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ACD Addiction and compulsive disorders interim 2 final exam summary
ACD Addiction and compulsive disorders interim 2 final exam summary
[Meer zien]Voorbeeld 4 van de 35 pagina's
Voorbeeld 4 van de 35 pagina's
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Voorbeeld van de inhoud
Addiction and Compulsive DisordersSummary Final Exam
Module 6
Background Module 6
To be diagnosed with a gambling disorder, one has to meet four of the following criteria during
the past year:
● Need to gamble with increasing amount of money to achieve the desired excitement
● Restless or irritable when trying to cut down or stop gambling
● Repeated unsuccessful efforts to control, cut back on or stop gambling
● Frequent thoughts about gambling (such as reliving past gambling experiences, planning
the next gambling venture, thinking of ways to get money to gamble)
● Often gambling when feeling distressed
● After losing money gambling, often returning to get even (referred to as “chasing” one’s
losses)
● Lying to conceal gambling activity
● Jeopardizing or losing a significant relationship, job or educational/career opportunity
because of gambling
● Relying on others to help with money problems caused by gambling
Living in a disadvantaged neighbourhood is predictive of the development of pathological
gambling, as is the physical proximity to a casino. GD is treated primarily with CBT.
- Focus on the clients' request for help and their motivation.
- Psychoeducation on pathological gambling.
- Functional analysis to identify both the triggering and sustaining factors of gambling.
- Exerting ‘stimulus control’ to stop gambling and regain control
- Challenging "gambling illusions" or irrational thoughts.
- Relapse prevention
,When it comes to food, there is an inevitable obesity epidemic. Neuroscience studies seem to
support the fact that overeating and obesity are associated with the same brain areas as drug
addiction. Seen from a trans-diagnostic perspective, the same psychological and neurobiological
mechanisms as seen in addiction could thus play an important role. Impulse control is not the
main cause of obesity, but, the fact that the prevalence of obesity has almost doubled globally
since 1980 indicates an important role of the environment. The cause could be partially
evolutionary (high fat and calorie foods in order to survive). A prominent brain region in that
network is the nucleus accumbens . From this evolutionary perspective, it is surprising that not
everyone is overweight in our current ‘obesogenic’ society.some are more sensitive than others
to the temptation of food. Food addiction seems to be compulsive given the negative
consequences and still continuing the way of living. Some researchers believe that only people
with binge eating disorder (BED) - and not obesity in general - meet the characteristics of an
addiction. BED has been described as: recurring episodes of eating significantly more food in a
short period of time compared to what most people would eat under similar conditions, with
episodes marked by feelings of losing control. Classification criteria:
Repeated episodes of binge eating. A binge-eating episode is characterized by both of the
following characteristics: 1. Eating during a certain amount of time (for example, two hours) and
an amount of food that is significantly larger than most people would eat under the same
conditions in such a period of time. 2. The feeling of having no control over food during the
period (for example, the feeling of not being able to stop or having control over what and how
much he or she eats).
The binge eating episodes are associated with three (or more) of the following characteristics:
● Eating much faster than usual.
● Continuing to eat until an unpleasant feeling arises of being full.
● Consuming large amounts of food without physical cravings.
● Eating secretly, out of shame of how much the person consumes
● Feeling disgusted afterwards, feeling gloomy or very guilty.
There is clear suffering from the binges.
The binge eating occurs on average at least once a week for three months.
,The binges are not accompanied by repeated inappropriate compensatory behavior as in bulimia
nervosa, and do not occur exclusively in the course of bulimia nervosa or anorexia nervosa.
Lecture 6
In the 60s-80s, people were struggling to categorise gambling in the DSM. In the NL, the
prevalence of pathological gambling is low (1% of general gambling). The definition of
gambling disorder led to its addition to addictive disorders (instead of impulse control). With
addiction behaviours, there is a risk of over-pathologizing (social online friendships). GD is
highly comorbid with drug and alcohol disorder. There is also a similarity in the genetic
component. Being young and male are risk factors. CBT and craving meds help. Gambling can
be measured with questionnaires (Problem gambling severity index and south oaks gambling
screen). The difference between SUD and GD is that SUD consists of consuming and GD
consists of spending. GD as a model of addiction is nice because it doesn't have the confound of
long term effects of drugs. A study with amphetamine has shown that drugs hijack the natural
reward system (high dopamine). SUD has direct reinforcing effects while GD has indirect
reinforcement to money. The unpredictability is the reinforcer in GD (SUD reinforces with
predictability). The fun in gambling comes from anticipation of winning, reward uncertainty,
arousal and excitement etc. things that make gambling addictive include games of chance
(machine design), individual differences (human design). The slot machines are one of the most
addictive. Reinforcement schedules: people gamble because of the schedule of reinforcement
that follows (variable/random ratio schedules). This is the gambler's fallacy. Shorting of the time
between the bet and outcome increases addiction. In NL this is regulated. Maximum loss is also
regulated here. Near miss: reinforcement without winning (almost winning). This produces even
more psychological responses than winning (maybe as a tease?). Losses disguised as wins (8
wins but actually 22 losses). Audiovisual effects are also reinforcers.
When it comes to human design features, In gambling, there is an illusion of control with
buttons, joysticks and superstitions (blowing dice). In a stop signal task GD patients showed
decreased prefrontal cortex response to inhibition. The Iowa Gambling task also shows gambling
behaviours. In delay discounting, the curve is the most steep one for GD. in the stroop task, GD
group revealed greater interference in incongruent trials. With problematic gamblers, in
gambling stimuli there is a cue reactivity in the visual areas. Gamblers show decreased activation
, of the mesolimbic reward system during reward anticipation (erotic and gambling cues). This is a
risk factor. Reward anticipation showed a greater activation in the dorsal striatum in gamblers.
Near misses led to increased NAcc activity in gamblers.
Literature Module 6: Disordered gambling: the evolving concept of
behavioral addiction (Clark)
In 2013, GD was moved from impulse control to addictive disorders in the DSM. this arised
from the similarities of addiction and GD.
Neurotoxicity
Long term substance abuse causes structural changes in the brain such as tissue shrinkage, cell
death, changes in inhibitory control etc. Impulsivity is a common factor of GD and SUD. other
executive functions are affected as well. For now, signs of structural brain changes can be
detected in gambling disorder, but these changes appear minor in comparison to most substance
addictions.
Dopamine is the core of the reward system. In a study with gambling and erotic stimuli, it was
found that addictions may be associated with an imbalance between different reward types, and
that the compatibility of the task reward with the abused commodity will critically determine
changes in the brain reward system. Another study investigated the impact of gambling cues on
decision making in GD. The gamblers made more impulsive choices (of smaller sooner rewards)
in the presence of the high-craving cues, and these cues also reversed the usual pattern of
subjective value coding in the midbrain and ventral striatum. Reduced striatal dopamine D2
receptor binding is a robust effect in individuals with drug addictions, but this couldn't be found
in GD yet. But another study has found increased dopamine release in males with GD compared
to males without GD. microdialysis studies collectively indicate greater evoked dopamine
response by drugs of abuse compared to natural rewards. In his model of addiction, Redish
proposed that, by exogenously stimulating the dopamine system, drugs of abuse continually elicit
response, giving rise to a kind of hyper-learning about associated cues. In an fMRI study patients
with gambling disorder and healthy controls played a card-guessing game for small (€1) or large
(€5) financial gains and losses. After an anticipatory delay, the financial outcome was revealed.
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