Biological Models of Addiction

Biological Models of Addiction

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Genetics of Addiction

Genetic explanations aim to suggest that the inidividual has a genetic predisposition in becoming more susceptible to addictive behaviours.

Lynskey et al (2006) found that when reviewing cases of illicit drug abuse and dependancy there was a high genetic influence with heritablility ranging from 45-79%

A1 Variant of the DRD2 Gene:

Individuals with the A1 variant appear to have fewer dopamine receptors in the pleasure part of the brain making it known as the 'Reward Gene' This means that even a little bit of dopamine would cause a lot of pleasure for these people.

A study looking at smokers found that a significantly higher number of smokers had the A1 variant at 48% where as 29% of the rest of the population did.

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Genetics Evaluation

Individual Differences:

The genetic explanation can explain why some people will become addicted to certain things like smoking and some wont be even though they've been exposed to the same environmental factors.

Inconsistent research findings:

Where as some studies such as Nobel (1998) who found alcoholics to be mooe likely to have the DRD2 Gene, others found no link what so ever or a very weak relationship.

Other Disorders:

The A1 variant of the DRD2 gene has been detected in other mental disorders such as Autism, this challenges the idea of it being a 'Reward Gene' as people with these disorders are not exactly pleasure seekers.

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The Disease Model - Dopamine

Initiation: Research has found that addictive drugs stimulate a reward circuit in the brain which triggers the release of dopamine and effectively tells the brain to do it again. For example crack cocaine triggers a rapid release of dopamine into the mesolimbic pathway which then gets the brain to link the pleasurable experiences with the drug.

Maintainance: Chronic exposure to drugs eventually results in a reduction of positive reward circuits in the brain (down regulation). The individual then creates a stress situation characterised by withdraw symptoms, this negative state then becomes the driving force in the drug craving as people no longer take the substance for the pleasurable effect, but instead as a way of avoiding having to experience the negative effects.

Relapse: Even though the drug no longer produces much of a reward the brain still recieves signals that says if you take it you will be rewarded due to the memories of it. Addicts try to abstain from it but are constantly surrounded by cues which trigger the same response, even though they know there is no reward coming there is still a release of dopamine. The frontal cortex is less effective at making decisions which heightens the risk of relapse.

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Volkow et al (2001) found that by giving participants a drug which slowly increases dopamine levels some of them liked the sensation while other hated it, he found that the ones whom liked it had fewer dopamine d2 receptors. This would explain why some people when exposed to the same thing might not get addicted.

There are limitations of the neurochemical explanation as they ignore the idea of other social factors making the approach reductionist. However as the addiction is seen as a disease, it can therefore be treated.

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Hey. Thanks for this. What does the "A1 variant" mean?

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