Explanations for nicotine addiction

The dopamine (or disease) model of addiction Syllabus Brain neurochemistry including the role of dopamine

Initiation of addictive behaviour: Dopamine is released in the mesolimbic dopamine system of the brain, to signal reward and pleasure. If a behaviour causes dopamine release then the brain knows to “do it again” – e.g. eating, drinking, keeping warm, having sex – these are adaptive behaviours in evolutionary terms as they help an organism/species to survive in its environment. Unfortunately other non-adaptive behaviours (i.e. behaviours that do not necessarily aid survival) can release huge amounts of dopamine (e.g. gambling and drug taking). Certain chemicals (e.g. amphetamines, alcohol, cocaine) can directly cause huge amounts of dopamine to be released. The effect of this dopamine release is to tell the brain that the behaviour is desirable and that it should seek to DO IT AGAIN! And according to incentive sensitisation theory, desire for the rewarding substance or behaviour persists even in the absence of the substance or behaviour.

Notes Dopamine release gives a feeling of pleasure (Eating). Possibly to strengthen positive behaviour (evolutionary). Other behaviours such as gambling, drug taking releases dopamine (reinforcing behaviour). We want to have that feeling of pleasure.

Maintenance of addictive behaviour: Repeated exposure to an addictive behaviour or substance causes reduced sensitivity to the dopamine release through a process known as down regulation. This means that more of the behaviour is needed to cause the same pleasurable psychological effect in the mesolimbic dopamine system. Stopping the behaviour altogether creates a state of disequilibrium in the dopamine system, and leads to withdrawal symptoms that can only be reduced by repeating the (now learned) behaviour. This disequilibrium, an increased need for dopamine stimulation, and the unpleasant withdrawal symptoms it causes now drive behaviour so that it is no longer pleasure (positive reinforcement), but the need to reduce withdrawal symptoms (negative reinforcement) that drives the addict’s behaviour.

Notes Down regulation: More behaviour required (smoking more) to get same pleasurable feeling. Leads to disequilibrium in the dopamine system, and leads to withdrawal symptoms. Which can be alleviated by taking the substance It can change from being a positive reinforcement I.e. giving pleasure. To negative reinforcement (reducing the withdrawal symptoms).

Relapse of addictive behaviour: When an addict finally manages to stop engaging in a behaviour or taking a substance, they are at risk of relapse. According to the dopamine model, relapse can be explained by addiction causing permanent brain changes that lead to lasting memories of the substance or behaviour. Environmental reminders of the addiction (e.g. being in a pub, watching horse racing, returning to a location where drugs were taken, being under stress) can release small amounts of dopamine, which in turn lead to the addicted person desiring a greater dopamine reward that can only be obtained by re-engaging in the addictive behaviour.

Notes Relapse due to permanent brain changes. Cannabis Environmental reminders of the addiction (e.g. being in a pub, watching horse racing, returning to a location where drugs were taken, being under stress) can release small amounts of dopamine which makes us want more.

The neurotransmitter dopamine is released into the mesolimbic system, which interacts with the nicotinic receptors to produce these feelings of euphoria and heightened pleasure to keep these feelings going you must increase the amount of nicotine.

Over time, the concentration of nicotine required to provoke deregulation increases periodically, and so the individual is said to have developed a tolerance towards nicotine.

There is evidence supporting the role of dopamine in the deregulation of nicotinic receptors, as suggested by McEvoy et al (1995). Patients taking the dopamine antagonist Haloperidol, which binds to and blocks dopamine receptors, smoked significantly more than those who were not taking the drug. This suggests a higher consumption of nicotine was needed to maintain the deregulation of nicotinic receptors, due the blocking of dopamine action. This in turn suggests that an increased level of nicotine is needed to compensate for decreased dopamine levels, thus supporting the role of dopamine in the maintenance of nicotine addictions.

Notes McEvoy et al (1995). If dopamine is blocked then people smoke more indicating that dopamine has an effect on nicotine addiction.

But However, Berrendero et al (2010) have suggested that there has been too much emphasis on the role of dopamine in the maintenance of nicotine addictions, and that there is not one isolated system or neurotransmitter which is solely responsible. For example, modern research has shifted their focus onto GABA and serotonin, as well as the role of endorphins which may produce the ‘euphoric’ and ‘painless’ feelings associated with a hit of nicotine. Therefore, a broader scope of research is required.

Notes Not Just nicotine could be other neurotransmitters such as GABA. Modern research has shifted their focus onto GABA and serotonin, as well as the role of endorphins which may produce the ‘euphoric’ and ‘painless’ feelings associated with a hit of nicotine.

Better An interactionist approach may be a better explanation for nicotine addiction, whilst acknowledging the role of biological factors. The key problem with a reliance on dopaminergic explanations, as suggested by Choi et al (2003) is the idea of biological reductionism, where nicotine addiction is reduced to the activity of neurotransmitters. Despite such neurotransmitter activity being a biological predisposition or ‘diathesis’ (tendency towards), psychosocial risk factors for the development of addictions may be more important, such as peer and family influences. This may therefore explain the statistic that only 50% of regular smokers develop a nicotine addiction, as they may be surrounded by ‘protective’ psychosocial factors e.g. a family with strong -anti-smoking’ views.

Interactionist approach taking into account: Genetics (predisposition) Social factors (peer group, family, socio-economic background) Neurotransmitters This may therefore explain the statistic that only 50% of regular smokers develop a nicotine addiction, as they may be surrounded by ‘protective’ psychosocial factors e.g. a family with strong -anti- smoking’ views.

Support for the dopamine model of addiction: Support for the dopamine model comes from many experimental studies, such as a study into the effects of ritaline (Volkow, 2001). Volkow gave a drug called ritalin to healthy volunteers and correlate their subjective experience of the drug with the density of dopamine receptors in their mesolimbic dopamine systems. Those that reported pleasurable feelings with ritalin had fewer dopamine receptors than those that hated its effects. This supports the theory that some people are more vulnerable to the effect of dopamine-releasing drugs than others.

Neurochemical explanations ignore social factors: An important point to note is that neurochemical explanations for addiction (e.g. the dopamine model) ignore social and environmental factors that may also contribute to addictive behaviour. However, they can lead to effective treatments for addictions, e.g. replacing cigarettes with nicotine patches.

Implications from animal research: Grant et al (1998) found that animals that lost social status also lost dopamine receptors, and offers therefore a possible explanation for social-class based addictions (e.g smoking in lower socio-economic groups). However, animal studies may not be generalisable to human addictive behaviour.

Inevitability of dopamine sensitivity leading to addiction: The dopamine model suggests that reduced dopamine sensitivity, as caused by fewer dopamine receptors, inevitably leads to addictive behaviour. However, there is likely to be a complex interaction between an individual's specific environment and whether or not dopamine sensitivity leads to addiction. A stimulating environment may provide enough dopamine reward to protect people from addiction, whereas a dull or boring environment may not (Volkow, 2003).

Neurochemical explanations are reductionist: Neurochemical explanations for addiction reduce addictive behaviour to a simple variance in the structure of the dopamine system, and so ignore social and cognitive factors that can influence addictions. However they can lead to effective treatments, so in this case it is useful to be reductionist.

Smoking Syllabus learning theory as applied to smoking behaviour including reference to cue reactivity

Why do people start smoking? Adolescents experiment with smoking for psychosocial reasons such as ‘I’m tough now because I smoke’. Within groups of adolescents smoking is seen as pleasurable and as making individuals more popular. According to Jarvis (2004) smoking is an act of rebellion that is more common in people who come from smoking backgrounds, and is more common in deprived areas. The desire to adopt an image as a ‘smoker’ is sufficient to overcome the unpleasantness of the first few cigarettes, after which physiological addiction (the dopamine system) takes over.

Do people start smoking because their parents do? There is a link between pregnant mothers smoking and their children becoming smokers themselves. Having a mum who smoked does not cause a greater chance of starting smoking, but it does double the chance of becoming addicted (Buka et al, 2003).

The role of self esteem in smoking Other factors that may start people smoking are low self-esteem (makes people vulnerable to any addictive behaviour), and even using nicotine as an appetite suppressant for weight loss.

Physical and psychological effects of nicotine Nicotine causes dopamine to be released in the brain which creates temporary feelings of pleasure for the smoker. The feelings of pleasure only last a short time (a few hours at most) before being replaced with withdrawal symptoms (e.g. loss of concentration, low mood, anxiety) that can only be relieved by having another cigarette.

Socioeconomic status and nicotine addiction Fidler at al (2008) found a strong link between low socioeconomic status and smoking – i.e. smoking is more prevalent among poorer people.

Commentary (evaluation) for smoking addiction

Smoking and popularity The idea that adolescents start smoking in order to be more popular is supported by Mayeux et al (2008) who found a positive link between smoking at age 16 and popularity at age 18, however this was only true for boys. Therefore adolescents start smoking to make themselves popular, which is the opposite to many other addictive behaviours (such as sex and drinking) that seem to be more likely among teenagers who are already popular. In other words, an adolescent may start smoking in order to fit in with his or her peers; but adolescents who are already popular may indulge in other addictive behaviours such as drinking or sex.

Physiological and psychological effects of nicotine Khaled et al (2009) found there may be permanent changes to brain chemistry that directly affects mood. Smokers had higher rates of depression than people who had never smoked, and smokers wanting to quit had the highest rate of depression. A problem with this study is cause and effect – do smokers smoke because they are depressed (i.e. self-medication), or does smoking cause depression?

Socioeconomic status and nicotine addiction Pertti-Watel et al (2009) found a link between poor housing conditions, low socio-economic status, and smoking. They suggested that improving smokers’ living conditions would be more successful at reducing smoking than other types of intervention.

Syllabus learning theory as applied to smoking behaviour including reference to cue reactivity I reckon you could do this without being taught.

Have a go

SLT Psychologists have suggested that nicotine addictions can be explained using social learning theory: it is a learned behaviour, and can be acquired through both classical and operant conditioning. A key feature of operant conditioning would be reinforcement, both negative and positive. This increases the likelihood of a certain behaviour being repeated.

Operant Conditioning Positive reinforcement suggests that we carry out certain behaviours because we are motivated by the consequent rewards. Smoking can be positively reinforced by the reward of the euphoric feelings of nicotine stimulating the dopaminergic mesolimbic system, increasing the likelihood that we will smoke again to achieve the same reward.

Negative reinforcement suggests that we carry out certain behaviours because we want to avoid unpleasant consequences. Smoking can be negatively reinforced by avoiding unpleasant withdrawal symptoms, through progressively increasing nicotine intake and therefore prolonging the period of desensitisation or deregulation of nicotinic receptors.

Cue reactivity suggests that there are certain environmental cues, such as attending parties or social gatherings, which increase the likelihood of engaging in addictive behaviours, such as smoking. These environments contain both primary reinforcers (the pleasurable effects of smoking) and secondary reinforcers which coincide with the benefits of smoking (such as the smell of cigars, the cardboard feel of the packet and the neat arrangement of cigarettes). Primary and secondary reinforcers work together, through the process of cue reactivity (made up of behavioural responses, physiological responses and our own personal attitudes towards smoking) to reinforce and maintain excessive smoking habits.

On the positive Learning theory is able to explain gender differences in smoking, as suggested by Carpenter et al (2014). Women are less likely to give up smoking and more likely to relapse, which may be due to their poor self-efficacy i.e. not believing that they are able to give up smoking. This may also be due to women potentially being more social than men, being engaged in more social events and caring about interpersonal relationships, all of which could increase their sensitivity to cues which trigger smoking, and thus more easily lead to an addiction through the mechanism of cue reactivity.

The use of learning theory as an explanation for nicotine addiction has particularly useful real life applications because aversion therapy and covert sensitisation is based upon these same principles. For example, Smith (1988) found that aversion therapy using electric shocks produced nicotine addiction recovery rates that were at least 32% higher compared to people who had simply decided to stop smoking. Therefore, an improved understanding of learning theory as an explanation for nicotine addiction may serve as economical implication of psychological research, where improved NHS and public health service guidelines for the treatment of such a common addiction could be beneficial for sufferers.

Negatives Biological approach. Discussion Interactionist approach.