The gateway hypothesis and the idea of common underlying liability represent two competing models to explain the relationship that is observed between different addictions and addictive behaviours.1
Within the former model, initial substance use acts as a gateway to the use of subsequent, ‘harder’ drugs, whereas the latter model focusses on the common underlying risk factors that are shared between several different forms of addiction.1
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Current evidence on the neurobiology of addictive behaviour highlights the transition from reward-driven to habitual drug use through alterations in mesolimbic dopamine, glutamatergic signalling, frontostriatal circuitry, and stress-related systems.
Functional neuroimaging studies commonly compare brain responses to substance-related cues versus neutral cues during fMRI or PET scanning and measure differential brain activation.
Recognition of addiction as a disorder of distributed brain circuits provides a framework for personalized assessment and treatment of addiction.