Running Head: ANXIETY DISORDER

Anxiety Disorder

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Anxiety disorder is a common disorder that affects people of different ages and races.

Over the last year, 18% of adults in the U.S were found to have an anxiety disorder (ADAA,

2018). However, anxiety disorder is at times exaggerated with victims often worried about

unrealistic issues. There is an extensive debate about the exact cause of anxiety disorder with

other people suggesting genetics as the predisposing factor to anxiety disorder. Therefore, this

paper evaluates the argument that “some individuals are born with genes that lead to an anxiety

disorder.”

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Anxiety disorder is a state of non-provoked severe worry and tension. The disease causes

regular worry about issues like disaster, family, and work. People suffering from an anxiety

disorder can develop suicidal thoughts at some point in their lives (Hoehn-Saric et al., 2004).

Anxiety disorder is characterized by irresistible fear and panic among other negative behaviors

which impact daily lives (Wong & Rapee, 2016), (American Psychiatric Association, 2013). The

exact cause of anxiety disorder is yet to be known though genetic inheritance is one of the

aspects attributed to the disorder. Some researchers claim that anxiety disorders can arise from

biological, social, and psychological elements in no particular definite or uniform pattern.

Studies show that one can inherit anxiety disorder from one or both parents and hence the

disorder can run in families (Drain, 2016).

Individuals who have a parent or sibling who has been diagnosed with an anxiety

disorder are vulnerable to developing the disorder themselves. Particular genetic variations

change levels of chemicals within the brain and may even impact nerve cell links, the growth of

nerve cells, and neural circuitry to the extent that they can predispose a person to anxiety (Cagni,

Goncalves, Ziller, Emile, & Barros, 2009). However, there is much unknown regarding genes
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and anxiety disorder. The situation becomes even more complicated for the reason that anxiety

and mood disorders like depression emerge from genetic variations that work in tandem with life

events as well as environmental factors (Newman, Llera, Erickson, Przeworski, & Castonguay,

2013).

Various genes can turn on or off in the life of a person. Genes are responsible for making

the right time at particular times. However, in the event genes get it wrong, a person’s biology is

altered to a level that the person’s mood becomes unstable. The biological propensity to anxiety

can be latent for some time until it is triggered by stressful events for its expression to manifest

(Kagan & Snidman, 1999). The genetic vulnerability of a person is mostly increased by anxiety-

triggering behaviors.

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Many reviews on predisposing factors for anxiety disorder and many interrelated

theoretical underpinning have been published over the past 20 years (Alfano & Beidel, 2011;

Kimbrel, 2008; Morrison & Heimberg, 2013; Ollendick & Hirshfeld-Becker, 2002; and Wong &

Rapee, 2015). Research studies on families that have had anxiety disorders in their lineup have

scrutinized genetic makeup of those families. Variants of genes and chromosomal regions have

been evaluated in such studies with the motive of determining common characteristics among

families with anxiety disorder history. No particular gene pattern has been observed to be

common in all cases of anxiety disorder in any research study. For instance, some research

studies discovered that doubling of the region associated with chromosome 15 was familiar to

families that have high levels of phobia as well as panic disorder (Mufson, 2019). Another study

found out that chromosomes genetic markers for anxiety disorder exist in chromosomes 1, 3, and

11 (Gottschalk & Domschke, 2017).

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There is extensive research on the link between genetics and anxiety disorder. Evidence

from some of the research works shows that genetic vulnerabilities and temperament have a

certain relationship to anxiety disorder. According to Abelson et al., (1991) the brain function

underlining depression is inherited. The study by Abelson and his company indicate that children

whose one or both parents have suffered depression are at high risk of developing an anxiety

disorder in their lifetime. If the argument in the study by Abelson et al., (1991) is valid, then

people who develop an anxiety disorder in the course of their lifetime inherited genes of anxiety

disorder from their parents.

Researchers have conducted studies on rhesus monkeys in an attempt to test whether

genes of anxiety disorder exist. The evaluation of the brain of rhesus monkeys found the

existence of anxious temperament within the brain structure. According to Kalin (2004), rhesus

monkey has three regions that are associated with anxiety. Kalin further argues that the presence

of areas associated with anxiety in monkeys is an indication that anxiety disorder is genetic and

hence evidence of inheritability. According to Charles Darwin and his theory of evolution,

human beings share the same genome with monkeys. Darwin argues that human beings are from

the family of monkeys and chimpanzees and hence share some genetic and biological

characteristics. Considering Darwin’s argument and the research study on rhesus monkey on

anxiety, then the features portrayed by monkeys regarding anxiety disorder are likely to be the

same in human beings.

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Another perspective on the cause of anxiety disorder on the brain sections, genetic

composition, and chromosomal regions. Some research works indicate that different genes, as

well as chromosomal regions, play home to an anxious brain. According to Pappas (2015), there
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is increased activity in the regions identified as the custodian of the anxious brain. Regions

identified as anxious brain are highly activated and experience activity that is twice the normal

activity range within those regions. The increased activity in the anxious brain serves as triggers

for response to mild threats. People with many anxious regions are highly sensitive to fear, and a

slight external triggering effect evokes panic in them. According to Shackman, Oler, Fox, &

Shelton (2013), the overactivity experienced in people with anxious brains is passed down from

parents to offsprings. The overactivity passed down to make the offspring vulnerable to develop

anxiety later. Additionally, chromosomes and the chromosomal composition is argued to have a

link to anxiety disorder. Scientists claim that chromosomes genetic markers for anxiety disorder

exist in chromosomes 1, 3, 11, and 15. Chromosomes are the carriers of genes of parents to

children. The traits of parents, whether positive or negative, are carried in chromosomes and

passed down to children before they are born. The genes of parents with anxious brains passed

down to children can predispose the latter to anxiety disorder. There is a possibility that the

inherited genes can remain dormant until they are triggered by some external factors (Morris-

Rosendahl, 2002). Regardless of the time, it takes for the symptoms of anxiety disorder to

manifest; there are high chances that victims inherited genes of the anxious brain from their

parents before they were born.

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Environmental factors have been proposed by some researchers to be the causative agents

of anxiety disorder. Unfavorable conditions that one is subjected to in the young life or even in

adulthood can have an impact on their emotional and social stability. Various types of abuse such

as sexual assault, domestic violence, and gender-based violence can result in the development of

anxiety (Vann, 2019). Additionally, traumatic events like being involved in fatal accidents,
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stress-awakening scenarios, limited social support, and household economic difficulties have

been observed to trigger anxiety. The moment triggers become extreme and the level of anxiety

rise to high scales, chances of developing an anxiety disorder in a person increases. The claim on

environmental factors causing anxiety disorder complicates the argument on genetics as the

cause of anxiety disorder.

The suggestion of other factors as predisposing elements to anxiety disorder gives

another perspective on the argument that individuals with an anxiety disorder are born with

certain causative genes. There is a chance that environmental factors are the sole causes of

anxiety disorders in people. Equally, there is a possibility that environmental factors only play a

triggering function to enable manifestation of the anxiety disorder symptoms. In any perspective

that can be adopted, the role of environmental factors in anxiety disorder cannot be overlooked.

The decision or conclusion between any of the two perspectives is not absolute, and it is

anchored on the scales of probability. Either the narrative of genetics or environmental factors

can be accepted or rejected, or a trade-off between the two aspects be adopted as the source of

anxiety disorder.

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In the many arguments revolving about people with anxiety disorder and the genetic

predisposition to anxiety disorder, no specific argument is exclusively conclusive. There seems

to be an interplay between genetics and a myriad of other elements in the development of anxiety

disorder. Some researchers show that anxiety disorder runs in families and hence it is a disorder

that is inherited and victims are born with the causative genes. Other research works present a

claim that the environment where people are subjected to and the experiences they encounter

have a bearing on the emotional and social state of a person and hence can trigger anxiety
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disorder. Furthermore, some studies propagate the view that anxiety disorder is genetic, but it

requires environmental factors to trigger it for manifestation. The implication of the various

stands regarding anxiety disorder is that no particular element can be conclusively said to cause

the disorder. The different claims only point to possible contributors to anxiety disorder in a

person. In the research works about genes causing anxiety disorder, there is no evidence that that

show genetic traits that are uniform in all families or individuals having anxiety disorders

(Barros, 2002). Thus, there are high chances that there is no particular “anxiety gene” that can be

singly linked to anxiety disorder. There is a possibility that various genes work together in a

reinforced scheme to stimulate stress response that leaves one more or less prospective to

becoming anxious. Therefore, the argument that “some individuals are born with genes that lead

to an anxiety disorder” is neither true nor wrong since anxiety disorder can be as a result of one

aspect or an interplay of more than one factor.

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References

Abelson L, Glitz D, Cameron G, Lee A, Bronzo M, Curtis C., (1991). Blunted growth hormone

response to clonidine in patients with generalized anxiety disorder. Arch Gen Psychiatry,

48,157–162.

ADAA. (2018). Facts and Statistics. Anxiety and Depression Association of America, 1.

Alfano, C., & Beidel, D. (2011). Social Anxiety in Adolescents and Young Adults: Translating

Developmental Science into Practice. American Psychological Association, 29-51.

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental

Disorders (5 ed.). Arlington: American Psychiatric Publishing.

Barros M, Tomaz C., (2002). Non-human primate models for investigating fear and

anxiety. Neuroscience Biobehavioral Review, 26, 187–201. 

Bethell J, Holmes A, MacLarnon A, Semple S., (2012). Evidence that emotion mediates social

attention in rhesus macaques. PLoS One, 7.

Cagni, P., Goncalves, I., Ziller, F., Emile, N., & Barros, M. (2009). Humans and natural

predators induce different fear/anxiety reactions and response pattern to diazepam in

marmoset monkeys. Pharmacology and Biochemical Behaviour, 93, 134-140.

Drain, K. (2016, October 14). What Caused Your Anxiety Disorder? Genes vs. Environment.

Medical Daily, p. 1.

Gottschalk, M., & Domschke, K. (2017). Genetics of generalized anxiety disorder and related

traits. Dialogues in Clinical Neuroscience, 19(2), 159-168.

Hoehn-Saric R, Schlund W, Wong H., (2004). Effects of citalopram on worry and brain

activation in patients with generalized anxiety disorder. Psychiatry Res.,131, 11–21.

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Kagan , J., & Snidman, N. (1999). Early childhood predictors of adult anxiety disorders.

Biological Psychiatry, 46, 1536-1541.

Kalin Ned (2004).Studying Non-Human Primates: A Gateway to Understanding Anxiety

Disorders, Primate Research in Anxiety Disorders, 2-6.

Kimbrel, N. (2008). A model of the development and maintenance of generalized social phobia.

Clinical Psychological Review, 592-612.

Morrison, & Heimberg. (2013). Social anxiety and social anxiety disorder. Annual Review of

Clinical Psychology, 249-274.

Mufson, M. (2019). Are anxiety disorders genetic? ShareCare: Psychiatry, 1.

Newman, M., Llera, S., Erickson, T., Przeworski, A., & Castonguay, L. (2013). Worry and

Generalized Anxiety Disorder: A Review and Theoretical Synthesis of Evidence on

Nature, Etiology, Mechanisms, and Treatment. Annual review of Clinical Psychology, 9,

275-297.

Ollendick, & Hirshfeld-Becker. (2002). The developmental psychopathology of social anxiety

disorder. Biological Psychiatry, 51, 44-58.

Pappas, S. (2015, July 8). Anxious Brains Are Inherited, Study Finds. LiveScience, p. 1.

Shackman, A., Oler, J., Fox, A., & Shelton, S. (2013). Neural mechanisms underlying

heterogeneity in the presentation of anxious temperament. Proceedings of the National

Academy of Sciences, 110(15), 6145–6150.

Wong, & Rapee. (2015). Social Anxiety and Phobia in Adolescents: Development, Manifestation

and Intervention Strategies. The developmental psychopathology of social anxiety and

phobia in adolescents, 11-37.

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Wong, Q., & Rapee, R. (2016). The aetiology and maintenance of social anxiety disorder: A

synthesis of complementary theoretical models and formulation of a new integrated

model. Journal of Affective Disorders, 203, 84-100.