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Addictions - Coggle Diagram
Addictions
Risk Factors in the Development of Addictions
Genetic vulnerability
Dopamine
Low D2 receptors, therefore compensating with addictive behaviours.
Nicotine metabolised by CYP2A6 enzyme
People are less likely to smoke if this enzyme is not fully functioning because nicotine levels are higher.
Research support
Kendler et al (2012) used data from National Swedish Adoption study. Those with addicted bio parent had a 8.6% increased risk compared to non addicted bio parent 4.2%.
Self control and emotional regulation may be genetic, a young person with less self control may be less likely to succeed, leading them into addictive behaviours. May gravitate towards friends with similar characteristics.
Stress
Childhood trauma
Epstein et al (1998) found strong correlation between instances of childhood rape and adult alcohol addiction
But only for women with PTSD- stress increases vulnerability.
Sensitive period
Anderson and Tiecher (2008) early experiences of distress damage the brain during a 'sensitive period'- creates vulnerability to addiction in adolescence.
Personality
Hostility
No "addictive personality" but some traits such as hostility are linked.
APD
Antisocial personality disorder strongly correlated with addiction related behaviours in adolescence.
Impulsivity
Key component of APD: risk taking, lack of planning and a preference for immediate gratification.
Ivanov et al (2008) suggested that impulsivity and addiction may share a genetic and neurological basis.
Family influences
Perceived parental approval
Livingston et al (2010) found that when parents allowed their children to drink alcohol at home during their final school year, children were more likely to drink excessively at college.
Parents may not care about children's behaviour often resulting in addiction.
Exposure
Adolescents are more likely to start using alcohol where it is an everyday part of family life, or when there is a history of addiction.
Peers
Rule breaking norms
SLT- a group norm that favours rule breaking can be influential.
Attitudes and opportunity
O'Connell et al (2009) three major elements to peer influence for alcohol addiction:
Attitudes about drinking are influenced by associating peers who use alcohol.
Peers provide more opportunities to use alcohol.
Individuals overestimate how much their peers are drinking and attempt to keep up with the perceived norm.
Practical application
Tobler et al (2000) created a peer pressure resistance programme to prevent young people taking up smoking.
Limitation
Risk factors interact
Different combinations of risk factors partly determine the nature and the severity of the addiction.
Furthermore, factors can make addiction less likely, understanding that there are many different pathways to addiction is a more realistic approach.
Cause and effect
Many studies have shown a strong correlation between stress and addiction.
However many addictions cause stress because of negative effects on relationships and finances.
This makes it difficult to separate the effects of one upon the other as many risk factors co relate.
Describing Addiction
Dependence
Physical
Occurs when a withdrawal syndrome is produced by stopping the drug.
Only possible to establish when someone has a physical dependence when they abstain from use.
Psychological
The compulsion to continue use.
For either an increase in pleasure or a reduction of discomfort.
Leads to behaviour becoming a habit despite harmful consequences.
Tolerance
Greater doses needed for the same effect, caused by repeated exposure.
Cross tolerance is when tolerance of one drug reduces the sensitivity of another.
E.g. people who have developed a tolerance to the sleep inducing effects of alcohol need higher doses of anaesthesia in surgery.
Withdrawal
Symptoms that develop after abstinence
Usually the opposite of the drugs effects
E.g. withdrawal from nicotine leads to irritability and anxiety.
Indicates a physical dependence
Motivation for taking the drug often stems from wanting to avoid these symptoms.
Explanations for Nicotine Addiction
Brain Neurochemistry
The Desensitisation Hypothesis
The role of nAChRs
Dani and Heinemann's (1996) hypothesis focuses on the neurotransmitter dopamine.
Some neurons that produce dopamine are in the ventral tegmental area of the brain (VTA).
These neurons have ACh receptors that also respond to nicotine called nicotinic receptors (nAChRs).
Desensitisation caused by nicotine
When nicotine binds to nAChRs:
the neuron is stimulated and produces dopamine.
The receptors shut down and cannot respond to neurotransmitters.
Leads to downregulation where fewer active neurons are available.
Supporting evidence
McEvoy et al (1995) found smoking behaviours increased in patients taking haloperidol (a dopamine antagonist).
Smoking increased as a form of self medication to achieve nicotine hit.
Also direct evidence for the importance of the dopamine reward system in brain imaging studies Ray et al (2008).
Effect of dopamine
Transmitted along the mesolimbic pathway to the nucleus accumbens to be released in the frontal cortex.
Mesolimbic pathway to the nucleus accumbens- reward centre
Mesolimbic pathway to be released in the frontal cortex.
Dopamine system creates a sense of reward and pleasure which is now associated with the intake of nicotine.
Limitation
Only considers dopamine, despite other neuro mechanisms being involved.
Actually a complex interaction of several systems including GABA and serotonin pathways and endogenous opioids.
Although dopamine is central we must acknowledge other systems.
Neurochemical explanations are reductionist
Ignores psychological differences.
Choi et al (2003) only 50% of smokers become dependant.
The Nicotine Regulation Model
Resensitisation of neurons leads to upregulation
When smokers go without nicotine for a prolonged period nicotine leaves the body.
nAChRs become functional again so neurons resensitise and become available (upregulation).
Upregulation leads to withdrawal symptoms
Because more nAChRs are available but not stimulated the smoker experiences acute withdrawal e.g. anxiety.
nAChRs are at their most sensitive which is why the first cigarette is the best.
This explains how dependence is maintained.
Chronic desensitisation increases tolerance
Persistent desensitisation of nAChRs leads to a permanent decrease in the number of active receptors.
Smoker requires more nicotine for same effects.
Therefore tolerance develops.
Real life application
Greater understanding of neurochemistry has led to the development of nicotine replacement therapies (NRT) in the form of patches and inhalers.
Understanding goes beyond nicotine addiction. Some diseases have high co morbidity with nicotine use e.g. depression.
Raises the prospect for further research and advances in treatments.
Learning theory
Operant conditioning
Positive reinforcement
If the consequence of the behaviour is rewarding they are more likely to do it again.
Mild euphoria produced by the dopamine reward system (mesolimbic pathway).
Negative reinforcement, to avoid withdrawal.
Classical conditioning
Smoking is a primary reinforcer as it is intrinsically rewarding.
Effects of smoking are biologically determined, nicotine on the reward system.
Secondary reinforcers include, pubs, smells, lighters, friends, etc.
Any other stimuli present at the same time or after smoking become associated with its pleasurable effects.
Certain environments create a sense of anticipation and pleasure thus becoming secondary reinforcers.
Even non pleasurable acts such as smoke in the back of you throat can become a secondary reinforcer as it is associated with nicotine.
Cue reativity
Cravings are triggered by cues related to smoking.
self reported desire to smoke
physiological signs of reactivity to a cue (e.g. heart rate)
objective behavioural indicators when cue is present (e.g. how many 'draws' are taken on a cigarette)
Supporting evidence
Non- human studies
Levin et al (2010) rats self administered nicotine due to positive reinforcement. Suggests they have similar mechanisms to humans.
Cue reactivity
Carter and Tiffany's (1999) meta analysis included measures of self reported cravings and physiological arousal in both non dependant and dependant smokers following exposure to smoking related cues.
Dependant smokers reacted strongly with high levels of arousal.
Findings were consistent with predictions therefore supporting theory.
Real life application
Aversion therapy works on the basis of counter conditioning by associating pleasurable effects with an aversive stimulus.
Smith (1988) found that 52% of participants who self administered electric shocks while engaged in smoking related behaviours were still abstaining after a year.
Practical benefits for the NHS.
Gender differences can be explained
Carpenter et al (2014) suggests that females struggle to give up smoking because they are more sensitive to cues.
The concept of self efficacy would suggest that female smokers have less confidence in their ability to quit.
Self efficacy is a learned behaviour.
Cannot explain why some do not become addicted.
Explanations for Gambling Addictions
Learning Theory
Vicarious reinforcement
One way people begin gambling is by seeing others being rewarded.
Through seeing others win in real life or in the news.
Direct reinforcement
Positive reinforcement can come from direct gain and the "buzz" that accompanies gambling.
Negative reinforcement occurs because gambling can offer a distraction from aversive stimuli e.g. anxiety.
Partial reinforcement
Skinners research found that partial reinforcement was more effective than continuous.
Once rewards stop behaviour stops (extinction).
In gambling only some bets will gain the reward. Unpredictability fuels the addiction.
Variable reinforcement
The variable reinforcement schedule is a partial reinforcement schedule where intervals between rewards vary.
Highly unpredictable.
E.g. slot machines pay out on 25th spin but not every time,
Very resistant to extinction.
Gambler learns that they will eventually win if they persist.
Cue reactivity
Gambling related atmospheres can trigger arousal.
Strengths
Research support
Dickerson (1979) high frequency gamblers in natural settings were more likely than low frequency to place bets in last 2 min of a race.
May delay to prolong the rewarding excitement.
Evidence for role of positive reinforcement in natural setting.
Learning theory explains failure to quit
Conscious desire to quit with motivational forces acquired through conditioning that drive them to continue.
Limitations
Lack of explanatory power
Explains certain types of gambling better than others.
Fruit machines are temporarily contagious, no delay between bet and outcome.
However poker requires skill and there is a greater delay, therefore more difficult to explain.
Individual differences
Griffiths and Delfabbro (2001) argue that people do not respond the same
Observations are difficult to explain without using cognitive features.
Doesn't explain all aspects of gambling
Conditioning processes may be less important at some points.