Substance Use Flashcards
DSM 5 Criteria
A: Problematic alcohol/substance use, clinical impairment/distress, within 12-month period.
Not enough evidence withdrawal feature for inhalant addiction.
A1: Uses larger amounts/longer periods than intended.
A2: Unsuccessful attempts to stop/cut down.
A3: Substantial time spent obtaining/using/recovering.
A4: Cravings/urges
A5: Failure to fulfil major roles (work/school/home)
A7: Gives up/reduces important social/occupational/recreational activities.
A8: Uses in hazardous environments.
A9: Continued used despite physical/psychological problems.
A10: Tolerance - diminished effect/need for increased amount
A11: Withdrawal - psychophysiological Sxs after stopping use/use relieves Sxs
Medical/disease model of addiction
Medical/disease model: impaired control over urges/cravings
- Clear biological effects of drug use
- Reduced stigma, blame
- Importance of treatment/rehabilitation emphasized
“A primary, chronic disease of brain reward, motivation, memory & related circuitry, with potential for both relapse & recovery”
“Addiction is a treatable, chronic medical disease involving complex interactions among brain circuits, genetics, the environment, and an individual’s life experiences. People with addiction use substances or engage in behaviors that become compulsive and often continue despite harmful consequences.” - Acknowledges interaction between external and internal forces in the etiology of addiction
- Substances exert their effects on consciousness through influencing our neurochemistry
- Repeated use results in changes to brain function (e.g., neurotransmitter systems) that persist beyond the acute effects of the drug (the ‘high’)
- These changes increase the likelihood of compulsive drug use (withdrawal, cravings, tolerance)
For example:
Alcohol affects a range of neurotransmitters, but most pronounced it upregulates GABA (inhibitory neuron) and downregulates glutamate systems (excitatory neurotransmitter). Body adapts to this by decreasing Gabba receptors and increasing glutamate receptors.
- This results in tolerance, need more alcohol to achieve same effect
Increased dopamine concentrations follows with repeated usage of drugs with hedonic properties.
“Although the development of addiction involve multiple areas and neurotransmitter systems that differ by drug-of-abuse, the DA system is of central importance to all”.
- Acute use of drugs results in upregulation of dopamine, while repeated used results in downregulation of dopamine (body expects an increased amount of dopamine)
Evidence 1: lower levels of D2 receptor in drug users from cocaine, methamphetamine and alcohol.
Evidence 2: 14 months of METH abstinence sees recovery of D2 receptor concentration.
Opponent process theory of addiction
- Drug activates A-process, Body activates B process as a homeostatic response.
- Over repeated use, B process begins to last longer and becomes more intense
- Drug use is continued in order to escape B process (negative reinforcement)
Liking vs Wanting: incentive-sensitization theory of addiction (Berridge et al., 1989)
“Liking” distinct/separate from “Wanting”
- It is therefore possible to begin wanting the drug despite not liking it anymore.
Dopamine mediates the “wanting” rather than “liking/pleasure” of something. This view is supported as dopamine is highest during ANTICIPATION of reward rather than DURING the experience.
I-RISA model of addiction (medical/disease perspective)
I-RISA: Impaired Response inhibition & Salience Attribution (Goldsten and Volkow, 2002)
- Imaging studies show structural changes to frontal lobe (morphological)
- Suppresses prefrontal cortex function (ability to self-regulate/monitor) and accentuates amygdala function
Four clusters of behaviors involved in I-RISA
Intoxication/excitement > Craving > Compulsive use > Withdrawal
- Characterized by attributing excessive salience to the drug and cues associated with using the drug
- Increased sensitivity to drug reinforcers and decreased sensitivity to non-reinforcers (other activities become less salient).
- Decreased ability to inhibit maladaptive behaviors.
IRISA in action:
Take a bite of cake –> VTA releases dopamine into the dopaminergic systems:
Amygdala: “This is delicious… this makes me very happy right now”
Hippocampus: Remembers experience and context
Prefrontal cortex: Focus attention on cake, to bite or not to bite?
Nucleus accumbens stimulated: “Pleasure center” causes you to take another bite.
Reward systems: Reactivated with each bite.
Addiction as a brain disease?
- Evidence of neurobiological adaptations in those with substance use disorders.
- Does this remove the stigma of addicted by choice?
- Conceptualizing as a disease argues against criminalization for use
Contention:
- Minimizes important social & environmental stresses like loneliness, poverty, violence, and other psychological factors
- Deflects responsibility (self-control/free will debate)
- Promotes fatalistic outlook
- Unhelpful perspective for therapy.
Biopsychosocial conceptualization of addiction (Solution to the I-RISA model)
Addiction is the result of multifactorial interaction between biopsychosocial factors.
Syndrome model of addiction (Shaffer et al. (2004)
- Each addictive disorder is a distinctive manifestation of the same underlying syndrome
- The Syndrome results from the interaction between common biopsychosocial factors
- The objects or foci of addiction are less important than we have previously assumed
- Not all symptoms are present in every manifestation
ANY DRUG OR SUBSTANCE OR ACTIVITY WITH HEDONIC PROPERTIES COULD BE THE FOCUS OF AN ADDICTION GIVEN RIGHT CIRCUMSTANCES
Addiction as a choice (rational choice/moral perspective)
Theory of rational addiction?
Self-medication model
Rational choice model
- Increased personal responsibility
- Increased sense of control and decision-making
- Many cases cease without treatment
Central arguments
- Evidence that addictive desires/cravings are not impervious to rational decision-making processes (1/3 of people get better with no intervention)
- Risk taking not unusual - we all assess costs & benefits when making decisions (driving, eating junk food)
- Spontaneous or natural recovery
Neurobiological correlates of substance use not unique to drugs.
Strong desires that result are not necessarily pathological.
Theory of rational addiction
- Argues that drugs have ‘lagged’ effects that unfold over time: individual takes current and future effects when making decision whether to take the drug (including decisions to increase)
Self-medication model
- Is it a choice?
- Arguments around the concept of “disease”, should it be viewed as a continuum?
Evidence-based treatment options for substance abuse?
Pharmacological:
- Naloxone (overdose); antabuse (disulfiram; Skinner et al., 2014); naltrexone; acamprosate
- Replacement therapies: methadone/suboxone
Therapy based:
- CBT
- Motivational interviewing
Individual may want to engage in Peer-based/recovery movement options:
- AA/NA (Project MATCH Research Group, 1998)
- Recovery centers
Management strategies need to be multifaceted and often integrates multiple domains of healthcare
- Need to address comorbidities
- Recovery is a long process and often involves relapse
Common barriers to successful treatment
- Psychiatric and medical comorbidities
- Acute and chronic neurocognitive deficits
- Social stresses
- Lack of resources
- Stigma
