Substance Use Disorder

Substance use disorder is a relapsing condition characterised by continued use despite harm, driven by neuroadaptation in reward, stress and executive control circuits rather than by weak willpower. The clinical picture varies by substance, but the treatment principles do not: the interventions that change mortality are pharmacological and behavioural, not nutritional. In opioid use disorder, buprenorphine and methadone roughly halve all-cause mortality, and withholding them in favour of abstinence-only approaches increases overdose deaths after periods of reduced tolerance. In alcohol use disorder, naltrexone and acamprosate have solid randomised evidence, and withdrawal itself can be fatal — seizures and delirium tremens require medical management, not self-detox. One nutritional intervention genuinely matters: high-dose parenteral thiamine prevents Wernicke encephalopathy, which becomes irreversible Korsakoff syndrome if missed. Glucose given before thiamine can precipitate it. Nutritional repletion supports recovery but does not treat the disorder.

• •Craving and preoccupation with use
• •Loss of control over amount or duration
• •Tolerance requiring larger amounts
• •Withdrawal symptoms on stopping
• •Continued use despite clear harm
• •Neglect of work, study or relationships
• •Repeated unsuccessful attempts to cut down

• •Genetic vulnerability and family history
• •Adverse childhood experiences and trauma
• •Co-occurring depression, anxiety, ADHD or PTSD
• •Early age of first use
• •Chronic pain and prescribed opioid exposure
• •Social isolation and unstable housing

Neuroadaptation in mesolimbic dopamine signalling, amplified stress reactivity through the extended amygdala, and impaired prefrontal inhibitory control, interacting with genetic vulnerability, trauma exposure and social environment.