- Describe the principal features of anxiety disorders.
- Describe the difference between fear and anxiety.
- Identify the major biological systems involved in anxiety and fear.
- Identify the biology thought to underlie the etiology of anxiety disorders.
Anxiety disorders are the most prevalent of all psychological disorders. Large scale surveys estimate that around 33% of the population is likely to suffer from an anxiety disorder at some point in their lives (Bandelow & Michaelis, 2015). The category of anxiety disorders encompasses a broad range of disorders marked by severe levels of fear and anxiety. Similar to the other disorders discussed in this chapter, the etiology of anxiety disorders is thought to be a complex combination of biological and environmental factors.
Introduction to Anxiety Disorders
The main feature common to all individuals suffering from an anxiety disorder is the experience of excessive anxiety. Similar to the emotion, fear, anxiety acts as a signal of danger, threat, or motivational conflict, and prepares the body for action. While fear is a physical and emotional response to a real or external imminent threat, anxiety is a generalized response to an unknown threat or internal conflict, often accompanied by bodily symptoms such as increased heart rate, muscle tension, a sense of unease, and apprehension about the future (APA, 2013). The category of anxiety disorders includes generalized anxiety disorder, panic disorder, specific phobia, social anxiety disorder (social phobia) (APA, 2013).
Like many psychological disorders, anxiety disorders are believed to arise from a complex blend of factors, both biological and environmental, that when combined with stress, lead to the development of a particular anxiety disorder.
Although all the anxiety disorders share the feeling of anxiety as a symptom, there are many different ways in which this anxiety may manifest in an individual, leading to the diversity seen among the disorders in this category.
Genetic and epigenetic factors in anxiety disorders
Anxiety disorders are believed to be highly complex and polygenic (Meier & Decker, 2019). While genetics have been known to contribute to the presentation of anxiety symptoms, the interaction between genetics and stressful environmental influences accounts for more anxiety disorders than genetics alone (Bienvenu, et al., 2011). Nevertheless, several genes have been identified that may contribute to the increased risk of the development of anxiety disorders.
One of the first promising genes to be identified was a serotonin transporter or SERT gene. The serotonin transporter is of major importance in regulating levels of serotonin in the synapse. Serotonin synapses play a central role in the neural circuitry controlling mood and temperament (Houwing, et al., 2017). Disturbances in the serotonin system are known to contribute to many psychological disorders (Andrews et al., 2015). Mutation of the SERT gene have been found to be related to a reduction in serotonin activity and an increase in anxiety-related personality traits (Munafo, et al, 2008).
In 2020, a large research study of over 200,000 participants identified a gene known as SATB1 (Levey, et al. 2020). This gene is believed to influence the activity ("expression") of multiple other genes involved in neuronal development, including a gene known as CRH1. The CRH1 gene codes for the protein, Corticotropin Releasing Hormone (CRH), which is a hormone that plays an essential role in our body’s HPA axis, the pathway modulates our stress and fear/anxiety responses.
Neural structures and neurotransmitters involved anxiety disorders
Researchers have identified several brain structures and pathways that are may be responsible for the excessive anxiety responses often seen in anxiety disorders. In particular, the atypical activation in the prefrontal cortex, hippocampus, and amygdala has been implicated in anxiety disorders (Shin & Liberzon, 2010, Maron & Nutt, 2017).
A region of the brain called the locus coeruleus has been of particular interest to researchers studying panic disorder. Located in the brainstem, the locus coeruleus is the brain’s major source of norepinephrine, a neurotransmitter that triggers the body’s fight-or-flight response (Figure 22.214.171.124). Research with nonhuman primates has shown that stimulating the locus coeruleus either electrically or through drugs produces panic-like symptoms (Charney et al., 1990). Such findings have led to the theory that individuals with panic disorder may have a hyperactive locus coeruleus, leaving them an increased likelihood of experiencing more intense and frequent physiological arousal than the general public (Gorman, et al., 2000). This theory is supported by studies in which individuals experienced increased panic symptoms following injection of norepinephrine (Bourin, et al., 1995).
Unfortunately, norepinephrine and the locus coeruleus fail to fully explain the development of panic disorder, and 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, et al., 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 projections from the amygdala to the hypothalamus activate endocrinologic responses to fear- releasing adrenaline and cortisol to help prepare the body to fight or flight (Gutman, et al. 2004).
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Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century. Dialogues in clinical neuroscience, 17(3), 327–335. https://doi.org/10.31887/DCNS.2015.17.3/bbandelow
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Levey DF, Gelernter J, Polimanti R, Zhou H, Cheng Z, Aslan M, Quaden R, Concato J, Radhakrishnan K, Bryois J, Sullivan PF; Million Veteran Program, Stein MB. (2020). Reproducible Genetic Risk Loci for Anxiety: Results From ∼200,000 Participants in the Million Veteran Program. Am J Psychiatry, 177(3), 223-232. doi: 10.1176/appi.ajp.2019.19030256
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Shin, L. M., & Liberzon, I. (2010). The neurocircuitry of fear, stress, and anxiety disorders. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 35(1), 169–191. https://doi.org/10.1038/npp.2009.83
Chapter 16, Biological Basis of Psychological Disorders, 17.3. Biological Bases of Anxiety Disorders, original material written by Amy E. Coren, PhD, Pasadena City College, is licensed under CC BY-NC-SA 4.0. Text of Section 17.3.4. Neural structures and neurotransmitters involved anxiety disorders modified and adapted by Amy E. Coren, Ph.D., Pasadena City College, from 4.6 Anxiety Disorders Etiology in Essentials of Abnormal Psychology, by Alexis Bridley & Lee W. Daffin Jr. at Washington State University;licensed under CC-BY-NC-SA 4.0 International License. Retrieved from: https://opentext.wsu.edu/abnormalpsy...g-information/
Figure 17.3.1 Public Domaine, Mohammad_Hassan, via Pixabay.
Figure 17.3.2 BrianMSweis, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons.
Figure 17.3.3 BruceBlaus, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons. File retrieved from: https://upload.wikimedia.org/wikiped...ine_Part_1.png