Two main approaches explain why some people develop addiction and others do not: a biological / genetic account and a learning (peer-pressure / social-learning) account. As with depression, the modern view integrates both.
Genetic vulnerability (Kaij and other twin studies)
Kaij (1960) studied alcoholism in twins:
- Compared concordance for alcoholism in monozygotic (MZ) and dizygotic (DZ) twin pairs.
- MZ concordance ~54%, DZ ~28% — substantial genetic contribution.
- Replicated by other studies (e.g. Goldberg et al. on Vietnam veterans; Pickens et al. 1991).
Adoption studies (Cloninger, 1981) — Swedish adoptees with biological alcoholic parents had ~3× the risk of developing alcoholism even when raised by non-alcoholic adoptive parents. Strong evidence for inherited vulnerability.
Specific mechanisms:
- Genes affecting alcohol metabolism (ADH and ALDH variants — common in East Asian populations protective against alcoholism via the "flushing" reaction).
- Variants of dopamine receptor genes (e.g. DRD2 A1 allele) linked to reward sensitivity.
- Genes affecting impulsivity and risk-taking.
Genetic risk is polygenic — many small contributions — and generally accounts for ~40–60% of variance in addiction risk. Therefore environment matters too.
Learning theory: peer pressure and reinforcement
The learning approach explains addiction through operant conditioning, classical conditioning and observational learning:
Operant conditioning
- The drug or behaviour produces a reward (dopamine release, social approval, anxiety relief). This positively reinforces future use.
- Removing withdrawal/anxiety by using again is negative reinforcement — making the user use again to feel "normal."
Classical conditioning
- Repeated pairing of cues (a particular pub, certain friends, time of day) with drug effects creates conditioned cravings when those cues appear later. Explains relapse triggered by environments associated with use.
Observational learning (social learning theory)
- Children and adolescents observe parents and peers using substances and model their behaviour.
- Bandura's social learning theory predicts modelling is more likely when the model is high-status, similar to the observer, or seen to be rewarded.
- Peer pressure — direct social influence: explicit invitations ("everyone's having one"); fear of social rejection; conformity (Asch-style normative pressure).
Evidence
- Akers et al. (1979) — adolescents' alcohol and drug use predicted by social learning variables (peer use, perceived approval, modelling).
- Sutherland's differential association theory in criminology — exposure to peers who endorse and use drugs predicts uptake.
- Observational studies of teenage onset show peer-group composition is the strongest single predictor of first use.
How they fit together
The modern view is diathesis–stress for addiction too: genetic vulnerability sets a baseline susceptibility; environmental learning experiences (family modelling, peer pressure, stress) determine whether the vulnerability is expressed.
Strengths and weaknesses
Genetic theory strengths: clear twin and adoption evidence; explains why some people become addicted on first exposure while others don't. Weaknesses: doesn't explain why addiction rates differ across cultures; doesn't account for psychological triggers.
Learning theory strengths: explains why addiction tends to start in adolescence (peer-driven); accounts for environmental cues and relapse; supports treatment by changing environments. Weaknesses: doesn't explain why people in similar environments differ (genetics); risks individualising what may be partly biological.
⚠Common mistakes— Common errors
- Treating either theory as sufficient on its own.
- Citing concordance without explaining what it means (rate at which both twins share the trait).
- Forgetting that peer influence works via modelling AND direct pressure AND perceived norms.
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