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 ------------------------------------------- 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.