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1.
Pediatr Pulmonol ; 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31571431

RESUMO

OBJECTIVE: The association of perinatal psychological adversity (ie, stressors and distress) with infant lung function (ILF) and development is not well studied in Africa and elsewhere. We determined the association between maternal perinatal psychological adversity and ILF in African infants. DESIGN: Prospective longitudinal follow up of the Drakenstein Child Health Study birth cohort. PARTICIPANTS: Seven hundred and sixty-two infants aged 6 to 10 weeks and 485 infants who had data for both maternal perinatal psychological adversity and ILF (measured at 6 to 10 weeks and 12 months). METHODS: The main analyses were based on cross-sectional measures of ILF at each assessment (6 to 10 weeks or 12 months), using generalized linear models, and then on the panel-data of both longitudinal ILF assessments, using generalised estimating equations, that allowed specification of the within-group correlation structure. RESULTS: Prenatal intimate partner violence (IPV) exposure was associated with reduced respiratory resistance at 6 to 10 weeks (beta coefficient [ß] = -.131, P = .023); postnatal IPV with reduced ratio of time to peak tidal expiratory flow over total expiratory time (tPTEF /tE ) at 12 months (ß = -.206, P = .016); and prenatal depression with lower respiratory rate at 6 to 10 weeks (ß = -.044, P = .032) and at 12 months (ß = -.053, P = .021). Longitudinal analysis found an association of prenatal IPV with reduced tPTEF /tE (ß = -.052, P < .0001); postnatal IPV with decreased functional residual capacity (FRC; ß = -.086, P < .0001); prenatal posttraumatic stress disorder with increased FRC (ß = .017, P < .0001); prenatal depression with increased FRC (ß = .026, P < .0001) and postnatal depression with increased FRC (ß = .021, P < .0001). CONCLUSION: Screening for psychological adversity and understanding the mechanisms involved may help identify children at risk of altered lung development and inform approaches to treatment.

2.
Cancer Res ; 79(19): 5113-5120, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31488422

RESUMO

Ovarian cancer is the deadliest gynecologic cancer. Chronic stress accelerates tumor growth in animal models of ovarian cancer. We therefore postulated that posttraumatic stress disorder (PTSD) may be associated with increased risk of ovarian cancer. We used data from the Nurses' Health Study II, a longitudinal cohort study with 26 years of follow-up, conducted from 1989 to 2015 with 54,710 subjects. Lifetime PTSD symptoms were measured in 2008. Self-reported ovarian cancer was validated with medical records. Risk of ovarian cancer was estimated with Cox proportional hazards models and further adjusted for known ovarian cancer risk factors (e.g., hormonal factors) and health risk factors (e.g., smoking). Fully prospective secondary analyses examined incident ovarian cancer occurring after PTSD assessment in 2008. In addition, we examined associations by menopausal status. During follow-up, 110 ovarian cancers were identified. Women with high PTSD symptoms had 2-fold greater risk of ovarian cancer versus women with no trauma exposure [age-adjusted HR = 2.10; 95% confidence interval (CI), 1.12-3.95]. Adjustment for health and ovarian cancer risk factors moderately attenuated this association (HR = 1.86; 95% CI, 0.98-3.51). Associations were similar or moderately stronger in fully prospective analyses (age-adjusted HR = 2.38; 95% CI, 0.98-5.76, N cases = 50) and in premenopausal women (HR = 3.42; 95% CI, 1.08-10.85). In conclusion, we show that PTSD symptoms are associated with increased risk of ovarian cancer. Better understanding of the underlying molecular mechanisms could lead to interventions that reduce ovarian cancer risk in women with PTSD and other stress-related mental disorders. SIGNIFICANCE: PTSD is associated with ovarian cancer risk, particularly in premenopausal women. Understanding the underlying molecular mechanisms will aid in formulating ways to reduce ovarian cancer risk associated with chronic stress.

3.
Mol Psychiatry ; 2019 Jul 24.
Artigo em Inglês | MEDLINE | ID: mdl-31341239

RESUMO

Although exposure to adversity increases risk for poor mental health outcomes, many people exposed to adversity do not develop such outcomes. Psychological resilience, defined broadly as positive emotional and/or behavioral adaptation to adversity, may be influenced by genetic factors that have remained largely unexplored in the era of large-scale genome-wide studies. In this perspective, we provide an integrative framework for studying human genome-wide variation underlying resilience. We first outline three complementary working definitions of psychological resilience-as a capacity, process, and outcome. For each definition, we review emerging empirical evidence, including findings from positive psychology, to illustrate how a resilience-based framework can guide novel and fruitful directions for the field of psychiatric genomics, distinct from the ongoing study of psychiatric risk and related traits. Finally, we provide practical recommendations for future genomic research on resilience, highlighting a need to augment cross-sectional findings with prospective designs that include detailed measurement of adversities and outcomes. A research framework that explicitly addresses resilience could help us to probe biological mechanisms of stress adaptation, identify individuals who may benefit the most from prevention and early intervention, and ascertain modifiable protective factors that mitigate negative outcomes even for those at high genetic risk.

4.
Nat Commun ; 10(1): 2548, 2019 06 11.
Artigo em Inglês | MEDLINE | ID: mdl-31186427

RESUMO

Epigenetic processes, including DNA methylation (DNAm), are among the mechanisms allowing integration of genetic and environmental factors to shape cellular function. While many studies have investigated either environmental or genetic contributions to DNAm, few have assessed their integrated effects. Here we examine the relative contributions of prenatal environmental factors and genotype on DNA methylation in neonatal blood at variably methylated regions (VMRs) in 4 independent cohorts (overall n = 2365). We use Akaike's information criterion to test which factors best explain variability of methylation in the cohort-specific VMRs: several prenatal environmental factors (E), genotypes in cis (G), or their additive (G + E) or interaction (GxE) effects. Genetic and environmental factors in combination best explain DNAm at the majority of VMRs. The CpGs best explained by either G, G + E or GxE are functionally distinct. The enrichment of genetic variants from GxE models in GWAS for complex disorders supports their importance for disease risk.


Assuntos
Metilação de DNA/genética , DNA/sangue , Interação Gene-Ambiente , Estudos de Coortes , Epigênese Genética , Feminino , Sangue Fetal , Genótipo , Humanos , Recém-Nascido , Masculino , Gravidez , Fatores de Risco
5.
Brain Behav Immun ; 81: 280-291, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31228611

RESUMO

Post-traumatic stress disorder (PTSD) is a debilitating mental disorder precipitated by trauma exposure. However, only some persons exposed to trauma develop PTSD. There are sex differences in risk; twice as many women as men develop a lifetime diagnosis of PTSD. Methylomic profiles derived from peripheral blood are well-suited for investigating PTSD because DNA methylation (DNAm) encodes individual response to trauma and may play a key role in the immune dysregulation characteristic of PTSD pathophysiology. In the current study, we leveraged recent methodological advances to investigate sex-specific differences in DNAm-based leukocyte composition that are associated with lifetime PTSD. We estimated leukocyte composition on a combined methylation array dataset (483 participants, ∼450 k CpG sites) consisting of two civilian cohorts, the Detroit Neighborhood Health Study and Grady Trauma Project. Sex-stratified Mann-Whitney U test and two-way ANCOVA revealed that lifetime PTSD was associated with significantly higher monocyte proportions in males, but not in females (Holm-adjusted p-val < 0.05). No difference in monocyte proportions was observed between current and remitted PTSD cases in males, suggesting that this sex-specific difference may reflect a long-standing trait of lifetime history of PTSD, rather than current state of PTSD. Associations with lifetime PTSD or PTSD status were not observed in any other leukocyte subtype and our finding in monocytes was confirmed using cell estimates based on a different deconvolution algorithm, suggesting that our sex-specific findings are robust across cell estimation approaches. Overall, our main finding of elevated monocyte proportions in males, but not in females with lifetime history of PTSD provides evidence for a sex-specific difference in peripheral blood leukocyte composition that is detectable in methylomic profiles and that may reflect long-standing changes associated with PTSD diagnosis.

6.
JAMA Netw Open ; 2(5): e193447, 2019 May 03.
Artigo em Inglês | MEDLINE | ID: mdl-31050786

RESUMO

Importance: There is a well-established negative association of educational attainment (EA) and other traits related to cognitive ability with posttraumatic stress disorder (PTSD), but the underlying mechanisms are poorly understood. Objectives: To investigate the association of PTSD with traits related to EA. Design, Setting, and Participants: Genetic correlation, polygenic risk scoring, and mendelian randomization (MR) were conducted including 23 185 individuals with PTSD and 151 309 control participants from the Psychiatric Genomics Consortium for PTSD and up to 1 131 881 individuals assessed for EA and related traits from UK Biobank, 23andMe, and the Social Science Genetic Association Consortium. Data were analyzed from July 3 through November 19, 2018. Main Outcomes and Measures: Genetic correlation obtained from linkage disequilibrium score regression, phenotypic variance explained by polygenic risk scores, and association estimates from MR. Results: Summary association data from multiple genome-wide association studies were available for a total of 1 180 352 participants (634 391 [53.7%] women). Posttraumatic stress disorder showed negative genetic correlations with EA (rg = -0.26; SE = 0.05; P = 4.60 × 10-8). Mendelian randomization analysis, conducting considering a random-effects inverse-variance weighted method, indicated that EA has a negative association with PTSD (ß = -0.23; 95% CI, -0.07 to -0.39; P = .004). Investigating potential mediators of the EA-PTSD association, propensity for trauma exposure and risk-taking behaviors were observed as risk factors for PTSD independent of EA (trauma exposure: ß = 0.37; 95% CI, 0.19 to 0.52; P = 2.57 × 10-5; risk-taking: ß = 0.76; 95% CI, 0.38 to 1.13; P = 1.13 × 10-4), while income may mediate the association of EA with PSTD (MR income: ß = -0.18; 95% CI, -0.29 to -0.07; P = .001; MR EA: ß = -0.23; 95% CI, -0.39 to -0.07; P = .004; multivariable MR income: ß = -0.32; 95% CI, -0.57 to 0.07; P = .02; multivariable MR EA: ß = -0.04; 95% CI, -0.29 to 0.21; SE, 0.13; P = .79). Conclusions and Relevance: Large-scale genomic data sets add further evidence to the negative association of EA with PTSD, also supporting the role of economic status as a mediator in the association observed.

8.
Psychol Med ; : 1-9, 2019 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-30982473

RESUMO

BACKGROUND: Whereas genetic susceptibility increases the risk for major depressive disorder (MDD), non-genetic protective factors may mitigate this risk. In a large-scale prospective study of US Army soldiers, we examined whether trait resilience and/or unit cohesion could protect against the onset of MDD following combat deployment, even in soldiers at high polygenic risk. METHODS: Data were analyzed from 3079 soldiers of European ancestry assessed before and after their deployment to Afghanistan. Incident MDD was defined as no MDD episode at pre-deployment, followed by a MDD episode following deployment. Polygenic risk scores were constructed from a large-scale genome-wide association study of major depression. We first examined the main effects of the MDD PRS and each protective factor on incident MDD. We then tested the effects of each protective factor on incident MDD across strata of polygenic risk. RESULTS: Polygenic risk showed a dose-response relationship to depression, such that soldiers at high polygenic risk had greatest odds for incident MDD. Both unit cohesion and trait resilience were prospectively associated with reduced risk for incident MDD. Notably, the protective effect of unit cohesion persisted even in soldiers at highest polygenic risk. CONCLUSIONS: Polygenic risk was associated with new-onset MDD in deployed soldiers. However, unit cohesion - an index of perceived support and morale - was protective against incident MDD even among those at highest genetic risk, and may represent a potent target for promoting resilience in vulnerable soldiers. Findings illustrate the value of combining genomic and environmental data in a prospective design to identify robust protective factors for mental health.

9.
Clin Neuropsychol ; : 1-18, 2019 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-30950749

RESUMO

Objective: Demographically corrected norms typically account for the effects of age, education, and in some cases, sex and other factors (e.g. race/ethnicity). However, generalizability of normative standards to different countries and ethnic groups is not universal. This study sought to determine whether demographically specific Zambian neuropsychological norms would generalize to a group of South African women. Method: 212 English-Xhosa bilingual, South African (SA) women were administered a comprehensive neuropsychological (NP) test battery in either English or Xhosa. We examined rates of "impairment" using Global Deficit Scores (GDS) based upon published, demographically corrected norms from a nearby African country (Zambia). Using multiple regression, we examined the extent to which Zambian norms "corrected" for the effects of age and education in this SA sample. Results: Compared to the normative standards from Zambia, the South African women performed somewhat worse than expected on a few test measures and better than expected on others, but their GDS and associated "impairment" rates were close to what was seen in Zambia. Demographically corrected Zambian norms adequately adjusted for the effects of age and years of education in this sample of SA women, with the exception that Zambian norms appeared to "under correct" for the positive effects of years of education on tests of information processing speed. Conclusions: Demographically corrected norms developed for Zambia may adequately adjust for the effects of age in SA women. Further research is needed to determine whether additional corrections for education are needed in SA, especially for tests of information processing speed.

10.
PLoS One ; 14(3): e0213441, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30897111

RESUMO

INTRODUCTION: The relation between TV viewing and posttraumatic stress disorder (PTSD) is controversial; prior work focused exclusively on whether TV viewing of disaster events constitutes a traumatic stressor that causes PTSD. This study evaluates a possible bidirectional relation between PTSD and TV viewing in community-dwelling women. METHODS: Data are from the PTSD subsample of the Nurses' Health II study, an ongoing prospective study of women aged 24-42 years at enrollment and who have been followed biennially (N = 50,020). Trauma exposure and PTSD symptoms (including date of onset) were assessed via the Brief Trauma Questionnaire and the Short Screening Scale for DSM-IV PTSD. Average TV viewing was reported at 5 times over 18 years of follow-up. Linear mixed models assessed differences in TV viewing patterns by trauma/PTSD status. Among women with trauma/PTSD onset during follow-up (N = 14,374), linear spline mixed models assessed differences in TV viewing patterns before and after PTSD onset. RESULTS: Women with high PTSD symptoms reported more TV viewing (hours/wk) compared to trauma-unexposed women at all follow-up assessments (ß = 0.14, SE = 0.01, p < .001). Among the women who experienced trauma during follow-up, significant increases in TV viewing (hours/day) prior to onset of high PTSD symptom levels were evident (ß = 0.15, SE = 0.02, p < .001). CONCLUSIONS: TV viewing following trauma exposure may be a marker of vulnerability for developing PTSD and also a consequence of having PTSD. High TV viewing levels may be linked with ineffective coping strategies or social isolation, which increase risk of developing PTSD.

11.
BMJ Open ; 9(2): e025469, 2019 Feb 19.
Artigo em Inglês | MEDLINE | ID: mdl-30782936

RESUMO

INTRODUCTION: Schizophrenia and bipolar disorder account for a large proportion of the global burden of disease. Despite their enormous impact, little is known about their pathophysiology. Given the high heritability of schizophrenia and bipolar disorder, unbiased genetic studies offer the opportunity to gain insight into their neurobiology. However, advances in understanding the genetic architecture of schizophrenia and bipolar disorder have been based almost exclusively on subjects of Northern European ancestry. The Neuropsychiatric Genetics of African Populations-Psychosis (NeuroGAP-Psychosis) project aims to expand our understanding of the causes of schizophrenia and bipolar disorder through large-scale sample collection and analyses in understudied African populations. METHODS AND ANALYSIS: NeuroGAP-Psychosis is a case-control study of 34 000 participants recruited across multiple sites within Ethiopia, Kenya, South Africa and Uganda. Participants will include individuals who are at least 18 years old with a clinical diagnosis of schizophrenia or bipolar disorder ('psychosis') or those with no history of psychosis. Research assistants will collect phenotype data and saliva for DNA extraction. Data on mental disorders, history of physical health problems, substance use and history of past traumatic events will be collected from all participants.DNA extraction will take place in-country, with genotyping performed at the Broad Institute. The primary analyses will include identifying major groups of participants with similar ancestry using the computation-efficient programme single nucleotide polymorphisms (SNP) weights. This will be followed by a GWAS within and across ancestry groups. ETHICS AND DISSEMINATION: All participants will be assessed for capacity to consent using the University of California, San Diego Brief Assessment of Capacity to Consent. Those demonstrating capacity to consent will be required to provide informed consent. Ethical clearances to conduct this study have been obtained from all participating sites. Findings from this study will be disseminated in publications and shared with controlled access public databases, such as the database of Genotypes and Phenotypes, dbGaP.

12.
Pediatrics ; 143(3)2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30718380

RESUMO

BACKGROUND: Research shows that the development of cardiometabolic disease can begin early in life with risk factors accumulating over time, but less is known about protective pathways to positive health. In this study, we use prospective data to test whether childhood assets predict a greater likelihood of being in optimal cardiometabolic health by age 17. METHODS: Data are from 3074 participants in the Avon Longitudinal Study of Parents and Children (mean age = 17.8). Four childhood assets were prospectively assessed via cognitive tests and parent report when children were between ages 8 and 10: strong executive functioning skills, prosocial behaviors, and low levels of internalizing and externalizing problems. Cardiometabolic health was assessed at ages 9 and 17 by using a composite dysregulation score derived from multiple biological parameters, including cholesterol, blood pressure, C-reactive protein, insulin resistance, and BMI. Associations between assets and optimal health at age 17 (ie, a dysregulation score of ≤1) were evaluated with Poisson regression models with robust error variances. RESULTS: After controlling for covariates (including sociodemographics, correlates of cardiometabolic health, and dysregulation scores at age 9), participants with multiple assets were 1.08 to 1.27 times more likely to be in optimal cardiometabolic health at age 17 compared with those with 0 or 1 asset. Each additional asset conferred a 6% greater likelihood of optimal health over time (relative risk = 1.06 [95% confidence interval: 1.01 to 1.11]). CONCLUSIONS: Childhood assets predicted cardiometabolic health with seemingly cumulative impacts. Identifying early assets may provide novel targets for prevention and elucidate pathways to positive adult health.

13.
J Affect Disord ; 245: 885-896, 2019 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-30699873

RESUMO

BACKGROUND: There have been considerable recent advances in understanding the genetic architecture of anxiety disorders and posttraumatic stress disorder (PTSD), as well as the underlying neurocircuitry of these disorders. However, there is little work on the concordance of genetic variations that increase risk for these conditions, and that influence subcortical brain structures. We undertook a genome-wide investigation of the overlap between the genetic influences from single nucleotide polymorphisms (SNPs) on volumes of subcortical brain structures and genetic risk for anxiety disorders and PTSD. METHOD: We obtained summary statistics of genome-wide association studies (GWAS) of anxiety disorders (Ncases = 7016, Ncontrols = 14,745), PTSD (European sample; Ncases = 2424, Ncontrols = 7113) and of subcortical brain structures (N = 13,171). SNP Effect Concordance Analysis (SECA) and Linkage Disequilibrium (LD) Score Regression were used to examine genetic pleiotropy, concordance, and genome-wide correlations respectively. SECAs conditional false discovery was used to identify specific risk variants associated with anxiety disorders or PTSD when conditioning on brain related traits. RESULTS: For anxiety disorders, we found evidence of significant concordance between increased anxiety risk variants and variants associated with smaller amygdala volume. Further, by conditioning on brain volume GWAS, we identified novel variants that associate with smaller brain volumes and increase risk for disorders: rs56242606 was found to increase risk for anxiety disorders, while two variants (rs6470292 and rs683250) increase risk for PTSD, when conditioning on the GWAS of putamen volume. LIMITATIONS: Despite using the largest available GWAS summary statistics, the analyses were limited by sample size. CONCLUSIONS: These preliminary data indicate that there is genome wide concordance between genetic risk factors for anxiety disorders and those for smaller amygdala volume, which is consistent with research that supports the involvement of the amygdala in anxiety disorders. It is notable that a genetic variant that contributes to both reduced putamen volume and PTSD plays a key role in the glutamatergic system. Further work with GWAS summary statistics from larger samples, and a more extensive look at the genetics underlying brain circuits, is needed to fully delineate the genetic architecture of these disorders and their underlying neurocircuitry.


Assuntos
Transtornos de Ansiedade/genética , Transtornos de Ansiedade/psicologia , Variação Genética/genética , Vias Neurais/fisiopatologia , Transtornos de Estresse Pós-Traumáticos/genética , Transtornos de Estresse Pós-Traumáticos/psicologia , Tonsila do Cerebelo/diagnóstico por imagem , Transtornos de Ansiedade/fisiopatologia , Encéfalo/diagnóstico por imagem , Feminino , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Humanos , Desequilíbrio de Ligação , Masculino , Polimorfismo de Nucleotídeo Único/genética , Fatores de Risco , Transtornos de Estresse Pós-Traumáticos/fisiopatologia
14.
Psychol Med ; : 1-10, 2019 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-30606272

RESUMO

BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with higher risk of incident hypertension, but it is unclear whether specific aspects of PTSD are particularly cardiotoxic. PTSD is a heterogeneous disorder, comprising dimensions of fear and dysphoria. Because elevated fear after trauma may promote autonomic nervous system dysregulation, we hypothesized fear would predict hypertension onset, and associations with hypertension would be stronger with fear than dysphoria. METHODS: We examined fear and dysphoria symptom dimensions in relation to incident hypertension over 24 years in 2709 trauma-exposed women in the Nurses' Health Study II. Posttraumatic fear and dysphoria symptom scores were derived from a PTSD diagnostic interview. We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each symptom dimension (quintiles) with new-onset hypertension events (N = 925), using separate models. We also considered lower-order symptom dimensions of fear and dysphoria. RESULTS: Higher levels of fear (P-trend = 0.02), but not dysphoria (P-trend = 0.22), symptoms were significantly associated with increased hypertension risk after adjusting for socio-demographics and family history of hypertension. Women in the highest v. lowest fear quintile had a 26% higher rate of developing hypertension [HR = 1.26 (95% CI 1.02-1.57)]; the increased incidence associated with greater fear was similar when further adjusted for biomedical and health behavior covariates (P-trend = 0.04) and dysphoria symptoms (P-trend = 0.04). Lower-order symptom dimension analyses provided preliminary evidence that the re-experiencing and avoidance components of fear were particularly associated with hypertension. CONCLUSIONS: Fear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.

15.
JAMA Psychiatry ; 76(4): 399-408, 2019 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-30673066

RESUMO

Importance: Increasing evidence shows that physical activity is associated with reduced risk for depression, pointing to a potential modifiable target for prevention. However, the causality and direction of this association are not clear; physical activity may protect against depression, and/or depression may result in decreased physical activity. Objective: To examine bidirectional relationships between physical activity and depression using a genetically informed method for assessing potential causal inference. Design, Setting, and Participants: This 2-sample mendelian randomization (MR) used independent top genetic variants associated with 2 physical activity phenotypes-self-reported (n = 377 234) and objective accelerometer-based (n = 91 084)-and with major depressive disorder (MDD) (n = 143 265) as genetic instruments from the largest available, nonoverlapping genome-wide association studies (GWAS). GWAS were previously conducted in diverse observational cohorts, including the UK Biobank (for physical activity) and participating studies in the Psychiatric Genomics Consortium (for MDD) among adults of European ancestry. Mendelian randomization estimates from each genetic instrument were combined using inverse variance weighted meta-analysis, with alternate methods (eg, weighted median, MR Egger, MR-Pleiotropy Residual Sum and Outlier [PRESSO]) and multiple sensitivity analyses to assess horizontal pleiotropy and remove outliers. Data were analyzed from May 10 through July 31, 2018. Main Outcomes and Measures: MDD and physical activity. Results: GWAS summary data were available for a combined sample size of 611 583 adult participants. Mendelian randomization evidence suggested a protective relationship between accelerometer-based activity and MDD (odds ratio [OR], 0.74 for MDD per 1-SD increase in mean acceleration; 95% CI, 0.59-0.92; P = .006). In contrast, there was no statistically significant relationship between MDD and accelerometer-based activity (ß = -0.08 in mean acceleration per MDD vs control status; 95% CI, -0.47 to 0.32; P = .70). Furthermore, there was no significant relationship between self-reported activity and MDD (OR, 1.28 for MDD per 1-SD increase in metabolic-equivalent minutes of reported moderate-to-vigorous activity; 95% CI, 0.57-3.37; P = .48), or between MDD and self-reported activity (ß = 0.02 per MDD in standardized metabolic-equivalent minutes of reported moderate-to-vigorous activity per MDD vs control status; 95% CI, -0.008 to 0.05; P = .15). Conclusions and Relevance: Using genetic instruments identified from large-scale GWAS, robust evidence supports a protective relationship between objectively assessed-but not self-reported-physical activity and the risk for MDD. Findings point to the importance of objective measurement of physical activity in epidemiologic studies of mental health and support the hypothesis that enhancing physical activity may be an effective prevention strategy for depression.

16.
Depress Anxiety ; 36(6): 490-498, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30681235

RESUMO

OBJECTIVE: Posttraumatic stress disorder (PTSD) is frequently associated with depression and anxiety, but the nature of the relationship is unclear. By removing mood and anxiety diagnostic criteria, the 11th edition of the International Classification of Diseases (ICD-11) aims to delineate a distinct PTSD phenotype. We examined the effect of implementing ICD-11 criteria on rates of codiagnosed depression and anxiety in survivors with recent PTSD. METHOD: Participants were 1,061 survivors of traumatic injury admitted to acute care centers in Israel. ICD-10 and ICD-11 diagnostic rules were applied to the Clinician-Administered PTSD Scale for DSM-IV. Co-occurring disorders were identified using the Structured Clinical Interview for DSM-IV (SCID). Depression severity was measured by the Beck Depression Inventory-II (BDI-II). Assessments were performed 0-60 ("wave 1") and 90-240 ("wave 2") days after trauma exposure. RESULTS: Participants identified by ICD-11 PTSD criteria were equally or more likely than those identified by the ICD-10 alone to meet depression or anxiety disorder diagnostic criteria (for wave 1: depressive disorders, OR [odds ratio] = 1.98, 95% CI [confidence interval] = [1.36, 2.87]; anxiety disorders, OR = 1.04, 95% CI = [0.67, 1.64]; for wave 2: depressive disorders, OR = 1.70, 95% CI = [1.00, 2.91]; anxiety disorders, OR = 1.04, 95% CI = [0.54, 2.01]). ICD-11 PTSD was associated with higher BDI scores (M = 23.15 vs. 17.93, P < 0.001 for wave 1; M = 23.93 vs. 17.94, P < 0.001 for wave 2). PTSD symptom severity accounted for the higher levels of depression in ICD-11 PTSD. CONCLUSIONS: Despite excluding depression and anxiety symptom criteria, the ICD-11 identified equal or higher proportion of depression and anxiety disorders, suggesting that those are inherently associated with PTSD.

17.
J Psychiatr Res ; 116: 172-177, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30553535

RESUMO

OBJECTIVE: Although childhood maltreatment has been reported to be associated with the incidence of cardiovascular diseases, its association with specific major cardiovascular events remains unclear. This study aimed to examine the relationship between different types of childhood maltreatment (CM) and myocardial infarction (MI) occurrence in a nationally representative sample. METHODS: We used data from the National Epidemiologic Survey of Alcohol and Related Conditions, a nationally representative US sample of adults aged 20 years and older (N = 34, 653). Logistic regression models were constructed to investigate the associations between five types of CMs including physical abuse, physical neglect, emotional abuse, emotional neglect, and sexual abuse and the risk of MI adjusting for sociodemographic variables. RESULTS: After adjusting for sociodemographic variables, childhood sexual abuse was significantly associated with increased odds of MI occurrence (adjusted odds ratio [aOR] = 1.85, 95%CI = 1.24-2.76, p = 0.003). Additionally, childhood physical abuse was significantly associated with increased odds of MI occurrence in men (aOR = 2.45, 95%CI = 1.35-4.44, p = 0.004) but this association was not observed in women (aOR = 0.72, 95%CI = 0.32-1.66, p = 0.440). Compared to those who did not experience CM, those who experienced more than three types of CMs showed increased odds of MI occurrence (adjusted OR = 2.08-3.05, all p < 0.05). CONCLUSIONS: Using data from a nationally representative US sample of adults, we found significant positive associations between CM and odds of MI occurrence in adulthood. Future longitudinal prospective studies are needed to confirm our findings.

18.
Artigo em Inglês | MEDLINE | ID: mdl-30383236

RESUMO

Context: Epidemiologic data link psychological stress to adiposity. However, the underlying mechanisms remain uncertain. Objectives: To test the hypotheses that: 1) higher activity of the amygdala, a neural center involved in the emotional and physiological response to stress, associates with greater visceral adipose tissue [VAT] volumes, and 2) this association is mediated by increased hematopoietic tissue activity. Setting: Massachusetts General Hospital, Boston, USA. Patients: 246 patients without active oncologic, cardiovascular, or inflammatory disease who underwent clinical 18F-FDG-PET/CT imaging were studied. VAT imaging was repeated ∼one year later in 68 subjects. Design: Metabolic activity of the amygdala [AmygA], hematopoietic tissue activity, and adiposity volumes were measured with validated methods. Main Outcome Measure: To evaluate the relationship between AmygA and baseline VAT and follow-up VAT. Results: AmygA associated with baseline: body mass index (standardized ß=0.15, p=0.01), VAT (0.19, p=0.002), and VAT to subcutaneous adipose tissue ratio (0.20, p=0.002), all remaining significant after adjustment for age and sex. Additionally, AmygA associated with hematopoietic tissue activity (0.15, p=0.01), which in-turn associated with VAT (0.34, p<0.001). Further, path analysis showed that 48% of the relationship between AmygA and baseline VAT was mediated by increased hematopoietic tissue activity (p=0.007). Moreover, baseline AmygA associated with achieved VAT after one year (p=0.02) in a model adjusted for age, sex, and baseline VAT. Conclusions: These results suggest the presence of a neurobiological pathway, involving the amygdala and bone marrow, linking amygdalar activity to adiposity in humans. Future studies should test whether targeting this mechanism may attenuate adiposity and its complications.

19.
Epigenomics ; 2018 Nov 20.
Artigo em Inglês | MEDLINE | ID: mdl-30456986

RESUMO

AIM: Trauma exposure is a necessary, but not deterministic, contributor to post-traumatic stress disorder (PTSD). Epigenetic factors may distinguish between trauma-exposed individuals with versus without PTSD. MATERIALS & METHODS: We conducted a meta-analysis of PTSD epigenome-wide association studies in trauma-exposed cohorts drawn from civilian contexts. Whole blood-derived DNA methylation levels were analyzed in 545 study participants, drawn from the three civilian cohorts participating in the PTSD working group of the Psychiatric Genomics Consortium. RESULTS: Two CpG sites significantly associated with current PTSD in NRG1 (cg23637605) and in HGS (cg19577098). CONCLUSION: PTSD is associated with differential methylation, measured in blood, within HGS and NRG1 across three civilian cohorts.

20.
Psychol Med ; : 1-10, 2018 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-30488818

RESUMO

BACKGROUND: Abnormal thyroid function is prevalent among women and has been linked to increased risk of chronic disease. Posttraumatic stress disorder (PTSD) has been linked to thyroid dysfunction in some studies; however, the results have been inconsistent. Thus, we evaluated trauma exposure and PTSD symptoms in relation to incident thyroid dysfunction in a large longitudinal cohort of civilian women. METHODS: We used data from 45 992 women from the ongoing Nurses' Health Study II, a longitudinal US cohort study that began in 1989. In 2008, history of trauma and PTSD were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, fourth edition, PTSD, and incident thyroid dysfunction was determined by participants' self-report in biennial questionnaires of physician-diagnosed hypothyroidism and Graves' hyperthyroidism. The study period was from 1989 to 2013. Proportional hazard models were used to estimate multivariable-adjusted hazard ratios and 95% confidence intervals (CIs) for incident hypothyroidism and Graves' hyperthyroidism. RESULTS: In multivariable-adjusted models, we found significant associations for PTSD only with hypothyroidism [p-trend <0.001; trauma with no PTSD symptoms, 1.08 (95% CI 1.02-1.15); 1-3 PTSD symptoms, 1.12 (95% CI 1.04-1.21); 4-5 PTSD symptoms, 1.23 (95% CI 1.13-1.34); and 6-7 PTSD symptoms, 1.26 (95% CI 1.14-1.40)]. PTSD was not associated with risk of Graves' hyperthyroidism (p-trend = 0.34). Associations were similar in sensitivity analyses restricted to outcomes with onset after 2008, when PTSD was assessed. CONCLUSIONS: PTSD was associated with higher risk of hypothyroidism in a dose-dependent fashion. Highlighted awareness for thyroid dysfunction may be especially important in women with PTSD.

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