Drug and Alcohol Dependence 59 Suppl. 1 (2000) S9 – S21
www.elsevier.com/locate/drugalcdep
Review
Current models of nicotine dependence: what is known and what
is needed to advance understanding of tobacco etiology among
youth
William G. Shadel a,*, Saul Shiffman b, Raymond Niaura a, Mark Nichter c,
David B. Abrams a
a
Brown Uni6ersity Center for Beha6ioral and Pre6enti6e Medicine, The Miriam Hospital, 164 Summit A6enue, Pro6idence, RI 02906, USA
b
Uni6ersity of Pittsburgh, Pittsburgh, USA
c
Uni6ersity of Arizona, Tucson, AZ, USA
Contents
1. Introductory remarks: the problem of youth smoking . . . . . . . . . . . . . . . . . . . . . . .
S10
2. Conceptual framework and organizational structure . . . . . . . . . . . . . . . . . . . . . . . .
S10
3. Features of substance dependence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1. Dependence producing substances have dose-dependent psychoactive effects . . . . . . .
3.2. Dependence producing substances act as positive reinforcers . . . . . . . . . . . . . . . .
3.3. Repeated exposures to a substance are necessary for dependence to develop. . . . . . .
3.4. Tolerance develops to the effects of dependence producing substances . . . . . . . . . .
3.5. Withdrawal symptoms appear upon cessation of dependence producing substance . . .
3.6. Cravings characterize dependence and motivate substance use . . . . . . . . . . . . . . .
3.7. Compulsive use is a behavioral marker of dependence . . . . . . . . . . . . . . . . . . .
3.8. Dependent users become ambivalent about their substance use . . . . . . . . . . . . . .
3.9. Dependence is a chronic condition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.10. Dependence producing substances can be used to manage stress and emotional upset
3.11. Comment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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S11
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S12
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S13
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S14
S14
4. Models of dependence . . . . . . . . . . . .
4.1. Neurobiological models . . . . . . . .
4.2. Classic learning models . . . . . . . .
4.3. Cognitive social learning models . . .
4.4. Social factors influencing dependence
4.5. Cultural contexts for dependence . . .
4.6. Comment . . . . . . . . . . . . . . . .
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5. Concluding remarks: a proposed research agenda . . . . . . . . . . . . . . . . . . . . . . . . . .
S18
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S19
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S19
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* Corresponding author. Tel.: +1-401-7933769; fax: + 1-401-3312453.
E-mail address: william – [email protected] (W.G. Shadel)
0376-8716/00/$ - see front matter © 2000 Elsevier Science Ireland Ltd. All rights reserved.
PII: S 0 3 7 6 - 8 7 1 6 ( 9 9 ) 0 0 1 6 2 - 3
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S10
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
Abstract
Youth smoking has risen dramatically during the last 5 years, leading one to the conclusion that prevention interventions have
not been particularly effective. This paper provides an examination of features that define adult nicotine dependence and argues
that these features need to be considered in any studied examination of youth etiology and development to nicotine dependence.
We review the historical context for the concept of nicotine dependence, features that define the concept and current models of
substance dependence more generally. Recommendations for future research are provided. © 2000 Elsevier Science Ireland Ltd.
All rights reserved.
Keywords: Adolescent; Children; Nicotine dependence; Etiology; Prevention; Tobacco
1. Introductory remarks: the problem of youth smoking
The majority of youth experiment with tobacco and
nicotine-containing products and over 25% of these
individuals proceed to regular tobacco usage as adults
(Escobedo et al., 1997; Giovino, 1997). After years of
decline, it is now apparent that smoking initiation is
rising dramatically among adolescents in the United
States (CDC, 1994, 1998) and throughout the world
(Winder et al., 1994; Villalbi, 1995; WHO, 1999).
Recent projections suggest that of the adolescents who
become regular smokers, nearly one-third will eventually die from a smoking related disease (CDC, 1996;
WHO, 1999). Clearly, then, tobacco use is among the
most serious of all pediatric health problems and is a
significant public health concern (Kessler et al., 1996)
that will have severe negative consequences for the
public health of the future (WHO, 1999).
Interventions designed to prevent youth adoption
and progression to tobacco dependence, on balance,
have not been particularly effective, whether in the
United States (Lichtenstein, 1997) or other parts of the
world (Van Wel and Knobbout, 1998; Bruce and van
Teijlingen, 1999). This lack of impact is due, in part,
to lack of knowledge about mechanisms that contribute
to youth initiation of cigarette smoking and the progression to regular usage in adulthood (Lichtenstein,
1997). In order to inform the next generation of tobacco prevention and cessation interventions, then, we
need to understand a great deal more about the mechanisms that regulate the etiology of youth tobacco
initiation and progression from occasional to regular
use of tobacco products (Abrams et al., 1991; Shiffman,
1993; Henningfield, 1997).
Nicotine is the major dependence producing agent in
tobacco products (USDHHS, 1988; Stolerman and
Jarvis, 1995) and nicotine dependence is widely regarded as one of the core elements which makes quitting smoking difficult (USDHHS, 1988). However, the
theoretical concept of nicotine dependence has not been
well studied among youth. A particular focus on
nicotine dependence, therefore, is a logical starting
point for advancing our understanding of what we
know and what we need to know about the etiology of
tobacco use, and ultimately, how to best inform the
next generation of prevention and cessation interventions for youth. The purpose of this essay is to review
current thinking and conceptions of substance dependence and to evaluate those conceptions with an eye
toward shaping definitions and conceptions of nicotine
dependence to better understand the etiology of youth
tobacco use.
2. Conceptual framework and organizational structure
The desired use of a concept will ultimately determine the manner in which it is defined (Garfinkel,
1981). By necessity, then, our first task in exploring the
theoretical concept of dependence is to ask what we
would like the concept to do for us. At the most basic
levels, we are interested in answering the following
questions:
1. What constitutes nicotine dependence?
2. How does nicotine dependence develop?
3. Who becomes nicotine dependent? and
4. Where does nicotine dependence lead?
In order to address the first two questions, our essay
will have a descriptive component (‘What’?) and be
developmentally relevant (‘How?’). The latter two questions are more difficult to answer for youth, however.
Rather than provide answers to these questions, then,
we will pose additional questions that may help to
identify high risk groups (‘Who?’) and to predict consequences of dependence for youth (‘Where?’).
As a starting point for our discussion, the concept of
dependence will be viewed as a syndrome (Edwards and
Gross, 1976; Hodgeson and Stockwell, 1985; APA,
1994), that is, a hypothetical construct designed to
summarize various behavioral and physiological
changes that occur when an individual uses substances
that have abuse liabilities. The syndromal conception
suggests that dependence is best viewed as a construct
summarized or indexed by combinations of symptoms
and behaviors. We will refer to these symptoms and
behaviors as features (Table 1), each with varying levels
of intensity and importance (WHO, 1964; Edwards and
Gross, 1976). The first section of our review will identify and define the features of substance depen-
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
dence more generally with an eye toward describing
nicotine dependence specifically. It is important to recognize that our choice of the term ‘feature’ was deliberate. This term is designed to underscore the notion
that a ‘transdisciplinary’ consensus (Abrams, 1999) exists which supports the existence of these features as
indices of a multidimensional construct that can be
labelled dependence.
We move from this descriptive phase to a hierarchical analysis of theoretical perspectives that have addressed dependence. Key differences emerge when we
consider the role that each feature plays within specific
theoretical models of dependence. Some models emphasize certain features over others, some relegate certain features to peripheral roles and favor other
features as causally central mechanisms of dependence,
and still other models nearly neglect features as
epiphenomena. However, if these models are analyzed
in a hierarchical fashion, the conceptual picture of
dependence becomes complementary and comprehensive. The second section of the essay places the features in several theoretical contexts in order to
illustrate the manner in which they work dynamically
together to index substance dependence. The theoretical models are presented within a framework of hierarchical levels of analysis in order to demonstrate
that seemingly disparate conceptions of dependence
are actually quite complementary. To this end, the
theories are presented in relatively ‘pure’ form to make
them as distinct from one another as possible. Extensive integrated reviews are available and the interested
reader is directed to these resources (Koob, 1997; Stolerman, 1997).
At the present time, we cannot readily answer for
youth the questions surrounding the identification of
groups at high risk for developing nicotine dependence
and questions about the consequences or implications
of being nicotine dependent. The final section of the
Table 1
Core conceptual features of nicotine dependence
1. Dependence producing substances have dose-dependent
psychoactive effects
2. Dependence producing substances act as positive reinforcers
3. Repeated exposures to a substance are necessary for
dependence to develop
4. Tolerance develops to the effects of dependence producing
substances
5. Withdrawal symptoms appear upon cessation of dependence
producing substances
6. Cravings characterize dependence and motivate substance use
7. Compulsive use is a behavioral marker of dependence
8. Dependent users become ambivalent about their substance use
9. Dependence is a chronic condition
10. Dependence producing substances are used to manage
negative affect and stress
S11
essay will therefore build upon the prior descriptive
and theoretical reviews to detail a series of questions
that may bring us closer to answers for these questions. We outline a research agenda for future prevention and cessation interventions and argue that any
such endeavors should be informed by this conceptual
review.
3. Features of substance dependence
This section reviews the prototypic features of substance dependence and relates these factors to conceptions of nicotine dependence. Several concerns need to
be kept in mind. First, the review is meant to describe
independently each feature as much as possible; we
reserve theoretical analyses of the dynamic relationship
between the features for a later section of this essay.
Second, our review of the literature here, and throughout, is necessarily selective, for the purposes of illustration. Comprehensive reviews are readily available
and the interested reader is directed to these resources
for further information (Tarter et al., 1998). Third, the
review is intentionally written at a moderate level of
complexity in order to facilitate transdisciplinary communication (Abrams, 1999) among persons not typically familiar with certain aspects of dependence.
3.1. Dependence producing substances ha6e
dose-dependent psychoacti6e effects
‘Psychoactivity’ will be used here as a summary
term used to refer to the acute behavioral, cognitive,
emotional, and physiological reactions that an individual experiences in response to use of a substance.
More precisely, psychoactivity can be viewed as a way
in which to summarize the acute positive and negative
changes in ‘normal’ functioning that are directly attributable to the pharmacological actions of the substance itself (Kaplan and Sadock, 1990). It is generally
seen as a time-limited and reversible phenomenon, and
the level of psychoactivity that results is generally proportional to the amount of the substance that has
been ingested. It can range from mildly euphoric reactions (generally positive) at low doses of the substance
to seriously incapacitating (aversive) reactions at high
doses of the substance (Kaplan and Sadock, 1990).
Nicotine exerts psychopharmacologic effects with a
wide variety of stimulant and depressant effects involving the central and peripheral nervous, cardiovascular,
endocrine, and other systems (USDHHS, 1988). At
standard (i.e. ‘normal’) doses, peripheral nervous system effects include skeletal muscle relaxation (USDHHS, 1988) and central nervous system effects include
electrocortical activation and increases in brain serotonin, endogenous opioid peptides, pituitary hormones,
catecholamines, and vasopressin (Pomerleau and
S12
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
Pomerleau, 1984, 1987; USDHHS, 1988). There is also
an apparent dose-response to these psychopharmacologic effects. Increased doses of nicotine (i.e. overdose)
have been reported to result in a host of symptoms not
normally associated with nicotine in relatively lower or
standard doses, for example, nausea, vomiting, weakness, tremor, and diarrhea (Benowitz, 1988). Taken
together, these findings indicate that nicotine produces
psychoactive effects.
3.2. Dependence producing substances act as positi6e
reinforcers
A positive reinforcer is anything that can be administered to increase the probability that a particular behavior will be repeated when the presentation of the
reinforcer is contingent on the performance of the
behavior. Substances act as positive reinforcers to the
degree that they activate so-called ‘reward systems’ in the
body; in short, substance use behavior is repeated because it is rewarded. Positive reinforcement may be
broken down into two components. A primary reinforcer
is a ‘natural’ reinforcer, rewarding because of the psychopharmacologic action of the reinforcer itself on
certain sections of the central nervous system involved
regulating reward. A secondary reinforcer is not necessarily rewarding due to the pharmacological actions of
the substance, but is rewarding as a consequence of
learning after repeated substance use. In either case, the
more quickly a reinforcer follows a specific act, the more
likely that act is to be repeated.
Recent research has focussed on the pharmacologic
actions that substances have on dopamine circuitry in the
central nervous system, circuitry that is thought to be
involved in the regulation of reward (Wise and Bozarth,
1987; Spyraki, 1988). The reinforcing properties of
nicotine may be related, in part, to nicotine’s moderating
effects on dopaminergic activity in the mesolimbic system
(Fuxe et al., 1987; Pert and Clarke, 1987; USDHHS,
1988; Clarke, 1990; Pich et al., 1997). One of the more
well-articulated pathways begins in the ventral tegmental
area, moves through the nucleus accumbens, and ends in
the prefrontal cortex (Wise and Bozarth, 1987). These
areas in particular are replete with dopamine receptors
(Wise and Bozarth, 1987). When these receptors are
stimulated (i.e. by dependence producing substances),
increased levels of dopaminergic activity, and thus,
reward, follow. With repeated use (and continued activation of dopaminergic pathways), the potential of the
substance to produce dependence may increase (Koob,
1992; Bozarth, 1994).
Nicotine is a potent reinforcer (Goldberg et al., 1981;
Corrigall and Coen, 1989; Stolerman and Jarvis, 1995).
Nicotine is readily absorbed from tobacco smoke in the
lungs (USDHHS, 1988) and rapidly accumulates in the
brain after cigarette smoking. It may take as little as 10
s for nicotine to reach the brain (USDHHS, 1988) and
significant brain nicotine concentrations may be reached
within 1 min of inhalation (i.e. bolus level; USDHHS,
1988). Repeated smoking throughout the day brings
blood nicotine concentrations to a plateau within 6–8 h
(Benowitz et al., 1982). Thus, nicotine smoked from
cigarettes reaches the brain extremely quickly and therefore serves to activate reward systems within only a few
seconds of use. It follows, then, that the behaviors
associated with cigarette smoking (e.g. striking a match,
lighting the cigarette, hand-to-mouth actions) are quickly
reinforced, and likely to be repeated.
3.3. Repeated exposures to a substance are necessary
for dependence to de6elop
Although the body is readily prepared to ‘accept’
substances — that is the substances bind more or less
easily to neuroreceptors in the body — there does not
appear to be a pre-existing condition or quality of the
organism per se that leads to immediate substance
dependence upon a single administration. Rather, multiple exposures seem to be necessary in order for use to
cross from intermittent to necessary and constant (Koob,
1992; Ouellette and Wood, 1998). In other words,
dependence develops over the course of many administration trials.
Repetitive use is among the most striking characteristics of cigarette smoking. In fact, cigarette smoking
develops into a behavior that is repeated with a regularity
that is unequalled by other substances of abuse. Because
smoking is possible throughout the day and because the
effects of nicotine are rapid but short-lived, smoking is
frequent: the average smoker in the United States — at
a pack a day — smokes more than 7000 cigarettes a year,
or more than 85 000 puffs a year. Even though smoking
patterns can vary within individuals over time (Shadel et
al., 2000), the number of cigarettes smoked per day
generally increases steadily over years of smoking (Chassin et al., 1996). Clearly, then, multiple exposures to
nicotine are easily achieved with cigarette smoking within
a relatively short period of time.
3.4. Tolerance de6elops to the effects of dependence
producing substances
Tolerance can be defined in two related ways: (1)
decreased reactivity, both physical and psychological, to
the same dose of a substance over time; or (2) the need
for a larger dose of the substance over time to achieve
the same physical and psychological effects. Robust
tolerance effects historically have been found across most
substances of abuse (Steinberg, 1969; Seigal, 1988). If
taken in the same dose over an extended period of time,
substances may cease to have the same reinforcing
effects. The development of tolerance is seen as the
adaptation of the body to the effects of the substance.
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
In general, acute and chronic tolerance develop to
many effects of nicotine (Perkins et al., 1994). The
development of chronic tolerance is thought to contribute to an increase in cigarette consumption, as
individuals smoke more to obtain desired effects of
nicotine over time (Henningfield et al., 1995). Over
repeated smoking trials, smokers generally report decreased subjective effects and lower heart rate reactivity
in response to subsequent cigarettes (Niaura, unpublished data; Russell, 1989; Gilbert and Meliska, 1991).
Tolerance may, in fact, be moderated by the valence of
the subjective output. Tolerance to subjectively felt
pleasant effects is not as strong as for tolerance to
subjectively felt negative effects (Perkins et al., 1994).
3.5. Withdrawal symptoms appear upon cessation of
dependence producing substance
Withdrawal effects can be reliably observed when
organisms are deprived of some substances after a period
of sustained use. In essence, the body becomes accustomed to (i.e. adapts to) continuous use of the substance,
and is cast into an aversive disequilibrium for a short
time, varying in periods of days to weeks, when the
substance is no longer used or administered (Tarter et
al., 1998). These symptoms can be both physical and
subjective (or psychological), and in some cases (e.g.
alcohol), fatal. Withdrawal symptoms can be relieved by
resuming substance use.
The nicotine withdrawal syndrome is well-defined
(Hughes and Hatsukami, 1986; Hughes et al., 1990;
APA, 1994). The syndrome includes irritability, frustration or anger, anxiety, difficulty concentrating, restlessness, decreased heart rate, and increased appetite or
weight gain (APA, 1994). The signs and symptoms of the
nicotine withdrawal syndrome can appear within 2 h
after the last use of tobacco, usually peak between 24
and 48 h after cessation, and last from a few days to a
few weeks (Hughes et al., 1990).
3.6. Cra6ings characterize dependence and moti6ate
substance use
There is general agreement that craving, a general
desire to use a substance, is an important part of
substance use (Pickens and Johanson, 1992). The mechanisms (i.e. biological, cognitive) which contribute to the
rise in cravings are not clear (Niaura et al., 1988; Tiffany,
1990), but cravings are generally regarded as the subjective manifestations of the felt ‘need’ for the substance.
Under conditions of deprivation, persons who smoke
report cravings for cigarettes that generally translate into
smoking and increasing levels of deprivation typically
lead to stronger cravings (Payne et al., 1996). Cravings
for cigarettes are commonly reported as motivators or
precursors to actual use (Marlatt and Gordon, 1985) and
S13
typically are triggered by a variety of internal (emotions,
thoughts) and external (situational) cues (Abrams et al.,
1987; Niaura et al., 1992, 1998; Shiffman et al., 1996).
Cravings reliably predict relapse to cigarettes (Killen and
Fortman, 1997; Shiffman et al., 1997) and precipitate
lapses and slips following abstinence (Shiffman et al.,
1996).
3.7. Compulsi6e use is a beha6ioral marker of
dependence
Not all substance use or substance abuse constitutes
substance dependence (e.g. intermittent use; Shiffman,
1991). Compulsive use is twofold (APA, 1994): (1)
compulsive in a ‘psychological’ sense that the user feels
‘driven’ to use the substance, perhaps even despite
(severe) negative consequences (USDHHS, 1988); and
(2) compulsive in the observable sense that behaviors are
repeatedly executed in order to procure the substance.
The substance becomes an increasingly important and
central part of the user’s life (Falk et al., 1983) — a
behavioral priority — to the exclusion of other behaviors
and activities to the point that negative consequences do
not ‘suppress’ the behavior (USDHHS, 1989).
Cigarette smoking is a compulsive behavior pattern
(Lichtenstein, 1982), whose frequency may be unequalled
by any other substance of abuse (Burton et al., 1990). A
fixed series of rituals (behavioral, cognitive, emotional,
physiological) come to define the process of preparing to
smoke, smoking, and the effects of smoking (Lichtenstein, 1982; Falk et al., 1983). Once learned, the maintenance of smoking behavior requires little effort (Tiffany,
1990) and takes on a quality of uncontrolled use.
3.8. Dependent users become ambi6alent about their
substance use
Substance users come to feel ambivalent towards their
own use. They may desperately want to stop using, but
feel compelled to continue (Orford, 1985). In effect, the
user becomes ambivalent about his or her own use of the
substance, and also about ceasing use of the substance
(Miller and Rollnick, 1991).
Cigarette smokers are no exception. Smokers typically
make multiple attempts to quit (Cohen et al., 1989) for
numerous reasons including decrements to health (CDC,
1994), yet they still will resume smoking despite these
well-known health consequences (USDHHS, 1989; Weinstein, 1998).
3.9. Dependence is a chronic condition
A chronic condition is one that is either constant or
intermittent and long lasting. It is very difficult for the
individual to stop using the substance, despite motiva-
S14
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
tion to not use the substance, external pressures not to
use (e.g. legal), and intensive treatment. The majority of
individuals (perhaps more than 75%) relapse following
a cessation attempt, the majority attempt to stop using
a substance multiple times during the course of their
lives, and even after continued — and perhaps even
lengthy — abstinence, periodic uses of the substance
(‘slips’ or ‘lapses’) can be expected (Hunt et al., 1971;
Marlatt and Gordon, 1985).
The characteristics and patterns of chronic nicotine
use have much in common with the use of other
psychotropic substances (Henningfield, 1984; USDHHS, 1988). Patterns of relapse to smoking after smoking cessation are quite similar to the relapse patterns
noted after treatment for other forms of substance
abuse and dependence (Hunt et al., 1971; Henningfield,
1984; USDHHS, 1988). Despite even the best, most
intensive treatments, the majority of smokers relapse
following a cessation attempt (Law and Teng, 1995).
The features reviewed above are often referred to in
discussions of substance dependence. Indeed, there is a
broad consensus that these features are observed in
dependent individuals, even though the precise picture
of dependence may change from person to person, from
time to time, and from one substance to another.
Nicotine, the main psychoactive ingredient in cigarette
smoke currently known, is associated with these same
features among smokers. Although the constellation of
features may distinguish nicotine dependence from
heroin or cocaine dependence, as they are distinguished
from each other, nicotine dependence is built from the
same blocks, and thus fits in well within the known
structure of substance dependence.
3.10. Dependence producing substances can be used to
manage stress and emotional upset
4. Models of dependence
Stress and negative affect are consistently linked with
increased substance use and onset of use (Newcomb
and Bentler, 1988), and relapse to the substance following a period of abstinence (Monti et al., 1989). Addictive substances are reported to be used in attempts to
provide some measure of stress relief to the habitual
user of the substance (Wills and Shiffman, 1985). The
mechanism of action is probably multifaceted. For
example, some dependence-producing substances act
pharmacologically to stimulate the release in the body
of endogenous opioids, which can be involved in abating stress reactions (Kreek, 1996). Alternatively, use of
the substance may alter cognitive processes in such a
way as to permit the user to focus more directly on
alleviating the source of their stress (e.g. the nicotine in
cigarettes can improve concentration, which may allow
an individual to engage in problem solving strategies
that will have the effect of reducing their stress; Wills
and Shiffman, 1985).
Evidence from both surveys and experimental studies
suggests that smokers smoke more during stressful situations or in situations involving negative mood (USDHHS, 1988). Smokers may smoke more when
confronted with these situations because nicotine consumption may decrease negative affect (USDHHS,
1988). Stress among junior high school students is
predictive of smoking initiation (Mitic et al., 1985), is
associated with increased smoking rates among regular
smokers (Epstein and Perkins, 1988), and is one of the
most commonly reported triggers for relapse (Shiffman,
1982; Bliss et al., 1989). This relationship has been
attributed to the coping value that individuals place on
smoking (Marlatt and Gordon, 1985; Shadel and Mer-
Independently listing and describing the features that
comprise dependence is somewhat of an atheoretical
enterprise; it does not comprise a theory of dependence.
The features represent the phenomenon to be explained
by theory, and theory ties together these seemingly
disparate features. Models of dependence do not typically differ in their acceptance of the existence of the
features. Rather, theories or models of dependence
differ in the emphasis or role they give each feature. In
one theory, a particular feature might be regarded as
fundamental or cardinal, while the others are minor or
epiphenomenal; a competing theory may reverse the
roles. The next section of this essay examines the manner in which these features of dependence are manifest
within the context of five levels of theoretical analysis.
Although each theory generally acknowledges the importance or the others, for the sake of argument and
presentation, our strategy is to present each of the
theories in its ‘pure’ form, that is with as little theoretical or conceptual overlap as possible (cf. Koob, 1997;
Stolerman, 1997).
In reviewing these theories, it is important to keep in
mind that genetics plays a role in influencing facets of
nicotine dependence (Collins, 1991; True et al., 1997).
Genetics do not comprise a separate theory per se, but
rather moderate different facets within each theory. For
example, there is evidence that receptors specific to
regulating reinforcement (Noble, 1998), sensitivity to
the effects of nicotine (Smolen et al., 1994), and individual differences in behavioral descriptors measured using
questionnaires (Gilbert and Gilbert, 1995) all have a
heritable component. Thus, while it is beyond the scope
of the present manuscript to review the important role
melstein, 1993) and also to the hypothesized anxiolytic
properties of nicotine (Gilbert et al., 1989).
3.11. Comment
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
of genetics in nicotine dependence (Collins, 1991; True
et al., 1997), any theory of dependence needs to consider
the role of a genetic influence in defining the construct.
4.1. Neurobiological models
Neurobiological models, as a group, emphasize the
direct effects of substances on the nervous system.
Several neurobiological models have been developed.
We review two classes of these theories below, a more
traditional theoretical perspective and a less well-known
perspective, to provide breadth to the discussion. It is
beyond the scope of this essay to provide in depth
coverage of these many models; the interested reader is
directed elsewhere (Clarke, 1990; Pomerleau, 1995).
Neuroadaptation models suggest that dependence,
broadly indexed by tolerance with withdrawal, occurs at
the neurocellular level. These models suggest that repeated exposures of a substance alter the sensitivity of
existing neuroreceptors that the substance binds to in
the central nervous system (Collins and Marks, 1991;
Pomerleau, 1995) and also increase the number of
receptors available to receive the substance (Robinson
and Berridge, 1993). Neurons become desensitized over
time to the same substance doses (i.e. adapt), and as a
result, the same doses of the substance come to elicit
markedly decreased effects (Collins and Marks, 1991).
Due to the neuroadaptation that has occurred, cessation
of the substance produces a withdrawal reaction as the
central nervous system rebounds in order to overcompensate, in a direction generally opposite of the substance effects, for the lack of substances at the neuronal
level (Pecknold, 1993). In these theories, the development of tolerance and appearance of withdrawal are
core markers of the adaptation of the body to the
substance. Having functionally adapted to the presence
of the substance, the nervous system finds itself maladapted to functioning without it, resulting in disequilibrium upon cessation. Attempts to avoid or relieve
withdrawal, therefore, are seen as the core determinants
for continued compulsive substance use, and as the
source of all the other observed features — for example,
relapse — of substance dependence.
Other neurobiological models (Frawley, 1988) suggest
that substances stimulate the reinforcement pathways of
the central nervous system (e.g. endorphin release, dopaminergic stimulation). Because of the speed with
which the substance activates this reinforcement system,
the substance is perceived as a powerful reinforcer and
the behaviors associated with using the substance are
powerfully rewarded. In a sense, addictive substances
‘hijack’ the reinforcement system, which fundamentally
controls motivation and behavior, to perpetuate their
own self-administration. Tolerance develops within the
reward system to the effects of the substance as the
‘normal’ (i.e. natural) reward systems of the body be-
S15
come shut down or suppressed. In this theory, then, it
is the positive neural consequences when the substance
is administered that perpetuate substance dependence.
In essence, then, neurobiological models — broadly
speaking — address a number of features of dependence at a very basic and reductionistic level. Tolerance
effects and withdrawal reactions are central to these
models, and are attributed to particular neurochemical
mechanisms. However, though implied, the precise
mechanism through which the behavioral manifestations of dependence (e.g. compulsive use parameters)
appear, and the resulting relapse and stress-relieving
features are not well-specified by this class of theories.
The burden remains for this class of models to translate
these basic processes into behavioral action features of
substance use.
4.2. Classic learning models
Classic learning models of substance dependence do
not attempt to explain dependence purely from behavioral principles without reference to pharmacological
effects, but rather take these effects as their starting
point and explain how behavioral processes build on
these effects to mould behavioral manifestations of
dependence. In this sense, ‘classic’ learning models
(rooted in classical and operant conditioning theories)1
complement — rather than compete with — neurobiological models of dependence. In particular, learning
models can help explain important observed phenomena
that generally are not adequately accounted for in
purely neurobiological models.
By way of brief overview, two classes of classic
learning models may be identified, under which several
substance dependence-specific theories may be subsumed. Classical (or Pavlovian) conditioning models are
predicated on the assumptions that: (1) substances of
abuse produce physiological and subjective reactions in
the user (both direct pharmacological effects and indirectly, withdrawal effects); and (2) substance administration occurs repeatedly in the same contexts (Childress
et al., 1992). As a result of this repeated pairing of
substance effects and particular contexts, the contexts
themselves come to elicit the substance effects in the
absence of substance administration (Childress et al.,
1992). Operant conditioning theories posit that reinforcers dictate and shape substance use behavior(s). The
1
What we have termed ‘classic learning models’ are more traditionally referred to as ‘behavioral models’. Our intent in using this label
rather than the more common one was to distinguish these models
from social learning models, which are behavioral models of sorts,
but which add additional variables and elements. Indeed, both classes
of models could be categorized as behavioral models, but for purposes of argument and illustration, we distinguish them via these
different labels. We are by no means arguing for an identifying label
change.
S16
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
behaviors that accompany substance use are immediately and powerfully reinforced, which increases the
probability that the behaviors that accompany substance use are repeated and that the substance will be
readministered.
Withdrawal symptoms are said to be classically conditioned (i.e. linked) to substance related cues (conditioned withdrawal; Wikler, 1965). The substance would
then be administered in the presence of substance use
cues in order to counteract the withdrawal effect. Due
to repeated pairings of the symptoms and the cues, the
cues would eventually come to trigger withdrawal
symptoms. This mechanism, in particular, provides an
explanation for relapse occurring long after acute withdrawal has subsided.
Some aspects of tolerance development are also explained by some conditioning theories (conditioned
compensatory responses; Seigal, 1988). In these theories, tolerance is viewed as a conditioned response,
intimately linked to the situations and cues in which the
substance use occurs. For example, under the same set
of conditions, increased substance doses are needed to
achieve the same effects — increased tolerance develops. However, once tolerance in one situation has
developed, if placed in a novel situation and given the
same substance dose, a toxic reaction — an overdose
— can occur.
Still other conditioning theories suggest that the positive effects of substances can become classically conditioned to substance use cues (appetitive motivational
theories; Goldberg, 1975; Young et al., 1981; Stewart et
al., 1984). Due to repeated pairings of the reinforcing
effects of substances with substance use cues, the cues
themselves come to elicit the same reinforcing events
that the substances elicit, and come to serve as priming
stimuli for substance use. Thus, in the presence of these
cues, a strong appetitive drive to increase use of the
substance occurs in order to achieve a stronger reinforcing effect. In this view, tolerance develops to the
negative effects of the substance, but not to the positive
effects of the substance.
In short, then, classic learning theories describe the
mechanisms through which features such as reinforcement translate into features such as compulsive use.
Although classic learning models do not specify the
precise neurobiological reinforcement mechanisms that
are important features of dependence, they invoke behavioral theory to explain the observable features of
dependence, and, therefore, fill the behavioral gaps in
neurobiological theories. However, a problem with such
classic learning theories is that they do not account well
for elements of cognition, such as thought and affect,
that have been demonstrated to have roles in regulating
behavior (Bandura, 1997), particularly substance use
behavior (Marlatt and Gordon, 1985).
4.3. Cogniti6e social learning models
Cognitive social learning models that have been applied to understanding substance dependence (Marlatt
and Gordon, 1985; Abrams and Niaura, 1987; Tiffany,
1990; Shadel et al., 2000) posit that the internal states
of humans mediate the relationship between the environment and the substance use behavior. Moreover,
there is an assumed interaction between the individual
and the social environment. The individual influences
his or her environment just as the environment shapes
and moulds his or her cognitive representations of and
emotional reactions to the environment (i.e. dynamic
reciprocal determinism).
Social learning models posit that substance use is
learned through observation and experiences with the
social environment (Bandura, 1986). More specifically,
the multidimensional effects of substance use in social,
cultural, psychological, and physical domains are
learned by observation, and in order to reap the
benefits of those multidimensional effects, the individual models the observed substance use. For example,
expectancies and attitudes about substance use are
learned through observation and modelling of the expectancies of significant others in the social environment. Direct experiences with the substance provide
knowledge through experiences about the effects of the
substance — for example, that it facilitates relaxation.
If used over a prolonged period of time, tolerance to
the effects of the substance will develop, as the individual learns to ingest greater amounts of the substance to
achieve the same effects. Dependence appears in both
physical and psychological domains. Physical dependence develops because the individual may use the
substance to avoid the experience of withdrawal, and
psychological dependence may develop because the individual comes to expect that use of the substance will
alleviate stress (Shadel and Mermelstein, 1993). Substance use results directly, then, from the interaction of
(1) expectations about the positive benefits of using the
substance and (2) decreased self-efficacy to execute
particular courses of action without the substance.
Cognitive social learning models thus provide insight
into the manner in which unobservable, though
testable, cognition translates into substance dependence. These models take reinforcement and behavioral
features as starting points, then invoke cognitive processes to explain them. In doing so, cognitive social
learning models fill a gap in prior models. However,
these models do not specify which social factors are
important for influencing cognition.
4.4. Social factors influencing dependence
Models of social influence articulate the immediate
environmental variables that give rise to substance
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
dependence. Cognitive social learning models imply
that such social factors are important and are internalized, so to speak, by the substance user in the form of
cognition, e.g. expectancies (Marlatt and Gordon,
1985), and cognitive self-regulatory systems (Shadel et
al., 2000). However, social factors are important to
consider independently in substance dependence. Social
factors may be broadly construed as those objective
environmental variables that have an impact on substance dependence. Such factors may not directly have
an impact on certain features — for example, psychoactivity, tolerance — but do have effects on features such as secondary reinforcement of the substance
and, indirectly, on compulsive use (that is, social factors
may make it more or less difficult to gain access to and
to use substances). For example, certain family interactional styles have been associated with increased risk of
substance use (Ablon, 1984; Hundleby and Mercer,
1987). Pricing structures, taxes, and legality of certain
substances may restrict or facilitate access to certain
substances (USDHHS, 1989). Socioeconomic status
also plays a role in determining risk for substance use
(USDHHS, 1988). In short, social factors broadly inform which variables in society at large are related to
substance dependence. However, they do little to explain the manner in which certain subgroups may be
more susceptible to these factors.
4.5. Cultural contexts for dependence
Culture is not a thing and is not to be used synonymously with ethnicity or race, but is a project in the
making undertaken by groups of people sharing what
they consider to be common and essential defining
characteristics at a particular point in time. Dependence
develops in specific cultural contexts where public and
private use of a substance such as tobacco takes on
meaning in relation to: (1) core values which dictate
consumption behavior; (2) the properties ascribed to
substances; (3) the exchange value of substances (their
relative worth in social exchanges); (4) use of a substance to facilitate valued forms of social interaction;
and (5) the manner in which substance use accords
identity (e.g. as a sign of social distinction).
Cultural aesthetics influence the manner in which
tobacco is prepared, what it is combined with to appeal
to certain groups, the preferred mode in which it is
ingested, and when and with what tobacco is consumed. These factors influence choice of tobacco products — smoked versus smokeless, mild versus harsher
blends of tobacco — which in turn influence patterns
of smoking topography and the relative perceived risks
associated with use. Patterns of daily, weekly, and
seasonal substance use are influenced by the way in
which time is structured around social activities and
particular times and spaces (Orcut, 1993). Unspoken
S17
rules about tobacco consumption related to when,
where, and in front of whom one may smoke may give
way to patterns of use subject to the discretion of
individual users.
Two of the prime objectives of campaigns designed
to market legal substances such as tobacco is to mainstream and normalize the perception of use — to
broaden public perception of when and where substance use and exchange are acceptable and to give the
perception that far more people are happily engaging in
product use than is actually the case (Lynch and Bonnie, 1994). When marketing is most effective, new temporal consumption rhythms are incorporated into
everyday life and legitimated, as is the case with coffee
and smoking breaks. What was once fashion becomes
entitlement as culture changes to accommodate perceived need. It is easy to see how such change can affect
the movement from low level substance use to dependency by increasing opportunities for consumption.
Proposed restrictions on the use of substances in public
places and work-sites raise cultural issues such as individual rights (Wagner, 1997). These are played upon by
the tobacco industry both in their lobbying efforts and
their marketing strategies aimed at youth in the name
of freedom of choice and the maturity to ‘smoke
responsibly’.
Cultural perceptions of what constitutes deviant use
of substances such as alcohol or tobacco are often
based as much on social as health related criteria.
Deviance may be determined as much on the basis of
the user’s ability to perform work roles, fulfill social
responsibilities, and maintain proper social composure
in public as on the quantity of a substance used and
frequency of use (Quintero and Nichter, 1996). Perceptions of normality and deviance involve two core sets of
expectations: expectations related to social behavior
and expectations related to the manner in which a
substance is thought to affect different people at different times. Cultural conceptualizations of why some
people do and do not become dependent on substances
such as tobacco influence personal evaluation of susceptibility and social evaluation of responsibility. Perceptions of personal susceptibility in turn influence
thinking about one’s capacity to maintain moderate
levels of substance use and the ability to quit or cut
down on levels of consumption.
Patterns of communication across gender and generation are influenced by cultural norms involving relations of respect, responsibility, and openness of
expression. The social relations of communication in
turn influence what feedback users of tobacco receive
from particular family members, friends, and community members. Patterns of communication involving
social sanction and support in turn contribute to patterns of use. Patterns of communication associated with
parenting styles may have an important cultural dimen-
S18
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
sion that influences both what kinds of messages youth
are exposed to and their response to the directives and
advice of elders. One factor influencing lower rates of
smoking among African American youth, for example,
appears to be parenting style and direct communication
about tobacco (Koepke et al., 1990; Royce et al. 1993;
Mermelstein et al., 1996).
4.6. Comment
If analyzed in a hierarchical fashion, it becomes clear
that differences between models do not necessary mean
that the models compete with one another, but rather
that they complement one another. The role that particular features play within particular theoretical conceptions is, however, open to debate. Indeed, the apparent
contrasts between the models lead one to the conclusion that although much is known about substance
dependence, many issues remain and that a comprehensive conceptual understanding is far from clear.
First, despite finding that most models share common features, each model assigns different weights to
these features. It is not clear which features should be
weighted most heavily in attempting to define dependence, and it certainly is possible that these weights
may differ for different persons over time. Second, a
syndromal conception of dependence suggests that
there should be substantial qualitative heterogeneity in
the profile of dependence, both between different individuals and within the same individuals over time. It
also suggests the possibility that different substances
might produce different profiles of dependence, differing not only in severity, but in the mix of features
manifested. Third, despite the framework that we have
provided, the relationships among the various features
are not completely specified by existent models, and it is
not clear how these features interact dynamically with
one another to result in some larger concept that can be
labelled dependence.
Finally, the emphasis on certain features as defining
dependence may vary not only according to one’s theoretical perspective, but also on one’s purpose in defining
it. For example, the objectives of making clinical diagnoses of dependence, preparing to treat dependence,
predicting the outcome of treatment, explaining dependence theoretically, and providing a basis for social and
judicial judgments of dependence, impose different demands and evoke different emphases in a definition.
Similarly, as dependence to particular substances is
recognized, attention is drawn to different features or
levels of analysis. For example, whereas study of opiate
addicts emphasizes tolerance, withdrawal, and negative
reinforcement models of dependence, attention to cocaine dependence highlights positive reinforcement features and models. The need for the construct of
dependence to flexibly address all of these phenomena
stresses the need for multidimensional definitions of the
construct and for multiple levels of analysis.
5. Concluding remarks: a proposed research agenda
This essay has provided a picture of substance dependence as it is manifest among adults. It is apparent,
however, that these models do little to address the
etiology of tobacco use and dependence among youth.
The data which support the various models of dependence are based primarily on research with adult populations and with adult animal samples. Very little
comprehensive theoretical information is available on
nicotine dependence as a concept among youth. A
developmental analysis of these features suggests at
least two alternative, yet related, lines of thinking for
understanding youth tobacco use. First, the features of
nicotine dependence are observable among youth users
of tobacco products. Strategies to assess each of these
features therefore need to be developed — either
adapted from existing adult measures or developed
through systematic study of youth users (Colby et al.,
2000). Second, the features have distinct developmental
trajectories. In other words, these features may not be
observable in ‘adult form’ among youth users, but
measurable ‘precursors’ may be found that predict corresponding adult features. In either case, the burden for
researchers of youth nicotine dependence is to examine
the role that the consensus features of adult dependence
play in youth dependence. Several important aspects of
a research agenda can be listed:
1. The order in which particular features of dependence appear needs to be identified. Which features
appear first? Is there a fixed sequence of appearance? Does this imply a causal chain, in which the
emergence of one feature causes the next one to
emerge?
2. The relationship of the adult conception of dependence needs to be related to the conception for
youth. Is the syndromal description of adult dependence adequate to describe early dependence and its
development? Are there some features of dependence, not observed among adults, that are important in the developmental trajectory of nicotine
dependence? Are there prodromal characteristics
(e.g. attitudes about substance use) that are not part
of dependence, per se, but which are important
milestones in the developmental trajectory?
3. The developmental relationship between the features
needs to be articulated. How do the features relate
to each other in the course of development? It seems
clear that some amount of chronic nicotine use is a
necessary condition for development of nicotine dependence, but how much is needed? What quantity
or frequency is necessary and/or sufficient? Is there
a threshold — a ‘point-of-no-return’ — past which
W.G. Shadel et al. / Drug and Alcohol Dependence 59 (2000) S9– S21
‘full-blown’ dependence can be said to emerge? Or
does the appearance of a particular feature or aspect of dependence signal the crossing of some
qualitative threshold?
4. The syndromal model of dependence has clear implications for assessment of dependence and for
research on its development. It suggests that assessment must be multi-variate, in order to be sensitive
to different dependence profiles that might be observed, especially as dependence develops or
emerges. It suggests that research may need to identify specific antecedents for more than one aspect of
dependence, rather than examining only a single
dependent variable, and that it must be sensitive to
the possibility of multiple pathways to adult dependence, rather than assuming a single route or
sequence.
5. More meaningful inquiry into patterns of substance
use may be gained from a consideration of what is
‘cultural’ (as an adjective) about such behavior,
than from a consideration of ‘culture’ (as a noun
designating the rather amorphous characteristics
thought to characterize a group, Appadurai, 1997).
An investigation of this type might, for example,
help us better understand differences in the age of
smoking initiation and smoking styles both: (a)
between groups of African American and Caucasian youth who share common social class backgrounds; and (b) within these populations when
epidemiological data identifies ‘inter-group’ differences.
This essay has provided an initial blueprint for basic
research that may advance an understanding of the
etiology of tobacco dependence among youth. In doing
so, it may serve as one step toward informing future
prevention and cessation efforts that ultimately will
curb youth experimentation with tobacco products and
halt the development of nicotine dependence among
youth.
Acknowledgements
The authors wish to thank the members of the Tobacco Etiology Research Network (Richard R. Clayton, Robert L. Balster, Linda M. Collins, Brian R.
Flay, Gary Giovino, Jack E. Henningfield, Mary
Jeanne Kreek, Robert J. McMahon, Kathleen R.
Merikangas, Stephen Tiffany) and The Robert Wood
Johnson Foundation (Marjorie A. Gutman, Nancy J.
Kaufman, Denis Prager) for their suggestions and
comments on versions of this manuscript. The
manuscript also benefited greatly from the suggestions
of John Hughes and Richard Brown. We also would
like to thank Susan Burnam for her administrative
assistance. Work on this manuscript was supported, in
S19
part, by the Tobacco Etiology Research Network and
The Robert Wood Johnson Foundation.
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