Written By Sydnee A. Fry
An Overview of Generalized Anxiety Disorder
GAD is often referred to as one of the most common psychological disorders, with a 21% rate in adults during their lifetime (Patriquin & Mathew, 2017). Characterized into a three-response system including verbal-subjective acts, overt motor acts, and somato-visceral activity, anxiety and fear interconnect with their symptoms and actions (Craske et al. 2011). Fear, commonly felt by the normal individual, is an alarm response to (real or perceived) danger, while anxiety is a future-oriented feeling associated with preparation for possible, upcoming negative events.
Using Pavlovian fear conditioning, where a neutral stimulus is paired with an aversive stimulus until the neutral stimulus alone can elicit a fear response, understanding anxiety becomes a much simpler task. In an article created by (Craske et al. 2011), they describe a newfound split in fear-based learning: explicit threat cue learning, which involves specific cues predicting imminent threat, and context learning, where the environment becomes associated with the threat. These types of learning correspond to different defensive responses and are mediated by different brain regions, such as the amygdala for explicit threat cues and the bed nucleus of the stria terminalis (BNST) for contextual cues. The hippocampus also plays a role, particularly in contextual fear conditioning. For example, a GAD patient may elicit a fear response upon driving during a stressful situation and begin to associate the car with a threat in a context-learning fashion. Some symptoms they could experience are anxiety symptoms such as excessive worry (verbal-subjective), avoidance (overt motor), tension (somato-visceral), and fear symptoms like racing, threatening thoughts (verbal-subjective), escape (overt motor), and strong autonomic surge resulting in physical symptoms such as sweating, trembling heart palpitations, and nausea (somato-visceral).
Potential Causes
Genetics and Epigenetic Factors
In a meta-analysis conducted by Hettema and Kendler (2001), the yielded heritability of generalized anxiety disorder was 0.32, or around 32%. This can be further explained by the epigenetic links of GAD based on environmental issues surrounding the patient. Based on a study revolving around childhood trauma and adult anxiety conducted by (Kascakova et al., 2020), reporting anxiety and pain was associated with a higher prevalence of emotional and physical abuse and emotional and physical neglect in the clinical population (Figure 1).
Figure 1
Prevalence of various childhood trauma types in the research groups
Note. Various groups report different symptoms. (A) Community sample reporting no chronic conditions; (B) Community sample reporting other chronic conditions; (C) Community sample reporting anxiety; (D) Clinical sample (respondents with a clinical diagnosis of anxiety or adjustment disorder who concurrently reported anxiety and some pain condition) (Kascakova et al., 2020).
Neurobiological Factors
Looking introspectively, a few potential disturbances in neurotransmitters such as serotonin, epinephrine, norepinephrine, and/or GABA have been found in diagnosed GAD patients (Bandelow et al., 2013). Recently, a study conducted by Kadosh and Johnstone (2024) investigated the brain chemistry behind anxiety in young women, observing important imbalances of GABA and glutamate. A problem in the delicate balance between the propelling of brain activity in glutamate and inhibition in GABA may explain constant irrational thoughts often found in anxiety symptoms, as well as lead to possible treatments to restore homeostasis. Furthermore, issues within the structure connectivity may be a leading cause of GAD. In an article detailing the neurobiological functions of GAD by (Patriquin & Mathew, 2017), they find that the resting-state functional connectivity (RSFC) between the amygdala and the prefrontal cortex (PFC) is reduced in GAD patients. The PFC holds an important role in the regulation of emotions, especially negative emotions such as anxiety. Without connectivity to the amygdala, which helps process perceived negative situations or threats, the PFC is unable to regulate an appropriate response.
References
Bandelow, B., Boerner, R. J., Kasper, S., Linden, M., Wittchen, H.-U., & Möller, H.-J. (2013). The diagnosis and treatment of generalized anxiety disorder. Deutsches Aerzteblatt Online, 110(17). https://doi.org/10.3238/arztebl.2013.0300
Craske, M. G., Rauch, S. L., Ursano, R., Prenoveau, J., Pine, D. S., & Zinbarg, R. E. (2011). What is an anxiety disorder? Focus, 9(3), 369–388. https://doi.org/10.1176/foc.9.3.foc369
Hettema, J. M., Neale, M. C., & Kendler, K. S. (2001). A review and meta-analysis of the genetic epidemiology of anxiety disorders. American Journal of Psychiatry, 158(10), 1568–1578. https://doi.org/10.1176/appi.ajp.158.10.1568
Is the secret to anxiety in young women hidden in our brain chemistry? | University of Surrey. (2024). Surrey.ac.uk. https://www.surrey.ac.uk/news/secret-anxiety-young-women-hidden-our-brain-chemistry
Kascakova, N., Furstova, J., Hasto, J., Madarasova Geckova, A., & Tavel, P. (2020). The unholy trinity: Childhood trauma, adulthood anxiety, and long-term pain. International Journal of Environmental Research and Public Health, 17(2), 414. https://doi.org/10.3390/ijerph17020414
Patriquin, M. A., & Mathew, S. J. (2017). The neurobiological mechanisms of generalized anxiety disorder and chronic stress. Chronic Stress, 1(1), 247054701770399. https://doi.org/10.1177/2470547017703993
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