Anxiety disorders are one of the most complex psychological disorders in existence and also one of the least understood, etiologically. It is extremely important to understand anxiety disorders from an etiologically genetic standpoint, because it often explains why those people who experience the same environment react differently- why some develop an anxiety disorder, whereas others don't. This is what is known as the GXE Interaction. For example, adults who suffered child abuse are susceptible to developing Post-Traumatic Stress Disorder, a type of anxiety disorder, as a result. However, some people will develop PTSD whereas others won't, even though they experienced the same trauma.
The research of GXE often separates the etiology and probability that any one person will develop an anxiety disorder as opposed to those who won't in the same environment, which is why it is so critical that we understand its effect on anxiety. There are two types of anxiety: state anxiety and trait anxiety; state anxiety is that anxiety which a person experiences from ordinary, normal', life events, such as job stress- it is temporary and tends to be mild to moderate. Trait anxiety however, is that anxiety that a person experiences constantly- it is moderate to severe and often debilitating (Belzung, Calatayud, and Clement, 2002). We will only be concerned with trait anxiety- which encompasses all of the anxiety disorders- for this essay.
[...] Genetic Vulnerability to Stress. Nature Neuroscience. Costa, P.T., Herbst, J.H., McCrae, R.R., and Zonderman, A.B. (2000). Do the Dimensions of the Character and Temperament Inventory Map a Simple Genetic Architecture? Evidence from Molecular Genetics and Factor Analysis. The American Journal of Psychiatry, 157, 1229-1235. Dugue, M. & Neugroschi, J. (2002). Anxiety Disorders: Helping Patients regain Stability and Calm. Geriatrics,57, 27-31. Skipper, M. (2002). Human genetics: It's all in the Mind. Nature Reviews Genetics, 3. Triunfol, M.L. (2002). Danger, danger…Will Robinson. [...]
[...] An inherited deficiency of GABA predisposes people to respond to a traumatic event with an anxiety disorder. This was determined in an animal study using mice, because “mice deprived of [the] gene that facilitates transmission of [the] specific chemical messages in the brain represent [the] potential animal model of anxiety-prone [humans].” When that particular gene was experimentally deleted in a laboratory assay, the mice exhibited a substantial reduction in GABA. The researchers then reserved a control group (of mice) and an experimental group of mice who were missing a copy of the GABA-receptor gene. [...]
[...] Kendler et al. (1992a; as cited by Boer & Lindhout, 2001) conclude: “Because the genes that influence vulnerability to major depression have the same effect on generalized anxiety disorder, and because familial environment plays no substantial role in their etiology, individual-specific experiences will decide whether somebody will suffer from generalized anxiety disorder or major depression.” (p.239) Kendler also states that when a particular comorbidity does occur, only 25% of it is influenced by genetic factors, whereas 75% is influenced by nonshared or specific environment (as cited by Boer & Lindhout, 2001). [...]
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