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Moral / Temperance Model*Addiction as Sin or Crime Personal Irresponsibility Disease Model *Genetic and Biological Factors 12-Step Framework; Abstinence.

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Presentation on theme: "Moral / Temperance Model*Addiction as Sin or Crime Personal Irresponsibility Disease Model *Genetic and Biological Factors 12-Step Framework; Abstinence."— Presentation transcript:

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2 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 Cognitive- Conditioning and Reinforcement Behavioral Models * Social Learning and Modeling Drug Expectancies and other Cognitive Factors / RP Family ModelsFamily Disease Family Systems Behavioral Marital/Family Tx MODELS OF ADDICTION: A SUMMARY

3 Psychological / PsychoanalyticDisordered /Addictive Personality Sociocultural ModelsCultural Factors Socioeconomics/ Social Policy Drug Subcultures Public Health ModelAgent, Host, Environment Interactions THE BIOPSYCHOSOCIAL MODEL: AN INTEGRATION MODELS OF ADDICTION: A SUMMARY

4 Medical / Disease Models of Addiction

5 BIOLOGY OF ADDICTION Introduction Why study addiction from a biological perspective? All Multicell Organisms Require Cell- to-Cell Communications Mammals Require a Variety of Sophisticated Systems for Chemical Communications

6 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

7 PET Scan 6-10 Copyright © The McGraw-Hill Companies, Inc. Positron Emission Tomography - Uses radioactive chemical injection

8 MRI Scan Magnetic Resonance Imaging - Computer processes (f MRI) magnetic field energy 6-11 Copyright © The McGraw-Hill Companies, Inc.

9 Information Movement in the Nervous System Figure 6-4 6-4 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

10 Chemical Signaling in the Nervous System Figure 6-2 6-2 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

11 Release of Neurotransmitter Molecules Figure 6-3 6-3 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

12 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

13 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

14 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

15 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 )

16 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

17 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

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19 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

20 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

21 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

22 Brainstorm What factors relate to the way drugs affect us?

23 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)

24 Brainstorm Drugs need to get into the body before exerting an effect...how many different ways can drugs enter the body and brain?

25 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)

26 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

27 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

28 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

29 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

30 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 ?)

31 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)

32 Early identification Education about diagnosis Acceptance of disease and overcoming “denial” Abstinence 12-steps essential for real recovery Disease Model - Treatment

33 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? _______________________

34 Adoption study of Goodwin 18% probands alcoholic vs. 5% controls Twin Studies male vs. female twin pairs Metabolic Studies P3 Wave Studies Disease Model - Research Support

35 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? ___________________


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