Phobias

Anxiety disorders: phobias

A phobic disorder involves extreme, persistent and irrational fear together with a lack of control, which is strongly out of proportion to the danger.

Three categories are distinguished by DSM-IV:

• Agoraphobia – Fear of open spaces or public places. In most cases, the panic disorder starts first, then the fear of having another attack makes the individual feel insecure about being in public. About 50% of all clinically-diagnosed phobics are suffering from agoraphobia with panic disorder.
• Social phobias, such as talking or eating in public, extreme concern about the individual’s own behaviour and the reactions of others towards that behaviour.
• Specific phobias such as zoophobias (animals), fear of water, fear of heights, etc. Specific phobias generally have little impact on overall quality of life.

1. Biological explanations of phobias

Genetic – Individuals may inherit a genetically-determined predisposition to develop phobias. This is supported by twin studies, such as Torgersen (1983), who found 31% concordance for panic disorder with agoraphobia in MZ twins versus zero concordance in DZ twins, though none of them shared the same phobias.

It is also supported by family studies. Solyom et al. (1974) found that 45% of phobic patients studied had a family history of the disorder, compared with 17% of ‘normal’ controls. A ‘concordance rate’ is the extent to which two things are related, in this case, how frequently both twins have the same disorder.

Evolutionary – Fear and anxiety are adaptive responses. A fear becomes a phobia when it interferes with normal functioning. The concept of biological preparedness (Seligman, 1971) proposes that there would be an adaptive advantage to develop certain (‘ancient’) fears more readily than others, for example, fear of heights or of strangers, because such fears would increase the survival (and ultimate reproduction) of an individual.

This explains why people acquire certain fears more readily than others, such as a fear of snakes rather than a fear of fast cars.

Evaluation:

• Kendler et al. (1992) concluded that specific phobias have only a small genetic component, whereas agoraphobia appears to be more related to genetic vulnerability.
• Genetic explanations are only part of the explanation. The diathesis–stress model is a fuller explanation. Kleiner and Marshall (1987) reported that 84% of agoraphobics had experienced family problems in the months before they had their first panic attack. This supports the diathesis–stress model. The diathesis–stress model suggests that illness occurs when a person has a genetic vulnerability or predisposition to develop a particular disorder (diathesis) but the disorder only develops if it is triggered by some environmental event or experience (a stressor).
• Bennett-Levy and Marteau (1984) found that fear was highly correlated with certain aspects of an animal’s appearance – the more the animal’s appearance was different to human form, the more the animal was feared. This suggests some innate predisposition – a tendency to fear strangeness.
• The concept of biological preparedness cannot explain fears of harmless situations or things.

2. Behavioural explanations of phobias

Classical conditioning – Watson and Rayner (1920) conditioned ‘Little Albert’ to fear white furry objects by pairing a loud noise with a furry object. It is likely that most phobias are learned through the association of trauma with some neutral stimulus. In addition, the fact that phobics avoid their feared situation means the response is never extinguished.

Operant conditioning – Mowrer (1947) proposed a two-process theory: the first stage of developing a phobia involves classical conditioning (as outlined above). The second stage is operant conditioning because the avoidance of the phobia stimulus reduces fear and is, therefore, reinforcing.

Social learning theory – Fears may be learned through imitation. Mineka et al. (1984) found that monkeys could develop snake phobias simply by watching another monkey experience fear in the presence of a snake.

Evaluation:

• Some fears may be innate (see above).
• Not everyone who is exposed to conditioning develops phobias. For example, DiNardo et al. (1988) found that as many people without dog phobias as those with dog phobias reported negative experiences with dogs.

3. Cognitive explanations of phobias

Phobias may be the result of irrational thoughts. For example, the sensation of crowding in a lift may develop into a cognition that lifts are associated with suffocation.

Eysenck (1997) reports research on biological challenges (e.g. breathing a mixture of carbon dioxide and oxygen). This often provokes a panic attack in patients suffering from panic disorder with agoraphobia, but rarely in normal controls. Panic attack patients may differ in the way they interpret their bodily symptoms. Cognitive explanations centre on irrational thinking and faulty cognition.

Evaluation:

• The success of behavioural and cognitive-behavioural therapies in treating phobias supports their value as explanations.

4. Psychodynamic explanations of phobias

Freud (1909) suggested that phobias arise when anxieties are displaced onto the phobic object that symbolises the initial conflict. If the conflict is resolved the phobia will disappear.

Freud used the classic case study of Little Hans to illustrate the process. Hans developed a fear of horses because the horse represented the boy’s unconscious fear of his father. He was also afraid of being bitten by a horse, whereas he was actually scared that his mother would leave him.

Evaluation:

• Freudian explanations lack falsifiability. There are other, possibly more plausible explanations, for example, Hans might have developed his fear through classical conditioning. Falsifiability refers to the ability to prove a theory wrong. It is possible to present a Freudian explanation to fit any facts.
• Data collection in such studies relies on retrospective recall, which may be unreliable.
• Such data is correlational and does not demonstrate a causal link.