746 research outputs found

    Alcohol use in adolescence as a risk factor for overdose in the 1986 Northern Finland Birth Cohort Study

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    Background Overdoses and poisonings are among the most common causes of death in young adults. Adolescent problem drinking has been associated with psychiatric morbidity in young adulthood as well as with elevated risk for suicide attempts. There is limited knowledge on adolescent alcohol use as a risk factor for alcohol and/or drug overdoses in later life. Methods Here, data from The Northern Finland Birth Cohort 1986 study with a follow-up from adolescence to early adulthood were used to assess the associations between adolescent alcohol use and subsequent alcohol or drug overdose. Three predictors were used: age of first intoxication, self-reported alcohol tolerance and frequency of alcohol intoxication in adolescence. ICD-10-coded overdose diagnoses were obtained from nationwide registers. Use of illicit drugs or misuse of medication, Youth Self Report total score, family structure and mother's education in adolescence were used as covariates. Results In multivariate analyses, early age of first alcohol intoxication [hazard ratios (HR) 4.5, 95% confidence intervals (CI) 2.2-9.2, P < 0.001], high alcohol tolerance (HR 3.1, 95% CI 1.6-6.0, P = 0.001) and frequent alcohol intoxication (HR 1.9, 95% CI 1.0-3.4, P = 0.035) all associated with the risk of overdoses. Early age of first intoxication (HR 5.2, 95% CI 1.9-14.7, P = 0.002) and high alcohol tolerance (HR 4.4, 95% CI 1.7-11.5, P = 0.002) also associated with intentional overdoses. Conclusions Alcohol use in adolescence associated prospectively with increased risk of overdose in later life. Early age of first intoxication, high alcohol tolerance and frequent alcohol intoxication are all predictors of overdoses.Peer reviewe

    Transport dynamics in a complex coastal archipelago

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    The Archipelago Sea (in the Baltic Sea) is characterised by thousands of islands of various sizes and steep gradients of the bottom topography. Together with the much deeper Åland Sea, the Archipelago Sea acts as a pathway to the water exchange between the neighbouring basins, Baltic proper and Bothnian Sea. We studied circulation and water transports in the Archipelago Sea using a new configuration of the NEMO 3D hydrodynamic model that covers the Åland Sea–Archipelago Sea region with a horizontal resolution of around 500 m. The results show that currents are steered by the geometry of the islands and straits and the bottom topography. Currents are highest and strongly aligned in the narrow channels in the northern part of the area, with the directions alternating between south and north. In more open areas, the currents are weaker with wider directional distribution. During our study period of 2013–2017, southward currents were more frequent in the surface layer. In the bottom layer, in areas deeper than 25 m, northward currents dominated in the southern part of the Archipelago Sea, while in the northern part southward and northward currents were more evenly represented. Due to the variation in current directions, both northward and southward transports occur. During our study period, the net transport in the upper 20 m layer was southward. Below 20 m depth, the net transport was southward at the northern edge and northward at the southern edge of the Archipelago Sea. There were seasonal and inter-annual variations in the transport volumes and directions in the upper layer. Southward transport was usually largest in spring and summer months, and northward transport was largest in autumn and winter months. The transport dynamics in the Archipelago Sea show different variabilities in the north and south. A single transect cannot describe water transport through the whole area in all cases. Further studies on the water exchange processes between the Baltic proper and the Bothnian Sea through the Archipelago Sea would benefit from using a two-way nested model set-up for the region.</p

    A population-based follow-up study shows high psychosis risk in women with PCOS

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    Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting up to 18% of women. Besides metabolic and fertility aspects, attention has lately been directed towards the detrimental effect of PCOS on psychological health. The objective of the study was to investigate whether women with PCOS are at higher risk for psychotic disorders. The study population derives from the Northern Finland Birth Cohort 1966 (N = 5889 women). The women with PCOS were identified by two simple questions on oligo-amenorrhea and hirsutism at age 31. Women reporting both symptoms were considered PCOS (N = 124) and asymptomatic women as controls (N = 2145). The diagnosis of psychosis was traced using multiple national registers up to the year 2016. Symptoms of psychopathology were identified using validated questionnaires at age 31. Women with PCOS showed an increased risk for any psychosis by age 50 (HR [95% CI] 2.99, [1.52-5.82]). Also, the risk for psychosis after age 31 was increased (HR 2.68 [1.21-5.92]). The results did not change after adjusting for parental history of psychosis, nor were they explained by body mass index or hyperandrogenism at adulthood. The scales of psychopathology differed between women with PCOS and non-PCOS controls showing more psychopathologies among the affected women. PCOS cases were found to be at a three-fold risk for psychosis, and they had increased psychopathological symptoms. PCOS should be taken into consideration when treating women in psychiatric care. More studies are required to further assess the relationship between PCOS and psychotic diseases.Peer reviewe

    Interaction between parental psychosis and early motor development and the risk of schizophrenia in a general population birth cohort.

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    BACKGROUND: Delayed motor development in infancy and family history of psychosis are both associated with increased risk of schizophrenia, but their interaction is largely unstudied. AIM: To investigate the association of the age of achieving motor milestones and parental psychosis and their interaction in respect to risk of schizophrenia. METHODS: We used data from the general population-based prospective Northern Finland Birth Cohort 1966 (n=10,283). Developmental information of the cohort members was gathered during regular visits to Finnish child welfare clinics. Several registers were used to determine the diagnosis of schizophrenia among the cohort members and psychosis among the parents. Altogether 152 (1.5%) individuals had schizophrenia by the age of 46 years, with 23 (15.1%) of them having a parent with psychosis. Cox regression analysis was used in analyses. RESULTS: Parental psychosis was associated (P<0.05) with later achievement of holding the head up, grabbing an object, and walking without support. In the parental psychosis group, the risk for schizophrenia was increased if holding the head up (hazard ratio [HR]: 2.46; degrees of freedom [df]=1; 95% confidence interval [95% CI]: 1.07-5.66) and touching the thumb with the index finger (HR: 1.84; df=1; 95% CI: 1.11-3.06) was later. In the group without parental psychosis, a delay in the following milestones increased the risk of schizophrenia: standing without support and walking without support. Parental psychosis had an interaction with delayed touching thumb with index finger (HR: 1.87; df=1; 95% CI: 1.08-3.25) when risk of schizophrenia was investigated. CONCLUSIONS: Parental psychosis was associated with achieving motor milestones later in infancy, particularly the milestones that appear early in a child's life. Parental psychosis and touching the thumb with the index finger had a significant interaction on risk of schizophrenia. Genetic risk for psychosis may interact with delayed development to raise future risk of schizophrenia, or delayed development may be a marker of other risk processes that interact with genetic liability to cause later schizophrenia.This study was supported by grants from the Brain and Behavior Research Foundation, Northern Finland Health Care Support Foundation, Sigrid Jusélius Foundation, and the Signe and Ane Gyllenberg Foundation, Finland. NFBC 1966 received financial support from the Academy of Finland (104781, 120315, 129269, 1114194, 24300796, 268336, 278286), Center of Excellence in Complex Disease Genetics and SALVE, Oulu University Hospital, Oulu, Finland, Biocenter of Oulu, Finland, University of Oulu, Finland (75617, 24002054, 2400692), Ministry of Social Affairs and Health (50459, 50691, 50842, 2749, 2465), NHLBI grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01), NIH/NIMH (5R01MH63706:02), ENGAGE project and grant agreement HEALTH-F4-2007-(201413), EU FP7 EurHEALTHAgeing (277849), EU FP7 EurHealth Epi-Migrant (279143), European Regional Development Fund 537/2010 (24300936) and the Medical Research Council, UK (G0500539, G0600705, G1002319, PrevMetSyn/SALVE).This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.eurpsy.2015.04.00

    Longitudinal regional brain volume loss in schizophrenia: Relationship to antipsychotic medication and change in social function.

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    BACKGROUND: Progressive brain volume loss in schizophrenia has been reported in previous studies but its cause and regional distribution remains unclear. We investigated progressive regional brain reductions in schizophrenia and correlations with potential mediators. METHOD: Participants were drawn from the Northern Finland Birth Cohort 1966. A total of 33 schizophrenia individuals and 71 controls were MRI scanned at baseline (mean age=34.7, SD=0.77) and at follow-up (mean age=43.4, SD=0.44). Regional brain change differences and associations with clinical mediators were examined using FSL voxelwise SIENA. RESULTS: Schizophrenia cases exhibited greater progressive brain reductions than controls, mainly in the frontal and temporal lobes. The degree of periventricular brain volume reductions were predicted by antipsychotic medication exposure at the fourth ventricular edge and by the number of days in hospital between the scans (a proxy measure of relapse duration) at the thalamic ventricular border. Decline in social and occupational functioning was associated with right supramarginal gyrus reduction. CONCLUSION: Our findings are consistent with the possibility that antipsychotic medication exposure and time spent in relapse partially explain progressive brain reductions in schizophrenia. However, residual confounding could also account for the findings and caution must be applied before drawing causal inferences from associations demonstrated in observational studies of modest size. Less progressive brain volume loss in schizophrenia may indicate better preserved social and occupational functions.Academy of Finland, Medical Research Council, Sigrid Jusélius Foundation and the Signe and Ane Gyllenberg Foundation, Finland, Stanley Foundation, Brain & Behavior Research Foundation. The work was partially completed within the University of Cambridge Behavioural and Clinical Neuroscience Institute, supported by a joint award from the Medical Research Council and Wellcome Trust.This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.schres.2015.06.01

    Serum C-reactive protein in adolescence and risk of schizophrenia in adulthood: A prospective birth cohort study.

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    OBJECTIVE: Meta-analyses of cross-sectional studies confirm an increase in circulating inflammatory markers during acute psychosis. Longitudinal studies are scarce but are needed to understand whether elevated inflammatory markers are a cause or consequence of illness. We report a longitudinal study of serum C-reactive protein (CRP) in adolescence and subsequent risk of schizophrenia and related psychoses in adulthood in the Northern Finland Birth Cohort 1986. METHOD: Serum high-sensitivity CRP was measured at age 15/16 years in 6362 participants. ICD-10 diagnoses of schizophrenia and related psychoses were obtained from centralised hospital inpatient and outpatient registers up to age 27 years. Logistic regression calculated odds ratios (ORs) for psychotic outcomes associated with baseline CRP levels analysed as both continuous and categorical variables using American Heart Association criteria. Age, sex, body mass index, maternal education, smoking, and alcohol use were included as potential confounders. RESULTS: By age 27years, 88 cases of non-affective psychosis (1.38%), of which 22 were schizophrenia (0.35%), were identified. Adolescent CRP was associated with subsequent schizophrenia. The adjusted OR for schizophrenia by age 27yearsfor each standard deviation (SD) increase in CRP levels at age 15/16yearswas 1.25 (95% CI, 1.07-1.46), which was consistent with a linear, dose-response relationship (P-value for quadratic term 0.23). Using CRP as a categorical variable, those with high (>3mg/L) compared with low (<1mg/L) CRP levels at baseline were more likely to develop schizophrenia; adjusted OR 4.25 (95% CI, 1.30-13.93). There was some indication that higher CRP was associated with earlier onset of schizophrenia (rs=-0.40; P=0.07). CONCLUSIONS: A longitudinal association between adolescent CRP levels and adult schizophrenia diagnosis indicates a potentially important role of inflammation in the pathogenesis of the illness, although the findings, based on a small number of cases, need to be interpreted with caution and require replication in other samples.Dr. Khandaker is supported by an Intermediate Clinical Fellowship from the Wellcome Trust (201486/Z/16/Z) and a Clinical Lecturer Starter Grant from the Academy of Medical Sciences, UK (grant no. 80354). Prof. Jones acknowledges grant support from the Wellcome Trust (095844/Z/11/Z & 088869/Z/09/Z) and NIHR (RP-PG-0606-1335). Prof. Veijola was supported by the Academy of Finland (grants no. 124257, 212828, 214273). Prof. Mäki has been supported by the Signe and Ane Gyllenberg Foundation, Finland. Prof. Miettunen was supported by the Academy of Finland (grant no. 268336). Dr. Stochl was funded by the Medical Research Council (MR/K006665/1) and the NIHR Collaboration for Leadership in Applied Health Research & Care (CLAHRC) East of England.This is the final version of the article from Elsevier via https://doi.org/10.1016/j.bbi.2016.09.00

    Lifetime antipsychotic medication and cognitive performance in schizophrenia at age 43 years in a general population birth cohort

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    This naturalistic study analysed the association between cumulative lifetime antipsychotic dose and cognition in schizophrenia after an average of 16.5 years of illness. Sixty participants with schizophrenia and 191 controls from the Northern Finland Birth Cohort 1966 were assessed at age 43 years with a neurocognitive test battery. Cumulative lifetime antipsychotic dose-years were collected from medical records and interviews. The association between antipsychotic dose-years and a cognitive composite score based on principal component analysis was analysed using linear regression. Higher lifetime antipsychotic dose-years were significantly associated with poorer cognitive composite score, when adjusted for gender, onset age and lifetime hospital treatment days. The effects of typical and atypical antipsychotics did not differ. This is the first report of an association between cumulative lifetime antipsychotic dose and global cognition in midlife schizophrenia. Based on these data, higher lifetime antipsychotic dose-years may be associated with poorer cognitive performance at age 43 years. Potential biases related to the naturalistic design may partly explain the results; nonetheless, it is possible that large antipsychotic doses harm cognition in schizophrenia in the long-term.Peer reviewe
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