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7.4: Anxiety Disorders - Etiology

  • Page ID
    161385
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    Learning Objectives
    • Describe the biological causes of anxiety disorders.
    • Describe the psychological causes of anxiety disorders.
    • Describe the sociocultural causes of anxiety disorders.

    Biological

    7.4.1.1. Biological – Genetic influences. While genetics have been known to contribute to the presentation of anxiety symptoms, the interaction between genetics and stressful environmental influences appears to account for more anxiety disorders than genetics alone (Bienvenu, Davydow, & Kendler, 2011). The quest to identify specific genes that may predispose individuals to develop anxiety disorders has led researchers to the serotonin transporter gene (5-HTTLPR). Mutation of the 5-HTTLPR gene is related to a reduction in serotonin activity and an increase in anxiety-related personality traits (Munafo, Brown, & Hairiri, 2008).

    7.4.1.2. Biological – 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 to ready 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 a threat is 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 the 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 responsible for 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.

    Psychological

    7.4.2.1. Psychological – Cognitive. The cognitive perspective on the development of anxiety related disorders centers around dysfunctional thought patterns. As seen in depression, maladaptive assumptions are routinely observed in individuals with anxiety-related disorders, as they often engage in interpreting events as dangerous or overreacting to potentially stressful events, which contributes to an overall heightened 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 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 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 primarily 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 to 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. This overestimation of social performance negatively reinforces future avoidance of social situations.

    7.4.2.2. Psychological – Behavioral. The behavioral explanation for the development of anxiety disorders is mainly reserved for phobias—both specific and social phobia. More precisely, behavioral theorists focus on respondent conditioning – when two events that occur close together become strongly associated with one another, despite their lack of causal relationship (see Module 2 for an explanation of respondent conditioning). Watson and Rayner’s (1920) infamous Little Albert experiment is an example of how respondent conditioning can be used to induce fear through associations. In this study, Little Albert developed a fear of white rats by pairing a white rat 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 respondent conditioning in the development of phobias.

    7.4.2.3. Psychological – Modeling is another behavioral explanation of the development of specific and social phobias. In modeling, an individual acquires a fear though observation and imitation (Bandura & Rosenthal, 1966). For example, when a young child observes their parent display irrational fear of an animal, the child may then begin to display similar behavior. Similarly, seeing another individual being ridiculed in a social setting may increase the chances of developing 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 object or situation is not something that should be feared.

    While modeling and respondent conditioning largely explain the development of phobias, there is some speculation that the accumulation of many these learned fears will develop into generalized anxiety disorder. Through stimulus generalization, or the tendency for the conditioned stimulus to evoke similar responses to other stimuli, a fear of one stimulus (such as the dog) may become generalized to other items (such as all animals). As these fears begin to grow, a more generalized anxiety will present, as opposed to a specific phobia.

    Sociocultural

    Seeing how prominent the biological and psychological constructs are in explaining the development of anxiety-related disorders, we also need to review the social constructs that contribute 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 significant contributors to anxiety disorders, additional sociocultural influences such as gender and discrimination have also received considerable attention, mainly due to the epidemiological nature of the disorder.

    Gender has largely been researched within anxiety disorders due to the consistent discrepancy in the 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 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 more often with anxiety-related disorders.

    Exposure to discrimination and prejudice, particularly relevant to ethnic minorities 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.

    Key Takeaways

    You should have learned the following in this section:

    • Biological causes of anxiety disorders include the serotonin transporter gene (5-HTTLPR); brain structures to include the amygdala, hippocampus, and prefrontal cortex; and the locus coeruleus and corticostriatal-thalamocortical (CSTC) circuit in relation to panic disorder.
    • Psychological causes of anxiety disorders include maladaptive assumptions, the linking of events through respondent conditioning, modeling, and stimulus generalization as it relates to generalized anxiety disorder.
    • Sociocultural causes of anxiety disorders include social pressures leading to a higher rate of diagnosis for women and discrimination and prejudice which affects ethnic minorities and other marginalized groups.
    Review Questions
    1. Discuss the biological etiology of panic disorders. What brain structures and neurotransmitters are involved?
    2. How does the cognitive model explain the development and maintenance of anxiety related disorders?
    3. What is the difference between emotion-focused and problem-focused coping strategies? How do these two coping strategies explain differences in anxiety related disorders?
    4. What are the effects of prejudice and discrimination on the development of anxiety disorders?

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