Addiction: a disorder in which an individual takesasubstanceor engages in a behaviour that is pleasurable but eventually becomes compulsive with harmful consequences. Marked by...
physiological and/or psychological dependence
tolerance
withdrawal
Physical dependence: a state of the body due to habitual substance abuse which results in withdrawal symptoms when use of the drug is reduced or stopped
Psychological dependence: a compulsion to continue taking a substance (or continue performing a behaviour) because its use is rewarding
Tolerance: a reductionofresponse to a substance, the need to take more of a drug to achieve the same effect as previously achieved at lower doses
Withdrawal syndrome: a set of symptoms that develop when an addicted person abstains from or reduces their substance abuse
Risk factors: any internalorexternalinfluence that increases the likelihood a person will start using addictive substances or start engaging in addictive behaviours
Types of tolerance:
behavioural tolerance
cross-tolerance
Behavioural tolerance: when an individual learns to adjusttheirbehaviour to compensate for the effectsofasubstance.
E.g. people addicted to alcohol can learn to walk more slowly to avoid falling over
Cross-tolerance: where creating a tolerance to one substance can reduce sensitivity to another substance.
E.g. an addicted alcoholic is likely tolerant to anaesthesia and need higher doses during surgery
Risk factors to developing an addiction:
genetic vulnerability
stress
personality
familyinfluence
peers
Phases of withdrawal:
acute withdrawal phase - within hours of abstaining, intense cravings are experienced, reflecting strong physiological and psychological dependence. Gradually fade over a few days.
prolonged withdrawal phase - involves symptoms that occur over long periods of times (weeks, months, years). Individual becomes highly sensitive to cuesassociated with the addiction (reason for common relapse)
Withdrawal symptoms are almost always the opposite of the ones created by the substance
Limitation of individual risk factors:
The effects of interactions are ignored, some positive effects can also be ignored. Combinations of risk matter more than single factors.
Mayes and Suchman point out that different combinations partly determine the nature and severity of an addiction.
Some risk factors e.g. personality can be protective
Looking at combinations of risk factors point to genesas dominant
Most risk factors are proximate (immediate influence on addiction), however genetics are the longest-standing risk factors.
Rey et al. proposed that our reactions to stress and the extent we seek novelty are both partly genetic.
Genetic vulnerability, two direct mechanisms...
The number of dopamine receptors an individual has are genetically controlled, people who are addicted have been found to have abnormally low numbers of D2 receptors. Fewer receptors means more compensation is needed for less dopamine activity.
The level of functioning of the nicotine enzyme (CYP2A6). Pianezza et al. found some people lack a fully functioning nicotine enzyme, these people smoke significantly less than those smokers with the fully functioning version.
Stress...
Andersen and Teicher highlight the role of adverse childhood experiences (ACEs) in later addiction. They argue early experiences of severe stress have a damaging effect on the developing brain which creates a greater vulnerability to addiction later in life.
Personality...
Most people with antisocial personality disorder (APD) are also addicted substance abusers (e.g. Petry).
Robins argues that APD is a causal risk factor for developing addiction as individuals with APD breaks social norms, are impulsive and may behave criminally.
Family influences...
Livingston et al. found that final-year-high-school students who were allowed by their parents to drink alcohol at home were significantly more likely to drink alcohol excessively during their first college year.
Adolescents who believe their parents have little or no interest in monitoring their behaviour are more likely to develop an addiction. Key determinant is the adolescent's perception
Peers...
Mary O'Connell et al. suggest there are 3 major elements...
At at-risk adolescent's attitudes and norms are influenced by associating with peers who drink alcohol
These experienced peers provide more opportunity for the at-risk individual to use alcohol
The at-risk individual overestimates how much their peers are drinking, which means they drink more to keep up with the perceived norm
Evaluate genetic vulnerability
Support from adoption studies:
Kendler et al. used data from the National Swedish Adoption Study. They looked especially at adults, who had been adopted as children, from biological families in which at least one parent had an addiction
These children had a significantly greater risk of developing an addiction, compared to adopted individuals with no addicted parents in their biological families
Evaluate stress
Issue of causation... many studies have shown a strongpositivecorrelation between stress and addiction, however the order of stress and addiction is more important. Stress can develop after the addiction. Correlational studies cannot be solely relied upon
Evaluate personality
Research support from many studies for the link between APD and addiction. Several studies show addiction and ADP are co-morbid.
Bahlmann et al. interviewed 55 alcohol-dependent people of which 18 were also diagnosed with APD.
On average, they found ADP developed 4 years before their addictions.
Evaluate family influence...
Madras et al found a strong positive correlation between parents' abuse of cannabis and their adolescent children's use of cannabis, nicotine, alcohol and opioids.
It may be their children observe and model their behaviour. They may also infer that their parents approve of drug use.
Evaluate peers...
Real-world application: Social norms marketing advertising (SNMA) is an intervention to change mistaken beliefs about how much peers are drinking. It uses mass media advertising to provide messages and statistics about how much people really drink.
Students/ adolescents can get a more accurate viewpoint and correct their overestimations.
Dani and Heinemann focused on dopamine in their desensitisation hypothesis of nicotine addiction.
Acetylcholine (ACh) is an important neurotransmitter which has many ACh receptors on the surfaces of many neurones in the CNS. One subtype of an ACh receptor is called the nicotinic acetylcholine receptor (nAChR). These receptors can be activated by ACh or nicotine
When nAChRs are activated by nicotine, the neurone transmits dopamine. The neurone then becomes desensitised.
When a neurone becomes desensitised, the receptors temporarily cannot respond to any neurotransmitters. This leads to downregulation, a decrease in the number of active neurones because less of them are available.
The brain compensates for this loss of function by increasing the production of new receptors. However, these new receptors have lower sensitivity than normal ones so they require higher levels of stimulants to activate them.
nAChRs are concentrated in the ventral tegmental area (VTA) of the brain
When nAChRs are stimulated by nicotine, dopamine is transmitted along the mesolimbic pathway to the nucleus accumbens (NA). This triggers the release of more dopamine from the NA to the frontal cortex
Simultaneously as dopamine is released from the NA, dopamine is also transmitted along the mesocortical pathway to be released directly into the frontal cortex.
The mesolimbic and mesocortical pathways are part of the brain's dopamine reward system
As long as a person is smoking, nAChRs are continually desensitised. However, when the person doesn't smoke for a prolonged period nicotine disappears from their body and nAChRs become functional again. This is called resensitisation and more nAChRs become available (upregulation).
Withdrawal symptoms can be explained by nAChRs becoming overstimulated by ACh during resensitisation.
Avoidance of withdrawal states means smokers will continually follow a cycle of daytime downregulation and night-time upregulation. This creates a long-termdesensitisation of nAChRs to nicotine. Continuous exposure can cause permanent damage to brain neurochemistry - number of active receptors decrease.
Evaluation for the dopamine hypothesis...
indirect support from McEvoy et al
limited research on only role of dopamine
NRT
doesn't fully explain withdrawal
Indirect support for the role of dopamine...
McEvoy et al. studied smoking behaviour in people with schizophrenia who were taking the antipsychotic drug Haloperidol. This drug is a dopamineantagonist. The people taking the drug showed a significant increase in smoking (presumably a form of self-medication to increase their dopamine levels)
Limited research on only dopamine...
The dopamine system is central but research increasingly shows a complex interaction of several neurochemical systems.
Watkins et al. claimed these include neurotransmitter pathways (e.g. GABA and serotonin) plus other systems such as endogenous opioids (endorphins).
So brain neurochemistry cannot be fully understood if only looking at dopamine
Nicotine replacement therapy...
NRT was developed to help smokers quit. NRT products contain a controlled dose of nicotine which act neurochemically by binding to nAChRs and mimicking the effect of nicotine from smoking.
This satisfies cravings and allows gradual reduction of nicotine dosage over weeks with minimal withdrawal symptoms