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Chapter: Psychology: Psychopathology

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Roots of the Anxiety Disorders

1. GENETIC RISK FACTORS 2. BRAIN BASES 3. PSYCHOLOGICAL RISK FACTORS

Roots of the Anxiety Disorders

 

As we have now seen, the DSM distinguishes among a number of different anxiety dis-orders. However, there is considerable comorbidity among these disorders, meaning that having one of these anxiety disorders makes it more likely that one will have another anxiety disorder. Indeed, more than half the people with one anxiety disorder will at some point also have some other anxiety disorder (T. Brown et al., 2001). This suggests that there are risk factors shared by the various anxiety disorders (factors that make a person vulnerable to more than one of these disorders) as well as specific risk factors (factors that make someone vulnerable to one of the disorders but not the others).

GENETIC RISK FACTORS

 

One cluster of risk factors involves the person’s genetic pattern, because twin studies clearly show a heritable basis for the anxiety disorders. Thus, the probability that one member of a twin pair will have an anxiety disorder if the other does (the concordance rate) is much higher for identical twins than for fraternal twins (or ordinary siblings) (Hettema, Neale, & Kendler, 2001).

 

A number of different genes are thought to contribute to the anxiety disorders (Binder et al., 2008; Kendler, Karkowski, & Prescott, 1999; Lesch et al., 1996; Noyes et al., 1992), and genetic factors may be particularly important in OCD (Black & Noyes, 1990; S. A. Rasmussen, 1993). In fact, different aspects of OCD seem to have separate inheritance paths so that, for example, someone may inherit a specific tendency toward hoarding, or a specific tendency toward excessive cleaning (Leckman, Zhang, Alsobrook, & Pauls, 2001; but see Holden, 2008b). However, here as elsewhere, it is important to emphasize that these genetic factors do not directly “cause” the anxiety disorders. Instead, the genetic factors provide part of the diathesis for these disorders, and the disorder itself will emerge only if the person with the genetic vulnerability is exposed to some sort of stressor (Binder et al., 2008; Stein, Schork, & Gelernter, 2008).

BRAIN BASES

 

Genetic factors clearly play a role in anxiety disorders, but what is this role? How does a person’s biology contribute to the problems we have discussed? We still have much to learn about the biological underpinnings of these disorders, but some intriguing findings recently have begun to emerge.

 

For example, functional neuroimaging studies show that the anxiety disorders, despite all they have in common, are quite different from each other in their biological underpinnings. Thus, the brain regions implicated in fear learning (including the amygdala and insula) seem to be especially active in people suffering from the specific phobias and social phobia (Etkin & Wager, 2007; Goldin et al., 2009). The pattern is different, though, in PTSD; here studies show that people with this disorder have less brain activation in prefrontal regions associated with emotion regulation. Yet a different pattern of brain activity is associated with panic disorder—one that involves apparent instability in the autonomic nervous system (Andreasen & Black, 1996; Wilhelm, Trabert, & Roth, 2001). OCD in turn may be linked to overactivity in three other brain areas—the orbitofrontal cortex, the caudate nucleus, and the anterior cingulate—although it is unclear whether this activity is the cause of the disease or one of its consequences (Micallef & Blin, 2001).

PSYCHOLOGICAL RISK FACTORS

 

So far, we have focused on genetic and biological risk factors. Other risk factors are psy-chological. Some of these, such as psychological maltreatment in childhood, seem to confer a general risk for several different anxiety disorders (Scher & Stein, 2003). Other psychological risk factors play a role in specific anxiety disorders, especially specific phobias and PTSD.

 

Many have proposed that specific phobias are the result of experiences that created a mental association between the phobic stimulus and a fearful idea, and often this proposal is cast in the language of Pavlovian conditioning. The broad notion is that, at some point in the past, the person who suffers from the phobia experienced a painful, frightening, or embarrassing event; this is the unconditioned stimulus, leading to the unconditioned response of fear. The conditioned stimulus, in turn, was an object or cue linked to the event. Perhaps, for example, the person was in a closed space when something frightening happened. As a result, he now associates the closed space with fear, in much the same way that the ringing of a bell that is followed by food delivery becomes a signal that the food will soon arrive. In this way, claustrophobia (fear of closed spaces) might be produced (Wolpe, 1958).

 

In fact, the onset of many phobias can be traced to a traumatic experience, just as the conditioning account requires (see, for example, Hackmann, Clark, & McManus, 2000). But we need more theory than this if we are to account for all the facts about phobias. For example, phobias sometimes emerge without a history of conditioning— so that, for example, someone can develop a snake phobia even if he has never had a frightening experience with a snake. In addition, a simple conditioning account does not explain why some phobias are rare while others are common. For example, cars, bathtubs, and hammers are all (statistically) dangerous; painful accidents involving them are not uncommon. In contrast, few people have been bitten by a snake or a spider. If associations with pain or trauma produce phobias, we would expect to see many hammer or bathtub phobias but relatively few snake or spider phobias. But the opposite is the case.

 

These puzzles are easily solved. A century ago, Ivan Pavlov argued that classical con-ditioning was necessarily rooted in an organism’s own experiences, but more recent studies have demonstrated vicarious conditioning, in which a person (or, in some stud-ies, a monkey) can acquire a conditioned response merely by observing someone else’s fear (e.g., Mineka & Ben Hamida, 1998). In addition, we discussed the fact that organisms seem “prepared” for some associations (and so learn them quickly) but “unprepared” for other associations (and so learn them more slowly if at all), and, in each case, the degree of preparedness is usually understandable in evolutionary terms.

 

How does this apply to phobias? Snakes and spiders were common dangers for our primate ancestors; natural selection may therefore have favored animals that were innately predisposed (i.e., prepared) to learn to fear snakes and spiders very quickly, after just one or two experiences with them (Öhman & Mineka, 2001; Seligman, 1971). If this was the case, limited but painful experience with these stimuli might still be enough to create and sustain a substantial number of phobias. With these relatively small modifications, then, we can preserve the claim that, in many cases, phobias are the product of learning—and, in particular, the product of classical conditioning (Mineka & Zinbarg, 2006).

 

With PTSD, the stress that precipitated the disorder is often obvious—a rape, a ter-rorist attack, a battlefield experience. But even when the trauma is easily identified, we need to consider more than just this immediate stress as the “cause” of the disorder. Not everyone who experiences a trauma develops PTSD. Indeed, according to one estimate, more than 90% of the U.S. population have experienced a trauma at some point, but only 5 to 12% develop PTSD (Lee & Young, 2001). Among Vietnam War vet-erans, many of whom were exposed to horrific violence, only one in ten developed PTSD (Dohrenwend et al., 2006).

 

Why is this? Part of the answer lies in the severity of the trauma; more severe trauma is more likely to produce the disorder (McNally, 2006; Sutker, Allain, & Winstead, 1993; E. Jones & Wessely, 2001). The individual’s level of social support is also relevant, with more and better support after a trauma associated with a decreased likelihood of later developing PTSD (Ozer & Weiss, 2004). Yet another factor is the diathesis inherent in the person’s genetic pattern. The odds of developing PTSD increase fivefold if a parent has had it (Radant, Tsuang, Peskind, McFall, & Raskind, 2001); identical twins who served in Vietnam were found to be far more similar to one another than fraternal twins in the like-lihood of developing PTSD, and,for those who did develop PTSD, in the type of symptoms they experienced (True et al., 1993).

 

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