Addiction

Gaming disorder = A pattern of behaviour where priority is given to gaming over all other activities. A person is unable to stop playing, despite the negative consequences it might have on a person’s health and life.

Symptoms of gaming disorder:

• Impaired control over gaming 

• Increased priority to gaming to the extent that gaming takes precedence over other life interests and daily activities

• Continuation or escalation of gaming despite the occurrence of negative consequences

To be diagnosed must display all above symptoms for 12 months. 

China and South Korea currently have a big problem with gaming disorder. Have set up military-style camps that have been disciplined for using extreme discipline and harsh punishments. 

The labelling of gaming disorder is meant to help doctors offer treatments and help. Not brandish the image of gaming.  

Addiction = a disorder in which an individual takes a substance or engages in a behaviour which is pleasurable but becomes compulsive with harmful consequences. 

1. Physical dependency - changes in the body

   1. starting the behaviour again reduces/stops the negative effects

1. Psychological dependency - the person feels as if they cannot cope with life without the drug or behaviour 

   1. causes anxiety, irritability or depression

1. Withdrawal symptoms - negative effects when they stop the substance/behaviour 

   1. stopping the addictive behaviour causes a lack of neurotransmitter and causes feelings which are opposite to those caused by the neurotransmitter

2. Tolerance - An individual's response to the substance/behaviour is reduced so they need an increased amount to experience the same effect

Risk factor = Any influence, internal or external, that may increase the likelihood that a person will become addicted to a substance or behaviour. 

5 risk factors of addiction:

1. Genetic vulnerability

Can be tested for by: Twin studies 

If we see that addiction is more likely in relatives we may assume that this behaviour is genetically controlled but this is an incorrect assumption because there is never 100% concordance even in MZ twins. 

Genes affecting neurotransmitters in addiction

• Neurotransmitters = Chemical messengers in the brain

• Dopamine = Rewarding chemical in the brain 

• If you have few receptor sites the the receiving neuron is less stimulated by the dopamine so the person repeats the behaviour more to increase the dopamine action

Genes affecting enzymes in addiction - People w/ a less efficient CYP2A6 enzyme are slower at metabolising nicotine so it stays in their system longer 

Kendler et al (2012) looked at adopted children in Sweden. 

• P’s were adults who had one addicted parent but had been adopted 

• 8.6% later developed an addiction compared to 4.6% of those adopted who had no addiction in their biological family 

• Supports the genetic basis of adoption

• Control group ensured the addiction was not down to the stress of being adopted 

Indirect effects = It may be that control of emotions is genetic which causes children to misbehave in school and then associate with people who have addictions and lead to themselves taking drugs. The genes play a role but only indirectly.

Early experiences of stress may have a damaging effect on the developing brain and cause a vulnerability for addiction later in life. Some may live their lives without addiction but the addition of another traumatic event may trigger the addiction. 

E.g. Epstein et al. found a strong correlation between childhood **** in women and adult alcohol addiction but only if the women had also been diagnosed with PTSD.

A strong link between Antisocial Personality Disorder and addictions. One big aspect of APD is impulsivity and instant gratification which may explain why APD is a risk factor for addiction. 

APD and addictions both begin in adolescence as the prefrontal cortex (responsible for impulse control)| is developing until 25. 

The strong link between impulsivity and addiction maybe because they share a common genetic or neurological cause.

• Parental attitudes to addictive behaviours, Livingstone et al found that high schoolers allowed to drink at home were then more likely to drink excessively at college the next year. 

• If the adolescent feels that the parent has little or no interest in their behaviour

• Family history of addiction

There are 3 elements to how peers can become a risk factor for alcohol addiction:

1. Their attitudes towards alcohol are influenced by their peers

2. Peers may provide more opportunities to access alcohol

3. The individual overestimates how much their peers use substances so they take more to keep up with the perceived norm

• A better understanding of neurochemistry can lead to the development of new treatments for nicotine addiction

  • E.g. nicotine replacement therapy or the possibility of nicotine immunisation

• For an experiment, the IV needs to be manipulated by the researcher. For an experiment into nicotine addiction, this means the researcher would have to enforce smoking. This would be unethical as we know that smoking causes long-lasting damage. 

• It may also be problematic to use correlational research as many of these studies show a strong correlation between stressful experiences and addiction-related behaviours. Some addictions can cause more stress due to their negative effects on relationships. Because risk-factors and addiction co-relate in these ways it can be difficult to separate out the effects of one on the other.

The role of dopamine:

• Dopamine is a neurotransmitter that causes short term feelings of euphoria

• When someone takes nicotine dopamine is released in the mesolimbic pathway

• This causes feelings of pleasure and reduction of stress so the addict repeats it 

The desensitisation hypothesis:

• Proposes that neurons in the brain that produce the neurotransmitter ACh have nicotinic receptors which can bind with nicotine. This causes the neuron to be temporarily stimulated but then these receptors shut down and temporarily cannot respond to neurotransmitters (downregulation). 

• When this process occurs in neurons, dopamine is released which leads to feelings of mild euphoria, increased alertness and reduced anxiety which makes the person want to continue to smoke. 

• The nicotine regulation model proposes that when smokers go without nicotine for a long time or at night, the drug is metabolised and re-sensitised. 

• This allows the ACh receptors to become re-sensitised (upregulation) however this results in acute withdrawal syndrome which includes anxiety and agitation due to decreased dopamine functioning. 

• Haloperidol reduces dopamine in the brain. McEvoy et al found that this drug caused patients to increase their smoking. This supports the neurochemical explanation as the patients seek to replace the dopamine that the drug is reducing. The body responded to having the dopamine levels artificially changed. 

• Reductionist view to break down a complex disorder into the production of dopamine, as this ignores the influence of GABA and serotonin. 

• Even if the biological explanations of nicotine addiction are true, they ignore the influences of social factors. Won Choi found that only around 50% of people who experimented with smoking became addicted. It was those who had friends that smoked and see themselves as bad at school that were more likely to become addicted. To include social factors provides a more holistic approach. This shows how the neurochemical theory can explain how the addiction occurs but not why.

1. Initiation

   1. The onset of smoking. Why people go from never smoking to trying. Especially as we are educated against it. 

2. Maintenance 

   1. Why people continue to smoke, even if they know it is bad for them

3. Relapse

   1. Why people return to smoking after a long time away from it and no longer addicted

SLT to explain smoking initiation

• Young people observe models receiving a reinforcement for smoking and so are vicariously reinforced themselves. The most likely models are those the young person identifies with. The reinforcement is the thought of being cool or attractive. 

Operant conditioning to explain smoking maintenance

• Positive reinforcement - People smoke to achieve the euphoric effects of dopamine acting on the mesolimbic pathway. Negative reinforcement - People continue to smoke because it reduces the unpleasant withdrawal effects they experience if they stop

Classical conditioning to explain smoking relapse: Cue reactivity

• The effects of nicotine are natural and unconditioned. Nicotine is then a primary reinforcer. When people smoke there are many other stimuli that are present, e.g. the smell of tobacco. The secondary reinforcers are then associated with the effects of nicotine. Cue reactivity occurs (the secondary reinforcer may lead to a similar physical and mental response as the nicotine itself). When someone is trying to quit smoking being exposed to these cues can trigger a craving so may relapse.

Karcher and Finn (2005)

• Teens who siblings smoked were 2.7 times more likely to smoke 

• Teens who peers smoked were 8 times more likely to smoke (then if no one around them smoked) 

• Peers are the biggest influence in the uptake of smoking in teenagers. SLT would explain this as teenagers are more similar to their peers than their siblings. 

• They may see their peers rewarded for smoking and be vicariously reinforced

Real-life application

• Advertising and media bans, e.g. James Bond no longer smokes

• Motor reproduction = make it harder for underage teenagers to buy nicotine

• Show role models be rewarded for not smoking

Social Learning Theory

SLT suggests that people start gambling from seeing others rewarded for their behaviour. 

Attention - how good are the rewards of gambling? 

Retention - will they be remembered?

Reproduction - does the person have the ability to create a good outcome? 

Motivation - are they driven to do it? 

Operant conditioning

If people gamble because it removes boredom then it is being negatively reinforced.

Positive reinforcement = money, more spins, fame. 

Reinforcement schedules

• Continuous reinforcement leads to the quickest learning but also the quickest extinction. 

• Variable reinforcement requires longer learning but lasts longer. 

• This is because the gambler doesn’t know when the reward is coming so will continue to gamble in the hope that the win will be soon. 

Classical conditioning

• Cue reactivity occurs in gambling, e.g. being in a casino, smoking inside, getting dressed up, floor music, bright lights