Unit 3: Addictive Behaviours

Characteristics of Addictive Behaviours

Addictive behaviour is defined by a repetitive, harmful compulsion to engage in a behaviour or use a substance, driven by an overwhelming desire despite negative consequences.

Key characteristics that define addiction suggested by Griffiths (2005) include Salience, where the addictive behaviour becomes the single most important activity in the individual’s life, dominating thoughts and feelings.

Individuals typically experience a significant Loss of Control, struggling to limit or stop the behaviour, which often leads to emotional distress, conflict with others and social/occupational impairment. Mood modification, where the activity is used to change emotional states such as stimulation or relaxation.

Over time, physical dependence develops, manifesting as Tolerance (the need for ever-increasing amounts of the substance or activity to achieve the same effect) and intense, distressing Withdrawal symptoms (involving unpleasant feelings, states and physical effects) when the behaviour is abruptly stopped.

The chronic nature of addiction means that even after a period of abstinence, the risk of Relapse remains high, making it a disorder that requires sustained psychological and/or biological intervention.

Diagnosis of addiction - Substance use disorder

Some types of addiction are classified as mental illnesses, and are included in the DSM. Other types of addiction do not meet the criteria for a full diagnosis.

Generally speaking, it is possible to develop an addiction to anything (although the DSM only specifies certain substances). However, all addictions have characteristics in common.

The DSM contains 10 categories of substance that can cause addiction. These are: alcohol, caffeine, cannabis, hallucinogens, inhalants, opioids, sedatives, stimulants, tobacco and “other”.

In addition to substances, the DSM also recognises the behaviour of gambling as a distinct addiction.

DSM-5

Substance Use Disorder (DSM-5) combines substance abuse and substance dependence into one disorder measured on a continuum from mild to severe, with each substance diagnosed separately. A diagnosis requires two to three symptoms for mild disorder from 11 criteria;

Including taking the substance in larger amounts or for longer than intended, wanting to cut down but not managing to, spending a lot of time getting, using or recovering from the substance, cravings and urges.

Failure to meet obligations, continued use despite relationship problems, physical or psychological problems, giving up important activities, repeated use in dangerous situations, tolerance, and withdrawal symptoms relieved by further use.

Biological Explanation: The role of Dopamine (Superhero)

The fundamental biological mechanism involves the brain's mesolimbic pathway, often called the reward or pleasure circuit.

• Initiation: All addictive substances and behaviours (e.g., drugs, gambling) trigger a large, rapid release of the neurotransmitter dopamine in the Nucleus Accumbens (NAc). (Wise, 2008) This surge produces intense pleasure or euphoria, and activates the mesolimbic pathway, reinforcing the behaviour. The brain learns that the behaviour leads to a powerful "reward”.

• Maintenance: Over time, repeated massive dopamine surges cause the brain to undergo neuroadaptation. If a drug is used regularly, the brain compensates and adapts to maintain the balance while the drug is present. This means that when the drug is no longer being taken, the brain becomes out of balance, causing withdrawal symptoms.

The role of Dopamine - Volkow 1997

• To protect itself from overstimulation, the brain reduces the number of dopamine receptors (down-regulation), meaning it produces less of its own dopamine. Volkow et al (1997) found that in users of cocaine, there was a reduction in both the number of D2 receptors in the brain, as well as reduction in the release of dopamine.

• When a drug is taken repeatedly, the effects of this drug will be diminished each time. Therefore, a higher and higher dose is needed in order to get the same effect. This is called tolerance.
  The individual must then continue or escalate the addictive behaviour just to reach a normal, non-addicted state, driving the compulsion and loss of control.

Frontal Cortex

The frontal cortex is also implicated in the maintenance of addiction. It has been proposed that the high levels of dopamine caused by addiction alter the functioning of parts of the frontal cortex, changes that persist even when the drug is no longer being taken or the behaviour no longer engaged in.

It is argued by Volkow and others that these changes to the frontal cortex can alter our attention, causing addicts to pay more attention to stimuli associated with their addiction, triggering relapse despite the negative effects of withdrawal and tolerance having disappeared.

Robinson and Berridge (2003) argue that changes to the frontal cortex causes the addict to want to engage in the addictive behaviour, rather than just like it. Many addicts report feeling compelled to engage in their addiction, even though they no longer gain any pleasure from it.

Evaluation of Biological Explanation (Dopamine)

Deterministic - (Wise, 2008) focus on biological factors, reduces blame for addicts

Reductionist - Volkow et al (1997) ignores individual differences/ social environmental factors, coercive treatment to reduce addiction

Application - Agonist/Antagonist substitution (method of modifying)

Cause and effect - Robinson and Berridge (2003), explains why addiction is maintained but doesn’t address what causes initiation (e.g taking drugs in the first place), insufficient explanation

Biological Explanation: Addiction Genes (Sidekick)

If genes play a part in the development of addictions, then people who are more closely related should share the behaviour.

A twin study by Prescott and Kendler (1999) found higher alcohol addiction concordance rates in identical (MZ) twins than fraternal (DZ) twins, suggesting about 48–58% of the risk for alcohol addiction is due to genetic factors.

Genes associated with addiction

A link has been found between the DRD2 dopamine receptor gene and addiction. Individuals with the A1 variant of the DRD2 gene have fewer D2 receptors in the brain’s pleasure centre.

The lower number of receptors leads to these individuals over compensating by engaging in addictive behaviours.

Comings (1996) found that 42.3% of drug and alcohol addicts carried the D2A1 variant in comparison with 29% of the control group.

Similarly in gambling addicts, 50.9% carried this variant of the DRD2 gene in comparison with 25.9% of non addicts.

Variations of the ADH gene have also been linked to increased risk of alcoholism, in individuals who break down alcohol much slower than others and so drink more of it, increasing their risk of dependence (Edenberg 2007).

Diathesis-Stress Model

The diathesis-stress model suggest that a disorder such as addiction only develops when a genetic predisposition is triggered by an environmental stressor.

Kaufamn (2007) found a link between the 5HTT (serotonin) gene and the development of alcoholism. However, this is not found on its own- it appears to interact with environmental factors such as childhood mistreatment.

Kendler et al (2012) conducted an adoption study showing that people with biological relatives who had addiction had a higher risk of addiction themselves, however, the risk was even greater when negative environmental factors (e.g., alcohol problems, criminality, divorce) were present in the adoptive family.

Evaluation of Addiction Genes

Deterministic - Comings (1996)

Reductionist - Prescott and Kendler (1999)

Cause and Effect - Kaufamn (2007)

Scientific - (Edenberg 2007), ADH Gene - treatments/ preventative measures

Individual Differences Explanation: Cognitive Biases (Superhero)

Addiction is often seen as irrational because people continue harmful behaviours even when they know the negative consequences.

Cognitive biases can distort thinking, leading individuals to act based on their own perceptions rather than reality.

While theories like Bandura’s Social Learning Theory suggest addiction is driven by expected rewards and low self-belief, many addicts are aware of the risks but still continue.

This gap between knowing and doing, known as loss of control, suggests addiction may be influenced by unconscious processes beyond deliberate choice.

Cognitive Biases: Heuristics - Representativeness

One of the key cognitive biases that may explain addiction is the effect of heuristics. Heuristics allow us to make mental shortcuts in order to make decisions quickly and with little effort.

While heuristics are vital for humans to function, they can lead to errors. These errors may be able to explain why some people engage in addictive behaviour, even though logically they should not.

The Representativeness Heuristic is a mental shortcut that we use when estimating probabilities. When we're trying to assess how likely a certain event is, we often make our decision by assessing how similar it is to an existing mental prototype.

An example of cognitive bias when applied to addiction is the Gambler's Fallacy (Karen and Lewis 1994). When it comes to gambling behaviour, after a run of losing bets, a gambler may feel that a bet is a "sure thing" due to the representativeness heuristic telling them that an outcome is due, and so may persist in gambling behaviour.

Cognitive Biases: Availability Heuristic + The Sunk-Cost Fallacy

The Availability Heuristic describes the mental shortcut where we make decisions based on emotional cues, familiar facts, and vivid images that leave an easily recalled impression in our minds.

The gambler’s own experiences can contribute to this heuristic. They will easily be able to remember the times when they won big, and it will be harder to remember the times when they lost.

As these memories of winning are more “available” than the ones of losing, the gambler will overestimate their chances of winning.

The sunk cost fallacy is a decision-making bias identified by Strough et al. (2008), which refers to the tendency to continue investing resources because of previous investment, even when it would be more rational to cut losses.

In gambling, this leads individuals to continue betting to recoup losses after spending large amounts of money, and it is often linked to representative bias, where gamblers believe that repeated losses mean they are “due” a win.

Evaluation of Cognitive Biases

Deterministic - Griffiths (1994) found that regular gamblers showed many more irrational verbalisations (14%) than non- regular gamblers (2.5%), many of which showed evidence of heuristics. Shows a clear difference between the cognitions of problem gambles and other gamblers, suggesting cognitive bias explains addiction.

Reductionist - (Strough et al, 2008)

Cause and Effect - (Karen and Lewis, 1994)

Individual Differences Explanation: Addictive Personality (Sidekick)

The addictive personality view suggests that some individuals have personality traits that predispose them to addiction in general, rather than to a specific addiction.

This means that if one addiction is overcome, it may be replaced by another behaviour. These predisposing factors are present before first exposure to drugs or addictive behaviours, making some individuals more vulnerable to use, abuse or dependence, while others may be more resistant.

Addictive Personality - Lang (1983)

Lang (1983) concluded that there is no single set of psychological characteristics common to all addictions. However, he identified several significant personality factors that may contribute.

These include impulsive behaviour, difficulty delaying gratification, antisocial personality traits and sensation seeking.

He also highlighted a high value on nonconformity and weak commitment to societal achievement goals, along with social alienation and tolerance for deviance.

Finally, heightened stress was identified as a risk factor, which may explain why adolescence and other stressful transition periods are often linked to more severe drug and alcohol problems.

Addictive Personality: Eysenck

Eysenck (1997) proposed that an addictive personality is linked to high psychoticism and neuroticism.

High psychoticism is associated with impulsivity, increasing the likelihood of engaging in risky behaviours, and De Wit (2009) found impulsivity can be both a cause and effect of drug abuse.

High neuroticism, linked to anxiety and stress, may lead individuals to use substances as self-medication, with Sinha (2001) highlighting stress in addiction and relapse.

Evaluation of Addictive Personality

Deterministic - Lang (1983)

Reductionist - Sinha (2001) ignores situational and environmental factors that also contribute to addictive behaviour.

Cause & Effect - De Wit (2009)

Application - Antagonist Substitution

Social Psychological Explanation: Peer Influences (Superhero)

Peers can act as role models that are imitated. Peers can establish social norms that mean that behaviour such as smoking and drinking are seen as acceptable.

Peer pressure may play a particularly important role in the initiation stage of addictive behaviour.

Experimentation often begins in adolescence, as does the process of addiction. Normal adolescent specific behaviours (such as risk taking, novelty seeking and response to peer pressure) increase the likelihood of use of legal and illegal drugs.

Adolescents may be particularly susceptible to social influences given the importance of school and peer groups in their life (Steinberg 2007).

Peer pressure or the direct or indirect encouragement from one’s own age group to engage in activities they may or may not want to engage in is a major factor in the development of risk taking behaviours e.g. alcohol, drug and tobacco use (Lewis and Lewis 1984).

Peer Influences: Social Learning Theory (SLT)

Social Learning Theory (Bandura, 1977) suggests that behaviour is learned through observation, imitation and modelling of a role model.

While traditional behaviourism explains addiction through classical conditioning (associating substances with pleasure) and operant conditioning (reinforcement through positive effects), SLT adds that people can learn addictive behaviours by watching others being rewarded. This is known as vicarious learning, where we learn through observing the rewards or punishments experienced by others, rather than through direct experience ourselves.

Imitation is more likely if the role model is the same gender, similar age or older, high status, powerful, or likeable, making SLT particularly useful in explaining peer influence in addiction.

Social Norms

It also recognises cognitive processes, as individuals think about and interpret what they observe.

Peer influence increases alcohol misuse through social norms, as individuals often overestimate descriptive norms (how much peers drink)

and injunctive norms (peer approval of drinking), leading them to drink more to fit in;

Perkins and Berkowitz (1986) found these misperceptions can result in higher alcohol consumption among students.

Evaluation of Peer Influences

Deterministic - (Lewis and Lewis 1984), adolescents peer groups —> positive peer pressure

Reductionist - Steinberg (2007), ignores biological factors

Cause & Effect - Bandura (1977), may seek out role models who are like them?

Prevention Strategies - Perkins and Berkowitz (1986) - Changing perceptions on alcohol misuse, informative sessions in university teaching that “most people drink moderately”

Social Psychological Explanation: The role of the media (Sidekick)

One social psychological explanation for addictive behaviour is the role of the media, which links closely to Bandura’s (1977) Social Learning Theory.

According to this theory, through vicarious reinforcement, an addict will imitate the behaviour of a celebrity role model who they admire, because their idol is being rewarded for addictive behaviour e.g. smoking or drinking leading to money for advertising such products and the idol engaging in drug behaviour that may win the admiration of others.

Gunasekera et al (2005) analysed 87 of the top 200 movies of the last 20 years. The use of alcohol and tobacco was common, but he also noted incidences of cannabis and other drug use.

The main focus was that the addictions tended to be portrayed positively, providing vicarious reinforcement for addicts who view their role models as engaging in exciting addictive behaviour with no negative outcome.

The role of the media: Addictive Behaviour Examples

Hanewinkel et al. (2014) found that 40% of teenagers aged 12-14 exposed to alcohol use in films tried drinking, even after controlling for other factors, such as personality and school performance.

Similarly, Glantz (2002) showed that as smoking in films decreased, tobacco sales also fell. Together, the studies suggest that media portrayals of addictive behaviours can influence viewers’ real-life behaviour.

In the UK, tobacco and alcohol advertising is tightly regulated, but gambling is less restricted.

Derevensky et al. (2010) found that most adolescents are exposed to gambling ads that portray winning as easy; while many recognise the risks, these ads tend to reinforce existing gambling habits, particularly among problem gamblers.

Evaluation of The Role of The Media

Deterministic - Hanewinkel et al. (2014), reduce exposure of such films to adolescents

Reductionist - Derevensky et al. (2010) Ignored peer influences

Cause & Effect - Gunasekera et al (2005) People with addictive behaviours may be more likely to watch TV shows and films which depict their behaviour.

Methods of Modifying Addictive Behaviours: Agonist and Antagonist Substitution (add study)

Agonist drugs: these are chemicals that bind to the postsynaptic receptor. They imitate the action of a synthetic chemical such as heroin.

Methadone is a drug that is most commonly used as a treatment for opioid addiction, particularly that of heroin. Heroin causes a large release of dopamine in the brain. Over time, the brain adapts by making dopamine receptors less sensitive and releasing less dopamine naturally.

As a result, the person becomes dependent on heroin and continues using it mainly to avoid withdrawal symptoms rather than to feel pleasure.

Methadone is a synthetic (man-made) replacement for heroin. It is an agonist drug. This means it occupies the dopamine receptors in the brain and thus mimics the effect of heroin minus the “high”.

It activates the dopamine receptors and therefore reduces the symptoms of withdrawal. One dose of methadone can reduce withdrawal symptoms for 24-36 hours.

Methadone showed efficacy in terms of reducing the use of heroin, reducing crime, limiting the spread of HIV infections and engaging users in treatment regimens (Lingford-Hughes et al 2004).

Method of Modifying: Antagonist Drugs

Antagonist drugs: these bind to a receptor but rather than causing a reaction, it blocks the action of a particular substance.

Similarly to methadone, naltrexone is a drug that is commonly used in the treatment of opioid addiction. However, while methadone is used to manage the symptoms of withdrawal, naltrexone is used to prevent recovering addicts from relapsing.

Gowing et al (2001) found that naltrexone is very effective for people who are highly motivated to quit, but not as useful for those who are less motivated.

Naltrexone is an antagonist substitution drug. This means that it occupies the dopamine receptor molecules but does not activate the receptors.

This prevents dopamine from attaching to the receptors and activating them. This means that if a patient who has taken naltrexone were to take an opioid such as heroin, they would not experience a “high” or pleasure because the dopamine receptors are blocked.

Therefore, this would make the drug less rewarding.

Evaluation of the Effectiveness of Agonist/ Antagonist Substitution

Strength - Effective - Gowing et al (2001) found that methadone programmes are very effective at reducing the physical and social harms associated with drug use. Typically, the longer that someone remains in treatment, the better their outcomes and the lower the chance ofrelapse.

Weakness - Antagonists not suitable for all & Issues with compliance (provides no pleasure) - Gowing et al (2001) found that naltrexone is very effective for people who are highly motivated to quit, but not as useful for those who are less motivated.

Strength - Economic Benefit - It has been estimated that investment in methadone leads to a threefold economic benefit in terms of reductions in NHS health and social care costs, reduced criminal activity and the price of policing. In addition, as methadone is much longer acting, it can be given once a day, rather than 2–4 times a day as required for heroin.

Weakness - Methadone is an addictive drug & can be fatal in overdose - Occasionally, the doses are found by children, who drink it as it is usually in a sugar solution and then die of overdose; this results in several deaths per year in the United Kingdom (Milroy and Forrest, 2000).

Evaluation of The Ethical Issues of Agonist/ Antagonist Substitution

Ethical Issue - Coercion - The view that drug addiction is caused by biological factors promotes the view that their behaviour is out of their own control and requires pharmacological intervention to treat it. However, Hall 2006 argues that this raises ethical issues regarding the rights of the individual with the possibility that the community will make greater use of coercive treatment to reduce addiction.

Ethical Strength - Less addicts on the streets - Methadone showed efficacy in terms of reducing the use of heroin, reducing crime, limiting the spread of HIV infections and engaging users in treatment regimens (Lingford-Hughes et al 2004) (less violence & harm/ crime).

Ethical Issue - Side effects of methadone: nausea, hallucinations, fainting & fast or pounding heartbeat. Interacts w/ antidepressants causing respiratory problems. Many addicts are depressed - discontinue with treatment

Evaluation of The Social Implications of Agonist/ Antagonist Substitution

Social Implication - Treats symptoms not causes - It could be argued that treatments such as methadone and naltrexone are really “papering over the cracks” of a wider issue of social deprivation. The Advisory Council for the Misuse of Drugs (1998) found that Deprivation is linked most strongly with the extremes of problematic use and least with casual, recreational or intermittent use of drugs. Does nothing to prevent people initiating an addiction in the first place, social problems are hard to solve, government find it easier to treat than address the root cause. Places blame inside criminal.

Positive Social Implication - Economic Benefit - It has been estimated that investment in methadone leads to a threefold economic benefit in terms of reductions in NHS health and social care costs, reduced criminal activity and the price of policing. In addition, as methadone is much longer acting, it can be given once a day, rather than 2–4 times a day as required for heroin.

Applying Biological explanation to methods of modifying: Dopamine Explanation

Initiation: All addictive substances and behaviours (e.g., drugs, gambling) trigger a large, rapid release of the neurotransmitter dopamine in the Nucleus Accumbens (NAc). (Wise, 2008) This surge produces intense pleasure or euphoria, and activates the mesolimbic pathway, reinforcing the behaviour. The brain learns that the behaviour leads to a powerful "reward”.

Maintenance: If a drug is used regularly, the brain compensates and adapts to maintain the balance while the drug is present. This means that when the drug is no longer being taken, the brain becomes out of balance, causing withdrawal symptoms. Over time, repeated massive dopamine surges cause the brain to undergo neuroadaptation.

When a drug is taken repeatedly, the effects of this drug will be diminished each time. Therefore, a higher and higher dose is needed in order to get the same effect. This is called tolerance.
The individual must then continue or escalate the addictive behaviour just to reach a normal, non-addicted state, driving the compulsion and loss of control.

The method of modifying should therefore work by replacing the activation of the mesolimbic pathways with a drug that does not provide the ‘high’ that substance misuse does. The method of modifying is Agonist/ Antagonist substitution.

Agonist & Antagonist Substitution

Agonist Drug: Methadone is a synthetic (man-made) agonist drug that is most commonly used as a treatment for opioid addiction.

This means it occupies the postsynaptic dopamine receptors in the brain and thus mimics the effect of the opioid drug minus the “high”.

It activates the dopamine receptors and therefore reduces the symptoms of withdrawal. One dose of methadone can reduce withdrawal symptoms for 24-36 hours.

Antagonist Substitution

Naltrexone is an antagonist substitution drug. This means that it occupies the dopamine receptor molecules but does not activate the receptors. This prevents dopamine from attaching to the receptors and activating them, therefore, it blocks the action of a particular substance.

This means that if a patient who has taken naltrexone were to take an opioid such as heroin, they would not experience a “high” or pleasure because the dopamine receptors are blocked.

Therefore, this would make the drug less rewarding. Generally speaking, naltrexone is often offered alongside psychological counselling to help prevent the risk of relapse.

Because it blocks the dopamine receptors, thus preventing activation of the mesolimbic pathway, naltrexone is starting to be used for other addictions, such as alcohol or even gambling.

Applying Individual Differences Explanation to methods of modifying: Addictive Personality Traits

Antagonist Substitution

The method of modifying should therefore work by blocking the activation of dopamine in the mesolimbic pathway, effectively ‘stopping’ the high from occurring at all. The method of modifying is Antagonist substitution.

Antagonist drugs: these bind to a receptor but rather than causing a reaction, it blocks the action of a particular substance.

Naltrexone is an antagonist substitution drug. This means that it occupies the dopamine receptor molecules but does not activate the receptors. This prevents dopamine from attaching to the receptors and activating them.

This means that if a patient who has taken naltrexone were to take an opioid such as heroin, they would not experience a “high” or pleasure because the dopamine receptors are blocked.

Therefore, this would make the drug less rewarding. Generally speaking, naltrexone is often offered alongside psychological counselling to help prevent the risk of relapse.

Because it blocks the dopamine receptors, thus preventing activation of the mesolimbic pathway, naltrexone is starting to be used for other addictions, such as alcohol or even gambling.

Applying Social Psychological Explanation to method of modifying: Peer pressure

Positive peer pressure & drug rehab

The method of modifying should therefore work by replacing negative peer pressure influences with more positive ones that the addict is able to interact with the positive influences to abstain from the addictive substance.

Method of modifying is Positive Peer Pressure & Drug Rehab.

We often have a negative connotation attached to the term “peer pressure”, which is understandable. However, it can also bring about a good change in someone’s life if it is positive. If people around you influence you to make healthy choices, it is known as positive peer pressure.

Many drug recovery programs make use of positive peer pressure to influence the behaviour of the patient. Just like a person surrounded by intoxicated friends uses drugs to fit in, an ex- addict surrounded by sober peers will naturally want to stop abusing so they can fit in. They’ll be motivated to lead healthy and happy lives.

Therefore, someone who is starting recovery must be surrounded with people who will encourage positive change. People who are in recovery must avoid meeting people who were once a source of negative peer pressure, as that can be a trigger for relapse. Creating a positive environment motivates an addict to be sober and positive peer pressure encourages individuals to abstain from addictive substances.