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Markku Koskenvuo - One of the best experts on this subject based on the ideXlab platform.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort a population based modeling study
    Archives of General Psychiatry, 1998
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Background The magnitude of heritability of Schizophrenia remains controversial, due in part to limitations of estimates derived from index twin pairs exclusively. We applied structural equation modeling in a total population of twins to determine the significance and magnitudes of the genetic and environmental contributions to Schizophrenia. Methods All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort
    Schizophrenia Research, 1997
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Methods: All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results: The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions: In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria. Arch Gen Psychiatry. 1998;55:67-74

John J Mcgrath - One of the best experts on this subject based on the ideXlab platform.

  • neonatal vitamin d status and risk of Schizophrenia a population based case control study
    Archives of General Psychiatry, 2010
    Co-Authors: John J Mcgrath, Darryl W Eyles, Carsten Bocker Pedersen, Cameron Anderson, Thomas H J Burne, Bent Norgaardpedersen, David M Hougaard, Preben Bo Mortensen
    Abstract:

    Context Clues from the Epidemiology of Schizophrenia suggest that low levels of developmental vitamin D may be associated with increased risk of Schizophrenia. Objective To directly examine the association between neonatal vitamin D status and risk of Schizophrenia. Design Individually matched case-control study drawn from a population-based cohort. Setting Danish national health registers and neonatal biobank. Participants A total of 424 individuals with Schizophrenia and 424 controls matched for sex and date of birth. Main Outcome Measures The concentration of 25 hydroxyvitamin D 3 (25[OH]D3) was assessed from neonatal dried blood samples using a highly sensitive liquid chromatography tandem mass spectroscopy method. Relative risks were calculated for the matched pairs when examined for quintiles of 25(OH)D3. Results Compared with neonates in the fourth quintile (with 25[OH]D3 concentrations between 40.5 and 50.9 nmol/L), those in each of the lower 3 quintiles had a significantly increased risk of Schizophrenia (2-fold elevated risk). Unexpectedly, those in the highest quintile also had a significantly increased risk of Schizophrenia. Based on this analysis, the population-attributable fraction associated with neonatal vitamin D status was 44%. The relationship was not explained by a wide range of potential confounding or interacting variables. Conclusions Both low and high concentrations of neonatal vitamin D are associated with increased risk of Schizophrenia, and it is feasible that this exposure could contribute to a sizeable proportion of cases in Denmark. In light of the substantial public health implications of this finding, there is an urgent need to further explore the effect of vitamin D status on brain development and later mental health.

  • new directions in the Epidemiology of Schizophrenia
    The Medical Journal of Australia, 2009
    Co-Authors: John J Mcgrath, Ezra Susser
    Abstract:

    New primary data and systematic reviews have prompted the review of some long-held views about the Epidemiology of Schizophrenia.

  • Schizophrenia a concise overview of incidence prevalence and mortality
    Epidemiologic Reviews, 2008
    Co-Authors: John J Mcgrath, Sukanta Saha, David Chant, Joy Welham
    Abstract:

    Recent systematic reviews have encouraged the psychiatric research community to reevaluate the contours of Schizophrenia Epidemiology. This paper provides a concise overview of three related systematic reviews on the incidence, prevalence, and mortality associated with Schizophrenia. The reviews shared key methodological features regarding search strategies, analysis of the distribution of the frequency estimates, and exploration of the influence of key variables (sex, migrant status, urbanicity, secular trend, economic status, and latitude). Contrary to previous interpretations, the incidence of Schizophrenia shows prominent variation between sites. The median incidence of Schizophrenia was 15.2/100,000 persons, and the central 80% of estimates varied over a fivefold range (7.7-43.0/100,000). The rate ratio for males:females was 1.4:1. Prevalence estimates also show prominent variation. The median lifetime morbid risk for Schizophrenia was 7.2/1,000 persons. On the basis of the standardized mortality ratio, people with Schizophrenia have a two- to threefold increased risk of dying (median standardized mortality ratio = 2.6 for all-cause mortality), and this differential gap in mortality has increased over recent decades. Compared with native-born individuals, migrants have an increased incidence and prevalence of Schizophrenia. Exposures related to urbanicity, economic status, and latitude are also associated with various frequency measures. In conclusion, the Epidemiology of Schizophrenia is characterized by prominent variability and gradients that can help guide future research.

  • myths and plain truths about Schizophrenia Epidemiology the nape lecture 2004
    Acta Psychiatrica Scandinavica, 2005
    Co-Authors: John J Mcgrath
    Abstract:

    Objective: Science needs to constantly match research models against the data. With respect to the Epidemiology of Schizophrenia, the widely held belief that the incidence of Schizophrenia shows little variation may no longer be supported by the data. The aims of this paper are (i) to explore data-vs.-belief mismatch with respect to the incidence of Schizophrenia, and (ii) to speculate on the causes and consequences of such discrepancies. Method: Based on a recently published systematic review of the incidence of Schizophrenia, the distribution of incidence rates around the world was examined. In order to examine if the incidence of Schizophrenia differed by sex, male vs. female risk ratios were generated. Results: The distribution of incidence rates for Schizophrenia is asymmetrical with many high rates skewing the distribution. Based on the central 80% of rates, the incidence of Schizophrenia varies in a five-fold range (between 7.7 and 43.0 per 100 000). Males have a significantly higher incidence of Schizophrenia compared with females (median male to female risk ratio = 1.4), and this difference could not be accounted for by diagnostic criteria or age range. Conclusion: The beliefs that (i) the incidence of Schizophrenia does not vary between sites and (ii) males and females are equally affected, may have persisted because of an unspoken deeper belief that Schizophrenia is an egalitarian and exceptional disorder. Our ability to generate productive hypotheses about the aetiology of Schizophrenia rests on an accurate appraisal of the data. Beliefs not supported by data should be identified and relabelled as myths.

  • the Epidemiology of Schizophrenia
    2003
    Co-Authors: John J Mcgrath
    Abstract:

    Schizophrenia is a group of disabling neuropsychiatric conditions that contributes substantially to the global burden of disease. While much has been discovered about Schizophrenia over the last 100 years, there are still many gaps in our knowledge base. In particular, epidemiological research has provided a range of clues to guide the generation of candidate nongenetic risk factors that may be in the causal pathway to Schizophrenia. In this thesis, various types of epidemiological studies are presented in order to advance our understanding of the nature and causes of Schizophrenia. The first part of the thesis includes two descriptive studies. In collaboration with senior colleagues from three other Australian sites, the author was involved in the first major study of the prevalence of Schizophrenia in Australia. The one-month prevalence for psychotic disorders in this study was 4 to 7 per 1000 with a weighted mean of 4.7 per 1000. The second descriptive study, which was based on community and inpatient samples, examined the fertility and fecundity of individuals with psychosis compared to their unaffected, same sex siblings. In keeping with many other studies, we found a marked reduction in the number of offspring in men with Schizophrenia, but no significant reduction in the women with Schizophrenia. The next section of the thesis explores selected nongenetic risk factors for Schizophrenia. After a general review of the literature, a season of birth study based on Queensland data is presented. By way of follow up, a systematic review and meta-analysis of season of birth studies from the southern hemisphere is also presented. While the Queensland study found a significant excess of Schizophrenia births in the third quarter of the year (winter/spring), the results of the meta-analysis did not identify a significant winter/spring excess. Apart from Schizophrenia birth rates, the month of first admission for Schizophrenia was also found to have marked seasonal variation, with a peak for first admissions in winter. A review of the literature on climate and Schizophrenia is presented, followed by a study examining perinatal sunshine duration and Schizophrenia birth rates. This study, based on Queensland and Dutch data, found an excess of male Schizophrenia births in periods with reduced sunshine. In addition, earlier age of onset was associated with reduced perinatal sunshine. Based on these studies, a novel candidate risk-modifying factor for Schizophrenia is presented - low prenatal vitamin D. The next section of the thesis presents two ecological studies examining viral epidemics and Schizophrenia birth rates (prenatal influenza, prenatal poliovirus). While the Queensland Influenza study was broadly supportive of an association with Schizophrenia, there was no association found for poliomyelitis. Two studies on minor physical anomalies in Schizophrenia are presented. The first paper reports the prevalence of minor physical anomalies in a sample from the United Kingdom and explores correlations between these anomalies and putative risk factors for Schizophrenia. Based on a large case-control study, we found that the psychosis group had (a) significantly more minor physical anomalies and (b) several quantitative differences related to measures of the head and face (patients with psychosis had a wider skull base and shorter lower facial heights). We speculate that these features may relate to the growth of the temporal lobes within the middle cranial fossa during early life. Based on the same case-control study, we examined two major risk indicators associated with Schizophrenia - migrant status and urban birth. We found a reduced odds of psychosis in those born overseas compared to Australian born, but no difference in the odds of psychosis in second generation migrants compared to second generation Australian born. Nor did we find an association between urban birth and psychosis. Differences between Australian studies and European/Scandinavian studies invite speculation on differentiating factors underlying the discrepancies. The final section of the thesis speculates about the primary prevention of Schizophrenia. In particular, a strategic plan is outlined linking candidate risk factors generated from Epidemiology with various tools from neuroscience in order to explore the biological plausibility of the candidate. Those interested in preventing Schizophrenia face an enormous challenge. We need to generate new candidate exposures and then test and reject them in as efficient a time frame as possible. Because of the substantial burden of unavertable disability associated with Schizophrenia, we need to maintain a sense of urgency about this task.

Tyrone D. Cannon - One of the best experts on this subject based on the ideXlab platform.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort a population based modeling study
    Archives of General Psychiatry, 1998
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Background The magnitude of heritability of Schizophrenia remains controversial, due in part to limitations of estimates derived from index twin pairs exclusively. We applied structural equation modeling in a total population of twins to determine the significance and magnitudes of the genetic and environmental contributions to Schizophrenia. Methods All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort
    Schizophrenia Research, 1997
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Methods: All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results: The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions: In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria. Arch Gen Psychiatry. 1998;55:67-74

Jouko Lonnqvist - One of the best experts on this subject based on the ideXlab platform.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort a population based modeling study
    Archives of General Psychiatry, 1998
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Background The magnitude of heritability of Schizophrenia remains controversial, due in part to limitations of estimates derived from index twin pairs exclusively. We applied structural equation modeling in a total population of twins to determine the significance and magnitudes of the genetic and environmental contributions to Schizophrenia. Methods All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort
    Schizophrenia Research, 1997
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Methods: All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results: The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions: In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria. Arch Gen Psychiatry. 1998;55:67-74

Matti O Huttunen - One of the best experts on this subject based on the ideXlab platform.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort a population based modeling study
    Archives of General Psychiatry, 1998
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Background The magnitude of heritability of Schizophrenia remains controversial, due in part to limitations of estimates derived from index twin pairs exclusively. We applied structural equation modeling in a total population of twins to determine the significance and magnitudes of the genetic and environmental contributions to Schizophrenia. Methods All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria.

  • the genetic Epidemiology of Schizophrenia in a finnish twin cohort
    Schizophrenia Research, 1997
    Co-Authors: Tyrone D. Cannon, Jaakko Kaprio, Jouko Lonnqvist, Matti O Huttunen, Markku Koskenvuo
    Abstract:

    Methods: All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results: The lifetime prevalence of Schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between Schizophrenia and no diagnosis was rejected. Conclusions: In a population-based twin study of Schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria. Arch Gen Psychiatry. 1998;55:67-74