Etiology Theories Causes of the Social Anxiety Disorder Research Paper

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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).

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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…

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…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).

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