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
