Internationally, schizophrenia remains a leading cause of disability. Kraepelin initially attributed schizophrenia as a course that inevitably leads to adverse behavioral and cognitive decline. Hence, most neuroscientists and clinicians view the condition as a progressive brain disorder that results in social incapacity. Current neuroimaging research has reinforced the perception by indicating progressive transformations to the brain structure (Zipursky et al., 2013). The disease has positive, negative, and cognitive dysfunction symptoms. The major cause of schizophrenia remains unclear, but recent studies indicate a combination of environmental and hereditary factors as the cause. Moreover, genetic predisposition is the key motive. However, external elements, including subdtance abuse and stressful life situations, can serve as schizophrenia triggers (Orsolini et al., 2022). The current schizophrenia construct remains non-exhaustive in explaining the complexity, heterogeneity, and complicated interplaying roles of additive elements, including environmental and genetic determinants, in schizophrenia pathogenesis. More so, the recent and past schizophrenia constructs cannot adequately offer individualized and dimensional insight into individuals suffering from the illness and cannot offer clinical characterization (Orsolini et al., 2022). Therefore, researchers should revise the traditional and recent schizophrenia construct to ensure enhanced psychiatry. The paper will focus on the role of biological and psychosocial elements in schizophrenia causation and provide a critique and a conclusion.
Niv et al. (n.d ) state that the psychopathological signs of schizophrenia include cognitive, negative, and positive symptoms, and the positive signs originate from an abnormality in functioning, including hallucinations, delusional thoughts, and disorganized behavior. In contrast, the negative signs entail alogia or lessening of speech productivity and fluency, affective flattening, or reduction in emotional expressiveness. Negative signs further involve avolition or inability to start goal-direct acts or behaviour. Anhedonia is the lack of pleasure from activities a person found interesting before. Moreover, cognitive symptoms entail low thinking, poor executive functioning, poor memory, and trouble concentrating (Loch, 2019).
Relevance and understanding
Neurotransmitters
Neurotramistters entail chemicals that transport messages between brain cells. Researchers link schizophrenia and neurotransmitters because medications that change the levels of the neurotransmitters in the brain relieve schizophrenia symptoms (Zipursky et al., 2013). Studies claim that schizophrenia may occur due to modifications in the serotonin and dopamine—an imbalance between serotonin and dopamine causes schizophrenia. More studies claim that changes in the body’s sensitivity to neurotransmitters can lead to schizophrenia (NHS, 2019).
Patel et al. (2015) highlight that neurotransmission abnormalities offer the foundation for theories on Schizophrenia pathophysiology. Most theories concentrate on the deficiency or excess neurotransmitters, including glutamate, serotonin, and dopamine. In contrast, some theories implicate GABA or gamma-aminobutyric acid, glycine, and aspartate as part of schizophrenia neurochemical imbalance. The dopamine receptor site, mostly D2, undergoes abnormal activities believed to cause most schizophrenia symptoms. Studies have implicated four dopaminergic pathways.
Moreover, the nigrostriatal pathways come from the substantia nigra ending in the caudate nucleus. Low levels of dopamine within the pathway impact the extrapyramidal system resulting in motor symptoms. More so, The mesocortical pathways expand from the VTA to the cortex. Low mesocortical level of dopamine leads to negative signs and cognitive deficits in schizophrenia (Patel et al., 2015). In addition, the tuberoinfundibular pathways extend from the hypothalamus to the pituitary glands. A blockage or decline in tuberoinfundibular dopamine leads to increased prolactin levels and minimizes libido, amenorrhea, and galactorrhea (Zipursky et al., 2013).
The serotonin hypothesis for schizophrenia development resulted from findings that LSD or lysergic acid diethylamide improved the serotonin impacts in the brain. More studies resulted in the development of medical compounds that blocked serotonin and dopamine receptors compared to traditional medications that impacted the dopamine receptors. The newer medication remains more effective in alleviating the negative and positive schizophrenia symptoms (Patel et al., 2015).
According to Patel et al. (2015), the theory of glutamate activity remains associated with schizophrenia symptoms. Glutamate entails the key excitatory neurotransmitter in the brain. The theory emerged in reaction to the finding that ketamine and phencyclidine, the non-competitive glutamate or NMDA antagonists, induce symptoms connected to schizophrenia. Moreover, the NMDA receptors remain inactive in the mesocortical dopamine neuron’s normal regulations leading to schizophrenia patients showing cognitive, affective, and negative symptoms. Subsequently, the brain tissues undergo noticeable physical transformations in schizophrenia patients, such as an increase in the lateral and third ventricles and a smaller medial temporal lobe.
Genetic
According to Kim (2016), the genetic theory gets utilized to explain the cause of schizophrenia. Epidemiological research, including studies with twins, verifies the genetic predisposition. The more closely a person is related to a person with schizophrenia, the more the risk of contracting the condition. Furthermore, the twin studies indicate that in identical twins, if one twin has schizophrenia, the second win has one in two chances of acquiring the condition. The outcome is true even if they were raised separately. More so, in non-identical twins with distinct genetic make-ups, when one suffers from the disease, the other twin possesses 0ne in eight chances of suffering from the condition (Naheed et al., 2012).
Kim (2016) claims that the illness happens internationally and with the same genetic risk estimates in all cultures and individuals. Moreover, the monozygotic twin of an individual with schizophrenia sharing a similar genome possesses 40 to 50 percent of contracting the disease. The number represents 50 percent genetic risk and 50 percent nongenetic risk, each functioning in the manifestation of the disease. More so, molecular genetics research such as candidate studies, genome-wide association research, and genome-wide linkage research have contributed to the genetic theories that explain schizophrenia development. The studies indicate that genes, including catechol-O-methyl transferase or COMT, neuregulin one, or NRG1, disrupted in schizophrenia 1 or NRG1, remain the primary genes that cause schizophrenia. Moreover, a meta-analysis study determined that locus 1q21-22, 12q22, and 6, 9, and 20 chromosomes are involved in schizophrenia development (Kim, 2016).
Environmental elements
Exposeme theory or paradigm was assessed in the schizophrenia field. The theory represents the environmental vulnerability entirety associated with schizophrenia spectrum disorder pathobiology in which a person gets exposed in their life (Lumen, n.d). The model observed that environmental elements are interlinked bi-directionally, including marijuana consumption connected to childhood diversity and the impacts of urbanicity, which can get influenced or changed by individual-level elements, including social diversity, discrimination, exclusion, or use of marijuana. The evidence further suggests that dose-response connection between mental health status severity and evidence (Lumen, n.d).
Orsolini et al. (2022) claim that various environmental elements include substance misuse and use, childhood adversity, birth season, prenatal complications, pregnancy complications, and urbanity. Ethnicity and minority status get connected to differential schizophrenia spectrum condition clinical manifestation (Murray et al., 2015). Drug or substance abuse is not directly connected to schizophrenia. However, research has found that drug or substance abuse increases the risks of acquiring schizophrenia or other similar diseases. Specific drugs such as amphetamines, LSD, cocaine, and cannabis triggers schizophrenia signs in susceptible individuals.
Moreover, cocaine and amphetamines can result in psychosis and cause a relapse in individuals recovering from past episodes. Studies indicate that adolescence and young adults consuming cannabis more often have a higher likelihood of developing schizophrenia in their adulthood (NHS, 2019). More so, meta-analysis indicates that substance use, especially progressive use remains considerably connected to higher rates of positive psychotic signs and increased likelihood of aggressive and violent behaviors (Orsolini et al., 2022). In contrast, stress remains the major psychological trigger of the condition. Stressful events, including termination of a relationship, emotional, sexual, and physical abuse, divorce, losing a job, losing a home, or bereavement, can lead to schizophrenia. The events may not cause schizophrenia, but they trigger the development of the illness in vulnerable individuals. More so, ethnic minority status remains correlated with adverse reality disorganization, distortion, and the start of negative symptomatology.
Additionally, individuals with schizophrenia are more likely to face complications during or before birth, such as lack of oxygen during birth, malnutrition, prenatal maternal stress, premature birth, infection, and low birth weight (Zhu et al., 2021). One study found that a mother with flu during the second of the first trimester increased the risk of their child who has schizophrenia. However, the research remains unclear. Infection and stress change neural development via a rise in pro-inflammatory cytokines.
Moreover, children born during spring or winter have an increased risk of developing schizophrenia because of prenatal viral infection or lack of Vitamin D. Infections such as Chlamydia and toxoplasma are associated with an increased risk of developing schizophrenia (Naheed et al., 2012). In addition, the brain’s viral infection during childhood remains connected to increased risks of schizophrenia in adulthood. Moreover, residing in an urban environment as a grown-up or as a child raises schizophrenia risks by a factor of 2 even after considering social group size, ethnic group and drug use, pollution, and urban setting may be the cause of high schizophrenia risks (Lumen, n.d).
Discussion and critique
Adaptive research supports the genetic element hypothesis claiming that it contributes to schizophrenia. However, the researchers indicated that the disorder is likely to arise from a combination of environmental and genetic elements instead of genes (Naheed et al., 2012). For instance, a research assessed schizophrenia rates among 303 adoptees. One hundred forty-five of the adoptees possessed biological mothers who had schizophrenia, and the group was considered the high-risk group. The remaining 158 adoptees had mothers without any psychiatric history, and the group comprised a low-risk genetic group. The adoptees were viewed to come from a disturbed family setting if they showed increased conflict and criticism and lacked problem-solving skills (Lumen, n.d).
The findings showed that adoptees with schizophrenia from mothers with high genetic risks raised in a disturbed family setting had a higher likelihood of developing psychotic disorders, including schizophrenia. The results got compared to adoptees with schizophrenia from biological mothers raised in a healthy family setting or those with low genetic risks raised in a healthy or disturbed setting (Patel et al., 2015).
From the research, adoptees at high genetic risks were likely to acquire schizophrenia only when in a disturbed family setting. Therefore, the study remains consistent with the biopsychosocial diathesis-stress schizophrenia interpretation. The model claims that environmental triggers, including drugs and stress, can trigger the development of schizophrenia in a genetically vulnerable individual. Moreover, the model shows the significance of the environment on the expression of genes. For instance, a young female in her 20s with a genetic vulnerability to suffering from schizophrenia can undergo a traumatic experience that triggers the onset of schizophrenia (Lumen, n.d).
Orsolini et al. (2022) state that epigenetic elements are obtained from the interplay between different environmental factors and genetic factors during the fetal development period that may influence and change the psychopathological trajectory of the disease and post-developmental elements. As a result, it influences the start of schizophrenia via an epigenetic mechanism. Subsequently, researchers have assessed various neurotransmitters, including glutamate, serotonin, and dopamine, acting via GPCRs or metabotropic G protein-coupled receptors that mediate induction of gene expression and intracellular signal transduction of gene expression to put antipsychotic activity in schizophrenia (Zhu et al., 2021). Genetic research has shown a connection between SNPs in genes linked to schizophrenia and GPCR. SNPs are connected to schizophrenia, treatment response to certain antipsychotics, and pathognomic measurable endophenotypes. However, more research is required to assess the role of SNPs and GPCRs variants in schizophrenia and treatment response to certain antipsychotics (van der Merwe et al., 2019).
Over the decades, various evidence-based schizophrenia guidelines have been developed. However, the treatment interventions for schizophrenia are ineffective, and various elements are involved in treatment response depending on the theoretical grounds (Orsolini et al., 2022). The recent schizophrenia approach in routine clinical settings remains stereotyped and prescribed as second-generation psychotic medicine. Since the 1950s, two antipsychotic medications, D2 receptor blockers, have been developed. However, the mechanisms used by D2 receptor blockers to influence therapeutic activity remain unclear (Khan et al., 2013).
Nonetheless, D2 receptor antagonism is viewed as unifying property for antipsychotic medications. However, the medications have limited effectiveness on negative and cognitive signs and demonstrate undesirable metabolic and neurological side effects (Khan et al., 2013). More so, despite the efficacy of the evidence-based cognitive behavioral approach, its utilization remains poor in schizophrenia individuals’ routine clinical practice. Moreover, family-based interventions and employment programs are not fully used in clinical practice. The management of schizophrenia demands a recovery-oriented approach to managing the illness. However, most mental health services lack resilience-promoting setting that incorporates interventions to enhance positive outcomes to implement well-being.
Suttajit et al. (2015) argue that functional psychosocial enhancement remains the ultimate objective for managing schizophrenia. However, it remains challenging to accomplish. Symptomatic remission may not get associated with functional improvement, and effective interventions in psychotic symptoms may not enhance functioning. Therefore, psychosocial functioning remains correlated with psychotic signs and other factors. Hence, concurrently directed toward the factors, therapeutic and preventive interventions may enhance functional outcomes.
Conclusion
In conclusion, the paper focused on the role of biological and psychosocial elements in schizophrenia causation and provided a critique and a conclusion. Researchers should revise the traditional and recent schizophrenia construct to ensure enhanced psychiatry. The major cause of schizophrenia remains unclear, but recent studies indicate a combination of environmental and hereditary factors as the cause. Moreover, genetic predispositions are the key motive. However, external elements, including substance abuse and stressful situations, can serve as schizophrenia triggers. The current schizophrenia conceptualization remains helpful in developing evidence-based principles for treatment and diagnosis (Zhu et al., 2021). Defining the illness by signs and symptoms will hinder a detailed understanding of the illness, its treatment outcomes, and heterogeneous clinical presentation and establishment of effective treatment (Murray et al., 2015). Current studies advocate for the revision of the schizophrenia concept, readapt and implement original and ancient schizophrenia constructs by creating new individualized and interactive approaches. It further advocates considering the unicity of individuals, clinically characterizing the onset of the disease, clinical manifestation, phenotypes, and individualized treatment intervention to an enhanced individualized and dimensional psychiatry (Orsolini et al., 2022).
References
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