What causes phobias?
For many years, it has been believed that we acquire our fears and phobias through a process of conditioning: that is, we learn them through a traumatic experience, usually in childhood. (To refresh your memory on conditioning, see pages 17—22.) Imagine, for example, that you are walking to school and a large and very aggressive dog suddenly leaps up from behind a garden fence. Fortunately, the animal is unable to escape the garden. But the incident leaves you with a deep fear of dogs; you have only to glimpse one to feel again the terror you experienced that morning long ago. Consequently, you avoid dogs at all costs — and thus fail to discover that the chances of being hurt are minimal.
Conditioning is still a useful theory. Innumerable laboratory experiments have demonstrated that it is a very effective way of inducing fear in both animals and humans (the most famous of these experiments involved Little Albert; you can read about it on p. 18). Moreover, many people with phobias do indeed trace them back to an early traumatic incident (though we might wonder whether their accounts are always accurate: in many cases, they are attempting to recall experiences from the distant past). And the psychological therapies employed to treat phobias rely heavily on insights derived from conditioning. Avoiding the situation we fear, or making a rapid exit from it, maintains and builds up our fear, so patients are helped to spend time in precisely the situations they dread (this is called exposure therapy). As they do so, and provided they aren’t using any safety behaviours (see p. 26), their anxiety naturally diminishes. It’s a remarkably effective treatment — and often a very rapid one too: just one three-hour session can eradicate a phobia that has been causing anxiety for years.
But the classical conditioning theory developed by scientists like J. B. Watson (1878—1958) comes up short in regard to certain important questions. Why, for example, do individuals often acquire phobias without undergoing any traumatic formative experience? Why is it that most of those who do suffer scares in childhood don’t develop a phobia? (One study, for example, found that people without dog phobias were just as likely to have been attacked by dogs as those with such a phobia.) And why are some fears much more common than others? According to classical conditioning theory, any object or situation ought to be able to cause a lasting fear. How then to explain why the fear of heights is much more prevalent than the fear of travelling in a car, or why so many people are terrified of snakes and so few are frightened of electrical appliances?
In light of these questions, psychologists have rethought aspects of conditioning theory. For example, it’s now understood that we don’t simply learn our fears through the events we experience. We also pick up signals transmitted by the people around us. We seem to be most susceptible to these signals as children, and usually it’s our parents who make the biggest impression. So if your father repeatedly tells you that dogs are dangerous, there is a fair chance that you will come to believe it.
But we don’t only develop our fears on the basis of what we are told (a process known as informational learning). We also mimic other people’s behaviour. For a good example of this vicarious acquisition of fear, have a look back at the experiment by Friederike Gerull and Ronald Rapee described on p. 44.
These kinds of learning may be more difficult to remember than a single dramatic and distressing event, not least because they may play out over several years. This perhaps helps explain why many individuals are unable to call to mind an explanation for their fear.
Why are some fears more prevalent than others? The answer, for some experts, lies in the concept of biological preparedness, summarized here by Arne Öhman and Susan Mineka:
We are more likely to fear events and situations that provided threats to the survival of our ancestors, such as potentially deadly predators, heights, and wide open spaces, than to fear the most frequently encountered potentially deadly objects in our contemporary environment, such as weapons or motorcycles.
According to Öhman and Mineka, biological preparedness draws on a ’fear module’ in the brain, centred on the amygdala. This fear module kicks in automatically and unconsciously. (For more on the role of the amygdala in anxiety, see pp. 30—32.)
In support of this idea, Mineka and Michael Cook conducted a series of experiments using laboratory-reared rhesus monkeys. The monkeys, who had never seen a snake before, displayed no fear when presented with both toy snakes and a real boa constrictor. That all changed, however, when they watched videotaped reactions of other monkeys responding fearfully to the real and artificial snakes. The lab monkeys learned to be afraid of snakes. On the other hand, footage which appeared to show monkeys reacting fearfully to flowers made no impression. If the lab monkeys could acquire a fear of snakes, why not a fear of flowers? The answer, according to Mineka and Cook, is that a fear of snakes is hard-wired in monkeys because of the danger they can pose. When the lab monkeys saw the other monkeys’ response to the snakes, their innate fear was activated. Flowers offer no such threat and therefore trigger no prepared fear.
Perhaps our evolutionary inheritance can also be detected in the close relationship that seems to exist between particular phobias and the feeling of disgust. Recent research has shown that people with phobias of certain small animals — such as spiders, rats, mice, cockroaches, slugs — and some blood-injection-injury phobias are abnormally susceptible to feelings of disgust. There is a logic here. Physical disgust is designed to prevent us coming into contact with substances that could cause illness. So a fear of rats, for example, might have its roots in the animal’s age-old reputation for spreading disease; a blood phobia might be based on a fear of contamination.
Conditioning clearly plays a big role in the development of fears and phobias. But, as with virtually all psychological problems, other factors are usually involved. For example, the cognitive perspective highlights the contribution of distinctive — and distinctly unhelpful — styles of thinking.
When researchers analysed the thoughts of people with a spider phobia, for instance, they unearthed some very pessimistic assumptions. Asked what they thought a spider might do if it was near them, the responses included: ’bite me’, ’crawl towards my private parts’, and ’crawl into my clothes’. When questioned as to their own likely reaction when encountering a spider, the participants believed they would ’feel faint’, ’lose control of myself’, ’scream’, or ’become hysterical’. In other words, fearful thoughts play a crucial role in causing phobias.
People with phobias tend to overestimate the likelihood of coming to harm and underestimate their ability to cope with the situation they fear. They are also constantly on the look-out for any sign of the situation they dread. As Cervantes wrote: ’Fear is sharp-sighted, and can see things underground, and much more in the skies.’ This threat-focused style of thinking, of course, serves only to fuel anxiety. (Incidentally, it’s difficult to reconcile these findings with the DSM’s stipulation that ’the [phobic] person recognises that the fear is excessive or unreasonable’. On the contrary, for many individuals, their anxiety appears absolutely justified.)
The final piece in the puzzle of phobia causation comprises biological factors. Scientists believe that susceptibility to anxiety problems may be linked to an imbalance in what we might call the ’fear system’ of the brain: the amygdala, the hippocampus, and the prefrontal cortex (see pp. 28—32 for more on this). That imbalance is partly genetic in origin.
One study of twins put phobia heritability at around 30% (to refresh your memory on the concept of heritability and the field of genetic epidemiology, see pp. 35—36). An analysis of male twins estimated heritability at 25—37%. A third experiment assessed how easily twins could be conditioned to fear a range of stimuli. Identical twins performed more similarly than fraternal twins, leading the researchers to conclude that the heritability of fear learning is around 35—45%.
Genetic make-up, then, is clearly part of the reason why some people develop phobias and others do not. Genes probably don’t play a dominant role; the heritability figures we’ve quoted suggest their contribution is moderate. But without a genetic vulnerability, we are much less likely either to learn to be afraid of something, or to see that fear develop into a full-blown phobia.