Is childhood cat ownership a risk factor for schizophrenia later in life?

Two previous studies suggested that childhood cat ownership is a possible risk factor for later developing schizophrenia or other serious mental illness. We therefore used an earlier, large NAMI questionnaire to try and replicate this finding. The results were the same, suggesting that cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill. If true, an explanatory mechanism may be Toxoplasma gondii. We urge our colleagues to try and replicate these findings to clarify whether childhood cat ownership is truly a risk factor for later schizophrenia.

Deinstitutionalization and the rise of violence.

The deinstitutionalization of individuals with serious mental illness was driven by 4 factors: public revelations regarding the state of public mental hospitals, the introduction of antipsychotic medications, the introduction of federal programs to fund patients who had been discharged, and civil libertarian lawyers. The result is approximately 3.2 million individuals with untreated serious mental illness living in the community. Beginning in the 1970s in the United States, there began to be reported increasing incidents of violent behavior, including homicides, committed by these untreated individuals. Such incidents became more numerous in the 1980s and 1990s, and have further increased since the turn of the century. Existing studies suggest that individuals with untreated severe mental illness are responsible for at least 10% of all homicides and approximately half of all mass killings. Studies have also shown that when these individuals are treated, the incidence of violent behavior decreases significantly. Examples of treatment mechanisms that have proven effective include assisted outpatient treatment (AOT), conditional release, and mental health courts.

Funcionamiento cognitivo antes del inicio de la psicosis: papel de la exposición fetal al virus de la gripe verificada con exámenes serológicos / Cognitive functioning prior to the onset of psychosis: The role of fetal exposure to serologically determined influenza infection

Fundamento. Los estudios previos han relacionado la exposición prenatal a la gripe con un mayor riesgo de padecer esquizofrenia; sin embargo, en ninguno se han examinado las secuelas del neurodesarrollo de esta agresión prenatal antes del inicio de los síntomas psicóticos con pruebas serológicas de la infección. En el presente estudio, entre niños que desarrollaron psicosis en la vida adulta, comparados con niños de control, no psiquiátricos, tratamos de examinar la contribución de la exposición prenatal al virus A y B de la gripe en el rendimiento cognitivo. Métodos. Los individuos eran 111 casos (70 con esquizofrenia y 41 con psicosis afectivas) y 333 individuos de control, emparejados, seguidos desde el embarazo hasta los 7 años de edad a través del Collaborative Perinatal Project. Se administró la escala de inteligencia de Wechsler para niños (7 años) y la morbilidad psiquiátrica en la vida adulta se valoró mediante la revisión de las historias clínicas y se confirmó mediante un estudio de validación. A partir de los sueros prenatales archivados de las madres, obtenidos en el momento del parto, se efectuaron análisis y la infección por gripe se determinó mediante unos títulos de anticuerpos inmunoglobulina G (>percentil 75). Resultados. Entre los casos expuestos en el período prenatal al virus B de la gripe, en comparación con los no expuestos, se identificaron disminuciones significativas del cociente intelectual verbal y del subtest de información, al igual que reducciones no significativas similares en las puntuaciones del cociente intelectual de la escala total y en los subtest de vocabulario, comprensión, aritmética e historietas. La exposición fetal al virus B de la gripe no dio lugar a diferencias significativas del rendimiento cognitivo entre niños del grupo de control. Conclusiones. En conjunto, estos hallazgos sugieren que un factor genético y/o ambiental asociado con la psicosis aumenta la vulnerabilidad del cerebro fetal a los efectos particulares del virus B de la gripe, dando lugar a un peor rendimiento cognitivo, incluso antes del inicio de los síntomas (AU)

Background.Previous studies have linked prenatal influenza exposure to increased risk of schizophrenia; however, no study has examined the neurodevelopmental sequelae of this prenatal insult before the onset of psychotic symptoms using serological evidence of infection. This study sought to examine the contribution of prenatal influenza A and B exposure to cognitive performance among children who developed psychoses in adulthood versus nonpsychiatric control children. Methods. Subjects were 111 cases (70 with schizophrenia and 41 with affective psychoses) and 333 matched control subjects followed from gestation until age 7 through the Collaborative Perinatal Project. The Wechsler Intelligence Scale for Children (age 7) was administered and adult psychiatric morbidity was assessed by medical records review and confirmed by a validation study. Assays were conducted from archived prenatal maternal sera collected at birth, and influenza infection was determined by immunoglobulin G (IgG) antibody titers 75th percentile. Results. Significant decreases in verbal IQ and the information subtest, as well as similar nonsignificant reductions in full scale IQ scores and vocabulary, comprehension, digit span, and picture arrangement subtests were found among cases who were prenatally exposed to influenza B versus cases who were not exposed. Fetal exposure to influenza B did not lead to any significant differences in cognitive performance among control children. Conclusions. Cumulatively, these findings suggest that a genetic and/or an environmental factor associated with psychosis rendered the fetal brain particularly vulnerable to the effects of influenza B, leading to poorer cognitive performance even before symptom onset (AU)

Toxoplasma and schizophrenia.

Research on infectious agents as a possible cause of schizophrenia has become prominent in the past decade. Toxoplasma gondii has emerged as a prime candidate for a variety of reasons; (i) many studies have reported that individuals with schizophrenia, compared to controls, have a higher prevalence of antibodies to T. gondii, (ii) some individuals with adult toxoplasmosis develop psychotic symptoms similar to those of schizophrenia, (iii) epidemiologically, there are many similarities between toxoplasmosis and schizophrenia, (iv) antipsychotic drugs known to be effective in schizophrenia also inhibit some parasites, including T. gondii, (v) Toxoplasma has been shown to induce elevated levels of dopamine in experimentally infected animals (elevated dopamine is commonly seen in individuals with schizophrenia) and (vi) studies have shown that individuals with schizophrenia, compared to controls, have had greater exposure to cats in childhood. A number of questions remain concerning a role for Toxoplasma in the aetiology of schizophrenia, including the roles of strain variation, the timing and source of infection, and the role of host genes in determining disease susceptibility. The establishment of a firm association between Toxoplasma and the aetiology of schizophrenia and related disorders would represent a major breakthrough in the understanding of these disorders and would lead to novel methods for their treatment and prevention.

The antecedents of psychoses: a case-control study of selected risk factors.

Winter birth, urban birth and/or childhood residence, and perinatal complications have each been identified as environmental risk factors for the later development of schizophrenia, schizoaffective disorder, and bipolar disorder. A preliminary case-control study also identified cat exposure in childhood as a possible risk factor. To assess selected environmental events, including childhood exposure to pets, as possible risk factors for these diseases, a case-control telephone survey was carried out by the University of Maryland Survey Research Center for 264 mothers of cases and 528 mothers of matched controls. The cases were randomly selected mothers who were members of the National Alliance for the Mentally Ill, and whose children had been diagnosed with schizophrenia, schizoaffective disorder, or bipolar disorder. The controls were mothers randomly selected from the same telephone exchanges. For five of the 19 major variables, there were statistically significant differences between cases and controls: fever during pregnancy, complications during delivery, city or suburban residence at birth, cat ownership between birth and age 13, and breast-feeding. In a multivariate logistic regression including these five variables, each variable made a significant contribution. The finding of perinatal complications, urban/suburban residence at birth, and cat ownership in childhood as risk factors for the later development of psychoses confirmed previous studies. Previous research on breast-feeding as a risk factor has yielded contradictory results. Additional research is needed to ascertain how such environmental risk factors interact with genetic risk factors. Understanding these could lead to better treatments and possible prevention strategies.

Familial and genetic mechanisms in schizophrenia.

A distinction should be made between genetic aspects of schizophrenia and familial aspects. Genetic aspects of the disease have been reviewed and found to be deficient in many respects. Until recent years, familial factors were assumed to be psychological in origin, but this assumption is now discredited. Research efforts should focus on familial factors that are biological, especially infectious agents that may be transmitted within the family. Most infectious agents are influenced by predisposing genes. The etiology of schizophrenia, then, may turn out to involve biological familial infectious agents that are influenced by susceptibility genes governing the infectious process and the clinical expression of the disease.