Lecture 16 Substance Use Flashcards
definition of addiction
-primary, chronic disease of brain reward, motivation, memory & related circuitry
-with potential for both
relapse & recovery
- physical and psychological dependence: adaptation resulting in tolerance and withdrawal, cravings, urges
- neuroadaptation: critical to transition to addiction but tolerance and withdrawal no longer deciding factor in whether an individual has an addiction
common components of addition
- salience: point of interest shrinks to use of substance, nothing else is important, preoccupation with drugs
- mood modification: use of substance to modify moods, reduce stress, withdrawal state
- tolerance: requirement of increasing doses in order to get same level of enjoyment
- withdrawal: once body lacking substance, craving and urges to consume to eliminate withdrawal symptoms
- conflict: to take it or not take it
- relapse: remain abstinent for a period of time but back to addiction
brain disease vs psychosocial factors
addiction as a brain disease:
– Concerns that it minimizes important social & environmental social stresses like loneliness, poverty, violence, & other psychological & environmental factors do not play an important role
– Deflects responsibility over actions: ‘My brain made me do it!’
• Self-control & free-will central to philosophical concepts
– Irresistible urge vs compulsive drive (craving as intuitive drive vs foreign urge)
– Desire centred vs. control centred accounts of impaired control
but dominant theoretical framework in addiction science is the biopsychosocial framework
biopsychosocial framework
- no single cause of addiction
- multifactorial interaction between biopsychosocial factors
- combination of symptoms and signs rather than unitary disorder
- not all signs and symptoms present in all cases, some have unique feature
risk factors
- anxiety, depression, low self-esteem, lack of resilience
- reward sensitivity: genetic, neurobiological
- environment: poverty, lifestyle, trauma exposure
distal antecedents
neurobiological (genetic, reward sensitivity)
psychosocial intrapsychic and environment
–> vulnerability
exposure leading desirable subjective shift (positive and negative reinforcement)
premorbid addiction syndrome
exposure & repeated use:
classical and operant conditioning
expression, shared manifestations and sequalae
drinking: cirrhosis
smoking: cancer
illicit drugs: hep C, HIV
signs/symptom
biological: tolerance, withdrawal, neuroanatomical changes
psychological: comorbid
social: social drift, criminality, disinhibition
natural history: relapse, recovery, progressive deterioration
response to intervention
object substitution: shift to other substances
distinction between medical/disease and rational choice model
medical: impaired control over urges/cravings
- reduced stigma, blame
- reduced personal responsibility, trust in behaviour (prone to relapse)
rational choice: voluntary behaviour under control
- increased personal responsibility
- increased sense of control
- majority cease without treatment
reward systems affected by drugs
- dopaminergic system
- endogenous opiod systems
concentration of dopamin increases following most drugs:
Alcohol, Nicotine, Cannabis,
Opioids, Cocaine, Amphetamines
drug effect at synapse
Drugs act like rubber stopper:
molecules block dopamine transporter & stop natural reuptake of dopamine into neurons
This causes a large excess of
dopamine in synapse & “overflow” of dopamine causes pleasure & euphoria
1 month and 4 month after cessation of use: low dopamine D2 receptors in striatum, after 4 months receptor levels increase but remain low
opponent process theory of addiction
- most people want to work towards normal level of homeostasis (stable state of functioning)
- take drug -> high (a state), increase in arousal, excitement
- body response: opponent process to bring arousal back down to homeostatic level (b state)
- process of habituation (effect of drug decreases, body responds)
- addictive stage: tolerance because b process has been magnified, reduced euphoria, increased unpleasance
- opponent process: A process provides increase, B process homeostatic attempt to draw it down, increased opponent process over time
–> reduced hedonic contrast
tolerance in substance dependence
Homeostatic state:
opponent-process (bprocess) balances the drug activation (aprocess). It can return to
the homeostatic state.
after repeated drug use, affective system transitions to a lower allostatic level
Impaired Response Inhibition and Salience Attribution (Goldstein & Volkow, 2002)
Drug addiction mediated by functional & structural changes in circuits modulated by dopamine
- Mesolimbic: amygdala, nucleus accumbens, hippocampus
• Acute reinforcing effects, memory & conditioning linked to craving, & emotional & motivational changes during withdrawal - Mesocortical: prefrontal cortex, orbito-frontal cortex & anterior cingulate
• Conscious experience of intoxication, salience, expectations, cravings, &
inhibitory control/decision-making
in one sense drug boosts up mesolimbic area, increases euphoria, excitement with release of dopamine
as excitement increases, inhibitory control and executive decision making becomes poor
four clusters/stages of behaviours
- Intoxication/excitement
• Higher extra-cellular dopamine concentrations in limbic circuits (nucleus
accumbens) & frontal lobe - Craving
• Classical & operant association of cues with pleasure
• Memory consolidated in amygdala & hippocampus (& thalamoorbitofrontal circuit in experience of craving)
3.Compulsive use
• Continued use when no longer perceived as pleasurable
- Withdrawal
• Dysphoria, anhedonia & irritability contributing to relapse
• Involvement of frontal cortical circuits
response when eating a piece of cake
VTA releases dopamine to all regions
- amygdala: delicious, makes me happy now
- hippocampus: remembers experience and context
- prefrontal cortex: focus attention on cake
- nucleus accumbens: pleasure centre, stimulated, causing you to take another bite
- reward system: reactivated with each bite
Addictive behaviors emerge if repeated too often
biological model
chronic substance use (conditioned response in amygdala)
–>
sensitisation (neuro-adaptation in reward circuit)
–>
changes in neurotransmitters (e.g. dopamine dysregulation)
–>
initial abstinence->withdrawal
or prolonged abstinence ->reward memory (hippo)
–>
craving (frontal cortex, decision making)
–>
relapse
negative affect and exposure to cues contribute
Addiction as choice
Medical model focus on impaired control: i.e., loss of normal capacities for rational self-control
Desire-centred models explain compulsion as an inability to resist acting on a
desire because the desire coerces her to choose the compulsive behaviour
- Rational informed stable choice (Vuchinich & Heather, 2003)
- Theory of rational addiction (Becker & Murphy, 1988)
- Self-medication model (Gelkopf et al., 2002)
- Choice theory (Skog, 2003)
- Challenges notion of “compulsive behaviour” as equivalent to “compelled behaviour”
choice model
Rationality/utility: subjective ST benefit outweights LT cost
Unstable preferences: Repeated failure to cease consumption, Self-control vs Self-regulation
opportunity --> perceived benefit and urges OR perceived cost and self-control -->addictive behaviour
public health approach
- limit access to and pattern of drug taking
- socioeconomic constraints: social norms, availability, price
- motivation to consume: reinforcement, peer group, genetic predisposition - acute consequence of drugs: health related, violence, public intoxication
- consequences of chronic drug use: drug dependency, addiction
Common barriers to successful treatment
- Psychiatric comorbidity,
- Acute or chronic cognitive deficits
- Medical problems
- Social stressors
- Lack of social resources
- Stigma
to break barriers
• Identify high risk situations & events
• (including people, places, internal cues such as
changes in affect)
• Reduce likelihood that these events are encountered
(providing alternative activities)
• Rehearsing non-drug alternatives to cues
Principles of effective treatment
- No single treatment is sufficient
- Treatment readily available & accessible
- Address multiple psychological, medical & social interventions & needs
(CBT, naloxone, antabuse, methadone, peer support) - Comorbid conditions treated in integrated manner
- Mandated treatment can lead to effect change
- Recovery a long term process & frequently requires
multiple episodes of treatment for lapses/relapse
