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Biological or medical model
It is worth mentioning at the outset that the medical model is generally
better at explaining chemical addiction than it is behavioural and it is
better at explaining maintenance of an addictive habit than its
acquisition.
In attempting to explain addictive behaviour the medical model assumes
the following:
Initiation
is due to a genetic vulnerability or predisposition which is triggered
by some environmental stressor
Maintenance
is via the dopamine and the activities of the brain’s reward system
Relapse
is due to physiological cravings and the need to avoid physical
withdrawal symptoms
We shall consider each in turn.
Genes and addiction (Initiation)
Clearly if there is a genetic factor we would expect to see trends for
the disorder in families and similarities between people most closely
related.
Sarafino (1990) found that children born of alcoholic parents were four
times more likely than usual to develop drinking problems themselves.
Clearly this in itself doesn’t rule out shared environment as a
contributory factor, but the tendency still remained true even when the
children had been adopted by non-alcoholic parents.
Agraval and Lynskey (2008) compared MZ and DZ twins and concluded that
there was a moderate to high concordance rate (0.3 to 0.7) for addiction
to a variety of drugs. However, they also reported that age, gender and
culture were also major contributory factors; all of which would be the
same for MZ twins!
More recent research by Wendy Slutske (2010) has looked at the
concordance rates of MZ and DZ twins in relation to gambling addiction.
She studied nearly 5,000 individuals and found that the concordance rate
for MZ twins was twice as high as the concordance rate for DZ twins.
However, as she herself points out, it isn’t possible to isolate the
genetic effects from environmental and social. Instead she describes a
‘perfect storm’ of inherited vulnerability combined with the presence of
gambling role models in the form of parents. Slutske’s is also
important in highlighting similar risks for both men and women.
Previous research has tended to focus on men.
Specific genes
Slutske believes that between 10 and 100 individual genes may be
involved in creating the vulnerability. Modern techniques with DNA have
allowed specific genes to be isolated for certain behaviours and
conditions. However, with psychological disorders these aren’t usually
so clear cut. Agraval et al (2008) believed that chromosomes 18 and 19
might be related to cannabis use. Higuchi et al (2008) reported that
Mpdz gene may predispose some animals to alcohol addiction. I’ll
consider the role of DRD2 in more detail on the next page. |
Evaluation
Fowler (2007) looked at the cases of over 1000 twins and found that
environmental and social factors were crucial in the initiating of
addictive behaviours (including nicotine, alcohol and cannabis) whereas
genetic and neurological factors were most closely linked with
maintenance and the behaviours becoming heavier.

Indirect effects
As with many behaviours, it may be difficult to pin down a specific gene
as predisposing to a specific
behaviour.
However, genes may be related to certain, broader personality types that
then may predispose certain behaviours.
With addiction, certain genes may predispose the individual to
antisocial and attention seeking behaviour. Attention seeking behaviour
has been linked with alcoholism (Jang et al 2008) and with gambling
(Comings et al 1996).
Evaluation of gene evidence
Some specific genes have been implicated in specific addictions, but
then subsequent research has found that many with that addiction don’t
possess that particular variant of gene.
DRD2 variant A1
One such gene is the DRD2 gene that codes for D2 dopamine receptors.
This variant has been linked with smokers (48%), alcoholics (42%),
gamblers (50%) as well as with other disorders, particularly autism.
However it is also found in 25% of the general population, many we have
to assume have no obvious psychological or behavioural issues.
However, its role in dopamine pathways makes it an obvious candidate for
involvement in addiction given the crucial role dopamine appears to play
in the addiction process.
Basically those with the A1 variant have significantly fewer dopamine
receptors, so think about what that might mean in practice. Fewer
dopamine receptors would seem to suggest less pleasure! It might
therefore follow that to get the same amount of pleasure as a ‘normal’
brain the person would need to engage in more of the pleasurable
behaviour, e.g. drink more alcohol.
This is similar to Eysenck’s physiological explanation of extroversion.
According to Eysenck, extroverts have lower levels of cortical arousal
so need to seek out additional stimulation. This appears to be true of
addicts but regarding lowered levels of pleasure
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