50.4 Understanding Anxiety Disorders, OCD, and PTSD

50-4 How do conditioning, cognition, and biology contribute to the feelings and thoughts that mark anxiety disorders, OCD, and PTSD?

Anxiety is both a feeling and a cognition—a doubt-laden appraisal of one’s safety or social skill. How do these anxious feelings and cognitions arise? Sigmund Freud’s psychoanalytic theory proposed that, beginning in childhood, people repress intolerable impulses, ideas, and feelings. This submerged mental energy sometimes, he thought, leaks out in odd symptoms, such as anxious handwashing. Few of today’s psychologists share Freud’s interpretation of anxiety. Most believe that three modern perspectives—conditioning, cognition, and biology—are more helpful.

Conditioning

Some bad events come with a warning. Your underdog team might lose the big game. You aren’t prepared and you may fail your quiz. You’re running late and might miss the bus. But when bad events happen unpredictably and uncontrollably, anxiety and other disorders often develop (Field, 2006; Mineka & Oehlberg, 2008). In a classic experiment, an infant called “Little Albert” learned to fear furry objects that were paired with loud noises. In other experiments, researchers have created anxious animals by giving rats unpredictable electric shocks (Schwartz, 1984). The rats, like assault victims who report feeling anxious when returning to the scene of the crime, became uneasy in their lab environment. The lab had become a cue for fear.

Such research helps explain why anxious people are hyperattentive to possible threats, and how panic-prone people come to associate anxiety with certain cues (BarHaim et al., 2007; Bouton et al., 2001). In one survey, 58 percent of those with social anxiety disorder experienced their disorder after a traumatic event (Ost & Hugdahl, 1981) .

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Through conditioning, the short list of naturally painful and frightening events can multiply into a long list of human fears. Can you recall a frightening event that left you fearful for a while? We can. I [DM] was headed home when my car was struck by another when its driver missed a stop sign. For months afterward, I felt a twinge of unease as a car approached from a side street. Likewise, I [ND] remember watching a terrifying movie about spiders, Arachnophobia, when a severe thunderstorm struck and the theater lost power. For months, I experienced anxiety at the sight of spiders or harmless cobwebs.

How might conditioning magnify a single painful and frightening event into a fullblown phobia? The answer lies in part in two conditioning processes: stimulus generalization and reinforcement.

Stimulus generalization occurs when a person experiences a fearful event and later develops a fear of similar events. Each of us [DM and ND] generalized our fears: One of us feared cars approaching from side streets and the other feared spiders. Those fears eventually disappeared, but sometimes fears can linger and grow. Marilyn’s thunderstorm phobia may have similarly generalized after a terrifying or painful experience during a thunderstorm.

Once fears and anxieties arise, reinforcement helps maintain them. Anything that helps us avoid or escape the feared situation can be reinforcing because it reduces anxiety and gives us a feeling of relief. Fearing a panic attack, we may decide not to leave the house. Reinforced by feeling calmer, we are likely to repeat that maladaptive behavior in the future (Antony et al., 1992). So, too, with compulsive behaviors. If washing our hands relieves our feelings of anxiety, we may wash our hands again when those feelings return.

Cognition

Conditioning influences our feelings of anxiety, but so does cognition—our thoughts, memories, interpretations, and expectations. By observing others, we can learn to fear what they fear. Nearly all monkeys raised in the wild fear snakes, yet lab-raised monkeys do not. Surely, most wild monkeys do not actually suffer snake bites. Do they learn their fear through observation? To find out, Susan Mineka (1985, 2002) experimented with six monkeys raised in the wild (all strongly fearful of snakes) and their lab-raised offspring (virtually none of which feared snakes). After repeatedly observing their parents or peers refusing to reach for food in the presence of a snake, the younger monkeys developed a similar strong fear of snakes. When the monkeys were retested three months later, their learned fear persisted. We humans learn many of our own fears by observing others (Helsen et al., 2011; Olsson et al., 2007).

Our past experiences shape our expectations and influence our interpretations and reactions. Whether we interpret the creaky sound in the old house simply as the wind or as a possible knife-wielding intruder determines whether we panic. People with anxiety disorders tend to be hypervigilant. A pounding heart signals a heart attack. A lone spider near the bed becomes a likely infestation. An everyday disagreement with a friend or boss spells possible doom for the relationship. Anxiety is especially common when people cannot switch off such intrusive thoughts and perceive a loss of control and a sense of helplessness (Franklin & Foa, 2011).

Biology

There is, however, more to anxiety disorders, OCD, and PTSD than conditioning and cognitive processes alone. Why will some of us develop lasting phobias or PTSD after suffering traumas? Why do we all learn some fears so readily? Why are some of us more vulnerable? The biological perspective offers insight.

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GenesGenes matter. Pair a traumatic event with a sensitive, high-strung temperament and the result may be a new phobia (Belsky & Pluess, 2009). Some of us have genes that make us like orchids—fragile, yet capable of beauty under favorable circumstances. Others of us are like dandelions—hardy, and able to thrive in varied circumstances (Ellis & Boyce, 2008; Pluess & Belsky, 2013).

Among monkeys, fearfulness runs in families. A monkey reacts more strongly to stress if its close biological relatives are anxiously reactive (Suomi, 1986). So, too, with people. If one identical twin has an anxiety disorder, the other is likewise at risk (Hettema et al., 2001; Kendler et al., 2002a,b; Van Houtem et al., 2013). Even when raised separately, identical twins may develop similar phobias (Carey, 1990; Eckert et al., 1981). One pair of 35-year-old female identical twins independently became so afraid of water that each would wade in the ocean backward and only up to the knees.

Given the genetic contribution to anxiety disorders, researchers are now sleuthing the culprit genes. One research team identified 17 gene variations associated with typical anxiety disorder symptoms (Hovatta et al., 2005). Other teams have found genes associated specifically with OCD (Taylor, 2013).

Genes can influence disorders by regulating neurotransmitters. Some studies point to an “anxiety gene” that affects brain levels of serotonin, a neurotransmitter that influences sleep, mood, and attention to negative images (Canli, 2008; Pergamin-Hight et al., 2012). Other studies implicate genes that regulate the neurotransmitter glutamate (Lafleur et al., 2006; Welch et al., 2007). With too much glutamate, the brain’s alarm centers become overactive.

Among PTSD patients, a history of child abuse leaves long-term epigenetic marks, increasing the likelihood that a genetic vulnerability to the disorder will be expressed (Mehta et al., 2013). Suicide victims show a similar epigenetic effect (McGowan et al., 2009).

The BrainOur experiences change our brain, paving new pathways. Traumatic fear-learning experiences can leave tracks in the brain, creating fear circuits within the amygdala (Etkin & Wager, 2007; Kolassa & Elbert, 2007; Herringa et al., 2013). These fear pathways create easy inroads for more fear experiences (Armony et al., 1998).

Anxiety-related disorders differ from one another, but they all involve biological events. In OCD, for example, when the disordered brain detects that something is amiss, it generates a mental hiccup of repeating thoughts (obsessions) or actions (compulsions) (Gehring et al., 2000). Brain scans of people with PTSD show higher-than-normal activity in the amygdala when they view traumatic images (Nutt & Malizia, 2004). Brain scans of people with OCD reveal elevated activity in specific brain areas during behaviors such as compulsive hand washing, checking, ordering, or hoarding (Insel, 2010; Mataix-Cols et al., 2004, 2005). These brain areas are not only more active among people with OCD, they are also enlarged (Rotge et al., 2010). As FIGURE 50.2 shows, the anterior cingulate cortex, a brain region that monitors our actions and checks for errors, seems especially likely to be hyperactive (Maltby et al., 2005). When deciding to get rid of one’s personal possessions, those with hoarding disorder also show elevated activity in the anterior cingulate cortex (Tolin et al., 2012).

Figure 50.2
An obsessive-compulsive brain Neuroscientists Nicholas Maltby, David Tolin, and their colleagues (2005) used functional MRI scans to compare the brains of those with and without OCD as they engaged in a challenging cognitive task. The scans of those with OCD showed elevated activity in the anterior cingulate cortex in the brain’s frontal area (indicated by the yellow area on the far right).

Some antidepressant drugs dampen this fear-circuit activity and its associated obsessive-compulsive behavior. Fears can also be blunted by giving people drugs as they recall and then rerecord (“reconsolidate”) a traumatic experience (Kindt et al., 2009; Norberg, et al., 2008). Although they don’t forget the experience, the associated emotion is largely erased.

Natural SelectionWe seem biologically prepared to fear threats faced by our ancestors. Our phobias focus on such specific fears: spiders, snakes, and other animals; enclosed spaces and heights; storms and darkness. (Those fearless about these occasional threats were less likely to survive and leave descendants.) Thus, even in Britain, with only one poisonous snake species, people often fear snakes. It is easy to condition and hard to extinguish fears of such “evolutionarily relevant” stimuli (Coelho & Purkis, 2009; Davey, 1995; Öhman, 2009). Some of our modern fears can also have an evolutionary explanation. A fear of flying may be rooted in our biological predisposition to fear confinement and heights.

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Fearless The biological perspective helps us understand why most of us have more fear of heights than does Felix Baumgartner, shown here skydiving from 24 miles above the Earth in 2012.

Compare our easily conditional fears to what we do not easily learn to fear. World War II air raids, for example, produced remarkably few lasting phobias. As the air blitzes continued, the British, Japanese, and German populations did not become more and more panicked. Rather, they grew more indifferent to planes outside their immediate neighborhoods (Mineka & Zinbarg, 1996). Evolution has not prepared us to fear bombs dropping from the sky.

Just as our phobias focus on dangers faced by our ancestors, our compulsive acts typically exaggerate behaviors that contributed to our species’ survival. Grooming gone wild becomes hair pulling. Washing up becomes ritual hand washing. Checking territorial boundaries becomes rechecking an already locked door (Rapoport, 1989).

RETRIEVAL PRACTICE

  • Researchers believe that conditioning and cognitive processes contribute to anxiety disorders, OCD, and PTSD. What biological factors also contribute to these disorders?

Biological factors include inherited temperament differences and other gene variations; learned fears that have altered brain pathways; and outdated, inherited responses that had survival value for our distant ancestors.