Biological Model of Addiction

A genetic factor could explain why some people develop addictions to things that many people are exposed to but do not normally develop an addiction.

There may be multiple genes involved or different genes for different addictions; nicotine addiction could be affected by a gene involved in nicotine addiction

Sayette & Hufford (1997) found a higher concordance rate for alcholism between MZ twins than DZ twins.

Kendler (1999) found in a twin study that heritability of nicotine addiction could be 60-70%

Not clear how a genetic link would work - the genes may affect the biological response to substances or affect the behavioural response.

Likely that genetics only cause a predisposition that would need to be triggered by environmental influences.

Twin studies don't show 100% concordance - other factors must be involved.

Altman et al (1996) found that dopamine is increased by nicotine and alcohol.

People with susceptibility to addiction may have a more sensitive mesolimbic dopamine pathway, so would gain more reward.

Research has found low levels of serotonin in addicts - serotonin might usually regulate impulsive behaviour by limiting reinforcing effects.

Opoid neurotransmitters such as endorphins are activated by pleasurable states and also by drugs. Naltrexone is a drug used to treat alcoholism and works by blocking opoid receptors, reducing pleasurable effects.

Naltraxone is an effective treatment so alcohol must affect the opoid system.

Krishnan-Sarin et al (1999) found that long-term smoking disrupts the opoid system.

Most data is correlational - cause and effect?

Deterministic: suggests that a person has very little control over their addiction so may discourage them from trying to quit.

Reductionist: fails to take into account the effects of environmental stimulus and the role of social learning.

Has implications for drug treatments.