Addicitve behaviours Flashcards
Describe the characteristics of Addictive Behaviours
- Salience, The activity that has become the most important thing in an individuals life. It dominates their thoughts, feelings and behaviour. Even when they are not engaged in the behaviour it will pre occupy them.
- Mood modification. When the individual engages in the addictive behaviour they expereince a change in their mood. This may be a ‘high’ or a ‘buzz; or perhaps a feeling of escape or numbness. It may even be that this changes at differnt times. Eg, a smoker may use nicotine for a boost at first then relaxation in the evening.
- Tolerence, as time goes on, the individual will need more of the drug or behviour to achieve the same amount effects as they have built a tolerance to it. This is usually associated with chemical addictions such as heroin or alcohol.
- Withdrawel Symptoms, if the behaviour is stopped an individual may begin to expereince withdrawel symptoms. These can be physical or psychological.
- Conflict, addicts will often expereince conflicts between themselves and friends or family by compromising their jobs or relationships at the expense of engaging in the behaviour.
- Relapse, addicts will have a strong tendancy to return to the addictive behaviour even after years of not engaging in it or after a seeming successful treatment.
What is the biological explanation of ‘ The role of Dopamine in Addiction?’
- The masolimic Pathway,The biological explanation of addiction highlights the role of dopamine in the brain’s reward pathway. The mesolimbic dopamine pathway, which includes the ventral tegmental area (VTA) and the nucleus accumbens, is central to this process. When engaging in addictive behaviors or substances, dopamine is released in the VTA, leading to feelings of pleasure in the nucleus accumbens. This reward pathway is typically an adaptive mechanism that reinforces behaviors beneficial for survival. However, in addiction, it becomes maladaptive, responding to harmful actions instead.
- TOver time, the repeated release of dopamine leads to tolerance, where dopamine receptors (such as D2 receptors) become less sensitive, and dopamine release decreases. As a result, more of the substance or behavior is needed to achieve the same pleasurable effect. Eventually, engaging in the behavior becomes more about avoiding withdrawal symptoms, such as irritability and discomfort, rather than seeking pleasure.
- Additionally, the frontal cortex plays a critical role in maintaining addiction and causing relapse. This part of the brain is responsible for higher cognitive functions like decision-making and memory. Research by Volkow et al. (1992) has shown that addiction can cause abnormalities in the frontal cortex, altering brain circuits that determine what to focus on. Addictive behaviors and their cues become more salient, leading to intense cravings even when the individual no longer finds the behavior enjoyable. These changes in the frontal cortex explain why addiction persists and is difficult to overcome.
Doesn’t explain all, Complex role, Method flaws, Animal issues.
C: Complexity
Evaluate Dopamine as a biological explanation for behaviour in Addiction.
-The dopamine explanation for addiction highlights the role of the mesolimbic pathway, where dopamine release in the ventral tegmental area (VTA) creates feelings of pleasure in the nucleus accumbens. While this explanation is supported by evidence, it is not without its limitations.
-One limitation is that not all addictive behaviors increase dopamine levels. While substances like cocaine and nicotine have been shown to elevate dopamine, research by Paul Stokes et al. (2009) found no significant increase in dopamine levels in participants consuming cannabis. This suggests that the dopamine explanation does not account for all addictions, especially behavioral ones such as gambling or video gaming. Consequently, it may not fully explain the complexity of addictive behaviors.
-Furthermore, the explanation has been criticized for oversimplifying the role of dopamine. Vaughn Bell (2013) famously referred to dopamine as the “Kim Kardashian of neurotransmitters,” highlighting how it has become fashionable to blame dopamine for numerous problems. This criticism points out that dopamine serves many other functions, such as regulating movement and motivation, making it overly simplistic to attribute addiction solely to dopamine dysregulation.
-Methodological issues also challenge the validity of the dopamine explanation. David Nutt et al. (2015) criticized the use of small sample sizes and the artificial conditions under which substances are administered in laboratory studies. For example, participants may be given substances in controlled environments that do not reflect real-world usage, meaning the findings may lack ecological validity. This raises questions about whether dopamine’s role in addiction is as significant in everyday contexts as it appears in laboratory settings.
-Additionally, much of the research into dopamine’s role in addiction relies on non-human animal studies. These studies allow for controlled experimentation that cannot ethically be performed on humans, but they present limitations. For example, the social and environmental contexts of human addiction are difficult to replicate in animal models. Behavioral addictions, such as gambling or video gaming, cannot be modeled accurately in animals, further limiting generalizability. This raises doubts about whether findings from such studies can be applied to human addiction.
-However, despite these limitations, the dopamine explanation is supported by evidence showing its involvement in addiction. Neuroimaging studies consistently demonstrate heightened activity in dopamine-related brain regions during substance use. This provides a biological basis for understanding addiction and supports the idea that dopamine plays a key role in the reward system.
- In conclusion, while dopamine is undeniably important in understanding addiction, it is not a complete explanation. Its inability to account for all addictions, the oversimplification of its role, and the methodological limitations of research highlight the need for a more nuanced approach that considers other factors, such as social and psychological influences. This multi-faceted view would better capture the complexity of addiction as a behavior.
Apply the biological explanation of ‘Dopamine’ to a method of modifying behaviour, using Varenicline
If dopamine is linked to the pleasure an individual feels as a result of the dopamine being released, then reducing this release could help to diminish cravings for the addictive behaviour. Vareicline is a drug prescribed to help those who are trying to quit smoking. It works by affecting dopamine made in the brain. By binding to nicotine receptors, alleviating cravings and withdrawal symptoms. It reduces the rewarding effects of nicotine by blocking the ability of nicotine to access the receptors and active dopamine release. Therefore, if someone is smoking a cigarette they will get less pleasure from it. Helping with quitting.
What is the biological explanation of ‘ Genetic Factors in Addiction?’
- Genetic factors are significant in explaining addiction, as research suggests that some individuals have a genetic predisposition to develop addictive behaviors. One of the key genes associated with addiction is the DRD2 gene, which codes for the D2 dopamine receptor. Individuals with the A1 variant of this gene have fewer dopamine receptors in the brain’s reward system, particularly in the nucleus accumbens, an area involved in pleasure and reinforcement. This reduced dopamine receptor activity may cause individuals to engage in addictive behaviors to compensate for the lower levels of stimulation. For example, Daniel Comings et al. (1996) found that 48.7% of smokers and ex-smokers carried the A1 variant of the DRD2 gene, compared to 25.9% of the general population, suggesting a link between this gene and addiction.- - Another set of genes involved in addiction is the ADH (alcohol dehydrogenase) and ALDH (aldehyde dehydrogenase) genes, which are responsible for alcohol metabolism. Normally, alcohol is metabolized into acetaldehyde by ADH and then further broken down by ALDH into acetic acid and water. However, certain variants of the ALDH and ADH genes slow down this process, leading to a build-up of acetaldehyde, which causes unpleasant effects like facial flushing and nausea. In populations with these variants, particularly East Asians, the unpleasant reaction to alcohol reduces the likelihood of developing alcoholism, as people are less likely to consume large quantities. Conversely, slower alcohol metabolism due to certain gene variants increases the risk of alcohol addiction.
- However, it is important to note that genetic factors alone do not fully explain addiction. The diathesis-stress model suggests that addiction is not caused by genetics alone but by an interaction between genetic vulnerabilities and environmental factors. For example, the Serotonin Transporter Gene (5HTT) has been associated with a predisposition to alcoholism, but this genetic risk is often triggered by environmental factors, such as childhood maltreatment or stress. Therefore, addiction develops when genetic predisposition interacts with specific environmental stressors.
Evaluate Genetic factors as a biological explanation for behaviour in Addiction.
The role of genetic factors in addiction has been widely researched and offers a biological explanation for why some individuals are more vulnerable to addictive behaviors. However, this explanation has strengths and limitations, particularly when considering its determinism and interaction with environmental factors.
Strengths of Genetic Explanations
Research Evidence from Twin Studies
Twin studies provide strong evidence for genetic influence in addiction, particularly regarding the maintenance of addictive behaviors. For example, Kendler and Prescott (1998) interviewed 2,000 twins and found that while environmental and social factors influenced the initiation of cocaine use, genetic factors played a key role in whether an individual became dependent. Concordance rates for cocaine initiation were higher in monozygotic (MZ) twins (54%) compared to dizygotic (DZ) twins (42%). However, for cocaine dependence, the concordance rates were significantly higher for MZ twins, indicating a stronger genetic influence on maintenance rather than initiation.
Genetic Links to Specific Substances
Studies have identified specific genes associated with addiction, such as the DRD2 gene (linked to dopamine regulation) and ADH genes (associated with alcohol metabolism). Shamisdeen Ojelade et al. (2015) found that the Rsu1 gene played a role in alcohol sensitivity in fruit flies, and further research demonstrated a connection between this gene and alcohol dependence in humans. Such findings highlight the biological complexity of addiction and provide a genetic basis for understanding individual differences in vulnerability.
Predictive Power
Genetic explanations help explain why only some individuals develop addictions despite being exposed to addictive substances or behaviors. This makes the explanation useful in identifying at-risk individuals and developing targeted prevention strategies.
Limitations of Genetic Explanations
Complexity of Genetic Influences
The idea of a single “gene for addiction” is overly simplistic. Research, such as that by Ojelade et al. (2015), shows that many genes contribute to addiction risk, each playing a small role. This complexity limits the explanatory power of genetic factors alone, as addiction likely results from the interaction of multiple genes and environmental influences.
Reductionism
Genetic explanations can be criticized for oversimplifying addiction by focusing solely on biological factors. This ignores psychological and social factors, such as peer pressure, stress, or cultural influences, which also play significant roles in addiction. For example, social learning theory emphasizes the role of observational learning and reinforcement, providing a more holistic understanding.
Causation vs. Correlation
While twin studies and genetic research indicate a strong correlation between genes and addiction, causation is difficult to establish. It is possible that genetic predispositions interact with environmental factors to increase the likelihood of addiction, but genes alone may not be sufficient to cause addictive behavior.
Determinism and Ethical Concerns
A deterministic view of genetic explanations suggests that individuals with certain genetic predispositions are fated to develop addictions. This raises ethical concerns, such as stigmatization or reduced personal accountability. However, this explanation may oversimplify the role of free will and ignores how environmental or psychological interventions can mitigate addiction risk.
Conclusion
Genetic factors provide valuable insight into why some individuals are more vulnerable to addiction, particularly regarding maintenance rather than initiation. Research evidence from twin studies and gene identification highlights the biological basis of addiction. However, the explanation is limited by its reductionist nature, lack of causation, and ethical concerns about determinism. Therefore, while genetic explanations are significant, they must be considered alongside psychological and environmental factors to provide a comprehensive understanding of addiction.
What is the individual differences explanation of ‘Personality’ in Addiction?’
Eysenck’s theory of personality suggests that there are three main dimensions of personality—Extraversion/Introversion, Neuroticism/Stability, and Psychoticism—which can be linked to addictive behaviors. These traits influence an individual’s susceptibility to addiction, with certain personality types being more prone to developing addictive habits.
Eysenck’s Theory of Personality:
Extraversion/Introversion: Extraverts are sociable and active, while introverts are more reserved and reflective.
Neuroticism/Stability: Neurotic individuals experience high levels of anxiety and emotional instability, while stable individuals are calm and resilient.
Psychoticism: This dimension includes traits like impulsivity and aggressiveness. High P scores indicate more impulsive and aggressive behavior.
Link to Addiction: Eysenck suggested that addiction can develop due to the personality traits an individual possesses. For example:
High Neuroticism: Individuals who score high on neuroticism may turn to substances or behaviors as a way to self-medicate their anxiety or emotional instability.
High Psychoticism: Those with high levels of psychoticism are more impulsive and aggressive, leading to more risky behaviors, such as drug use.
Research supports this theory. For instance, a study by Gossop and Eysenck (1980) found that drug addicts scored higher on psychoticism and neuroticism and lower on extraversion compared to a control group.
Evaluate Personality as an Individual Differences explanation for behaviour in Addiction.
-Difficulty establishing cause and effect.
Key issue with research inti the relationships between addiction and personality is that it is mainly correlational. Personality tests are usually given once the individual has already developed the addiction therefore cause and effect can not be established. Addiction has made the individual more stressed or moe impel;sive or not the other way round. However, Dong et al (2013) carried out a study on Chinese Uni students. They were given the EPQ just after entering uni, and 2 years later their addiction on the internet was assessed. Researchers found that higher N and P scores were linked to addiction.
-Role of personality depends on the addictive behaviour. Ruth McNamara et al (2010) found that in rats, impulsivity meant that the animals were more likely to self- administer cocaine but not heroin. Paul Rosin and Caryn Stroess (1993) looked at individuals tendency to become addicted to a range of different activities and could not find a common pattern. Therefore, the type of personality involved might depend on the specific addictive behaviour being investigated.
-The myth of addictive personalities. There are numerous traits that have been linked to addiction, and this makes it very difficult to reach a definite conclusion about what is meant by an addictive personality. In addition many of the traits are not unique to addiction. eg, Eyesneck also found high N and P scores in criminals. John Kerr refers to the idea of an addictive personality as one of the ‘myths of addiciton’. So many traits listed that they would be typical to most at some degree.
What is the Individual explanation of ‘Cognitive Biases’ in Addiction?’
Daniel Kahneman and Ames Tversky, proposed humans have a particular way of decision making called heuristics. Which are mental shortcuts used to solve a problem quickly.
- Applying these to gambling; 2 of the heuristics identified by Kahenman and Tvesky are; Represetaivness and Avalibality. These can explain why some people gamble. If a particular heuristic is selected on the wrong occasion this can cause problems. Contributing to a gambling addiction.
- Representativeness. This is the belief that random events have a pattern, and in particular that a series of events drawn from a small sample should represent what would be found in a larger sample. Eg, if people are asked to create a random sequence of 20 coin tosses they will suggest that the ratio should be 50/50 of heads to tails, but in reality it may take many more throws to reach this pattern. Gamblers fallacy is the beielf that if something happens more frequency than normal it will happen less frequently in the future, eg, Monte Carlo 1913. 1 Roulette showed a run of black for 26 times. Gamblers believe that a red was due and there was a rush to bet on red. Leading to money being lost. Gamblers may adapt this king of thinking pattern and believe that they are ‘;due;’ a win or predict the outcome of the next bet.
-Avaliability. This heuristic works on the principle that an event is seen as more likely if it is easier to recall from memory. The way people make decisions is often based on how often they hear about something and how available information is rather than the actual probability. Eg, over estimate the frequency of death if they have experienced it in close relatives. In the case of gambling it might encourage people to engage and continue in the behaviour in the mistaken belief that they are likely to win. eg, media reports on big wins by lottery winners. Make it seem events are more likely to happen than they are. Which may be why casinos and slot machines are close to each other.
Evaluate Cognitive Biases as an individual explanation for behaviour in Addiction.
- Supporting evidence. Mark Griffiths (1994) compared the verbalisations of 30 regular gamblers with 30 non-regular gamblers while they were plying on a fruit machine. He found that the regular gamblers showed many more irrational verbalisations than the non-regular gamblers (14% compared to 2.5%). In addition the verbalisations showed evidence of many of the heuristics and biases. Showing a clear difference in the cognitions of problem gamblers and other gamblers, suggesting that cognitive biases could be a useful explanation for the addiction. However, it is not an experiment so no cause or effect can be established.
- Issues with research. Research into cognitive biases requires participants to report to researchers whilst they are thinking, this creates a range of problems.eg, in research like that carried out by Griffiths (1994), researchers have to decide what bias is being shown, which may be susceptible to researcher bias. Questionnaires rely on the gambler being honest about what they are thinking, which could be subject to issues such as demand characteristics and social desirability. If a gambler is aware that they are thinking is irrational they may be reluctant to admit it. As well as this it ignores individual differences. Gamblig+Males. =Bingo +Females
- Description or explanation, one issue with cognitive biases as an explanation of gambling is that they may merely provide a description of the thoughts of gamblers rather than a true explanation. Explanations of behaviour should be able to predict what will happen in certain circumstances, and one of the features of cognitive biases is that it is impossible to predict when a particular bias might be used.’Grittiths (2013); triple rollover in lottery. This illustrates that using cognitive biases as an explanation does not allow predictions about behaviour to be accurately made.
What is the Social Psychological explanation of ‘Peer Influences’ in Addiction?’
The social psychological explanation of addiction focuses on the significant role of peer influences in the initiation and continuation of addictive behaviors. These influences involve processes such as role modeling, vicarious reinforcement, and perceived social norms.
Role modeling is a central concept, derived from Bandura’s Social Learning Theory (1977, 1986), which states that individuals imitate behaviors observed in those they identify with, such as peers. For example, an individual may observe a friend smoking or drinking and perceive them as popular or socially influential. This can motivate the individual to mimic these behaviors in hopes of achieving similar social rewards.
Vicarious reinforcement occurs when an individual observes a peer being rewarded for engaging in addictive behaviors, such as receiving attention, social status, or group acceptance. For example, seeing someone gain popularity for smoking may encourage imitation, as the observer anticipates similar benefits without directly experiencing the behavior.
Perceived social norms also play a key role. These are an individual’s perceptions of how prevalent and acceptable certain behaviors are within their peer group. Descriptive norms refer to beliefs about how common a behavior is (e.g., “Most people drink alcohol at parties”), while injunctive norms relate to perceptions of approval for the behavior (e.g., “Everyone thinks it’s normal to drink at parties”). Students often overestimate both types of norms within their social groups, which may lead them to engage in behaviors like drinking to align with these perceived expectations.
Research supports the impact of peer influences on addiction. For instance, Keizer et al. (2020) studied 359 emerging adults and found that individuals exposed to negative peer groups were more likely to engage in lifetime drinking compared to those in non-peer groups. This highlights how perceived peer behaviors and attitudes can strongly influence the development of addictive behaviors.
Evaluate ‘Peer Influences’ as a social psychological explanation for addictive behaviours.
-Research Evidence. Bruce Simons-morton and Tilada Earhart ( 2010( reviewed 40 prospective studies into the relationship between peers and smoking and found that all but one showed a positive correlation between the 2. This research supports the link between the behaviour of peers and engagement in addictive behaviour.
- Peer influence or peer selection. A key problem with research into peer influences on addictive behaviour is whether the peers influence the individual to engage int heir addictive behaviour (peer influence) or whether individuals choose friends because they also engage in the behaviour. (peer selection). It is likely they intersect. Ennett and Bowman (1994) found that pp who were non-smokers at the start of the study who had smoking friends were more likely to smoke at the follow up. Also evidence of selection. so both peer influence and selection are important processes.
-The role of other psychological facts. Mat may be too simplistic to say that peers are the only social factor that influence the development of addictive behaviour. Kimberly Kobe’s (2003) suggests we need to consider larger social contexts like family and neighbourhood. In addition, the exact mechanisms involved are unclear. Social learning theory and perceived social norms are just 2 explanations; may be other processes. eg, conformity and social identity.
What is the Social Psychological Explanataion of ‘the role of the media’ in addiction?
- Social learning theory. This is the same principles as peers. But film celebs. These act as the role model. The vicarious reinforcement would, eg, be the portrayal of the character as popular or glameruous in the film.
- How the media portrays addiction. Exposure to addictive behaviours in the media. A number of studies have showed that the potraytol of potentially addictive behaviours, partially smoking and alcohol use, is very common in films and TV. Eg, alcohol use was seen in 86% of popular UK films and 40% of TV programmes. Vicarious reinforcement. Not only are these behaviours seen frequently, but also the behaviours are often presented in a positive light. Hasantha Gunasekra et al (2005) analysed 87 of the top 200 movies of the last 20 years using a content analysis method. Tobacco and alcohol use were moe common and the researchers also noted incidences of cannabis and other drug use. The main finding is that positive potrayal= no negative consequences therefore vicarious reinforcement.
- Whether the exposure has effect: Robert Hellman et al (2006) reviewed a number of studies looking at how exposure to tobacco advertising and use of cigarettes influenced children’s attitudes to smoking and their smoking habits,. The researchers found that, across a variety of studies, that exposure to marketing and media promoting smoking increased positive attitudes and even doubted the chances of starting to smoke.
Evaluate the role of the media as a social psychological explanation for addictive behaviours.
-Difficulty establishing a casual link. The majority of the research into the media and addiction is correlational, and therefore cause and effect cannot be established,. It might not be the ‘media’ causing the addiction; eg, may be friends or family. However, Cornelia Pechman et al (1999) used an experimental method to assess the effect of smoking potrayol on attitudes to smoking. 2 v. Same film. 1 smoking, 1 none. Smoking v reported more positive attitudes and increased personal intentions to smoke. The use of this expermental method provides support for a casual relationship between the media and smoking.
- Lack of population validity. Matt lack population validity as much of it is conducted with adolescents. As they are more susceptible to social influences and effects. It is more easily detected. May be difficult in adults. Jamieson and Romeo (2015) suggest similar results are seen. Looked at trends in tobacco on TV and compared to smoking they found a clear correlation between tobacco use on TV and adult cigarette consumption.
- The media can have positive effects as well. Research so far has focused on an increase in addiction. It is important to note that the media can also have positive effects. May reduce addictive behaviours. Eg, Pechmann and Shah study, any effects of showing smoking in the film were cancelled out by showing an anti-smoking ad before. Also, many aspects of media report on the negative consequences. Many films show negative effects= Vicarious punishment, discouraging behaviours.
What is the method of modifying behaviour ‘Agonist and Antagonist Substitution’ for addictive behaviours?
- Agonist substitution: Methadone. An against is a chemical that binds to a post synaptic receptor and activates that receptor to produce a response. Agonsits are designed to imitate the action of another substance such as heroin.
Methadone is used as part of a maintenance treatment. The aim is that by giving heroin users methadone as a substitute, it will reduce cravings and prevent withdrawal symptoms. It has some of the same effects as heropin. Not the same ‘high’ should be reduced over time. (Detoxification) until the individual stops using it completely ( abstinence).
Dosage: Initial dosage of 10-4mg a day. Increased by up to 10mg a day. Until no signs of withdrawal. Maintenance dose of 60-120mg a day. - Antagonist substitution; An antagonist substitution binds to a receptor. But rather than causing a reaction, it blocks the usual function of a particular substance. Eg, naltrexone. Primarily used in the abstinence stage of recovery from addiction. It blocks euphoric and pleasurable effects associated with opioids and makes them less rewarding.
Naltrexone should be used by people who have stopped using opioids and have demonstrated they are highly motivated to stay free from drugs. Orally given. It may also be given in cases of alcohol addiction. Recommended to be taken alongside a psychological intervention and after withdrawal has occurred. It can be used for up to a 6 month period/
Evaluate the method of modifying behaviour ‘Agonist and Antagonist Substitution’ for addictive behaviours in terms of Effectiveness, Ethical and social implications.
- effectiveness; NICE assessed 31 reviews of effectiveness, including 27 randomised controlled trials. They found a higher level of retention for people using methadone than placebo/no treatment. One meta-analysis of studies into the effectiveness of a range of treatments concluded that as long as the dosage is adequate then methadone is effective as a maintenance treatment.
- Comparing methadone and buprenorphine. One alternative to methane is burprenophine. It’s a milder medication, has both aganoist and antagonist properties. Which means it partially activates the dopamine receptors, reducing the withdrawal symptoms. But is also blocks the receptors preventing the euphoria associated with the opioids. One advantage is that there is less risk of overdose due to its ‘ceiling’ effect. Meaning that taking large quantities will not increase its treatment. Marleau et al (2015) analysed data for 5 years and concluded that it was 6 times safer than methadone. However, methadone is preffered.
- Naltrexone. NICE reviewed 17 studies concerning the effectiveness of naltrexone for heroin addiction. Overall, they found conflicting results, and many of the randomised trials showed no significant difference between naltrexone and a control treatment for retention on the programme.However, when the results were pooled they did not find that naltrexone was associated in a reduction in relapse rates. Particularly in those that were highly motivated and where the patients were closely monitored and offered extra support. Issue with effectiveness is that it does not follow up over. along period of time. Relapse occurs after a few years_ weeks. Sample attention is common. Some people drop out the treatment and study.
- ethical implications. There are ethical criticisms of the uses of methadone. Side effects need to be taken into consideration. eg, methadone may interact with other drugs such as aldol and antidepressents= respiratory problems. Also a danger of overdose. The office for national statistics reported that in 2013, methadone was responsible for 429 deaths in the uk. Naltrexone, there is a greater risk of overdose. If the individual returns to taking a drug they will need more of it to feel the same effects and therefore less likely to overdose. People also need to be monitored for issues with liver function. If opioid dependent= withdrawal. It also treats the symptoms not cause.
- Social implications. Financial costs of methadone to society. A report by the centre for policy studies said that prescribing methadone was expensive failure and costs to society money and also drug users on benefits. It suggested greater success would be activated by funding rehabilitation units. However, drug scope disputed the claims, saying that the report overestimated the cost.
Methadone and criminality. According to a report by the National Treatment agency (2009). treating heroin users with methadone has an immediate positive effect on society by reducing their criminality. They suggest that rates of offending are reduced by half when addicts are in treatment. However, CFPS claimed that drug-related reoffending has continued to rise despite the availability of drug treatments for methadone.
What is the method of modifying behaviour ‘Aversion Therapy’ for addictive behaviours?
Aversion therapy is based on the principles of classical conditioning. An addict will learn to associate the thing they are addicted to with an unpleasant stimulus. Overtime, the thing they previously addicted to = an unpleasant response. To stop addiction.
- Antabuse (disulfiram). Țo treat alcohol addiction, ppl can be given a drug. Antabuse acts as the aversive stimulus. It works by affecting how the body metabolises alcohol. Normally alcohol goes to acetaldehyde which goes to enzymes in the liver called aldehyde dehydrogenase. Antabuse causes a reaction known as the disulfirom reaction, which stops this enzyme from working and causes a build up of acetedyde in the blood stream. This causes a range of unpleasant symptoms such as sweating, heart preparations, headaches and vomiting. It occurs within 10 minutes of consuming alcohol. Association made= avoid contact. Before learrring; Antabuse (UCS) goes to vomiting (UCR)
During learning; Antabuse (UCS) and Alcohol (NS) goes to vomiting (UCR)
After learning; Alcohol (now CS) GOES TO VOMITINING (now a CR).
NICE suggests that treatment begins after withdrawal. Dose of 200mg, can be increased. Should remain under supervision. Need to be careful about alcohol from other sources. eg, food or mouthwash = may cause unpleasant reaction.
- Rapid smoking, this is a form of aversion therapy used to help smokers overcome their addiction. Smokers sit in a closed room and take a puff on a cigarette every 6 months. Until they finish a certain number or feel sick. Unconditioned stimulus= not a drug. It is intensive smoking. As with the use of Antabuse, the theory is that the smoker will associate this unpleasant feeling with smoking and develop aversion to it. May be repeated= stronger aversion. it was popular in 19702.
Evaluate the method of modifying behaviour ‘Aversion Therapy’ for addictive behaviours in terms of Effectiveness, Ethical and social implications.
- Effectiveness.
Antabuse; hemet Neiderhafer and Wolfgang Staffed (2000s) compared Antabuse to a placebo and assessed their ppt using self report methods and screening for 90 days. The Antabuse patients have has significantly greater abstinence duration that the placebo group. Morgan et al (2011) found that those treated w Antabuse had more days until relapse and fewer drinking days. However, studies that look at the effectiveness of Antabuse in the long term are rare and they tend to lack scientific rigour as they are not full randomised controlled trials. - Rapid smoking. Recent research into the effectiveness of rapid smoking is limited as the treatment is less popular now. However, Hayden Mcrobbie (2007) carried out a study on 100 smokers attending a cessation clinic where rapid smoking was compared with a control condition of watching a video about giving up smoking. The rapid smoking group showed a significant increase in their urge to smoke in the 24 hours and week after the procedure. At 4 weeks the difference between the groups was no longer significant and therefore the impact of rapid smoking on long-term abstinence remains unclear.
- Behaviour is treated not the problem.
-Ethical implications;
Risk of harm. Taking Antabuse can clearly cause negative effects to an individual if they drink alcohol while on the med. Reid smoking is also a very unpleasant experience. On the other hand, this is the way the treatment is designed to work and those taking it will have given the valid consent prior. - More ethical alternatives such as the use of covert sensitisation. Individuals may be encourages to imagine feelings of being sick and vomiting.
-Social Implications; - Financial implications. In an article in the Telegraph newspaper (Devlin, 2008) highlights the dramatic increase in spending an Antabuse and other drugs to treat alcholosim. In 2008 the NHS spent just under £2.25 mill on the medication, up from £1.08 mill in 1998. However, alcohol concern responded by saying that this w`s a small amount compared with the money spent on treating alcoholism and related problems on the NHS.
- Social cost of not treating addictions. Alcohol costs the UK £21 billion a year. eg., lead to unemployment and may lead to individuals claiming benefits.
