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background module 1
Intro
Substance and alcohol use range from non-pathological levels to substance abuse, diagnosed as
a mental health disorder in the Diagnostic Statistical Manual of Mental Disorders (DSM) .
Substance use disorders are characterized by a compulsive and chronically relapsing pattern of
drug use, impaired control over substance use, continuation of use despite negative
consequences, craving, tolerance and withdrawal. it poses a significant burden on the quality of
life, physical health, mental health, social relationships and professional functioning (e.g., due to
absence through illness and under-performance). It also increases the risk for mortality.
Substance use disorders also leads to substantial costs to society as a result of increased health
care expenditure, drug-related crime, lost productivity, social welfare, and other social
consequences. Therefore, substance use disorder is an important disorder to understand.
Effective, evidence-based prevention and treatment of alcohol and substance use disorders is
important for not only the health and well-being of addicted people, but also for creating healthy
and safe families and communities. In the first part of the ACD course, you will learn about
underlying psychological and neurobiological processes, treatment, comorbidities, and the role of
loved ones.
Models of addiction
The National Institute on Drug Abuse (NIDA) ([Link] in the USA
defines addiction as: "a chronic, relapsing disorder, characterised by compulsive drug seeking,
continued use despite harmful consequences, and long-lasting changes in the brain". According to
the brain disease model, the latter changes are responsible for extreme drug cravings (Module 1),
and the formation of rigid drug habits (Module 2), as well as impaired cognitive control (or
'executive') functions, which lie at the heart of uncontrolled drug use as well as relapse after a
period of abstinence.
How society understands addiction - and people with addictions - has changed dramatically over
time. Below is a simplified, chronological overview of major models of addiction, based on a
historical review by Wim van den Brink (2006; in Justitiële Verkenningen) and later developments.
Each model places a different emphasis on certain drivers of addiction (e.g., neurobiological,
learning-related, or social/structural), and has implications for how we look at individuals with a
substance use disorder and associated stigma's.
The moral model (19th century)
For much of history, addiction and drug-seeking behavior were seen as moral failings. Addiction
was understood as a sign of weak character or bad values. People with addictions were often
punished, imprisoned, or sent to institutions for "re-education", sometimes under harsh conditions.
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Although this model is not supported by scientific evidence, traces of it still appear today in
attitudes that frame addiction mainly as a matter of personal responsibility or moral weakness.
The pharmacological model (mid-19th century)
In the mid-1800s, in the U.S. and Western Europe, a new idea emerged: perhaps the substance
itself was to blame, rather than the person. According to this model, drugs are inherently addictive,
and exposure to them is the main cause of addiction.
Therefore, the most effective countermeasure was to prevent people from becoming involved with
these dangerous substances. The most famous example of this thinking is alcohol Prohibition in
the U.S. (1920-1933). Today, most researchers view this model as incomplete. Simply having
access to a drug is not enough to explain why some people develop addiction and others do not.
However, this way of thinking still strongly influences policies toward illegal drugs, such as the
“War on Drugs”, often with similar unintended consequences like increased organized crime.
The symptomatic model (1930s-1950s)
Influenced by psychoanalytic ideas, addiction came to be seen as a symptom of deeper
psychological problems, such as personality disturbances or unresolved conflicts. Addiction itself
was not considered the main problem, but rather a sign of something underlying.
Treatment therefore focused on long-term psychotherapy aimed at gaining insight into these
deeper issues. Versions of this approach are still used in some therapeutic communities.
The disease model (1940s-1960s)
The disease model (propagated by Jellinek ) proposed that some people have fundamental
biological and psychological differences that make them unable to use substances in moderation.
Addiction is viewed as a chronic illness characterized by loss of control, tolerance, and
withdrawal.
An important implication of this model is that while many people can use substances moderately,
those with addiction must aim for complete abstinence. Alcoholics Anonymous (AA) and the
Minnesota Model are well-known examples based on this perspective.
The learning theory model (1960s-1970s)
During this period, addiction began to be understood as learned behavior. According to this view,
repeated substance use is reinforced by its effects and becomes habitual over time.
If addiction is learned, then it should also be possible to unlearn it. Behavioral interventions such
as aversion therapy and cue exposure were developed, although their effectiveness has generally
been limited.
The bio-psycho-social development model (1970s–1990s)
Research increasingly showed that there is no clear line separating “addicts” from “non-addicts.”
Social context, life experiences, and environment play major roles. For example, many U.S.
soldiers who became addicted to heroin in Vietnam stopped using after returning home. This led
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to the bio-psycho-social model, which views addiction as developing through interactions between
biological vulnerability, psychological development, and social circumstances. Substance use is
seen as existing on a continuum, ranging from use to harmful use to addiction.
This model supports multi-modal treatment, combining medication, psychotherapy, and social
interventions such as housing and employment support.
The brain disease model (since ~1990)
Advances in neuroscience and genetics have strengthened the focus on brain processes in
addiction. Many researchers began to describe addiction as a brain disease, involving long-lasting
changes in brain circuits related to reward, motivation, and self-control. Within this model,
neurobiological vulnerability forms the indispensable basis for repeated use of psychoactive
substances, while the repeated use of these substances in turn leads to important, difficult to
reverse, changes in the brain. Pharmacological and behavioral therapeutic interventions are seen
as the most promising within this model.
Ongoing Debate
While the brain disease model remains influential, it has also increasingly been criticized. By
labeling addiction as a brain disease we risk that insufficient attention is paid to social,
environmental, and structural factors that shape addiction. Relatedly, in recent years complex
systems models of mental health have gained interest and support. From this perspective,
addiction emerges from dynamic interactions among biological, psychological, and social factors
over time (Scheffer et al., 2025, JAMA Psychiatry). Each person’s pattern of addiction - and
resistance to change - is unique (Griffiths & Larkin, 2004). Rather than searching for a single
cause, this approach emphasizes how multiple influences combine and reinforce each other.
Tolerance and withdrawal symptoms
With repeated substance use, tolerance may develop. Tolerance refers to a reduction in a
substance’s effect following chronic administration. As the body and brain become less sensitive
to the substance, increasingly higher doses are required to achieve the same effect. As a
consequence, escalating use substantially increases the risk of overdose, including fatal
overdose. In addition, after prolonged substance use, withdrawal symptoms may emerge when
use is reduced or discontinued. Withdrawal symptoms that are common across many substances
of abuse include anxiety, irritability, malaise, dysphoria, hyperkatifeia (i.e., heightened sensitivity to
emotional distress), a pervasive sense that “everything is gray,” and alexithymia (i.e., difficulty
identifying or expressing one’s emotions).
Traditional theories of addiction place these withdrawal symptoms at the center of addiction
development and maintenance. According to these accounts, drugs are initially used because
they produce pleasure or relief (a form of positive reinforcement). Over time, however, tolerance
develops and drug use becomes increasingly motivated by the desire to avoid the unpleasant
emotional and physical states associated with withdrawal (a form of negative reinforcement). One
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influential framework that formalizes this transition is the opponent-process model of addiction
(Solomon & Corbit, 1974).
The opponent-process model proposes that every drug-induced emotional or physiological
response (the a-process) automatically elicits a secondary, opposing response (the b-process)
that serves to restore homeostasis. During initial drug use, the a-process - such as euphoria or
relief from distress - is rapid and strong, whereas the b-process is relatively weak and short-lived.
As a result, the net subjective experience is predominantly positive. With repeated drug exposure,
however, the b-process strengthens, becomes more enduring, and is triggered more rapidly, while
the a-process shows comparatively little change. This growing opponent process counteracts the
drug’s pleasurable effects, producing tolerance and diminishing the hedonic impact of drug
use. Crucially, when the drug is no longer present, the b-process persists, giving rise to a negative
emotional state that is experienced as withdrawal. Therefore, within this framework, addiction is
conceptualized as a shift from pleasure-driven drug use to a state in which drug taking is primarily
motivated by the avoidance of distress. Over time, the absence of the drug becomes increasingly
aversive, while the presence of the drug provides diminishing relief, effectively trapping the
individual in a cycle of compulsive use aimed at alleviating negative affect rather than achieving
pleasure (Solomon & Corbit, 1974; Koob & Le Moal, 2008).
Figure: opponent process theory of addiction (Roura Turet, 2015). The top panels illustrate the experienced
(appetitive/aversive) state that results from the underlying a- and b-processes that are illustrated in the bottom panels.
Although the opponent-process model provides an elegant explanation for tolerance, withdrawal,
and escalation of use, it has important limitations. In particular, it cannot fully account for the
observation that relapse frequently occurs after long periods of abstinence, when acute
withdrawal symptoms and opponent processes have largely subsided. This suggests that while
negative reinforcement processes contribute to the maintenance of addiction - especially during
periods of frequent use - they are insufficient to explain the persistence and recurrence of
addictive behavior. Instead, relapse appears to be strongly influenced by additional mechanisms,
including cue-induced craving driven by Pavlovian conditioning (Module 1), the development of
habitual drug-seeking behaviors, and impairments in cognitive control functions that limit the
ability to inhibit drug use (Module 2).
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Major substance classes
Different substances affect the brain and mental functioning in different ways due to their chemical
properties. They also differ in other important respects: the reasons for initially taking them vary,
as do the associated risks for developing an addiction, their 'addiction potential' (i.e., how likely it
is to lead to problematic, compulsive use; e.g., nicotine, heroin and cocaine have higher addiction
potential than most hallucinogens), the long-term psychological effects, the impact on risk-taking
and bodily harm, the danger of overdose, and relapse rates.
In terms of acute psychological effects, patterns also differ across major substance classes. While
this is not exam material, these effects are briefly described here for context. Alcohol is
commonly associated with euphoria, reduced anxiety, lowered inhibitions, and impaired judgment.
Caffeine increases alertness and reduces fatigue. Cannabis (THC-containing products) often
produces relaxation, altered sensory perception, and short-term memory impairment, and may
increase anxiety in some individuals. Classic hallucinogens (e.g., LSD, psilocybin) alter
perception and thought processes, sometimes intensifying emotions and producing visual
distortions, whereas dissociative hallucinogens (e.g., ketamine, PCP) are more likely to
produce detachment from the self or environment and confusion. Inhalants can cause brief
euphoria, dizziness, and perceptual disturbances. Opioids (e.g., morphine, fentanyl) are
associated with euphoria, warmth, relaxation, and emotional blunting. Sedatives, hypnotics, and
anxiolytics (e.g., benzodiazepines, barbiturates) produce calmness and sedation along with
slowed cognition. Stimulants (e.g., cocaine, amphetamines) increase energy, alertness, and
confidence but may also provoke anxiety or irritability. Nicotine produces mild stimulation and
enhanced attention, often accompanied by relief of withdrawal-related irritability.
Pavlovian (or 'classical') conditioning
Pavlovian conditioning is a learning mechanism that plays an important role in addiction. Here,
previously neutral stimuli (such as drug paraphernalia, particular people,internal states or drug-
associated contexts) that predict the effects of a drug come to evoke conditioned responses and
craving. Craving is considered an essential driving force in substance abuse by many researchers
and clinicians, and it has been incorporated into the DSM-V as one of the criteria. Pavlovian
conditioned stimuli (CSs) evoke an anticipation of the unconditioned (drug) stimulus (US) and
elicit craving and approach, and can reinforce and sustain drug seeking by acting as conditioned
reinforcers. Drug-associated CSs can also capture attention and elicit sign tracking.
One of the most prominent theories of addiction also regards craving as central to addiction is the
incentive-sensitization theory of Berridge & Robinson (2011). According to this theory, drug-
associated stimuli gradually acquire incentive salience. This means that these stimuli attract the
attention of the person with the addiction and become attractive in themselves. These stimuli will
lead to "wanting" of the drug, which in turn elicits targeted behavior to acquire the drug. According
to this model, "wanting" and liking don't always occur together. In addiction, the craving/"wanting"
of a substance increases, while the hedonic experience during consumption (liking) - if anything -
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decreases. This theory may explain relapse, as exposure to drug-associated cues (e.g.,
paraphernalia, certain friends with whom the drug has been used in the past, a pub, or selling
point) incite craving for the drug long after withdrawal symptoms have disappeared.
Pavlovian processes, overdose risk and tolerance. Repeated drug use in consistent
environments can produce Pavlovian (classical) conditioning effects that increase overdose risk.
Environmental cues that reliably precede drug administration become conditioned stimuli that over
time elicit anticipatory physiological responses that are compensatory, meaning they oppose the
drug’s pharmacological effects in an effort to maintain homeostasis. For example, with repeated
opioid use, cues associated with use may trigger increases in arousal or respiratory drive that
partially counteract opioid-induced respiratory depression. These conditioned compensatory
responses contribute to tolerance in familiar settings. However, if the drug is taken in a novel
context where the usual cues are absent or altered, the compensatory response may not occur.
As a result, a previously tolerated dose can produce a stronger-than-expected effect, increasing
the risk of overdose. Following a similar logic, CS-elicited compensatory responses can also
contribute to the development of tolerance: in familiar settings, the same dose produces a smaller
net effect because the body has already begun compensating.
The role of dopamine in addiction
Despite their different chemical properties, an important feature which substances of abuse have
in common is that they directly or indirectly result in release of dopamine in the nucleus
accumbens, which plays an important role in their addictive effect. The nucleus accumbens is part
of the mesolimbic dopamine pathway that has evolved throughout our evolution and has many
adaptive functions. It enables us to anticipate certain rewards (e.g. food, sex) in our environment,
but also reinforces desirable/adaptive behavior: behavior followed by a reward is repeated. To
illustrate, when we encounter a reward-associated stimulus (e.g., the smell of a tasty snack),
dopamine is released and enhances our motivation to approach the reward. Drugs however, lead
to much stronger dopamine activity than natural rewards such as food or sex. Therefore, it has
been said that drugs 'hijack the dopamine reward system', driving addictive behaviour even when
the actual drug consumption has become less pleasurable over time. Accordingly, the incentive-
sensitization theory posits that the mesolimbic pathway plays a crucial role in drug "wanting" (but
not liking). The role of dopamine in substance use disorders will be discussed further in the
lectures and reading material of the first two modules: Module 1 will focus on its role in craving
and Module 2 in habits.
Research has shown that people with addiction are less sensitive to natural rewards (Franken et
al., 2007). Neuroscientific PET research suggests that people with a low density of dopamine D2
receptors in the ventral striatum (nucleus accumbens) are less sensitive to simple natural
rewards. According to the reward deficiency syndrome (RDS) account, these people may look for
stronger stimuli to compensate this, such as through the use of drugs (or perhaps also gambling
or eating extra sweet/fatty food). As a vulnerability factor for addiction, RDS has also been linked
to a genetic predisposition. Conversely, people with a high D2 receptor density are very sensitive
to natural rewards and are therefore less likely to take drugs. In addition, the effect of drugs may
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even be unpleasant for these people because the effect is too powerful. On the other hand,
dopamine D2 receptor density may be down-regulated as a consequence of substance abuse.
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