Biological preparedness helps explain this easily acquired phobia

Biological preparedness helps explain this easily acquired phobia

This factor helps explain why rats don't learn to associate a visual stimulus with illness. Biological preparedness helps explain the easily acquired phobia. Phobia. Extreme, irrational fear of a specific object animal or situation..; Subjects Preparedness theory is one of the most influential ideas in explaining the origin of specific phobias. The theory proposes that fear conditioning is selective to animals that have posed a threat to survival throughout human evolution, and that acquired fear memories to such threats are resistant to blogger.com by: 13 May 10,  · For example, it has been suggested that biological preparedness explains why certain types of phobias tend to form more easily.   We tend to develop a fear of things that may pose a threat to our survival, such as heights, spiders, and snakes. Those who learned to fear such dangers more readily were more likely to survive and blogger.comted Reading Time: 3 mins

Cognitive processes during fear acquisition and extinction in animals and humans

Try out PMC Labs and tell us what you think. Learn More, biological preparedness helps explain this easily acquired phobia. Department of Psychology, Boston University, Beacon Street, 6th Floor, Boston, MAUnited States. Anxiety disorders are highly prevalent. Fear conditioning and extinction learning in animals often serve as simple models of fear acquisition and exposure therapy of anxiety disorders in humans.

This article reviews the empirical and theoretical literature on cognitive processes in fear acquisition, extinction, and exposure therapy. It is concluded that exposure therapy is a form of cognitive intervention that specifically changes the expectancy of harm. Implications for therapy research are discussed. Anxiety disorders, such as social phobia, specific phobias, panic disorder, and post-traumatic stress disorder are among the most common mental disorders in the population.

The most effective strategies for treating biological preparedness helps explain this easily acquired phobia disorders include exposure therapy with or without cognitive strategies, and pharmacotherapy, such as selective serotonin reuptake inhibitors for a review, see Barlow, Exposure therapy is rooted in behaviorism and learning theories in psychology that began in the early s Watson, Especially influential was Mowrer who hypothesized that fears are acquired through repeated presentations of a neutral stimulus conditioned stimulus; CS and a pain-producing or fear-eliciting stimulus unconditioned stimulus; US.

He observed that the strength of the fear response in rats is determined by the number of repetitions of association between the CS and US, biological preparedness helps explain this easily acquired phobia, and the intensity of the unconditioned response.

Mowrer further noted that the repeated presentation of the CS in the absence of the US leads to extinction, the gradual decrease of the conditioned response.

For example, Davis et al. In this review, I will biological preparedness helps explain this easily acquired phobia the processes of fear acquisition and extinction learning and will later discuss novel pharmaceutical approaches to enhance the extinction processes during exposure therapy.

Animal research suggests that extinction is a form of acquired inhibition that suppresses a fear response. In other words, extinction is probably not simply an unlearning or forgetting but rather a new form of learning that changes the CS-US contingency in such a way that the CS no longer signals an aversive event and thereby inhibits the expression of the fear response e. Laboratory studies implicate the amygdala during fear extinction. It will be argued that extinction learning and exposure therapy are forms of cognitive intervention that specifically changes harm expectancy.

It should be noted that I will not present an exhaustive review of learning processes, but rather a focused, clinically relevant discussion of models that are derived from Pavlovian conditioning and their associations with cognitive theory and therapy.

The idea that direct conditioning is primarily responsible for fear acquisition in humans was the dominant view for many decades. For example, the study of Little Albert by Watson and Rayner has frequently been used as an biological preparedness helps explain this easily acquired phobia of fear conditioning in humans. In the experiment, Watson and Biological preparedness helps explain this easily acquired phobia first presented Little Albert, an month old orphan with several objects including a rat, a rabbit, a fur coat, and a dog.

Little Albert did not show any signs of fear or other negative emotional reactions towards these objects, biological preparedness helps explain this easily acquired phobia. However, the infant cried in response to the US, which was a loud noise made by banging a heavy hammer against a steel bar.

During the conditioning trial, the experimenters presented the infant with a rat CS. Each time the infant reached for the rat, biological preparedness helps explain this easily acquired phobia, the US was also presented. After seven trials over the course of 1 week, the subject was presented with only the rat. As predicted, the boy exhibited signs of fear and avoidance.

The experimenters then presented Albert with other hairy objects, biological preparedness helps explain this easily acquired phobia, including a rabbit, a fur coat, and a dog. The boy reacted similarly distressed to each of these objects, suggesting that the response generalized to other objects with hair.

A similar reaction was observed 5 days and, to a lesser degree, 31 days after the initial conditioning trial. When the subject was tested in a different context by moving him to a different room the fear response was still noticeable but significantly decreased.

Other authors, however, identified a number of methodological limitations that make the findings ambiguous and difficult to interpret. A more in depth critique of Little Albert and its relevance to classical fear conditioning can be found in Harris For example Rescorla assumed that the crucial aspect in conditioning is the information that one stimulus gives about another i.

According to this view, conditioning only occurs if the probability of the US in the presence of the CS is different than in its absence. Other theorists, in contrast, argue that contingency is neither necessary nor sufficient for conditioning e.

In addition to traditional Pavlovian conditioning, fear can also be acquired without directly experiencing the CS and US. For example, Mineka and colleagues demonstrated that young Rhesus monkeys learn quickly to acquire a fear of snakes simply by observing another monkey responds fearfully to them. Similarly, observing another monkey responding nonfearfully can effectively prevent the acquisition of this fear following later exposure to models behaving fearfully e.

In other words, fear can be acquired by observing two events contiguous in time: the snake and the fear response to the snake exhibited by another monkey. Moreover, fear can be prevented or inhibited through observation, suggesting the involvement of higher-order cognitive processes. Common fears are not randomly distributed. For example, cars are considerably more dangerous to pedestrians than are dogs or snakes.

This had led some researchers to assume that animals and humans specifically acquire fears of objects that were once potentially harmful or dangerous e. This model was developed to explain the rapid acquisition and seeming irrationality of common phobias, biological preparedness helps explain this easily acquired phobia, as well as their high resistance to extinction.

Phobic fear was seen as a noncognitive and irrational response that is fundamentally different from conditioned fear in the laboratory Seligman, However, a number of experimental studies question the validity of various postulations of the model see McNally,for a review.

For example, latent inhibition has been used to explain the belongingness between stimuli and fear response. Latent inhibition is the phenomenon that simple prior exposure to a CS before the CS and US are ever paired together reduces the amount of subsequent conditioning to the CS when paired with the US e.

Another postulation by the model that has not been supported is the assumption that fear acquisition of prepared stimuli is a primitive form of learning with little cognitive involvement. For example, Dawson, Shell, and Banis measured skin conductance response and US expectancy online i. The results showed that US expectancy ratings mirrored skin conductance response and both measures suggest the same resistance to extinction effect.

Similar findings were also reported by Davey The author argued that the heightened expectation of aversive outcomes following the presentation of feared stimuli may generate and maintain a learned association between fear and expectation.

This cognitive bias could explain why some stimuli, but not others, become associated with aversive outcomes Davey, Learning through verbal communication and observation seems to be particularly common in humans e. As a result, theorists have considered modifications of the simple conditioning models to explain how fear in humans can be acquired. These modifications place a particular emphasis on cognitive processes.

The indirect pathway allows for conditioning to occur even when CS and US are separated in time, as long as the subject learns the relationship between events Rachman, However, a number of other retrospective and prospective studies raised questions about the validity of this model.

Furthermore, when giving the choice, most phobic individuals choose panic attacks as the most important reason for their phobia Hofmann et al. Some studies defined a conditioning event as the CS-US pairing in which the US is a potentially harmful or traumatizing event such as a car accident or dog bite. In contrast, others used a more liberal definition and considered a panic attack as a possible US in the presence of the CS e. This obviously raises the important question why uncued panic attacks happen in the first place for a discussion, see Bouton et al.

Öhman and Mineka present evidence for a selective associative model and the existence of an evolutionarily evolved fear module that shows four characteristics, each shaped by evolutionary contingencies: 1 selectivity with regard to the input i. A further elaboration of the contemporary learning theory perspective on the etiology of anxiety disorders was provided by Mineka and Zinbarg This model assumes that, aside from direct or vicarious traumatic conditioning experiences, a number of other factors influence CS-US conditioning.

These factors include the perceptions of controllability and predictability of stressful events, the properties of the CS such as fear relevance, temporal proximity to stressful events, etc. The case of post-traumatic stress disorder PTSD might illustrate some of these factors. PTSD is the only anxiety disorder that includes a direct conditioning event in its diagnostic definition. Consistent with the conditioning model, war veterans with PTSD who are exposed to trauma cues by watching a video clip of a combat scene typically show intense emotional responses that are elicited by the specific trauma cues, which are the conditioned stimuli that were previously paired with the traumatic event e.

However, exposure to trauma is not sufficient to develop PTSD. Although the majority of individuals in a large community sample These data suggest that trauma exposure is not sufficient to develop PTSD.

The modern learning perspective of fear acquisition by Öhman and Mineka and Mineka and Zinbarg places a particular emphasis on cognitive processes, such as the controllability and predictability of the aversive event. At the same time, however, Öhman and Mineka assume that the fear module is impenetrable to conscious cognitive control i. In other words, once confronted with a snake, the fear module of a snake phobic is activated and cannot be aborted easily by any cognitive strategies.

Öhman and Mineka hypothesize that the fear module originated and is neurologically located in the subcortical areas of the brain, especially the limbic structure. However, Öhman and Mineka caution that the encapsulation assumption should not be taken to imply that cognitions are unimportant in phobias, because the amygdala, the neural node of the fear network in humans, is reciprocally connected with areas of the frontal lobe that serve to regulate emotions.

Therefore, the fear circuitry in rats suggests that the amygdala and its projections are involved biological preparedness helps explain this easily acquired phobia both the acquisition and expression of conditioned fear e. In sum, the simple Pavlovian conditioning model Mowrer, ; Watson, shows a number of significant weaknesses as a model of fear acquisition in humans.

As a result, a number of alternative models were discussed, including the preparedness theory e. Bouton et al. As pointed out by McNally bnone of these theories can fully account for all cases, and some of them became so complex that it has been difficult to test them in the laboratory, let alone in clinical practice.

Common features of contemporary theories of fear acquisition include the consideration of temperamental variables, such as anxiety sensitivity McNally, aand cognitive processes. These cognitive processes are evident in observational and informational learning, as well as during direct conditioning events. Specifically, it has been demonstrated that US expectancies and the perception of controllability and predictability about stressful events are essential aspects of fear conditioning in humans.

For the remainder of this discussion, I will refer to US expectancies and the perception of controllability and predictability of future events as cognitive processes.

The goal is to identify these processes in extinction learning and exposure therapy and to discuss the implications for clinical research. It remains unclear whether these cognitive processes causally implicate fear mechanisms or whether they are simply epiphenomenal correlates to the actual mediator. Nevertheless, there is sufficient evidence to conclude that extinction learning and exposure therapy are not simply automatic, unconscious, and low-level processes.

Instead, higher-order cognitive processes that modulate harm expectancy and the perception of control are closely linked to extinction learning and exposure therapy.

Therefore, although often attempted in treatment component analyses, I will conclude that it is impossible to conduct successful exposure therapy without also changing these cognitive processes. Fear acquisition and extinction involve the learning of associations between passively observed events. It is typically assumed that animals only learn about causal relations by using basic associative mechanisms.

Causal reasoning allows the animal to predict outcomes on the basis of observation.

Phobia, Causes, Signs and Symptoms, Diagnosis and Treatment.

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May 10,  · For example, it has been suggested that biological preparedness explains why certain types of phobias tend to form more easily.   We tend to develop a fear of things that may pose a threat to our survival, such as heights, spiders, and snakes. Those who learned to fear such dangers more readily were more likely to survive and blogger.comted Reading Time: 3 mins This “preparedness theory” (Seligman, ) was an early attempt to explain human fears in the context of evolutionary psychology. The theory (also known as the “selective association model”) states that humans are biologically “prepared” to acquire the fear of certain objects or situations that used to threaten the survival of our blogger.com by: This factor helps explain why rats don't learn to associate a visual stimulus with illness. Biological preparedness helps explain the easily acquired phobia. Phobia. Extreme, irrational fear of a specific object animal or situation..; Subjects