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1.
PLoS Genet ; 15(7): e1008245, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31306407

RESUMO

Major depression is a common and severe psychiatric disorder with a highly polygenic genetic architecture. Genome-wide association studies have successfully identified multiple independent genetic loci that harbour variants associated with major depression, but the exact causal genes and biological mechanisms are largely unknown. Tissue-specific network approaches may identify molecular mechanisms underlying major depression and provide a biological substrate for integrative analyses. We provide a framework for the identification of individual risk genes and gene co-expression networks using genome-wide association summary statistics and gene expression information across multiple human brain tissues and whole blood. We developed a novel gene-based method called eMAGMA that leverages tissue-specific eQTL information to identify 99 biologically plausible risk genes associated with major depression, of which 58 are novel. Among these novel associations is Complement Factor 4A (C4A), recently implicated in schizophrenia through its role in synaptic pruning during postnatal development. Major depression risk genes were enriched in gene co-expression modules in multiple brain tissues and the implicated gene modules contained genes involved in synaptic signalling, neuronal development, and cell transport pathways. Modules enriched with major depression signals were strongly preserved across brain tissues, but were weakly preserved in whole blood, highlighting the importance of using disease-relevant tissues in genetic studies of psychiatric traits. We identified tissue-specific genes and gene co-expression networks associated with major depression. Our novel analytical framework can be used to gain fundamental insights into the functioning of the nervous system in major depression and other brain-related traits.

2.
Nat Neurosci ; 22(7): 1196, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31168101

RESUMO

Several occurrences of the word 'schizophrenia' have been re-worded as 'liability to schizophrenia' or 'schizophrenia risk', including in the title, which should have been "GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal effect of schizophrenia liability," as well as in Supplementary Figures 1-10 and Supplementary Tables 7-10, to more accurately reflect the findings of the work.

3.
Nat Genet ; 51(6): 933-940, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31086352

RESUMO

The genetic architecture of psychiatric disorders is characterized by a large number of small-effect variants1 located primarily in non-coding regions, suggesting that the underlying causal effects may influence disease risk by modulating gene expression2-4. We provide comprehensive analyses using transcriptome data from an unprecedented collection of tissues to gain pathophysiological insights into the role of the brain, neuroendocrine factors (adrenal gland) and gastrointestinal systems (colon) in psychiatric disorders. In each tissue, we perform PrediXcan analysis and identify trait-associated genes for schizophrenia (n associations = 499; n unique genes = 275), bipolar disorder (n associations = 17; n unique genes = 13), attention deficit hyperactivity disorder (n associations = 19; n unique genes = 12) and broad depression (n associations = 41; n unique genes = 31). Importantly, both PrediXcan and summary-data-based Mendelian randomization/heterogeneity in dependent instruments analyses suggest potentially causal genes in non-brain tissues, showing the utility of these tissues for mapping psychiatric disease genetic predisposition. Our analyses further highlight the importance of joint tissue approaches as 76% of the genes were detected only in difficult-to-acquire tissues.


Assuntos
Perfilação da Expressão Gênica , Estudos de Associação Genética , Predisposição Genética para Doença , Transtornos Mentais/genética , Transtornos Mentais/psicologia , Transcriptoma , Algoritmos , Biologia Computacional/métodos , Regulação da Expressão Gênica , Redes Reguladoras de Genes , Estudos de Associação Genética/métodos , Estudo de Associação Genômica Ampla , Humanos , Transtornos Mentais/diagnóstico , Especificidade de Órgãos , Polimorfismo de Nucleotídeo Único , Locos de Características Quantitativas , Característica Quantitativa Herdável
5.
Psychol Med ; 49(7): 1218-1226, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30929657

RESUMO

BACKGROUND: Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC. METHODS: Linkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals). RESULTS: Positive genetic correlation was observed between MD and AD (rgMD-AD = + 0.47, P = 6.6 × 10-10). AC-quantity showed positive genetic correlation with both AD (rgAD-AC quantity = + 0.75, P = 1.8 × 10-14) and MD (rgMD-AC quantity = + 0.14, P = 2.9 × 10-7), while there was negative correlation of AC-frequency with MD (rgMD-AC frequency = -0.17, P = 1.5 × 10-10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10-6). There was no evidence for reverse causation. CONCLUSION: This study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.

6.
Psychol Med ; : 1-15, 2019 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-30874500

RESUMO

BACKGROUND: Frequency and quantity of alcohol consumption are metrics commonly used to measure alcohol consumption behaviors. Epidemiological studies indicate that these alcohol consumption measures are differentially associated with (mental) health outcomes and socioeconomic status (SES). The current study aims to elucidate to what extent genetic risk factors are shared between frequency and quantity of alcohol consumption, and how these alcohol consumption measures are genetically associated with four broad phenotypic categories: (i) SES; (ii) substance use disorders; (iii) other psychiatric disorders; and (iv) psychological/personality traits. METHODS: Genome-Wide Association analyses were conducted to test genetic associations with alcohol consumption frequency (N = 438 308) and alcohol consumption quantity (N = 307 098 regular alcohol drinkers) within UK Biobank. For the other phenotypes, we used genome-wide association studies summary statistics. Genetic correlations (rg) between the alcohol measures and other phenotypes were estimated using LD score regression. RESULTS: We found a substantial genetic correlation between the frequency and quantity of alcohol consumption (rg = 0.52). Nevertheless, both measures consistently showed opposite genetic correlations with SES traits, and many substance use, psychiatric, and psychological/personality traits. High alcohol consumption frequency was genetically associated with high SES and low risk of substance use disorders and other psychiatric disorders, whereas the opposite applies for high alcohol consumption quantity. CONCLUSIONS: Although the frequency and quantity of alcohol consumption show substantial genetic overlap, they consistently show opposite patterns of genetic associations with SES-related phenotypes. Future studies should carefully consider the potential influence of SES on the shared genetic etiology between alcohol and adverse (mental) health outcomes.

7.
Transl Psychiatry ; 9(1): 117, 2019 03 15.
Artigo em Inglês | MEDLINE | ID: mdl-30877270

RESUMO

The major depressive disorder (MDD) working group of the Psychiatric Genomics Consortium (PGC) has published a genome-wide association study (GWAS) for MDD in 130,664 cases, identifying 44 risk variants. We used these results to investigate potential drug targets and repurposing opportunities. We built easily interpretable bipartite drug-target networks integrating interactions between drugs and their targets, genome-wide association statistics, and genetically predicted expression levels in different tissues, using the online tool Drug Targetor ( drugtargetor.com ). We also investigated drug-target relationships that could be impacting MDD. MAGMA was used to perform pathway analyses and S-PrediXcan to investigate the directionality of tissue-specific expression levels in patients vs. controls. Outside the major histocompatibility complex (MHC) region, 153 protein-coding genes are significantly associated with MDD in MAGMA after multiple testing correction; among these, five are predicted to be down or upregulated in brain regions and 24 are known druggable genes. Several drug classes were significantly enriched, including monoamine reuptake inhibitors, sex hormones, antipsychotics, and antihistamines, indicating an effect on MDD and potential repurposing opportunities. These findings not only require validation in model systems and clinical examination, but also show that GWAS may become a rich source of new therapeutic hypotheses for MDD and other psychiatric disorders that need new-and better-treatment options.

8.
Artigo em Inglês | MEDLINE | ID: mdl-30456828

RESUMO

Obsessive-compulsive disorder (OCD) is a highly heritable complex phenotype that demonstrates sex differences in age of onset and clinical presentation, suggesting a possible sex difference in underlying genetic architecture. We present the first genome-wide characterization of the sex-specific genetic architecture of OCD, utilizing the largest set of OCD cases and controls available from the Psychiatric Genomics Consortium. We assessed evidence for several mechanisms that may contribute to sex differences including a sex-dependent liability threshold, the presence of individual sex-specific risk variants on the autosomes and the X chromosome, and sex-specific pleiotropic effects. Furthermore, we tested the hypothesis that genetic heterogeneity between the sexes may obscure associations in a sex-combined genome-wide association study. We observed a strong genetic correlation between male and female OCD and no evidence for a sex-dependent liability threshold model, suggesting that sex-combined analysis does not suffer from widespread loss of power because of genetic heterogeneity between the sexes. While we did not detect any significant sex-specific genome-wide single nucleotide polymorphisms (SNP) associations, we did identify two significant gene-based associations in females: GRID2 and GRP135, which showed no association in males. We observed that the SNPs with sexually differentiated effects showed an enrichment of regulatory variants influencing expression of genes in brain and immune tissues. These findings suggest that future studies with larger sample sizes hold great promise for the identification of sex-specific genetic risk factors for OCD.

9.
Drug Alcohol Depend ; 194: 197-204, 2018 Nov 06.
Artigo em Inglês | MEDLINE | ID: mdl-30447512

RESUMO

BACKGROUND: The prevalence of smoking varies across ethnic groups in developed countries, but little is known about ethnic variations in specific aspects of nicotine dependence (ND). We conducted item-response analyses in current smokers to compare ND factors across five ethnic groups. METHODS: Data were obtained from a population-based, multi-ethnic cohort study conducted in the Netherlands. The Fagerström Test for Nicotine Dependence (FTND) was assessed in 1147 Dutch, 991 South-Asian Surinamese, 1408 African Surinamese, 1396 Turkish, and 584 Moroccan smokers (N = 5526). We tested whether the factorial structure of the FTND was invariant across ethnic groups using a multi-group confirmatory factor analysis. FTND item and total scores and factor means were compared across groups. RESULTS: The two-factor model representing "morning smoking" and "smoking patterns" provided an adequate fit. The items "Cigarettes smoked daily" and "Time until first cigarette" showed differential item functioning (DIF) as a function of ethnicity. Three out of four ethnic minority groups scored significantly higher on both factors compared to the Dutch origin group (all p < 0.001) before and after taking DIF into account, while the African Surinamese scored higher only on "morning smoking" when DIF was accounted for. DISCUSSION: The factor structure of the FTND is not measurement invariant across ethnic groups in this population-based sample. Accounting for DIF affecting the nicotine dependence factor scores, although South-Asian Surinamese, Turkish, and Moroccan groups showed higher levels of dependence than the Dutch origin group, genetic as well as environmental factors may account for the observed differences.

10.
PLoS One ; 13(9): e0203483, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30212480

RESUMO

AIM: To investigate whether items of the SF-12, widely used to assess health outcome in clinical practice and public health research, provide unbiased measurements of underlying constructs in different demographic groups regarding gender, age, educational level and ethnicity. METHODS: We included 23,146 men and women aged 18-70 of Dutch, South-Asian Surinamese, African Surinamese, Ghanaian, Turkish, or Moroccan origin from the HELIUS study. Both multiple group confirmatory factor analyses (MGCFA), with increasingly stringent model constraints (i.e. assessing Configural, Metric, Strong and Strict measurement invariance (MI)), and regression analysis were conducted to establish comparability of SF-12 items across demographic groups. RESULTS: MI regarding gender, age and education was tested in the ethnic Dutch group (N = 4,615). In each subsequent step of testing MI, change in goodness-of-fit measures did not exceed 0.010 (RMSEA) or 0.004 (CFI). Moreover, goodness-of-fit indices showed good fit for strict invariance models: RMSEA<0.055; CFI>0.97. Regarding ethnicity, RMSEA values of metric and subsequent models fell above 0.055, indicating violation of measurement invariance in factor loadings, thresholds and residual variances. Regression analysis revealed possible age-, education- and ethnicity-related DIF. Adjustment for this DIF had little impact on the magnitude of age and educational differences in physical and mental health, but ethnic inequalities in physical health-and to a lesser extent mental health-were reduced after DIF adjustment. CONCLUSIONS: We found no evidence of violation of measurement invariance of the SF-12 regarding gender, age and educational level. If minor DIF would remain undetected in our MGCFA analyses, we showed that this would have negligible effect on the magnitude of demographic health inequalities. Regarding ethnicity, the SF-12 was not measurement invariant. After accounting for DIF, we observed a reduction of ethnic inequalities in health, in particular in physical health. Caution is warranted when comparing SF-12 scores across population groups with various ethnic backgrounds.

11.
Nat Neurosci ; 21(9): 1161-1170, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30150663

RESUMO

Cannabis use is a heritable trait that has been associated with adverse mental health outcomes. In the largest genome-wide association study (GWAS) for lifetime cannabis use to date (N = 184,765), we identified eight genome-wide significant independent single nucleotide polymorphisms in six regions. All measured genetic variants combined explained 11% of the variance. Gene-based tests revealed 35 significant genes in 16 regions, and S-PrediXcan analyses showed that 21 genes had different expression levels for cannabis users versus nonusers. The strongest finding across the different analyses was CADM2, which has been associated with substance use and risk-taking. Significant genetic correlations were found with 14 of 25 tested substance use and mental health-related traits, including smoking, alcohol use, schizophrenia and risk-taking. Mendelian randomization analysis showed evidence for a causal positive influence of schizophrenia risk on cannabis use. Overall, our study provides new insights into the etiology of cannabis use and its relation with mental health.

12.
Nat Genet ; 50(7): 956-967, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29955180

RESUMO

We apply integrative approaches to expression quantitative loci (eQTLs) from 44 tissues from the Genotype-Tissue Expression project and genome-wide association study data. About 60% of known trait-associated loci are in linkage disequilibrium with a cis-eQTL, over half of which were not found in previous large-scale whole blood studies. Applying polygenic analyses to metabolic, cardiovascular, anthropometric, autoimmune, and neurodegenerative traits, we find that eQTLs are significantly enriched for trait associations in relevant pathogenic tissues and explain a substantial proportion of the heritability (40-80%). For most traits, tissue-shared eQTLs underlie a greater proportion of trait associations, although tissue-specific eQTLs have a greater contribution to some traits, such as blood pressure. By integrating information from biological pathways with eQTL target genes and applying a gene-based approach, we validate previously implicated causal genes and pathways, and propose new variant and gene associations for several complex traits, which we replicate in the UK BioBank and BioVU.

13.
Drug Alcohol Depend ; 188: 94-101, 2018 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-29758381

RESUMO

BACKGROUND: Alcohol and tobacco use are heritable phenotypes. However, only a small number of common genetic variants have been identified, and common variants account for a modest proportion of the heritability. Therefore, this study aims to investigate the role of low-frequency and rare variants in alcohol and tobacco use. METHODS: We meta-analyzed ExomeChip association results from eight discovery cohorts and included 12,466 subjects and 7432 smokers in the analysis of alcohol consumption and tobacco use, respectively. The ExomeChip interrogates low-frequency and rare exonic variants, and in addition a small pool of common variants. We investigated top variants in an independent sample in which ICD-9 diagnoses of "alcoholism" (N = 25,508) and "tobacco use disorder" (N = 27,068) had been assessed. In addition to the single variant analysis, we performed gene-based, polygenic risk score (PRS), and pathway analyses. RESULTS: The meta-analysis did not yield exome-wide significant results. When we jointly analyzed our top results with the independent sample, no low-frequency or rare variants reached significance for alcohol consumption or tobacco use. However, two common variants that were present on the ExomeChip, rs16969968 (p = 2.39 × 10-7) and rs8034191 (p = 6.31 × 10-7) located in CHRNA5 and AGPHD1 at 15q25.1, showed evidence for association with tobacco use. DISCUSSION: Low-frequency and rare exonic variants with large effects do not play a major role in alcohol and tobacco use, nor does the aggregate effect of ExomeChip variants. However, our results confirmed the role of the CHRNA5-CHRNA3-CHRNB4 cluster of nicotinic acetylcholine receptor subunit genes in tobacco use.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Éxons/genética , Predisposição Genética para Doença/genética , Variação Genética/genética , Uso de Tabaco/genética , Consumo de Bebidas Alcoólicas/epidemiologia , Alcoolismo/diagnóstico , Alcoolismo/epidemiologia , Alcoolismo/genética , Estudos de Coortes , Feminino , Predisposição Genética para Doença/epidemiologia , Humanos , Masculino , Proteínas do Tecido Nervoso/genética , Polimorfismo de Nucleotídeo Único/genética , Receptores Nicotínicos/genética , Fatores de Risco , Uso de Tabaco/epidemiologia , Tabagismo/diagnóstico , Tabagismo/genética
14.
Soc Psychiatry Psychiatr Epidemiol ; 53(6): 629-638, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29644388

RESUMO

PURPOSE: To examine the association between obesity and depressed mood in a large multi-ethnic population and check for consistency in this association across six ethnic groups. METHODS: Data of 21,030 persons (18-70 years) were sourced from the HELIUS study. Cross-sectional relationships between obesity measures [body mass index (kg/m2) and waist circumference (cm)] and depressed mood (PHQ-9 score ≥ 10) were analysed. Consistency of associations was investigated across ethnic groups by interaction terms (ethnicity*obesity measures) in basic (age, sex, education) and fully (health behaviours and somatic health) adjusted models. RESULTS: Obesity was prevalent in all ethnic groups, but varied substantially. After sociodemographic adjustment, obesity measures were associated with increased odds of depressed mood but this was inconsistent across ethnic groups. Obesity (BMI ≥ 30 or highest waist circumference quartile) was strongly and significantly associated with depressed mood in the Dutch [Odds Ratio (OR) = 1.72; 95% Confidence intervals (CI) 1.24-2.40, and OR = 1.86; 95% CI 1.38-2.50], respectively, and African Surinamese (OR = 1.60; 95% CI 1.29-1.98 and OR = 1.59; 95% CI 1.27-2.00, respectively) but had a weaker, non-significant association in other ethnic groups (South-Asian Surinamese, Ghanaian, Moroccan, Turkish groups). Adjustment for health behaviours and somatic health had limited effect on this pattern. CONCLUSION: Obesity was associated with a higher risk of depressed mood. However, ethnic differences were found: the obesity-depressed mood association was strong in the Dutch and African Surinamese populations, but not in other ethnic groups. Future studies should explore whether differential normative values or pathophysiology across ethnic groups explain why the obesity-depression association is inconsistent across ethnic groups.

15.
Nat Genet ; 50(5): 668-681, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29700475

RESUMO

Major depressive disorder (MDD) is a common illness accompanied by considerable morbidity, mortality, costs, and heightened risk of suicide. We conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype.

16.
Nicotine Tob Res ; 20(6): 766-774, 2018 May 03.
Artigo em Inglês | MEDLINE | ID: mdl-29617888

RESUMO

Introduction: To understand smoking behaviors among ethnic minority groups, studies have largely focused on societal factors, with little attention to family influences. Yet studies among majority groups have identified parental smoking as an important risk factor. It is unknown whether this applies to ethnic minority groups. We investigated the association between parental smoking and adult offspring's smoking behaviors among ethnic minority groups with an immigrant background. Methods: We used data from the Healthy Life in an Urban Setting study from Amsterdam (the Netherlands) from January 2011 to December 2015. The sample consisted of 2184 parent-offspring pairs from South-Asian Surinamese, African Surinamese, Turkish, Moroccan, and Ghanaian origin. We collected self-reported smoking data: current status, duration of exposure to parental smoking, number of daily cigarettes, heavy smoking ( > 10 cigarettes/day), and nicotine dependency (using the Fagerström Test). Analyses were stratified by offspring's age, cohabitation with parent, education (parent/offspring), offspring's cultural orientation, and gender concordance within pairs. Logistic regression was used. Results: Overall, parental smoking was associated with offspring's smoking behaviors (eg, current smoking: odds ratio 2.33; 95% confidence interval 1.79-3.03), with little ethnic variation. We found dose-response associations between exposure to parental smoking and offspring's smoking. The associations were similar across different strata but stronger in gender-concordant pairs (3.16; 2.12-4.51 vs. 1.73; 1.15-2.59 in gender-discordant pairs; p-value for interaction .017). Conclusions: Parental smoking is associated with offspring's smoking behaviors in ethnic minority groups across different strata but particularly in gender-concordant pairs. Similar to majority groups, family influences matter to smoking behaviors in ethnic minority groups. Implications: Our findings have deepened our understanding of smoking behaviors among ethnic minority groups. Future studies should simultaneously consider societal factors and parental influences, to comprehensively understand their impact on smoking among ethnic minority groups. Also, smoking patterns among family members should be addressed in individual counselling, irrespective of ethnicity.

17.
Int J Methods Psychiatr Res ; 27(2): e1608, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29484742

RESUMO

OBJECTIVES: Genome-wide association studies (GWAS) have become increasingly popular to identify associations between single nucleotide polymorphisms (SNPs) and phenotypic traits. The GWAS method is commonly applied within the social sciences. However, statistical analyses will need to be carefully conducted and the use of dedicated genetics software will be required. This tutorial aims to provide a guideline for conducting genetic analyses. METHODS: We discuss and explain key concepts and illustrate how to conduct GWAS using example scripts provided through GitHub (https://github.com/MareesAT/GWA_tutorial/). In addition to the illustration of standard GWAS, we will also show how to apply polygenic risk score (PRS) analysis. PRS does not aim to identify individual SNPs but aggregates information from SNPs across the genome in order to provide individual-level scores of genetic risk. RESULTS: The simulated data and scripts that will be illustrated in the current tutorial provide hands-on practice with genetic analyses. The scripts are based on PLINK, PRSice, and R, which are commonly used, freely available software tools that are accessible for novice users. CONCLUSIONS: By providing theoretical background and hands-on experience, we aim to make GWAS more accessible to researchers without formal training in the field.

18.
Behav Genet ; 48(2): 95-108, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29460079

RESUMO

The American Psychological Association defines gender identity as, "A person's deeply-felt, inherent sense of being a boy, a man, or a male; a girl, a woman, or a female; or an alternative gender (e.g., genderqueer, gender nonconforming, gender neutral) that may or may not correspond to a person's sex assigned at birth or to a person's primary or secondary sex characteristics" (American Psychological Association, Am Psychol 70(9):832-864, 2015). Here we review the evidence that gender identity and related socially defined gender constructs are influenced in part by innate factors including genes. Based on the data reviewed, we hypothesize that gender identity is a multifactorial complex trait with a heritable polygenic component. We argue that increasing the awareness of the biological diversity underlying gender identity development is relevant to all domains of social, medical, and neuroscience research and foundational for reducing health disparities and promoting human-rights protections for gender minorities.


Assuntos
Disforia de Gênero/genética , Identidade de Gênero , Feminino , Humanos , Masculino , Caracteres Sexuais , Comportamento Sexual/psicologia , Pessoas Transgênero/psicologia
19.
BMJ Open ; 7(12): e017873, 2017 Dec 14.
Artigo em Inglês | MEDLINE | ID: mdl-29247091

RESUMO

PURPOSE: Ethnic minority groups usually have a more unfavourable disease risk profile than the host population. In Europe, ethnic inequalities in health have been observed in relatively small studies, with limited possibilities to explore underlying causes. The aim of the Healthy Life in an Urban Setting (HELIUS) study is to investigate the causes of (the unequal burden of) diseases across ethnic groups, focusing on three disease categories: cardiovascular diseases, mental health and infectious diseases. PARTICIPANTS: The HELIUS study is a prospective cohort study among six large ethnic groups living in Amsterdam, the Netherlands. Between 2011 and 2015, a total 24 789 participants (aged 18-70 years) were included at baseline. Similar-sized samples of individuals of Dutch, African Surinamese, South-Asian Surinamese, Ghanaian, Turkish and Moroccan origin were included. Participants filled in an extensive questionnaire and underwent a physical examination that included the collection of biological samples (biobank). FINDINGS TO DATE: Data on physical, behavioural, psychosocial and biological risk factors, and also ethnicity-specific characteristics (eg, culture, migration history, ethnic identity, socioeconomic factors and discrimination) were collected, as were measures of health outcomes (cardiovascular, mental health and infections). The first results have confirmed large inequalities in health between ethnic groups, such as diabetes and depressive symptoms, and also early markers of disease such as arterial wave reflection and chronic kidney disease, which can only just partially be explained by inequalities in traditional risk factors, such as obesity and socioeconomic status. In addition, the first results provided important clues for targeting prevention and healthcare. FUTURE PLANS: HELIUS will be used for further research on the underlying causes of ethnic differences in health. Follow-up data will be obtained by repeated measurements and by linkages with existing registries (eg, hospital data, pharmacy data and insurance data).


Assuntos
Grupos Étnicos/estatística & dados numéricos , Nível de Saúde , Disparidades em Assistência à Saúde/etnologia , Estilo de Vida Saudável , Adolescente , Adulto , Idoso , Doenças Cardiovasculares/etnologia , Doenças Transmissíveis/etnologia , Comparação Transcultural , Estudos Transversais , Feminino , Humanos , Masculino , Transtornos Mentais/etnologia , Pessoa de Meia-Idade , Países Baixos/epidemiologia , Estudos Prospectivos , Fatores de Risco , Fatores Socioeconômicos , População Urbana , Adulto Jovem
20.
BMC Psychiatry ; 17(1): 349, 2017 10 24.
Artigo em Inglês | MEDLINE | ID: mdl-29065874

RESUMO

BACKGROUND: In Western European countries, the prevalence of depressive symptoms is higher among ethnic minority groups, compared to the host population. We explored whether these inequalities reflect variance in the way depressive symptoms are measured, by investigating whether items of the PHQ-9 measure the same underlying construct in six ethnic groups in the Netherlands. METHODS: A total of 23,182 men and women aged 18-70 of Dutch, South-Asian Surinamese, African Surinamese, Ghanaian, Turkish or Moroccan origin were included in the HELIUS study and had answered to at least one of the PHQ-9 items. We conducted multiple group confirmatory factor analyses (MGCFA), with increasingly stringent model constraints (i.e. assessing Configural, Metric, Strong and Strict measurement invariance (MI)), and regression analysis, to confirm comparability of PHQ-9 items across ethnic groups. RESULTS: A one-factor model, where all nine items reflect a single underlying construct, showed acceptable model fit and was used for MI testing. In each subsequent step, change in goodness-of-fit measures did not exceed 0.015 (RMSEA) or 0.01 (CFI). Moreover, strict invariance models showed good or acceptable model fit (Men: RMSEA = 0.050; CFI = 0.985; Women: RMSEA = 0.058; CFI = 0.979), indicating between-group equality of item clusters, factor loadings, item thresholds and residual variances. Finally, regression analysis did not indicate potential ethnicity-related differential item functioning (DIF) of the PHQ-9. CONCLUSIONS: This study provides evidence of measurement invariance of the PHQ-9 regarding ethnicity, implying that the observed inequalities in depressive symptoms cannot be attributed to DIF.


Assuntos
Depressão/epidemiologia , Grupos Étnicos/estatística & dados numéricos , Grupos Minoritários/estatística & dados numéricos , Questionário de Saúde do Paciente/normas , Adulto , Idoso , Depressão/psicologia , Grupos Étnicos/psicologia , Análise Fatorial , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Grupos Minoritários/psicologia , Países Baixos/epidemiologia , Prevalência , Fatores Socioeconômicos
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