Transcript Cannabis sativa

Chapter 13 Health
Psychology: Addiction,
Emotion, and Stress
Impact of Psychological
Factors on Health
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Copyright © 2007 by Allyn and Bacon
Health Psychology
 An
area of psychological research
that focuses on the effects of
psychological factors on physical
health
 Multidisciplinary
 Two major areas addressed here –
addiction and emotion
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Drug Tolerance

Decreased sensitivity to a drug as a
consequence of exposure to it

Shift in the dose-response curve
Cross tolerance – exposure to one drug
can produce tolerance to similar drugs
 Tolerance often develops to some effects
and not others
 More than one form of tolerance

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Copyright © 2007 by Allyn and Bacon
Drug Tolerance
 Metabolic
Less
drug is getting to the site of action
 Functional
Decreased
responsiveness at the site of
action - fewer receptors, decreased
efficiency of binding at receptors,
receptors less responsive
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Physical Dependence

Indicated by occurrence of withdrawal
 Seen
when drug use is terminated
 Symptoms are the opposite of the drug’s
effects
 Body has made changes to compensate for
drug’s presence – functions normally with the
drug present
 Severity varies with drug and pattern of use
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Copyright © 2007 by Allyn and Bacon
Drug Tolerance and Conditioning
Situational specificity of drug tolerance is
well-documented
 Cues associated with drug-taking become
conditioned stimuli that elicit conditioned
compensatory responses, producing
tolerance prior to drug use or withdrawal in
the absence of the drug

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Addiction: What Is It?
 “Addicts”
are those who continue to
use a drug despite its adverse
consequences
 Nobody is immune to the addictive
effects of drugs
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Biological Theories of Addiction

Physical-Dependence Theory –
 Use
continues to avoid withdrawal
Why relapse after detoxification? Why begin use?
 Why does addiction develop to drugs that do not
produce severe withdrawal?


Positive-Incentive Theories
 Use
continues due to craving (anticipated
pleasure) for drug effects
 Supported by research
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Causes of Relapse
 Stress
Drug
use as a coping mechanism
 Priming
A
single exposure leads to a relapse
 Environmental
cues
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5 Commonly Abused Drugs
Tobacco
 Alcohol
 Marijuana
 Cocaine
 Opiates

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Tobacco
Nicotine – major psychoactive ingredient
 About 70% of those who experiment with
smoking become addicted
 Only about 20% of attempts to stop are
successful

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Effects of Long-Term Tobacco Use
Smoker’s syndrome – chest pain, labored
breathing, wheezing, coughing, increased
susceptibility to respiratory infections
 Susceptible to various lethal lung disorders
– pneumonia, bronchitis, emphysema, lung
cancer

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Alcohol
A depressant
 High heritability estimate for alcohol
addiction - ~55%
 Metabolic and functional tolerance
develops
 Attacks almost every tissue in the body

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Effects of Chronic Alcohol
Consumption

Severe withdrawal – 3 phases
 5-6
hrs post-drinking: tremors, nausea,
sweating, vomiting, etc.
 15-30 hrs: convulsive activity
 24-48 hrs: delirium tremens – may last 3-4
days
Korsakoff’s syndrome
 Cirrhosis

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Fetal Alcohol Syndrome (FAS)
 Alcohol
readily penetrates the
placental membrane
 Alcohol disrupts brain development
 No known “safe” amount
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Marijuana
Cannabis sativa – common hemp plant
 THC – primary psychoactive constituent –
although over 80 others are present
 High doses impair short-term memory and
interfere with tasks involving multiple steps
 Addiction potential is low
 Negative effects are far less severe than
those associated with alcohol and tobacco

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Adverse Effects of Heavy
Marijuana Use
problems – cough,
bronchitis, asthma
 Single large doses can trigger heart
attacks in susceptible individuals
 No evidence that marijuana causes
permanent brain damage
 Respiratory
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Medicinal Uses of Marijuana
 Treat
nausea
 Block seizures
 Dilate bronchioles of asthmatics
 Decrease severity of glaucoma
 Reduce some forms of pain
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THC
 Fat-soluble
 Binds
to receptors in basal ganglia,
hippocampus, cerebellum, and
neocortex
 Endogenous ligand is anandamide
 Function of anandamide is not known
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Stimulants
Increase neural and behavioral activity
 Cocaine and its derivatives – commonly
abused
 Crack – a potent, cheap, and smokable
form of cocaine
 Cocaine is an effective local anesthetic

 Synthetic
analogues procaine and lidocaine
used today
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Cocaine

Cocaine binges or sprees may lead to
cocaine psychosis
 Looks
like paranoid schizophrenia
While tolerance may develop to some
effects of cocaine, sensitization is seen to
motor and convulsive effects
 Although highly addictive, withdrawal is
relatively minor

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Amphetamine
AKA “speed” – another abused stimulant
 Effects are comparable to those of cocaine
– also can produce psychosis
 MDMA (ecstasy) – a relative of
amphetamine
 Evidence suggests that stimulants are
neurotoxins

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Ecstasy (MDMA)
Studies of lab animals find that MDMA has
toxic effects on serotonergic and
dopaminergic neurons
 But are the doses used in studies
comparable to what humans use?
 Human studies do find abnormalities of
serotonergic function and deficits in
memory, mood, and psychomotor tasks

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Opiates: Heroin and Morphine



Morphine and codeine obtained from the opium
poppy
Opiates – these drugs and others with similar
structures or effects
Medicinal uses
 Analgesics
(painkillers)
 Treatment of cough and diarrhea

High risk of addiction
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Factors Increasing Opiate
Popularity

China’s ban of tobacco smoking led to
opium smoking
 More

addicting than eating opium
Isolation of morphine
 Opium’s

most potent constituent
The hypodermic needle
 During
the Civil War morphine addiction came
to be known as “soldiers’ disease”
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U.S. Opiate History
Readily available in a variety of “potions”
until 1914
 Harrison Narcotic Act (1914)

 Illegal to sell or use opium
 Heroin, a synthetic opiate,
was still legal
Structure similar to morphine, but better able to
cross the blood-brain barrier
 More addictive


Heroin illegal as of 1924
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Opiate Addiction






Drawn to use by the rush following IV injection
Tolerance and physical dependence develop
Desire to avoid withdrawal adds to motivation to
use
Although highly addictive, direct health hazards
are relatively minor
Many health hazards related to use of needles
Severity of withdrawal has been exaggerated
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Comparison of the Health Hazards
Which drug is our biggest “drug
problem”?
 Which drug harms the individual
the most?
 Which drug harms society the
most?

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Addiction and the Neural
Mechanisms of Motivation
 How
has drug-produced
reinforcement been studied in
nonhumans?
Drug
self-administration
Conditioned place-preference
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Behavioral preference tests
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Involvement of Dopamine in Drug
Addiction
 Dopamine
antagonists
block
self-administration of, or
conditioned preference for addictive
drugs
reduce reinforcing effects of food
 Dopamine
might signal
reward/pleasure
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The Dopamine (DA) System

Cell bodies of neurons composing the
brain’s DA system are in two midbrain
nuclei
 Substantia
nigra
 Ventral tegmental area

Two mesotelencephalic DA pathways
 Projecting
from the midbrain to areas in the
telencephalon
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Mesotelencephalic Dopamine
System

Nigrostriatal pathway
 Substantia
nigra > Dorsal striatum
 Degeneration here seen in Parkinson’s

Mesocorticolimbic pathway
 Ventral
tegmental area (VTA) > cortical and
limbic sites
 Involved in reward – VTA > nucleus
accumbens
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Evidence of Dopamine’s Role in
Reinforcing Effects of Drugs




Lab animals will press a level to self-administer
addictive drugs to the nucleus accumbens
Lab animals will develop conditioned place
preferences with microinjections of addictive
drugs to the nucleus accumbens
Addicts only report a high when cocaine is
effectively blocking DA reuptake, increasing
extracellular dopamine
IV amphetamine study – euphoria reported
correlated with DA levels in nucleus accumbens
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Human Studies
PET studies find that many addicts have
reduced cerebral dopamine levels
 Dopamine levels increase when addicts
are exposed to their drug of choice
 Dopamine may be involved in the
expectation of reward, rather than its
experience – a signal, perhaps

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Expectation-of-reward Theory




Dopamine neurons in monkey VTA – respond to
unpredicted reward
An expected reward did not lead to a release of
dopamine
A conditioned stimulus does lead to release of
dopamine
Consistent with dopamine as a signal of a
reward to come, as opposed to a response to a
reward
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Introduction of the Biopsychology
of Emotion
Phineas Gage provides an elegant
demonstration of the brain’s role in
emotion
 Why would a tamping iron through the
skull lead to dramatic changes in
personality?
 Damage to the medial prefrontal lobes

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Darwin’s Theory of the Evolution of
Emotional Expression
 Expressions
of emotion evolve from
behaviors that indicate what an
animal is likely to do next
 If emotional signals are beneficial,
they will evolve to more effectively
communicate and may lose their
original meaning
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Evolution of Emotional
Expression
 Opposite
messages are often
signaled by opposite movements.
“Principle of antithesis”
 Threat displays, for example, are
beneficial – intimidate victims without
the costs and risks of fighting
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Theories of Emotion

James-Lange
 Stimulus
> autonomic/skeletal response > emotion
 Autonomic/skeletal response necessary for emotion

Cannon-Bard
 Stimulus
> autonomic/skeletal response & emotion
 Autonomic/skeletal response independent of emotion

Both of these extreme positions are wrong
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Theories of Emotion
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Bard – Sham Rage
Decorticated cats exhibit extreme and
unfocused aggressive responses
 Hypothalamus must be intact
 Perhaps hypothalamus is needed for
expression of aggression and cortex
serves to inhibit and direct responses
 Papez proposed emotional circuit – limbic
system, that includes hypothalamus

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Copyright © 2007 by Allyn and Bacon
Kluver-Bucy Syndrome
 Rare
cerebral neurological disorder
 Major symptoms - urge to put objects
into mouth, memory loss, extreme
sexual behavior, placidity, visual
distractibility
 Bilateral temporal lobes
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Stress and Health
– reaction to harm to threat
 Stressors – stimuli that cause stress
 Chronic psychological stress – most
clearly linked to ill health
 In the short-term stress is adaptive, in
the long-term it is maladaptive
 Stress
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Selye and the Stress Response
Activation of the anterior-pituitary adrenalcortex system
 Selye neglected the role of the
sympathetic nervous system
 All common psychological stressors are
associated with high levels of
glucocorticoids, epinephrine, and
norepinephrine

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Effects of
Stress
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Stress and Gastric Ulcers
Gastric ulcers – lesions of stomach lining
and duodenum
 More common in those who are stressed
and readily created in the lab
 Ulcers are caused by a bacteria – but it
appears that stress makes the body
susceptible to this bacteria
 75% of healthy subjects have the bacteria

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Psychoneuroimmunology
 Study
of the interaction of
psychological factors, nervous
system, and immune system
 Antigens – cell proteins that identify
them as native or foreign
 Immune system protects with specific
and nonspecific barriers
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Immune System

Nonspecific barriers
 Mucous
membranes
 Phagocytosis – consume and destroy foreign
matter

Specific barriers
 Cell-mediated
(T lymphocytes)
 Antibody-mediated (B lymphocytes)

Lymphocytes – white blood cells
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Copyright © 2007 by Allyn and Bacon
Stress and Immune Function
If stress affects immune function,
how might it do so?
 Why is stress initially adaptive
and then, when chronic, harmful?

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Meta-Analysis of Stress Studies

Effects of stress on immune function
depend on the kind of stress
 Acute
stressor improve immune function
 Chronic stressor impair

Many ways that stress could impact
immune function
 Physiological
 Behavioral
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Why might decreased immune function
not cause an increase in disease?



Redundancy exists in the immune
system
Stress-produced immune changes
in test subjects may be too shortlived to have any impact
Declines in some aspects of
immune function may lead to
compensatory increases in others
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Early Experience of Stress
Early exposure to stress may result in
increased intensity of subsequent stress
responses
 While prenatal stress has a negative
effects, early neonatal stress can have
lasting positive effect – if the stress leads
to increased maternal grooming

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Stress and the Hippocampus
Hippocampus has many glucocorticoid
receptors
 Following stress

 Dendrites
of pyramidal cells are shorter and
less branched
 Adult neurogenesis of granule cells reduced

Effects seen with only a few hours of
stress
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Brain Mechanisms of Emotion
What can fear conditioning tell
us about the brain’s role in
emotion?
 What does the amygdala do for
us?

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Fear Conditioning
 Auditory
fear conditioning blocked
with medial geniculate nucleus (MGN)
lesions – not affected by auditory
cortex lesions
 Critical pathways: MGN to amygdala
 Amygdala lesion blocks fear
conditioning
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Auditory Fear Conditioning
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Contextual Fear Conditioning and
the Hippocampus
Just as fear of an auditory stimulus can be
learned, so can fear of a place
 Hippocampus involved

 Lesion
before conditioning prevents
development of contextual fear
 Lesion after blocks retention of contextual fear
response
 Other fear responses intact
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Role of the Amygdala is Human
Emotion

Structure most frequently associated with
emotion
 Kluver-Bucy
syndrome
 Study of those with amygdalar damage
Damage > problems with recognition of
facial expressions of fear
 Urbach-Wiethe – bilateral amygdala
damage > unable to identify fear

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Emotion
What unique challenges must be
overcome in the study of emotion?
 Why is it important to develop an
understanding of the brain
mechanisms that underlie emotion?

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