A person who has had good experiences with a potentially phobic stimulus, such as the little girl playing here with her dog, is likely to be immunized from later acquiring a fear of dogs even if she has a traumatic encounter with one.
Events that occur during a conditioning experience, as well as before it, are also important in determining the level of fear that is conditioned. For example, experiencing an inescapable and uncontrollable event, such as being attacked by a dog that one cannot escape from after being bitten, is expected to condition fear much more powerfully than experiencing the same intensity of trauma that is escapable or to some extent controllable (e.g., by running away after the attack; Mineka, 1985a ; Mineka & Zinbarg, 1996 , 2006 ). In addition, the experiences that a person has after a conditioning experience may effect the strength and maintenance of the conditioned fear (Rescorla, 1974 ; White & Davey, 1989 ). For example, the inflation effect suggests that a person who acquired, a mild fear of driving following a minor crash might be expected to develop a full-blown phobia if he or she later were physically assaulted, even though no automobile was present during the assault (Dadds et al., 2001 ; Mineka, 1985b ; Mineka & Zinbarg, 1996 , 2006 ). Even verbal information that later alters one’s interpretation of the dangerousness of a previous trauma can inflate the level of fear (e.g., being told, “You’re lucky to be alive because the man who crashed into your car last week had lost his license due to a record of drunk driving leading to fatal car crashes”; Dadds et al., 2001 ). Another way in which fear of a CS can be inflated following conditioning is if the organism later is exposed to uncontrollable stress (Baratta et al., 2007 ). These examples show that the factors involved in the origins and maintenance of fears and phobias are more complex than suggested by the traditional, simplistic conditioning view, although they are nevertheless consistent with contemporary views of conditioning (Mineka & Oehlberg, 2008 ; see also Coelho & Purkis, 2009 ; Laborda & Miller, 2011 ).
It has also been shown that our cognitions, or thoughts, can help maintain our phobias once they have been acquired. For example, people with phobias are constantly on the alert for their phobic objects or situations and for other stimuli relevant to their phobia (McNally & Reese, 2009 ). Nonphobic persons, by contrast, tend to direct their attention away from threatening stimuli (see Mineka, Rafaeli, & Yovel, 2003 ). In addition, phobics also markedly overestimate the probability that feared objects have been, or will be, followed by frightening events. This cognitive bias may help maintain or strengthen phobic fears with the passage of time (Muhlberger et al., 2006 ; Öhman & Mineka, 2001 ; Tomarken, Mineka, & Cook, 1989 ).
Evolutionary Preparedness for Learning Certain Fears and Phobias Consider the observation that people are much more likely to have phobias of snakes, water, heights, and enclosed spaces than of motorcycles and guns, even though the latter objects may be at least as likely to be associated with trauma. This is because our evolutionary history has affected which stimuli we are most likely to come to fear. Primates and humans seem to be evolutionarily prepared to rapidly associate certain objects—such as snakes, spiders, water, and enclosed spaces—with frightening or unpleasant events (e.g., Mineka & Öhman, 2002 ; Öhman, 1996 ; Seligman, 1971 ). This prepared learning occurs because, over the course of evolution, those primates and humans who rapidly acquired fears of certain objects or situations that posed real threats to our early ancestors may have enjoyed a selective advantage. Thus “prepared” fears are not inborn or innate but rather are easily acquired or especially resistant to extinction. Guns and motorcycles, by contrast, were not present in our early evolutionary history and so did not convey any such selective advantage.
There is now a large amount of experimental evidence supporting the preparedness theory of phobias. In one important series of experiments using human subjects, Öhman and his colleagues (see Öhman, 1996 ; Öhman, 2009 ; Öhman & Mineka, 2001 , for reviews) found that fear is conditioned more effectively to fear-relevant stimuli (slides of snakes and spiders) than to fear-irrelevant stimuli (slides of flowers and mushrooms). These researchers also found that once the individuals acquired the conditioned responses to fear-relevant stimuli, these responses (including activation of the relevant brain area, the amygdala) could be elicited even when the fear-relevant stimuli (but not the fear-irrelevant stimuli) were presented subliminally (i.e., presentation was so brief that the stimuli were not consciously perceived; e.g., Carlsson et al., 2004 ; Öhman et al., 2007 ). This subliminal activation of responses to phobic stimuli may help to account for certain aspects of the irrationality of phobias. That is, people with phobias may not be able to control their fear because the fear may arise from cognitive structures that are not under conscious control (Öhman & Mineka, 2001 ; Öhman & Soares, 1993 ).
Another series of experiments showed that lab-reared monkeys in a vicarious conditioning paradigm can easily acquire fears of fear-relevant stimuli such as toy snakes and toy crocodiles but not of fear-irrelevant stimuli such as flowers and a toy rabbit (Cook & Mineka, 1989 , 1990 ). Thus, both monkeys and humans seem selectively to associate certain fear-relevant stimuli with threat or danger. Moreover, these lab-reared monkeys had had no prior exposure to any of the stimuli involved (e.g., snakes or flowers) before participating in these experiments. Thus, the monkey results support the evolutionarily based preparedness hypothesis even more strongly than the human experiments. For example, human subjects (unlike the lab-reared monkeys) might show superior conditioning to snakes or spiders because of preexisting negative associations to snakes or spiders rather than because of evolutionary factors (Mineka & Öhman, 2002 ).
Biological Causal Factors
Genetic and temperamental variables affect the speed and strength of conditioning of fear (e.g., Gray, 1987 ; Hettema et al., 2003 ; Oehlberg & Mineka, 2011 ). That is, depending on their genetic makeup or their temperament and personality (all of which are clearly related; see Chapter 3 ), people are more or less likely to acquire fears and phobias. For example, Lonsdorf and colleagues ( 2009 ) found that individuals who are carriers of one of the two variants on the serotonin-transporter gene (the s allele, which has been linked to heightened neuroticism) show superior fear conditioning relative to individuals who do not carry the s allele. However, those with one of two variants of a different gene (the COMT met/met genotype) did not show superior conditioning but did show enhanced resistance to extinction (see also Lonsdorf & Kalisch, 2011). Relatedly, Kagan and his colleagues ( 2001 ) found that behaviorally inhibitedtoddlers (who are excessively timid, shy, easily distressed, etc.) at 21 months of age were at higher risk of developing multiple specific phobias by 7 to 8 years of age than were uninhibited children (32 versus 5 percent). The average number of reported fears in the inhibited group was three to four per child (Biederman et al., 1990 ).
Several behavior genetic studies also suggest a modest genetic contribution to the development of specific phobias. For example, a large female twin study found that monozygotic (identical) twins were more likely to share animal phobias and situational phobias (such as of heights or water) than were dizygotic (nonidentical) twins (Kendler et al., 1999b ). Very similar results were later also found for men (Hettema et al., 2005 ). However, the same studies also found evidence that nonshared environmental factors (i.e., individual specific experiences not shared by twins) also played a very substantial role in the origins of specific phobias, a result that supports the idea that phobias are learned behaviors. Another study found that the heritability of animal phobias was separate from the heritability of complex phobias such as social phobia and agoraphobia (Czajkowski et al., 2011).
A form of behavior therapy called exposure therapy —which is the best treatment for specific phobias—involves controlled exposure to the stimuli or situations that elicit phobic fear (Choy et al., 2007 ; Craske & Mystkowski, 2006 ). Clients are gradually placed—symbolically or increasingly under “real-life” conditions—in those situations they find most frightening. In treatment, clients are encouraged to expose themselves (either alone or with the aid of a therapist or friend) to their feared situations for long enough periods of time so that their fear begins to subside. One variant on this procedure, known as participant modeling, is often more effective than exposure alone. Here the therapist calmly models ways of interacting with the phobic stimulus or situation (Bandura, 1977 , 1997 ). These techniques enable clients to learn that these situations are not as frightening as they had thought and that their anxiety, while unpleasant, is not harmful and will gradually dissipate (Craske & Mystkowski, 2006 ; Craske & Rowe, 1997 ). The new learning is probably mediated by changes in brain activation in the amygdala, which is centrally involved in the emotion of fear.