Division of Psychiatry, University of Bristol
Department of Social Medicine, University of Bristol
Department of Psychiatry, University of Nottingham
Correspondence: Glynn Harrison, Division of Psychiatry, 41 St Michael's Hill, University of Bristol BS8 3JT, UK
Declaration of interest The study was funded by Trent Regional Health Authority.
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ABSTRACT |
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Aims To investigate the relationship between adult-onset schizophrenia and two indicators of social inequality at birth: social class and area of residence.
Method A matched casecontrol design was used with data from birth certificates of first-episode cases and age- and gender-matched controls.
Results Risk increased with increasing levels of deprivation at birth. Subjects whose fathers were social class IVV or who were born in deprived areas were at increased risk of schizophrenia (odds ratio=2.1; 95% Cl=0.8-5.5). Risk was greater in those with both of these indicators (odds ratio=8.1; 95% Cl=2.7-23.9). There was some evidence that associations were stronger in older subjects. Exclusion of AfricanCaribbeans or cases with positive family history somewhat attenuated the association.
Conclusions Indicators of social inequality at birth are associated with increased risk of adult-onset schizophrenia, suggesting that environmental factors are important determinants of schizophrenic disorders.
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INTRODUCTION |
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METHOD |
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Study design
A matched casecontrol design was used. Of 168 incident cases arising
over the 24-month study recruitment period, 94 had been born in the study
catchment area and these form the basis of this analysis. The birth
certificate of each of these cases was located from local birth registers and
four age-gender-matched controls were obtained by selecting the next four
births registered at the same registry office. Cases and controls thus were
matched for date of birth (to within 6 weeks) and area of birth registration.
Because our cases were incident episodes of psychotic disorder in people who
had been born in Nottingham, to ensure comparability of the source populations
for cases and controls we eliminated, before analysis, those controls (43% of
the total) who were no longer resident in Nottingham (according to the Family
Health Services Authority register) at the time of case ascertainment.
We extracted father's occupation and mother's address from the birth certificates for cases and controls. Father's occupation was assigned to a social class on the basis of the Registrar General's Classification of Occupations (Office of Population Censuses and Surveys, 1991). We used the mother's address to assign each individual to an area measure of socio-economic deprivation, the Nottinghamshire County Council index of need. This was based mainly upon 1971 census data (Nottinghamshire County Council, 1975), corresponding to the median birth year of the study sample. The county was divided into zones, composed of combinations of enumeration districts, designed to cover areas of broadly similar social character. Each of the zones was scored on 20 indicators representing income, unemployment, crime, housing and other dimensions of deprivation. The scores then were aggregated to give a single (unweighted) summary measure of deprivation, allowing them to be ranked and stratified into four broad categories. Because of the relatively small numbers in the present study, we decided a priori to create a two-level indicator of deprivation by collapsing these four groups into two broad categories of above average or below average social need.
Analysis
We analysed associations of the two indicators with all psychotic
disorders. Then we assessed separately the associations for non-affective,
non-substance-related psychosis (broadly defined schizophrenia,
ICD-10 F20-29) and non-schizophrenic psychosis (ICD-10 F30-33 and F1x).
Conditional logistic regression analyses were carried out using the Stata
software package (StataCorp,
1999). Tests for linear trend across social class categories were
based on the continuous measure for social class. Because no information on
the ethnicity or family history of controls was available, the potential
confounding effects of these factors were assessed by repeating the main
analyses but excluding AfricanCaribbean cases as well as cases with a
family history of schizophrenia.
A three-level childhood deprivation score, combining information on place of birth and parental occupation, then was produced as follows: 0, if the father was social class IIII and the mother lived in a non-deprived area; 1, if the father was social class IV/V or the mother lived in a deprived area; 2, if the father was social class IV/V and the mother lived in a deprived area.
Appropriate interaction terms were fitted to the models to investigate whether associations between childhood socio-economic deprivation and schizophrenia differed by gender or age (categorised into two groups above or below the median age of 25 years for the sample).
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RESULTS |
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Table 2 shows the odds ratios (95% CI) for the association of adult-onset psychosis with paternal social class and area-level deprivation. For all psychoses there were significant associations with the two indicators examined independently: social class and area of residence at birth. When associations with broad schizophrenia and other psychoses were examined separately there was some evidence that associations are stronger in relation to area of residence for broad schizophrenia. The small number of cases limited the power of analyses examining relationships with other psychotic disorders.
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The combined childhood deprivation score showed a highly significant linear association with all psychoses and for broad schizophrenia, although the association was weaker for non-schizophrenic psychoses. For the latter group, confidence intervals were wide and, as stated above, the analysis lacked statistical power. There was no significant interaction between gender and the combined deprivation score with respect to overall risk of psychosis (P=0.81). There were weak interactions between age and the summary deprivation score with respect to all psychosis (P=0.16) and the broad schizophrenia grouping (P=0.18). In a stratified analysis the odds ratio for broad schizophrenia per unit increase in deprivation score was 4.6 (95% CI=1.9-10.9) for subjects aged >25 years and 2.1 (95% CI=1.0-4.2) for subjects aged <25 years.
Family history of psychosis and AfricanCaribbean family
background
The association between indicators of deprivation at birth and adult-onset
psychosis could be explained by family history of psychotic illness. Parental
illness would have led to reduced occupation status and geographical
segregation in deprived urban areas. There is also an increased risk of
psychosis in those with a family background of migration to the UK from the
Caribbean (Harrison et al,
1997), and AfricanCaribbean families might be more likely
to reside in areas of higher deprivation. To assess these possible confounding
effects, analyses were repeated for cases without a family history of
psychosis in a first-degree relative (Table
3) and cases with neither a family history of psychosis nor
AfricanCaribbean ethnicity (Table
4). Because both of these analyses are based on smaller numbers of
cases, they have lower statistical power than those based on the complete
data-set. Restriction of the analysis to these subgroups without a positive
family history did not alter greatly the strength of the observed associations
reported in Table 2, although
the magnitude of the odds ratios was attenuated after exclusion of the
AfricanCaribbean cases and their matched controls, suggesting some
confounding of the main effects. An analysis excluding only
AfricanCaribbean cases showed a similar degree of attenuation.
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DISCUSSION |
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Methodological issues
The strengths of our study design include a well-defined first-episode
cohort from a delineated catchment area, with almost complete and
comprehensive case ascertainment and assessment. A high proportion of face to
face interviews at baseline and follow-up was achieved and standardised
assessment tools with high interrater reliability and operationalised criteria
for diagnosis were used throughout. The record of family history of psychotic
disorder was the weakest aspect of the methodology: we did not carry out a
systematic interview with all first-degree relatives, but relied upon
interviews with patients, case notes and, where available, an interview with
an informant. It is possible that this resulted in some underreporting.
Several other methodological limitations require consideration. Although the study design was a population-based casecontrol study, case finding was based upon contact with secondary services rather than a systematic community survey. The observed association with social deprivation may have been for risk of making contact with secondary mental health services when developing psychotic symptoms, rather than for risk of psychotic illness per se. Although we cannot eliminate this possibility altogether, we think that this is unlikely in view of evidence from community surveys that most cases make contact with specialist services at some point in the course of the disorder (Link & Dohrenwend, 1980).
The selection of controls required consideration. First, no attempt was made to determine whether controls had schizophrenia. However, because the population prevalence of schizophrenia is low (Office of Population Censuses and Surveys, 1995), the effects of any possible misclassification of controls would be small. Furthermore, such misclassifications would tend to reduce the size of any effect and bias our findings towards the null hypothesis. Second, Nottingham has three birth registry offices and, because both cases and controls would be more likely to register locally, we probably overmatched for geographical area. This also would tend to bias our findings towards the null hypothesis of no difference in area of residence. Finally, confounding could be explored only in a limited way because we were unable to obtain information on the ethnicity and family history of the controls.
A further issue in the interpretation of these data is the potential effect of possibly different migration patterns among cases and potential controls. Although we excluded controls that had migrated out of Nottingham, it is possible that socio-economic factors may influence the migration patterns of people during the prodromal period of psychotic illness: the outward migration from Nottingham of preschizophrenia cases could have been greater among more affluent cases, producing a biased distribution of social class and area of residence among the remaining cases. We believe that this is an unlikely explanation, but the issue remains incapable of being resolved conclusively within the design and sample sizes available in our study.
We based our deprivation score upon available data close to the median birth date of our sample and we do not have data for the longer term stability of this scoring distribution, covering the age range of our sample. There is evidence from other studies, however, that an area's socio-economic characteristics remain relatively stable over long time periods (Dorling et al, 2000). Finally, it should be recognised that the exclusion of cases that were not born in Nottingham resulted in a sizeable reduction in the number of cases eligible for inclusion in our sample. Our findings therefore only apply to people with schizophrenia who continue to reside in a local area after birth: the association cannot be generalised to all schizophrenic disorders.
Previous studies
Although Goldberg & Morrison
(1963) and Hare et al
(1972) found that social class
distribution by paternal background was comparable to that of the general
population, our findings are similar to those of Turner & Wagenfield
(1967) and Castle et
al (1993), who reported
associations with lower paternal social class. Recent British
(Done et al, 1994;
Jones et al, 1994)
and Finnish (Makikyro et al,
1997) studies, which take advantage of well-defined birth cohorts
followed through part of the risk period for schizophrenia, report an
association with high paternal socio-economic status. However, in the study by
Jones et al (1994)
the number of cases was small (n=30) and in both Done's (1994) and
Makikyro's (1997) studies the subjects were followed for only part of the risk
period (to age 28 and age 23 years, respectively) for developing
schizophrenia. These analyses thus were confined to early-onset cases. It is
possible that any association between parental social class and schizophrenia
is stronger for later-onset cases, which would be consistent with our finding
of borderline interactions between age and the summary deprivation score with
respect to all psychosis. Larger, carefully defined samples are required to
clarify these complex issues and, although we developed a combined measure to
illustrate accumulated risk (after reporting separate analyses for our two
indicators), future studies should continue to examine these (and other)
markers separately.
Social inequalities and the aetiology of schizophrenia
Measures of socio-economic position are, at best, proxy markers for factors
linked more directly to the risk of schizophrenia. There are a number of
causal possibilities, including biological risk factors such as exposure to
infections and other toxic agents, and non-biological factors such as social
and psychological stressors linked to the degree of social fragmentation and
individual social capital (Hare,
1956; Van Os et al,
2000). It is becoming increasingly difficult to distinguish
between causes that have a clear material basis and those that might be
located in the environment or in mental activity. In addition,
although our data suggest that there are independent associations with
individual-level and area-level characteristics, cumulative effects are likely
to accrue over the life course and it is probable that causal relationships in
schizophrenia are mediated by complex geneenvironment interactions.
Whatever the nature of the risk factors involved, our data suggest that
environmental factors play a significant role in the aetiology of
schizophrenia.
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Clinical Implications and Limitations |
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LIMITATIONS
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REFERENCES |
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Received for publication November 20, 2000. Revision received April 20, 2001. Accepted for publication April 26, 2001.
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