Comparison with the previous literature

Overall, incidence rates observed in this Chapter are consistent with the literature, although between- study heterogeneity in methodologies, inclusion criteria and diagnoses studied make direct comparisons difficult. For example, the incidence of broadly-defined schizophrenia in the WHO 10-country study (Jablensky et al., 1992) varies from 15 to 42 per 100,000 person-years, although that study used a different age range (15-54 years) and did not consider affective psychoses (Jablensky et al., 1992). In our study, comparable rates of non-affective psychoses vary from 5 to 41 per 100,000 person-years after

standardisation for age, sex and migrant status. The systematic review presented in Chapter 2 observed a pooled crude incidence of all psychotic disorders of 28.3 (95%CI: 23.4-34.3) per 100,000 person-years, somewhat higher than the overall crude incidence rate I observed here (21.4). Such comparisons should be interpreted cautiously, given heterogeneity in estimation methods, and setting; few incidence studies have been conducted in southern Europe until recently (Lasalvia et al., 2014; Mulè et al., 2017; Tarricone et al., 2012), where rates appeared uniformly low, despite inclusion of urban catchment areas.

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The higher rates of disorder observed in men (van der Werf et al., 2014), younger age groups (Thorup et al., 2007; van der Werf et al., 2014; Kirkbride, Hameed, Ankireddypalli, et al., 2017) ethnic minorities (Bourque et al., 2011), and for non-affective psychoses (Kirkbride et al., 2012), are also frequently reported in the literature. The present study provides further robust evidence of a secondary peak in psychosis risk for women between 45-60 years old, building on previous observations (Bromet et al., 1992; Jackson et al., 2013; Kirkbride et al., 2006). This effect warrants further investigation, with previous research

hypothesizing a protective role for estrogen prior to menopause (Grigoriadis & Seeman, 2002), or the potential for an increase in psychosocial stressors experienced during this stage of the life course. Our findings add further evidence to the observation that early intervention services with an upper age limit of 35 years (or lower) may lead to gendered mental health inequalities (Lappin et al., 2016): only 50.8% of women with psychosis were identified before age 35 in our settings, compared with 67.9% of men (Figure 4.1).

Incidence not only varied by person, but importantly, by place, suggesting that the social environment may shape incidence patterns of FEP. The best-fitting models of all FEP and non-affective psychoses suggested that owner-occupancy levels predicted incidence, although residual variation at the setting-level was not explained by other catchment area-level measures. Although I can’t exclude the possibility of reverse causality, owner-occupancy may also be a proxy for a variety of social exposures, most obviously socioeconomic position (Kirkbride et al., 2007), but extending to the social stability and cohesiveness, previously associated with psychosis (Allardyce et al., 2005). The incidence of FEP appeared to be lower in southern Europe, but I found no evidence of variation by latitude in multivariable models. Nevertheless, settings were located within a narrow band (38° to 53°north of the equator), except for Brazil (21° south of the equator). This location may have contributed to the null finding, and the absence of high rates of psychosis in our southern European settings, particularly in major urban centres, requires further

investigation; in southern Europe incidence patterns with respect to population density appear to diverge from those observed in northern Europe (Table 4.8). Variation in the incidence of affective disorders, with lower rates in catchment areas with higher levels of unemployment is counterintuitive and unexpected. Whilst this might be explained by the inclusion of Spain, where rates of affective disorder were uniformly low and unemployment was a range of magnitude larger than in other countries, the finding may be a chance finding and further research is required to replicate and explain it.

Our study was predominantly based in Europe, and will be complemented by studies in other settings, including low and middle income [LAMI] settings (Morgan et al., 2017). Outside of Brazil, the only non- European country included in the present study, a dearth of high quality epidemiology data exists on psychotic disorders. Findings in Brazil were congruent with previous research (Menezes & Scazufca, 2007), and tentatively suggested that psychosis morbidity in LAMI countries could be considerable.

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4.5.4 Conclusion

In this international, multi-centre study I found that treated incidence of psychotic disorders varied eight- fold between catchment areas after standardisation for age, sex and minority status. Rates were higher in younger people, in men, minorities, and areas with lower levels of owner-occupied housing, although substantial variation between catchment areas, and by broad diagnosis, remained. These results suggest that there is pronounced variation in the healthcare burden of psychosis worldwide.

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- Searching for the cause of higher rates of psychosis in

ethnic and other minority groups

5.1 Introduction

The research synthesised and presented in Chapters 2 and 4 demonstrated that there is substantial variation in incidence of psychosis across person and place. One persistent finding is that ethnic minorities have a higher incidence of psychosis than the (White) majority. In the remaining Chapters of my thesis I aim to investigate why this is the case.

This Chapter is a temporary departure in my thesis, both in writing style and in content. This Chapter will adopt a philosophical perspective to outline a theory of causality suited to explain the proposed model of why rates of psychosis are higher in (ethnic) minorities. In the next Section, I will outline a theory of causality adequate to explain why rates of psychosis are higher in ethnic minorities. I will then critically review the epidemiological evidence as described in Section 1.4, and conclude that epidemiology alone is insufficient to solve our causal puzzle: we need both epidemiology and the social sciences. I subsequently examine literature from the social sciences and use this to form a background to Chapters 6 and 7, where I will return to epidemiology to formulate and empirically test the hypotheses as theorised in this Chapter.