Lecture 6
Anxiety Disorders: Etiology
Psycho-Social Factors
Lecture Outline
I. Introduction
II. Learning
A. Learning Theory
B. Socio-cultural factors
III. Cognition
A. Attribution and related theories
B. Network Theories
IV. Conclusions
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I. Introduction
To understand the etiology of Anxiety Disorders, we must look at a
complex interaction of factors: Learning, Physiology, Neurobiology,
Cognition, and more. There is still much to learn about the causes of
these disorders - many questions remain.
As we shall see throughout this course, the manner in which one
conceptualizes the etiology of a disorder has direct and important
implications for how one carries out research and how one conceptualizes
and conducts the treatment of that disorder (discuss Handout 6-1).
In today's lecture we will examine a number of possible
explanations for the Anxiety Disorders: learning theories and cognitive
theories.
II. Learning
A. Learning Theory
Learning Theories of the Anxiety Disorders have a relatively long
history in modern psychology, especially in the branch of psychology
known as behaviorism. John B. Watson, often known as the "father of
behaviorism", was one of the first to demonstrate that fears can be
learned, and in precisely the same manner that other things are learned
in our lives. The important point is that fears, even irrational ones,
are learned - there is nothing mysterious about them.
There are two related issues when we talk about the etiology of the
Anxiety Disorders: 1. What was the initial cause of the learned fear?
and 2. Why does the fear persist once it's learned?
1. Acquisition: Classical Conditioning Model
The idea here is that phobias are learned through "traumatic
conditioning" (Wolpe, 1958) - the person learns to associate a
threatening stimulus with a nonthreatening stimulus, so that
the latter by itself can trigger anxiety.
Some definitions:
US = unconditioned ("unlearned") stimulus (a threatening
stimulus)
UR = unconditioned response (the anxiety response to the US
CS = conditioned ("learned") stimulus (initially a nonthreatening
stimulus, but comes to be threatening)
CR = conditioned response (the learned response to the CS)
If the US is paired with a CS enough times, the CS will
eventually be able to elicit the response that originally
happened just with the US. Here is a diagram to show how this
works...
The Process of Learning:
Stage Process Example (a dog phobia)
-----------------------------------------------------------
Prior to US ---> UR Pain ---> Anxiety
Learning
Learning US ---> UR Pain ---> Anxiety
+ +
CS Dog (eg: dog bites me - pain
associated with sight of the
dog)
Successful CS ---> CR Dog ---> Anxiety
Learning
According to this model, the fear can be "unlearned" by
simply reversing the process. That is, by repeatedly
presenting the CS without the US, eventually the fear will no
longer be elicited by the CS. This is known as the process of
extinction.
2. Maintenance: Avoidance model
The behavioral model of fear acquisition emphasizes the
association of two stimuli: the CS and the US. It follows
from this model that if that association can be broken the
fear will be extinguished. However, for many people, once a
phobia is learned, it is often very resistent to extinction:
Once I learned to be afraid of dogs, I remained afraid for
years. To account for this, we need to look at more than one
factor of learning.
Factor 1: Fear is initially learned through classical conditioning.
Factor 2: Fear is then maintained through avoidance - because the
individual avoids the thing he/she is afraid of, there are no
opportunities for "reality testing" and new learning. As a
consequence, the fear does not extinguish. (eg: I never
learn that most dogs are OK because I never get near enough
to find out).
3. Social Learning
Acquisition and Maintenance of fears is undoubtedly more
complex than mere traumatic conditioning. People learn by
watching others, they don't necessarily need to directly
experience something to learn it. Thus, people also learn
fears by watching what happens to other people. If you grow
up with a father who is deathly afraid of dogs, and you
repeatedly observe his fear reactions when dogs are present,
then it is likely that you too will learn to be afraid of dogs
- this is known as modeling (your father modeled the fear, and
you "picked it up" from him). Similarly, it is likely that an
overanxious parent, say, will subtly communicate fearfulness
to his/her child, thereby planting the seeds of an anxiety
disorder.
There is some interesting animal research on this (see Agras,
1985): in one study, young monkeys who had been raised in a
laboratory (and therefore had no fear of snakes) were allowed
to watch their parents (who had been raised in the wild and
had normal a fear of snakes) react fearfully to toy and real
snakes. After only eight minutes, the young monkeys had
developed a strong fear of snakes.
B. Socio-cultural factors
1. Acquisition: Socialization/Internalization
Another possible explanation for the learning of fears and
phobias is the effect of sex-role stereotyping. Women are
taught to be helpless and dependent which leads them to be
more vulnerable to learn phobic responses (Fodor, 1974). Men,
although they may be fearful, have been taught that "real men"
face their fears.
2. Maintenance: Social Sanctions
Sex-role stereotyping may also explain why phobias maintain
themselves, at least for women (and as we have seen, the
prevalence of anxiety disorders is greater in women). A woman
who tries to break out of the helpless and dependent role and
confront her fears and act assertively may be met by social
sanctions: implicit and explicit disapproval or punishment
from others.
As I list these theories separately I do not mean to imply that either
one or another might someday be found to be the true and correct
explanation of Anxiety Disorders. Although these theories and those we
turn to next are presented in succession, the best explanation of
Anxiety Disorders will undoubtedly combine aspects of each of the
separate theories.
III. Cognition
A. Attribution and related theories
1. Mistaken beliefs: The basic idea here is that our fear is
caused by the things we say to ourselves about the world and
about ourselves. Anxiety arises because we interpret a
stimulus as threatening - the interpretation is more important
than the actual stimulus. There are many theories that are
variations and elaborations on this theme (eg: Beck & Emery,
1985; Ellis & Harper, 1976). They include as the crucial
cognitive variable: irrational thoughts, misinterpretations,
misattributions, and mistaken appraisals. This type of
thinking is characterized by the tendency to catastrophize,
overgeneralize, and magnify the significance of an event.
Ellis and Beck both note that such thinking is often
absolutistic in nature: The person sees things way out of
proportion and only in black or white (a situation is either
Very Bad or Very Good). One of the major anxiety producing
cognitions seems to be the belief that one has lost control
over the situation and one's own reactions (Barlow, 1988).
This diagram illustrates the chain of events:
Stimulus ----> Interpretation ----> Anxiety
Some researchers (eg: Lazarus, 1984) suggest that the
interpretive/attribution/appraisal process may occur
unconsciously or automatically in certain situations, making
this process all the more complex (certainly more difficult to
study, not to mention treat!). Such unconscious/automatic
processing would explain why irrational beliefs persist - they
never really make themselves available for rational, conscious
scrutiny and correction.
2. Generalized Arousal: Attribution theories and their
variants first became popular with the work of Stanley
Schachter in the 60's (eg: Schachter, 1964). Schachter's
theory of anxiety (actually, of emotion in general) includes a
biological component: An event will trigger a generalized,
undifferentiated state of physiological arousal ("a kind of
bubbling physiological soup"! [Lang, 1979, p. 507]). Which
emotion is experienced depends on how you then appraise the
arousal (dangerous, good, bad, loving...). So, the process
looks like this:
S ----> Generalized Arousal ----> Appraisal ----> Emotion
(anxiety...)
The concept of Generalized Arousal, although initially a
promising attempt at bringing cognition and biology together,
has not in fact been supported by research evidence (even
though many textbook fail to mention this). Rarely is there a
generalized arousal; rather, the various indices of arousal
(sweating, heart rate, blood pressure, etc) can vary in
independent ways (Schwartz, 1986). In addition, there is now
quite reliable evidence that the emotions are in fact
physiologically differentiated. Variables such as heart rate,
facial EMG (measures of muscle activity) and blood pressure
differ across the various emotions. For example, diastolic
blood pressure (ie: as the heart fills with blood) is higher
in anger than in fear (Schwartz, 1986). Even within the
category of anxiety, there are differences: skin conductance
(sweating) and blood pressure indices are highest in panic and
agoraphobia, whereas these indices are not particularly high
in simple phobias (Zahn, 1986). In addition, the concept of
generalized arousal doesn't make sense given the evidence that
people will sometimes say that they are anxious and even act
anxious, yet not be physiologically aroused (Lang, 1968).
3. Self-Fulfilling Prophecies: It may seem strange that
someone would so tenaciously hold onto and continue making
misattributions that cause so much distress. We've noted that
one reason for this may be that the whole process goes on
automatically and unconsciously. An additional reason may be
that it is our beliefs that allow us to make sense out of the
world. They're part of our self-concept and our world view,
and to change them means changing all that. As long as we
stick with our beliefs, no matter how distressing they may be,
they provide us with a sense of stability: They bias what we
see in such a way as to make what we see consistent with our
self-concept and world view - a self fulfilling prophecy. To
do away with these beliefs would mean jeopardizing that
stability for an unknown and unpredictable world (Wegner &
Vallancher, 1977).
B. Network Theories
Much of what we are discussing has been elaborated by
associative network models of emotion (eg: Bower, 1981; Foa &
Kozak, 1985; Lang, 1979). The basic idea: Fear is a network of
concepts, tendencies, or informational nodes stored in memory that
represent stimuli, responses, and their meanings. Think of what a
network is: a bunch of things all connected, somehow related.
Human memory can be modeled in terms of a network (see, for
example, Bower, 1981). Each event and experience (including
emotions) is represented in memory as a cluster of descriptive
thoughts, beliefs, ideas, or what we can call "nodes". Now, what
is important is that each of these nodes are connected to other
related nodes. So, "school" node is connected to "exams" node in
my mental network. If I think of "school", it is much more likely
that I will think of "exams" than if I didn't think of "school".
When one of these thoughts, feelings (or other nodes) comes to
consciousness, it is said to be activated. And once activated,
other nodes nearby in the network are likely to be activated.
Handout 6-2 illustrates a possible network for an emotion.
"Emotion 3" is connected to various other nodes: nodes representing
thoughts, behaviors, physiological patterns, events, and so on that
have to do with "emotion 3".
From this network perspective, fear is seen as residing in a
network, made up of nodes which are all associated or connected, so
activation of one node makes others more likely to be activated.
Fear isn't a simple process where one thing leads to another, but
rather a complex network of things. The more of the network
activated, the more likely fear will occur. And fear can begin at
various places - beliefs, physiology, response patterns - all parts
of the network.
This network then is like a computer program that, when run,
outputs fear behavior.
The network is generally thought to be learned, bit by bit,
although some aspects of it may be innate (Barlow, 1988) [and as we
shall see in our discussion next time of "preparedness"].
Abnormal fear networks differ from normal ones in a number of
important ways (Steketee & Foa, 1985):
1. Re: the stimulus: erroneous attributions/appraisals of
threat
2. Re: meaning: unusually high fearfulness associated with an
event
3. Re: responses: excessive response elements, such as
avoidance behaviors
4. Re: treatment: resistent to modification
Why resistant?:
a) processing is unconscious
b) impairment of physiological, neurological or
cognitive processes
c) failure to access the fear network, or only
incomplete access - eg: access just cognitions, not
physiological components. Such incomplete accessing
has been argued to lead to incomplete "emotional
processing" - ie: the fear doesn't subside or become
absorbed, but persists unduly long (Rachman, 1980).
IV. Conclusions
As is becoming clear, there are "multiple pathways" (Barlow, 1988)
to Anxiety Disorders. Today we have discussed some of these paths:
1. Learning
2. Social Factors
3. Attributions
4. Network Theories
A question to begin pondering: "Are patients and nonpatients
qualitatively different from one another, or just quantitatively
different?" We often think of an abnormal person as somehow
qualitatively different than us. It may, in fact be simply a matter of
degree.
In the next lecture, we will continue our discussion of the
etiology of anxiety.