Understanding urbanicity: how interdisciplinary methods help to unravel the effects of the city on mental health

Abstract

Twenty-first century urbanization poses increasing challenges for mental health. Epidemiological studies have shown that mental health problems often accumulate in urban areas, compared to rural areas, and suggested possible underlying causes associated with the social and physical urban environments. Emerging work indicates complex urban effects that depend on many individual and contextual factors at the neighbourhood and country level and novel experimental work is starting to dissect potential underlying mechanisms. This review summarizes findings from epidemiology and population-based studies, neuroscience, experimental and experience-based research and illustrates how a combined approach can move the field towards an increased understanding of the urbanicity-mental health nexus.

Explaining the association between urbanicity and psychotic-like experiences in pre-adolescence: The indirect effect of urban exposures

“…Many of these experiences would fit within a social defeat model (Selten et al, 2013) whereby socio-economic disadvantage, and the consequences we speculate about above, promote the marginalization and subordination of disadvantaged individuals, leaving them socially isolated and more vulnerable to stress. Whatever the mechanisms, taken with other work, our findings suggest that urbanicity may set the physical and social context for experiences that are linked with increased PLE risk (Krabbendam et al, 2020). It is notable and disconcerting that the association between these exposures and PLE are already present in late childhood.…”

“…Despite the clear etiological importance of the urban environment for psychosis, one of the most critical issue related to this association remains poorly understood: what is the mechanism through which urbanicity impacts risk? Urban environments involve a wide variety of physical (e.g., pollution) and social (e.g., poverty) exposures, and it may be these exposures that explain, in part, why urban environments impact psychosis risk (Abrahamyan Empson et al, 2019;Brown, 2011;Lydia Krabbendam et al, 2020). To this point, a variety of urban-related physical exposures have been shown to increase risk for and exacerbate psychotic symptoms including air pollution (Antonsen, Mok, Webb, Mortensen, McGrath, Agerbo, Brandt, Geels, Christensen, & Carsten Bøcker Pedersen, 2020;Gao et al, 2017;Lary et al, 2015;Liang et al, 2019;Tong et al, 2016), and xenobiotic heavy metal (i.e., lead) exposure (Arinola et al, 2010;Opler et al, 2004Opler et al, , 2008.…”

The Influence of the Urban Environment on Mental Health during the COVID-19 Pandemic: Focus on Air Pollution and Migration—A Narrative Review

“…To note, living in urban centers was also found to be associated with the development of psychiatric symptoms among different populations during the pandemic [ 21 , 22 ]. This could be connected with the fact that urbanicity (being born or raised in cities) represents a possible risk factor for the development of serious mental illnesses, such as schizophrenia spectrum disorders and other psychotic disorders [ 23 , 24 ]. Different explanations were sought for this association, including not only social stressors such as inequalities and low social cohesion [ 25 , 26 ], but also possible influences of urbanicity on brain structure [ 27 ] and coping styles [ 28 ].…”

Placing poverty-inequality at the centre of psychiatry

“…13 We also concede that most people who grow up in poverty do not develop a life-changing episode of depression, let alone SMI. But the antecedents of SMI are complex, and our understanding of why people develop psychosis is changing, building on the seminal work of Jim Van Os on the toxic effects of urbanicity 14 with consistent evidence of the cumulative effects of social disadvantage. Work with case-control groups in south London showed odds ratios (ORs) for subsequent psychosis in people below the poverty line of 4.50 (95% CI 2.89-7.00) and 2.95 (1.89-4.61), for 1-year and 5-year pre-symptom onset, respectively.…”