Section Learning Objectives
- Describe the biological causes of anxiety disorders.
- Describe the psychological causes of anxiety disorders.
- Describe the sociocultural causes of anxiety disorders.
188.8.131.52 Genetic Influences
While genetics have been known to contribute to the presentation of anxiety symptoms, the interaction between genetics and stressful environmental influences accounts for more of anxiety disorders than genetics alone (Bienvenu, Davydow, & Kendler, 2011). The quest to identify specific genes that may predispose individuals to develop anxiety disorders has lead researchers to the serotonin transporter gene (5-HTTLPR). Mutation of the 5-HTTLPR gene has been found to be related to a reduction in serotonin activity and an increase in anxiety-related personality traits (Munafo, Brown, & Hairiri, 2008).
184.108.40.206 Neurobiological Structures
Researchers have identified several brain structures and pathways that are likely responsible for anxiety responses. Among those structures is the amygdala, the area of the brain that is responsible for storing memories related to emotional events (Gorman, Kent, Sullivan, & Coplan, 2000). When presented with a fearful situation, the amygdala initiates a reaction in efforts to prepare the body for a response. First, the amygdala triggers the hypothalamic-pituitary-adrenal (HPA) axis to prepare for immediate action— either to fight or flight. The second pathway is activated by the feared stimulus itself, by sending a sensory signal to the hippocampus and prefrontal cortex, to determine if the threat is real or imagined. If it is determined that no threat is present, the amygdala sends a calming response to the HPA axis, thus reducing the level of fear. If there is a threat present, the amygdala is activated, producing a fear response.
Specific to panic disorder is the implication of the locus coeruleus, the brain structure that serves as an “on-off” switch for norepinephrine neurotransmitters. It is believed that increased activation of the locus coeruleus results in panic like symptoms; therefore, individuals with panic disorder may have a hyperactive locus coeruleus, leaving them more susceptible to experience more intense and frequent physiological arousal than the general public (Gorman, Kent, Sullivan, & Coplan, 2000). This theory is supported by studies in which individuals experienced increased panic symptoms following injection of norepinephrine (Bourin, Malinge, & Guitton, 1995). Unfortunately, norepinephrine and the locus coeruleus fail to fully explain the development of panic disorder, as treatment would be much easier if only norepinephrine was implicated. Therefore, researchers argue that a more complex neuropathway is likely implicated in the development of panic disorder. More specifically, the corticostriatal-thalamocortical (CSTC) circuit, also known as the fear-specific circuit, is theorized as a major contributor to panic symptoms (Gutman, Gorman, & Hirsch, 2004). When an individual is presented with a frightening object or situation, the amygdala is activated, sending a fear response to the anterior cingulate cortex and the orbitofrontal cortex. Additional projection from the amygdala to the hypothalamus activates endocrinologic responses to fear- releasing adrenaline and cortisol to help prepare the body to fight or flight (Gutman, Gorman, & Hirsch, 2004). This complex pathway supports the theory that panic disorder is mediated by several neuroanatomical structures and their associated neurotransmitters.
The cognitive perspective on the development of anxiety disorders centers around dysfunctional thought patterns. Maladaptive assumptions are routinely observed in individuals with anxiety disorders, as they often interpret events as dangerous and overreact to potentially stressful events, which contributes to a heightened overall anxiety level. These negative appraisals, in combination with a biological predisposition to anxiety likely contribute to the development of anxiety symptoms (Gallagher et al., 2013).
Sensitivity to physiological arousal not only contributes to anxiety disorders in general, but also for panic disorder where individuals experience various physiological sensations and misinterpret them as catastrophic. One explanation for this theory is that individuals with panic disorder are actually more susceptible to more frequent and intensive physiological symptoms than the general public (Nillni, Rohan, & Zvolensky, 2012). Others argue that these individuals have had more trauma-related experiences in the past, and therefore, are quick to misevaluate their physical symptoms as a potential threat. This misevaluation of symptoms as impending disaster likely maintain symptoms as the cognitive misinterpretations to physiological arousal creates a negative feedback loop, leading to more physiological changes.
Social anxiety is also largely explained by cognitive theorists. Individuals with social anxiety disorder tend to hold unattainable or extremely high social beliefs and expectations. Furthermore, they often engage in preconceived maladaptive assumptions that they will behave incompetently in social situations and that their behaviors will lead to terrible consequences. Because of these beliefs, they anticipate social disasters will occur and therefore, avoid social encounters (or limit them to close friends/family members) in efforts to prevent the disaster (Moscovitch et al., 2013). Unfortunately, these cognitive appraisals are not only isolated before and during the event. Individuals with social anxiety disorder will also evaluate the social event after it has taken place, often obsessively reviewing the details (i.e., ruminating over social events). This over-evaluation of social performance negatively reinforces future avoidance of social situations.
The behavioral explanation for the development of anxiety disorders is largely reserved for phobias- both specific and social phobia. More specifically, behavioral theorists focus on classical conditioning – when two events that occur close together become strongly associated with one another, despite their lack of causal relationship. Watson and Rayner’s (1920) infamous Little Albert experiment is an example of how classical conditioning can be used to induce fear through associations. In this study, Little Albert developed a fear of white rats by pairing a white rate with a loud sound. This experiment, although lacking ethical standards, was groundbreaking in the development of learned behaviors. Over time, researchers have been able to replicate these findings (in more ethically sound ways) to provide further evidence of the role of classical conditioning in the development of phobias.
Modeling is another behavioral explanation of the development of specific and social phobias. In modeling, an individual acquires a far through observation and imitation (Bandura & Rosenthal, 1966). For example, when a young child observes their parent display irrational fears of an animal, the child may then begin to display similar behaviors. Similarly, observing another individual being ridiculed in a social setting may increase the chances of the development of social anxiety, as the individual may become fearful that they would experience a similar situation in the future. It is speculated that the maintenance of these phobias is due to the avoidance of the feared item or social setting, thus preventing the individual from learning that the item/social situation is not something that should be feared.
While modeling and classical conditioning largely explain the development of phobias, there is some speculation that the accumulation of a large number of these learned fears will develop into GAD. Through stimulus generalization, or the tendency for the conditioned stimulus to evoke similar responses to other conditions, a fear of one item (such as the dog) may become generalized to other items (such as all animals). As these fears begin to grow, a more generalized anxiety may present, as opposed to a specific phobia.
Finally, we will review the social constructs that contribute to and maintain anxiety disorders. While characteristics such as living in poverty, experiencing significant daily stressors, and increased exposure to traumatic events are all identified as major contributors to anxiety disorders, additional sociocultural influences such as gender and discrimination have also received a great deal of attention.
Gender has largely been researched within anxiety disorders due to the consistent discrepancy in diagnosis rate between men and women. As previously discussed, women are routinely diagnosed with anxiety disorders more often than men, a trend that is observed throughout the entire lifespan. One potential explanation for this discrepancy is the influence of social pressures on women. Women are more susceptible to experience traumatic experiences throughout their life, which may contribute to anxious appraisals of future events. Furthermore, women are more likely to use emotion-focused coping, which is less effective in reducing distress than problem-focused coping (McLean & Anderson, 2009). These factors may increase levels of stress hormones (e.g., cortisol) within women that leave them susceptible to develop symptoms of anxiety. Therefore, it appears a combination of genetic, environmental, and social factors may explain why women tend to be diagnosed with anxiety disorders more often than men.
Exposure to discrimination and prejudice, particularly relevant to ethnic minority and other marginalized groups, can also impact an individual’s anxiety level. Discrimination and prejudice contribute to negative interactions, which is directly related to negative affect and an overall decline in mental health (Gibbons et al., 2014). The repeated exposure to discrimination and prejudice over time can lead to fear responses in individuals, along with subsequent avoidance of social situations in efforts to protect themselves emotionally.
Chapter 4 covered the topic of anxiety disorders. This discussion included Generalized Anxiety Disorder, Specific Phobias, Agoraphobia, Social Anxiety Disorder, and Panic Disorder. As with other chapters in this book, we discussed the clinical presentation, epidemiology, comorbidity, and treatment of the anxiety disorders. Etiology was also discussed in the context of biological, psychological, and sociocultural theories.