The Veins of the City: Environmental Influences of Schizophrenia


Did you know the environment you lived in affects your gene expression? Specifically, the environment in which we live can act as a trigger or catalyst in activating certain genes. We see this with the onset of schizophrenia, and new studies have shown a connection with the development of schizophrenia (especially the expression of psychosis) and urban life (Krabbendam 2005). Currently, the connection between the city and the development of schizophrenia is known as the “geographical drift,” meaning that people who are at-risk for/currently are developing schizophrenia are moving into the city. Although the geographical drift is the dominant hypothesis that this describes this association, studies are now showing that living in the city is “turning on” genes that induce schizophrenia (Lewis et al 1992). This phenomenon is known as epigenetics; the environment in which we live in alters gene expression. To put it simply, genes are “switched” on or off depending on different influences, such as the environment, the food we eat, and a number of other factors (Holliday 2006).

Although cities both hurt and benefit physical health, the nature of city life has had adverse effects on mental health as well. A variety of mental health illnesses are found in increasing numbers in the city rather in suburban or rural life, such as anxiety and mood disorders, in addition to schizophrenia. Some scientists hypothesize that the stress related to city life causes negative effects on neural processes, specifically on the amygdala (Lederbogen et al 2011). When altered, the amygdala influences the development of schizophrenia (Bogerts et al 1993). Specifically, the amygdala plays a role in human emotions and the development of hallucinations. Any unwanted modifications to this part of the brain (specifically in its volume) can cause disruptions leading to the onset of schizophrenia (Mahon et al 2012).

Urban life has accounted for more than 30% of cases of schizophrenia in America. Living in the city as a baby and during early adolescence increases one’s chance of developing schizophrenia later in life by 2-folds (Haddad et al 2014). In addition, stress can affect our development during upbringing through the decrease in grey matter volume and other structural abnormalities that play into early development of schizophrenia (Haddad et al 2014). These differences manifest differently in both men and women, with brain studies showing that men have more brain morphological differences (Haddad et al 2014). It’s important to understand this difference so we can create different treatment methods specifically catered to men and women.

There are also precursors, or higher risks, for developing schizophrenia that are increased in the city. For example, there is a higher about of obstetric complications in the city, which can lead to developmental impairments associated with schizophrenia (Howes et al 2004). There is also higher drug abuse in the cities. Psychoactive drugs that release dopamine can cause an increase in the likelihood of developing psychosis. In the city especially, a trend of abusing these drugs at a younger age when the brain is still developing can be observed. For example, the youth are increasingly engaging in cannabis with no physical symptoms of ailment. However, studies show that cannabis can cause psychosis, therefore acting as a pathway to schizophrenia (Howes et al 2004).

A large amount of immigrants move to the city, and this may affect their development of schizophrenia. Social isolation is thought to increase the risk of psychosis, and researchers observed social isolation largely in non-white, minority migrants (Howes et al 2004). Making a move into an unfamiliar land requires social support to adjust to the new environment. However, sometimes these groups of people are ostracized, especially in today’s polarized political climate. This increase in social isolation causes schizophrenia, which may itself cause an increase in further social isolation; the two continue to feed each other in an negative cycle.

 

References

Bogerts, B., Lieberman, J. A., Ashtari, M., Bilder, R. M., Degreef, G., Lerner, G., … & Masiar, S. (1993). Hippocampus-amygdala volumes and psychopathology in chronic schizophrenia. Biological psychiatry33(4), 236-246.

Haddad, L., Schäfer, A., Streit, F., Lederbogen, F., Grimm, O., Wüst, S., … & Meyer-Lindenberg, A. (2014). Brain structure correlates of urban upbringing, an environmental risk factor for schizophrenia. Schizophrenia bulletin41(1), 115-122.

Holliday, R. (2006). Epigenetics: a historical overview. Epigenetics1(2), 76-80.

Howes, O. D., McDonald, C., Cannon, M., Arseneault, L., Boydell, J., & Murray, R. M. (2004). Pathways to schizophrenia: the impact of environmental factors.

Kohn, M. L., & Clausen, J. A. (1955). Social isolation and schizophrenia. American Sociological Review20(3), 265-273.

Krabbendam, L., & Van Os, J. (2005). Schizophrenia and urbanicity: a major environmental influence—conditional on genetic risk. Schizophrenia bulletin31(4), 795-799.

Lederbogen, F., Kirsch, P., Haddad, L., Streit, F., Tost, H., Schuch, P., … & Meyer-Lindenberg, A. (2011). City living and urban upbringing affect neural social stress processing in humans. Nature474(7352), 498.

Lewis, G., David, A., Andréassson, S., & Allebeck, P. (1992). Schizophrenia and city life. The Lancet340(8812), 137-140.

Mahon, P. B., Eldridge, H., Crocker, B., Notes, L., Gindes, H., Postell, E., King, S., Potash, J. B., Ratnanather, J. T., … Barta, P. E. (2012). An MRI study of amygdala in schizophrenia and psychotic bipolar disorder. Schizophrenia research138(2-3), 188-91.

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