Inequalities in the Incidence of Psychotic Disorders Among Racial and Ethnic Groups.

OBJECTIVE: The authors examined recent trends in incidence of psychotic disorders, demographic characteristics, and comorbid psychiatric and medical conditions among six racial/ethnic groups. METHOD: A retrospective cohort study design was used to examine the incidence of psychotic disorders across race/ethnicity groups and comorbid psychiatric and medical conditions among members of Kaiser Permanente Northern California from 2009 to 2019 (N=5,994,758). Poisson regression was used to assess changes in annual incidence, and Cox proportional hazards and logistic regression models adjusted for age and sex were used to test correlates and consequences. RESULTS: Overall, the incidence of nonaffective psychotic disorders decreased slightly over the study period. Compared with White members, the risk of nonaffective psychosis diagnosis was higher among Black (hazard ratio=2.13, 95% CI=2.02-2.24) and American Indian or Alaskan Native (AIAN) (hazard ratio=1.85, 95% CI=1.53-2.23) members and lower among Asian (hazard ratio=0.72, 95% CI=0.68-0.76) and Hispanic (hazard ratio=0.91, 95% CI=0.87-0.96) members, as well as those whose race/ethnicity was categorized as "other" (hazard ratio=0.92, 95% CI=0.86-0.99). Compared with White members, the risk of affective psychosis diagnosis adjusted for age and sex was higher among Black (hazard ratio=1.76, 95% CI=1.62-1.91), Hispanic (hazard ratio=1.09, 95% CI=1.02-1.16), and AIAN (hazard ratio=1.38, 95% CI=1.00-1.90) members and lower among Asian (hazard ratio=0.77, 95% CI=0.71-0.83), Native Hawaiian or other Pacific Islander (hazard ratio=0.69, 95% CI=0.48-0.99), and "other" (hazard ratio=0.86, 95% CI=0.77-0.96) members. Psychotic disorders were associated with significantly higher odds of suicide (odds ratio=2.65, 95% CI=2.15-3.28), premature death (odds ratio=1.30, 95% CI=1.22-1.39), and stroke (odds ratio=1.64, 95% CI=1.55-1.72) and lower odds of health care utilization (odds ratio=0.44, 95% CI=0.42-0.47). CONCLUSIONS: This study demonstrates racial and ethnic variation in incident psychotic disorder diagnoses in the United States, compared with non-Hispanic Whites. Individuals diagnosed with psychosis face a greater burden of other negative health outcomes and lower odds of health care utilization, reflecting personal and economic impacts. Identifying risk factors for elevated rates and protective influences in subgroups can inform strategies for prevention and interventions to ameliorate severe consequences of psychotic syndromes.

First episode psychosis and weight gain a longitudinal perspective in Cheshire UK: a comparison between individuals with nonaffective versus affective psychosis.

Early weight gain following initiation of antipsychotic treatment predicts longer-term weight gain, with attendant long-term consequences including premature cardiovascular events/death. An important question is whether there is a difference in weight change over time between people with affective versus nonaffective psychosis. Here we describe the results of a real-world analysis of the BMI change in the months postdiagnosis with affective versus nonaffective psychosis. Methods: We undertook an anonymised search across one Primary Care Network in Cheshire, UK with a total population of 32 301 individuals. We reviewed the health records of anyone who had been diagnosed over a 10-year period between June 2012 and June 2022 for the first time with first episode nonaffective psychosis versus psychosis associated with depression or bipolar affective disorder (affective psychosis). Results: The overall % change in BMI was +8% in nonaffective psychosis individuals and +4% in those with a diagnosis of affective psychosis - however, the distribution was markedly skewed for nonaffective psychosis patients. Using caseness as >30% increase in BMI; affective = 4% cases and nonaffective = 13% cases, there was a three-fold difference in terms of increase in BMI. In regression analysis, the r2 linking the initial BMI to % change in BMI was 0.13 for nonaffective psychosis and 0.14 for affective psychosis. Conclusion: The differences observed here in the distribution of weight change over time between individuals with affective versus nonaffective psychosis may relate to underlying constitutional differences. The phenotypic and genetic factors underlying this difference remain to be defined.

Origins of spousal cross-concordance for psychiatric disorders: a test of the social stress theory for alcohol use disorder.

BACKGROUND: The authors sought to clarify the impact of spousal psychiatric disorders of differing severity [major depression or anxiety disorders (DAD) v. bipolar disorder or nonaffective psychosis (BPN)] on proband risk for alcohol use disorder (AUD) during marriage. METHODS: In a Swedish cohort (N = 744 628), associations between spousal DAD and BPN and proband AUD were estimated with Cox proportional hazards; associations between parental AUD, proband premarital AUD, and spousal lifetime DAD and BPN were estimated with logistic regression; and whether spousal DAD or BPN causally increased risk for AUD was evaluated with frailty models. RESULTS: Spousal premarital DAD, spousal marital-onset DAD, and spousal BPN (premarital or marital-onset) were associated with proband AUD during marriage [hazard ratios (HR) range 1.44-3.72]. Those with a parental or premarital history of AUD (v. without) were more likely to marry a spouse with DAD or BPN (odds ratios 1.22-2.77). Moving from an unaffected first spouse to a DAD-affected second spouse increased AUD risk in males (HR 2.90). Moving from an unaffected first spouse to a BPN-affected second spouse increased AUD risk (HRmales 3.96; HRfemales 5.64). Moving to an unaffected second spouse from a DAD-affected first spouse decreased AUD risk, with stronger evidence in females compared to males (HRmales 0.59; HRfemales 0.28). CONCLUSIONS: Associations between spousal DAD or BPN and proband AUD reflect both selection and causal effects. Marriage to a BPN-affected spouse has a particularly strong effect on AUD risk, with more modest effects for spousal DAD.

Assessing behavior and cognition in rodents, nonhuman primates, and humans: where are the limits of translation?
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New psychopharmacological treatments are needed for affective and nonaffective psychoses, especially for the associated negative and cognitive symptoms. Earlier developments mostly failed, probably partly because of limitations in behavioral models used for validation. Now, deeper understanding of the genetics underlying disease pathogenesis and progress in genetic engineering will generate many rodent models with increased construct validity. To improve these models' translational value, we need complementary data from nonhuman primates. We also have to improve and streamline behavioral test systems to cope with increased demand. Here, we propose a comprehensive neurocognitive test battery that should overcome the disadvantages of single tests and yield cognitive/behavioral profiles for modeling subsets of patient symptoms. Further, we delineate a concept for classifying disease-relevant cognitive endophenotypes to balance between face and construct validity and clinical diagnostics. In summary, this review discusses new concepts and the limitations and future potential of translational research on cognition in psychiatry.
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Se requiere de nuevos tratamientos psicofarmacológicos para las psicosis afectivas y no afectivas, especialmente para los síntomas negativos y cognitivos asociados. La mayoría de los desarrollos anteriores fallaron; en parte debido, probablemente, a las limitaciones en los modelos conductuales empleados para la validación. Ahora, una comprensión más profunda de la genética subyacente a la patogénesis de la enfermedad y el progreso en la ingeniería genética generará muchos modelos de roedores con una mayor validez de constructo. Para mejorar el valor de estos modelos translacionales se requiere de datos complementarios de primates no humanos. También hay que mejorar y racionalizar los sistemas de pruebas conductuales para hacer frente a una mayor demanda. En este artículo se propone una batería completa de pruebas neurocognitivas que debería superar las desventajas de las pruebas individuales y generar perfiles cognitivo-conductuales para modelar subconjuntos de síntomas del paciente. Además, se plantea un concepto para clasificar los endofenotipos cognitivos relevantes para la enfermedad a fin de equilibrar la validez aparente y de constructo con el diagnóstico clínico. En resumen, esta revisión analiza nuevos conceptos, y las limitaciones y el potencial futuro de la investigación translacional sobre la cognición en psiquiatría.

De nouveaux traitements psychopharmacologiques sont nécessaires pour les psychoses dysthymiques ou non, surtout pour les symptômes associés négatifs et cognitifs. Par le passé, la plupart des développements ont échoué, probablement en partie en raison des limites des modèles comportementaux utilisés pour la validation. Aujourd'hui, une meilleure compréhension de la génétique de la pathogenèse de la maladie et les progrès du génie génétique vont produire de nombreux modèles de rongeurs mieux construits. Des données supplémentaires issues de primates non humains sont nécessaires pour améliorer la valeur traductive de ces modèles. Afin de satisfaire une demande croissante, nous devons aussi améliorer et rationaliser les systèmes de tests comportementaux. Nous proposons ici une batterie complète de tests neurocognitifs susceptible de palier les inconvénients des tests isolés et de fournir des profils cognitifs/comportementaux pour des sous-groupes de modélisation des symptômes des patients. En outre, nous définissons un concept pour classer les endophénotypes cognitifs pertinents pour la maladie afin de trouver un équilibre entre une validité de façade et de construit et les diagnostics cliniques. En résumé, cet article analyse de nouveaux concepts ainsi que les limites et les futures possibilités de la recherche translationnelle sur la cognition en psychiatrie.