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.

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, physical or psychological problems, giving up important activities, repeated use in dangerous situations, tolerance, and withdrawal symptoms relieved by further use.

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, 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, 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. 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

It has been proposed that the frontal cortex is also implicated in the maintenance of addiction.

The frontal lobe is involved in higher order tasks, such as reasoning, planning of behaviour and memory. 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.

Prescott and Kendler (1999) Used personal interviews to assess alcohol abuse and dependence among 3,516 twins from male-male pairs born in Virginia between 1940 and 1974.

Concordance rates were much higher between MZ twins when compared to DZ twins. The authors concluded that 48-58% of the variance in alcohol addiction is genetic.

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.

He also found that 48.7% of those who smoked carried this gene in comparison with 25.9% of non- smokers. 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

It is important to consider how genetic factors may interact with the environment. 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 a large-scale adoption study and found that children of biological parents or who had genetic full and half siblings who had a drug addiction had a significantly higher risk of drug addiction themselves.

However, they also noted that the risk was much higher if there were environmental factors in the adopted family such as criminal activity, divorce, alcohol problems or death.

Evaluation of Addiction Genes

Deterministic - Comings (1996)

Reductionist - Prescott and Kendler (1999)

Cause and Effect - Mental illness may cause addiction (Regier, et al 1990) found that 84% of people with anti social behaviour disorder have some for, of substance abuse in their lifetime.

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

Individual Differences Explanation: Cognitive Biases (Superhero)

Addiction is often seen as irrational because individuals continue behaviours with clear negative outcomes, suggesting problems in how addicts think about and judge their behaviour.

Cognitive biases, which involve systematic deviations from rational judgment, lead individuals to construct a subjective social reality that guides behaviour rather than objective facts.

Although traditional theories based on Bandura’s Social Learning Theory argue that addiction is maintained by positive outcome expectancies, reduced negative expectancies and low self-efficacy, evidence shows addicts often recognise negative consequences yet continue the behaviour.

This desynchrony between intentions and behaviour, known as loss of control, suggests addictive behaviour may be driven by processes outside conscious awareness and intentional control.

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)