Risk Factors in Addiction

Genetic Vulnerability

Twin and molecular genetic studies suggest a heritable component to addiction vulnerability. McGue (1999) reviewed twin studies of alcohol dependence and found concordance rates of approximately 50-60% for MZ twins and 30% for DZ twins, indicating significant genetic contribution. Kendler et al. (2000) estimated the heritability of tobacco smoking at around 60-70% in a large Virginia twin registry. At the molecular level, the ALDH2*2 allele, common in East Asian populations, encodes a deficient form of aldehyde dehydrogenase, causing an aversive flushing reaction to alcohol — providing natural protection against alcohol use disorder. Variants in dopamine receptor genes (DRD2, DRD4) have been associated with individual differences in reward sensitivity, potentially mediating vulnerability across substance and behavioural addictions.

Stress

Koob and Le Moal (2008) proposed that chronic stress activates the corticotropin-releasing factor (CRF) system and the HPA axis, producing a state of negative affect (anxiety, dysphoria). Substances that relieve this negative affect provide powerful negative reinforcement — a key mechanism maintaining addiction. Under stress, the threshold for relapse is significantly reduced. Wills and Shiffman (1985) developed the stress-coping model: substances are used as a coping strategy to regulate negative emotional states. Individuals with fewer alternative coping resources are therefore at greater risk of developing or maintaining addiction.

Personality

Zuckerman (1994) identified sensation seeking — a trait characterised by the need for novel, varied, and intense experiences, and willingness to take risks — as a key personality risk factor for substance use. High sensation seekers are drawn to substances precisely because they produce rapid and intense reward. Verdejo-García et al. (2008) conducted a systematic review and identified impulsivity as the personality characteristic most consistently associated with substance misuse across drugs and populations. Impulsive individuals struggle to delay gratification and to inhibit responses despite adverse consequences — both features that increase addiction risk.

Family Influences

Orford (2001) emphasised that family environments shape addiction risk through social learning: children who observe parents or siblings using substances as coping strategies are more likely to adopt the same patterns. Beyond modelling, family dysfunction — including parental neglect, permissive attitudes to substance use, and exposure to domestic conflict — elevates risk. Flores (2004) proposed that insecure attachment is a significant pathway: individuals with disrupted early attachment relationships may use substances or addictive behaviours as a substitute form of emotional regulation, providing comfort and relief in the absence of secure relational bonds.

Peers

Peer influence is particularly powerful during adolescence, when identity formation and social conformity pressures are at their peak. Simons-Morton et al. (2001) found that peer substance use was the strongest single predictor of adolescent smoking initiation, outperforming parental smoking, availability, and advertising exposure. Peers shape addictive behaviour through direct pressure, normative beliefs ('everyone does it'), social facilitation (substances consumed in social contexts are experienced as more rewarding), and modelling. Social exclusion and peer rejection may also push vulnerable adolescents towards substance-using peer groups as a form of belonging.

Evaluation

Risk factors interact: genetic vulnerability may increase the rewarding properties of substances (diathesis); stress, family dysfunction, and peer influence provide the environmental triggers (stress). No single risk factor is deterministic — most individuals exposed to even multiple risk factors do not develop addiction, reflecting the role of protective factors (secure attachment, social support, self-regulation skills). A biopsychosocial model integrating genetic, psychological, social, and environmental factors is most consistent with the evidence.

Key Takeaways

  • Genetic: McGue (1999) — alcohol MZ 50-60%, DZ 30%; Kendler et al. (2000) — tobacco heritability 60-70%. ALDH2*2 protective in East Asian populations; DRD2/DRD4 variants linked to reward sensitivity.
  • Stress: Koob & Le Moal (2008) — stress → negative affect → substance use as negative reinforcement. Wills & Shiffman (1985): stress-coping model — substances regulate negative emotion.
  • Personality: sensation seeking (Zuckerman, 1994) and impulsivity (Verdejo-García et al., 2008) most consistently linked to addiction.
  • Family: Orford (2001) — social learning of parental substance use. Flores (2004) — insecure attachment → substance use as emotional regulation.
  • Peers: Simons-Morton et al. (2001) — peer smoking strongest predictor of adolescent smoking initiation. Operates via modelling, norms, social facilitation.
  • No single factor is deterministic. Diathesis-stress model: genetic vulnerability + environmental triggers interact to produce addiction.