Extensive evidence indicates that rates of psychotic disorder are elevated in more urban compared with less urban areas, but this evidence largely originates from Northern Europe. It is unclear whether the same association holds globally. This study examined the association between urban residence and rates of psychotic disorder in catchment areas in India (Kancheepuram, Tamil Nadu), Nigeria (Ibadan, Oyo), and Northern Trinidad.

Comprehensive case detection systems were developed based on extensive pilot work to identify individuals aged 18–64 with previously untreated psychotic disorders residing in each catchment area (May 2018–April/May/July 2020). Area of residence and basic demographic details were collected for eligible cases. We compared rates of psychotic disorder in the more v. less urban administrative areas within each catchment area, based on all cases detected, and repeated these analyses while restricting to recent onset cases (<2 years/<5 years).

We found evidence of higher overall rates of psychosis in more urban areas within the Trinidadian catchment area (IRR: 3.24, 95% CI 2.68–3.91), an inverse association in the Nigerian catchment area (IRR: 0.68, 95% CI 0.51–0.91) and no association in the Indian catchment area (IRR: 1.18, 95% CI 0.93–1.52). When restricting to recent onset cases, we found a modest positive association in the Indian catchment area.

This study suggests that urbanicity is associated with higher rates of psychotic disorder in some but not all contexts outside of Northern Europe. Future studies should test candidate mechanisms that may underlie the associations observed, such as exposure to violence.

To examine food and beverage purchasing patterns across formal and informal outlets among Mexican households’ and explore differences by urbanicity and income.

Cross-sectional study of a nationally representative sample of households. We calculated the proportion of total food and beverage expenditure in each household by food outlet type overall and by urbanicity and income. We defined informal outlets as those which are not registered or regulated by tax and fiscal laws. Since some of the outlets within community food environments do not fall in clear categories, we defined a continuum from formal to informal outlets, adding mixed outlets as a category.

Mexico.

Mexican households (n 74 203) from the 2018 National Income and Expenditure Survey.

Of the total food and beverage purchases, outlets within the formal food sector (i.e. supermarkets and convenience stores) accounted for 15 % of the purchases, 13 % of purchases occurred in outlets within the informal food sector (i.e. street markets, street vendors and acquaintances) and 70 % in fiscally mixed outlets (i.e. small neighbourhood stores, specialty stores and public markets). Across levels of urbanicity and income, most food and beverage purchases occurred in mixed outlets. Also, purchases in informal and mixed outlets decreased as levels of urbanicity and income increased. In contrast to informal outlets, purchases in formal outlets were most likely from richer households and living in larger sized cities.

Understanding where Mexican households shop for food is relevant to create tailored interventions according to food outlet type, accounting for regulatory and governance structures.

While extensive recent data details risk factors for psychoses in urban milieu, insights regarding recovery processes in cities are scarce. This hampers the translation of promising epidemiological and neuroimagery findings into effective therapeutic strategies. Given the twofold higher incidence of psychoses in cities and the fact that 68% of world population will be urban by 2050, it becomes an urgent matter of psychiatric care.

This presentation details specific targets for therapeutic interventions in city context to further discuss a pioneering participatory project with the aim to conceive a novel city specific recovery-oriented program.

Based on most recent research data, some of which our own, a comprehensive survey of urbanicity studies and an overview of main avenues for developments will be presented.

Urban milieu is a complex dwelling space made of protective and disruptive features. During each life course they may form unique combinations hampering or enhancing psychological well-being. Urban living is not only correlated with higher prevalence of psychoses, but also with better access to health care and lower rates of treatment resistant schizophrenia, pointing to some beneficial aspects of city living on recovery processes. The interplay between personal characteristics, urban resources and supportive social environments seems pivotal to recovery calling for multilevel interventions (CBT interventions, peer-support, go-alongs, resocialization) and integration of different stakeholders (patients, peer-practitioners, community actors).

Participatory approach (design thinking, urban lab etc.) represents an important means of innovation and ensures the best match between patients needs and therapeutic propositions.

No significant relationships.

To investigate acquisition and mobility experiences of food-insecure individuals across urbanicity levels (i.e., urban, suburban, rural) in the early months of the COVID-19 pandemic.

Cross-sectional study using a nationally representative online panel to measure where food-insecure individuals acquired food, food acquisition barriers and mobility to food sources, which were evaluated across urbanicity levels using chi-squared tests and 95 % CI.

USA.

2011 adults (18 years or older).

Food insecurity impacted 62·3 % of adults in urban areas, 40·5 % in rural areas and 36·7 % in suburban areas (P < 0·001). Food acquisition barriers that were significantly more prevalent among food-insecure adults in urban areas were a change in employment status (34·2 %; 95 % CI 27·2 %, 41·1 %; P < 0·0001) and limited availability of food in retailers (38·8 %; 95 % CI 31·7 %, 45·9 %; P < 0·001). In rural areas, food-insecure adults primarily acquired food for the household from supercentres (61·5 %; 95 % CI 50·4 %, 72·5 %; P < 0·05), while locally sourced foods were less common among food-insecure adults in rural areas (6·9 %; 95 % CI 0·01 %, 13·0 %) compared to urban areas (19·8 %; 95 % CI 14·3 %, 25·4 %; P < 0·01). Transportation as a barrier did not vary significantly by urbanicity, but food-insecure adults across urbanicity levels reported utilising a range of transportation modes to acquire food.

A planning approach that links urban and rural areas could address food insecurity by enhancing the integration of food production, transportation and food distribution, building towards a more resilient and equitable food system for all Americans.

Associations of socioenvironmental features like urbanicity and neighborhood deprivation with psychosis are well-established. An enduring question, however, is whether these associations are causal. Genetic confounding could occur due to downward mobility of individuals at high genetic risk for psychiatric problems into disadvantaged environments.

We examined correlations of five indices of genetic risk [polygenic risk scores (PRS) for schizophrenia and depression, maternal psychotic symptoms, family psychiatric history, and zygosity-based latent genetic risk] with multiple area-, neighborhood-, and family-level risks during upbringing. Data were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 British twins born in 1994–1995 and followed to age 18 (93% retention). Socioenvironmental risks included urbanicity, air pollution, neighborhood deprivation, neighborhood crime, neighborhood disorder, social cohesion, residential mobility, family poverty, and a cumulative environmental risk scale. At age 18, participants were privately interviewed about psychotic experiences.

Higher genetic risk on all indices was associated with riskier environments during upbringing. For example, participants with higher schizophrenia PRS (OR = 1.19, 95% CI = 1.06–1.33), depression PRS (OR = 1.20, 95% CI = 1.08–1.34), family history (OR = 1.25, 95% CI = 1.11–1.40), and latent genetic risk (OR = 1.21, 95% CI = 1.07–1.38) had accumulated more socioenvironmental risks for schizophrenia by age 18. However, associations between socioenvironmental risks and psychotic experiences mostly remained significant after covariate adjustment for genetic risk.

Genetic risk is correlated with socioenvironmental risk for schizophrenia during upbringing, but the associations between socioenvironmental risk and adolescent psychotic experiences appear, at present, to exist above and beyond this gene-environment correlation.

Several factors may contribute to duration of untreated psychosis (DUP): patient-delay, referral-delay and treatment-delay caused by mental health care services (MHS-delay). In order to find the most effective interventions to reduce DUP, it is important to know what factors in these pathways to care contribute to DUP.

To examine the relationship of the constituents of treatment delay, migration status and urbanicity.

In first episode psychotic patients (n = 182) from rural, urban and highly urbanized areas, DUP, migration status and pathways to care were determined.

Mean DUP was 53.6 weeks (median 8.9, SD=116.8). Patient-delay was significantly longer for patients from highly urbanized areas and for first generation immigrants. MHS-delay was longer for patients who were treated already by MHS for other diagnoses.

Specific interventions are needed focusing on patients living in highly urbanized areas and first generation immigrants in order to shorten patient delay. MHS should improve early detection of psychosis in patients already in treatment for other diagnosis.

The association between schizophrenia and decreased vitamin D levels is well documented. Low maternal and postnatal vitamin D levels suggest a possible etiological mechanism. Alternatively, vitamin D deficiency in patients with schizophrenia is presumably (also) the result of disease-related factors or demographic risk factors such as urbanicity.

In a study population of 347 patients with psychotic disorder and 282 controls, group differences in vitamin D concentration were examined. Within the patient group, associations between vitamin D, symptom levels and clinical variables were analyzed. Group × urbanicity interactions in the model of vitamin D concentration were examined. Both current urbanicity and urbanicity at birth were assessed.

Vitamin D concentrations were significantly lower in patients (B = −8.05; 95% confidence interval (CI) −13.68 to −2.42; p = 0.005). In patients, higher vitamin D concentration was associated with lower positive (B = −0.02; 95% CI −0.04 to 0.00; p = 0.049) and negative symptom levels (B = −0.03; 95% CI −0.05 to −0.01; p = 0.008). Group differences were moderated by urbanicity at birth (χ2 = 6.76 and p = 0.001), but not by current urbanicity (χ2 = 1.50 and p = 0.224). Urbanicity at birth was negatively associated with vitamin D concentration in patients (B = −5.11; 95% CI −9.41 to −0.81; p = 0.020), but not in controls (B = 0.72; 95% CI −4.02 to 5.46; p = 0.765).

Lower vitamin D levels in patients with psychotic disorder may in part reflect the effect of psychosis risk mediated by early environmental adversity. The data also suggest that lower vitamin D and psychopathology may be related through direct or indirect mechanisms.

Evidence suggests that cannabis use, childhood adversity, and urbanicity, in interaction with proxy measures of genetic risk, may facilitate onset of psychosis in the sense of early affective dysregulation becoming ‘complicated’ by, first, attenuated psychosis and, eventually, full-blown psychotic symptoms.

Data were derived from three waves of the second Netherlands Mental Health Survey and Incidence Study (NEMESIS-2). The impact of environmental risk factors (cannabis use, childhood adversity, and urbanicity) was analyzed across severity levels of psychopathology defined by the degree to which affective dysregulation was ‘complicated’ by low-grade psychotic experiences (‘attenuated psychosis’ – moderately severe) and, overt psychotic symptoms leading to help-seeking (‘clinical psychosis’ – most severe). Familial and non-familial strata were defined based on family history of (mostly) affective disorder and used as a proxy for genetic risk in models of family history × environmental risk interaction.

In proxy gene–environment interaction analysis, childhood adversity and cannabis use, and to a lesser extent urbanicity, displayed greater-than-additive risk if there was also evidence of familial affective liability. In addition, the interaction contrast ratio grew progressively greater across severity levels of psychosis admixture (none, attenuated psychosis, clinical psychosis) complicating affective dysregulation.

Known environmental risks interact with familial evidence of affective liability in driving the level of psychosis admixture in states of early affective dysregulation in the general population, constituting an affective pathway to psychosis. There is interest in decomposing family history of affective liability into the environmental and genetic components that underlie the interactions as shown here.

Considering existing knowledge on the relationship between certain environmental factors and incidence rates of psychosis, we carried out a systematic review to provide a broad and updated picture of the incidences of different psychotic disorder subgroups worldwide and how some environmental factors influence these rates.

Studies with original data related to the incidence of psychosis (published between 2000 and 2015) were identified via searching electronic databases (CINAHL, MEDLINE, PSYCINFO, PUBMED, and SCOPUS). Data on the following risk factors were extracted: gender, urbanicity, immigration and socio-economic level. Descriptive appraisals of variation in incidence rates (IR) and incidence rate ratios (IRR), with a 95% confidence interval were calculated. In addition, a meta-analysis was performed to calculate IR pooled by diagnosis group and IRR pooled by diagnosis and gender, urbanity, immigration and socio-economic level, using a random effects model.

We identified 33 reports to analyse. Overall IR per 100 000 persons for non-affective psychoses (IR pooled = 22.53 (16.51–28.54)) were higher than affective psychoses (IR pooled = 7.12 (5.03–9.22)). There was an increase in rates of psychosis in men v. women (IRR pooled = 1.54 (1.37–1.72)), in urban v. rural areas (IRR pooled = 1.64 (1.38–1.95)), in immigrants v. natives (IRR pooled = 3.09 (2.74–3.49)), and in lower socio-economic level areas (IRR pooled = 1.78 (1.43–2.22)).

IR among different psychotic disorders was found to vary depending on gender, urbanicity, and immigration (as most of the previous literature focuses on non-affective psychosis or schizophrenia).

Studies have indicated that the association of urbanicity at birth and during upbringing with schizophrenia may be driven by familial factors such as genetic liability. We used a population-based nested case–control study to assess whether polygenic risk score (PRS) for schizophrenia was associated with urbanicity at birth and at age 15, and to assess whether PRS and parental history of mental disorder together explained the association between urbanicity and schizophrenia.

Data were drawn from Danish population registries. Cases born since 1981 and diagnosed with schizophrenia between 1994 and 2009 were matched to controls with the same sex and birthdate (1549 pairs). Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of a separate, large meta-analysis.

Those with higher PRS were more likely reside in the capital compared with rural areas at age 15 [odds ratio (OR) 1.19, 95% confidence interval (CI) 1.01–1.40], but not at birth (OR 1.09, 95% CI 0.95–1.26). Adjustment for PRS produced almost no change in relative risks of schizophrenia associated with urbanicity at birth, but slightly attenuated those for urban residence at age 15. Additional adjustment for parental history led to slight attenuation of relative risks for urbanicity at birth [incidence rate ratio (IRR) for birth in capital = 1.54, 95% CI 1.18–2.02; overall p = 0.016] and further attenuation of relative risks for urbanicity at age 15 (IRR for residence in capital = 1.32, 95% CI 0.97–1.78; overall p = 0.148).

While results regarding urbanicity during upbringing were somewhat equivocal, genetic liability as measured here does not appear to explain the association between urbanicity at birth and schizophrenia.

Evidence suggests that in affective, non-psychotic disorders: (i) environmental exposures increase risk of subthreshold psychotic experiences (PEs) and strengthen connectivity between domains of affective and subthreshold psychotic psychopathology; and (ii) PEs are a marker of illness severity.

In 3021 adolescents from the Early Developmental Stages of Psychopathology cohort, we tested whether the association between PEs and presence of DSM-IV mood disorder (MD)/obsessive–compulsive disorder (OCD) would be moderated by risk factors for psychosis (cannabis use, childhood trauma and urbanicity), using the interaction contrast ratio (ICR) method. Furthermore, we analysed whether the interaction between environment and PEs was mediated by non-psychotic psychopathology.

The association between PEs and MD/OCD was moderated by urbanicity (ICR = 2.46, p = 0.005), cannabis use (ICR = 3.76, p = 0.010) and, suggestively, trauma (ICR = 1.91, p = 0.063). Exposure to more than one environmental risk factor increased the likelihood of co-expression of PEs in a dose–response fashion. Moderating effects of environmental exposures were largely mediated by the severity of general non-psychotic psychopathology (percentage explained 56–68%, all p < 0.001). Within individuals with MD/OCD, the association between PEs and help-seeking behaviour, as an index of severity, was moderated by trauma (ICR = 1.87, p = 0.009) and urbanicity (ICR = 1.48, p = 0.005), but not by cannabis use.

In non-psychotic disorder, environmental factors increase the likelihood of psychosis admixture and help-seeking behaviour through an increase in general psychopathology. The findings are compatible with a relational model of psychopathology in which more severe clinical states are the result of environment-induced disturbances spreading through a psychopathology network.

To evaluate dietary intake based on the Chinese Food Pagoda (CFP) and to determine what factors may be associated with adherence to CFP guidelines for older Chinese.

This cross-sectional population-based study used 24 h recall over three consecutive days to assess dietary intake and adherence to CFP among older Chinese participating in the China Health and Nutrition Survey 2009.

Nine provinces across four diverse regions (Northeast, East Coast, Central and West).

A total of 2745 older Chinese, aged 60–69 years (n 1563) and ≥70 years (n 1182), with dietary data.

None of the participants reached all ten food group recommendations. More than half of the participants exceeded the recommended amount for grains (63 %), oil (62·8 %) and salt (55·7 %). Ten per cent of the participants consumed dairy, while merely 0·5 % met the recommended amount. Average Chinese Food Pagoda Score (CFPS) was 3·3 in men and 3·5 in women, far below the maximum possible score of 10. Women had 0·26 higher CFPS than men (P<0·001; 95 % CI 0·16, 0·36). People living in medium and high urbanicity areas had significantly higher scores than those living in low urbanicity areas (P<0·001). Also, there were significant differences in CFPS according to gender, BMI, work status, education level and region.

Few older Chinese are meeting the intake of the various food groups based on the recommendations in the CFP guidelines, thus increasing the risk of malnutrition and non-communicable diseases. Action is needed to increase dissemination and uptake of nutrition education, with interventions targeted at socio-economic regions. Moreover, specific dietary guidelines for older Chinese people should be developed.

The extent to which different symptom dimensions vary according to epidemiological factors associated with categorical definitions of first-episode psychosis (FEP) is unknown. We hypothesized that positive psychotic symptoms, including paranoid delusions and depressive symptoms, would be more prominent in more urban environments.

We collected clinical and epidemiological data on 469 people with FEP (ICD-10 F10–F33) in two centres of the Aetiology and Ethnicity in Schizophrenia and Other Psychoses (AESOP) study: Southeast London and Nottinghamshire. We used multilevel regression models to examine neighbourhood-level and between-centre differences in five symptom dimensions (reality distortion, negative symptoms, manic symptoms, depressive symptoms and disorganization) underpinning Schedules for Clinical Assessment in Neuropsychiatry (SCAN) Item Group Checklist (IGC) symptoms. Delusions of persecution and reference, along with other individual IGC symptoms, were inspected for area-level variation.

Reality distortion [estimated effect size (EES) 0.15, 95% confidence interval (CI) 0.06–0.24] and depressive symptoms (EES 0.21, 95% CI 0.07–0.34) were elevated in people with FEP living in more urban Southeast London but disorganized symptomatology was lower (EES –0.06, 95% CI –0.10 to –0.02), after controlling for confounders. Delusions of persecution were not associated with increased neighbourhood population density [adjusted odds ratio (aOR) 1.01, 95% CI 0.83–1.23], although an effect was observed for delusions of reference (aOR 1.41, 95% CI 1.12–1.77). Hallucinatory symptoms showed consistent elevation in more densely populated neighbourhoods (aOR 1.32, 95% CI 1.09–1.61).

In people experiencing FEP, elevated levels of reality distortion and depressive symptoms were observed in more urban, densely populated neighbourhoods. No clear association was observed for paranoid delusions; hallucinations were consistently associated with increased population density. These results suggest that urban environments may affect the syndromal presentation of psychotic disorders.

Social capital has been considered aetiologically important in schizophrenia but the empirical evidence to support this hypothesis is absent. We tested whether social capital, measured at the neighbourhood level, was associated with the incidence of schizophrenia (ICD-10 F20).

We administered a cross-sectional questionnaire on social capital to 5% of the adult population in 33 neighbourhoods (wards) in South London (n=16 459). The questionnaire contained items relating to two social capital constructs: social cohesion and trust (SC&T) and social disorganization (SocD). Schizophrenia incidence rates, estimated using data from the Aetiology and Ethnicity in Schizophrenia and Other Psychoses (AESOP) study, provided the outcome. We used multi-level Poisson regression to test our hypothesis while controlling for individual- and neighbourhood-level characteristics.

We identified 148 cases during 565 576 person-years at-risk. Twenty-six per cent of the variation in incidence rates was attributable to neighbourhood-level characteristics. Response from the social capital survey was 25.7%. The association between SC&T and schizophrenia was U-shaped. Compared with neighbourhoods with medial levels of SC&T, incidence rates were significantly higher in neighbourhoods with low [incidence rates ratio (IRR) 2.0, 95% confidence interval (CI) 1.2–3.3] and high (IRR 2.5, 95% CI 1.3–4.8) levels of SC&T, independent of age, sex, ethnicity, ethnic density, ethnic fragmentation and socio-economic deprivation.

Neighbourhood variation in SC&T was non-linearly associated with the incidence of schizophrenia within an urban area. Neighbourhoods with low SC&T may fail to mediate social stress whereas high SC&T neighbourhoods may have greater informal social control or may increase the risk of schizophrenia for residents excluded from accessing available social capital.