INITIATION is the process where the individual starts to become addicted.
MAINTAINANCE is the process where people continue to behave in an addicted way, even in the presence of negative consequences
RELAPSE is where an individual has managed to abstain from their addictive behaviour, but has started to show signs and symptoms of the behaviour again.
There is some evidence to suggest that addictions are caused by a genetic predisposition. This is where an individual may have inherited the addiction and therefore be genetically predisposed / more vulnerable to develop the addictive behaviour.
MERIKANGAS ET AL (1998) found that in 36% of the cases they looked at, where an individual had been diagnosed with an alcohol-use disorder, they also had genetic relatives who were diagnosed with an alcohol-use disorder.
TWIN STUDIES and probably more crucially, ADOPTION STUDIES have provided strong evidence to suggest that genetics do play a vital role in the development of addictive behaviours. HEATH AND MARTIN (1993) found 39 - 60% heritability for alcohol dependence.
Researchers have identified two pathways that seem to be particularly important in the development of addictive behaviour, notably substance addictions.
DOPAMINE REWARD SYSTEM: Dopamine is one neurotransmitter that has been at the centre of lots of research into psychological behaviours. There are a number of dopamine systems in our brains and the MESOLIMBIC DOPAMINE SYSTEM seems to be involved in motivation (reward).
When functioning normally, the mesolimbic dopamine system releases small amounts of dopamine. As it releases just small amounts this could explain why most of us maintain a relatively stable mood. It has also been found that alcohol and nicotine seem to increase the amount of dopamine released (ALTMAN et al., 1996). Consequently, the increased level of dopamine motivates the individual to want more alcohol and / or nicotine resulting in addictive behaviour.
OPIOID SYSTEM: Opioid neurotransmitters include ENKEPHALIN (associated with feelings of pleasure and euphoria) and ENDORPHINS (also associated with pleasure and pain relief). The opioid system is directly activated by drugs such as nicotine, alcohol and heroin.
Another theory suggests that when individuals take psychoactive drugs (cocaine, nicotine and caffeine) it can actually result in changes in brain chemistry. Therefore when an individual stops taking the drugs, the biochemical changes no longer occur. This could explain withdrawal symptoms and also why people sometimes develop a drug tolerance where they need to take more and more drugs in order to produce the same effects.
USING BIOLOGICAL MODELS TO EXPLAIN SMOKING AND PRO
- Biochemical: Nicotine increases levels of dopamine which acts as a reward and could explain why an individual may become addicted to smoking once trying it.
- Genetics: It may also be that they have a genetic predisposition to developing an addiction once exposed – eg fewer dopamine receptors.
Biochemical: The release of serotonin and increased heart rate gives the person a ‘high’ and this and may explain why they develop an addiction.
Genetics: They may also have a genetic predisposition – eg lower serotonin levels.
USING BIOLOGICAL MODELS TO EXPLAIN SMOKING AND PRO
Biochemical: The increased release of dopamine is rewarding and may therefore explain why individuals may maintain an addiction – encouraging them to smoke particularly when stressed/upset
Biochemical: Individual is encouraged to maintain gambling due to increased serotonin/heart rate experienced when playing and even more so when winning. Use gambling when feeling down.
Individual is encouraged to maintain gambling due
Neuroadaptation: When the individual abstains from smoking they experience withdrawal symptoms. The individual may choose to smoke again in order to avoid withdrawal symptoms.
Neuroadaptation: The experience of withdrawal symptoms leads them to relapse in order to get rid of unpleasant symptoms.
EVALUATION OF BIOLOGICAL MODELS AND SMOKING
SHIELDS (1962) looked at 42 twin pairs who lived apart and found that in all but 9 cases they were concordant (where one twin was a smoker, so was the other). Provides support to suggest there is a genetic vulnerability because the twins lived apart, to a large extent ruling out environmental factors. However, there were 9 cases where they were not both smokers suggesting they may have been genetically more vulnerable, yet the addiction had not (yet) been triggered by any environmental influences.
LI ET AL (2003) also found that heritability for nicotine addiction is high (39-80%).
KENDLER ET AL (1999) found that nicotine dependence shows 60 – 70% heritability
PERGADIA ET AL (2006) identified a genetic link to the experience of withdrawal from nicotine.
None of the evidence shows 100% concordance/heritability therefore unable to completely rule out environmental factors – ignores the role of nurture.
Volkow et al: (2001) Ritalin administered to adult volunteers to raise dopamine levels. Some loved it some hated it. Those that loved it had fewer dopamine receptors.
- This shows that some are more vulnerable to the effect of dopamine enhancing drugs so are more vulnerable to addictions.
- Nicotine reaches the brain in less than 10 seconds, which is quicker than if it had been injected straight into the bloodstream. It is also known that nicotine acts as a stimulant as well as a depressant therefore it has both an arousing and a relaxing effect on an individual’s mood: something smokers enjoy. Nicotine is thought to activate the mesolimbic dopamine pathway, which would explain why it is found to be motivating (rewarding) and addictive.
EVALUATION OF BIOLOGICAL MODELS AND GAMBLING
EISEN, LIN AND LYONS (1999) found evidence for a genetic vulnerability to gambling.
EISEN ET AL (2001) investigated a genetic basis for pathological gambling and found twins have a similar incidence and severity of gambling problems (and this co-occurred with alcohol misuse).
BLACK ET AL (2006) found that gambling was more prevalent in close relatives.
COMINGS ET AL (2001) has suggested that some genes may control the activity of neurotransmitters such as dopamine and serotonin.
These studies suggest that gambling may have a biological cause. This supports both a genetic role in gambling and an underlying physiological explanation for addictions in general.
Shinohara, Yanagisawa and Kagota (1999) have found that there is an increase in the level of serotonin when gamblers are on a winning streak and they experience a ‘high’.
In addition, Meyer et al. (2004) compared the level of neurotransmitters secreted whilst a group of problem gamblers engaged in gambling (experimental condition) or played cards but not for money (control condition). They found that in both conditions their heart rate and level of serotonin increased, but this was even greater in the condition where they were playing for money.
Rosenthal and Lesieur (1992) found that 60% of gamblers experienced physical withdrawal symptoms (insomnia, loss of appetite, muscle weakness, breathing difficulties). They also found that in some cases these withdrawal symptoms were more severe than those associated with drugs – supports neuroadaptation.
- Evidence based on scientific research – falsifiable.
- Blood tests, ECG’s, etc, are well controlled so have high internal validity, but artificial settings may lack external validity. some very realistic so improves external validity