Pregnancy burdens maternal folate reserves. Postpartum restoration to normal folate values may take up to 1 year. Maternal folate deficiency during early pregnancy has been hypothesized as a cause of schizophrenia in the offspring. We investigated whether the risk of schizophrenia is increased in persons conceived shortly after another birth. A population-based cohort was established of 1.43 million persons born in Denmark between 1950 and 1983, yielding 17.6 million person-years of follow-up. Schizophrenia in cohort members (5095 cases) and their siblings and parents was identified by linkage with the Danish Psychiatric Case Register. Relative risks of schizophrenia were estimated by use of log-linear Poisson regression. As compared to intervals of 45 months and longer, the schizophrenia risk ratio was 1.14 (95% confidence interval [CI], 0.97 to 1.35) for interbirth intervals of up to 15 months, 1.32 (95% CI, 1.12 to 1.56) for intervals of 15 to 17 months, 1.38 (95% CI, 1.18 to 1.61), for intervals of 18 to 20 months and 1.13 (95% CI, 1.00 to 1.29) for intervals of 21 to 26 months. Relative risks did not essentially change after adjustment for age, sex, calendar year of diagnosis, maternal and paternal age, history of mental illness in a parent or sibling, sibship size, place of birth, and distance to younger sibling. These results show an association between short birth intervals and schizophrenia in the offspring. Although maternal folate depletion may play a role in this association, we cannot rule out other explanations such as maternal stress during pregnancy and childhood infections.
Psychotic experiences (PE) in individuals of the general population are hypothesized to mark the early expression of the pathology underlying psychosis. This notion of PE as an intermediate phenotype is based on the premise that PE share genetic liability with psychosis. We examined whether PE in childhood was predicted by a family history of mental disorder with psychosis rather than a family history of nonpsychotic mental disorder and whether this association differed by severity of PE. The study examined data on 1632 children from a general population birth cohort assessed at age 11-12 years by use of a semistructured interview covering 22 psychotic symptoms. The Danish national registers were linked to describe the complete family history of hospital-based psychiatric diagnoses. Uni- and multivariable logistic regressions were used to test whether a family history of any mental disorder with psychosis, or of nonpsychotic mental disorder, vs no diagnoses was associated with increased risk of PE in offspring (hierarchical exposure variable). The occurrence of PE in offspring was significantly associated with a history of psychosis among the first-degree relatives (adjusted relative risk [RR] = 3.29, 95% CI: 1.82-5.93). The risk increased for combined hallucinations and delusions (adjusted RR = 5.90, 95% CI: 2.64-13.16). A history of nonpsychotic mental disorders in first-degree relatives did not contribute to the risk of PE in offspring nor did any mental disorder among second-degree relatives. Our findings support the notion of PE as a vulnerability marker of transdiagnostic psychosis. The effect of psychosis in first-degree relatives may operate through shared genetic and environmental factors.
Notes
Cites: Nat Genet. 2013 Sep;45(9):984-9423933821
Cites: Ugeskr Laeger. 2013 May 13;175(20):139923663392
OBJECTIVE: This study replicated a previous report that there may be substantial synergism between urbanicity (a proxy environmental risk factor) and familial clustering of psychotic disorder (a proxy genetic risk factor). METHOD: The amount of synergism was estimated from the additive statistical interaction between urbanicity of place of birth and family history of schizophrenia or family history of any severe mental disorder in a population-based Danish cohort of 1,020,063 individuals. RESULTS: There was significant interaction between urbanicity and family history; between 20% and 35% of individuals who had been exposed to both of these risk factors had schizophrenia possibly because of their synergistic effects. CONCLUSIONS: The results suggest that a substantial proportion of the population morbidity force of schizophrenia may be the result of gene-environment interactions associated with urbanicity.
ECEVE, UMRS 1123, Université Paris Diderot, Sorbonne Paris Cité, INSERM, Paris, France; AP-HP, URC-Eco, DHU Pepsy, F-75004 Paris, France; Foundation FondaMental, French National Science Foundation, Créteil, France. Electronic address: jeanbaptiste.hazo@urc-eco.fr.
As part of the Roamer project, we aimed at revealing the share of health research budgets dedicated to mental health, as well as on the amounts allocated to such research for four European countries. Finland, France, Spain and the United Kingdom national public and non-profit funding allocated to mental health research in 2011 were investigated using, when possible, bottom-up approaches. Specifics of the data collection varied from country to country. The total amount of public and private not for profit mental health research funding for Finland, France, Spain and the UK was €10·2, €84·8, €16·8, and €127·6 million, respectively. Charities accounted for a quarter of the funding in the UK and less than six per cent elsewhere. The share of health research dedicated to mental health ranged from 4·0% in the UK to 9·7% in Finland. When compared to the DALY attributable to mental disorders, Spain, France, Finland, and the UK invested respectively €12·5, €31·2, €39·5, and €48·7 per DALY. Among these European countries, there is an important gap between the level of mental health research funding and the economic and epidemiologic burden of mental disorders.
Knowledge on the significance of childhood psychotic symptoms and experiences (PE) is still limited. This study aimed to investigate the prevalence and clinical significance of PE in preadolescent children from the general population by use of in-depth psychopathological interviews and comprehensive diagnostic assessments.
We investigated 1,632 children from the general population-based Copenhagen Child Cohort 2000. PE were measured by semistructured interviews using the K-SADS-PL-items on psychotic and affective symptoms, each symptom scored as not present versus likely or definitely present. The Development and Well-Being Assessment (DAWBA) was used independently to diagnose DSM-IV-mental disorders. Puberty development and sleep disturbance were self-reported. The associations between PE (any lifetime hallucination and/or delusion) and various mental problems and disorders were examined by multivariable binomial regression analyses, adjusting for gender and onset of puberty.
The weighted life time prevalence of PE at age 11-12 years was 10.9% (CI 9.1-12.7). The majority of children with PE (n = 172) either had a diagnosable DSM-IV-mental disorder (31.4%) or self-reported mental health difficulties in absence of a diagnosis (31.4%). The risk of delusions increased with onset of puberty. The risk of PE increased with emotional and neurodevelopmental disorders, subthreshold depressive symptoms, sleep problems and lack of sleep, regardless of whether PE were expressed as hallucinations and/or delusions. The highest correlations were seen for emotional and multiple disorders.
Psychotic experiences are particularly prevalent in the context of affective dysregulation and sleep disturbance, increase with onset of puberty and represent a trans-diagnostic marker of psychopathology.
