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Clinical and Neuropsychology 2 > CPch10 - Substance Use Disorder > Flashcards

CPch10 - Substance Use Disorder Flashcards

1
Q

Some statistics on substance use

A
  • almost 8 in 10 Dutch adults sometimes drink alcohol
  • the prevalence of alcohol/drug differs by country
  • alcohol is the most used substance
  • from 2016 to 2019 the use of illigit drugs has increased but the use of pharmacological substances nonmedically has decreased (because now they cannot be bought without a prescription)
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2
Q

What is the use of drugs associated with?

A
  • cardiovascular diseases
  • mental health problems
  • accidents
  • infectious diseases (HIV, …)
    !! major cause of mortality among young people in Europe
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3
Q

What are the most used drugs?

A
  • cannabis
  • cocaine
  • Ecstasy (MDMA)
  • amphetamines
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4
Q

how much is cannabis used?

A
  • 15% of people between 15-35 y.o. in EU use cannabis
  • highest in France and Italy (20%)
  • 1%of adults in the EU are daily users
  • it has increased in Denmark, Finland, France and Germany
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5
Q

Do men or women use substances more?

A

Men, but the gap is narrowing
(differences among cultures, race and ethnicity as well)

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6
Q

what is tolerance indicated by?

A
  1. large doses of substance needed to produce the desired effect
  2. effects of the drug becoming markedly less if the usual amount is taken
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7
Q

What is withdrawal?

A

negative physical and psychological effects developed after stopping taking the substance or when the amount is reduced

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8
Q

What are some common withdrawal symptoms?

A

muscle pain and twitching, sweating, vomiting, diarrhea and insomnia

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9
Q

What is the order of the most used substances? (US)

A
  • alcohol
  • cigarettes
  • marijuana
  • psychotherapeutics (misuse)
  • cocaine
  • hallucinogens
  • inhalants
  • heroin
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10
Q

What are the defining symptoms of substance use disorder?

A
  • trouble meeting obligations
  • keep using even if dangerous
  • ongoing relationship problems linked to the use of substance
  • keep using even if causes problems in person’s life
  • tolerance
  • withdrawal
  • more substance taken than originally intended
  • efforts to reduce or control use don’t work
  • lots of time spent trying to acquire the substance
  • giving up or reducing social events, hobbies and work
  • strong cravings to use substance
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11
Q

Gambling Disorder
- is it a disorder? why?

A
  • in DSM-V under “substance-related and addictive disorders”
  • similar patterns of brain activation as people with substance use disorder
  • criteria for the two disorders are related (-> gambling is part of broader addiction concept)
  • can be impairing
    > especially Massively multiplayer online role-playing games (MMORGP)
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12
Q

What are some similarities and differences between substance use disorder and gambling disorder?

A

Difference:
- gambling does not involving taking substances -> difficult to determine whether someone with G.D. can have withdrawal symptoms
Similarities:
- tolerance
- consequences of the behaviour (e.g. on school, work and relationships)

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13
Q

Do people with gambling disorder participate in some types
of gambling more often than those without a gambling disorder?

A
  • no
  • playing the lottery is most common type of gambling for all people (with or without disorder)
  • people with disorder are likely to have participated in wider variety of gambling activities
  • frequency of gambling is the important factor that predicts likelihood of going from recreational to compulsive gambling
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14
Q

what distinguishes professional gamblers from people with g. disorder?

A
  • professional g. won more money than those with disorder
  • people with disorder had no income from gambling
  • people with disorder reported more stressful life events, lower quality of life, more impulsivity and more comorbidity with other psychological disorders
    ! (professional gamblers gamble even more than people with g. disorder)
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15
Q

Alcohol Use Disorder

A
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16
Q

What are some common withdrawal symptoms of alcohol use disorder?

A
  • feeling anxious, depressed, weak, restless and unable to sleep
  • muscle tremors (fingers, face, eyelids, lips and tongue)
  • elevated pulse, blood pressure and temperature
  • delirium tremens (DTs) when drinking heavily for several years and levels of alcohol in blood drop suddenly
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17
Q

What do DTs include?

A
  • delirium + tremors + hallucinations (visual and tactile)
  • unpleasant and active creatures may appear to be crawling on walls or person’s body or be filling the room
    > e.g. snakes, cockroaches and spiders
    → person might start frantically clawing at their skin to get rid of creatures
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18
Q

what other substances is alcohol use disorder associated with? how?

A
  • 80-85% of people with a.u.d. are also smokers
    > alcohol and nicotine are cross-tolerant (nicotine can create tolerance to alcohol and vice versa)
    → consumption of both drugs may be increased to maintain rewarding effects
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19
Q
  • what age group is most affected by a.u.d?
  • for what type of drinking? (+ definitions)
A
  • college-age adults
    → for binge drinking
    = having five or more drinks in a short period of time
    → for heavy-use drinking
    = having five or more drinks on the same occation five or more times in a 30-day period
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20
Q

Gender difference in prevalence of a.u.d.

A
  • varies by gender, race and education level
  • more prevalent in men (11.2) than women (8.9), but difference is shrinking (from 3 times more likely to 1.2)
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21
Q

Ethnicity difference in prevalence of a.u.d.

A
  • two or more races: 12.3
  • white: 11.5
  • native american or alaska native: 10.3
  • hispanic or latino: 9.4
  • asian: 9.1
  • black or african american: 5.6
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22
Q

education difference in prevalence of a.u.d.

A
  • college degree: 13.1
  • high school degree: 8.2
  • less than high school degree: 7.5
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23
Q

what is the pathway of alcohol once ingensted?

A
  • metabolized by enzymes in the stomach
  • goes to small intestines and is absorbed into the blood
  • broken down by the liver
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24
Q

what do the effects of alcohol depend on?

A

the concentration of alcohol in the bloodstream
- amount of alcohol in particular period of time
- how much food is in the stomach
- weight and body fat of person
- efficiency of the liver

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25
Q

how is alcohol concentration based on gender?

A
  • women have higher blood alcohol concentrations (even after adjustment of weight)
    → bc of differences in:
    > body water content
    > the enzyme that breaks down alcohol (alcohol dehydrogenase)
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26
Q

how does alcohol produce its effects?
- specific neurotransmitters + relative effect

short-term effects of alcohol

A

through interaction with several neurotransmitters:

  • stimulates GABA receptors (for ability to reduce tension)
  • increased level of dopamine and serotonin (for ability to produce pleasurable effects)
  • inhibits glutamate receptors (cause cognitive effects of alcohol intoxication - e.g. memory loss and slowed thinking)
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27
Q

study about effect of alcohol on brain and behavior (driving)

short-term effects of alcohol

A
  • low and high dose of alcohol administred to participants + simulation of driving
    = low dose→ small impairment in motor functioning
    = high dose→ significant motor impairment
    = any dose→ effects in ACC and orbitofrontal cortex (making decisions and monitoring mistakes)
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28
Q

how does prolonged consumption affect tissues and organs?

A
  • impairs digestion of food and absorption of vitamins
  • cirrhosis of the liver (if together with reduction of protein intake)
    > liver cells become engorged and prevent functioning
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29
Q

fetal alcohol syndrome

A
  • heavy alcohol consumption during pregnancy
  • accounts for less than 20% of fetal alcohol spectrum disorders
  • leading known cause of intellectual disability among children
  • slowed growth of fetus + cranial, facial and limb anormalities
  • even moderate drinking can produce detrimental effects on fetus
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30
Q

what are some long-term health effects of moderate alcohol consumption?

A
  • lower risk if coronary heart disease and diabetes (only for women in wealthier countries)
  • great alcohol consumption predicts less gray matter density (particularly hippocampus)
  • many associations with cancer, self-harm, accidents (across the world and no matter of wealth)
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31
Q

Tobacco use disorder

A
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32
Q

how has the number of smokers changed from 1990 to 2015?

A

it declined about a third
- 83% decline in people with college degreee
- 39% decline in people with less than high school degree
!! despite the decline, smoking remains the single most preventable cause of premature death

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33
Q

what are the main medical problems arising from smoking cigarettes?

A
  • emphysema
  • cancers of the larynx, esophagus, pancreas, bladder, cervix and stomach
  • complications during pregnancy
  • sudden infant death syndrome
  • periodontitis
  • cardiovascular disorders
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34
Q

what are the most harmful components in the smoke from burning tobacco?

A
  • nicotine
  • carbon monoxide
  • tar (hydrocarbons→ carcinogens)
    ! study: people that smoke even just one cigarette a day are more likely to die from any cause than people who never smoked
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35
Q

statistics about smoking

A
  • tobacco use among people 18-25 has declined between 2015-2018
  • smoking is more prevalent among people in lower socioeconomic classes
  • difference in addiction across race and ethnicity
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36
Q

gender differences in smoking

A
  • men: 48.2
  • women: 31.4
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37
Q

ethnicity differences in smoking

A
  • native american or alaska native: 51.3
  • white: 39.2
  • black or african american: 29.4
  • hispanic or latino: 28
  • asian: 21.2
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38
Q

why are african american cigarette smokers:
- less likely to quit
- more likely to get lung cancer?

A
  • they retain nicotine in their blood longer than European Americans do
  • they metabolize more slowly
  • they are more likely to smoke menthol cigarettes (due to advertising)
    → with menthol cigarettes, they inhale more deeply and hold in the smoke for longer time (more deleterious effects)
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39
Q

secondhand smoke

A
  • smoke coming from the burning end of a cigarette
  • also called “envoronmental tobacco smoke” (ETS)
  • it contains higher concentrations of ammonia, carbon monoxide, nicotine and tar (than does the smoke inhaled by the smoker)
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40
Q

why are cancer rates lower in chinese americans than european americans and latinos?

A

chinese americans metabolize less nicotine from cigarettes

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41
Q

what are the effects of ETS? (in nonsmokers)

A
  • prolonged exposure to smoke can lead to lung cancer and cardiovascular disease
  • precancerous lung abnormalities and development of allergies
  • babies of nonsmoker women exposed to smoke are often born premature and with low birth weight and birth defects
  • children of smokers are more likely to have upper respiratory infections, asthma, bronchitis and inner-ear infections
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42
Q

Electronic cigarettes

A
  • made with plastic or metal and filled with nicotine and toher chemicals (often with flavours)
  • battery-operated→ heats up the nicotine
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43
Q

statistics on e-cigarettes

A
  • half the amount of people that smoke normal cigarettes smoke e-cigarettes
  • adolescents that use e-cigarettes are more likely to use alcohol and marijuana
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44
Q

what are the differences between e-cigarettes and normal cigarettes?

A
  • e-cigarettes are less toxic than traditional combustible cigarettes
  • e-cigarettes can be helpful tools to stop smoking (only for adults)
  • young people who use e-cigarettes are more likely to transition to smoking cigarettes
  • secondhand aerosols from e-cigarettes contain nicotine and other chemicals (ETS)
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45
Q

Cannabis use disorder

A
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46
Q

Marijuana

A

dried and crushed leaves of the plant cannabis sativa
- in DSM-V under “cannabis use disorder”

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47
Q

Hashish

A
  • much stronger than marijuana
  • removing and drying the top of cannabis sativa
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48
Q

synthetic marijuana

A

artificially created chemicals that are sprayed on plant (illegal)

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49
Q

Statistics on marijuana

A
  • in 2018, 27.7 million people reported using marijuana in the past month
  • most common drug used across age groups
  • equivalent across ethnic groups
  • 7.6 million people have daily use (2012)
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50
Q

What are cannabinoids?
What are the two major ones?

A
  • cannabinoids are active chemicals in marijuana
  • THC is major cannabinoid
  • cannabidiol (CBD) -> second most common cannabinoid
    + also contains carcinogens
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51
Q

What are psychological effects of marijuana?

A

> intoxicating effects depend on the potency and size of dose
- usually feel more relaxed and sociable
- larger dose: rapid shifts in emotion, dull attention, fragment thoughts, impaire memory, time moving slowly
- extremely large dose: hallucinations, panic
- marijuana can interfere with cognitive functioning
- when high, impaired complex psychomotor skills necessary for driving (“high” can last for 8 hours but not felt anymore-> dangerous for driving)

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52
Q

Does chronic use of marijuana affect cognitive functioning even when the person is not using the drug?

A
  • longitudinal study assessed cognitive functioning at 13 and 38 y.o.
    = less IQ and poorer working memory and processing if used marijuana persistently
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53
Q

what are the physical consequences of marijuana?

A
  • bloodshot, itchy eyes, dry mouth and throat, increased appetite, reduced pressure within the eye, raised blood pressure
  • longterm use-> impair lung structure and function
  • tolerance and withdrawal symptoms (depression, anxiety, restlessness, tension, stomach pains, insomnia, …)
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54
Q

how does marijuana affect the brain?

A
  • CB1 and CB2 cannabinoid receptors in the brain
  • cognitive problems are associated with effect of marijuana on CB1 receptors in hippocampus
  • regular users show different patterns of connectivity between amygdala and frontal cortex when trying to regulate emotions
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55
Q

what are the therapeutic effects of marijuana?

A
  • reduction in nausea and in loss of appetite that come with chemotherapy
  • alleviation of glaucoma, chronic pain, muscle spasms and discomfort for people with aids
  • can help symptoms of Tourette’s syndrome, social anxiety, dementia, sleep disorders
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56
Q

did legalization of marijuana increase the number of users?

A
  • more adolescent users in states with legalized marijuana
  • difference in use was there before legalization
  • increase in recreational use in states with early legalization
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57
Q

What is the gateway hypothesis of marijuana?

A
  • marijuana dangerous because it’s first step of young people towards use of other drugs
  • not much evidence
  • cocaine and heroin users are likely to have started with marijuana
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58
Q

Opioid use disorder

A
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59
Q

Opioids

A
  • opium, morphine, heroin and codeine
  • can relieve pain in moderate doses
  • in 2018 over 9 million people misused prescription pain medications
  • in DSM-V: “Opioid use disorder”
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60
Q

What are some opioid medications that can be legally described?

A
  • hydrocodone (eg for vicodin)
  • oxycodone
  • fentanyl (causes the most deaths by misuse of opioids)
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61
Q

Waves of deaths by opioids

A
  1. started in 1990s (prescription pain medications)
  2. started in 2010 (heroin)
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62
Q

prevalence of opioid use

A
  • more than 800.000 people over 12 y.o. in US in 2018
  • more men than women
  • usually start after prescription meds
  • misuse of prescription meds more common in white americans
  • overdose deaths from syntetic opioids have risen deamatically since 2015
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63
Q

effects of opioids

A
  • euphoria, drowsiness, lack of coordination, increased self confidence
  • letdown and stupor (later on)
    !! these effects produced by stimulating neural receptors of body’s own opioid system or by acting on nucleus accumbens
  • withdrawal symptoms are similar to influenza, + vomiting, no sleep, diarrhea, …
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64
Q

Stimulants

A
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65
Q

Stimulants

A
  • increase altertness and motor activity
  • amphetamines (synthetic), cocaine (natural, from coca leaf), caffeine
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66
Q

Caffeine addiction

A
  • caffeine can create tolerance and withdrawal symptoms
  • most common effects: metabolism, body temperature and blood pressure increase, sleepiness and appetite diminishes and hand tremors created
  • excess use can cause death
  • addiction start early on (caffeine also in hot cocoa, soft drinks, …)
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67
Q

Amphetamines - how do they work?

A
  • release of norepinephrine and dopamine
  • block reuptake of these neurotransmitters
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68
Q

What are some effects of amphitamines?

A
  • heighten wakefulness, inhibit intestinal functions and suppress appetite (used in diets)
  • (less common) quicken heart rate and constrict blood vessels
  • person becomes euphoric, more self-confident, agitated, confused, …
  • tolerance built only 6 days after repeated use
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69
Q

Methamphetamines

A
  • derivative of amphetamines
  • most come from illecit sources
  • men more likely to misuse methamphetamines (less gender differences in amphetamines)
  • person becomes very agitated when drug wears off
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70
Q

what are the effects of methamphetamines on the brain?

A
  • damage to dopamine and serotonin system
  • reduction in brain volume in temporal and frontal cortices
  • smaller volume of hippocampus (poorer performance on memory test)
  • areas impacted are associated with reward and decision-making (insula, striatum and frontal and temporal cortex)
    > unclear whether these areas were damaged before methamphitamine use or only after
    !! difficult to find participants that use only one drug (confounds)
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71
Q

Cocaine

A
  • from leaves of coca shrub
  • “crack” is a form of cocaine (rock-crystal that is melted and smoked)
  • cocaine use is declining
  • men use cocaine and crack more often than women
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72
Q

How does cocaine act?

A
  • blocks reuptake of dopamine in mesolimbic areas
  • dopamine left in synapse facilitates neural transmission -> pleasurable state
  • vasoconstrictor (causes blood vessels to narrow)
    > prenatal exposure makes grey matter smaller in frontal cortex
  • increases risk for stroke, causes cognitive impairments
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73
Q

Hallucinogens

A
  • include LSD, psilocybin, mescaline
  • main effect: hallucinations (recognized by user as caused by the drug)
  • in DSM-V: “hallucinogen persisting perception disorder”
    > experience of flaschbacks and perceptual symptoms felt during drug even when not under the effect
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74
Q

LSD

A
  • increased use in past years
  • tolerance developed quickly
  • no signs of withdrawal
    ! alters a person’s sense of time (slower)
    ! sharp mood swings and extended consciousness
    ! increases anxiety because you feel that you are going crazy, but reduces anxiety in people with life-threatening illnesses
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75
Q

Ecstasy

A
  • made from MDMA
  • in DSM-V: “other hallucinogen use disorder”
  • as a pill, but added to other substances
  • neurotoxic effects on serotonin system because it reduces availability of SERT transporter in brain
    ! enhances intimacy and insight, improves interpersonal relationships, elevates positive emotion and self-confidence, and promotes aesthetic awareness
    ! causes muscle tension, rapid eye movements, jaw clenching, nausea, faintness, chills or sweating, anxiety, depression, depersonalization, and confusion
76
Q

PCP

A
  • “angel dust”
  • in DSM-V: “phencyclidine use disorder”
  • more men than women
  • severe paranoia and violence, coma and death
77
Q

Etiology of S.U.D.

A
  • genetic
  • neurobiological
  • psychological
  • sociocultural
    ! differently related based on the different substance
78
Q

Genetic influences

A
  • heritability: 0.4-0.6
  • twin studies: genetic component in alcohol use disorder, smoking, heavy use of marijuana and general drug use disorders
79
Q

genetic influences

What is the influence of peers on substance use?

A
  • peers are particularly important environmental variable
    > higher heritability for alcohol problems among adolescents that have many drinking peers
    > higher heritability for alcohol and smoking among adolescents whose best friend smokes or drinks
    > higher heritability in schools where the “popular crowd” smokes or drinks
80
Q

genetic influences

Why do some ethic groups have lower rate of alcohol problems?

A
  • asians have lower rate of alcohol problems because of physiological intolerance
    > inherited deficency in enzymes for alcohol metabolism (alcohol dehydrogenases - ADH)
  • mutations in ADH2 and ADH3 gene code proteins that make ADH enzyme, and these genes have been linked with alcohol use disorders
    = many asians lack ADH which metabolizes alcohol; they experience flushing (unpleasant sensation), which may protect them from becoming dependent on alcohol
81
Q

genetic influences

how does nicotine lead to dependence to smoking?

A
  • nicotine stimulates dopamine release and inhibits its reuptake
  • people who are more sensitive to this effect are more likely to become regular smokers
82
Q

genetic influences

what genes have been linked to smoking dependence?

A
  • link between smoking and SLC6A3 gene, which regulates reuptake of dopamine
    > people with this gene have lower likelihood of smoking & higher likelihood of quitting
  • gene CYP2A6 codes for enzymes that metabolize nicotine
    > faster metabolism of nicotine leads to smoking more
    > this gene is also associated with more lung cancer likelihood
83
Q

genetic influences

what is the influence of genes on marijuana dependence?

A

four different genes have been associated with marijuana dependence, but not enough evidence

84
Q

Neurobiological Influences

A
  • vulnerability model
    > problems in dopamine system increase the vulnerability to becoming dependent to substances
  • toxic effect model
    > problems in the dopamine system are the consequences of taking substances
    ! people continue to take drugs to avoid negative symptoms of withdrawal
85
Q

Neurobiological influences

What are the contingencies of stress in people with S.U.D.?

A

People with Alcohol use disorder that recently stopped drinking have larger physiological responses to unpredictable stress

86
Q

Neurobiological influences

How can the cravings for the drug be explained?

A

Incentive-sensitization theory

87
Q

Neurobiological influences

what is the Incentive-sensitization theory?

A
  • dopamine system (pleasure, liking) becomes super sensitive to direct effects of drug and to cues of such drug (e.g. spoons, needles)
  • sensitivity to cues induces craving (wanting)
  • liking decreases, but wanting remains very intense
    !! transition from liking to wanting maintains addiction (transition accomplished by pathways involving dopamine)
88
Q

Neurobiological influences

how important are cues in the dependence?

A
  • cues can elicit similar responses to drug itself
    > e.g. changes in physiological arousal, increase in craving and “high feeling” in response to cue
  • cues activate reward and pleasure areas of the brain implicated in drug use
    > e.g. looking at a cigarette before stressful task lessened the physiological and perceived stress more than actually smoking the cigarette
89
Q

Neurobiological influences

Do people with stronger cravings for a substance actually use it more, even when they are trying to quit?

A
  • yes
  • more craving and liking of alcohol at baseline assessment the more A.U.D. symptoms they had 6 years later
  • more craving predicts use of cigarettes
90
Q

Neurobiological influences

what are the results of the fMRI study on go/no-go task?

A
  • in go/no-go task, when refraining from pressing the no-go button, basal ganglia, inferofrontal gyrus and premotor areas are activated
  • people that show greater brain activation when refraining from pressing button were less likely to act on craving
91
Q

Neurobiological influences

short term vs long term rewards

A
  • people with substance dependence often value immediate and impulsive pleasure and reward coming from taking a drug more
  • lab setting where people offered 1$ now or 10$ in the day
    > delay discounting: extent to which people opt for smaller immediate rewards
    > people with S.U.D. have more delay discounting
92
Q

Neurobiological influences

What brain regions are associated with short-term or long-term rewards?

A
  • valuing short-term rewards: amygdala and nucleus accumbens
  • valuing long-term rewards: prefrontal cortex
    ! these brain regions compete with one another when evaluating which reward to accept
93
Q

Neurobiological influences

what are the contingencies of risk taking for people with S.U.D.?

A
  • people who have low tolerance for ambiguous risk but not for known risk were more likely to relapse
    > predict relapse through computer game that assesses tolerance for known vs ambiguous financial risks
  • risky decision making associated with orbitofrontal cortex, parietal cortex and rostral parts of ACC
  • tolerance for ambiguity is associated with the dorsolateral prefrontal cortex, parietal cortex, and dorsal parts of the ACC
94
Q

Psychological Influences

A
  • emotion regulation
  • expectancies about alcohol and drug effects
  • personality traits
95
Q

Psychological influences

Emotion Regulation

A
  • people with S.U.D are less able to regulate negative emotions (cause or effect?)
  • alcohol reduces self-reported and physiological indicators of anxiety (particularly when uncertainty about negative event)
  • alcohol lessens positive emotions in response to anxiety-provoking situations
96
Q

Psychological influences

why is alcohol consumed in social situations? (an hypothesis)

A
  • as emotion regulation tool
  • it helps calm down thoughts of being rejected and focus instead on the pleasures of being around others
97
Q

Psychological influences

emotion regulation and nicotine

A
  • some studies found that nicotine reduces negative emotions, others didn’t
  • this is because it depends on stage of smoking (just started? tried to stop and failed?)
  • greater reduction in negative emotions when starting to smoke than when regularly smoking or when in relapse
    > (study) greater relief in negative emotions when smoking after not smoking for 12 hours
98
Q

Psychological influences

emotion regulation and other aspects of smoking

A
  • suggested that it’s act of smoking (e.g. inhaling) that reduces negative emotions (and not nicotine)
  • many studies have proved that negative emotions are relieved even if cigarettes did not contain nicotine
99
Q

Psychological influences

what is another explanation for reduced negative emotions followed by substance use?

A
  • distraction theory
  • alcohol impairs cognitive processing and narrows attention to most immediatly available cues
    = alcohol myopia
    -> intoxicated person has less cognitive capacity, so focuses on immediate situation, does not think about negative emotion, negative emotion decreases
100
Q

Psychological influences

what are the benefits of distraction for relieving anxiety with substances?

A
  • reduction in anxiety perceived when smoking during a distracting activity (not if no distraction)
    ! alcohol and nicotine might increase negative emotions when distraction is not present
    > e.g. if drinking alone, limited cognitive capacity is focused on negative emotions, and they become stronger
  • effects of alcohol are stronger than expectancy of alcohol
101
Q

Psychological influences

what are the effects of expectancies about alcohol and drug effects?

A
  • people that expect alcohol to reduce anxiety and relieve stress are more frequent users
  • expectancies about alcohol and its effects begin at age four
  • expectancies become more positive throughout development and after first exposure
  • more aggressiveness even when you believe you’re drinking alcohol
  • the higher expectancy of danger of the drug, the lower the rates of consumption
102
Q

Psychological influences

Personality factors

A
  • neuroticism (negative emotionality)
  • persistent desire for arousal + increased positive affect
  • constraint (cautious behavior, harm avoidance, conservative moral standards)
    ! low constraint and high neuroticism predicted onset of alcohol, nicotine and drug use disorders
    + strong associations with low levels of agreeableness and conscientiousness
103
Q

Sociocultural influences

A
104
Q

What are the most commonly used substances across the world?

A
  • alcohol is the most used substance in countries studied (differences in levels of use across cultures)
  • marijuana is next common substance (most countries)
  • higher rates of amphetamines, ecstasy and cocaine in countries with higher rates of marijuana
    ! other research documented other differences in substance use
105
Q

what is the consumption of substances based on?

A
  • acceptable social norms of the community and culture
  • social setting also influences use (e.g. peer influences)
  • social networks influence use of substance, but also inclination to use substances makes person select networks where substance is used
106
Q

how can the influence of social environment on substance use disorder be explained?

A
  • social influence model (media)
  • social selection model (networks)
107
Q

Does advertising change substance use patterns among young people?

A
  • adolescents exposed to ads about e-cigarettes were more likely to try them
  • advertising about ill effects of smoking has opposite effect
108
Q

A.U.D. treatment

Treatment of Alcohol Use Disorder

A
  • inpatient hospital treatment
  • alcoholics anonymous
  • couples therapy
  • motivational interventions
  • moderation in drinking
  • medications
109
Q

Treatment of Substance Use Disoder

A
  • typically chronic and often relapse
  • first step: admitting that there is a problem
    > several treatment programs require addict to stop using before starting the program to show commitment
  • medication approved for alcohol, tobacco and opioids
  • only 1 out of 10 addicts receive treatment
110
Q

A.U.D. treatment

Inpatient hospital treatment

A
  • first step of treatment: detoxification
  • often happens in hospitals because of supervised setting
  • inpatient treatment is much more expensive
111
Q

A.U.D. treatment

Alcoholics anonymous

A
  • more than 2 million people around the world
  • half of the people that receive treatment do so through AA (2018)
  • also narcotics anonymous, cocaine anonymous and marijuana anonymous
  • still “alcoholic” even if not had a drink in 15 years
112
Q

A.U.D. treatment

does AA work? how?

A
  • group provides understanding, emotional support, close counseling and social network
  • AAs principles outlined in 12 steps
  • most effective line of treatment
  • goal: complete abstinence (reached for at least 3 years)
  • often “attrition” (dropping out)
113
Q

A.U.D. treatment

Couples Therapy

A
  • reduction in problem drinking
  • improvement in couples’ distress generally
  • effective for couples of all sexualities
  • individual cognitive skills + dealing with stress as a couple
114
Q

A.U.D. treatment

motivational interventions
(what are the steps?)

A
  • intervention in college
    1. comprehensive assessment including TimeLine Follow Back (to assess drinking in the past three months)
    2. brief motivational treatment
    > including individualized feedback about person’s drinking in relation to community and national averages, education about effects of alcohol, tips for reducing harm and moderating drinking
  • TLFB works, but if add motivational intervention, longer lasting results
115
Q

A.U.D. treatment

moderation in drinking

A
  • “controlled drinking”: goal of the treatment approach “guided self-change”
  • assumption:
    > people can exercise control over their drinking than they typically believe
    > more awareness of the negative effects of drinking too much can help and awareness of the benefits of drinking less
  • e.g. delay of 20 minutes before taking second drink can help
  • effective treatment!
116
Q

A.U.D. treatment

medications

A
  • antabuse: induces violent vomiting after ingesting alcohol
  • very harsh, very high drop-out rates and not effective (study)
  • naltrexone (opiate antagonist) blocks activity of endorphins stimulated by alcohol -> reduces craving
    > proven to be effective if together with CBT
  • acamptosate reduces drinking and cravings by impacting glutamate system
117
Q

Treatments for smoking

A
  • if people in the social network stop smoking, it is easier to stop
  • only half of people that go to a smoking cessation program stop smoking when the program ends
  • only small percentage keeps abstaining after one year
    > psychological treatments
    > nicotine replacement treatments and medications
118
Q

treatments for smoking

Psychological treatments

A
  • most widespread psychological treatment is physician telling person to stop smoking
  • …because of lung disease, hypertension, heart disease, diabetes, …
  • motivational interviewing only moderately effective
  • some smells quite down craving for five minutes (e.g. apple, lemon, chocolate, …)
  • school interventions and cognitive behavioural approaches (on coping skills and problem solving) are effective
  • stopping all at once is too difficult
119
Q

treatments for smoking

statistics about smoking

A

by 18 years old:
- 2/3 of cigarette smokers regret starting
- 1/2 have already tried stopping
- 40% show interest in obtaining treatment to stop

120
Q

treatments for smoking

Nicotine Replacement Treatments and medication

A
  • nicotine replacement therapy: different gradual delivery of nicotine to reduce cravings
  • e.g. gums, pathces, inhalers or e-cigarettes
121
Q

treatments for smoking

how do the nicotine replacements work?

A
  • nicotine gum release nicotine more slowly but causes cardiovascular changes (e.g. increased blood pressure)
  • nicotine patches release nicotine through the skin and carried to the brain
    > only one a day and not remove before new one (advantage compared to gum)
    > treatment effective after 8 weeks of use, no longer than three months
    > dangerous levels of nicotine if smoking while wearing patch
    > effective for both genders
  • abstinence rates are less than 50% at 12-months follow-up
  • not effective for adolescents
122
Q

treatments for smoking

are e-cigarettes an effective NRT?

A
  • evidence is mixed
  • no statistical difference between results of gum, patches and e-cigarettes
123
Q

treatments for smoking

What medications are effective in stopping to smoke?

A
  • antidepressant burpropion (NRT more effective than burpropion alone; more effective than varenicline alone)
  • varenicline (effective alone or in combination with behavioural treatment or NRT)
124
Q

Treatment of Drug Use Disorders

A
  • psychological treatment
  • medication
125
Q

Treatment of Drug Use Disorders

is CBT effective? what does it focus on?

A
  • CBT (effective)
    > learn to avoid high-risk situations
    > recognize lure of the drug
    > develop alternatives to using the drug
    > strategies to cope with craving and resisting the tendency to regard slip as catastrophe
    ! CBT on computer was even more effective than one in person + less dropout rate
126
Q

Treatment of Drug Use Disorders

Contingency management

A
  • learn to reinforce behaviours inconsistent with drug use (eg taking medication in trigger situations)
  • learn to avoid situations associated with drug use in the past
  • vouchers given if “clean”, to buy things person wants
    ! based on belief of importance of environmental contingencies
    ! effective (greater likelihood of abstinence and better quality of life)
127
Q

Treatment of Drug Use Disorders

motivational interviewing

A
  • CBT + techniques to help person to generate solutions for themselves
  • effective
128
Q

Treatment of Drug Use Disorders

self-help residential programs

A
  1. separation of people from previous social contacts
    > assumption that these relationships have been instrumental in maintaining use disorder
  2. new environment without drugs and with support to transition to no drugs
  3. presence of former drug addicts
  4. direct and intense confrontation in group therapy (accept own responsability and change behaviour)
  5. setting in which people are respected and not stigmatized
129
Q

Treatment of Drug Use Disorders

are self-help residential programs effective?

A
  • obstacles in evaluating efficacy
  • high drop-out rate -> remaining people not representative of population (their motivation is stronger and it’s possible cause of getting better)
130
Q

Treatment of Drug Use Disorders

why don’t some people receive treatment?

A
  • 90% of people needing treatment do not get it
  • many end up in prison and don’t get treated
  • option to get treated instead of going to prison is less costly and 4/10 people succeed
131
Q

Treatment of Drug Use Disorders

Matrix treatment

A
  • 16 CBT group sessions
  • 12 family education sessions
  • 4 individual therapy sessions
  • 4 social support group sessions
132
Q

Treatment of Drug Use Disorders

is Matrix treatment effective?

A
  • more effective than TAU (treatment as usual)
  • no lower rates of relapse after 6 months than TAU
133
Q

Treatment of Drug Use Disorders

What is MAT? What types of medications?

A
  • “medication assisted treatment” (MAT)
  • opioid substitutes (agonists)
    > stimulates neurotransmitters
    > chemically similar to opioids and lower the cravings
  • opioid antagonists
    > dampens activity of neurotransmitters
    > prevent user from experiencing the high
  • often not provided because of stigma around it
134
Q

Treatment of Drug Use Disorders

what are some benefits and disadvantages of using opioid substitutes?

A
  • opioid substitutes: methadone and buprenorephine
  • also addictive (controversy)
  • weaker withdrawal symptoms
  • lower risk of overdose death
135
Q

Treatment of Drug Use Disorders

methadone - does it work?

A
  • methadone works best when together with psychological treatment
  • has to be taken in clinic in front of physician
  • does not produce “high”: people return to heroin
  • methadone + contingency management
  • side effects: constipation, sweating, insomnia, diminished sexual functioning
136
Q

Treatment of Drug Use Disorders

buprenorphine - does it work?

A
  • advantage: can be taken at home rather than a clinic
  • not as powerfully addicting
  • to combat potential of abuse of drug: drug created containing buprenorphine and naloxone (to fight against overdose effects)
137
Q

Treatment of Drug Use Disorders

naltrexone - how does it work?

A
  • prevent feeling “high” if use opioids later
  • binds to opiod receptors without stimulating them
  • when surgically implanted, works best
138
Q

Prevention of Substance Use Disorders
- what measures work?

A
  • 1/2 of adult smokers started smoking before age 15, and almost all before age 19
  • prevention is important from early age
  • same measures for smoking also work for drugs and alcohol
    > brief family interventions
    > state measures (smoke-free zones, tobacco control programs, taxes on cigarettes, restricting tobacco advertising, public education campaign, …)
  • graphic warning labels on cigarettes packages
139
Q

Flashcards from the slides

A
140
Q

how many people in the Netherlands use substances?

A
  • 8 in 10 Dutch adults sometimes drink alcohol
  • many Dutch adults have used drugs in their life
  • prevalence depends on the country
141
Q

What reinforcements play a role in addiction?

A
  • positive reinforcement
    > rewarding/mood-enhancing effects of the drug
  • negative reinforcement
    > drug use reduces negative affect (self-medication)
    > drug use prevents withdrawal symptoms
142
Q

What are some harmful effects of alcohol?

A
  • 18% of suicides
  • 18% of interpersonal violence
  • 27% of traffic injuries
  • 13% of epilepsy
  • liver cirrhosis, mouth cancers, pancreatitis, tuberculosis, colorectal cancer, breast cancer, hypertensive heart disease, …
143
Q

what is the difference between people who use and abuse?

A
  • only a minority of people who use develops a full-blown substance abuse disorder
  • e.g. for every 250 people that use, 25 abuse
144
Q

What is the lifetime prevalence of substance abuse in the Netherlands?

A
  • 17% of people suffer from substance abuse at some point in their life
  • alcohol: 12.8%
  • drugs: 6.6%
145
Q

why is it important that we understand addiction better?

A
  • substance and alcohol abuse are prevalent
  • it has a destructive impact on individual’s wellbeing and mental health, social relationships and professional functioning
  • society pays a price for substance abuse
    > healthcare resources, lost productivity, spread of diseases, crime and homelessness
146
Q

what is the pathway from use to abuse?

A
  1. positive attitude
  2. experimentation
    (craving)
  3. regular use
    (habit)
  4. heavy use
  5. substance abuse
    (compulsive drug seeking)
  6. maintenance
  7. (recovery and) relapse
147
Q

what are the rates of relapse?

A

40 to 60%

148
Q

what qualifies as “abuse”?

A

problematic pattern of substance leading to clinically significant limitations or suffering
(DSM-V)

149
Q

What are the criteria of S.U.D.?
(part 1)

A
  • at least 2 of 11 features occurring within 1 year
  • 2-3 mild, 4-5 moderate, >6 severe
    1. taking the substance in larger amounts or for longer than what you’re meant to
    2. wanting to cut down or stop using the substance but not managing to
    3. spending a lot of time getting, using or recovering from use of the substance
    4. cravings and urges to use the substance
    5. not managing to do what you should at work, home or school because of substance
150
Q

What are the criteria of S.U.D.?
(part 2)

A
  1. continuing to use, even when it causes problems in relationships
  2. giving up important, social, occupational or recreational activities because of substance abuse
  3. using substances again and again, even when it puts you in danger
  4. continuing to use, even when you know you have a physical or psychological problem that could have been caused or made worse by the substance
  5. needing more of the substance to get the effect you want (tolerance)
  6. development of withdrawal symptoms, which can be relieved by taking more of the substance
151
Q

What are behavioral addictions?

A
  • e.g. Gambling Disorder
    > in “substance-related and addictive disorders”
  • more research needed for Internet Gaming Disorder (might be related to other mental disorders)
  • neurological processes are similar to other addictions
152
Q

why do some people become addicted?

A
  • addictive effect on the brain
    > brain disease model
153
Q

History models of addiction

A
  • 1850 Moral (re-education institutions)
  • 1920 Pharmacological (drug causes addiction-> prohibition)
  • 1940 Symptomatic (psychoanalysis; personality disorder)
  • 1950 Disease (genetic, biological and psychological premorbid differences between addicts and normal users; some people should not use)
  • 1975 Learning (maladaptive learnt behavior -> behavioral intervention)
  • late ’70s Social
  • 1980 Biopsychosocial (multimodal intervention: housing, relocation, …)
  • 1990 Brain Disease (not much different from Biopsychosocial model; neurobiological and genetic basis of addiction)
154
Q

Brain Disease Model

A
  • “addiction might be better considered and treated as an acquired disease of the brain”
  • addiction:
    > complex, chronic, relapsing brain disease
    > genetic and neurobiological basis
    > compulsive drug seeking and use despite harmful consequences
155
Q

what is the pattern of the Brain Disease Model?

A

(see picture)

156
Q

what are some prominent critics of the B.D.M?

A
  • “people take drugs out of choice and can stop out of choice”
  • “addicts are not blameless vicitms of some terrible illness they have no control over”
157
Q

what do all substances have in common? (to some degree)

A
  • role of dopamine
    > abused substances increase dopamine much more than natural reinforcers
    > brain’s natural reward system becomes highjacked
158
Q

What stimuli can induce craving? How?

A

.. external stimuli (places, things, people)
.. internal stimuli (stress, anxiety, depression)
- through pavlovian learning (classical conditioning), stimuli become associated with substance
= these stimuli in envoronment become potent triggers of craving

159
Q

How does liking and wanting change throughout addiction?

A
  • incentive-sensitization theory
    1. repeated use sensitizes the brain
    2. drug and stimuli become more able to elevate dopamine activity
    3. increased “wanting” and decreased “liking” (liking sometimes stays the same)
    = brain becomes desensitive to drug and sensitive to craving
160
Q

What are the main driving forces of addiction?

A
  • cravings
  • “chasing the first high”
  • unnatural disconnection between wanting and liking
  • (see graph)
161
Q

how can stimuli be associated with drug seeking behaviors?

A
  • instrumental learning (operant conditioning)
  • stimuli-> behavior-> habit
  • it happens with natural rewards as well, but more with drugs because of dopamine system
162
Q

how does operant conditioning associate stimuli and habit?

A
  • repeated performance in behavior in presence of certain stimuli-> stimulus-response (S-R) habits become stronger
  • rewards reinforce S-R learning
  • because of dopamine, stronger association between stimulus and habit
  • once formed, habits are automatically triggered by stimuli, independent of one’s motivation for outcome
163
Q

important summary of conditionings

A
  • from stimuli to craving: pavlovian (classical) conditioning
    > stimuli trigger craving
  • from stimuli to habit: instrumental (operant) conditioning
    > stimuli trigger behavior to get drug
164
Q

what cognitive control functions are affected by substance abuse?

A
  • impaired response inhibition
  • steeper delay discounting
  • risky decision making
    ! these impairments can be both:
    > consequence of neurotoxic effects of substances (on prefrontal cortex particularly)
    > vulnerability factors for the development of an addiction
165
Q

Disrupted dual processes

A
  • bottom up processes (craving and habits)
  • top down processes (cognitive control functions)
    > disrupted reward system + impaired executive functions = compulsive drug seeking
166
Q

Risk Factors

what are some sociodemographic factors associated with greater substance abuse? (in NL)

A
  • gender (men greater risk)
  • young age
  • living alone
  • being unemployed
  • very high degree of urbanization
167
Q

Risk Factors

what are personality risk factors?

A
  • sensation-seeking (desire for increased arousal and positive affect)
  • low impulse control (cognitive control functions)
168
Q

Risk Factors

what are some cultural risk factors?

A
  • drug availability
  • advertising and media (16% less consumption if ads portraying danger)
169
Q

Risk Factors

what are some risk factors regarding family and peers?

A

Family:
- substance abuse by caregivers
- marital discord, psychiatric or legal problems in the family
- lack of parental monitoring
- lack of emotional support by parents
Peers:
- social influences (become role models)

170
Q

Risk Factors

what is S.U.D. comorbid with?

A
  • depression (especially with alcohol abuse)
  • anxiety, PTSD, ADHD, bipolar disorder, borderline and anti-social personality disorder
    ! when dual diagnosis, there’s greater risk of addiction, more severe development of S.U.D. and more resistance towards treatment
171
Q

Risk Factors

what are the two contrasting hypothesis of disorders?

A
  • self-medication hypothesis (mental disorder > substance use)
  • high-risk hypothesis (substance use > mental disorder)
172
Q

Risk Factors

Risk factors - general overview

A
  • no single factor can predict whether a certain individual will develop substance abuse
  • interplay between genetic, environmental and developmental factors influences risk for addiction
  • the more risk factors, the greater the chance that alcohol/drug use spirals out of control
  • the more protective factors, the greater the resilience of an individual against developing addiction
173
Q

Treatment

Treatment demand distribution (NL, 2015)

A
  • 45% alcohol
  • 14% opioids
  • 11% cocaine
  • 17% cannabis
  • …
    ! stigma is the barrier (a lot of people don’t seek out treatment)
174
Q

Treatment

Most common treatments

A
  • aim: breaking through pattern of problematic substance use (reducing or quitting)
  • protocolled treatment + workbook
  • CBT + motivational interview (most common, strong evidence)
  • potentially in combination with medication
175
Q

Treatment

CBT for S.U.D. and Gambling disorder

A
  1. enhance motivation for treatment
  2. self-control measures and contingency management
  3. functional analysis
  4. dealing with craving
  5. prevention of relapse
  6. declining/refusing substances
176
Q

Treatment

1) Motivation for treatment

A
  1. Motivational Interviewing
    > helps people to believe in their ability to change (intrinsic motivation)
    > important because some people are still ambivalent when starting treatment (they don’t believe they can change)
    > collaborative, goal-oriented conversation style with special focus to change language
  2. Cost/Benefit Balance
    - disadvantages of use
    - benefits of decreasing/stopping use
177
Q

Treatment

what are the main causes of relapse?

A
  • withdrawal symptoms (only at the beginning)
  • exposure to external or internal stimuli (!)
178
Q

Treatment

3) Functional analysis of substance abuse

A
  • table where you have to write down external situation, internal situation, behaviour and consequences
  • to learn how to identify and deal with triggers
179
Q

Treatment

2.1) Self-control measures

A
  • Stimulus Control
    > avoid risk situations/triggers
  • Stimulus-Response Prevention
    > link the risk situations/triggers with alternative behaviour (preferably one with same function; e.g. relaxation techniques)
180
Q

Treatment

2.2) Contingency Management

A
  • desirable behaviour is reinforced or rewarded (e.g. with vaucher)
    > abstinence
    > attendance (to meetings)
    > positive activities
  • not applied systematically at addiction treatment centers
    (it is effective, but there’s problems with insurance)
181
Q

Treatment

4) Dealing with cravings

A
  • seek distraction or social support when experiencing craving
  • “urge surfing” (wait out urge)
    > trigger→rise→peak→fall
182
Q

Treatment

  1. prevention of relapses
    - what is the problem with “slips”?
A
  • a slip after a period of abstinence may cause person to feel guilt, shame and self-doubt
  • this may increase risk of complete relapse
    ! see slips as part of recovering process
    ! perform task that is effortful/unpleasant but that makes you feel better at the end (e.g. exercising)
183
Q

Treatment

  1. Declining offered substances
A
  • often strong social aspect to substance abuse
  • CBT treatment may involve role play with the therapist to practice declining substances
184
Q

Treatment

Medication

A
  • aversion drugs
    > antabuse (disulfram): nausea and vomiting if alcohol is consumed
  • anti-craving drugs
    > naltrexone
    > acamprosate
  • detoxification and/or maintenance drugs
    > methadone
185
Q

Treatment

Alcoholics Anonymous

A
  • largest self-help group
  • also Narcotics anonymous
  • goal: complete abstinence
  • 12-step program
  • regular meetings with other addicts
  • provides support, understanding and acceptance
186
Q

Treatment

CRAFT

A
  • community, reinforcement and family training
    > protocolized, evidence-based treatment based on CBT principles
  • aims:
    > help close relatives to adjust their behaviour in order to motivate patient to recover from their addiction
    > improve quality of life of close relatives
    ! not reinforcing unwanted behavior, but positive reinforcement of desirable behaviour

Clinical and Neuropsychology 2 (12 decks)

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