Theories of Etiology Research Paper 10 pages

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Theories of Etiology (Causes) of the Social Anxiety Disorder

Subordination Stress Model

Primates depend on establishing social relationships, and like men, laboratory assessments can be conducted to study their behavior. Studies that focused on nonhuman primates in an informal setting concerning dominance and subordination targeted female cynomolgus monkeys. The study established that subordinates dedicated more time living alone where they scanned their social world with fear. This is unlike the dominants who displayed directly opposite of the behavior. Biological analysis focusing on the subordinates further revealed hyperactive hypothalamic-pituitary-adrenal (HPA) axis activity, impaired dopaminergic neurotransmission, and serotonergic functions. A different challenge study on social subordinates registered HPA axis activation and hyper-secreted cortisol. A challenge test about fenfluramine on cynomolgus macaques (housed) showed low response on prolactin, which indicates a fall in central serotonergic response. These monkeys’ strata were subjected to low social interactions and reduced body contact compared to those with high prolactin activity. A haloperidol test using dopamine antagonist, which promotes prolactin’s secretion into the tuberoinfundibular pathways, exhibited prolactin reduction in subordinates (Shively, 1998). The implication of the results is a reduced postsynaptic dopamine receptors response towards subordinates’ pathways. Post emission tomography studies registered reduced striatal dopamine D2 binding analogous to the neuroendocrine data, indicating abnormal neurotransmission in the central dopaminergic. These results imitate single-photon emission computerized tomography (SPECT) conducted on humans exhibiting anxiety disorder (Mathew, Coplan & Gorman, 2001, p.1558).

Studies conducted on wild and socially oriented subordinate baboons indicated abnormalities in the neuroendocrine with the results similar to those of depressed and anxious humans. Both hypercortisolemia and resistance to inhabitation feedback arising from dexamethasone were also registered. Subordinate males of the baboon-ancestry were also found to contain lower growth factor 1 levels than the dominants (Sapolsky & Spencer, 1997). The revelations can explain the relationship between anxiety disorder and short stature (Mathew, Coplan & Gorman, 2001).

Variable-Foraging-Demand Model

Variable-foraging-demand-model is also applicable in nonhuman primates. The model was developed by Paully and Rosenblum to achieve non-assertiveness and social timidity through the exposure of nursing mums to impulsive foraging-demand situations and later invoking uneven attachment procedures to the infants (Paully & Rosenblum, 1984). Adult animals that excelled under the demand conditions showed stable growth in social timidity compared to certainly raised subjects of comparison; for example, reduced species huddling, subordination, and exception to antagonistic encounters. These elements were evident when compared to the reared subjects.

From a biologist’s perspective, subjects in the variable-foraging-demand-model display raised CSF (cerebrospinal fluid), CRF (corticotropin-releasing factor), HVA (homovanillic acid), and 5-HIAA (5-hydroxyindoleacetic acid). Only those under the model registered correlation in CRF and both 5-HIAA and HVA levels of all the subjects. It suggests that there is a functional connection between CRF status and both serotonergic and dopaminergic systems. Additionally, of the group under the model, there was increased CRF levels that showed close correlation with fall in the development of growth hormone and its response to ?2 adrenergic agonist clonidine. Further, there was a correlation in anxiety activity to yohimbine, which is an ?2 antagonist (Mathew, Coplan & Gorman, 2001).

A neurochemical dimension indicated significant relevance in the social anxiety disorder and associated alteration of dopaminergic CSF metabolites for primates housed under the foraging model. It tallies with various dopaminergic abnormalities present in patients exhibiting social anxiety disorder. In terms of behavior, primates (young children) in the variable-foraging demand situations exhibited unfamiliar behavioral inhibition. They registered over-pronounced heart rates, raised stress levels, and increased levels of salivary cortisol. Behavioral inhibition also showed a correlation with the activity of high total norepinephrine. Thus, variables in the foraging models can be useful in suggesting that the affective nature of environmental stress may lead to a shift in both behavior and neurobiology in the direction of socially anxious characteristics (Mathew, Coplan & Gorman, 2001, p.1559).

Animal Attachment Models

From the historical perspective, lack of attachment behavior has close links with schizoid and autistic disorders. The difference between patients with the two disorders and those with social anxiety occurs in their degree to be attached or relate to others. Due to their closeness with the variant avoidant disorder, patients with anxiety disorder desire attachments and connections but fear the associated interactions. On the other hand, schizoid and autistic persons lack interest in the attachments. They also do not show interest in affiliative characters. Given these differences, attachment models have no significant contribution to understanding social anxiety disorder (Mathew, Coplan & Gorman, 2001).

Various studies have been conducted in the neurotransmitter systems about affiliations and attachments among people with autism. Improved serotonergic effects gave enhanced affiliative characteristics among primates. A reduced level of serotonin led to avoidance. In a different yet related study, primates (free-ranging) with reduced CSF 5-HIAA levels demonstrated low social competence and an increased likelihood of exiting their social groups at a tender age (Mehlman et al., 1995). This was in comparison with those with higher CSF 5-HIAA levels.

Though limited in their explanations and misappraisals that touch on social anxiety disorder, preclinical models offer important constructs that help understand the affiliative nature of aberrant social behavior among those with an anxiety disorder (Raleigh, Brammer & McGuire, 1983). They also offer a platform to help enhance future studies of the neurobiological disorder. One of the shortcomings regarding neurobiology attachments is the sparsity of data that would otherwise be useful in the replication process. At least at this time, direct use of such animal models is limited in offering social anxiety disorder (Mathew, Coplan & Gorman, 2001).

Associated Factors in the Development of Social Anxiety Disorder (genetic, environmental, familial, lifestyle)

Genetic

Low, Cui and Merikangas (2008) carried out a study on 1053 parents affected by Social anxiety disorder (SAD) in their Community versus clinic sampling: effect on the familial aggregation of anxiety disorders published in Biological psychiatry. In-depth analysis revealed a heightened risk of acquiring SAD, especially with five years of early adolescence (Low, Cui & Merikangas, 2008). The research identified a set of three groups among parents who were believed to have offspring with a high risk of developing the disorder. In the first group, the parents had no history of mental disorders. The second has parents with a history of mental illness but not a social phobia. The third group comprised parents with a complete disorder diagnosis (Sundaram, 2019).

Other genetic studies were conducted along the same research line to assess risk factors and possibly associated genetic, social anxiety disorders (Lebowitz et al., 2016; Hitchcock, Chavira & Stein, 2009; Sundaram, 2019). It was revealed that:

The social anxiety of shyness among children correlates with the shyness factor of the biological mother.

In the learning process of SAD-affected parents, children could develop social anxiety disorders.

The degree of SAD occurrence is greater in genetically identical (monozygotic) twins than fraternal (dizygotic) twins. This is according to statistics recorded from 2163 female twins with preformed anxiety (Sundaram, 2019).

Several types of genes could lead to the development of SAD. These include:

SLC6A4 gene

SLC6A4, by definition, falls under the category of serotonin transporters. Research has shown a strong association between it and SAD development. It has been demonstrated that SLC6A4 and SNP have major contributions to SAD development (University of Bonn, 2017). SLC6A4 also assumes other names like SERT or 5-HTT (5-hydroxytryptamine). Defects in the process of serotonin transformations have also been linked with a social anxiety disorder (Frick et al., 2015). Serotonin involved in neurotransmission is crucial in the definition of different moods. Blockage in neurotransmitters’ release can cause serotonin imbalances, leading t anxiety disorder alongside conditions such as depression (Sundaram, 2019).

ADRB1 gene

Also known as beta-1 adrenergic receptor (?1 adrenoreceptor) can also lead to the development of SAD. There is no scientific backup to ascertain its association with the development of social anxiety disorder (Sundaram, 2019).

CRF receptor gene

Corticotropin-releasing factor (CRF) constitutes one of the genetic components available in the CRHR2 CRF receptor. Genetic mutation of CRHR2 leads to social anxiety (Reul & Holsboer, 2002). The mutation also inhibits the binding process between CRF and CRF2 receptors. The process is viral in stress reduction. The gene encoding regulator of G protein signaling 2 (Rgs2) is a quantitative trait gene that influences mouse anxiety behavior, making its human ortholog (RGS2) a compelling candidate gene for human anxiety phenotypes (Smoller et al., 2008). Some documentation associated the RGS2 gene with SAD, but details remain scanty (Sundaram, 2019).

Environmental

SAD is associated with the constant fear of performing in social environments. These elements arise from the environmental implications and etiological characteristics of the disorder.

1. Parenting Factors

Evidence exists that attribute parent-child engagement as one of the SAD predisposing factors. Further investigations of the onset of the disorder at an early age have more to do with parenting factors than other anxiety disorders. Parents can develop social models that lead to negative responses, which can be catastrophic in social life. Faulty and fearful social modeling exposes them to negative judgment. True to this theory, SAD patients report that at their time of development (Norton & Abbott, 2017), the parents emphasized both the appearance and opinions of others (Khetrapal, 2019).

Parents who exercise over-control and tend to be over-protective over the kids set a culture of restrictions that cause social autonomy and self-efficacy. They also suppress the growth of social abilities. This parenting style also conveys to the children that they lack the powers to overcome challenging situations and only exist when offered protection against the scary world. On the other end, parents who relax parenting behavior and encourage them to protect themselves make them develop a sense of social ability and significantly reduce SAD development. This has been proven in kids around four years old (Majdandzic et al., 2014).

2. Negative and Traumatic Life Experiences

SAD has also been linked to difficult or traumatic experiences in life. Though SAD development can lead to trauma, research indicates that prior development and experiences of difficult conditions accelerate SAD-related risk such as psychopathology (Smoller et al., 2008). SAD has neem linked to negligence and emotional abuse in childhood compared to other traumatic conditions such as physical and sexual abuse. (Norton & Abbott, 2017).

Lifestyle

People experiencing social anxiety depict it differently, and symptoms do not have to manifest in all social situations. If the environment is friendly such as with personal friends, family, and relatives, and people they are accustomed to, the symptoms may not appear at all. Even when such categories of people are requested to speak about a subject publicly, they have some expertise; they can confidently do some with some merit. However, in other situations, the same faces major anxiety and distress, even situations that do not pose any threat to anyone (Bridges to Recovery).

Pathology of social anxiety disorder.

Research projects between 30 and 50 percent of cases of anxiety disorders arise from genetic contributions. It implies that non-genetic factors contribute between 50 to 70 percent of the disorders (Patriquin & Mathew, 2017). Disorders accelerated by the environmental conditions emanate from epigenetic methods, even at utero (Patriquin & Mathew, 2017). Such environmental factors include situations like trauma and stress. Detailed understanding of Generalized anxiety disorder (GAD) both in epigenetic and genetic dimensions form important tools for building neurobiological measures to create both treatment and preventive methods.

One known study targeting GAD symptoms revealed a close association between a single-nucleotide intronic (rs78602344) to thrombospondin into thrombospondin 2 (THBS2) and its symptoms GAD (Patriquin & Mathew, 2017). This was done on a population of Latino/Hispanic adults (Dunn et al., 2017). A study that was not tied directly to GAD that assesses non-anxious versus non-anxious adults indicates that DNA methylation intensity was more among anxious adults than non-anxious ones (Patriquin & Mathew, 2017).

Disturbed brain coordination has been quoted as the principal neurobiological feature that leads to Generalized Anxiety Disorder (GAD) (Martin et al., 2009). Precisely, reduced resting-state functional connectivity (RSFC) for the prefrontal cortex (PFC) and amygdala. This happens in both adolescents and adults with GAD. The differences, both functional and structural neuroimaging, between healthy and GAD control groups exist beyond frontolimbic contexts. They also penetrate the downstream way from the amygdala (anterior cingulate cortex). Scientific investigations reveal a reduced association between PFC and amygdala for adulthood and adolescence and GAD diagnosis (Martin et al., 2009). The PFC is particularly critical because of its regulatory role in the ventromedial areas to cope with anxiety and negative emotional effects. PFC’s activity has also been known to enhance limbic structural regulations following psychological and pharmacological GAD effects (Patriquin & Mathew, 2017).

Examples of Treatment Options Pharmacological and Nonpharmacological Treatments

Pharmacological interventions

SAD medication process utilizes three categories of drugs. 1) Anticonvulsants 2) antidepressants, and 3) benzodiazepines (WebMD, 2019). Other categories, such as antipsychotics, cognitive enhancers, beta-antagonists, and St John’s wort, have also helped treat SAD (Cassano, Baldini Rossi & Pini, 2002). Antidepressants are associated with enhanced serotonin and dopamine levels in the brain (WebMD, 2019).

Selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) are used for SAD and common anxiety disorders. Of all SNRIs, the only venlafaxine has been extensively researched and proven to positively affect handling social anxiety disorder. The effects occur through variations in prescribed serotonin dosage levels (WebMD, 2019).

Monoamine oxidase inhibitors (MAOIs) are involved in inhibiting melatonin, dopamine, tyramine, serotonin, and noradrenaline breakdown. These effects take part in any body part rich in MAO, not just the brain. A typical example is gut. MAO inhibition can lead to dangerous effects caused by tyramine interactions, and in the case of some medications, blood pressure can rise significantly. Moclobemide is known to reduce this effect through reversing functionalities (National Collaborating Centre for Mental Health UK, 2013).

Benzodiazepines affect gamma-aminobutyric acid, which plays the chief neurotransmitter inhibitory role in the brain. Persistent use of benzodiazepines can lead to dependence and tolerance and hence faces restrictions in its use. (National Collaborating Centre for Mental Health UK, 2013).

Anticonvulsants precisely alpha2delta calcium-gated channel blockers play an important role in the reduction of neuronal excitability. It is also instrumental in addressing neuropathic pain. However, its operation mechanism remains unknown (National Collaborating Centre for Mental Health UK, 2013).

Nonpharmacological

Exposure in vivo encourages socially anxious person to confront challenging situations without fear. It often takes a hierarchical approach beginning from the least feared to the most. Repeated exposure may result in habituation. The technique of exposure also aids in disconfirming beliefs that are mostly maladaptive. Exposure practices take real-life confrontation (in vivo) in the context of social circumstances through therapy, assignments, and multiple exercises (National Collaborating Centre for Mental Health UK, 2013).

Applied relaxation focuses on training individuals to compose themselves in situations uncomfortable to them. It begins with the traditional ways that mimic muscle relaxation and then followed by progressive steps, all anchored on relaxation’s fundamental goal. The last step often involves adopting intense relaxation techniques in the social environment (National Collaborating Centre for Mental Health UK, 2013).

Social skills training assumes that people get anxious because of uncertainty about the behavior to adopt. Principally, this form of training concentrates on non-verbal skills such as posture and eye contact and verbal skills such as initiating and maintaining a conversation ((National Collaborating Centre for Mental Health UK, 2013). These skills are realized through therapeutic practices achieved through different roles of the sessions and the assignments. In cases of exposure, skills may arise through suppressing negative beliefs or habituation.

Cognitive-behavioral therapy (CBT) assumes in vivo exposure and restructuring of the cognitive statuses and relaxation training techniques. It also incorporates conversational training. CBT is served through group or individual methods(Bandelow, Michaelis & Wedekind, 2017).

Cognitive therapy (CT) is closely related to CBT. Its main focus areas include negative individual beliefs of SAD people, low self-imagery, and behavioral and cognitive challenges. In practice, the treatment is customized to meet individuals. Even though the therapist should invite different people to participate by adopting longer sessions (National Collaborating Centre for Mental Health UK, 2013).

Short-term psychodynamic psychotherapy identifies SAD symptoms by reviewing relationships in conflicts present in previous experiences. In this process, the therapy helps the individual realize the association between symptoms and conflicts. The identification is an essential attribute of change (National Collaborating Centre for Mental Health UK, 2013).

Diagnostic and Research Technologies Employed in Clinical Diagnosis, Clinical and Behavioral Health Care, and Basic Science Research

The role of diagnosis in clinical settings is essential in offering appropriate care to the patients and enhancing both policies and research. It takes both a classification and process scheme or even pre-existing standards set by medical professionals. These standards are customized depending on the condition being diagnosed. Once a patient approaches health care services, what follows in a repeated information gathering process, consolidation, interpretation, and later determination of diagnosis process. Other processes to gather vital information involve interviews and review of clinical history, testing, and physical examination. All these details link to the health of the patient. These are not the only ways to gather information, and the diagnostic process can employ a varied approach. Before these processes, there should be a generation of hypotheses and updates on past probabilities. Other attributes essential in the clinical process in communication among the clinicians, patients, and family engagement. They enhance the process of harvesting information, consolidation, and interpretation (Balogh, Miller & Ball, 2015).

Tools and technologies involved in medical care are commonly used for health improvement. They can utilize a diagnostic approach. The interaction amid various elements contributes to the functionality of the entire health system. For example, a variation in the physical environment could limit health information technologys (IT’s) accessibility and the same for changes in the diagnostic team, affecting the assigned tasks. The set systems of work influence how the process of diagnosis takes place. Health IT comprises, among others, electronic health records (EHRs), computerized order entries, patient engagement tools, clinical decision support, imaging tools, and medical devices (Balogh, Miller & Ball, 2015). The IT tools play critical roles in the entire diagnostic procedures. It aids in gathering important information such as history, tests and results, physical examination, and the shaping of clinical workflow. All these come together to facilitate the process of information exchange.

References

Balogh, E. P., Miller, B. T., & Ball, J. R. (2015). Improving diagnosis in health care.

Bandelow, B., Michaelis, S., & Wedekind, D. (2017). Treatment of anxiety disorders. Dialogues Clin Neurosci, 19(2), 93-107. DOI: 10.31887/DCNS.2017.19.2/bbandelow

Bridges to Recovery. (n.d.). Causes of Social Anxiety. Retrieved November 14, 2020, from https://www.bridgestorecovery.com/social-anxiety/causes-social-anxiety/

Cassano, G. B., Baldini Rossi, N., & Pini, S. (2002). Psychopharmacology of anxiety disorders. Dialogues in clinical neuroscience, 4(3), 271285.

Dunn, E. C., Sofer, T., Gallo, L. C., Gogarten, S. M., Kerr, K. F., Chen, C. Y., … & Qi, Q. (2017). Genome?wide association study of generalized anxiety symptoms in the Hispanic Community Health Study/Study of Latinos. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 174(2), 132-143.

Frick, A., hs, F., Engman, J., Jonasson, M., Alaie, I., Bjrkstrand, J., … & Wahlstedt, K. (2015). Serotonin synthesis and reuptake in social anxiety disorder: a positron emission tomography study. JAMA psychiatry, 72(8), 794-802.

Hitchcock, C. A., Chavira, D. A., & Stein, M. B. (2009). Recent findings in social phobia among children and adolescents. The Israel journal of psychiatry and related sciences, 46(1), 3444.

Khetrapal, A. (2019). Neural mechanisms of Social Anxiety Disorder. Retrieved from https://www.news-medical.net/health/Neural-Mechanisms-of-Social-Anxiety-Disorder.aspx

Lebowitz, E. R., Leckman, J. F., Silverman, W. K., & Feldman, R. (2016). Cross-generational influences on childhood anxiety disorders: pathways and mechanisms. Journal of neural transmission (Vienna, Austria : 1996), 123(9), 10531067. https://doi.org/10.1007/s00702-016-1565-y

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Majdandi?, M., Mller, E. L., de Vente, W., Bgels, S. M., & van den Boom, D. C. (2014). Fathers’ challenging parenting behavior prevents social anxiety development in their 4-year-old children: A longitudinal observational study. Journal of Abnormal Child Psychology, 42(2), 301-310.

Martin, E. I., Ressler, K.J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatric Clinics, 32(3), 549-575.

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