Who becomes addicted: genes, stress and dopamine receptors
Explains why some people use drugs without developing addiction while others do: genetics (including opioid and dopamine receptor differences), chronic stress, comorbid mental illness and social context.
Where this fitsConnects to 2 · Unlocks 2
- Connects to
- The course lens: biopsychosocial, and no 'chemical imbalance' — This is the biopsychosocial lens applied to addiction.
- Dose-response curves: potency, efficacy, slope and variability — Receptor density differences are one source of variability.
- Unlocks
- From use to addiction: receptor loss, hypofrontality, craving and relapse — Low receptor density can be a cause — or a consequence — of heavy use.
- Treating addiction: substitution, antagonists, glutamate, vaccines — and the model's limits — Genetic differences can predict who a treatment helps (naltrexone and alcohol).
Walk through
Four sources of risk
Genetic differences, stress (especially chronic), comorbid mental illness and social context all change the odds of moving from use to addiction.
Analogy and worked example
Analogy: Two people stand in the same rain. One has a good umbrella (protective genes, low stress, support), the other has holes in theirs (a risk variant, chronic stress, isolation). Same storm, very different outcome — the drug is the rain, not the whole story.
Why might a person with low D2 receptor density find a stimulant more rewarding than someone with high density?
- Fewer D2 receptors = less dopamine signaling at baseline for the same release.
Tip: the ← and → keys move through the lesson.