You are viewing a free preview of this lesson.
Subscribe to unlock all 10 lessons in this course and every other course on LearningBro.
If addiction is, in large part, a matter of what substances do to the brain's reward and receptor systems, then it follows that drugs which modulate those systems should be able to help reduce it — and this is the logic of drug therapy, the principal biological treatment for addiction. Pharmacological treatments do not work by persuasion or insight; they work by altering the neurochemistry of craving, reward and withdrawal so that abstinence becomes achievable. This lesson examines the main classes of drug therapy through the lens of agonists and antagonists: agonist and substitute therapies that supply or mimic the substance to ease withdrawal and craving (nicotine replacement therapy; methadone and buprenorphine for opioid dependence), antagonist therapies that block the reward of using (naltrexone), and aversive drug therapy that makes use unpleasant (disulfiram for alcohol). It considers each drug's mechanism, its effectiveness, and the wider harm-reduction and clinical-guidance (NICE) context that shapes how these treatments are actually used. A recurring theme is the contrast between treatments that manage the symptoms of addiction — withdrawal, craving, reward — and the psychological and social factors that a drug alone leaves untouched, and the consistent finding that combined treatment outperforms medication used in isolation. Substance misuse is treated clinically and objectively throughout, in the standard academic register of A-Level teaching.
Key Definition: In addiction pharmacology, an agonist binds to and activates a receptor, mimicking the substance (used to reduce withdrawal and craving); an antagonist binds to a receptor and blocks it, so that the substance no longer produces reward; and an aversive drug makes using the substance produce unpleasant effects, adding a deterrent.
This lesson addresses the Edexcel 9PS0 — Paper 2, Topic 8: Health Psychology content on the biological (drug) treatment of addiction: agonist and substitute drug therapies (nicotine replacement therapy; methadone and buprenorphine in opioid dependence), antagonist drug therapy (naltrexone), and aversive drug therapy (disulfiram), including their mechanisms, their effectiveness and the harm-reduction and clinical-guidance context in which they are prescribed. In assessment-objective terms, you should be able to describe how agonist, antagonist and aversive drug therapies work at the level of receptors and neurochemistry (AO1), apply this knowledge to a described case — for example, selecting or explaining an appropriate drug therapy for a person with a particular addiction (AO2), and evaluate drug therapy, including its strong evidence base and scalability, its symptom-focused and compliance-dependent nature, its ethical and harm-reduction dimensions, and its limited applicability to behavioural addictions (AO3).
Connects to…
Drug therapies follow from the biological explanation: if addiction is driven by the action of substances on reward and receptor systems, then medications that modulate those systems should help. They divide into three broad strategies, each attacking a different point in the addiction cycle.
| Strategy | What it does | Point in the cycle targeted |
|---|---|---|
| Agonist / substitute | Supplies or mimics the substance in a controlled, safer form to reduce withdrawal and craving | Removes withdrawal and craving as obstacles to abstinence |
| Antagonist | Blocks the receptors the substance acts on, so using no longer produces reward | Removes the reinforcement — using no longer "pays" |
| Aversive | Makes using the substance produce unpleasant physical effects | Adds a deterrent cost to using |
Understanding this three-way logic is the key to the whole lesson: substitution eases the path to abstinence by removing withdrawal; antagonists attack the reward so relapse is less rewarding; and aversives attach a penalty to use. Which is chosen depends on the substance, the evidence base, and the individual's circumstances and preferences.
Nicotine replacement therapy (NRT) is an agonist/substitute treatment: it supplies controlled nicotine without the harmful combustion products of cigarette smoke, via patches, gum, lozenges, inhalers or nasal sprays. Because it delivers nicotine — an agonist at nicotinic acetylcholine receptors — it directly occupies the receptors that drive craving. It works by:
NRT maps neatly onto the neuroadaptation account from the biological explanation: by keeping nicotinic receptors gently and steadily stimulated, it prevents the acute craving state that drives the next cigarette, then reduces the level slowly enough for the upregulated receptors to readjust. A further advantage of separating the nicotine from the cigarette is that it begins to break the conditioned behavioural habit — the hand-to-mouth ritual, the cues of lighting up — even while withdrawal is being managed. This is one reason NRT is markedly more effective when combined with behavioural support, and why some smokers use a combination of a slow-release patch (for steady background nicotine) with a fast-acting form such as gum or spray (to manage sudden cue-triggered cravings). NRT is a harm-reduction treatment in the clearest sense: even where full abstinence is not immediately achieved, replacing smoked tobacco with clean nicotine removes the tar and combustion toxins responsible for most smoking-related harm.
For opioid dependence, the leading agonist/substitute treatments are methadone and buprenorphine. Both act on the same opioid receptors as heroin, but in a controlled, medically supervised way that transforms the pattern of use.
Both are cornerstones of opioid substitution therapy (OST), a harm-reduction approach whose aims extend beyond abstinence: by stabilising the person on a legal, oral, known-dose medication, OST reduces injecting and needle-sharing (and hence the transmission of blood-borne viruses such as HIV and hepatitis C), reduces overdose deaths, reduces drug-related crime, and retains people in treatment where other health and social needs can be addressed. This reframing — from "cure" to reducing the harm associated with continued dependence — is central to how these drugs are understood clinically.
graph TD
A[Opioid dependence] --> B[Substitution therapy]
B --> C[Methadone: full agonist, long-acting]
B --> D[Buprenorphine: partial agonist, ceiling effect]
C --> E[Prevents withdrawal, reduces craving]
D --> E
E --> F[Harm reduction: less injecting, fewer overdoses, retention in treatment]
Key Definition: Harm reduction is an approach to addiction whose primary aim is to reduce the health, social and economic harms associated with substance use — not necessarily to achieve immediate abstinence. Substitute therapies (NRT, methadone, buprenorphine) are its main pharmacological tools.
Antagonist drug therapy works by blocking the receptors that the addictive substance acts on, so that using the substance produces little or no reward. The principal example is naltrexone, an opioid antagonist.
The contrast with substitution is instructive. A substitute (methadone) satisfies the receptor to remove withdrawal; an antagonist (naltrexone) blocks the receptor to remove reward. Antagonist therapy therefore depends heavily on the person's motivation and compliance — nothing physically compels them to keep taking a drug whose only effect they notice is the absence of a high they are trying to give up — which is a central theme in its evaluation. Because gambling engages the same opioid-modulated reward circuitry, opioid antagonists have also been trialled for gambling urges, with some promising results, though there is no established, approved pharmacological treatment specific to gambling disorder.
Aversive drug therapy takes the opposite approach to substitution: rather than easing use, it makes use unpleasant. The principal example is disulfiram, used in alcohol dependence.
Disulfiram works by blocking an enzyme in the normal metabolism of alcohol (aldehyde dehydrogenase). As a result, when a person taking disulfiram drinks, a toxic metabolite (acetaldehyde) accumulates, producing a highly unpleasant reaction: flushing, throbbing headache, nausea and vomiting, palpitations and breathlessness. The knowledge that drinking will produce this reaction is intended to deter alcohol use — the person abstains to avoid the aversive consequence. Two features are important. First, disulfiram is properly understood as an aversive/deterrent, not a reward-blocker: it does not reduce craving, and it works entirely through the anticipated unpleasantness of drinking. Second, and consequently, it is entirely dependent on compliance — it only deters drinking on the days it is actually taken, and a person who wishes to drink can simply stop taking it a day or two beforehand, which is why it is often most effective when taken under supervision (for example, administered by a pharmacist or a family member).
Key Definition: An aversive drug therapy such as disulfiram makes consuming the addictive substance produce unpleasant physical effects, so that the person abstains to avoid the aversive consequence. Unlike an antagonist, it does not block reward or reduce craving — it works purely as a deterrent, and only while it is being taken.
| Drug therapy | Class | Substance | Mechanism |
|---|---|---|---|
| Nicotine replacement (NRT) | Agonist / substitute | Nicotine | Supplies clean nicotine; eases withdrawal and craving; tapered |
| Methadone | Full agonist / substitute | Opioids | Occupies opioid receptors steadily; prevents withdrawal, no "rush" |
| Buprenorphine | Partial agonist / substitute | Opioids | Partially activates + tightly binds opioid receptors; ceiling effect; lower overdose risk |
| Naltrexone | Antagonist | Opioids; alcohol | Blocks opioid receptors; removes the "high"/dampens reward of use |
| Disulfiram | Aversive | Alcohol | Blocks alcohol metabolism; drinking causes an unpleasant reaction |
Drug therapies are not prescribed in a vacuum; in UK practice their use is shaped by clinical guidance — most influentially that issued by the National Institute for Health and Care Excellence (NICE) — and by the harm-reduction philosophy that underpins much addiction treatment. Several principles recur. First, drug therapy is generally recommended alongside psychological and behavioural support, not as a stand-alone treatment, reflecting the consistent evidence that combined treatment outperforms medication alone. Second, treatment goals are understood on a spectrum from immediate abstinence to reduced harm, so a treatment such as opioid substitution is judged not only by whether it achieves abstinence but by whether it reduces injecting, overdose and disease transmission and retains the person in services. Third, the choice of drug is individualised — matched to the substance, the person's history, their risk profile and their own goals — rather than applied uniformly. Understanding this context is important for evaluation: it means the "effectiveness" of a drug therapy has to be judged against the aim it is being used to serve, and it explains why treatments that fall short of curing addiction can still be strongly endorsed as effective harm-reduction tools.
A practical consequence of the three-way logic is that the same substance can be treated with different drugs depending on the person's stage, motivation and goals. Consider opioid dependence. A person who is not yet ready or able to stop, and for whom the priority is to reduce the immediate dangers of injecting street heroin, is a candidate for a substitute (methadone or buprenorphine): the aim is harm reduction and stabilisation, and the drug works whether or not the person is highly motivated, because it directly relieves withdrawal. By contrast, a person who has already completed detoxification and is strongly motivated to stay abstinent is a candidate for an antagonist (naltrexone): there is no withdrawal to relieve, the aim is relapse prevention, and the treatment leans on the person's own motivation to keep taking a drug whose only felt effect is to block a high they are trying to renounce. The same distinction runs through alcohol treatment, where a reward-dampening antagonist (naltrexone) and a deterrent aversive (disulfiram) suit different patients — the former reducing craving and the "pull" of drinking, the latter deterring a motivated abstainer who values a supervised external check on impulsive drinking. Seeing drug therapy as a menu matched to the individual, rather than a single standard prescription, is exactly the reasoning that scenario questions reward, and it is the clinical reality that guidance such as NICE's is designed to support.
Subscribe to continue reading
Get full access to this lesson and all 10 lessons in this course.