Gambling Addiction Flashcards

1
Q

Neurophysiological basis of addiction

A
  • If you continue to do something for a long period of time, neurophysiological changes in the brain occur
  • Different areas of the brain activates during pleasurable activities
    • Ex. alcohol floods the brain with NTs, but the more you do it, the less responsive your system is -> brain no longer responds in same way -> can constitute a disease process (b/c you need more and more of that thing to stimulate brain and get feeling of excitement)
  • – Over time, brain can go back to normal state
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2
Q

Psychological factors contributing to addiction

A
  • Early childhood experiences
  • Trauma
  • Mental health issues
  • Affect regulation
  • Impulsivity/sensation seeking
  • Cognitive distortions (ex. Illusion of control, Attributional bias, Gambler’s fallacy)
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3
Q

Sociological factors

A
  • Access to desirable alternatives
  • Social norms (ie. modeling, culture)
  • Exposure (accessibility/availability, habituation/social adaptation)
  • Implications of punitive action
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4
Q

Research on access to desirable alternatives

A
  • Bruce Alexander: looked at old experiment (rats in cage with cocaine/morphine, rats self-administered until they died -> perpetuated idea that addiction was chronic and inevitable); Bruce hypothesized it was because they had nothing else to do -> created experiment where he build rat park in cages, then put rats in, and rats didn’t self-administer -> reinforced sociological component of addiction
  • Carl Hart: had people come into lab who were already users of cocaine/heroin -> gave them choice of injecting in the lab or getting a desirable alternative -> many chose desirable alternative over the substance
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5
Q

Biopsychosocial model of addictive processes

A
  • Biological: genetics, neurophysiological reward system, changes in neurochemical action, development brain changes, learning
  • Social: social norms, access to desirable alternatives, access to money
  • Psychological: early childhood experiences, trauma, mental health conditions, impulsivity/sensation-seeking, affect regulations, cognitive distortions
  • PLUS repeated exposure that produces a desirable subjective shift
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6
Q

Gambling in the DSM

A
  • In DSM-IV, put with kleptomania, trichotillomania, pyromania, intermittent explosive disorder
  • In DSM-5, under substance-related and addictive disorder -> conceptualized as addiction
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7
Q

Hallmarks of gambling disorder

A
  • Needs to gamble with increasing amounts of money in order to achieve the desired excitement
  • Is restless or irritable when attempting to cut down or stop gambling
  • Has made repeated unsuccessful efforts to control, cut back, or stop gambling
  • Is often preoccupied with gambling
  • Often gambles when feeling distressed
  • After losing money gambling, often returns another day to get even
  • Lies to conceal the extent of involvement
  • Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling
  • Relies on others to provide money to relieve a desperate financial situation caused by gambling
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8
Q

Problem Gambling Severity Index

A
  • used to measure severity of gambling problem
  • includes questions, person ranks how often they occur from (0/never-3/almost always)
  • ex. how often have you bet more than you could afford to lose? Borrowed money to gamble with? etc.
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9
Q

Casino employee identification of problematic behaviour

A
  • Direct solicitation of advice
  • Direct behaviour
  • Indirect behaviour
    • What level of responsibility should employees have?
    • When to intervene?
    • What to do?
    • What to say?
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10
Q

Red flag behaviours

A
  • Signs:
    • anger/aggression
    • Signs of distress
    • Myths and distorted thinking
    • Signs of excessive involvement
  • More than one time point
  • Better in conjunction with quantitative data
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11
Q

Definitions of addiction

A
  • Comes from Latin “enslaved by” or “bound to”
  • DSM-5 – Substance Use Disorders: a problematic pattern of using alcohol or another substance that results in impairment in daily life or noticeable distress
  • Repeated failure to refrain from drug use despite prior resolutions to do so; decision-making, ambivalence (part of you wants to do it, part of you doesn’t), and conflict as central features
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12
Q

Delay discounting

A
  • Drug users prefer immediate rewards -> steeper delay discounting
    • Drug users discount money more steeply than controls, and discount drug of choice more steeply than money
  • Robust findings across all studies of drugs of abuse (heroin, cocaine, alcohol, cigarettes)
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13
Q

Delay discounting: evidence of ecological validity

A
  • Odum et al: heroin users who admitted using dirty needles discounted more steeply than those who did not
  • Field et al: 13-hour abstinence from smoking significantly increased discounting rates
  • Krishnan-Sarin et al: steeper discounting predicted relapse in adolescent smokers starting smoking cessation program
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14
Q

why do people use drugs?

A
  • To feel good/euphoria:
    • Positive reinforcement – response increased when a pleasant stimulus occurs (operant conditioning)
  • To escape low mood or alleviate unpleasant withdrawal symptoms
    • Negative reinforcement: response increases with an aversive stimulus is removed (also operant conditioning)
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15
Q

intra-cranial self-stimulation (ICSS)

A
  • related to brain mechanisms of operant reinforcement
  • researchers put electrode in rat brain that stimulated medial forebrain bundle (driven by dopamine to nucleus accumbens)
    • Rat can control it by pressing lever, and would spend hours doing it -> no satiation point
    • ISCC curves: drugs of abuse shift the ICSS curve to the left -> rat will work harder for lower level of stimulation -> more sensitive to reward
  • – Antipsychotic medication that blocks dopamine receptors has opposite effect
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16
Q

how do drugs “hijack” brain reward system?

A

Drug-induced dopamine release is higher amplitude, more sustained, and robust to motivational state (as compared to dopamine release from natural rewards like food and sex) -> hits the same system, but much more potent

17
Q

dopamine theory

A
  • Main example of brain disease model of addiction
  • States that drugs of abuse act directly or indirectly to increase dopamine levels in nucleus accumbens
    • These effects are greater and markedly stronger than effects of the natural rewards (although natural rewards do work on the same system)
    • Animals will self-administer drugs of abuse at the expense of natural rewards
  • Drugs “hijack” brain reward system to create an addiction system
18
Q

how to measure dopamine in humans

A
  • Using PET (Positron Emission Tomography) -> relies on injecting a radioactive tracer
  • Inject participant with [11C]raclopride (dopamine D2 receptor antagonist that is carbon labelled) -> will bind to D2 receptors in striatum
    • PET scanner acts as camera to see how many dopamine receptors participant has in striatum
19
Q

Dopamine and addiction (Volkov study)

A
  • Saw that people with substance use disorders have lower levels of dopamine D2 receptors in the brain
    • Consistent across many substance use disorders (cocaine, meth, heroin, alcoholism, etc.)
    • Seen during early and long-term abstinence (so not withdrawal-related)
20
Q

Dopamine receptors and activity in vmPFC - cocaine users study

A

Large group of cocaine users put in PET scan -> people with lower levels of dopamine receptors also had lower levels of metabolic activity in vmPFC -> could be linked to impaired decision-making

21
Q

influence of Pavlovian/classical conditioning

A
  • Robins et al.: In Vietnam, it was estimated that 20% of US military were using opioids, but post-war, an addiction epidemic never happened
    • This is because Vietnam became a conditioned stimulus -> without the cues of its sights, smells, and sounds, there were less urges to take the drugs back in the USA
22
Q

dopamine and pavlovian conditioning

A
  • Think back to monkey/juice experiment
  • “Hyper-learning” to exogenous drugs
    • Someone who just starts smoking initially has no response to seeing cigarette packet, but eventually will release dopamine at sight of packet
    • Dopamine won’t go away at the sight of cigarette though, because it’s designed to drive dopamine response -> double-hit of dopamine (contrasts with monkey, who stops showing dopamine to juice) -> perpetual increases of dopamine
23
Q

possible factors that make gambling addictive

A
  • Early big wins sensitize reinforcement learning
  • “State splitting”: separate learning rules applied to gains and losses
  • Under maximal uncertainty, cognitive distortions take hold (ie. Gambler’s fallacy)
24
Q

fMRI of reward in addictions

A

Ventral striatum is underactive during reward anticipation (of money rewards) in groups with substance abuse disorders

25
Q

reward deficiency vs. incentive salience

A
  • Reward Deficiency (Volkow): people with developmentally under-active reward system are drawn to intense and risky activities such as drug-taking
  • Incentive salience: cues associated with the drug acquire value, so users are hyper-sensitive to these cues
  • These theories do not sit easily together, but:
    • Reward deficiency is a theory of vulnerability, incentive salience is a theory of disorder
    • Reward deficiency is domain general (all rewards), incentive salience is domain specific (drug cues)
26
Q

low dopamine receptors: cause and effect?

A
  • Drugs of abuse increase dopamine levels, and this may cause a drop in receptor levels as a compensation (“neuroadaptive changes”)
  • Also possible that lowered dopamine is a risk factor for addictions - the reward deficiency hypothesis
27
Q

toxic effects of chronic drug use

A

Evidence from:

  • Post-mortem tissue (ie. Methamphetamine users -> prefrontal cortex)
  • Animal models (ie. Cocaine administration -> prefrontal cortex)
  • Longitudinal MRI scans (ie. Alcohol dependence -> whole brain)
28
Q

evidence of vulnerability: individual differences in subjective effects

A

In health participants, lower D2 receptor binding is associated with a more pleasurable experience of Ritalin

29
Q

evidence of vulnerability: impulsive rats

A
  • Highly impulsive rats show differences in ventral striatum
  • Put high impulsive and low impulsive rats on cocaine self-administration session -> high impulsive administer more cocaine (impulsivity predicts drug use)
30
Q

evidence of vulnerability: “addictive personality” in prospective studies

A
  • Measure people’s impulsivity through a personality questionnaire (Multidimensional Personality Questionnaire) at age 18
    • 3 superfactors: “negative emotionality”, “positive emotionality”, “constraint” (opposite of reactivitiy)
    • Reassessed at age 21:
  • – 10% developed alcohol dependence, 9% developed cannabis dependence, 18% developed nicotine dependence, 6% became problem gamblers
  • – Could we predict this based on their earlier results? -> People who go on to develop these problems have low levels of constraint and high levels of negative emotionality
31
Q

Drug use =/= drug addiction

A
  • Across all drugs, only a minority of users become addicted -> Important to understand why some ppl are vulnerable
  • A ‘bio-psycho-social’ model - some vulnerability seems to be hard-wired / inherited - Early environment and social factors also play important roles