ABC Horizon
Level 5 — 18 sessions
The term "addiction" is often used loosely in everyday language to describe anything from a love of chocolate to excessive use of social media. However, in a clinical and psychological context, addiction is a specific and serious condition. It is a complex, chronic disease of the brain's reward, motivation, and memory systems. It is not a moral failing or a lack of willpower. A helpful way to conceptualize addiction is through the "Four Cs":
To provide a standardized and reliable framework for diagnosis and research, clinicians use two main diagnostic manuals: the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the World Health Organization's International Classification of Diseases (ICD-11). Both manuals have moved away from the separate categories of "abuse" and "dependence," instead using the concept of a "Substance Use Disorder" (SUD) measured on a spectrum of severity (mild, moderate, severe).
A problematic pattern of substance use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:
Two other key characteristics often associated with addiction are tolerance and withdrawal, which fall under the pharmacological criteria in the DSM-5:
It is crucial to understand that while tolerance and withdrawal are common in severe SUDs, they are neither necessary nor sufficient for a diagnosis. A person can be addicted without significant physical withdrawal (e.g., cannabis use disorder), and a person can experience withdrawal from a substance they are not addicted to (e.g., a patient taking prescribed opioid painkillers as directed). The core of addiction lies in the compulsive use and loss of control.
Instructions: In breakout rooms, discuss the following scenarios. Using the "Four Cs" and the DSM-5 criteria, decide whether each person's behaviour likely constitutes a Substance Use Disorder. Be prepared to justify your reasoning.
Teacher Guidance: Facilitate a discussion. Scenario 1 is likely a mild to moderate SUD (risky use, consequences). Scenario 2 is physical dependence, but not addiction (no loss of control, compulsion, or negative consequences beyond the intended medical use). Scenario 3 is a clear example of a behavioural addiction (Gambling Disorder), demonstrating all the core features.
The DSM-5 includes "craving" as a diagnostic criterion for the first time. Why is this significant? How does the inclusion of a subjective, psychological experience like craving change our understanding of addiction compared to a model that focuses only on observable behaviours like tolerance and withdrawal? Does it make the diagnosis more or less reliable?
After establishing a clinical definition, a critical question arises: is this concept actually useful? The idea of "addiction" as a distinct category of behaviour serves several important functions:
Despite its utility, the concept of addiction is fraught with problems and controversy. Critics argue that the label itself can be harmful and that the concept is often oversimplified.
The stigma associated with being labeled an "addict" is a major barrier to seeking help. It can lead to discrimination in housing, employment, and social relationships. Furthermore, some argue that the label can become a harmful part of a person's identity, fostering a sense of powerlessness.
Perhaps the most significant scientific criticism of the addiction concept is its categorical nature. The label "addict" implies a black-and-white distinction: you either are one or you are not. However, modern research increasingly views substance use, and the problems associated with it, as existing on a continuum. The DSM-5's shift to a "Substance Use Disorder" with a severity rating (mild, moderate, severe) is a direct response to this criticism. It acknowledges that there is a vast grey area between occasional, non-problematic use and severe, compulsive addiction. The question remains: is it more useful to think of addiction as a discrete category or as the extreme end of a spectrum?
How might treating addiction as a continuum rather than a category change public health policy? For example, would it encourage more focus on harm reduction and early intervention for "mild" or "moderate" problems, rather than focusing only on severe cases?
Instructions: This is a structured debate. Divide the class into two groups.
Teacher Guidance: Moderate the debate, ensuring both sides address the key points from the lecture. The goal is not to reach a definitive answer but to have students engage deeply with the pros and cons of this powerful label. This directly addresses AC 1.2.
Consider the term "cancer." Like addiction, it is a medicalized term for a spectrum of diseases. Does the label "cancer patient" carry the same level of social stigma as "addict"? Why or why not? What does the difference in public perception of these two "diseases" tell us about the role of perceived personal responsibility and morality in how we view health conditions?
A psychoactive substance is any chemical that, when taken, alters brain function, resulting in changes in perception, mood, consciousness, cognition, or behaviour. This is a very broad category that includes everything from caffeine and nicotine to prescription medications and illegal drugs. The key feature is their ability to cross the blood-brain barrier and directly influence the central nervous system.
Many psychoactive substances have a dual nature. The same drug can be a valuable therapeutic tool in one context and a dangerous substance of abuse in another. The distinction often lies in the dose, the route of administration, the user's intent, and the social and legal context.
Cannabis is increasingly being legalized for both medical and recreational use. How does this dual legal status complicate our understanding of it as either a "medicine" or a "drug of abuse"?
Why are some substances so powerfully reinforcing? The answer lies deep within the brain in a circuit known as the mesolimbic dopamine pathway, often called the "reward pathway." This is not a single spot, but a set of interconnected brain structures that are crucial for motivation, reinforcement learning, and survival. Its purpose is to make us repeat behaviours that are essential for life, such as eating, drinking, and procreating, by associating them with feelings of pleasure.
The key players in this pathway are:
Process: When you engage in a rewarding activity (e.g., eating a delicious meal), the VTA releases a surge of the neurotransmitter dopamine into the nucleus accumbens. This dopamine signal essentially tells the brain, "That was good! Remember what you did, and do it again."
Addictive drugs are so powerful because they artificially and dramatically increase dopamine in the reward pathway. They "hijack" this natural system, creating a surge of pleasure far more intense and reliable than natural rewards. Different drugs do this in different ways:
This artificial overstimulation teaches the brain that the drug is more important than natural rewards. Over time, the brain adapts to these massive dopamine surges by reducing its own dopamine production or decreasing the number of dopamine receptors. This leads to tolerance (needing more of the drug to get the same effect) and anhedonia (the inability to feel pleasure from natural rewards), driving the cycle of addiction.
Instructions: In breakout rooms, assign each group one of the following substances: 1) Cocaine, 2) Heroin, 3) Nicotine. Each group must prepare a short (2-minute) explanation for the class on how their assigned drug "hijacks" the reward pathway.
Your explanation should answer:
Teacher Guidance: This activity forces students to engage with the specific neurobiological mechanisms. Provide them with simplified resources or diagrams for each drug. After the presentations, summarize the common theme: all addictive drugs converge on the same final pathway of increasing dopamine in the nucleus accumbens.
If addiction is a disease of the reward pathway, why aren't all pleasurable activities (like eating cake or playing sports) considered "addictive" in the same way as drugs? What is the difference between a natural reward and a drug-induced reward in terms of the brain's response? (Hint: Think about the magnitude, speed, and reliability of the dopamine signal).
A common misconception is that drugs are made illegal because they are scientifically proven to be the most dangerous. In reality, the legal status of a drug is a complex issue shaped by historical, cultural, political, and economic factors, not just pharmacology. For example, alcohol and tobacco are legal in most countries, yet they are responsible for far more deaths and societal harm than many illegal substances combined. Conversely, substances like psilocybin (magic mushrooms) and LSD, which have a very low potential for physical addiction and overdose, are strictly illegal in most places. It is essential to understand that legality is not a reliable indicator of a drug's potential for harm or addiction.
A more scientific way to classify drugs is based on their primary effect on the central nervous system (CNS). The three main categories are depressants, stimulants, and hallucinogens. Opiates are often considered a sub-category of depressants but are significant enough to warrant their own discussion.
| Class | Primary Effect on CNS | Psychological/Behavioural Effects | Examples |
|---|---|---|---|
| Depressants | Slows down CNS activity (often by enhancing the effect of the inhibitory neurotransmitter GABA). | Reduced anxiety, sedation, impaired coordination and judgment, sleepiness. | Alcohol, Benzodiazepines (e.g., Xanax, Valium), Barbiturates. |
| Stimulants | Speeds up CNS activity (often by increasing levels of dopamine and norepinephrine). | Increased alertness, energy, and confidence; euphoria; decreased appetite. | Caffeine, Nicotine, Cocaine, Amphetamines (e.g., Adderall, Methamphetamine). |
| Hallucinogens (Psychedelics) | Alters perception, thought, and mood (often by acting on serotonin receptors). | Profound sensory distortions, altered sense of time and self, mystical experiences. | LSD, Psilocybin (mushrooms), Mescaline, DMT. |
| Opiates/Opioids | Depresses CNS activity by binding to opioid receptors. | Pain relief (analgesia), intense euphoria, drowsiness, respiratory depression. | Heroin, Morphine, Codeine, Fentanyl, Oxycodone. |
Instructions: Below is a list of user-reported effects. In breakout rooms, for each set of effects, identify the most likely class of drug (Depressant, Stimulant, Hallucinogen, or Opiate) and explain your reasoning.
Teacher Guidance: This activity tests students' understanding of the distinct psychological and behavioural profiles of each drug class. The answers are: 1) Depressant (e.g., Alcohol), 2) Stimulant (e.g., Amphetamine), 3) Hallucinogen (e.g., Psilocybin), 4) Opiate (e.g., Heroin).
Some drugs don't fit neatly into one category. For example, MDMA (Ecstasy) has both stimulant (increased energy) and hallucinogenic (empathy, sensory enhancement) properties. Cannabis can also have effects across different categories. How does the existence of these "hybrid" drugs challenge our classification system? Does it suggest that the categories are oversimplifications of complex neurochemical interactions?
For most of history, excessive substance use was viewed through a moral model. The "drunkard" or "addict" was seen as a person with a weak character, a sinful nature, or a lack of willpower. The solution was punishment, shame, or religious conversion. The mid-20th century saw a revolutionary shift in thinking with the emergence of the disease model of addiction. This model reframed addiction not as a choice, but as an involuntary, chronic, and progressive medical illness, similar to diabetes or heart disease.
The disease model was popularized by the work of E.M. Jellinek in the 1940s and 50s. Based on his studies of members of Alcoholics Anonymous (A.A.), Jellinek proposed that alcoholism was a predictable, progressive disease with distinct phases. His work was groundbreaking because it moved the problem of alcoholism from the church and the jailhouse into the realm of medicine. He argued that the "alcoholic" was a sick person who deserved treatment, not a bad person who deserved punishment.
Jellinek's most famous contribution is the "Jellinek Curve," a U-shaped diagram that maps the progression of alcoholism and the potential path to recovery. While originally based on a specific subset of male alcoholics and now considered an oversimplification, it remains a powerful visual tool used in many treatment centers.
The left side of the curve shows the downward spiral into addiction, marked by increasing dependence and negative consequences. The bottom represents "hitting rock bottom," a point of crisis that often precedes the "uphill" path of recovery on the right side.
The disease model has had a profound and lasting impact on how society views and treats addiction. However, it is also heavily criticized for being oversimplified and potentially disempowering.
Instructions: In breakout rooms, create a T-chart listing the pros and cons of viewing addiction as a disease.
Teacher Guidance: After the groups have brainstormed, facilitate a class discussion. This debate is central to the unit and directly addresses AC 2.1. Encourage students to see the complexity—that the model can be both helpful (reducing stigma) and potentially harmful (reducing agency) at the same time.
The disease model implies a loss of control, which seems to contradict the idea that recovery requires personal choice and effort. How can these two ideas be reconciled? Can a person be suffering from a disease that impairs their ability to choose, yet still be required to make a choice to get better? This is known as the "paradox of control" in addiction.
While Jellinek's model was a crucial social and political step, the modern Brain Disease Model of Addiction (BDMA) is a neurobiological theory grounded in decades of neuroscience research. It builds on the disease concept by identifying the specific, measurable changes in brain structure and function that are caused by chronic substance use and that underlie the symptoms of addiction. The BDMA argues that addiction is a disease of the brain's reward, stress, and self-control circuits.
Leading researchers, particularly from the National Institute on Drug Abuse (NIDA), have proposed a three-stage model to explain the neurobiology of the addiction cycle. This cycle becomes more and more severe over time as drugs physically alter the brain.
This diagram illustrates a vicious cycle where each stage feeds into the next, making it increasingly difficult to break free.
Instructions: Read the following brief case study. In your breakout rooms, map the character's experiences onto the three stages of the addiction cycle.
Case Study: Alex started using opioids recreationally. At first, it was just for the intense euphoric high on weekends (Stage 1). After several months, Alex found that life seemed grey and joyless without the drug and felt intensely anxious and sick when not using. Alex started using every day just to feel "normal" and stop the withdrawal symptoms (Stage 2). Now, even after a week of being clean, seeing a movie where someone uses a needle is enough to trigger an overwhelming urge, and Alex's resolve to stay clean crumbles (Stage 3).
Discussion Points:
Teacher Guidance: This activity helps students translate the abstract neurobiological model into a concrete human experience. It reinforces their understanding of how the motivation for drug use shifts from positive reinforcement (seeking pleasure) to negative reinforcement (avoiding pain).
The BDMA suggests that the prefrontal cortex (PFC) is "hijacked" or impaired in addiction. This raises a profound philosophical question about free will. If the part of the brain responsible for self-control is compromised by a disease process, to what extent is the person truly "choosing" to use the drug? How does this neurobiological evidence challenge or support the legal and moral concepts of personal responsibility?
The Brain Disease Model of Addiction (BDMA) is the dominant paradigm in addiction science and medicine. However, it is not without its powerful critics. While few dispute that chronic drug use changes the brain, many sociologists, psychologists, and philosophers argue that the BDMA is a form of neuro-reductionism—that is, it reduces a complex human problem to a simple matter of brain chemistry, ignoring the psychological, social, and existential dimensions of addiction.
As a counterpoint to the disease model, some theorists propose a choice model of addiction. This model does not necessarily deny the biological changes that occur but places a much stronger emphasis on human agency and rational decision-making. Key tenets include:
Instructions: This debate will tackle the central controversy. In breakout rooms, consider the following statement: "Addiction is fundamentally a matter of choice, not a disease."
Teacher Guidance: This debate directly prepares students for their summative assessment. Encourage them to move beyond simple assertions and use evidence and concepts from the previous sessions to support their arguments.
Are the disease and choice models mutually exclusive? Could they be two sides of the same coin? Perhaps addiction is a "disease that affects the organs of choice." In this view, the disease process (the neurobiological changes) makes it incredibly difficult to choose otherwise, but it does not make it impossible. How does this synthesized view change our approach to treatment? (Hint: It might suggest a dual approach that combines medical interventions to heal the brain with psychological therapies to strengthen self-control and build a meaningful life).
The debate between the disease model and the choice model is not just a philosophical one; it is a scientific one that rests on evidence. But what counts as "evidence"? And how do we evaluate its quality? This session is a practical workshop designed to develop your skills in critically evaluating the scientific evidence used to support theoretical arguments about addiction. This directly addresses AC 2.2 and prepares you for the summative assessment.
Addiction researchers use a variety of methods, each with its own strengths and limitations:
When you encounter a piece of scientific evidence, you must think like a critic. Don't just accept the conclusion; question the method. Key questions to ask include:
Instructions: Below are two simplified abstracts from hypothetical research studies. For each one, work in your breakout groups to answer the critical evaluation questions above.
Abstract 1: "Using fMRI, we scanned the brains of 20 individuals with severe cocaine use disorder and 20 healthy controls while they viewed images of cocaine paraphernalia. The cocaine users showed significantly reduced activation in the prefrontal cortex (PFC) and heightened activation in the nucleus accumbens compared to controls. We conclude that addiction is a brain disease characterized by an overactive reward system and an underactive control system."
Abstract 2: "A large-scale survey of 5,000 adults found a strong positive correlation between the number of adverse childhood experiences (ACEs) and the likelihood of developing a substance use disorder in adulthood. We conclude that childhood trauma is a major cause of addiction."
Teacher Guidance:
For Abstract 1, guide students to see that while it provides strong evidence for the neural correlates of craving (supporting the BDMA), it is still correlational. Does the PFC dysfunction cause the addiction, or does the addiction cause the PFC dysfunction?
For Abstract 2, guide students to identify the classic "correlation is not causation" problem. While trauma is clearly a risk factor, there could be a third variable (e.g., genetic predisposition, poverty) that causes both trauma and addiction.
How would a proponent of the disease model and a proponent of the choice model interpret the findings from Abstract 1 differently? The disease model proponent would say, "See? The brain is broken." The choice model proponent might say, "This just shows the brain of someone who has repeatedly made a certain choice. It doesn't prove they can't make a different choice in the future." This highlights how the same evidence can be interpreted through different theoretical lenses.
This is one of the most fundamental questions in addiction science. If two people try the same drug, why might one go on to develop a severe addiction while the other does not? The answer is that addiction is not caused by a single factor. There is no single "addiction gene" or "addictive personality." Instead, addiction results from a complex interplay of multiple risk factors. The best framework for understanding this complexity is the biopsychosocial model.
The biopsychosocial model is a holistic perspective that posits that health and illness are determined by the dynamic interaction of biological, psychological, and social factors. It moves away from simple, linear explanations ("genes cause addiction") to a more comprehensive, multi-layered understanding.
A useful metaphor for understanding how these factors interact is the "Swiss Cheese Model," often used in accident analysis. Imagine a stack of Swiss cheese slices. Each slice represents a layer of protection (e.g., stable family, good mental health, no genetic risk). The holes in each slice represent a risk factor. An adverse outcome—like the development of addiction—occurs only when the holes in all the slices line up, allowing a trajectory of risk to pass through all the layers of protection.
This model illustrates a key concept: cumulative risk. It's rarely one thing that leads to addiction, but rather the accumulation of multiple risk factors across the biological, psychological, and social domains. Conversely, protective factors (like a supportive family or strong coping skills) can "block the holes" and prevent addiction even in the presence of other risks.
Instructions: As a class, using a collaborative digital whiteboard, let's build a "Swiss Cheese" model for addiction.
Teacher Guidance: This is a highly visual and collaborative way to introduce the biopsychosocial model. It helps students see that addiction is not a simple cause-and-effect issue but a result of complex interactions. This activity directly addresses AC 3.1.
The biopsychosocial model is dynamic. The factors can influence each other over time. For example, a biological predisposition (Bio) might lead to psychological traits like anxiety (Psych), which in turn leads a person to seek out a peer group that uses drugs (Social), which then leads to brain changes from chronic use (Bio). How does this concept of a feedback loop make the problem of addiction even more complex to treat?
While biology and psychology are important, they don't happen in a vacuum. The social and environmental context in which a person lives is a powerful determinant of their risk for developing an addiction. This session explores these "nurture" factors, from broad cultural influences to the immediate impact of family and peers.
The immediate social environment of family and peers is one of the most powerful predictors of substance use, especially during adolescence.
Instructions: Consider the following two individuals, who are cousins with a similar genetic background. In breakout rooms, use the social and environmental factors discussed today to explain their different outcomes.
Discussion Questions: Identify at least three social/environmental risk factors that contributed to Mike's outcome and three protective factors that contributed to Leo's outcome.
Teacher Guidance: This activity clearly illustrates the power of context. Guide students to identify factors like parental monitoring, peer group norms, socioeconomic environment, and modeling of substance use.
Peer influence is often seen as a one-way street ("bad kids" corrupting "good kids"). However, research shows it's often a matter of selection vs. socialization. Do peers cause a person to use drugs (socialization), or do individuals who are already predisposed to using drugs seek out peers who are similar to them (selection)? How do these two processes likely work together in a feedback loop?
While the social environment provides the context, individual psychological factors and personality traits play a crucial role in determining a person's vulnerability to addiction. Why do some people thrive in high-stress environments while others turn to substances? Why are some people more drawn to risky behaviours than others? This session explores the internal, psychological landscape of addiction risk.
One of the strongest predictors of developing a substance use disorder is the presence of another mental health condition. This is often referred to as co-occurring disorders or dual diagnosis. The relationship is complex and can work in several ways:
Common co-occurring disorders include depression, anxiety disorders, PTSD, and personality disorders.
Exposure to high levels of stress, particularly chronic or traumatic stress, is a major psychological risk factor. Stress impacts the same brain circuits involved in addiction, particularly the prefrontal cortex and the stress-response system (the HPA axis). Individuals who have experienced significant trauma (e.g., abuse, violence, combat) have a much higher risk of developing addiction, often as a way to numb emotional pain or manage the symptoms of PTSD.
While there is no single "addictive personality," research has identified several personality traits that are consistently linked to a higher risk of substance use disorders:
One influential model is Cloninger's Tridimensional Theory of Addictive Behaviour, which proposes that vulnerability to addiction is influenced by three key personality dimensions:
Cloninger proposed that different combinations of these traits could predict the risk for different types of addiction (e.g., high novelty-seeking predicting early-onset alcoholism).
Instructions: Let's return to our case study of Mike from the previous session. We already identified his social risk factors. Now, let's build a more complete biopsychosocial profile. In your groups, add potential biological and psychological risk factors that could have contributed to his cannabis use disorder.
Recap: Mike grew up in a low-income area with an absent parent and drug-using siblings/peers. He developed a severe cannabis use disorder.
Brainstorming Prompts:
Teacher Guidance: This activity requires students to synthesize information from the last three sessions. The goal is to create a rich, multi-layered explanation for Mike's addiction, demonstrating a full understanding of the biopsychosocial model.
How do personality traits and social factors interact? For example, a highly impulsive person (psychological risk) might be fine in a low-risk environment (e.g., supportive family, no drugs available). However, place that same impulsive person in a high-risk environment (e.g., a peer group that encourages drug use), and the risk of addiction skyrockets. This is an example of a gene-environment interaction (or more broadly, a person-environment interaction). The risk is not in the person or the environment alone, but in the combination of the two.
Research is essential for advancing our understanding and treatment of addiction. However, conducting research with individuals who have substance use disorders presents a unique and complex set of ethical challenges. People with active addictions are considered a vulnerable population in research ethics. This is because their ability to make fully informed and voluntary decisions may be compromised by factors such as cognitive impairment from drug use, the compulsion to obtain drugs, or socioeconomic desperation.
All human research is guided by core ethical principles, but they take on special significance in the context of addiction:
One of the most difficult ethical issues in clinical trials for addiction treatment is the use of a placebo control group. The "gold standard" for testing a new medication is a randomized controlled trial (RCT) where one group gets the new drug and another group gets a placebo (a sugar pill). However, is it ethical to give a placebo to a person seeking help for a life-threatening condition, thereby denying them a potentially effective treatment for the duration of the study?
To manage this, researchers often use an "active control," where the new drug is compared to the current standard treatment rather than a placebo. This ensures that no one is denied treatment altogether.
Instructions: In breakout rooms, you will act as an ethics review board. Discuss the following two research proposals and decide whether you would approve them. You must justify your decision based on the core ethical principles.
Proposal 1: The Relapse Study. "A researcher wants to study the brain activity associated with relapse. The plan is to recruit individuals who have been abstinent from heroin for one month. In the lab, they will be exposed to heroin-related cues (videos, paraphernalia) to induce craving while in an fMRI scanner. Participants will be paid £100 for their time. The goal is to identify brain markers that predict relapse."
Proposal 2: The Ayahuasca Trial. "A researcher believes the hallucinogen Ayahuasca may be an effective treatment for alcoholism. The plan is to recruit individuals with severe alcohol use disorder. One group will receive several guided Ayahuasca sessions with psychotherapeutic support. The control group will receive only the psychotherapeutic support (no placebo, as the effects are obvious). The study will last three months."
Teacher Guidance:
For Proposal 1, guide the discussion towards the conflict between beneficence (the knowledge gained could help future patients) and non-maleficence (exposing people in early recovery to powerful cues could trigger a real-world relapse). Is the payment coercive?
For Proposal 2, focus on the risks. Ayahuasca can be psychologically and physically risky, especially for people with co-occurring health problems. How can the researchers ensure participant safety? Is it ethical to use a powerful, illegal substance in research, even with a therapeutic goal?
Consider the issue of stigma in research reporting. Imagine a study finds a gene that is weakly associated with a higher risk for addiction. How could the media misinterpret and sensationalize this finding? What responsibility does the researcher have to communicate their findings to the public in a way that is accurate and avoids promoting a deterministic or stigmatizing view (e.g., the idea of a single "addiction gene")?
Just as there is no single cause of addiction, there is no single "cure." Effective treatment must be tailored to the individual's specific needs, addressing their unique combination of biological, psychological, and social problems. Modern addiction treatment is best understood as a continuum of care, with different levels of intensity and support.
Treatment can range from brief interventions to long-term residential care:
For many individuals with physical dependence on a substance, the first step before engaging in psychological therapy is detoxification (detox). Detox is the process of safely managing the acute physical symptoms of withdrawal that occur when a person stops using a substance. This is often done under medical supervision, where medications can be used to ease the symptoms and prevent dangerous complications.
It is absolutely critical to understand that detox is not treatment. It is a preparatory step. Detox manages the physical crisis of withdrawal, but it does nothing to address the underlying psychological, social, and behavioural problems that caused the addiction in the first place. A person who only completes detox without engaging in further therapy has an extremely high probability of relapsing.
Detox addresses the body's immediate reaction to the absence of the drug. Treatment addresses the brain disease of addiction—the compulsive thoughts and behaviours.
Medical supervision during detox is particularly important for two classes of drugs:
Instructions: In breakout rooms, read the following patient profiles and decide on the most appropriate initial level of care (e.g., Outpatient, Residential, Medically Managed Inpatient). Justify your choice.
Teacher Guidance:
Patient A needs Medically Managed Inpatient treatment due to the severity and risk of life-threatening withdrawal.
Patient B is a good candidate for Outpatient treatment or brief intervention.
Patient C might be a good candidate for Intensive Outpatient (IOP) or standard Outpatient, possibly combined with medication-assisted treatment. Residential treatment could be an option, but her responsibilities at home make outpatient a more practical first choice.
The "Minnesota Model" of treatment, popularized by the Hazelden Betty Ford centers, advocates for a 28-day inpatient stay as the standard. This model is highly influential in the US. Based on the continuum of care model, what are the potential problems with a "one-size-fits-all" 28-day approach? For whom might it be too much, and for whom might it be too little?
If addiction is a disease of the brain, psychological therapies are the "software updates" designed to help rewire it. These therapies don't just involve talking; they are structured, evidence-based interventions that teach individuals concrete skills to manage cravings, change destructive thought patterns, and build a life in recovery. This session focuses on two of the most widely used and effective psychological therapies: Cognitive Behavioural Therapy (CBT) and Motivational Interviewing (MI).
Cognitive Behavioural Therapy (CBT) is a type of psychotherapy based on the idea that our thoughts, feelings, and behaviours are interconnected, and that changing negative thought patterns can lead to changes in behaviour. In the context of addiction, CBT helps individuals identify and change the dysfunctional thoughts and beliefs that contribute to their substance use.
CBT works by breaking this cycle. Key techniques include:
Many people with addiction are ambivalent about changing. Part of them wants to stop, but another part of them doesn't. A traditional, confrontational approach ("You have to quit!") often backfires, making the person defensive. Motivational Interviewing (MI) is a collaborative, person-centered counseling style designed to explore and resolve this ambivalence. It is not about persuading the person to change, but about helping them find their own motivation to change.
MI is guided by a "spirit" of partnership, acceptance, compassion, and evocation (drawing out the person's own wisdom). The core skills are summarized by the acronym OARS:
Instructions: Pair up. One person will be the "client," and the other the "therapist." The client's role is to express ambivalence about a common behaviour (e.g., "I know I should exercise more, but I'm always so tired after work and I just want to watch TV.").
Class Discussion: As the client, how did each round feel? Which approach made you feel more understood? Which one made you more or less likely to consider changing?
Teacher Guidance: This simple exercise powerfully demonstrates the core principle of MI. Students will almost universally report that the advice-giving felt judgmental and unhelpful, while the reflective listening felt supportive and made them more open to exploring their own motivations.
CBT and MI are often used together. MI is frequently used in the early stages of treatment to build motivation and get the person "ready" for change. Once the person is committed to changing, the more structured, skill-building techniques of CBT are introduced. Why is this sequential approach often more effective than starting with CBT right away, especially for someone who is highly ambivalent?
While CBT and MI focus on the internal world of thoughts and motivations, other therapies focus more directly on changing behaviour through conditioning or on changing the social system in which the individual lives. This session explores these behavioural and systemic approaches, including aversion therapy, contingency management, and family and group therapy.
Behavioural therapies are based on the principles of classical and operant conditioning. They aim to change the addictive behaviour directly by altering its associated rewards and punishments.
Systemic therapies recognize that an individual's addiction does not exist in isolation. It affects, and is affected by, the social systems they are part of, particularly their family and peer group.
Instructions: Consider a 22-year-old client with a severe cocaine addiction. He is highly ambivalent about quitting, lives at home with parents who often give him money (enabling), and most of his friends use cocaine.
In your breakout rooms, design a multi-component treatment plan for him. For each of the following therapies, explain what specific goal it would target:
Teacher Guidance: This activity requires students to synthesize their knowledge of the last two sessions.
1. MI would be used to address his ambivalence and build motivation.
2. CM could provide tangible rewards for clean urine tests.
3. CBT would teach him to identify triggers and develop coping skills.
4. Family therapy would address the parents' enabling behaviour and improve the home environment.
Contingency Management is sometimes criticized as "paying people not to use drugs." Critics argue it's an external bribe that doesn't produce internal change. A proponent of CM would argue that it's a powerful tool to initiate a period of abstinence, which then gives other therapies (like CBT) a chance to work. How does this debate reflect the broader tension in psychology between behaviourist (external reinforcement) and cognitive (internal change) approaches?
If addiction is a brain disease, it follows that we should have medicines to treat it. Pharmacotherapy involves using medications to help manage addiction. These medications are not a "cure," but they can be powerful tools to reduce cravings, manage withdrawal, and prevent relapse, often used in combination with psychological therapies. This session explores the main pharmacological strategies and emerging brain stimulation techniques.
Medications for addiction generally work in one of three ways:
| Strategy | Mechanism of Action | Goal | Example(s) |
|---|---|---|---|
| Agonist Therapy (Replacement) |
The medication is a weaker, slower-acting agonist that binds to the same receptors as the drug of abuse. | Prevents withdrawal and reduces cravings without producing the intense "high." Stabilizes the person so they can engage in therapy. | Methadone or Buprenorphine for opioid addiction. Nicotine patches/gum for tobacco addiction. |
| Antagonist Therapy (Blocking) |
The medication is an antagonist that blocks the drug of abuse from binding to its receptors. | Removes the rewarding effect of the drug. If the person uses, they feel nothing, which extinguishes the behaviour over time. | Naltrexone for opioid or alcohol addiction. |
| Aversive Therapy | The medication produces a highly unpleasant reaction if the drug of abuse is consumed. | Creates a powerful deterrent based on punishment (classical conditioning). | Disulfiram (Antabuse) for alcohol addiction (causes severe nausea, vomiting, and flushing if alcohol is consumed). |
The most prominent use of pharmacotherapy is in Medication-Assisted Treatment (MAT) for opioid use disorder. This is a highly effective, evidence-based approach that combines medication with counseling and behavioural therapies.
MAT is often controversial, with some critics incorrectly viewing it as "substituting one addiction for another." However, scientific consensus is clear: MAT is a life-saving medical treatment that dramatically reduces illicit drug use, overdose deaths, and the spread of infectious diseases.
As our understanding of the neurocircuitry of addiction improves, researchers are exploring ways to directly modulate the brain circuits that are dysfunctional in addiction. These techniques are still largely experimental but hold future promise:
Instructions: For each of the following clinical goals, decide which pharmacological strategy (Agonist, Antagonist, or Aversive) would be most appropriate. Explain your choice.
Teacher Guidance:
1. Antagonist (Naltrexone) is a good choice. It blocks the pleasure and can be taken as a pill.
2. Agonist (Methadone or Buprenorphine) is the standard of care. It provides stability.
3. Aversive (Disulfiram) is the correct answer, as its purpose is to create a punishing physical reaction.
Antagonist therapy (like Naltrexone) has a major practical problem: patient compliance. For the medication to work, the person has to choose to take it every day. A person in the midst of a craving might simply choose not to take their Naltrexone so they can get high. How does this compliance issue highlight the limitations of a purely biological approach and reinforce the need for integrated psychological therapy to build motivation and coping skills?
So far, we have focused on addiction to substances. But can a person be addicted to a behaviour? The concept of behavioural addiction (or process addiction) proposes that individuals can develop a compulsive, out-of-control relationship with certain behaviours that produce a short-term reward, leading to significant negative consequences. This is a controversial but rapidly growing area of psychology.
For a long time, pathological gambling was classified as an "Impulse-Control Disorder." However, in a landmark decision, the DSM-5 reclassified it as Gambling Disorder and placed it in the chapter on "Substance-Related and Addictive Disorders." This was the first time a non-substance-related behaviour was officially recognized as an addiction. The rationale was the overwhelming evidence that Gambling Disorder looks remarkably similar to a substance use disorder:
What about other behaviours? The most debated potential behavioural addiction is Internet Gaming Disorder, which was included in the appendix of DSM-5 as a condition requiring further study. Proponents argue that some individuals' relationship with online gaming shows all the classic signs of addiction: compulsion, loss of control, withdrawal symptoms when not playing, and severe impairment in social, occupational, and academic functioning. Opponents argue that this is over-pathologizing a common hobby and that the problem is often a symptom of other underlying issues, like depression or social anxiety, rather than a primary addiction itself.
Other proposed behavioural addictions include compulsive shopping, sex addiction, and exercise addiction, though none of these are currently recognized as formal diagnoses in the DSM-5.
Instructions: In your breakout rooms, you will again act as an ethics/diagnostic committee. Your task is to debate whether "Internet Gaming Disorder" should be moved from the appendix of the DSM-5 and made an official diagnosis.
Teacher Guidance: This is a very current and relevant debate. Encourage students to apply the core definition of addiction from Session 1. Does excessive gaming meet the criteria of compulsion, craving, consequences, and loss of control in a way that is clinically significant? This directly addresses AC 4.3.
Where do we draw the line between a passion and a behavioural addiction? A professional musician might spend 10 hours a day practicing, sacrificing their social life. A marathon runner might experience "withdrawal" if they can't run. Why do we view these as dedication, but spending 10 hours a day gaming as a potential pathology? What is the key difference? (Hint: The crucial factor is often the presence of significant, ongoing negative consequences and the subjective experience of loss of control).
This session serves as a capstone for the unit, bringing together our knowledge of addiction theories with the critical evaluation skills we have been developing. The ability to read a research paper, understand its methods, and critically assess its conclusions is the single most important skill in psychology. Today, we will practice this skill in preparation for both of your final assignments.
As we've seen, the evidence for any single theory of addiction is complex and often contradictory. There is no single study that "proves" the disease model or the choice model. Instead, scientists build a case by looking for a convergence of evidence from many different types of studies. A strong theory is one that is supported by findings from animal research, neuroimaging, genetic studies, and clinical trials. A critical thinker must be able to weigh the strengths and weaknesses of each piece of evidence to evaluate the overall strength of a theoretical argument.
Let's revisit the framework from Session 8. When you read a study, you should ask:
Instructions: Below is a simplified abstract for a real, influential study in addiction research. Read it carefully. In your groups, use the 6-point framework above to prepare a brief critical evaluation.
Study: The "Rat Park" Experiment (Alexander et al., 1978)
Abstract: Previous research showed that rats housed alone in small, barren cages would readily self-administer morphine until they died, which was taken as evidence for the powerful addictive properties of the drug itself. We hypothesized that this behaviour was an artifact of the impoverished environment. We created two conditions: rats in isolated, standard lab cages, and rats in "Rat Park," a large, naturalistic environment with ample space, toys, and other rats for social interaction. Both groups had access to two water bottles: one with plain water and one with morphine-laced water. We found that rats in the isolated cages consumed significantly more morphine than rats in Rat Park. Furthermore, when rats were first forced to consume only morphine for several weeks and then moved to Rat Park, they voluntarily reduced their morphine consumption. We conclude that the environment, not the drug itself, is the primary driver of addiction.
Teacher Guidance: This is a classic study that challenges the simple disease model. Guide students to see:
- Strength: It's an experiment, so it can make causal claims. It has high theoretical importance.
- Weakness: It's an animal study. Can we generalize from rats to humans? It pits two extreme environments against each other; what about the shades of grey in human environments?
- Implication: It provides powerful evidence for the role of social and environmental factors, suggesting that treatment should focus on improving a person's environment and opportunities, not just on the individual.
How does the Rat Park study directly challenge the Brain Disease Model of Addiction (BDMA)? A strict BDMA might predict that once the rats' brains were "hijacked" by the forced morphine exposure, they would continue to seek the drug compulsively regardless of the environment. Yet, they didn't. What does this suggest about the brain's "plasticity" and its ability to recover when provided with rewarding alternatives?