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Genetics And Environmental Factors In Schizophrenia

  • 5 days ago
  • 5 min read

Author: Yogita Sanwal


SUMMARY

Schizophrenia is a severe mental disorder that affects thinking, perception, emotions and behavior. It is not caused by a single factor but develops due to the combined influence of genetic vulnerability and environmental exposure. Research has consistently shown that individuals with a family history of schizophrenia are at a higher risk, indicating a strong genetic basis. However, genetics alone cannot fully explain the occurrence of the disorder, as many people with genetic risk never develops schizophrenia. Environmental factors such as prenatal complications, childhood trauma, substance use and social stressors significantly contribute to the onset and course of the illness. Modern research emphasizes the interaction between genes and environment, suggesting that environmental stressors may activate underlying genetic susceptibility. Understanding this interaction is essential for early identification, prevention and improved treatment strategies. From a psychological. point of view schizophrenia cannot be understood only through biological causes, as life experiences and surroundings conditions strongly influence how the disorder develops and progresses.





KEY DEFINITIONS


SCHIZOPHRENIA:

A chronic psychiatric disorder characterized by disturbances in thought, perception, emotions and behavior, often presenting with hallucinations, delusions, and impaired functioning.


GENETIC FACTORS:

Inherited biological characteristics passed from parents to offspring that increase an individual’s susceptibility to developing schizophrenia.


ENVIRONMENTAL FACTORS:

External conditions and life experiences such as stress, trauma, infections or substance use that influence mental health outcomes.


GENE – ENVIRONMENT INTERACTION:

A process in which environmental influences affect individuals differently depending on their genetic makeup.


NEURODEVELOPMENT:

The process of brain growth and maturation from prenatal life through adulthood which may be disrupted in schizophrenia.


POLYGENIC INHERITANCE:

A pattern in which multiple genes collectively contribute to the risk of developing a disorder rather than a single gene.



INTRODUCTION

Schizophrenia is a complex mental illness that affects approximately one percent of the population worldwide. It usually begins it in late adolescence or early adulthood and often leads to long term impairment in social, occupational and personal functioning. For many years, researchers attempted to identify a single cause of schizophrenia but current scientific understanding recognizes it as a multiple factorial disorder. Both genetic and environmental factors contribute significantly to its development. While genetic factors create a vulnerability to the disorder, environmental influences determine whether and how this vulnerability is expressed. In my view, focusing only on genetics or only on environment gives an incomplete picture because both factors work together in shaping mental health outcomes. Studying both expects together provide a more comprehensive understanding of schizophrenia and support the development of effective prevention and intervention strategies.


GENETIC FACTORS IN SCHIZOPHRENIA

Evidence for the genetic basis of schizophrenia comes from family, twin and adoption studies. Individual with a close relative diagnosed with schizophrenia are at a higher risk compared to the general population. Twin studies demonstrate higher concurrence rates among identical twins then fraternal twins, indicating a strong heredity component. However, the fact that concurrence is not 100 percent also highlight the role of non genetic influences.

Advances in molecular genetics have revealed that schizophrenia is a polygenic disorder. This means that many genes each contributing a small effect, collectively increase vulnerability. These genes are often involved in brain development, neurotransmitter functioning and synaptic connectivity. Rather than one defective gene causing schizophrenia or combination of genetic variation creates a predisposition. 

In addition to common genetic variations, rare mutations and structural changes in chromosomes known as copy number variations, have been linked to schizophrenia. Certain chromosomal deletions and duplication significantly increase the risk of developing the disorder. These finding support the idea that disruption in early brain development are central to schizophrenia.

This clearly suggests that having a genetic risk does not mean a person will definitely develop schizophrenia, but it increases vulnerability under certain conditions.



ENVIRONMENTAL FACTORS IN SCHIZOPHRENIA

Environmental influences play a crucial role in determining whether genetic vulnerability leads to schizophrenia. Prenatal and perinatal factors are among the earliest environmental risk. Complications during pregnancy such as maternal infection, malnutrition or high stress levels can interfere with fetal brain development. Birth related complications including oxygen deprivation, have also been associated with an increased risk of schizophrenia later in life.

Many studies show that long term stress during childhood can quietly affect emotional regulation and coping ability, which may later contribute to psychotic symptoms. 

Social factors also contribute significantly. Growing up in urban environments, experiencing social isolation or belonging to marginalized communities have been associated with higher rates of schizophrenia. Migration and discrimination may increase exposure to social stress, which can trigger symptoms in vulnerable individuals.

Substance use, specially cannabis using during adolescence, is a well established environmental risk factor. Research suggests that early and heavy cannabis use increase the risk of psychosis, particularly in individuals who already have a genetic predisposition. This highlights the importance of preventive education and early intervention.


INTERACTION BETWEEN GENETIC AND ENVIRONMENTAL FACTORS

Current models of schizophrenia emphasize the interaction between genetic susceptibility and environmental stressors. The diathesis - stress model proposes that individuals inherit a vulnerability that remain inactive until triggered by environmental challenges. For example, a person with genetic risk may develop schizophrenia following severe stress, trauma or substance use while another individual without such vulnerability may not.

Environment interaction explains why people expose to similar environmental condition do not experience the same outcomes. Genetic makeup influences how individuals respond to stress, infection or drugs. Environmental factors may activate or suppress certain genes, leading to changes in brain functioning.

This interruption helps explain why two individuals exposed to similar stressors may show very different psychological outcomes.


BIOLOGICAL PATHWAYS LINKING GENENS AND ENVIRONMENT

Several biological mechanisms explain how genetic and environmental factors interact. One key pathway involves abnormal neurodevelopment. Genetic risk factors may disrupt normal brain maturation while environmental stressors further impair sympathetic pruning and connectivity.

Neurotransmitter systems, particularly dopamine and glutamate, are also involved genetic variations affecting these systems may increase sensitivity to stress or substances, leading to psychotic symptoms. Environmental triggers such as stress can further dysregulate these pathways.

The immune system has emerged as another important link. Prenatal infections and chronic inflammation may interact with genetic susceptibility to alter brain development and function. Immune - related genetic variations may increase sensitivity to environmental infections, contributing to schizophrenia risk.


IMPLICATIONS FOR RESEARCH AND PRACTICE

Understanding the combined role of genetics and environment has important implications for mental health care. Early identification of individuals at risk can help implement preventive strategies such as stress management and substance use prevention. Genetic research may guide the development of personalized treatment approaches tailored to individual risk profiles.

Therefore, understanding schizophrenia requires looking beyond a single cause and considering the combined influence of biological vulnerability and real life experiences.


REFERENCES

  1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). American Psychiatric Publishing.

  2. Brown, A. S. (2011). The environment and susceptibility to schizophrenia. Progress in Neurobiology, 93(1), 23–58.

  3. Cannon, M., Jones, P. B., & Murray, R. M. (2002). Obstetric complications and schizophrenia. American Journal of Psychiatry, 159(7), 1080–1092.

  4. Caspi, A., Moffitt, T. E., Cannon, M., et al. (2005). Cannabis use and psychosis risk. Biological Psychiatry, 57(10), 1117–1127.

  5. Gottesman, I. I. (1991). Schizophrenia genesis: The origins of madness. W. H. Freeman.

  6. Marconi, A., Di Forti, M., Lewis, C. M., Murray, R. M., & Vassos, E. (2016). Cannabis use and psychosis. Schizophrenia Bulletin, 42(5), 1262–1269.

  7. van Os, J., Kenis, G., & Rutten, B. P. (2010). The environment and schizophrenia. Nature, 468(7321), 203–212

 
 
 

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