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Psychology of addictive behaviour
Definition of addition: Most of these only consider addiction to drugs (chemical addiction): World Health Organisation (WHO): ‘a state of periodic or chronic intoxication produced by repeated consumption of a drug; natural or synthetic.’ Concise Oxford Dictionary: ‘An addict is a person addicted to a habit, especially one dependent on a specific drug.’ However, although most early research centred on drug taking, other behavioral addictions are now recognized, for example: gambling, eating, sex, exercise, work, internet, shopping etc… Most modern definitions of addictive behaviour involve ‘loss of control’ or ability to regulate behaviour: ‘A repeated habit pattern that increases the risk of disease and/or associated personal and social problems. Addictive behaviours are often experienced subjectively as ‘loss of control’ – the behaviour contrives to occur despite volitional attempts to abstain or moderate use.’ Krivanck (1988) believes addiction is best seen as a process rather than a behaviour or entity and also best explained on a spectrum of severity. However, loss of control is subjective and raises ethical issues since it suggests a certain level of culpability and blame.
Addiction as Disease (AAD) Our stereotypical view of an addict is likely to be based on one addicted to drugs, particularly alcohol. This view sees an individual compelled to continually take the substance to avoid symptoms of withdrawal and who undergoes changes in behaviour, willing for example, to commit crimes and neglect their job and loved ones in order to feed their habit. Criticisms of AAD
Behavioural addictions Can behavioural addictions such as gambling be classified similarly to chemical addiction? Clinical criteria of addiction (Carnes 1991):
Griffiths (1996) believes these ten criteria can be subsumed nicely into the following six:
1. Salience: The behaviour becomes the most important thing to the person and they have it on their minds for much of the time. Alcohol and nicotine addicts tend not to be so obvious in this regard, since they are able to combine their addiction with other behaviours in social settings. However, once deprived of their fix, salience becomes far more apparent. 2. Mood modification The addict gets a rush or buzz when engaged in the behaviour. The addict is also able to use their behaviour to bring about a mood change. Interestingly, the same chemical or behaviour can alter mood in different directions depending on time or setting. Nicotine can stimulate in the morning or relax before sleep. 3. Tolerance Usually associated with chemical addiction such as alcohol or heroin, this one can also be applied to behaviours. Basically the addict needs bigger and bigger hits to get the same effect as they did initially with smaller amounts. Risk-taking behaviour, for example, tends to get more extreme over time. 4. Withdrawal symptoms Changes in mood, shakes, irritability etc. as a result of cessation. Applies to behavioural as well as chemical addiction. 5. Conflict The pursuit of short term pleasure can cause conflict with other; parents, spouse, friends and can also result in conflict within the person. 6. Relapse A tendency to return to the behaviour, months or even years after an apparent ‘cure.’ Again this is just as common with behavioural addiction as it is with chemical. Griffiths believes that all six need to be present for a diagnosis of addiction. However, others disagree, believing that addiction doesn’t always result in undue disruption to a person’s lifestyle and occasionally no withdrawal symptoms are experienced on cessation. Addiction or enthusiasm? If it adds quality to a person’s life: Enthusiasm If it detracts from a person’s life: Addiction
The main thrust of this topic is synoptic and looks, yet again, at the main theoretical approaches or perspectives to psychology:
Models of addiction Biological or Medical model: Addiction is the result of something physical. This could be genes, brain chemicals or brain structure. The biological model of addiction is unusual however, in that it has some overlap with the behaviourist explanation. Psychological models Behaviourist: Considers addictions to be learned either by operant or classical conditioning, or perhaps by social learning and vicarious reinforcement. Cognitive: Considers the role of decision making, faulty thinking, perceptual biases and relapse prevention. Social: Considers the importance of social and situational variables (experiential model) and of weak character (moral 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 it is acquisition. 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. Addiction to chemical substances is due to physiological changes in brain structure and changes in brain chemistry. Neurotransmitters Addictive chemicals tend to be chemically very similar to naturally occurring brain chemicals such as dopamine. They are therefore able to activate nerve pathways in the brain and send abnormal messages; for example cannabis and heroin. Cocaine on the other hand works by stimulating nerve endings into producing very large amounts of natural neurotransmitters that have a stimulating effect on areas of the brain.
Reward centres (mesolimbic system) Be warned this isn’t easy stuff, and introduces you to a few brain areas, not before encountered. Olds and Miller (1954) found that rats will press a lever to electrically stimulate certain brain areas, and will do so in preference to food and even sex! It is worth pointing out that pleasure is a very adaptive experience. If we didn’t find food and sex pleasurable we’d starve to death or not reproduce!
Ventral tegmental area (VTA) The VTA is comprised of dopamine neurons. Nearly all drugs that result in addiction increase levels of dopamine in the MLS. Dopamine neurons respond when stimulation similar to reward is present. Dopamine is released into the forebrain and nucleus accumbens (NAcc). Nucleus accumbens (NAcc) The NAcc is comprised of mostly GABA neurons. It seems that the NAcc is involved in acquiring and triggering conditioned behaviours and seems to be involved in increased sensitivity to drugs as addiction progresses.
Prefrontal cortex (PFC) The PFC is responsible for executive functions; cast your memory back to the working memory model at AS. The central executive appears to be located in the PFC. It seems that the PFC is able to override or moderate our baser instinctive drives that may be triggered by the lower centres of the brain including the limbic system. However, it seems that some drugs can block these higher functions leaving us unable to suppress less appropriate responses and control our behaviour. Certain areas of the PFC appear to have quite specific functions, for example there seems to be areas responsible for inhibiting behaviours that may bring short term reward at the expense of long term losses; which would include most drug-taking habits. Damage or impairment to these areas would lead us prone to making bad choices for short term gain. There is evidence from some addicts that this is the case. However, there is the usual issue of cause and effect. It could be that addiction leads to brain damage in these locations. Other areas such as the basolateral amygdala seem to be involved in motivation. The hippocampus has a role in memory and learning and seems to alter dopamine levels in the NAcc and VTA. Regardless of the complex pathways involved, what seems clear is that addictive drugs over-stimulate dopamine pathways and flood the brain with dopamine. This is associated with feelings of intense pleasure, resulting in euphoria and repeated use.
Tolerance (desensitisation) Repeated drug use will result in consistently high levels of dopamine. Eventually the brain will adapt by producing less dopamine resulting in a dampening down and less experience of pleasure. To achieve the same result, increased quantities of the drug will be needed. Not only does the pleasure disappear but it can be replaced by unpleasant effects, particularly anxiety. The drug user now has to take drugs, not to get the pleasure as initially, but to stave off the unpleasant side effects and withdrawal symptoms (in behaviourist terms the drug is now acting as a negative reinforcer… removing the unpleasant).
Genetics of addictive behaviour 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!
Specific genes 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.
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.
Evaluation of medical model As always the medical model offers a reductionist model of a complex behaviour. It fails to take into account social and cultural factors as well as other situational and dispositional factors to be considered when we look at vulnerability. For example, self esteem and the attribution process. The brain mechanisms involved in any behaviour seem to be multifarious. A particular chemical can effect many different pathways in the brain and sometimes even result in what appear to be incongruous results. For example nicotine appears to be able to increase arousal whilst decreasing stress, which if you cast your minds back to AS would seem to be impossible.
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. 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. Interestingly, it might also explain why those brought up in poverty (both in terms of wealth and environment) may be more prone to taking drugs. A lack of environmental pleasure is compensated for by taking chemicals. Those in more stimulating surroundings don’t need the extra buzz, even if their brains lack the D2 receptors. The medical model therefore might explain individual differences and why some people who experience the same situational stimuli are less likely to develop addictive behaviours. Psychological explanations of addictive behaviour
As you’d expect, here we shall consider the idea that addictive behaviour is learned. In practice this has proved to be the most successful approach in treating addiction so would appear have some validity. First, by way of background information we shall consider the idea of schedules of reinforcement. I shall explain these mostly in terms of Skinner’s work on lever-pressing rats, however, similar patterns can be seen in human behaviour. As always with the behaviourist approach it is useful to consider Mowrer’s two stage approach when explaining the acquisition and maintenance of any behaviour:
Schedules of reinforcement
Continuous schedule Operant conditioning is based on the idea of a behaviour reinforced is likely to be repeated. However, the behaviour does not need to be reinforced every time it is performed for the learning to take place. In fact if a rat were to be fed every time it pressed a lever (continuous reinforcement) it would very soon become full and lose interest. Drinks machines operate on this schedule. Put money into a drinks machine you expect to get something out every time. If you don’t you stop the behaviour straight away… it becomes extinguished. If you want to maintain a behaviour, in the absence of reward, for example as is needed in casinos, bingo halls, amusement arcades, you need to adopt a more irregular schedule of reinforcement. Other schedules can be based on time (interval) or number of behaviours performed (ratio).
Interval schedules A behaviour may be rewarded every 5 minutes providing the behaviour has occurred in that time. This is called fixed interval. Payment at the end of the month would be a human example. Alternatively, reward may be on a variable interval schedule. Reward may be after 5 minutes, or sometimes 15, perhaps sometimes 2 minutes etc. This is less predictable and leads to slower extinction. If after 5 minutes there is no reward the animal keeps pressing. Perhaps reward may be after 25 minutes this time. Ratio schedules Time is no longer an issue. In rat terms reward occurs after so many presses. This may be every 10 presses (fixed interval) or it may be variable ratio.
Operant conditioning of this sort is better at explaining maintenance as opposed to initial acquisition. However, it is effective at explaining both chemical and behavioural addiction via the process of reinforcement. Chemical addiction can also be explained in terms of avoidance of the punishment of withdrawal. The behaviourist model always emphasises the role of environmental factors in shaping our behaviour. It has long been known that environment is crucial in relapse following treatment so the behaviourist approach has been one of the more successful approaches in the treatment of addictive behaviour. As early as 1948, Wikler found that heroin addicts were far more likely to relapse when in a similar situation or with the same people as when indulging in the habit originally. Shiffman (1996) asked former smokers to record when and where they relapsed and foud it was always in situations were readily available and when with other smokers.
Evaluation of behaviourist approach Operant conditioning is very good at explaining the maintenance of addictive behaviour and at its persistence via the deliberate use of variable ratio schedules of reinforcement. However, classical conditioning is not so useful in explaining behavioural addictions. If addiction is due to an association between gambling behaviour (for example) and winning, then why do addicts continue to gamble even after a very long losing streak? Why doesn’t the behaviour become extinguished? With chemical addiction the association of behaviour followed by buzz remains so will not extinguish. However, classical can explain spontaneous recovery of the behaviour. Following a long period of abstinence, one slip can cause relapse since it triggers the long-lost association. As always the model can be criticized for being reductionist. It takes a complex human behaviour and attempts to explain it in terms of contingencies and patterns of reward. It takes no account of individual differences or thought processes. We are all exposed to similar media pressures and gambling opportunities so why do some of us resist and others succumb?
No surprises from the cognitive perspective either. This approach always emphasizes the importance of perceptions and thinking as well as schemas. In its simplest form the cognitive approach assumes that addiction behaviour is due to irrational beliefs. For example regular gamblers have the irrational belief that the odds are not stacked against them and tend to over-estimate the extent to which their behaviour can affect outcomes. In particular they tend to under-estimate the money they put in whilst over-estimating their winnings. Unlike the medical and behaviourist models the cognitive model considers the thinking that underlies the behaviour. Self-medication This approach assumes there are reasons for the person’s choice of ‘addiction.’ Although they don’t set out with the intention of becoming addicted , there is a reason why, for example, alcohol is the drug of choice rather than cigarettes. The person may be overly anxious or feel that they’re lacking in confidence. Alcohol would therefore be seen as a way of overcoming these problems. If the issue is stress, nicotine may be the drug of choice. However, although there may be some face validity here, very often the drug of choice does not have the desired effect. Nicotine increases stress levels and former smokers who have kicked the habit generally experience less stress. However, as always with the cognitive model, it is the individuals perception that is important. Parrott (1988) explains this in terms of withdrawal symptoms. Abstaining from nicotine, even for a brief period, causes increased stress and anxiety in the form of cravings. Smoking immediately removes this anxiety and in the very short term reduces the perception of stress. Longer term use however, increases stress but this isn’t noticed. Evaluation The model does assume an underlying or prior psychological problem, such as stress. This isn’t always apparent in addicts. However, Sanjun et al (2009) reported that some women who suffer frequent sexual abuse drink excessively often do develop drinking problems. In this case the alcohol acts to help remove their sexual inhibitions, making the abuse that little bit more tolerable.
Griffiths’ Heuristics Much more familiar ground now, for those of you who understand the usual workings of the cognitive model. As we saw at AS and then again with Piaget, schemas play an important role in mental process (cognition) and are useful in explaining all manner of behaviours. Schemas (I refuse to use that horrible word ‘schemata’ as the plural) Schemas are essentially ‘mental representations’ that allow us to picture, visualize etc. all manner of situations, events, objects. We all have a schema for ‘dog’ that kicks in when one is mentioned. Schemas allow us to be ‘cognitive misers’ providing us with existing templates and saving valuable mental processing time. Remember that stereotypes are essentially schemas for people (individuals or groups). So where is this leading? Heuristics A heuristic (like a schema or stereotype) is a mental shortcut that allows us to make judgments and decisions, with minimal thinking effort involved. Heuristics of addictive behaviour are perhaps easiest understood if we apply them to gambling. Gambling is surely a perfect example of irrational thinking. Its very premise seems to be built on a falsehood; the erroneous belief that an individual can beat the odds. Griffiths suggests a number of such heuristics. We shall consider a few of them: Gambler’s fallacy seems to be an obvious starting point: the idea that random events equal themselves out over time. “I haven’t had a win for three months so it’s my turn soon.” With the lottery, the idea that a number hasn’t been drawn for twelve weeks so it must come up this time. Availability bias: is in some respects the above heuristic in reverse. The notion that because something has happened in the past it will occur again in the future. Big winners on the lottery get oodles of coverage leading us to think it’s a common occurrence and hence likely to happen to us too. In the early days of the lottery it soon became apparent that the number 44 was being drawn more than the others. Result, everyone was picking the number 44! Sunk cost bias: another possible explanation of the gambler’s fallacy. Playing a game costs money, we expect something in return sooner or later. Having made that initial investment and not had a return we feel obliged to continue so we don’t lose out. Long term we could potentially lose a lot more! Representativeness bias: the tendency to confuse a representative sample with a random sample. Clearly games like the lottery require a random drawing of numbers. However, when we come to chose a random sample we tend to pick numbers that best represent the spectrum 1 to 49. As a result we are likely to chose a single number, one from the twenties, thirties etc. The exception to this is the estimated thousands that pick 1,2,3,4,5,6! Illusion of control: gamblers tend to over-estimate the amount of control they have. With the lottery this is minimal, however, I suppose being able to chose your numbers provides some semblance of control. The illusion of control is more likely with fruit machines which give the impression of control with features such as ‘nudge’ and ‘hold’ even though in practice very little skill is involved.
As well as heuristics there is also a tendency by many gamblers to make it personal. Gamblers will switch from one bandit to another, claiming the first one doesn’t like them. Some thin k they can con the machine by only putting in £1 at the outset.
Evaluation As is usually the case with cognitive explanations it’s difficult to disentangle cause and effect (chicken and egg if you will). Research disagrees over what comes first the irrational thinking and heuristics (which the model assumes are causes of addiction) or the addiction, making the heuristics mere symptoms of the addiction. Think of similar problems we’ve seen before: Does faulty perception of body image create anorexia or is it a symptom? Does negative thinking cause depression or is it a symptom? Assuming that the heuristics pre-date the addiction then how do they arise? Why don’t we all develop this way of thinking? What makes some people more susceptible than others? Individual factors such as these seem best explained by the biological model and the possibility of some brains being more or less sensitive to dopamine and its rewarding effects; this in turn being determined by our genes. Or perhaps dispositional factors such as the fabled ‘addictive personality’ that again predisposes some of us to all manner of addictive behaviours. It would seem logical to conclude that games based on skill (or at least the perception of skill) would be more addictive given the cognitive explanation and its ideas of illusions of skill etc. In games that are clearly random such as the lottery, the illusion of skill and control is going to be minimal in comparison to other forms of gambling such as cards (perhaps excluding pontoon). Fruit machines employ what are called structural techniques to make repeat gambling more likely. Lots of flashing lights and near wins to provide reinforcement (without money) and features such as nudge and ladders that give the impression of control. Where does this leave us? It is clear from all that has preceded, that neither cognitive, biological, behavioural nor structural characteristics are sufficient in their own right to explain the complexity of addiction. In some way or other all of them combine to create addiction. See the biopsychosocial model at the end of vulnerability to addiction!
Explaining specific addictions 1. Smoking Starting to smoke… the initial draw perhaps? Acquisition of a new behaviour is often usefully explained using classical conditioning, and smoking is no exception. Smoking is associated with the behaviour of adults and in films associated with the cool or the ‘hard.’ Jarvis believes this strong association with things positive is sufficient to get children especially past the horrible experience that is that first cigarette. Because the association with cool etc is so powerful they’re prepared to stick at it and have a few more. Quicker than expected they then become addicted. In fact DiFranza (2008) believes nicotine can create addiction within a few days. It used to be thought that addiction took years to develop. Some studies have suggested that 10% of children start showing the early signs of addiction within two days! Parents can also be a powerful influence. This time we have the other favourite (neo) behaviourist SLT, also good at explaining acquisition. Children are twice as likely to smoke if they have parents that smoke. However, the effect is even more powerful if the parent shows fervent anti-smoking tendencies; this time children are seven times less likely to smoke than average. SLT also impacts through peer pressure. Ogden (2008) found that children from poorer backgrounds were more likely to smoke. Other factors such as poor performance in class, not being involved in sports and low self-esteem were also contributory factors. Surprisingly therefore it seems that children with high self esteem, who are sports captains and popular with peers, are also more likely to smoke! Personality can also play a role obviously. Furnham and Heaven (1999) compared incidence of smoking with Eysenck’s three personality factors: extroversion (E), neuroticism (N) and psychoticism (P). Not only are those high in extroversion more likely to some but there’s also a positive correlation between the two. Those with the highest levels of E smoke the most. Neuroticism, not surprisingly perhaps is also associated with smoking, with those highest in N being the deepest inhalers! The link with psychoticism is a little more obscure. Patton et al (1993) found those who still smoke score higher on P than ex smokers and those who have never smoked.
Maintenance This is probably best explained by the medical model. Nicotine stimulates some acetyl choline receptors which results in production of dopamine by the nucleus accumbens (NAcc). As we saw at the start this is very rewarding. After a few hours the pleasant feelings that result wear off stimulating the need for another cigarette. 2. Gambling: see examples already provided under behaviourist and cognitive
The syllabus specifies self esteem, attribution for addiction and social context Again there appears to be some confusion reading through the different text books aimed at this specification. Eysenck spends a lot of time discussing biosocial influences, whereas Flanagan and Gross devote half of their coverage specifically to media. I’ve tried to disentangle this and present it in, what to me at least, seems a more logical manner.
This first section (rest of this page) is designed for background information only. It isn’t tackling the issue of addiction, merely providing a little explanation of what attribution theory is and what it seeks to explain. Therefore to keep the usual moaning Minnies happy (you know who you are), I shall italicize the offending material J Attribution is an interesting topic in its own right. Basically it considers the means by which we seek to explain the behaviour of others as well as our own. Generally speaking we tend to use dispositional factors to explain the behaviour of those we don’t know and situational factors to explain our own behaviour. I’ll explain with the most obvious example. You see a person being rude in Sainsburys queue. A little old granny pushes in front of you, let’s say! Having never met her before, we assume she’s rude. We attribute (that word) her rudeness to dispositional (in this case personality) factors. However, if we have our own rudeness pointed out we are likely to attribute it to an environmental or situational factor. Something that emphasizes the peculiarity of the situation we found ourselves in. We were in a hurry, we didn’t see the queue etc. This is called the fundamental attribution error (FAE). Other explanations for the FAE might include:
Actor-observer bias: We see ourselves as complex and unpredictable and certainly object to attempts to categorise us. As a result we like to see our own behaviour as flexible and adapting to our circumstances. On the other hand we feel happier being able to predict the behaviour of others so we look for more straight forward and unchanging explanations of their behaviour based on the more constant characteristics of personality and disposition. Self serving bias Acts to protect self esteem. We can explain other people’s behaviour in any way we see fit. However, we like to see our own behaviour in as positive a way as possible. When we know we’ve done wrong we protect our ego by looking for the positives.
Relating this to addiction Davies (1996) believes the way addicts attribute their behaviour passes through five distinct stages:
Davies didn’t consider this a true stage theory however. He recognised that there could be movement in either direction, e.g. from stage 4 back to stage 3 etc. However, he believed that stage three always followed on from stage two.
The Davies experiment Davies interviewed twenty drug and alcohol users. He passed the transcripts of the interviews onto others to rate in terms of the five stages, to see the extent to which they would agree. He found an average of 71% agreement between the raters, none of whom ever disagreed by more than one stage. This does suggest a high degree of reliability. In this case inter-rater reliability.
Evaluation of attribution theory of addiction Despite Davies’ theory being based on many years of observing addicts of one sort or another, his research on just twenty participants seems woefully inadequate. Since our attributions vary depending on context, such as the situation we are in, it would seem a much larger sample of different substance abusers, in different contexts would be needed to test the theory adequately. Assuming the stages of attribution are valid, do they predict change in addictive behaviour or simply reflect what the person is going through. For example does the person admitting they are an addict signal that perhaps they are ready for treatment or is it simply being used to make sense of their past behaviour? Nelson believes this attribution-behaviour cycle is important in trying to understand the changing behaviour of the addict, and sadly is an area that is often neglected during trying to understand the complexities of addictive behaviour. Nelson (2004) believes the following attributions hold true:
Eiser (1982) provided evidence for this last point. Heavy smokers labeled as addicts tend to see their behaviour as being outside of their control. Labeling people in this way becomes self-fulfilling and is easy to use as an excuse for the behaviour. 'Of course I can’t stop smoking… I’m addicted to nicotine!' McAllister and Davies (1992) take it a stage further suggesting that heavy smokers use the term ‘addiction’ to absolve themselves of any blame, since being an addict suggests they can’t be expected to control their behaviour. Hatgis et al (2008) found that our attributions of other people’s addictions depends on the substance they are addicted to. For example those addicted to cannabis should accept more responsibility for their behaviour since cannabis is seen as less addictive than heroin or nicotine. Finally, we have the ever-present issue of causality. The researchers into attribution theory are generally assuming that these attributions are then the cause of subsequent behaviour. For example, it was found that prisoners tended to blame their crimes of theft on the fact that they were drug users; ie. They are attribyting their life of crime to their addiction. In fact research suggests that it is more likely for the criminal behaviour, such as theft, to predate the drug use. If anything being involved in petty crime is more likely to lead to subsequent drug use.
There has been lots of research linking low self esteem with such things as depression and eating disorders. Research also suggests that self esteem is related to more general health behaviour, particularly in teenagers. However, there has been relatively little research into self esteem and addiction. The research that has been done has tended to produce contradictory findings. Taylor et al (2007) carried out a longitudinal study of nearly 900 boys, following them for 9 years. Those who scored low on self-esteem at eleven years of age were more likely to have become drug addicts by the age of twenty. However, although this suggests a possible link we cannot establish a causal relationship. Many other factors could be influencing the later problems, such as poverty and deprivation or lack of education. Niemz et al (2005) found that ‘pathological internet users’ (presumably those who use the internet too much) tended to have lower levels of self esteem, though again it would be difficult to establish a cause and effect relationship. In 1993, Van Hesselt et al found that although drug users were more likely to be depressed they were no different to a control group in terms of their self esteem. Newcombe et al (1986) believed lower self esteem may be a contributory factor, however, it was low down on the list of causes, coming as it did behind peers taking drugs, deviance, early alcohol use, sensation seeking, poor relationships with parents, ‘low religion,’ poor academic attainment and psychological distress. So very low down as a risk factor! McCurran (1994) supported these findings, believing other factors such as culture, parents, social group, lifestyle, environment, behavioural skills, thoughts, feelings and physical factors all to be crucial. In short, not an easy web to disentangle and control.
Triadic influence theory (Sussman et al (2000)) As you guessed this considers three factors, but they do seem to be catch-all criteria:
They looked at over 700 high risk youths from a collection of ‘alternative high schools’ in California. Basically these were set up to provide additional support for those seen as being at risk either due to poor academic achievement or behavioural and emotional factors. They provide an education grounded in more practical skills and a higher teacher to student ration.
They essentially found that the best predictors of drug addiction were
the students themselves. Those who had used drugs or intended to use
drugs or were concerned about later drug use, were, twelve months later.
The most likely to have become addicts. Extrapersonal and Intrapersonal Sussman and Ames (2001) simplified the above three factors down to just these two Extrapersonal This covers demographic (such as age and gender), environmental, cultural and social. I won’t cover the whole list but rather concentrate on a few examples from each area. Environmental
Cultural Determines what is available and our prevailing ideas and attitudes about the behaviours.
Cannabis The Netherlands are famous for their liberal attitude to cannabis. In other parts of the World, including the UK, it isn’t even available fore medical use. There has been widespread criticism in recent years for the confused message coming from the British government who first down-graded cannabis from category B to C (2004), but in 2008 reinstated its grade B status.
Alcohol In Europe there tends to be a more relaxed view of alcohol consumption. The French particularly are famed for allowing children to drink alcohol at the table, almost regarding wine as food. In the USA however, there are far stricter views. Most states have a minimum drinking age of 21. Barbara Bush (daughter of George W) was sentenced to eight hours community service in 2001 for consuming alcohol at the dangerously young age of 19! What kind of crazy bitch is she!!! Note: the USA’s hard line approach to alcohol isn’t new. In 1919 the eighteenth amendment to the constitution banned alcohol from public sale. Prohibition wasn’t repealed until 1933, despite being largely flouted in the latter stages.
Social context Alcohol also provides a very good example of how social norms can impact on attitudes and behaviour towards addictive habits.
Opiate use really took off around the turn of the eighteenth into the nineteenth century. It was widely used recreationally and seen as a cure-all or panacea for a wide range of illnesses. Examples of its marketing include: Dover’s Powders, marketed as a cure for gout and Godfey’s Cordial which was sold as a “soother” for crying babies! Usually it was taken as a tincture with alcohol and referred to as laudanum. Apparently it was particularly popular in the Fens. The city of Ely was known as the ‘opium eating city.’ It wasn’t until 1868 that availability was restricted to use by pharmacists only. Recently smoking has become increasingly socially unacceptable and numbers of smokers in the UK has declined significantly in the past thirty years.
In this section we shall consider the extent to which the media portrayal of addiction influences addictive behaviour in the observer and the effectiveness of anti-addiction messages and government information campaigns. Portrayal of addiction in the media Films: Sulkunen (2007) looked at 140 scenes taken from 47 films that portrayed drugs, alcohol, nicotine, gambling and sex. Some of these scenes concentrated more on use of rugs etc. rather than on addiction per se, so the final number of scenes was whittled down to 61. According to the findings, most of these films, e.g. American Beauty, tended to focus on the positive effects of addiction, for example contrasting the fun and enjoyment of taking drugs with the mundane nature of everyday life. Gunasekera et al (2005) looked at 87 of the most popular films of the past twenty years. Use of cannabis featured in 8%, tobacco (68%) and drunken behaviour (32%). Again they concluded that portrayal tended to be positive and the dangers of associated behaviors such as unprotected sex were not considered. However, Boyd (2008) disagrees and believes many films do consider the negative effects; listing: physical deterioration, prostitution and rape, theft and murder and moral decline such as stealing from friends and family. However, although theses studies consider the actual portrayal, relatively few studies consider the extent to which they influence attitudes and behaviour. Sargent and Hanewinkel (2009) looked at the effects of film portrayal of smoking on over 4,000 adolescents. They questioned them at the start of the study and then returned a year later. Those who had taken up smoking in the intervening twelve months often cited the influence of smoking in films as a contributory factor. However, clearly this is self-report. Finally, Byrne (1997) makes an interesting point. Films play a major role in determining our ideas about a whole range of topics, particularly those we wouldn’t normally encounter. He believes films create our stereotyped view of what it is to be an addict. He likens this to the person’s view of ECT, learned not through direct experience or from any educational source, but rather from its negative portrayal in ‘One Flew Over the Cuckoo’s Nest.’
Media, creativity and drug use As well as media portrayal of drug use, there are many reported cases of drug-use influencing the media. This is particularly the case in popular music but surely also relates to film and to painting and art. Many song-writers and performers attribute their creativity to use of one or other drugs. Famously Brian Wilson, the creative ‘genius’ behind 60s and 70s legends the Beach Boys, attributed many of his ideas to the use of cannabis. Later he cites the use of LSD as an influence on his writing of the album ‘Pet Sounds.’ The Beatles went through an LSD phase which probably influenced writing of later albums such as Sergeant Pepper’s Lonely Hearts Club Band and the White Album. Some of the tracks such as ‘A Day in the Life’ make overtly obvious mention of drugs; ‘I went upstairs and had a smoke, and somebody spoke and I went into a dream.’ Later some of Lennon’s work was probably influenced by heroin. His track ‘Cold Turkey’ on the album ‘Shaved Fish’ was about his experiences coming off of heroin. In an interview published in Uncut in 2004, McCartney admitted drugs "informed" much of the Beatles' music. He said the song Got To Get You Into My Life was "about pot - although everyone missed it at the time", and Day Tripper was "about acid".
He added it was "pretty obvious" that Lucy in the Sky with Diamonds was inspired by LSD, and other songs made "subtle hints" about narcotics. .
Media and Health Campaigns Television is an ideal medium for getting across messages about the dangers of alcohol, drugs, tobacco and gambling. Not only does it provide easy access to a large number of people but it also provides the capability to target campaigns at particular groups of people. If you want the over 60s to get your message about the dangers of skunk you schedule your showing for the ad breaks in Countdown. This way it will be shown alongside advertisements for Saga Holidays, stair lifts and easy ways of getting wrinklies in and out of the bath. In the more likely event of wanting to target teenagers show it straight after Hollyoaks or the like. Examples of campaigns ‘Psst… the really useful guide to alcohol’ was a six part 30 minute TV series aired by the BBC in 1989. Research into its effectiveness carried out in 1991 by Bennett et al concluded that it had increased people’s awareness of alcohol related issues but had had little or no impact on their behaviour or consumption of alcohol. More recently Frank has been used to inform younger people about the dangers of taking drugs. Recently Frank has introduced the dog Pablo. The ads show Pablo on a quest to find out the truth about the drug by questioning the key players from the world of coke including the dealer, the user, a bag of cocaine, a heart, a nostril and a bank note. The TV ad, created by Mother, first airs tonight on Channel 4, and will continue to be broadcast on Channel 4 and satellite channels in programming which targets the 15- to 18-year-old audience.
Tying it all together Addiction is complex! A whole host of factors, be they intrapersonal and extrapersonal combine to create the likelihood of addictive behaviour. In this book and the previous one on models of addiction we have seen how the following all seem to play their part: Biological and genetic predisposition: The idea that an addictive personality might be inherited and areas of the mesolimbic system might predispose some more than others to become addicted. Personality factors such as level of self esteem may also make it more likely that some people will become addicted. Situational and environmental factors may trigger addictive behaviour. For example being around others that themselves are addicted. Being in areas where drugs are widely available etc. The Media may provide unsuitable role models, for example in films that glorify drug taking and minimize its negative consequences. Seeing others rewarded for their addictive behaviours acts as vicarious reinforcement or SLT. Structural characteristics may be deliberately created to draw us in. This is most widely seen in gambling where machines are designed to be attractive and convince us that a e=win is just around the corner. Cognitive biases or heuristics may explain why some people may become addicted when others remain unaffected by pressures to partake. Although these heuristics may simply be convenient excuses or attempts to rationalize what otherwise is seen as irrational behaviour. Attitudes and attributions may impact particularly on how the person perceives and explains their behaviour which in turn will influence their chances of recovery or relapse. Together these are referred to as the biopsychosocial approach which seeks to combine biological, psychological and social explanations to provide a more holistic explanation of what is, undoubtedly a very complex pattern of behaviour.
Models of Prevention and Types of Intervention Not the most clearly defined of AQA topics it has to be said, but broadly speaking they want us to look at ways in which addiction can be understood in terms of personal intention and then the ways psychologists or others can intervene to alter these intentions. Hopefully it will all make more sense as we wade through the topic. Be warned however, enjoyable this topic is not! Overview: Methods of Prevention: Two strikingly similar theories:
Types of Intervention More familiar ground
Here goes
Methods of Prevention 1. Theory of Reasoned Action (TRA) A cognitive theory first proposed by Azjen and Fishbein (1975) Assumption A person’s decision to perform a particular behaviour (such as stopping smoking) can be predicted by their intentions. Immediately you can hopefully spot the weakness in this theory, nicely summed up by the saying ‘the road to hell is paved with good intentions.’ All too often our behaviour falls well short of our intentions. Labour Party Manifesto (1997) made a lot of their intended ‘ethical foreign policy.’ The same policy that led to an illegal war! (Don’t quote obviously lol) According to the theory, intentions are determined by two variables:
1. Individual Attitude (Personal perspective if you like) This is our personal attitude towards the target behaviour. It is the sum of all our knowledge, attitudes, prejudices etc. that we think of when we consider the behaviour. For example, our individual attitude to alcohol might include, pleasurable, relaxing, nice taste, makes us feel good, makes us brave, can cause hangovers, makes us aggressive, too many calories etc. We weigh up the good and the bad and form an overall impression. 2. Subjective norms Considers how we view the ideas of other people about the target behaviour. For example the attitude of family and friends to alcohol. We consider whether they approve of alcohol, their drinking habits, their past experiences etc. The closer the friends the greater the influence of their attitudes upon us. The theory has been widely applied to many health-related issues and in marketing. However, this is a huge over-simplification of human behaviour. As already mentioned, intentions would not appear to be the best predictor of eventual behaviour. Although an intention may be necessary it certainly isn’t sufficient. Albarracin et al (2005) for example, found that attitudes, as determined by a questionnaire, were not usually good predictors of behaviour in real life situations. All too often with smoking and eating behaviour, the intention to change is there but social situations, low moods etc. prevent the intention becoming practice. Alcohol has particular issues associated with it. The intention to reduce our drinking is usually decided under sober conditions (or perhaps hungover). However, once we’re out with friends and have enjoyed a few pints of real ale we get what Steel and Josephs refer to as ‘alcohol myopia’ (alcohol short-sightedness if you like. Alcohol reduces inhibitions and really messes up our cognitions. Intentions decided in the cold light of a sober morning go out of the window when the ale starts having its wicked way with our minds. And of course, alcohol doesn’t just interfere with alcohol-related intentions but also intentions relating to smoking, eating and unprotected sex.
Theory of Planned Behaviour (TPB) Basically this takes the previous theory (TRA) and adds ‘self-efficacy.’ In practice this means adding the extent to which you believe the change in behaviour is possible. So for example, if you have been trying for 28 years to stop eating kebabs (with chilli sauce) after a night out drinking, then you’re not going to rate your chances too highly this time. The theory believes that this perception of behavioural control acts on either the intention or directly on the behaviour itself. This has two effects:
Evaluation At present this is the most widely used and applied model of social cognition used in health psychology. This would suggest it has a fair amount in its favour. All three components (individual attitude, subjective norm and perceived behavioural control) correlate with intentions. It has proved to be especially useful in predicting intentions relating to testicular self-examination, dieting and weight loss, smoking, alcohol consumption, increasing exercise and as the following study shows, intention to wear sun protection: White et al (2008) measured assessed the individual attitudes, subjective norms and perceived behavioural control of over a thousand teenagers in Australia (where else) as they all related to issues of skin cancer and skin protection. Two weeks later he assessed their behavioural intentions and their eventual behaviour. The researchers found that the three factors were significant predictors not only of intentions but also of eventual behaviour. However, this is not always the case and its essential weakness is the same as TRA; intentions not being the nest predictors of eventual behaviour. Have I said this before? Armitage and Conner (2001) in a meta-analysis, concluded that it was a better predictor of intentions and of eventual behaviour than TRA. Many see it as too rational, ignoring as it does, feelings, motivations and real-life pressures. Completing a questionnaire in the cold light of day is never likely to be a good predictor of eventual real-life behaviour.
Introduction We shall now consider steps that can be taken by professionals or by governments to intervene and attempt to influence intentions and/or behaviour. Essentially these measures are aimed at subjective norms and personal attitudes in an attempt to strengthen or support our intentions.
Biological Interventions These tend to be limited and based around drugs of one sort or another. They are most commonly applied to drug addicts, alcoholics and smokers. Drugs can fall into one of three basic categories:
1. Aversion These are drugs that produce unpleasant consequences such as vomiting and nausea especially when taken alongside other drugs. Example: antabuse (disulfiram) for the treatment of alcoholics. 2. Agonist These act as a less harmful replacement for the dependent drug, resulting in fewer side effects and allowing gradual and controlled withdrawal from the substance. Ideally they should be accompanied by counselling and rehabilitation. Example: methadone for the treatment of heroin addiction. 3. Antagonist These block the effects of the target drug and prevent them from having the desired effect. Example: naltrexone for the treatment of opiate addictions We shall now consider each one in more detail as we look at ways of treating various addictions:
Biological interventions for alcoholism Alcoholics can suffer severe withdrawal symptoms including delirium tremens (DTs) if alcohol is removed completely. Often patients are admitted to hospital during detoxification and given anxiolytics such as benzodiazepines (e.g. valium) to prevent fits and to reduce the anxiety of being withdrawn. The patient can then gradually be withdrawn from the anxiolytics. Occasionally if the symptoms aren’t too severe the process can be performed as an outpatient under the supervision of the patient’s GP.
Maintaining abstinence. Once withdrawn the patient may be treated with antabuse. Under normal circumstances alcohol is broken down in the liver. The breakdown consists of two main stages, both obviously carried out by enzymes. Firstly, the alcohol is broken into acetaldehyde and later into acetic acid (vinegar). Antabuse prevents this second stage. As a result, acetaldehyde builds up in the bloodstream and can reach up to 10 times the normal level. This is not good! Acetaldehyde is the main component of a hangover. Small levels are uncomfortable and painful. High levels are horrible! Imagine the mother of all hangovers! Typically antabuse combined with even small levels of alcohol will result in severe throbbing headache, increased heart rate, palpitations, nausea and vomiting. Nice! Detoxification really needs to come first. The patient should not take antabuse if they have consumed alcohol in the previous twelve hours. The effects of one treatment of antabuse can remain in the system for up to two weeks. Clearly the patient needs to be fully informed of the consequences and give their consent for treatment. They also need to be highly motivated to stop drinking. However, although the chemical is effective in reducing alcohol intake the drop-out rate from treatment is as high as 80%. Side effects of the chemical alone include a persistent metallic taste in the mouth. In some cases patients can be treated at home under the supervision of the GP, however, often patients need to be treated in hospital making it less cost-effective. Recently, antabuse has been trialled as a treatment for cocaine addiction since it also blocks the breakdown of dopamine.
Naltrxone is an opiate antagonist; it blocks the effects of the brains natural opiates (endorphins) so prevents the feeling of pleasure that the release of these chemicals usually creates. In the UK naltrexone is used for the treatment of heroin addiction, however, in the USA it is becoming more widely used for the treatment of alcoholics under the trade names Revia or Depade. A 50mg tablet taken once a day interrupts brain pathways and prevents alcohol producing pleasure. Essentially the chemical blocks the effects of endorphins that are released in response to alcohol and create the pleasurable sensations associated with drink. In this case ‘associated’ is the key word! Naltrexone allows the person to drink without pleasure so that eventually the link between alcohol and pleasure is broken. It is known as the ‘Sinclair Method’ after David Sinclair who first discovered this use. He claims a 78% success rate, which is ridiculously high and may even explain its lack of widespread acceptance. Professionals working with alcoholics generally adhere to the twelve steps approach of the AA. Essentially this claims that alcoholics must abstain completely to be successful. For the Sinclair method to be successful it requires the patient to take the drug with alcohol so the association can be broken. It has even been suggested that the alcohol rehabilitation industry has to much to lose by embracing a potential ‘cure’ (Times Online 2009).
A similar opiate antagonist naloxone works in a similar way.
Attempts have also been made to treat alcoholics with SSRIs such as Prozac. The underlying assumption appears to be that alcoholics drink for a reason, such as depression or low mood. Improve the state of mind and it may reduce or remove the need to drink. Anxiolytics such as valium might be effective for similar reasons.
Patches, gum and inalers These replace nicotine (the addictive chemical in cigarettes) in a less harmful manner. However, it is worth pointing out that reducing withdrawal symptoms from cigarettes is only minimally related to success. Nicotine patches release the chemical slowly and although it does increase heart rate and blood pressure it isn’t being taken with the cocktail of other harmful chemicals that are found in cigarettes.
Both patches and gum produce cardiovascular changes so need to be taken with care. Patches are seen as being more convenient since only one is needed per day, whereas the effects of gum are shorter lived so need to be taken at regular intervals to overcome the nicotine craving.
Biological interventions for heroin abuse The agonist
methadone is most widely used. Methadone is a man-made (synthetic)
opioid which produces similar effects to heroin but avoids the
over-powering rush associated with heroin itself. Essentially the idea
is to replace heroin with methadone to prevent withdrawal symptoms and
then gradually reduce the levels o methadone given. This allows for
safer and controlled reduction and withdrawal under supervision.
Psychological Interventions Here we shall consider methods suggested by the behaviourists and by cognitive psychologists.
Behaviourist approach Cast your minds back to abnormality in year 12. Behaviourist methods of treatment can be split into those based on classical conditioning (such as aversion therapy) and those based on operant conditioning (such as token economy) Aversion therapy Classical (Pavlovian) conditioning centres on learning through association. In this case the idea is to associate the undesirable behaviour with something unpleasant. Aversion therapy has been most widely applied to alcoholism so we shall concentrate on this. A warm salty solution containing an emetic is given to the patient. An emetic is a drug designed to make you throw up! Behaviourists have a ‘law of contiguity’ which states that two actions that occur together will become associated. Immediately prior to vomiting the patient is given a shot of alcohol, usually whisky which has a strong and distinctive smell as well as taste. Ideally the vomiting should then occur just after the drink. The process is repeated on a regular basis with subsequent treatments involving larger doses of emetic and perhaps various other alcoholic beverages.
As with antabuse (used by the medical model) inducing vomiting is not a method preferred by patients, so as with antabuse there is a very high drop out rate from treatment. Aversion therapy has been used for a host of ‘disorders’ including homosexuality. It has also been used in an attempt to treat gambling addiction. McConaghy et al 1983, got gamblers to read out lists of words. Each time a word associated with gambling was read they were given an electric shock! Success rate was put at around 50%.
Contingency Management This is sometimes referred to as community reinforcement approach and I still think of it as token economy. The Board and texts however, seem to prefer contingency management so CM it is J The method is based on operant conditioning so rewards are the order of the day. Patients and those that deal with them socially or professionally are encouraged to provide rewards when behaviours ‘inconsistent’ with the addictive behaviour are performed. Usually rewards consist of vouchers (hence ‘token economy’) which can be swapped for goods. In prisons this is often cigarettes (though this would be unlikely in the case of tackling nicotine addiction).
Evaluation Davison et al (2004) believes it to be one of the most effective treatments for addiction. Petry et al compared the outcomes of two groups of alcoholics, one receiving ‘standard outpatient’ care, the other having the same but coupled with CM. The relapse rate for those getting the CM was significantly lower, 26% compared to 61% for the standard treatment group. CM has been used to treat other addictions, for example heroin. Sindelar et al (2007) compared groups of heroin users. All were getting the standard daily treatment with methadone but half were also given CM. Those receiving the CM were far more likely to test negative for heroin use. (Note: in this case the reward was entry into a draw for those who tested negative. Winners were given various amounts o money). Overall Behaviourist methods, like their theories I guess, are superficial. They tackle the behaviour but not the underlying causes or predisposition. As a result, although their interventions produce some short term success, in the long term there is a high rate of relapse. Cognitive (and Cognitive Behavioural) Interventions Although usually used to treat depression, as we’ve already seen, CBT has also been applied successfully to the treatment of a variety of addictions. The basis of CBT is that behaviour is determined largely by our thoughts and although the patient may not be able to change their situation they can certainly change the way they think about it. When applied to alcohol and other drug dependence, CBT teaches the patient how to recognise and then avoid high risk situations in which they are more likely to drink or use drugs. Although there are a variety of CBTs (rational emotive therapy, rational behaviour therapy, dialectic behaviour therapy etc) when applied to addiction they all share to main components.
Functional Analysis The patient (client) and therapist work together to try and recognise under what circumstances the behaviour occurs. They explore the feelings and motivations before, during and after the event in an attempt to help the patient determine the risk factors. Functional analysis is useful in helping the patient identify possible reasons for the behaviour.
Skills training The therapist teaches the patient better or more appropriate coping strategies. This involves unlearning old habits and replacing them with healthier ones. Unlike other forms of therapy such as psychoanalysis, CBT is very structured and shorter in duration. The more open ended psychodynamic techniques can take many months or even years whereas CBT usually lasts 10-15 sessions. When applied to gambling, we saw earlier in the topic that erroneous beliefs (heuristics) such as an over-perception of control and under-estimate of losses help to maintain the gambling behaviour. The therapist will help the patient test these faulty beliefs and replace them with healthier and realistic ideas that hopefully will reduce the urge to gamble.
Effectiveness Carroll et al (1994) This was a 12 week study that compared the effectiveness of drug treatment and CBT to control cocaine addiction. Patients were either given the drug desipramine (tricyclic antidepressant) or CBT that taught the patient how to avoid high-risk situations and develop alternatives to cocaine use. Both the drug and the CBT were effective at treating patients with a high level of depression (possible cause of the addiction). However, generally the CBT was more effective than the antidepressant in treating cocaine addiction and this was maintained twelve months later. It is also worth mentioning that Carroll et al (and many other researchers in the field) believe that therapy needs to vary from patient to patient. This is a break with the traditional ‘one size fits all’ approach of the medical model. Some patients respond better to certain techniques than others. Other studies have been less favourable. Morgenstern et al (2001) compared CBT with the 12-step approach favoured by Alcoholics Anonymous and found little difference in effectiveness. Although it is widely assumed that learning of coping skills is crucial to the success of CBT in treating addiction, some research seems to question this. Morgenstern and Longabaugh (2000) reviewed ten studies in which CBT was compared to other interventions. The link between coping strategies and success was questioned for two reasons:
Ladouceur et al (2001) randomly allocated 66 gamblers to either:
86% of those who completed the CBT were no longer seen as pathological gamblers (as defined by the DSM-IV. Furthermore, in the longer term the patients who underwent CBT had higher self efficacy and were still coping better at a one year follow up. Conclusion CBT is one of the most widely evaluated methods of treating addiction, When compared to no treatment it is clearly more effective. When compared to other methods the results are not quite so conclusive, however, it is certainly seen as being one of the most effective methods. It appears to be most effective when combined with other forms of therapy such as support groups.
Self-help interventions The most popular self-help therapy Worldwide is the one adopted by Alcoholics Anonymous (AA) and their offshoots Gamblers, Narcotics and even Sexaholics Anonymous. Their motto is ‘One day at a time’ since they believe that addiction can only be arrested never cured. They all take the Minnesota 12-step programme as the basis of their intervention. The sessions are run by former addicts and all those attending must be at rock bottom. They must also attend voluntarily and show a commitment to overcoming their addiction. Treatments are based on group therapy in which each addict has to self-disclose the issues they are facing. Others offer advice and support. Addicts are encouraged to exchange phone numbers and keep in touch between sessions as well.
It is clear from the steps above that the Minnesota approach does rely heavily on spiritually and the power of belief. This does act as a bar to some people.
Evaluation As its name suggests, all information is anonymous. As a result there are no records so any information collected is self-report making it any assessment of the success notoriously unreliable. The only measure of success that the technique adopts is total abstinence. There is no follow up studies on those that drop out so there is no reliable method of judging success, relapse rate or cure.
Unlike other methods suggested so far, public health initiatives are not just aimed at addicts. According to Ogden (2004) they target all members of the population so that everyone is aware of the risks and the information/help that is on offer. We shall look at four types: 1. Doctor’s advice Russell et al (1979) carried out a study in five doctors’ surgeries over a four week period. Patients were being encouraged to give up smoking and were placed in one of four treatment groups:
Clearly the doctor’s advice to quit was influential even though the percentages are low. However, this was only over a four week period. Apparently the success rate was better if the doctors had been trained in client-centred (humanistic) therapy.
2. Workplace interventions These can either be government-led, for example the no smoking in enclosed places legislation introduced in the UK in 2007 or they can be smaller, localised initiatives adopted by the workplace. An example would be new guidelines for the canteen or discouraging lunchtime drinking by its employees. These tend to have an advantage in that potentially they could have a large target population meaning dozens or even millions could be involved and with things like the smoking ban there is built-in social support. Since everybody in the company is affected then people can rally round and offer encouragement. In the case of the smoking ban there is evidence that it has drastically reduced smoking whilst at work. The downside is that it’s probably increased smoking at home as people compensate for their lack of nicotine earlier in the day. This could be having an adverse effect on children for example. An Australian study that investigated attitudes immediately and six months after a similar ban in 44 government buildings suggested immediate resentment and inconvenience which diminished with time. Despite this the ban only resulted in 2% quitting completely. In the UK the ban was introduced in July 2007. Between April and December of that year an estimated 250,000 people quit. Most of these were in the nine months prior to the ban being introduced.
3. Community-based initiatives The Stanford Five City Project was a large scale community-based intervention designed to test whether a comprehensive program of community organization and health education would positively alter the behaviour of those involved. Two cities were targeted and the results compared to three other cities that had not undergone the intervention. A six year intervention targeted all residents in the two treatment cities and involved a multiple risk factor strategy delivered through multiple educational channels. The results showed that the treatment cities produced significantly greater improvements in cardiovascular disease knowledge, blood pressure, and smoking than the control cities. For example there was a 13% reduction in the number of smokers. A similar study in North Karelia was launched in 1972 in response to a local petition to get urgent and effective help to reduce the very high rates of CHD in the area. In cooperation with local and national authorities and experts as well as with WHO, the North Karelia Project was formulated and implemented to carry out a comprehensive intervention through the community organizations and the action of the people themselves. The 25-year results and experiences of the North Karelia Project show that a determined and well thought out intervention programme can have a major impact on health-related lifestyles and on population risk factors. By 1995 the annual mortality rate of coronary heart disease in North Karelia in the working age population had fallen approximately 75%, compared with the rate before the Project. 4. Government initiatives Broadly speaking governments can intervene in one of two ways.
Harm minimisation In recent years public health initiatives have adopted a more realistic harm-minimisation approach. As we saw in the section on media, very often anti-drug campaigns and pro-health campaigns such as ‘five a day’ increase knowledge but have little impact on behaviour. As a result, addicts are made aware of the risks but continue the habit. Many campaigns have therefore focused on making the behaviours safer rather than attempting to stop them. An obvious example would be increasing awareness of the dangers of sharing needles and ensuring heroin addicts can either obtain clean needles or know the correct message of sterilization. They may also advertise the benefits of safer or replacement drugs such as methadone that doesn’t contain unknown contaminants and can be correctly dosed. Many, however, resent such information, believing that it seeks to condone the behaviour rather than prevent it from happening at all.
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