Phobias and Preparedness Theory - Essay Example

Running Head: PHOBIAS AND PREPAREDNESS THEORY Phobias and Preparedness Theory [The [The of the Institution] Phobias and Preparedness Theory There is an evolutionary predisposition for humans to acquire fears of angry, critical, or rejecting faces. According to the preparedness theory of phobias, humans have a biologically based predisposition to fear objects or situations that once threatened the survival of the species throughout its evolutionary history. (Seligman, 1971) Thus, individuals who easily developed fears of dangerous objects or situations could have had a selective advantage in the struggle for survival. Furthermore, it is theorized that social anxiety disorder, like specific phobias, develops as a consequence of one or more traumatic conditioning experiences. The gaze aversion demonstrated by individuals with social anxiety disorder also makes sense in light of preparedness theory. Direct eye contact seems to be very frightening or threatening among our close relatives, the primates. Although this response is greatly altered by contextual and learning factors among humans, experimental evidence shows that angry faces directed at the individual are highly salient. Thus, one can avoid the threat of angry, critical, or rejecting faces by looking away. In a critical review of experimental literature, McNally (1987) posed some strong challenges to the preparedness theory of phobias. According to preparedness theory, phobias are supposed to be rapidly acquired, irrational, highly resistant to extinction, and differentially associable with stimuli of evolutionary significance (Seligman, 1971). However, McNally indicated that the rate at which phobias are acquired varies widely. He also argued that phobic avoidance is not necessarily irrational in those who fear anxiety and its consequences. Thus, although socially anxious persons recognize they have no physical threat to avoid, they are avoiding the likelihood of becoming extremely anxious in encountering a feared situation. McNally also showed that, while skin conductance responses established to fear-relevant CSs are highly resistant to extinction in laboratory conditioning, behavioral treatment research demonstrates that "prepared" phobias are eliminated at least as easily as "unprepared" ones, with fears of heights and of animals among the easiest phobias to treat through exposure therapy. Furthermore, several alternative explanations for the experimental resistance to extinction effect need to be tested. McNally asserted that only one of the original assumptions of preparedness theory remains unaltered by the data and critical analyses: Most phobias are associated with threats of evolutionary significance. Other plausible hypotheses for experimental findings that need to be ruled out are ontogenetic (i.e., cultural) preparedness, stimulus significance (preparedness effects occur because fear-relevant stimuli are more significant than fear-irrelevant stimuli), and CS prepotency (humans are innately predisposed to respond with high levels of attention and arousal, not necessarily fear, to stimuli of evolutionary significance). The pattern of initial vigilance for highly aversive information, followed by avoidance, is of potential clinical significance because it may promote the conditions under which sensitization, rather than extinction (or fear reduction), takes place (Marks, 1989). Consequently, it may play an important role in the maintenance of excessive fear and anxiety. If so, this suggests it would be therapeutically helpful to target specifically this subsequent cognitive avoidance because avoidant processing may impede an individual's ability to reevaluate the threat stimulus and to reappraise it as less threatening. Thus, secondary avoidance strategies may interfere with cognitive treatment interventions. Experiments on traumatic stimulation in humans are not fully supportive of classical conditioning of fears. de P. Silva, Rachman S., & Seligman M. ( 1977) were able to condition fears in humans through electric shock pairings, but they were weak, incomplete, and transient. However, these weak results may arise from insufficiently severe "traumas" in the laboratory setting. Fear is conditioned in humans with more intense stimuli, of which naturalistic examples include the development of anticipatory nausea and vomiting due to chemotherapy or fears of drugs due to negative or allergic reactions during drug ingestion ( Siddle & ' Bond, 1988). Furthermore, the basic principle of classical conditioning is supported by reports of traumatic onset for phobias. For example, Lautch ( 1971) reported that every one of 34 dental phobics related the onset of his or her phobia to a traumatic dental experience. st and Hugdahl ( 1981, 1983) found that 88% of agoraphobics attributed their disorder to a traumatic experience, as did 69% of claustrophobics, 48% of animal phobics, and 58% of social phobics. Withers and Deane ( 1995) found 77.5% of nonclinical individuals who had clear memories of onset attributed their strongest fears to direct conditioning experiences. In contrast, other studies show that traumatic experiences are equally common among nonphobic persons. It was found that two thirds of dog phobic as well as nonphobic groups had experienced traumatic incidents with dogs. Furthermore, several studies fail to find evidence for traumatic incidents as significant precursors to fears and phobias. Inconsistencies across studies are due in large part to their retrospective nature and imprecise questioning. Cognitive therapy assumes that emotions are based on cognitive processes that can be corrected or manipulated via conscious reasoning. McNally ( 1987) asserted that cognitive therapies are unlikely to be effective due to the unconscious and involuntary nature of anxious cognitive processes. Verbal mediation is necessary but not sufficient to correct primal or automatic modes of information processing. One of the most effective ways of deactivating the primal threat mode is to counter it with more elaborative, strategic processing of information resulting from the activation of the constructive, reflective modes of thinking. Indeed, there is evidence that elaborative cognitive processes, such as those rehearsed in cognitive therapy, can override involuntary, automatic processes. For example Siddle and Bond ( 1988) cite evidence showing that instructions alone alter conditioned responses. Cognitive therapy is effective for many anxiety disorders. Safety signals, or conditioned inhibitors, signal the absence of the aversive unconditional stimulus, or, in other words, signal safety. Common safety signals for anxiety disorder patients are the presence of another person, medications, and food or drink. Although providing relief and enabling confrontation with feared stimuli in the short term , safety signals contribute to fear and avoidance behavior over the long term (Siddle & Bond, 1988). Medications can be safety signals even when not consumed, because their availability reassures the individual that the dangers of extreme fear are controllable. At the same time, however, attribution of safety to medications impedes correction of misperceived danger. Thus, anxiolytics may be detrimental to behavioral therapy to the extent that they assume the function of safety signals. Again, direct investigation of this hypothesis is yet to be conducted. An interesting caveat arises with respect to safety signals in that they tend to lose their inhibitory properties with the passage of time. Thus, conceivably, occasions when anxiolytics inexplicably lose their effectiveness over time may be in part due to gradual depletion of their power to signal safety. Trait anxiety is associated with increased estimates of risk for all negative events whereas state anxiety is associated with increased risk estimates for specific threats. Support for the notion of entrenchment of cognitive biases with the onset of anxiety disorders derives from findings that whereas non-clinically anxious individuals are able to override automatic processing of threat stimuli of which they are aware (Lovibond, P.E., Siddle, D.A.T. & Bond, N. (1993), clinically anxious populations retain selectivity of attention to conscious as well as preconscious threat stimuli. Treatments that fail to reduce fears of bodily sensations have higher rates of relapse. On the other hand, as noted earlier, Williams and colleagues find that self-efficacy predicts changes in agoraphobic behavior over and above the effects of shifts in catastrophic cognitions. With respect to social phobia, Mattia, Heimberg, and Hope ( 1993) showed that responders to cognitive-behavioral treatment, medications, and placebo had significant reductions in modified Stroop response latencies for social threat words. Also, changes in Fear of Negative Evaluation scores and Irrational Beliefs Test scores predict outcome for social phobics treated with cognitive therapy, behavioral therapy, or a combination of the two. Indeed, changes in Fear of Negative Evaluation scores account for most outcome variance. On the other hand, this test is considered by some to be a measure of anxiety rather than cognition approximately 65% of outcome variance was unexplained, suggesting that factors other than cognitive modification are important as well. Most of the research on cognitive mediation of treatment effects pertains to generalized anxiety disorder. Recovered generalized anxiety disorder patients interpret ambiguous statements in much the same way as controls, with relatively benign meanings, in comparison to currently anxious patients. Also, recovered patients are more likely to complete stems of words with neutral than with threatening words in comparison to currently anxious patients. Individuals often engage in disorder-maintaining safety-seeking behaviors during panic attacks. These behaviors typically include some kind of escape or avoidance. Avoidance and escape behaviors can include frank agoraphobic avoidance, taking benzodiazapines, and subtle safety-seeking behaviors. Safety-seeking behaviors tend to provide immediate anxiety relief but maintain the disorder. Individuals who are afraid of a mental collapse during attacks may do any of the following. They may touch the ground, pinch themselves, look for signs that their perception is not crazy by scanning the visual field, or attempt to suppress disturbing cognitions. Those individuals who are afraid of losing control and embarrassing themselves during attacks often isolate themselves from others. During panic attacks, individuals with any catastrophic cognition may look for an escape route or ask for help. The learned helplessness hypothesis accounts for this pattern of results by assuming that subjects learn the contingency to which they are exposed during pretreatment and respond accordingly during testing. Specifically, unpredictable, uncontrollable shock is assumed to represent the area in an instrumental contingency space which corresponds to response-reinforcer independence. Subjects learn the independence between responding and shock termination during exposure to inescapable shock and develop an expectation that future events will be similarly uncontrollable. This expectation of helplessness works in two ways to impair later escape performance. First, learning that responding and outcomes are independent proactively interferes with the learning of the positive escape contingency that exists during testing. Second, the expectation that responding will be ineffective in modifying test shocks reduces the motivation to engage in the type of instrumental behavior that would increase contact with the escape contingency. Thus, the expectation of helplessness serves as a cognitive mediator of later associative and motivational deficits. Learned helplessness theory made an important contribution to the study of stress effects in several ways. Differential pathology following experience with an aversive event was tied directly to a definable experimental contingency. The explanation for performance deficits was simple and internally consistent. Moreover, Seligman's ( 1971) elaboration on the emotional impact of uncontrollable aversive events served to stimulate research on the environmental causes of depression and related pathology. References de P. Silva, Rachman S., & Seligman M. ( 1977). "Prepared phobias and obsessions: Therapeutic outcome". Behaviour Research and Therapy, 15, 65-77. Hugdahl K., & hman A. ( 1977). "Effects of instruction on acquisition and extinction of electrodermal responses to fear-relevant stimuli". Journal of Experimental Psychology: Human Learning and Memory, 3, 608-618. Lautch H. ( 1971). "Dental phobia". British Journal of Psychiatry, 119( 549), 151-158. Marks, I. M. (1989). Learning of Fear. In I.M.Marks, "Fears, Phobias and Rituals", New York: Oxford University Press. Mattia J. I., Heimberg R. G., & Hope D. A. ( 1993). "The revised Stroop color-naming task in social phobics". Behaviour Research and Therapy, 31(3), 305-313. McNally, R.J. (1987). Preparedness and Phobias: A Review. 'Psychological Bulletin', 101, 283-303. Seligman, M.E.P. (1971). Phobias and preparedness. "Behavior Therapy, 2", 307-320. Lovibond, P.E., Siddle, D.A.T. & Bond, N. (1993) Resistance to extinctionof fear-relevant stimuli: Preparedness or selective sensitization. "Journal of Experimental Psychology, 122" 449-461. Siddle D. A.T., & Bond N. W. ( 1988). Avoidance learning, Pavlovian conditioning, and the development of phobias. Biological Psychology, 27, 167-183. Withers R. D., & Deane F. P. ( 1995). Origins of common fears: Effects of severity, anxiety responses and memories of onset. Behaviour Research and Therapy, 33, 903-915. Read More