Written by Sarya Gulec
Imagine having a life and memories with your family and friends. What if one day,
someone tells you they are not real. Schizophrenia is one of the most serious and frightening of all mental illnesses. No other disorder arouses as much anxiety among the public, medical professionals and inevitably the media.
Effective treatments are available, yet patients and their families often find it hard to access good care (1). Researchers have not identified one single cause of the disorder. Researchers have theorised that an interaction between genes and a range of environmental factors may cause schizophrenia (2).
Different studies highlight that the greatest risk factor is the presence of family history. While the lifetime risk of Schizophrenia is just below 1%, it is 6.5% for first degree relatives of patients. The monozygotic twins of patients have more than %40 chance of developing the illness.
There have been researches about the association between schizophrenia drug usage, particularly cannabis, the evidence that patients with established schizophrenia smoke more cannabis than the general population is overwhelming. Cohort studies show that cannabis use increases the future risk of schizophrenia— fourfold a meta-analysis of prospective studies reported a doubling of the risk (1). But there are also ideas that might cause a reverse causality. Individuals with vulnerability to psychosis, such as social anxiety may be more likely to start using cannabis so as to “self-medicate” their distress. This is a reasonable hypothesis and must be examined before it can be concluded that cannabis contributes causally to the risk of psychosis (3). A study in Greece tested the subtle psychotic experiences with distress and cannabis' association and the subtle psychotic experiences without distress’ association with cannabis.The authors, however, found stronger associations between cannabis and psychotic experiences in the absence of distress, making self-medication unlikely. Actually, both the self-medication hypothesis and the causal hypothesis may be true. In fact, such a bidirectional relationship between risk factor and disease is not unusual for psychiatric disorders such as psychotic illnesses (3).
Being born premature is associated with heightened risk of negative neurological outcomes. It’s also considered as a risk factor to psychiatric disorders including psychosis. Preterm adolescents are at a 3-to-4-fold increased risk of being diagnosed with any psychiatric disorder compared to their term-born peers (4).
In adulthood, studies have found that risk of psychiatric disorder and hospitalisation is significantly related to the degree of prematurity. One of the most commonly observed abnormalities in premature babies is ventricular enlargement. Ventricular enlargement has also been observed in preterm adolescents and adults (4). Increased ventricle size is also one of the most replicated neuroimaging findings in chronic schizophrenia. Studies have found associations between ventricular abnormalities and history of obstetric complications in patients with schizophrenia— with a strong likelihood that complications during delivery interact with genetic risk for psychosis in contributing to these abnormalities. Ventricular enlargement following preterm birth may therefore represent a marker of increased underlying vulnerability to psychosis.
Many theories have related schizophrenia with disorder at neural connectivity, in which communication disorder between brain regions leads to the associated symptoms and cognitive changes. White matter forms the structural connections between brain regions, and thus, not surprisingly there are impairments observed in people with schizophrenia. The differences in the white matter are present in the first episode of the illness and are present in subjects at the risk group for the disorder, indicating that they are not secondary to the later progression of the disease or to treatment effects but may be a core contributor to the disease’s onset (5).
References:
Picchioni, M. M., & Murray, R. M. (2014, July 14). Schizophrenia. PubMed Central (PMC). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1914490/
World Health Organization. (2022, January 10). Schizophrenia. https://www.who.int/news-room/fact-sheets/detail/schizophrenia
Henquet, C., Murray, R., Linszen, D., & Ons, J. (2005, January 1). The environment and schizophrenia: The role of cannabis use. OUP Academic. https://academic.oup.com/schizophreniabulletin/article/31/3/608/1894455
Vanes, L. D., Murray, R. M., & Nosarti, C. (2022, September). Adult outcome of preterm birth: Implications for neurodevelopmental theories of psychosis. Science Direct. https://www.sciencedirect.com/science/article/pii/S0920996421001523#ab0005
Karlsgodt, K. H., Sun, D., & Cannon, T. D. (2010, August). Structural and functional brain abnormalities in schizophrenia. PubMed Central (PMC). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4235761/
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