Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Addiction Biological models The genetics of addiction Family and twin studies Agrawal and Lynskey (2006) – illicit drug abuse and dependence affected by genetic influences, heritability estimates between 45% and 79% Kendler et al. (2003) common genetic factor influences alcohol abuse, drug abuse and dependence, and adult antisocial behaviour Specific genes, specific drugs Kendler and Prescott, (1998) Variant of the D2 receptor gene DRD2 in ⅔ deceased alcoholics compared to only ⅕ of deceased non-alcoholics (Noble et al., 1991). Individuals with this A1 variant have fewer dopamine receptors in pleasure centres in brain, hence become addicted to drugs that increase levels of dopamine. Biological models The genetics of addiction Inconsistent research findings Individual differences Genetic explanations can explain why some people become addicted yet others with same experiences do not using diathesis-stress model. Meta-analysis by Noble (1998) – 48% of severe alcoholics, 32% of less severe alcoholics and only 16% of controls had A1 variant of the DRD2 gene. However, subsequent studies have found no relationship or no relationship between this variant and addiction to alcohol. DRD2 and Tourettes A1 variant also occurs with several other disorders including Tourettes (45% of cases). Creates a problem for idea of DRD2 being a ‘reward’ gene. Biological models The genetics of addiction Tatum O’Neill, was arrested in New York for trying to buy cocaine (she eventually pleaded guilty to disorderly conduct). “Addiction runs in families. It’s a disease,” she said. Biological models Dopamine and addiction INITIATION RELAPSE Drug-taking triggers the release of dopamine. Mesolimbic pathway in the brain creates memories that link drugs such as cocaine to the rewarding nature of their activation of dopamine receptors. Permanent recovery made difficult because of druginduced changes that create lasting memories of the drug. This is made even more difficult by reminders of the drug and the promise of imminent reward. MAINTENANCE Chronic exposure to drugs results in a reduction of these reward circuits. This creates withdrawal symptoms so user must now take higher doses of the drugs to avoid this unpleasant state (negative reinforcement). Biological models Dopamine and addiction Supporting evidence Social stress and dopamine Volkow et al. (2001) gave adults Ritalin which raises dopamine levels. Some loved the feeling and some hated it. Those who loved it had fewer dopamine receptors than those who hated it. Explains why some people, after experimenting with drugs become addicted and others don’t. Research with monkeys (Grant et al., 1998) showed that dopamine system can be influenced by social interaction. Animals that lost social status also lost dopamine receptors. Suggests that stress of poverty makes some people more vulnerable to addiction. Limitation This explanation ignores the social context of drug taking although it does allow for treatment IDA Synoptic issues Cognitive models Self-medication Initiation This proposes that individuals intentionally use drugs to ‘treat’ psychological symptoms (e.g. loneliness, depression) from which they suffer. The choice of drug depends on the effect the individual desires. Maintenance and relapse ‘Stress relief’ often cited as reason why people smoke. However, smokers report higher levels of stress. When they stop, stress levels decrease, only to rise again when smoking again. Each cigarette has an immediate effect on decreasing withdrawal symptoms but ongoing smoking increases stress levels once more. Cognitive models Self-medication Research support Gottdiener et al. (2008) – meta-analysis to test assumption that substance abuse is due to a failure of ego control, i.e. the inability to control the impulse to self-medicate. Participants with substance abuse disorders showed significantly lower levels of ego control than control group of non-alcoholics. Problems of cause and effect Self-medication model predicts that distress must precede need for self-medication. Supported by research with sexually abused women who used alcohol to remove resulting sexual inhibitions (Sanjuan et al., 2009), but other studies have found no preceding distress prior to self-medication. Cognitive models Expectancy theory Initiation Drug or alcohol use escalates into addiction as a result of the expectations that an individual has about the costs and benefits of that activity. Among heavy drinkers, drinking has been shown to be associated with expectations of social and physical pleasure, tension reduction, enhanced cognitive and motor performance and greater sociability (Brown, 1985). Maintenance and relapse As an addiction develops, it is maintained less by conscious expectations and more by unconscious expectations involving automatic processing. This explains the loss of control that many addicts report concerning their addictive behaviour and the difficulties they face in abstaining. Cognitive models Expectancy theory Subjective evaluation Most research measures the likelihood of experiencing certain effects, but Leigh (1987) suggests subjective evaluation of outcomes more important determinant of drinking behaviour. Addiction or consumption? Few studies distinguish between ‘problematic behaviour’ such as bingedrinking or drug-taking and addictive (involving loss of control) behaviour. Synoptic issues IDA Learning models Operant conditioning Initiation and positive reinforcement Behaviours that lead to consequences that the individual finds rewarding are likely to be repeated. Crack cocaine produces massive activation of dopamine receptors in mesolimbic system which is rewarding. Maintenance and relapse After repeated exposure to drug, withdrawal symptoms develop which are the body’s compensatory reactions. Taking the drug is now necessary to avoid these unpleasant sensations, an example of negative reinforcement. Learning models Operant conditioning Strengths of explanation Can explain how process of addiction develops and is maintained without conscious choice or awareness and why addicts experience conflict when they try to abstain. Also explains why many addicts report a decrease in other drives such as eating. Addiction creates drives that are hard to satisfy therefore take priority over other drives. Problems of explanation There are aspects of addiction that are not explained by this explanation. Robinson and Berridge (1993) point out that many people take potentially addictive drugs at some times in their lives yet relatively few become addicts. This suggests that there are other psychological and physiological factors are involved in the transition from consumption to addiction. Learning models Classical conditioning Initiation and secondary reinforcers Stimuli that precede or occur at the same time as a learned stimulus become secondary reinforcers, deriving their influence by association. To an alcoholic, sights and sounds of a pub elicit same physiological responses (e.g. arousal) as alcohol itself. To a heroin addict, the drug paraphernalia (syringe, lighter, teaspoon) has the same effect. Drug effect Bodily response Drug effect Bodily response No response Bodily response Maintenance and relapse Drug habit is maintained through threat of withdrawal symptoms. Drug effect is now UCS, body’s response as it tries to restore equilibrium is the UCR. Stimuli that precede the drug dose become CS. If presented alone, CS causes CR but this creates disequilibrium if no drug dose. Learning models Classical conditioning Research support Implications for treatment Major claim is that stimuli that occur at same Drummond et al. (1990) propose the use of cue exposure (presenting cues without opportunity to engage in drug-taking. This leads to stimulus discrimination, as without the reinforcement of the actual drug, the association between cue and drug is extinguished, reducing the cravings. time produce same response. Evidence in support of this prediction from study of soldiers returning from Vietnam who were less likely to relapse because sights and sounds associated with their drug-taking were now different. Synoptic issues IDA Smoking addiction Starting smoking Effects of nicotine Smoking initially symbolic act conveying messages such as ‘I’m tough’ or ‘I’m rebellious’. Desired image sufficiently powerful to put up with unpleasantness of smoking until physical effects take over. Nicotine activates receptors in the brain which leads to the release of dopamine. This creates feelings of pleasure for, but is short-lived and must be repeated to avoid withdrawal symptoms. Socioeconomic status and addiction Research suggests an association between addiction to nicotine and social disadvantage (Fidler et al., 2008), which would explain why poorer smokers find it difficult to quit (they have a higher nicotine intake). Smoking addiction Socioeconomic status Link between socioeconomic status and nicotine intake supported in French study with poor housing conditions linked to greater nicotine intake. Suggests that interventions must also attempt to improve poor smokers’ living conditions to lower incidence of smoking. Smoking and popularity Peer popularity and smoking link supported in study which found positive relationship between smoking at age 16 and boys’ popularity two years later (Mayeux et al., 2008). This was not the case for other risky behaviours such as the use of alcohol and sexual activity at age 16. Effects of nicotine Khaled et al., (2009) study supports possibility that longterm smoking has adverse effect on mood. Incidence of depression was highest among smokers and lowest among ‘never smoked’. Gambling addiction Genetic factors Pathological gambling appears to run in families. Twin study (Shah et al., 2005), using adult participants found evidence of genetic transmission of gambling among men. Black et al. (2006) found first degree relatives of pathological gamblers were more likely to suffer from pathological gambling than were more distant relatives Sensation seeking and boredom avoidance Zuckerman (1979) – individual differences in need for optimal amounts of stimulation. High sensation seekers have lower appreciation of risk and anticipate arousal as more positive than do low sensation seekers. Blaszczynski et al. (1990) – pathological gamblers had higher boredom proneness scores than control group of non-gamblers. Gambling addiction Genetics or environment? Difficult to disentangle the relative influences of genetics and environment, but Slutske et al., (2000) estimates that 64% of the variation in risk for pathological gambling can be accounted for in terms of genetic factors alone. What is inherited? A genetic predisposition for gambling may work indirectly through the trait of impulsivity. A number of studies have found supporting evidence for this relationship, i.e. that impulsivity as an inherited trait is a significant predictor of the development of pathological gambling. Lack of research support The claim that gamblers should be higher sensation seekers appears to be true for casino gamblers but not for gamblers who bet on horse racing in a betting shop (Coventry and Brown, 1993). This challenges the view of gambling as a homogenous activity. Synoptic issues IDA THEORY OF REASONED ACTION THEORY OF REASONED ACTION Attitude An individual's positive or negative feeling associated with performing a specific behaviour. They will hold a favourable attitude toward a behaviour if they believe that the performance of the behaviour will lead to mostly positive outcomes. Subjective Norm (plus descriptive norm) Determined by an individual's normative beliefs that significant others think they should or should not perform the behaviour, plus motivation to comply with these norms. Intention The likelihood of doing something, like buying a brand or losing weight. It is a type of judgment about how an individual will behave toward a particular object or their intention to engage in a particular behaviour. THEORY OF PLANNED BEHAVIOUR THEORY OF PLANNED BEHAVIOUR A person’s intention to carry out a particular behaviour is only possible if they believe they have some behavioural control over that behaviour. This will be determined by their past experiences or perceived obstacles. If the individual has favourable attitudes and subjective norms toward a particular behaviour, the likelihood of them actually performing behaviour in question increases with their perceived behavioural control. 10. Reasons for her addiction include (150 words): Social modeling (parents and friends), need for peer acceptance, rebelliousness, nicotine addiction etc. 11. Theory of reasoned action (125 words): Attitude: A positive or negative feeling associated with performing a specific behaviour, e.g. Sally may believe that smoking will make her popular or may help to lose weight. Subjective Norm: What she believes others significant others think about her acting in this way and her motivation to comply. Intention: The likelihood of her doing something. 12. Two examples of public health interventions (100 words): e.g. Shock tactics showing cigarettes dripping fat to demonstrate the effect of smoking on arteries (Tobacco Education Campaign, 2004) 13. Effectiveness (250 words): e.g. Interventions such as the TEC have quadrupled the effectiveness of the government's anti-smoking campaign, according to the tracking study. The study found advertising campaigns prompted 32% of recent attempts to stop smoking compared to GP’s 21%.