Biological Model of Gambling Initiation
Initiation: genetic predisposition to gambling addictions.
Black et al (2006): 1st degree relatives of pathological gamblers are more likely to develop the same addiction than more distant relatives.
A1 variant of DRD2 gene: this gene determines amount of dopamine receptors. People with the variant have fewer dopamine receptors, leading to less feelings of pleasure which dopamine is responsible for. They may therefore try to make up for this by gambling.
Biological Model of Gambling Maintenance
Maintenance: change in neurochemistry and tolerance while gambling.
Gambling has been found to increase dopamine and noradrenaline in players' brains, giving them a rush of pleasure.
Shinohara et al (1999): measured neurochemisty of problem gamblers during a winning streak and found the above to be true. After time, our receptors develop a tolerance to these neurotransmitters, making us feel the need to gamble more for the same original rush.
Biological Model of Gambling Relapse
Relapse: withdrawal symptoms from stopping gambling.
As gambling causes excess amounts of dopamine and noradrenaline, a process called homeostasis occurs.
This causes neuroadaption, which makes our brain produce less natural dopamine and noradrenaline to compensate for the increased amount. When problem gamblers stop, they have lower than average amounts of dopamine and noradrenaline.
This causes negative physical and psychological withdrawal symptoms such as insomnia, muscle weakness, breathing problems and appetite loss.
Rosenthal (1992): 60% of recovering problem gamblers experience these symptoms.
The fastest way to remove these symptoms is to relapse, forcing dopamine and noradrenaline production.
Evaluation of the Biological Model of Gambling
Strength: explains individual differences.
Genes can act as a biological predisposition to a form of behaviour, such as gambling. Therefore, genetic differences can explain why some people might develop a gambling addiction while others don't, despite exposure to similar environments. The environment acts as a trigger for the addiction, but only to those who have the genetic predisposition. (Diathesis-Stress Model)
Weakness: cannot explain levels of addictiveness.
The approach cannot explain why some forms of gambling are more addictive than others.
Breen & Zimmerman (2001): online gamblers developed an addiction in about a year while it took sports/horse gamblers an average of 3 and a half years to develop an addiction. The biological model cannot explain these differences, therefore weakening the validity of the approach.
Biological Model of Smoking Initiation
Initiation: genetic predisposition to smoking addiction.
Studies have shown that smoking addiction may run in families as heritability is between 40% and 80%.
A1 variant of DRD2: this gene determines amount of dopamine receptors. People with the variant have fewer dopamine receptors, leading to less feelings of pleasure which dopamine is responsible for. They may therefore try to make up for this by smoking.
Biological Model of Smoking Maintenance
Maintenance: change in neurchemistry and tolerance while smoking.
Cigarettes contain nicotine which binds to nAchR receptors in the brain, releasing dopamine (eliciting a rush of feelings of pleasure).
After repeated use, nAchR receptors build up a tolerance to nicotine and less dopamine is produced.
Therefore, smoking is maintained to achieve the same original rush of pleasure produced by nicotine/dopamine production.
Biological Model of Smoking Relapse
Relapse: withdrawal symptoms from stopping smoking.
As the nicotine in cigarettes causes excess amounts of dopamine, a process called homeostasis occurs.
This causes neuroadaption, which makes our brain produce less natural dopamine to compensate for the increased amount. When smokers stop, they have lower than average amounts of dopamine.
This causes negative physical and psychological withdrawal symptoms. The easiest way to remove these is to smoke, therefore relapse occurs to remove withdrawal symptoms.
Evaluation of the Biological Model of Smoking
Mixed Evidence: Vink et al. (2005)
Studied 1572 Dutch twin pairs for smoking habits. Found that initiation was 44% caused by genetics and 56% caused by the environment. Conclusion: while initiation of smoking may be more down to environmental factors, the likelihood of an addiction forming is definitely determined by biological differences.
Strength: real world application
One way to undo homeostasis while avoiding withdrawal is by gradual weaning, giving your body time to adjust to the amount of dopamine that it produces. This has led to nicotine replacement therapies.
Weakness: reductionist view
The biological model attempts to reduce the cause of addiction to simple mechanisms, ignoring other factors such as the environment (peer pressure). This lowers the validity of the approach.
Cognitive Model of Gambling Initiation
Initiation: false expectation of gambling.
Gambling is used to self-medicate for depression. This doesn't help, but if the user percieves it to, then the addiction initiates.
Cognitive Model of Gambling Maintenance
Maintenance: change in processing the risks and benefits of gambling.
A con of gambling is the risk of losing. However, an addict develops irrational beliefs about gambling which gives them a sense of control from supersition e.g. wearing lucky socks.
Therefore, the addiction is maintained as the user percieves control and fails to see the risks.
Cognitive Model of Gambling Relapse
Relapse: overestimation of pros and underestimation of cons in gambling.
Gambling addicts may overestimate the good times and underestimate the bad, as a result of recall bias - focus on the times they won, and not the times they lost, putting the gambling in a positive light.
Therefore, relapse occurs because of a faulty perception of the positives of gambling.
Li et al. (2008) - Research Support
Method: compared 2 groups of gamblers - one who gambled for pleasure, and one who gambled to "escape reality".
Findings: those who gambled to escape reality were more likely to suffer from other forms of addiction.
Conclusion: self-medicators are likely to suffer from an overall addiction problem due to their faulty thought processes about addictive acts
Evaluating the Model
A key point of the model is that addiction is used as a self-medication to treat a negative psychological symptom such as depression. This is supported by research that shows the majority of pathological gamblers also suffer from some form of depressive disorder.
However, studies only show a correlation. It is possible these people are depressed because of their gambling problem, or because of a third variable such as biology which causes the problem.
Cognitive Model of Smoking Initiation
Initiation: false expectation of smoking.
It is reported that people smoke when they experience a negative mood and that smoking will replace it with a positive one. It is argued that people become addicted because they develop a false expectation that smoking can be used as self-medication to treat their negative moods.
Cognitive Model of Smoking Maintenance
Maintenance: change in processing the risks and benefits of smoking.
Brandon et al. (1999): argues that smoking addiction is maintained due to unconscious automatic processing.
As the addiction develops, when we are in a bad mood, we automatically smoke to alleviate the negative emotions. This also explains why it is so hard to quit.
Cognitive Model of Smoking Relapse
Relapse: overestimation of pros and underestimation of cons of smoking.
Once a person has quit, a common reason for relapse is that a user finds more reasons to go back to smoking than to stay quit. If a user percieves great benefit, they will find little motivation to resist the urge.
Relapse occurs due to a faulty perception of the benefits of smoking.