Substance use disorders are chronic, treatable medical conditions — not failures of willpower. Pharmacotherapy is one component of care alongside counselling, peer support (AA, SMART Recovery, NA), regular clinical review, and management of co-occurring mental-health conditions. The medications below address three distinct dependencies through complementary mechanisms; the best choice for a given patient depends on which substance is being treated, the goal (abstinence vs reduction), comorbid conditions, organ function, motivation, and the availability of behavioural support.
Smoking cessation — nicotinic-receptor partial agonist. Champix (varenicline 1 mg) is one of the most effective single agents for tobacco dependence, producing 1-year abstinence rates roughly two to three times placebo. As a partial agonist at the α4β2 nicotinic-acetylcholine receptor it both dampens cravings and blocks the rewarding effect of any cigarette smoked during the course. The 12-week protocol titrates from 0.5 mg once daily to 1 mg twice daily with a quit date set 8–14 days into therapy; 12 weeks of additional maintenance roughly doubles 1-year abstinence. The original 2009 FDA black-box was removed in 2016 after the EAGLES trial found no significant excess of neuropsychiatric events. Renal-dose adjustment is required at eGFR < 30.
Alcohol use disorder — aldehyde-dehydrogenase inhibition (deterrence). Cronotol 500 mg, Esperal 250 mg, Dizone 250 mg, and Firam 250 mg are all disulfiram: the oldest licensed AUD pharmacotherapy, in clinical use since 1949. By irreversibly inhibiting aldehyde dehydrogenase, disulfiram causes acetaldehyde to accumulate when any alcohol is consumed — the disulfiram–ethanol reaction (flushing, nausea, palpitations, hypotension). It is a deterrent rather than a craving-reduction drug and works best in motivated patients with structured supervision. The 500 mg strength (Cronotol) is used in the loading phase; the 250 mg formulations (Esperal, Dizone, Firam) are the standard maintenance dose. Patients must be alcohol-free for at least 12 hours before the first dose, must avoid hidden ethanol sources (mouthwash, cough syrup, vinegar, after-shave, hand-sanitiser, fermented foods), and require baseline + 2-week + monthly LFT monitoring for the first 3 months because of rare idiosyncratic hepatotoxicity. Do not co-prescribe with metronidazole, tinidazole, or isoniazid.
Alcohol or opioid use disorder — opioid-receptor antagonism (craving reduction). Nalsign, Nalcon, Nodict, and Naltima are naltrexone 50 mg, a long-acting μ-opioid receptor antagonist. In alcohol use disorder it dampens the reward of drinking (COMBINE study, 2006); in opioid use disorder it blocks the effect of any opioid taken. Unlike disulfiram, naltrexone produces no aversive reaction — a slip is uneventful, which is therapeutically useful. Patients must be opioid-free for 7–10 days (14 days for methadone) before starting for OUD or naltrexone precipitates severe withdrawal; most prescribers run a naloxone-challenge test before the first dose. Major operational consideration: opioid analgesia is largely blocked while on naltrexone — surgical, dental, and emergency-department teams must be informed, and a wallet card carried.
Alcohol use disorder maintenance — NMDA / glutamate modulation. Acamptas 333 mg en Acamprol 333 mg are acamprosate calcium, the second first-line oral pharmacotherapy for AUD alongside naltrexone. After chronic heavy drinking, the brain up-regulates NMDA glutamate receptors and down-regulates GABA-A receptors as adaptation; on cessation this leaves a relative glutamate hyperactivity producing the protracted post-cessation syndrome (insomnia, anxiety, irritability, dysphoria) that drives late relapse. Acamprosate modulates NMDA-receptor function and helps the brain re-equilibrate. Standard dose is two 333 mg tablets three times daily (1,998 mg/day) with food; the dose is halved at eGFR 30–50 and acamprosate is contraindicated below eGFR 30. The interaction profile is exceptionally clean (no hepatic metabolism, no CYP activity), making it the preferred AUD agent in patients with established liver disease.
Off-label adjunct — multi-mechanism anticonvulsant. Topamac (topiramate 25 / 50 mg) is licensed for epilepsy and migraine prophylaxis but has substantial evidence (Johnson 2007) for off-label use in alcohol use disorder, particularly in patients who have not responded to naltrexone or acamprosate or who have comorbid migraine. Multi-mechanistic action (sodium-channel blockade, GABA-A potentiation, glutamate AMPA antagonism, carbonic anhydrase inhibition) is thought to dampen reward circuitry. Slow titration (25 mg per week over 8 weeks to a 100–300 mg/day target) is essential because cognitive side effects (“topa-dopa”: word-finding difficulty, mental slowing) are dose-limiting. Specific safety considerations: 2–3-fold increase in oral cleft malformation in first-trimester pregnancy (effective contraception is mandatory), nephrolithiasis (~1.5%, mitigated by aggressive hydration), rare acute angle-closure glaucoma (any eye pain or visual change in the first month is an emergency), and metabolic acidosis. Renal-dose adjusted.
Hoe te kiezen: for tobacco dependence, varenicline is first-line monotherapy; for alcohol use disorder, current guidelines (NICE, APA, ASAM) place naltrexone and acamprosate as first-line — choose naltrexone where craving and reward are the dominant relapse driver, choose acamprosate where the protracted post-cessation glutamate-hyperactivity syndrome (sleep, anxiety, dysphoria) dominates, or in established liver disease. Disulfiram is a strong second-line option for highly motivated patients with structured daily supervision. Topiramate is a reasonable off-label option after first-line failure or with comorbid migraine. For opioid use disorder, naltrexone is the non-controlled option; opioid-agonist therapy (methadone, buprenorphine) is the alternative and often preferred where adherence is uncertain. All pharmacotherapy works substantially better when paired with structured behavioural support — the medication does not treat the disorder alone.
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