Theories of Etiology of Schizophrenia Disorder

Running head: MENTAL HEALTH 1
Theories of Etiology of Schizophrenia Disorder
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Introduction
Schizophrenia (SZ) is a severe mental condition where a person with the illness
interpreted the real things in an abnormal manner. A person with mental disorder will think that
someone either, a public speaker, a famous person, or anyone giving some general life situation
examples is directing the speech or written message to him her. Some of the signs and symptoms
of the disease include hallucinations, extreme thinking disorders, and abnormal behavior, which
interfere with daily functioning. Treatment of the condition is a long-term life process
(McCarthy-Jones et al., 2017).
The current theoretical models of schizophrenia that can be useful in this paper to analyze
Jess’s condition include environmental, genetic-vascular inflammation theory, and genetic theory
of schizophrenia. Jess is a 26 years’ old who was diagnosed with schizophrenia while at the age
of 20 years. Jess receives care from her parents, support from the NDIS disability workers, and a
local general practitioner. Since there was an informed history of the illness in Jess’s family, a
genetic theory of the etiology of schizophrenia can apply to this condition. The gene-
environmental interaction theory can refer to Jess’s condition, whereby it is reported that she
acquired the abusive behavior from a grandmother who her primary caregiver. Hospitalization
due to Jess’s usage of cannabis and alcohol abuse shows the importance of analyzing the
theoretical implications of the inflammatory genetic etiology of the disease, which interconnect
the genetic and environmental factors that lead to the development of the disease (Li et al.,
2017). The etiology of this mental disorder has been poorly understood for the past several years.
Still, there is a current accumulation of evidence that has revealed that it is associated with a
range of brain abnormalities. Several postmortem studies have shown that structural post-
morphologies have been noted in enlargement of lateral and third ventricles, loss of brain frontal,

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grey matter, temporal lobe volume, and decrease in the brain size (Edwards, Bacanu, Bigdeli,
Moscati & Kendler, 2016).
Genetic Theory of Schizophrenia
The genetic etiology of schizophrenia has been intensely studied. It was found to the
subject of the conjecture during the pre-genomic period, though the field of molecular genetics
was limited. This theory relates to the case study of Jess, where it is reported that there is a
history of schizophrenia disease with the family. Jess’s grandmother also seems to have had the
illness since the case study shows that Jess acquired the abusive behavior from her grandmother,
who was her primary care caretaker while she was a child. The dopamine 2 receptor (D2)
subtypes have been studied widely due to their contribution to the risk of SZ after the
antipsychotics drugs, and their pharmacological effects in the brain were discovered.
Antipsychotics interfered with the synapses by altering the dopamine levels leading to boosting
the schizophrenia symptoms such as delusions, thought disturbances, and hallucinations. Intense
research was then shifted to the candidate genes, which were found to have relations with
dopamine production, signaling, and release (Lawford et al., 2016).
Genes associated with the neurodevelopment process, vascular inflammation, and
glutamine regulation strengthened the rationalization of the several candidate genes and the
fundamental hypothesis of SZ. A meta-analysis of the candidate gene was a major step towards
identifying the risk factors of the disease, although it is a difficult process. The venturing of the
achievement of genetic hits as a result of the candidate gene proved to be risky, and there was a
low rate. Earlier studies showed underpowered, and this was the main problem that limited the
capacity to separate true signals from noise. Further research showed that simple samples of
hundreds of thousands of genes could bring a significant effect on the variation related to SZ.

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They also proved more statistical power for those associations to reach sufficient investigation
level replication (Maxwell et al., 2019).
The advancement of technology has enhanced the integrative mapping of the human
genome leading to a cost-effective means of studying various complex traits through the wide-
genome assays. This technological revolution leads to a crucial breakthrough in the genetics of
the SZ. The heritable risk of the disease is known to be contributed by the genes that are indexed
by the single strand nucleotide that is located on the minor allele frequency (MAF) spectrum.
There is also a problem of chromosomal duplication that is known as copy number variants
(CNVs) has been demonstrated in SZ, and it has assisted in the expansion of the pathology of SZ
disease. The disease appears to have run in the lineage of the family of Jess, and it is a result of
genetic mutation. The clinical practitioner can help Jess by organizing for a genetics specialist
who can be of much importance in the long-term treatment of Jess's condition. This genetic
professional uses the family history, which includes health information of both the first and the
second degree, to determine whether the disorder has some genetic element (Liu, Tian, Li, Li &
Zhuo, 2019.
Implications of the Theory
Schizophrenia has led to some substantial comorbidity between several disorders such as
anxiety, tic, oppressive-compulsive, and depression disorders. Depending on the presence of the
gene modifiers, what maps the genome has to prove to be a simple cluster of complex symptoms
than those in diagnostic manuals of risks that can be converted into depression and anxiety
disorders. Some phenotypes that are currently used to study genetics are the neurobiological
differences, which include the abnormalities in the eye movements, and are associated with