Transcript CHEMICAL MESSENGERS

MODELS OF ADDICTION:
A SUMMARY
Moral / Temperance Model *
Addiction as Sin or Crime
Personal Irresponsibility
Disease Model *
Genetic and Biological Factors
12-Step Framework; Abstinence
Education as Treatment
Behavioral and CognitiveBehavioral Models *
Conditioning and Reinforcement
Social Learning and Modeling
Drug Expectancies and other
Cognitive Factors / RP
Family Models
Family Disease
Family Systems
Behavioral Marital/Family Tx
MODELS OF ADDICTION:
A SUMMARY
Psychological / Psychoanalytic
Disordered /Addictive Personality
Sociocultural Models
Cultural Factors
Socioeconomics/ Social Policy
Drug Subcultures
Public Health Model
Agent, Host, Environment
Interactions
THE BIOPSYCHOSOCIAL MODEL:
AN INTEGRATION
Medical / Disease
Models of Addiction
BIOLOGY OF ADDICTION
• Introduction
• Why study addiction from a biological perspective?
All Multicell Organisms Require Cellto-Cell Communications
Mammals Require a Variety of
Sophisticated Systems for Chemical
Communications
CHEMICAL MESSENGERS
 Chemical Messengers
 Hormones—Released from glands and
affect other cells, including other glands
 Neurotransmitters—More discrete and
targeted than hormones
 Receptors—Cell structures that receive
the chemical message
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PET
Scan
6-10
Positron Emission Tomography - Uses radioactive
chemical injection
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MRI Scan
(f MRI)
6-11
Magnetic Resonance Imaging - Computer processes
magnetic field energy
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Information Movement in the Nervous System
Figure 6-4
6-4
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Chemical Signaling in the Nervous System
Figure 6-2
6-2
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Release of Neurotransmitter Molecules
Figure 6-3
6-3
7 Neurotransmitters Related to Drug Effects
The 3 Monoamines
1. Dopamine - common and pervasive chemical important in
regulation of motor movements, emotional and cognitive
processes, and reinforcement
- schizophrenia (increased dopamine activity)
- Parkinson’s Disease (decreased activity)
• Different drugs affect dopamine levels in different ways:
 stimulants like cocaine and amphetamines
increase dopamine activity
7 Neurotransmitters Related to Drug Effects
2. Serotonin - important in regulation of sleep and mood
monoamine theory of depression supported by:
drugs that reduced Monoamines produce depression
drugs effective in treating depression act on serotonin
or norepinephrine
3. Norepinephrine - important in the regulation of hunger,
alertness and arousal; implicated in depression
7 Neurotransmitters Related to Drug Effects
4. Acetylcholine (ACh) - important in the functions of muscular
activity, regulation of thirst and memory
(e.g. Alzheimer’s Disease is related to loss of cholinergic
function in brain)
5. Endorphins - thought to modulate pain relief and to be
associated with naturally occurring pleasures or “highs”
6. GABA - (gamma-aminobutyric acid) referred to as an inhibitory
transmitter because when it binds to receptor sites it stops the
neuron from firing.
What drugs act on the GABA system? ____________
7. Glutamate – throughout brain; excitatory
BIOLOGY OF ADDICTION
• neuron is like a rechargeable battery, can fire again after
either:
enzymes break down transmitter substance so it cant
occupy receptor site anymore or
reuptake: substance taken back into terminal button
•
agonists and antagonists
agonist is any chemical (naturally occurring in brain or
introduced) that fits a receptor lock and activates it;
in general, agonists increase the activity of the
transmitter systems they operate on
(ex. morphine is an agonist for the endorphins )
BIOLOGY OF ADDICTION
antagonists - don’t activate receptor sites and neurons to fire
but still occupy site, preventing other chemicals
from sitting there
ex. naloxone is an opiate antagonist
Some
Mechanisms of
Drug Action
- drug can decrease or
increase synthesis of
neurotransmitters
- neurotransmitter
transport interference
- neurotransmitter
reuptake is blocked
(pictured)
- receptor activation;
drug mimics
neurotransmitter
- receptor blocking
NEURAL BASIS OF REWARD & ADDICTION
• studies of stimulation of rat brains: in some areas the rats
loved the electrodes! rats could be trained to lever press to
self-stim and to have cocaine delivered to them
• possibly a final common pathway for positive stimulation and
reward; this pathway is dopamine-rich;
• most drugs produce changes in this system, but “broccoli”
(food) does not produce dramatic changes, presumably
because it does not have the intensity and immediacy of
reinforcement being delivered to the brain by drugs
NEURAL BASIS OF REWARD & ADDICTION
 some research (Anna Childress) suggests that craving is a
type of feeling or “body” memory because exposure to
strong, previously learned cues can trigger dopamine
release even before a drug enters the body (e.g., location
where drug previously bought and used)
amygdala activated prior to drug ingestion in cocaine
users compared to controls
 some evidence that the “addicted brain” is qualitatively
different from non-drug users even after drug use is
discontinued
e.g. dopamine depletion present after
methamphetamine use for up to a year after last
use among frequent users
A Few Definitions
Psychopharmacology - study of the effects of drugs on behavior
Pharmacology -
the study of drugs and their effects;
• Pharmacokinetics - the study of how drugs are absorbed,
distributed, transformed and excreted in animals and humans
• Pharmacodynamics - study of the biochemical effects of drugs
and their mechanisms of action
Brainstorm
What factors relate to the way drugs affect
us?
Brainstorm
What factors relate to the way drugs affect
us?
dose, route of admin., body weight, gender, age, inherited predispositions,
psychological characteristics; absorption, distribution & elimination
processes; interactions between drugs, tolerance, expectancies (e.g.
social and cultural expectations in particular contexts)
Brainstorm
Drugs need to get into the body before
exerting an effect...how many different
ways can drugs enter the body and brain?
The 4 major routes of drug administration

Oral

Injection
subcutaneous - beginning drug users; steady
absorption rate
intramuscular - faster but obviously can be
painful
intravenous - into veins; “mainlining”; immediate
effects but most complications
(e.g. death)
The 4 major routes of drug administration

Inhalation - absorbed through lungs; fast & effective;
drug gets wasted though, can only absorb a
small amount

Absorption
intranasal - mucous membranes of nose, sinus
sublingual - under the tongue; absorbed through
mouth’s mucous membranes
(e.g nitroglycerin; dip or chew
tobacco to get nicotine)
transdermal - through the skin; examples?
(nitro and nicotine patches)
rectal - suppositories
Pharmacodynamics
 dose-effect curve
effective doses - % of people who experience
effect of drug at given doses
 ED - 50 ; 50% of people taking specific dose
will be experiencing the effect
lethal doses - effect of interest is death! Defined
as % of animal subjects who die
LD - 50
•
•
the diff b/n ED and LD MAY NOT BE THAT LARGE!
drug interactions
Pharmacokinetics
 Absorption: rate and extent to which drug leaves its site
of administration;
bioavailability: portion of drug that reaches its site of action
 Distribution: where the blood flows most is where most
of the drug goes (where? _________)
 Elimination: liver enzymes play biggest part in expelling
drugs; kidneys as well
 where excreted? Urine, feces, perspiration,
mother’s milk, lungs
 drug half-life: time it takes for 50% of drug to be
excreted
Behavioral Pharmacology and Tolerance
Behavioral Pharmacology - specialty area within pharmacology
that concentrates on drug use as learned behavior
General Definition of tolerance - reduced response to a drug after
repeatedly taking it
Types of Tolerance:

Dispositional tolerance - increase in the rate of
metabolizing a drug after repeated use

Functional (cellular) tolerance- brain becomes
less sensitive to drug
• acute tolerance: occurs within single dose or first few
doses of drug
(e.g., Alcohol
cocaine)
• vs. protracted:occurs after regular,chronic use
Behavioral Pharmacology and Tolerance
• Behavioral tolerance - person adjusts or compensates for
their drug-induced behavior
EX. We compensate for intoxicated behavior in diff ways
_______
• Issue of cross-tolerance EX. alcohol and depressant drugs
• tolerance to some effects of drug but not others
(EX. Appetite suppressant effect of amphetamine absent after few weeks)
• tolerance syndrome doesn’t develop to some drugs
(Hallucinogens? Pot?)
•
reverse tolerance - becoming more sensitive with repeated
use (examples ?)
MODELS OF ADDICTION
Assumptions of Disease Model
addiction seen as a “primary” disease process
alcoholics qualitatively different from non
alcoholics: can’t drink in moderation
central symptom of addiction is loss of control
(e.g., one drink, one drunk)
addiction is chronic and progressive; no cure,
can only be arrested with total abstinence
(e.g. progression models - Johnson…learning &
seeking the mood swing; harmful dependence;
drinking to feel normal)
Disease Model - Treatment
• Early identification
• Education about diagnosis
• Acceptance of disease and
overcoming “denial”
• Abstinence
• 12-steps essential for real recovery
CRITIQUE OF DISEASE MODEL
Strengths
-
perception shift: from sin to TX
-
eases guilt, self-blame
-
disease is a good metaphor that fits the experience
-
12-step support and framework works for many
(prevalence of meetings; 24-hour support…)
-
Other strengths? _______________________
Disease Model - Research Support
• Adoption study of Goodwin
• 18% probands alcoholic vs. 5% controls
• Twin Studies
• male vs. female twin pairs
• Metabolic Studies
• P3 Wave Studies
CRITIQUE OF DISEASE MODEL
Limitations
- Assumptions not all data-based
addiction as “primary”
loss of control
chronic / progressive
alcoholics qualitatively different
-
Dichotomous thinking dangerous; no middle ground
(you’re an alcoholic or not)
-
Loss of control and responsibility paradox
-
Other flaws? ___________________