Biological Model of Addiction

• Physical dependence theory- people become addicted because doing without the item or behaviour is so unpleasant.
•  An important concept associated with physical dependency theory is tolerance. E.g. a person continues to smoke because he/ she becomes tolerant, and needs to engage in the activity more and more to maintaine the positive feeling.
• Stopping the activity can result in withdrawal symptoms.

• Forshaw (2002) inicated that the initiation of smoking can be explained by a combination of several approaches e.g. biological, behavioural and cognitive.
•  There is evidence to suggest that the reason people take up smoking in the first place may well be because of their genetics.
• Lerman et al (1999) have shown that people with a particular gene are less likely to take up smoking than others. The gene is called SLC6A3-9 and works on the dopamine system.
• This gene can be discussed more in maintenance...

Whatever the reason is for starting smoking (the biological approach cannot really explain this), the reason for continuing the behaviour can be explained in the form of a chemical addiction.

We all know that cigerettes contain nicotine within the tobacco. Nicotine is an extremely addictive drug producing changes in how our brain functions... (see next card).

• Shachter (1977) asserts that the physical dependancy theory (continuing to behave in a certain way because not repeating the behaviour is so unpleasant) is relevant to smokers.
• In the nicotine regulation model, he argues that the smokers continue to smoke to maintain nicotine in the body at a level high enough to avoid any negative withdrawal symptoms.
• In his research he compared how many cigarettes different smokers needed to consume each week.
• Each of his p's were given cigarettes with a low nicotine content, and some, cigarettes with a high nicotine content.
• Those with the low nicotine cigarettes smoked more than those with the high content. Heavy smokers smoked on adverage 25% more low nicotine cigarettes.
• The high nicotine content allowed smokers to reach the level of nicotine required with fewer cigarettes. 
• This study supports the biological model as the results are based purely on physiological findings and not on social reasons... i.e. if people smoked 'to look cool' then they would have all smoked the same amount.

• Earlier I mentioned that Lerman et al showed that those carrying the gene SLC6A3-9 were less likely to take up smoking, and that the gene worked on the dopamine system in the brain.
• Sabol et al (1999) went on to show that this gene was extremely important in enhancing people's ability to stop smoking, and that those not carrying it were mre likely to remain smokers, maintaining their addictive behaviour.
• Dopamine is a neurostransmitter that is responsible for communication in different parts of the brain, including the 'reward system'.
• Nicotine has been shown to biologically increase dopamine production in the brain, thus maintaining addictive smoking behaviour continues to provide the smoker with this positive feeling.
• Coen et al (1991) showed that it is possible to train rats to self administer nicotine through implants directly into the reward centres of their brain, to provide themselves with positive feelings. Injecting the rats with a drug that prevents dopamine release decreases this nicotine self-administration.
• However, this animal research isn't generalisable to humans as we have different physiologies and we have social factors that influence our choice to smoke e.g. we know it can cause cancer. The study can also be accused of being unethical.

• A physical dependance on a drug such as nicotine can mean a quite high tolerance to it. Stopping long- term use of smoking at high tolerance levels can result in severe withdrawal symptoms. The unpleasant feelings of withdrawal can be avoided if the person relapses and resumes the addictive behaviour.
• Lerman et al (2007) have shown that smokers who are deprived of nicotine during withdrawal show increased activity in certain parts of their brain.
• After a night without smoking, there was an increased blood flow to parts of the brain concerned with attention, memory and reward in the p's. They concluded that these parts of the brain become particularly active when the person is craving a cigarette.
• The researchers also suggested that some people are more prone than othersto cravings because of changes in the brain chemistry.
• This researched demonstartes what encourages a smoker to relapse and why some people do more easily than others.

• Genetics:
• Commings et al (1996) found a specific variant of dopamine D2 receptor gene called DRD2A1 was found more often in pathological gamblers than in the general population.
• Eisen et al (1998) over 3000 male- male twin pairs of which both twins served in the US military it was found that inherited factors plus shared environmental experiences might explain 46-55% of the variance in pathological gambling. Although this study lacks external validity because of the sample.
• Winters and Rish (1998) did a study involving both males and females and found that the role of genetics might be very different for men and women, for different types of gambling activity and for different gambling criteria.
• Positive reward theory:
• Adrenaline rush that follows a bet can be addictive. It is a pleasurable experience and can be gained again and again simple by just placing another bet.
• Bergh et al (1997)- there is a link between pathological gambling, the reward centre, genetics and impulsive behaviour.

• The increase in dopamine levels when gambling is a reinforcing experience. The brain learns to repeat a behaviour in order to gain the increase in dopamine again.
• Cohen et al (2005) demonstrated that low levels of dopamine induced by a drug enhances reinforcing effects of the slot machines in pathological gamblers.
• Bennet (2006) found that dopamine is increased in excessive gamblers just when experiencing an environmental cue e.g. sounds of fruit machine.
• There has been research done into brain activities of those who gamble and those who don't. Potenza et al (2003) investigated craving states in men who were diagnosed with pathological gambling. When viewing gambling tapes, the gamblers showed different blood flow in their brains when compared with non- gamblers.

• Wray and Dickerson (1981) found that gamblers report withdrawal symptoms that are similar to those addicted to smoking. Avoiding withdrawal symptomes by continueing to gamble maintains gambleing behaviour.
• Orford et al (1996) compared alcoholcs and problem gamblers. The two groups reported similar levels of percieved strengths of addictions.
• Ciarrochi et al (1987) note another point that is relevant here. Those addicted to gambling often have other problems such as addiction to alcohol and shopping. It has been reported that when giving up gambling, people switch their attention to another of rheir addictive behaviours. When that behaviour becomes too much of a problem, they switch back to gambling. And so on...

• The biological approach is reductionist as it doesn't consider the role that psychology has to play. Explaining addiction by reference to brain structure and function implies that once identified, addiction is fully explained. But identicle brain activity is also triggered when addicts are not directly involved in addictive behaviour, suggesting that psychological factors, like conditioned responses and cognitive processes are also involved.
• Addiction to one drug can produce cross- tolerance to other related drugs and withdrawal symptoms can be addressed by taking a similar drug e.g. methadone for heroin withdrawal. This suggests that similar drugs act on the nervous system in the same way, supporting the biological model.
• The biological model is deterministic because it says that a) some people have a pre- disposition to be drug addicts (genetic) and that b) once you are addicted to a particular drug/ behaviour, you will always relapse. This is socially sensitve and the latter is proven wrong by many people.