Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population

Congenital or early life infection with Toxoplasma gondii has been implicated in schizophrenia aetiology. Childhood cat ownership has been hypothesized as an intermediary marker of T. gondii infection and, by proxy, as a risk factor for later psychosis. Evidence supporting this hypothesis is, however, limited. We used birth cohort data from the Avon Longitudinal Study of Parents and Children (ALSPAC) to investigate whether cat ownership in pregnancy and childhood (ages 4 and 10 years) was associated with psychotic experiences (PEs) in early (age 13, N = 6705) and late (age 18, N = 4676) adolescence, rated from semi-structured interviews. We used logistic regression to examine associations between cat ownership and PEs, adjusting for several sociodemographic and socioeconomic factors, household characteristics and dog ownership. Missing data were handled via multiple imputation. Cat ownership during pregnancy was not associated with PEs at age 13 years [adjusted odds ratio (OR) 1.15, 95% confidence interval (CI) 0.97–1.35] or 18 years (OR 1.08, 95% CI 0.86–1.35). Initial univariable evidence that cat ownership at ages 4 and 10 years was associated with PEs at age 13 years did not persist after multivariable adjustment (4 years: OR 1.18, 95% CI 0.94–1.48; 10 years: OR 1.12, 95% CI 0.92–1.36). There was no evidence that childhood cat ownership was associated with PEs at age 18 years. While pregnant women should continue to avoid handling soiled cat litter, given possible T. gondii exposure, our study strongly indicates that cat ownership in pregnancy or early childhood does not confer an increased risk of later adolescent PEs

Trajectories of Neighborhood Cohesion in Childhood, and Psychotic and Depressive Symptoms at Age 13 and 18 Years

OBJECTIVE: Exposure to adverse social environments has been associated with psychotic and depressive symptoms in adolescence in cross-sectional studies, but the longitudinal relation is unclear. This study examined whether longitudinal trajectories of exposure to adverse social environments across childhood are associated with psychotic experiences and depressive symptoms in adolescence. METHOD: Data on participants from the Avon Longitudinal Study of Parents and Children (ALSPAC) were used to estimate longitudinal trajectories of childhood exposure to neighborhood cohesion (NC), discord (ND), and stress (NS) using latent class growth modeling. Logistic regression was used to examine the association between these trajectories and psychotic experiences and depressive symptoms at 13 and 18 years of age, adjusting for maternal psychopathology, participant sociodemographic and socioeconomic characteristics, and area-level deprivation. RESULTS: A dose-response association was observed between higher NS and the odds of psychotic experiences at 13 years (medium NS, adjusted odds ratio [aOR] 1.25, 95% CI 1.05–1.49; high NS, aOR 1.77, 95% CI 1.30–2.40), whereas high levels of ND predicted psychotic experiences at 18 years (aOR 1.50, 95% CI 1.10–2.07). High levels of NC (aOR 1.43, 95% CI 1.02–1.71) and NS (aOR 1.55, 95% CI 1.07–2.26) were associated with increased odds of high depressive symptoms at 18 years in a dose-response fashion. CONCLUSION: Prolonged and more severe exposure to adverse social environments is associated with greater odds of developing psychotic and depressive symptoms in late adolescence

Association of neighbourhood migrant density and risk of non-affective psychosis: a national, longitudinal cohort study

BACKGROUND: Elevated risk of psychotic disorders in migrant groups is a public mental health priority. We investigated whether living in areas of high own-region migrant density was associated with reduced risk of psychotic disorders among migrants and their children, and whether generation status, probable visible minority status, or region-of-origin affected this relationship. METHODS: We used the Swedish registers to identify migrants and their children born between Jan 1, 1982, and Dec 31, 1996, and living in Sweden on or after their 15th birthday. We tracked all included participants from age 15 years or date of migration until emigration, death, or study end (Dec 31, 2016). The outcome was an ICD-10 diagnosis of non-affective psychosis (F20-29). We calculated own-region and generation-specific own-region density within the 9208 small areas for market statistics neighbourhoods in Sweden, and estimated the relationship between density and diagnosis of non-affective psychotic disorders using multilevel Cox proportional hazards models, adjusting for individual confounders (generation status, age, sex, calendar year, lone dwelling, and time since migration [migrants only]), family confounders (family income, family unemployment, and social welfare), and neighbourhood confounders (deprivation index, population density, and proportion of lone dwellings), and using the Akaike information criterion (AIC) to compare model fit. FINDINGS: Of 468 223 individuals included in the final cohort, 4582 (1·0%) had non-affective psychotic disorder. Lower own-region migrant density was associated with increased risk of psychotic disorders among migrants (hazard ratio [HR] 1·05, 95% CI 1·02-1·07 per 5% decrease) and children of migrants (1·03, 1·01-1·06), after adjustment. These effects were stronger for probable visible minority migrants (1·07, 1·04-1·11), including migrants from Asia (1·42, 1·15-1·76) and sub-Saharan Africa (1·28, 1·15-1·44), but not migrants from probable non-visible minority backgrounds (0·99, 0·94-1·04). Among migrants, adding generation status to the measure of own-region density provided a better fit to the data than overall own-region migrant density (AIC 36 103 vs 36 106, respectively), with a 5% decrease in generation-specific migrant density corresponding to a HR of 1·07 (1·04-1·11). INTERPRETATION: Migrant density was associated with non-affective psychosis risk in migrants and their children. Stronger protective effects of migrant density were found for probable visible minority migrants and migrants from Asia and sub-Saharan Africa. For migrants, this risk intersected with generation status. Together, these results suggest that this health inequality is socially constructed. FUNDING: Wellcome Trust, Royal Society, Mental Health Research UK, University College London, National Institute for Health Research, Swedish Research Council, and FORTE

Refugee migration and risk of schizophrenia and other non-affective psychoses: cohort study of 1.3 million people in Sweden.

OBJECTIVE:  To determine whether refugees are at elevated risk of schizophrenia and other non-affective psychotic disorders, relative to non-refugee migrants from similar regions of origin and the Swedish-born population. DESIGN:  Cohort study of people living in Sweden, born after 1 January 1984 and followed from their 14th birthday or arrival in Sweden, if later, until diagnosis of a non-affective psychotic disorder, emigration, death, or 31 December 2011. SETTING:  Linked Swedish national register data. PARTICIPANTS:  1 347 790 people, including people born in Sweden to two Swedish-born parents (1 191 004; 88.4%), refugees (24 123; 1.8%), and non-refugee migrants (132 663; 9.8%) from four major refugee generating regions: the Middle East and north Africa, sub-Saharan Africa, Asia, and Eastern Europe and Russia. MAIN OUTCOME MEASURES:  Cox regression analysis was used to estimate adjusted hazard ratios for non-affective psychotic disorders by refugee status and region of origin, controlling for age at risk, sex, disposable income, and population density. RESULTS:  3704 cases of non-affective psychotic disorder were identified during 8.9 million person years of follow-up. The crude incidence rate was 38.5 (95% confidence interval 37.2 to 39.9) per 100 000 person years in the Swedish-born population, 80.4 (72.7 to 88.9) per 100 000 person years in non-refugee migrants, and 126.4 (103.1 to 154.8) per 100 000 person years in refugees. Refugees were at increased risk of psychosis compared with both the Swedish-born population (adjusted hazard ratio 2.9, 95% confidence interval 2.3 to 3.6) and non-refugee migrants (1.7, 1.3 to 2.1) after adjustment for confounders. The increased rate in refugees compared with non-refugee migrants was more pronounced in men (likelihood ratio test for interaction χ(2) (df=2) z=13.5; P=0.001) and was present for refugees from all regions except sub-Saharan Africa. Both refugees and non-refugee migrants from sub-Saharan Africa had similarly high rates relative to the Swedish-born population. CONCLUSIONS:  Refugees face an increased risk of schizophrenia and other non-affective psychotic disorders compared with non-refugee migrants from similar regions of origin and the native-born Swedish population. Clinicians and health service planners in refugee receiving countries should be aware of a raised risk of psychosis in addition to other mental and physical health inequalities experienced by refugees

Suicide risk among refugees compared with non-refugee migrants and the Swedish-born majority population

BACKGROUND: It has been hypothesised that refugees have an increased risk of suicide. AIMS: To investigate whether risk of suicide is higher among refugees compared with non-refugee migrants from the same areas of origin and with the Swedish-born population, and to examine whether suicide rates among migrants converge to the Swedish-born population over time. METHOD: A population-based cohort design using linked national registers to follow 1 457 898 people born between 1 January 1970 and 31 December 1984, classified by migrant status as refugees, non-refugee migrants or Swedish-born. Participants were followed from their 16th birthday or date of arrival in Sweden until death, emigration or 31 December 2015, whichever came first. Cox regression models estimated adjusted hazard ratios for suicide by migrant status, controlling for age, gender, region of origin and income. RESULTS: There were no significant differences in suicide risk between refugee and non-refugee migrants (hazard ratio 1.28, 95% CI 0.93-1.76) and both groups had a lower risk of suicide than Swedish born. During their first 5 years in Sweden no migrants died by suicide; however, after 21-31 years their suicide risk was equivalent to the Swedish-born population (hazard ratio 0.94, 95% CI 0.79-1.22). After adjustment for income this risk was significantly lower for migrants than the Swedish-born population. CONCLUSIONS: Being a refugee was not an additional risk factor for suicide. Our findings regarding temporal changes in suicide risk suggest that acculturation and socioeconomic deprivation may account for a convergence of suicide risk between migrants and the host population over time. DECLARATION OF INTEREST: None

An integrative view of mammalian seasonal neuroendocrinology

This is the peer reviewed version of the following article: Dardente, H., Wood, S.H., Ebling, F. & Sáenz de Miera, C. (2019). An integrative view of mammalian seasonal neuroendocrinology. Journal of neuroendocrinology. Journal of Neuroendocrinology, 31(5), e12729, which has been published in final form at https://doi.org/10.1111/jne.12729. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.Seasonal neuroendocrine cycles that govern annual changes in reproductive activity, energy metabolism and hair growth are almost ubiquitous in mammals that have evolved at temperate and polar latitudes. Changes in nocturnal melatonin secretion regulating gene expression in the pars tuberalis (PT) of the pituitary stalk are a critical common feature in seasonal mammals. The PT sends signal(s) to the pars distalis of the pituitary to regulate prolactin secretion and thus the annual moult cycle. The PT also signals in a retrograde manner via thyroid‐stimulating hormone to tanycytes, which line the ventral wall of the third ventricle in the hypothalamus. Tanycytes show seasonal plasticity in gene expression and play a pivotal role in regulating local thyroid hormone (TH) availability. Within the mediobasal hypothalamus, the cellular and molecular targets of TH remain elusive. However, two populations of hypothalamic neurones, which produce the RF‐amide neuropeptides kisspeptin and RFRP3 (RF‐amide related peptide 3), are plausible relays between TH and the gonadotrophin‐releasing hormone‐pituitary‐gonadal axis. By contrast, the ways by which TH also impinges on hypothalamic systems regulating energy intake and expenditure remain unknown. Here, we review the neuroendocrine underpinnings of seasonality and identify several areas that warrant further research

Inferring Population Preferences via Mixtures of Spatial Voting Models

Understanding political phenomena requires measuring the political preferences of society. We introduce a model based on mixtures of spatial voting models that infers the underlying distribution of political preferences of voters with only voting records of the population and political positions of candidates in an election. Beyond offering a cost-effective alternative to surveys, this method projects the political preferences of voters and candidates into a shared latent preference space. This projection allows us to directly compare the preferences of the two groups, which is desirable for political science but difficult with traditional survey methods. After validating the aggregated-level inferences of this model against results of related work and on simple prediction tasks, we apply the model to better understand the phenomenon of political polarization in the Texas, New York, and Ohio electorates. Taken at face value, inferences drawn from our model indicate that the electorates in these states may be less bimodal than the distribution of candidates, but that the electorates are comparatively more extreme in their variance. We conclude with a discussion of limitations of our method and potential future directions for research.Comment: To be published in the 8th International Conference on Social Informatics (SocInfo) 201

A Holder Continuous Nowhere Improvable Function with Derivative Singular Distribution

We present a class of functions $\mathcal{K}$ in $C^0(\R)$ which is variant of the Knopp class of nowhere differentiable functions. We derive estimates which establish \mathcal{K} \sub C^{0,\al}(\R) for 0<\al<1 but no $K \in \mathcal{K}$ is pointwise anywhere improvable to C^{0,\be} for any \be>\al. In particular, all $K$'s are nowhere differentiable with derivatives singular distributions. $\mathcal{K}$ furnishes explicit realizations of the functional analytic result of Berezhnoi. Recently, the author and simulteously others laid the foundations of Vector-Valued Calculus of Variations in $L^\infty$ (Katzourakis), of $L^\infty$-Extremal Quasiconformal maps (Capogna and Raich, Katzourakis) and of Optimal Lipschitz Extensions of maps (Sheffield and Smart). The "Euler-Lagrange PDE" of Calculus of Variations in $L^\infty$ is the nonlinear nondivergence form Aronsson PDE with as special case the $\infty$-Laplacian. Using $\mathcal{K}$, we construct singular solutions for these PDEs. In the scalar case, we partially answered the open $C^1$ regularity problem of Viscosity Solutions to Aronsson's PDE (Katzourakis). In the vector case, the solutions can not be rigorously interpreted by existing PDE theories and justify our new theory of Contact solutions for fully nonlinear systems (Katzourakis). Validity of arguments of our new theory and failure of classical approaches both rely on the properties of $\mathcal{K}$.Comment: 5 figures, accepted to SeMA Journal (2012), to appea

Longitudinal associations between psychotic experiences and disordered eating behaviours in adolescence: a UK population-based study

BACKGROUND: Psychotic experiences might represent non-specific markers of poor mental health in adolescence. However, only a few predominantly cross-sectional studies have tested their association with disordered eating behaviours in adolescent and adult populations. The aim of this study was to explore the association between psychotic experiences at age 13 years, and disordered eating behaviours and body-mass index (BMI) at age 18 years. METHODS: We used data from the Avon Longitudinal Study of Parents and Children, a longitudinal birth cohort based in Avon (England, UK) including mothers with an expected delivery date between April 1, 1991, and Dec 31, 1992, and their children. Psychotic experiences (such as delusions and hallucinations) and BMI were measured at clinical assessments when children were nearly aged 13 years, and data on disordered eating behaviours (ie, presence of binge eating, purging, fasting, or excessive exercise for weight loss; any of these behaviours [included to increase statistical power]; and number of behaviours [included to investigate severity]) were obtained via a postal questionnaire that used adapted questions from the Youth Risk Behaviour Surveillance System questionnaire at approximately age 18 years. For each outcome, we ran a univariable model and four multivariable models (logistic, linear [for BMI], or negative binomial [for the number of behaviours] regression), progressively adjusting for child and maternal sociodemographic, physical, and mental health characteristics (including child's sex, and maternal age, marital status, and highest academic qualification); autistic traits at age 7 years (measured with the Social and Communication Disorder Checklist); baseline BMI at age 13 years, and depressive symptoms at baseline (ie, at age 13 years when psychotic experiences were measured: childs' symptoms measured with the Moods and feelings Questionnaire, and maternal symptoms measured at 32 weeks' gestation with the Edinburgh Postnatal Depression Scale). We imputed missing outcome and covariate data. FINDINGS: Our sample included 6361 children, of whom 734 (12%) reported psychotic experiences at age 13 years. In univariable models, psychotic experiences were associated with greater odds of reporting any disordered eating behaviours (odds ratio [OR] 1·92, 95% CI 1·46–2·52; p<0·0001), and more severe symptoms (as measured by the number of disordered eating behaviours: 0·58, 0·32–0·84; p<0·0001) at age 18 years. These associations were slightly attenuated by adjustment for maternal and child characteristics (any disordered eating behaviours OR 1·82, 95% CI 1·35–2·44, p<0·0001; number of disordered eating behaviours 0·49, 95% CI 0·23–0·75, p<0·00001), autistic traits at age 7 years (any disordered eating behaviours OR 1·80, 95% CI 1·34–2·41, p<0·0001; number of disordered eating behaviours 0·48, 95% CI 0·22–0·74, p<0·00001), and BMI (any disordered-eating behaviours OR 1·83, 95% CI 1·36–2·46, p<0·0001; number of disordered-eating behaviours 0·32, 95% CI 0·06–0·57, p<0·00001) Adjusting for baseline depressive symptoms attenuated, but not removed, these associations (any disordered eating OR 1·50, 95% CI 1·10–2·03, p=0·010; more severe symptoms 0·32, 0·06–0·57, p=0·017). Psychotic experiences were also associated with greater binge eating, purging, and fasting behaviours, although some associations weakened after controlling for depressive symptoms. We noted no associations between psychotic experiences and excessive exercise or BMI in any of the models. INTERPRETATION: Our findings suggested that psychotic experiences are markers of increased risk for several disordered eating behaviours in late adolescence, possibly by indicating more severe psychopathology in early adolescence. More research investigating shared risk factors for psychotic experiences and eating disorders is warranted to elucidate shared and specific causal pathways. FUNDING: Wellcome Trust, the Royal Society, University College London Hospitals National Institute for Health Research Biomedical Research Centre, UK Medical Research Council, and the University of Bristol