Addic on 1
WEEK 1
Chapter 1: The History of Addiction Concepts: From ‘Addiction’ to ‘Addictions’
addic on was first associated with substances (e.g. alcohol, nico ne) and only recently applied to behaviors
(e.g. gambling, gaming)
there used to be no clear dis nc on between medical and moral understandings of addic on
used to be a disagreement over the roots of addic on (characteris cs of person vs proper es of the
substance)
the standardiza on of addic on concepts happened around the 1950s-1980s
the DSM first described it as a personality disorder, then as a behavioral disorder
emergence of the term dependence (1970s)
>> clearer dis nc on between compulsion and physical effects
>> more a en on to the nature and impact of dependence (<> only the physical consequences)
>> understanding that addic on to different substances have the same underlying mechanisms
(emergence of neuroimaging also confirms this)
today, people link dependence with addic on (<> dependence can be a normal bodily response to a
substance)
Chapter 2: Addiction, Brain Disease, and Free Will
addic on as weak will vs brain disease
Brain Disease Model
long-term use of a drug >> changes in the brain >> behavior goes from voluntary to compulsive >> free will
can no longer be exercised
<> neuroscience of addic on is actually s ll in its infancy
<> downplays environmental factors
<> people with addic on can actually control their drug use if given incen ves
drug-induced changes in the structure and func on of the brain:
blun ng of normal dopamine func on
reduced ac vity in the prefrontal regions
structural and func onal abnormality in prefrontal regions, especially in anterior cingulate
cortex/medical prefrontal cortex
disrup ons to cogni on and emo onal processing (may also be a risk factor in the development of
addic on, not long-term consequence of it)
3 models of neuroadapta on:
subcor cal regions underlying responsiveness become desensi zed
>> tolerance: rewarding effect of drug is diminished
>> disengagement from ac vi es that used to be rewarding
>> reduced enjoyment (anhedonia)
desensi zed regions become ac vated by drug-related cues
>> triggers powerful cravings
>> a rac on to drug-related cues
>> induc on of behaviors to take the drug (even if not wishing to)
prefrontal cortex becomes hypoac ve
>> ability to modulate ac vity in subcor cal regions is lost
>> impairment of execu ve func ons (e.g. inhibi on, goal/plan ini a on and execu on)
= losing interest in ac vi es that used to be rewarding, drug cues are more mo va ng, reduced ability to
resist cravings
The Case of Free Will
Heather’s ‘strong’ sense: free will has been completely eroded
‘Weak’ sense: free will is only par ally eroded
, Addic on 2
sources of evidence for (par al) loss of free will:
many drug users try to stop but are unable
high levels of relapse
behavioral automa city
weaker inhibitory control
craving undermines a empts to curtail drug use
dual process theory of addic on: mo vated behaviors are ini ally goal-directed and are under cogni ve
control >> shi to more automa c
Counter Argument: Not Brain Disease, Free Will Remains
why not brain disease:
brain changes in addic on are not consistent across different people (i.e. we cannot detect or
diagnose addic on from brain scans alone)
many neuroadapta ons of addic on are also present in other contexts (e.g. ea ng, love)
we don’t have a full understanding of brains in general, so we aren’t equipped to dis nguish between
healthy and diseased brains
the priorisa on of neuroscien fic explana ons generated few new treatments and increased s gma
alterna ve ideas & evidence:
unable to control vs difficult to control?
switching the focus from free will or no free will to reward processing (and other cogni ve processes)
many PWA can control their use if given financial incen ves
many PWA recover (majority even)
drug use is partly maintained by perceived benefits of drug use
Integra on of the two Arguments
cravings are an important feature of addic on and are increasingly difficult to resist over the longer term
chance of recovery is influenced by the environment
contextualized reinforcer pathology model: drug valua on is rela ve to the availability of alterna ve
reinforcers in the environment (>> emphasizes the use of community-based interven ons)
the automa za on vs control of thought processes is a con nuum and is constantly under change (not all-or-
nothing)
>> there is a constant balancing of control, weighing on the availability of the drug and alterna ve reinforcers
Chapter 5: The Developmental Epidemiology of Substance Use and Disorder
huge heterogeneity in the developmental epidemiology of substance use and disorder
importance of
developmental ming (childhood/adolescence/adulthood)
stage or extent of substance involvement (onset, experimenta on, escala on, disorder, decelera on,
recovery)
period (e.g. historical influences like covid)
cohort effect (intersec on of the above)
early onset (< 15 years) is a strong predictor of nega ve substance use related consequences/disorder
substance use and disorder peak between 18 and 24 (like other health risk behaviors)
substance use could be an extension (= heterotypic expression) of underlying adap ve challenges involving
behavioral disinhibi on (externalizing pathway) or emo onal dysregula on (internalizing pathway)
stronger associa ons between substance use/disorder and externalizing pathway
social marginaliza on/discrimina on >> intrapersonal distress >> higher risk processes >> higher mo va on
for substance use
period and cohort effects:
availability of new substances
delivery mechanisms for substances
changes in laws and policies governing use
altered social contexts in which use takes place
, Addic on 3
notable comorbidity between substance use disorder and other mental health disorder
Lecture 1 - What is Addiction: An Introduction
men make up 80% of the people with substance use disorders
societal relevance of substance use: health, crime, public safety, work-related produc vity
addic on and substance use cannot be understood apart from the social and historical context
Types of Substances
Tobacco (cigare es)
S mulants (cocaine, amphetamines) >> s mulate the nervous system
Depressants (alcohol, benzodiazepines) >> relaxing
Opioids (heroin, prescrip on drugs) >> s mulate the opioid system
Hallucinogens (LSD, cannabis, ketamine) >> s mulate the perceptual systems
agonist: mimic the response of neurotransmi ers
antagonist: block the response of neurotransmi ers
Lecture 2 - Social and Cultural Aspects of Addiction
The Neurocogni ve Profile of Addic on
reduced cogni ve control
increased mo va on (craving, a en onal biases)
>> imbalance between approach-oriented mo va onal system
and regulatory control system
the environment plays an important role in these processes
Risk Factors Drug Use and Addic on
social environment + physical environment + individual differences >> risk for substance use and addic on
The Social Environment
one’s immediate environment (peer influence, family dynamics, social norms)
affects the likelihood that an individual will use drugs or develop an addic on
we are not equally affected by social influence:
age (e.g. adolescents are most sensi ve to it)
peer group (e.g. level of pressure/acceptance within group)
individual differences
social a unement: the tendency to harmonize with one’s social environment
WEEK 1
Chapter 1: The History of Addiction Concepts: From ‘Addiction’ to ‘Addictions’
addic on was first associated with substances (e.g. alcohol, nico ne) and only recently applied to behaviors
(e.g. gambling, gaming)
there used to be no clear dis nc on between medical and moral understandings of addic on
used to be a disagreement over the roots of addic on (characteris cs of person vs proper es of the
substance)
the standardiza on of addic on concepts happened around the 1950s-1980s
the DSM first described it as a personality disorder, then as a behavioral disorder
emergence of the term dependence (1970s)
>> clearer dis nc on between compulsion and physical effects
>> more a en on to the nature and impact of dependence (<> only the physical consequences)
>> understanding that addic on to different substances have the same underlying mechanisms
(emergence of neuroimaging also confirms this)
today, people link dependence with addic on (<> dependence can be a normal bodily response to a
substance)
Chapter 2: Addiction, Brain Disease, and Free Will
addic on as weak will vs brain disease
Brain Disease Model
long-term use of a drug >> changes in the brain >> behavior goes from voluntary to compulsive >> free will
can no longer be exercised
<> neuroscience of addic on is actually s ll in its infancy
<> downplays environmental factors
<> people with addic on can actually control their drug use if given incen ves
drug-induced changes in the structure and func on of the brain:
blun ng of normal dopamine func on
reduced ac vity in the prefrontal regions
structural and func onal abnormality in prefrontal regions, especially in anterior cingulate
cortex/medical prefrontal cortex
disrup ons to cogni on and emo onal processing (may also be a risk factor in the development of
addic on, not long-term consequence of it)
3 models of neuroadapta on:
subcor cal regions underlying responsiveness become desensi zed
>> tolerance: rewarding effect of drug is diminished
>> disengagement from ac vi es that used to be rewarding
>> reduced enjoyment (anhedonia)
desensi zed regions become ac vated by drug-related cues
>> triggers powerful cravings
>> a rac on to drug-related cues
>> induc on of behaviors to take the drug (even if not wishing to)
prefrontal cortex becomes hypoac ve
>> ability to modulate ac vity in subcor cal regions is lost
>> impairment of execu ve func ons (e.g. inhibi on, goal/plan ini a on and execu on)
= losing interest in ac vi es that used to be rewarding, drug cues are more mo va ng, reduced ability to
resist cravings
The Case of Free Will
Heather’s ‘strong’ sense: free will has been completely eroded
‘Weak’ sense: free will is only par ally eroded
, Addic on 2
sources of evidence for (par al) loss of free will:
many drug users try to stop but are unable
high levels of relapse
behavioral automa city
weaker inhibitory control
craving undermines a empts to curtail drug use
dual process theory of addic on: mo vated behaviors are ini ally goal-directed and are under cogni ve
control >> shi to more automa c
Counter Argument: Not Brain Disease, Free Will Remains
why not brain disease:
brain changes in addic on are not consistent across different people (i.e. we cannot detect or
diagnose addic on from brain scans alone)
many neuroadapta ons of addic on are also present in other contexts (e.g. ea ng, love)
we don’t have a full understanding of brains in general, so we aren’t equipped to dis nguish between
healthy and diseased brains
the priorisa on of neuroscien fic explana ons generated few new treatments and increased s gma
alterna ve ideas & evidence:
unable to control vs difficult to control?
switching the focus from free will or no free will to reward processing (and other cogni ve processes)
many PWA can control their use if given financial incen ves
many PWA recover (majority even)
drug use is partly maintained by perceived benefits of drug use
Integra on of the two Arguments
cravings are an important feature of addic on and are increasingly difficult to resist over the longer term
chance of recovery is influenced by the environment
contextualized reinforcer pathology model: drug valua on is rela ve to the availability of alterna ve
reinforcers in the environment (>> emphasizes the use of community-based interven ons)
the automa za on vs control of thought processes is a con nuum and is constantly under change (not all-or-
nothing)
>> there is a constant balancing of control, weighing on the availability of the drug and alterna ve reinforcers
Chapter 5: The Developmental Epidemiology of Substance Use and Disorder
huge heterogeneity in the developmental epidemiology of substance use and disorder
importance of
developmental ming (childhood/adolescence/adulthood)
stage or extent of substance involvement (onset, experimenta on, escala on, disorder, decelera on,
recovery)
period (e.g. historical influences like covid)
cohort effect (intersec on of the above)
early onset (< 15 years) is a strong predictor of nega ve substance use related consequences/disorder
substance use and disorder peak between 18 and 24 (like other health risk behaviors)
substance use could be an extension (= heterotypic expression) of underlying adap ve challenges involving
behavioral disinhibi on (externalizing pathway) or emo onal dysregula on (internalizing pathway)
stronger associa ons between substance use/disorder and externalizing pathway
social marginaliza on/discrimina on >> intrapersonal distress >> higher risk processes >> higher mo va on
for substance use
period and cohort effects:
availability of new substances
delivery mechanisms for substances
changes in laws and policies governing use
altered social contexts in which use takes place
, Addic on 3
notable comorbidity between substance use disorder and other mental health disorder
Lecture 1 - What is Addiction: An Introduction
men make up 80% of the people with substance use disorders
societal relevance of substance use: health, crime, public safety, work-related produc vity
addic on and substance use cannot be understood apart from the social and historical context
Types of Substances
Tobacco (cigare es)
S mulants (cocaine, amphetamines) >> s mulate the nervous system
Depressants (alcohol, benzodiazepines) >> relaxing
Opioids (heroin, prescrip on drugs) >> s mulate the opioid system
Hallucinogens (LSD, cannabis, ketamine) >> s mulate the perceptual systems
agonist: mimic the response of neurotransmi ers
antagonist: block the response of neurotransmi ers
Lecture 2 - Social and Cultural Aspects of Addiction
The Neurocogni ve Profile of Addic on
reduced cogni ve control
increased mo va on (craving, a en onal biases)
>> imbalance between approach-oriented mo va onal system
and regulatory control system
the environment plays an important role in these processes
Risk Factors Drug Use and Addic on
social environment + physical environment + individual differences >> risk for substance use and addic on
The Social Environment
one’s immediate environment (peer influence, family dynamics, social norms)
affects the likelihood that an individual will use drugs or develop an addic on
we are not equally affected by social influence:
age (e.g. adolescents are most sensi ve to it)
peer group (e.g. level of pressure/acceptance within group)
individual differences
social a unement: the tendency to harmonize with one’s social environment
