To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Ethnic inequalities in health outcomes are often explained by socioeconomic status and concentrated poverty. However, ethnic disparities in psychotic experiences are not completely attenuated by these factors.
We investigated whether disparities are better explained by interactions between individual risk factors and place-based clustering of disadvantage, termed a syndemic.
We performed a cross-sectional survey of 3750 UK men, aged 18–34 years, oversampling Black and minority ethnic (BME) men nationally, together with men residing in London Borough of Hackney. Participants completed questionnaires covering psychiatric symptoms, substance misuse, crime and violence, and risky sexual health behaviours. We included five psychotic experiences and a categorical measure of psychosis based on the Psychosis Screening Questionnaire.
At national level, more Black men reported psychotic experiences but disparities disappeared following statistical adjustment for social position. However, large disparities for psychotic experiences in Hackney were not attenuated by adjustment for social factors in Black men (adjusted odds ratio, 3.24; 95% CI 2.14–4.91; P < 0.002), but were for South Asian men. A syndemic model of joint effects, adducing a four-component latent variable (psychotic experiences and anxiety, substance dependence, high-risk sexual behaviour and violence and criminality) showed synergy between components and explained persistent disparities in psychotic experiences. A further interaction confirmed area-level effects (Black ethnicity × Hackney residence, 0.834; P < 0.001).
Syndemic effects result in higher rates of non-affective psychosis among BME persons in certain inner-urban settings. Further research should investigate how syndemics raise levels of psychotic experiences and related health conditions in Black men in specific places with multiple deprivations.
Declaration of interest
K.B. is Editor in Chief of the British Journal of Psychiatry but played no part in the review and decision process.
Major depressive disorder (MDD) is a leading cause of disability worldwide and influenced by both environmental and genetic factors. Genetic studies of MDD have focused on common variants and have been constrained by the heterogeneity of clinical symptoms.
We sequenced the exome of 77 cases and 245 controls of Han Chinese ancestry and scanned their brain. Burden tests of rare variants were performed first to explore the association between genes/pathways and MDD. Secondly, parallel Independent Component Analysis was conducted to investigate genetic underpinnings of gray matter volume (GMV) changes of MDD.
Two genes (CSMD1, p = 5.32×10−6; CNTNAP5, p = 1.32×10−6) and one pathway (Neuroactive Ligand Receptor Interactive, p = 1.29×10−5) achieved significance in burden test. In addition, we identified one pair of imaging-genetic components of significant correlation (r = 0.38, p = 9.92×10−6). The imaging component reflected decreased GMV in cases and correlated with intelligence quotient (IQ). IQ mediated the effects of GMV on MDD. The genetic component enriched in two gene sets, namely Singling by G-protein coupled receptors [false discovery rate (FDR) q = 3.23×10−4) and Alzheimer Disease Up (FDR q = 6.12×10−4).
Both rare variants analysis and imaging–genetic analysis found evidence corresponding with the neuroinflammation and synaptic plasticity hypotheses of MDD. The mediation of IQ indicates that genetic component may act on MDD through GMV alteration and cognitive impairment.
Email your librarian or administrator to recommend adding this to your organisation's collection.