By Anthony Nedelman & Micheal Calderon
Anxiety disorders are the most common type of mental illness in the United States (Simmons, 2008). The British Journal of Psychiatry describes General Anxiety Disorder (GAD) as a serious and chronic illness; consisting of excessive worry, poor concentration, restlessness, sleep disturbance, and muscle tension (Butters, 2011). Recent research has linked anxiety to processes in the anterior cingulate cortex (ACC). According to University of Toronto professor Michael Inzlicht, the ACC is involved in alerting people when something is out of the ordinary or unexpected in their environment (Wood, 2012). These feelings of confusion or error causes anxiety, worry, and stress. In a study performed by the University of California San Diego, researchers used a method called ambiguity processing. Ambiguity processing occurs when an individual makes a decision based on information that does not clearly suggest the selection of one option over another (Simmons, 2008). The data from the test reveal that those prone to higher anxiety showed greater activation of the dorsal anterior cingulate cortex than those with less anxiety. Older adults that suffer from depression and/or comorbid anxiety have elevated activation in a variety of brain areas, including an increase in activation of the dorsal anterior cingulate cortex. Left untreated, it's possible for an individual to become vulnerable to long term cognitive impairment due to homeostatic mechanisms that prevent excessive biological stress response (Butters, 2011). In other words, biological systems that regulate balance between neurological hormone releases begin to decrease.
Another area of the brain that is often associated with higher levels of anxiety and psychophysiological responses is the hypothalamic-anterior pituitary-adrenocortical (HPA) axis. Major activation of the HPA axis is linked with the release of cortisol; often referred to as the stress hormone. Many studies have been devoted to examining the increases in cortisol levels to both naturalistic stressors and those imposed in the lab environment (Ring 2002; Dickerson and Kemeny 2004). It's also believed that cortisol levels increase in the anticipation of a stressful event; such as prior to public speaking (Garcia-Leal et al. 2005). Cortisol is a chemical associated with permanent brain changes that lead to increased levels of stress, high blood pressure, and heart rate. According to an article in Biological Psychiatry, "early parental separation (EPS) increases the risk for emotional disorders in adulthood (Meinlschmidt, 2007). According to the archives of General Psychiatry, high levels of cortisol may be associated with depression and may also lead to neuronal death and cognitive decline. Women with high cortisol levels or other manifestations of HPA axis dysregulation might have depressive symptoms and poor cognitive function (Browner, 1999).
A Look at Current Research
A fascinating study that examines the effects of cortisol both pre- and post-stressor is titled "The effects of exposure to an acute naturalistic stressor on working memory, state anxiety, and salivary cortisol concentrations (Robinson, Sünram-Lea, Leach, & Owen-Lynch 2007)."
Robinson's team wanted to examine the activation of the HPA axis both before and after the exposure of a stressor; their study used a helicopter evacuation simulation. The helicopter underwater evacuation training (HUET) simulator is used in the UK's military training and other helicopter-related occupations. "During this training students are strapped into a helicopter simulator that is suspended over an environmental pool. On command the students adopt the crash position whereupon the helicopter undergoes a rapid but controlled ditching into the water, submerges and rotates 180 degrees (Robinson et al., 2007)." The students involved in the simulation are required to remain strapped in their seats until the helicopter stops moving, then they are allowed to release their harnesses, evacuate the helicopter, and inflate their life preservers.
Before and after the HUET simulator, the participant's saliva was then collected and examined for cortisol concentrations. One of the findings that stand out above the others revolves around the cortisol levels and it's timing. There were much higher state anxiety levels during the anticipation stage of the training and immediately following the exposure to the stressor, however there were only increased levels of cortisol recorded 25 minutes after exposure to the stressor; not before nor immediately after (Robinson et al., 2007). Robinson and colleagues believe that a possible reason for this is because the participants may not have seen the HUET exercise as a strong enough threat to activate the HPA axis. However, the anticipation of the HUET elevated the state anxiety of the participants prior to the stressor, which leads researchers to believe the HPA axis was activated. They later discovered that the timing the saliva was collected did not coincide with when the cortisol was at it's peak, nor when anxiety levels were at their peak (Robinson et al., 2007) Further research is needed to ascertain how the timing of cortisol, anxiety, and the HPA axis are interrelated as well as how this dissociation in timing can be accurately measured.Summary
The combination of anxiety disorders and its physiological effects on the brain can cause damaging long term defects such as memory impairments. Excessive worry, poor concentration, and restlessness can also lead to depression or other mood disorders. However, treatments for anxiety disorders have been known to improve cognitive function (Butters, 2011).
Dickerson SS, Kemeny ME. 2004. Acute stressors and cortisol reactivity: A meta analytic review. Psychosom Med 64:85-174.
Garcia-Leal C, Alexandre CBV, Parente C, Del-Ben CM, Guimara ̃es FS, Moreira CA, Elias LLK, Graeff FG. 2005. Anxiety and salivary cortisol on symptomatic and nonsympto- matic panic patients and healthy volunteers performing simulated public speaking. Psychiatry Res 133:239-252.
Ring C, Harrison LK, Winzer A, Carroll D, Drayson M, Kendall M. 2002. Secretory immunoglobulin A and cardiovascular reactions to mental arithmetic, cold pressor, and exercise: Effects of alpha-adrenergic blockade. Psychophysiology 37:634-643.
Robinson, S. J., Sünram-Lea, S. I., Leach, J., & Owen-Lynch, P. (2008). The effects of exposure to an acute naturalistic stressor on working memory, state anxiety and salivary cortisol concentrations. Stress: The International Journal on the Biology of Stress, 11(2), 115-124.
Browner, W., Blackwell, T., Gore, R., Sands, L., Reus, V., Yaffe, K. (1999). Depressive symptoms and cognitive decline in nondemented elderly women. Archives of General Psychiatry, 56 (5), 425-430.
Butters, M., Andreescu, J., Begley, A., Bhalla, R., Mantella, R., Wetherell, J. (2011). Changes in neuropsychological functioning following treatment for late-life generlised anxiety disorder. The British Journal of Psychiatry, 199: 211-218.
Simmons, A., Matthews, S., Feinstein, J., Hitchcock, C., Paulus, M., Stein, M. (2008). Anxiety vulnerability is associated with altered anterior cingulated response to an affective appraisal task. NeuroReport, 19 (10): 1033-1037.
Wood, C. (2012). Religious belief reduces anxiety response. Retrieved from www.ibcsr.org.