitive measures of impulsivity, and whether these
changes mediate long-term behavioural changes [11].
Other novel therapeutic approaches target neurocognitive
dimensions of impulsivity. Some of the most promising
approaches in this area are based on behavioural economic
principles and dual-system models of decision-making that
involve executive and impulsive decision systems [158,159].
Increased delay discounting reflects greater control of the
impulsive over the executive decision system and character-
izes reinforcement pathologies, such as SUDs [160]. Delay
discounting has recently been considered a genetically-influ-
enced target for drug abuse prevention [161]. Therapeutic
approaches based on dual system models use computerized
working memory training and episodic future thinking to
modify delay discounting and expand the constricted
temporal horizon characterizing the addictive state [162].
Such training has the strongest effects in substance-dependent
individuals who display the steepest delay discounting [163].
According to this review, such interventions hold promise
for reducing risk for substance misuse and psychopathologi-
cal symptoms generally. A number of other neurocognitive
intervention strategies also show promise as adjunct treat-
ment for addictions. For example, response inhibition and
working memory training have been found to curb impulsive
drinking in problem drinkers, particularly in individuals who
score low on these functions [164– 166]. Cognitive bias modi-
fication has also shown promise in the treatment of
addictions and other forms of psychopathology [167]. Neuro-
cognitive measures of impulsivity might be more suitable
than trait measures for use in tracking treatment effects and
outcomes, owing to their state-dependent nature. For
example, excessive delay discounting predicts initiation of
drug use, improves with treatment, and returns within the
normal range with abstinence [141].
Another promising intervention approach stemming from
the neurocognitive understanding of impulsivity is the use of
repetitive Transcranial Magnetic Stimulation (TMS), which is
a non-invasive, and safe, human brain stimulation technol-
ogy based on electromagnetic induction [168] used to
depolarize brain neurons [169]. Repetitive high-frequency
(5 Hz) TMS can modulate long-term cortical excitability,
repetitive TMS (rTMS) at a low frequency (about 1 Hz) pro-
duces inhibitory effects on neurons. Systematic reviews
suggest that excitatory rTMS produces distinct effects on
different impulsivity subdomains: small-to-moderate effects
on response inhibition/impulsive action and moderate effects
9 Phil. Trans. R. Soc. B 374: 20180137
on delay discounting/choice impulsivity [170]. Whether
these effects translate to changes in substance use behaviour
is less well investigated, but it has been suggested that rTMS
might produce small reductions in some relevant addiction
outcomes, such as impulsivity [151] and craving [171].
There is also evidence that combining the excitatory and
inhibitory effects of rTMS in relation to different environ-
mental stimuli (e.g. drug versus natural reward cues) can
reverse the reward sensitivity resulting from neurophysiolo-
gical changes from repeated drug exposure [172]. What has
yet to be investigated is whether these effects are mediated
by changes in impulsivity or subdomains of impulsivity as
outlined in this review.
Finally, considering that some reviews suggest that meta-
cognitive executive function training for externalizing
problems is effective when combined with supervised coach-
ing with parents [173], more studies are needed in which
modular combinations of neurocognitive and cognitive-
behavioural interventions are evaluated and tested. There is
an unexplored therapeutic potential of integrating personal-
ity with neurocognitive and other intervention modules,
based on individual risk factors, which may optimize the
precision and efficacy of targeted intervention approaches
for addictions.
Data accessibility. This article has no additional data.
Competing interests. We declare we have no competing interests.
Funding. This study was supported by the Institute of Neurosciences,
Mental Health and Addiction (frn114887 and frn126053), by the
National Institute on Drug Abuse (NIDA) and the Fogarty Inter-
national Center at NIH under award number R01DA021421 to
Jasmin Vassileva, by a Canada Research Chair awarded to Patricia
Conrod, and by a Canadian Health Research Institutes Project
Grant (FRN 126053).
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