41-4 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 hand washing. Few of today’s psychologists interpret anxiety this way. Most believe that three modern perspectives—conditioning, cognition, and biology—are more helpful.

Some bad events come with a warning. You’re running late and might miss the bus. But when bad events happen unpredictably and uncontrollably, anxiety or other disorders often develop (Field, 2006; Mineka & Oehlberg, 2008). In a classic experiment, infant “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, learn to become uneasy in their lab environment. The lab had become a cue for fear.

Such research helps explain how panic-prone people learn to associate anxiety with certain cues, and why anxious people are hyperattentive to possible threats (Bar-Haim et al., 2007; Duits et al., 2015). In one survey, 58 percent of those with social anxiety disorder said their disorder began after a traumatic event (Ost & Hugdahl, 1981).

How might learning magnify a single painful and frightening event into a full-blown 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. My [DM’s] car was once struck by another whose driver missed a stop sign. For months afterward, I felt a twinge of unease when any car approached from a side street. Likewise, I [ND] was 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 cobwebs. Those fears eventually disappeared, but sometimes fears linger and grow. Marilyn’s thunderstorm phobia may have similarly generalized after a terrifying or painful experience during a thunderstorm.

Once fears and anxieties are learned, reinforcement helps maintain them. Anything that helps us avoid or escape the feared situation reduces anxiety. This feeling of relief can reinforce phobic behaviors. 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.

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Conditioning influences our feelings of anxiety, but so does cognition—our thoughts, memories, interpretations, and expectations. We learn some fears by observing others. 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 interpretations and expectations also shape our 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. They attend more to threatening stimuli. They more often interpret ambiguous stimuli as threatening: a pounding heart signals a heart attack, a lone spider near the bed indicates an infestation, and an everyday disagreement with a friend or a boss spells doom for the relationship. And they more readily remember threatening events (Van Bockstaele et al., 2014). 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).

Some aspects of anxiety disorders, OCD, and PTSD are not easily understandable in terms of conditioning and cognitive processes alone. Why do some of us develop lasting phobias after suffering traumas, but others do not? Why do we all learn some fears more readily? Our biology also plays a role.

GENES Among monkeys, fearfulness runs in families. A monkey reacts more strongly to stress if its close biological relatives have sensitive, high-strung temperaments (Suomi, 1986). So, too, with people. Some of us are predisposed to anxiety. 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 separated identical twins independently became so afraid of water that, at age 35, they would wade into the ocean backward and only up to their knees.

Given the genetic contribution to anxiety disorders, researchers are now sleuthing the culprit genes. Among their findings are 17 gene variations associated with typical anxiety disorder symptoms (Hovatta et al., 2005), and others that are associated specifically with OCD (Taylor, 2013).

Some genes influence anxiety disorders by regulating brain levels of neurotransmitters. These include serotonin, which influences sleep, mood, and attending to threat (Canli, 2008; Pergamin-Hight et al., 2012), and glutamate, which heightens activity in the brain’s alarm centers (Lafleur et al., 2006; Welch et al., 2007).

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So genes matter. 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).

But experience affects gene expression. Among PTSD patients, a history of child abuse leaves long-term epigenetic marks, which are often organic molecules. These molecular tags attach to our chromosomes and turn certain genes on or off. Thus, experiences such as abuse can increase the likelihood that a genetic vulnerability to a disorder will be expressed (Mehta et al., 2013). Suicide victims show a similar epigenetic effect (McGowan et al., 2009).

THE BRAIN Our 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; Herringa et al., 2013; Kolassa & Elbert, 2007). These fear pathways create easy inroads for more fear experiences (Armony et al., 1998). Some antidepressant drugs dampen this fear-circuit activity and associated obsessive-compulsive behaviors.

Anxiety-related disorders all involve biological events. Brain scans of people with PTSD show higher-than-normal activity in the amygdala when they view traumatic images (Nutt & Malizia, 2004). When the disordered brain of an OCD patient detects that something is amiss, it generates a mental hiccup of repeating thoughts (obsessions) or actions (compulsions) (Gehring et al., 2000). Brain scans 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). As FIGURE 41.2 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).

NATURAL SELECTION We seem biologically prepared to fear the threats our ancestors faced—spiders and snakes, enclosed spaces and heights, storms and darkness. (In the distant past, those who did not fear these threats were less likely to survive and leave descendants.) Thus, in Britain, which has only one poisonous snake species, people often fear snakes. Even 9-month-olds attend less to modern danger sounds than to sounds signaling ancient threats—hisses, thunder, angry voices (Erlich et al., 2013). Our Stone Age fears are easy to condition and hard to extinguish (Coelho & Purkis, 2009; Davey, 1995; Öhman, 2009). Some of our modern fears may also have an evolutionary explanation. A fear of flying may be rooted in our biological predisposition to fear confinement and heights.

Compare our easily conditioned 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 strikes continued, the British, Japanese, and German populations did not become more and more panicked. Rather, they grew increasingly indifferent to planes outside their immediate neighborhoods (Mineka & Zinbarg, 1996). Evolution has not prepared us to fear bombs dropping from the sky.

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Our phobias focus on dangers our ancestors faced. Our compulsive acts typically exaggerate behaviors that helped them survive. Grooming had survival value; it detected insects and infections. Gone wild, it becomes compulsive hair pulling. Washing up helped people stay healthy. Out of control, it becomes ritual hand washing. Checking territorial boundaries helped ward off enemies. In OCD, it becomes checking and rechecking an already locked door (Rapoport, 1989).