A meta-analysis of sex differences in human navigation skills

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There are inconsistent reports regarding behavioral sex differences in the human navigation literature. This meta-analysis meta the overall magnitude of sex differences in large-scale navigation skills in a variety of paradigms and populations, and examines potential moderators, using effect sizes from studies and a multilevel analytic approach. The type of task, the type of dependent variable and the testing environment significantly contribute to variability in effect sizes, although there are only a few situations in which differences are either nonexistent or very large.

Sex and recall tasks and the deviation scores associated with them show larger sex differences than distance estimation tasks or learning to criterion. We discuss the implications of these meta for understanding sex differences in human spatial navigation and identify avenues for future navigation research.

Nora Newcombe. The authors have no competing interests in the current manuscript. Skip to main content. Advertisement Hide. A meta-analysis of sex differences in human navigation skills. Theoretical Review Meta Online: 03 July This is a preview of subscription content, log in to check access.

Abstract and scenographic imagery: The effect of environmental form on wayfinding. Journal of Environmental Psychology, 18— Apolipoprotein E4 meta sex affect neurobehavioral performance in primary school children. Pediatric Research, 67— Acredolo, L. Developmental Psychology11— Individual differences in the use of strategy in spatial orientation: Acquiring sex and configural knowledge in virtual environments Order No. Allen, G. Developmental issues in cognitive mapping: The selection and utilization of environmental landmarks.

Child Development, 50— The need for controlled information processing in the visual acquisition of route knowledge. Journal of Environmental Psychology, 18sex Interaction of task difficulty and gender stereotype threat with a spatial orientation task in a virtual nested environment.

Learning and Motivation5722— Anooshian, L. Developmental changes meta cognitive maps of a familiar neighborhood. Child Development, 52, — Human sex differences in solving a virtual navigation pro blem.

Behavioural Brain Research, — Astur, R. A characterization of performance by men and women in a virtual Morris water task: A large and reliable sex difference. Behavioural Brain Research93— Humans with hippocampus sex display severe spatial memory impairments in a virtual Morris water task. Behavioural Brain Research,77— Meta differences and correlations in a virtual Morris water task, a virtual radial arm maze, and mental rotation.

Guided navigation impairs spatial knowledge: Using aids to improve spatial representations Order No. Barkley, C. Sex differences in cue perception in a visual scene: Investigation of cue type. Behavioral Neuroscience, — Age-related decline in route learning Developmental Neuropsychology, 10 Wayfinding in an unfamiliar environment: Different spatial settings of two polyclinics. Environment and Behavior36— Mental travel primes place orientation in spatial meta.

Stachniss, K. Uttal Eds. Berlin, Germany: Springer. Google Scholar. Bateman, I. Contrasting conventional with multi-level modeling approaches to meta-analysis: Expectation consistency in UK woodland recreation values. Land Economics, 79— Keeping track of where we are: Spatial working memory in navigation. Visual Cognition, 25— Are there gender-specific neural substrates of route learning from different perspectives?.

Cerebral Cortex14 Boccia, M. Neuropsychology of environmental navigation in humans: Review and meta-analysis of FMRI studies in healthy participants. Neuropsychology Review24— Sex differences in sex strategy and efficiency. Borenstein, M. Introduction to meta-analysis. Gender effects in spatial orientation: Cognitive profiles and mental strategies. Brake, W. Sex differences in spatial navigation: The role of gonadal hormones. Current opinion in behavioral sciencessex— Egocentric and allocentric navigation strategies in Williams sex and typical development.

Developmental Science17— Sequential egocentric sex and reliance on landmarks in Williams syndrome and typical development. Frontiers in Psychology6 Going to town: Visualized perspectives and navigation through virtual environments. Computers in Human Behavior28— Navigation in 3D virtual environments: Effects of user experience and location-pointing navigation aids.

International Journal of Human-Computer Studies, 65— Evidence for the influence of testosterone in the performance of spatial navigation in sex virtual meta maze in women but not in men. Hormones and Behavior51— How sense-of-direction and learning intentionality relate to spatial knowledge acquisition in the environment. Cognitive Research: Principles and Implications2 Effect of reference frames and number of cues available on the spatial orientation of males and females in a virtual memory task.

Sex differences in spatial cognition among Hadza foragers. Evolution and Human Behavior, 33— Spatial navigation in large-scale virtual environments: Gender differences in survey tasks.

Computers in Human Behavior24— Chai, X. Sex differences in directional cue use in a virtual landscape. Behavioral Neuroscience, Effects of cue types on sex differences in human spatial memory. Meta Brain Research, Gender differences in landmark learning for virtual navigation: The role of distance to a goal.

Behavioural Processes8820— Gender differences in relation to wayfinding strategies, navigational support design, and wayfinding task difficulty. Journal of Environmental Psychology29— Sex-specific relationships between route-learning strategies and abilities in a large-scale environment.

Environment and Behavior, 38— Cohen, J. Statistical power analysis for the behavioral sciences 2nd. Hillsdale: Erlbaum. Coluccia, E. Gender differences in spatial orientation: A review.


The sex-related differences in the clinical outcomes of rhythm and safety after catheter ablation remain unclear. The purpose of this study was to compare the clinical outcomes of catheter ablation for atrial fibrillation AF in women and men. Studies that met our predefined inclusion criteria were included. Nevertheless, for the endpoint of all-cause mortality, there was no significant difference between the two genders in the subgroup of prospective studies OR: 1.

The reasons for these sex-related differences need to be further studied. The sex-related differences in the clinical outcomes of rhythm and safety after catheter ablation of atrial fibrillation AF remain unclear. Our data provided physicians and their patients with real-world information sex sex-specific outcomes of catheter ablation of AF. Over the past two decades, catheter ablation has emerged as a safe and effective therapy for the management of atrial fibrillation AF and has been associated with a reduction in AF burden and stroke, as well as with improvement in symptoms and quality of life.

Catheter ablation is currently recommended dex a reasonable alternative first-line therapy for the treatment of drug-resistant AF. However, there is a paucity of data mfta the effectiveness and safety of catheter ablation in a large cohort study of women. Therefore, we conducted a systematic review and meta-analysis to investigate the clinical outcomes associated with sex ablation of AF in women vs.

To identify all the published clinical studies that compared outcomes of catheter ablation of AF in women keta men, we performed a eex online sed of the meta through the Medline and EMBASE databases to Decemberwithout language restriction. The bibliographies of the reviewed manuscripts were manually retrieved ssx avoid missing relevant data.

Studies were included if they reported primary endpoints of interest in patients undergoing catheter ablation of AF and if they provided detailed information on women vs. Catheter ablation was defined as an endocardial ablation procedure radiofrequency or cryoablation.

Inclusion criteria were as follows: i studies had to provide reliable data on the assessment of at least one of the primary endpoints; ii to minimize the risk of small-study effects, all studies were required to have a minimum of individuals; and iii endpoints were reported as numerical events metaa than only as hazard mrta, relative risk, or odds rate. If relevant data were not reported in the published articles, we tried to contact the corresponding authors to acquire further information.

To ensure that studies were eligible for the prespecified inclusion criteria, retrieval results were reviewed by three authors C. Acute coronary syndrome was defined as acute myocardial infarction MI or unstable angina. PV stenosis was defined as moderate to severe stenosis of PV or PV stenosis requiring therapeutic intervention. Data extraction and presentation for the preparation of this manuscript followed the recommendations of the Preferred Reporting Items meha Systematic Reviews and Meta-Analyses Supplementary material onlineTable S1.

The following study- patient- ssex procedure-related data were extracted from the main paper. Any discrepancies meta resolved by discussion among the authors. In view of the intrinsic differences in study design and demographics, a random-effects model was used to estimate the pooled effects of our meta-analyses.

For the primary endpoints, prespecified sensitivity analyses were performed by iteratively removing sex study at a time to confirm that jeta results were not significantly affected by any single study. Multiple subgroup analyses according to study design, study quality, and age of patients were performed to further test the stability of our meta-analysis. To srx the effect of preselected covariates on the overall effect, we sex a random-effects meta-regression analysis.

The logarithm of OR for the primary endpoints, weighted by the inverse variance of each study, was regressed metaa age, percentage of hypertension, diabetes mellitus DMcoronary artery disease Srxstroke, smoking history, left ventricular ejection fraction LVEFand size of left atrial LA diameter in both groups.

To detect any publication bias in the primary endpoints, we examined in detail the meta of the funnel plots and further meta them sex the Begg adjusted rank correlation test and the Egger regression asymmetry test. Initially, potentially relevant studies were identified by our search strategy. After critical sex, 19 studies nine prospective meta 10 retrospective observational studies published between and met our eligibility criteria and reported desired clinical endpoints of catheter sex in women compared with men.

Flow diagram of the study selection process. AF, meta fibrillation; TIA, transient ischaemic attack. For the endpoints of safety, women undergoing catheter ablation were more likely to be older and to have previous DM, hypertension, stroke, chronic kidney disease, and valvular heart disease.

There were 0. CI, confidence interval; TIA, transient ischaemic attack. Pooled analysis showed that female sex was associated with a higher risk of all-cause mortality compared with male sex 0. The sex-related difference in the risk of sexx mortality was still significant during the in-hospital stay OR: 0.

There was no significant difference at 1-year follow-up OR: 1. CI, confidence sex. Moreover, after excluding the largest sample size study by Elayi et al. Mwta the excluded studies with more than patients six studies involving patients were included in the quantitative synthesis, we found that the result of each primary endpoint was still similar to previous findings Supplementary material onlineFigure S6.

In the subgroup of retrospective studies, the risk of all-cause mortality was higher in women than in men OR: 2. However, there was no significant difference between the two genders in the subgroup meta prospective studies OR: 1. For sex primary endpoints, meta-regression indicated that sxe significant correlation between the preselected metq and the overall treatment effect of catheter ablation was observed Supplementary material onlineTable S5.

For the primary endpoints, visual inspection of the funnel plot including all studies showed symmetry, indicating a low risk of publication bias Supplementary material onlineFigure Metta. In agreement with a prior study, 25 our data showed that Despite a higher prevalence of paroxysmal AF and less enlargement of LA diameter, long-term success rates were lower in females than males. Patel et al. It was noted that females scheduled to undergo ablation in mwta study were older and had less paroxysmal AF and more comorbidities, which were attributed to more advanced structural remodelling and led to lower success rates.

Meta, two studies with comparable baselines also found that women experience higher recurrence than men. Sex-specific differences in physiological, metaa, and structural characteristics of the atria, which might result in mta AF recurrence in the female than male sex, include lower meta ion currents, prolonged action potential duration in female atria, greater frequency of non-pulmonary triggered activity, and more pronounced AF-associated fibrotic remodelling.

It is well established meat females with AF have an increased risk for stroke in comparison with males even sex adjustment for emta factors. First, women undergoing PV isolation were older with increased comorbidities. Second, the long-term success rate was lower in women. Third, genetic factors, vascular biology, hormonal, or thromboembolic factors that differ between women and men might lead to a higher risk of stroke.

These findings were in line with the 0. It was notable that the findings of these studies were limited by small sample sizes. The increased risk of death may be mrta explained by the fact that women undergoing catheter ablation were older and had increased comorbidities and major complications. Nevertheless, there was no significant difference between the two genders in the subgroup of prospective studies.

Thus, considering the discrepancy of baseline characteristics and the inconsistent findings between retrospective and prospective studies, our metx on all-cause mortality still need to be confirmed in eex future.

Our data showed that female sex was associated with a significantly increased risk of major complications after catheter ablation, which agreed with previous findings. The increased risk of major bleeding might be due to the higher prevalence of chronic kidney disease in women than men. The increased risk mefa PMI in women may be explained by the fact that women were more often prescribed AAD therapy than invasive catheter ablation, 33 and excessive use of AAD may potentially trigger symptomatic bradycardia.

A possible explanation for sex-related differences in major complications in women sez that females were more wex to be older and to have increased comorbidities. Nevertheless, Ayoub et al. Meta higher complication risk in women suggested that incremental caution and preoperative discussion of anticipated risk in women are completely necessary. Our analysis included 19 studies available in the literature to date from multiple centres and countries. It is the largest study aiming to provide physicians and their patients with real-world information about sex-specific outcomes of catheter ablation.

However, this meta-analysis has several limitations. First, 10 of these included studies are retrospective in nature, subjecting our results to possible bias. Although we tried to conquer this limitation by the fulfilment of multiple sensitivity and subgroup analyses and meta-regression analyses, selection bias could still not be ruled out.

Second, for clinical endpoints of safety, female sex undergoing meta ablation had increased preoperative cardiovascular risk. Whether the poorer in-hospital and long-term outcomes after catheter ablation in women can be counterbalanced by these increased risks of intervention are unclear. Therefore, sfx confounders may exist in our findings. Lastly, the available data in studies did not allow for a separate analysis for cardiac and non-cardiac death, haemorrhagic, and non-haemorrhagic stroke.

In addition, major complications were more often in the female sex. The reasons for these sex-related differences in catheter ablation of AF need to be further studied. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, sed, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search.

Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents. Eex differences in catheter ablation of atrial fibrillation: a systematic review and meta-analysis Xiaocheng Cheng. Oxford Academic. Google Scholar. Qiongwen Hu. Lei Gao. Jian Liu. Shu Qin. Dongying Zhang. Corresponding author. E-mail address : cqmezdy yeah. Cite Citation. Permissions Icon Permissions.

Regional plots of the six genomic regions can be found in Supplementary Figs. The six leading markers show odds ratios of 1. This is supported by PM-plots posterior probability that a SNP effect exists in a given study showing a high consistency of effects among the studies predicted to have an effect 13 Supplementary Figs.

No evidence of replication was found by directly comparing the six leading markers, nor by investigating the larger genomic regions harboring the signal Supplementary Figs. Gene-based analyses in AFA did not result in genome-wide significant loci. We show evidence that the African-ancestry-specific SNP rs seems to capture a genomic region that may influence the expression of non-coding RNAs from this PTSD risk locus in response to increased glucocorticoid receptor signaling, thus linking this African-specific genetic variant to stress response and non-coding RNA expression Supplementary Fig.

PRS generated from well-powered GWAS have recently become a tool of high relevance for polygenic disorders and traits e. Analyses include only subjects of European ancestry. Analysis of shared heritability across common disorders of the brain 17 and specific genetic correlations of psychiatric disorders with cognitive, anthropomorphic and behavioural measures 10 , 18 , 19 , 20 has been facilitated greatly by the development of a centralized database of GWAS results including a web interface for LDSC LD Hub Genetic variation associated with PTSD was positively correlated with PRS from other psychiatric traits including depressive symptoms, schizophrenia and neuroticism, as well as epidemiologically comorbid traits such as insomnia, smoking behavior, asthma, hip-waist ratio and coronary artery disease.

Significant positive correlations were also found for reproductive traits such as the number of children ever born, and, as previously reported for women 22 , PTSD was negatively correlated with age at first birth.

Only traits with at least one significant correlation with the 5 psychiatric disorders are shown. Solid points indicate significant correlation after Bonferroni correction.

These findings are not surprising, as pleiotropic effects i. SNPs impacting multiple traits have been widely reported for psychiatric disorders. In order to test to what degree genome-wide significant findings from our GWAS meta-analyses were specific to PTSD rather than driven by correlated traits as identified above, we adjusted the top hits from our analyses for the effects of genetically correlated psychiatric traits.

These findings indicate that the genetic variants identified here are specific to PTSD when tested in the context of the three psychiatric disorders genetically most significantly correlated with PTSD. PTSD is a common and debilitating condition influenced by genetic factors, yet common genetic risk variants for PTSD have not been robustly identified.

These results show this is also true of PTSD. This increased power has led us to draw several major conclusions. First, our genetic findings squarely place PTSD among the other psychiatric disorders in terms of heritability and genetic relationship with other disorders. While this statement may seem obvious to some, there remains debate about whether PTSD is entirely a social construction We found substantial SNP-based heritability i.

The heritability results and pattern of genetic correlations are also consistent with our initial findings 10 and with those from twin studies.

PTSD shares common variant risk with other psychiatric disorders, which show substantial sharing of common variant risk with one another PTSD was most significantly genetically correlated with major depression, but also with schizophrenia, both of which have genome-wide significant loci implicated in brain function. These loci pointed to a number of different target genes that merit further investigation.

The dopaminergic system has a critical role in fear conditioning which is important in the development and maintenance of PTSD Finally, the HLA-B complex may be related through the known role of immunity and inflammation in stress-related disorders 42 , However, preliminary work from our group including imaging and psychophysiology highlights the value of deep phenotyping in conducting functional investigations into the meaning of GWAS findings 8.

Extensive follow-up work is needed to replicate our findings and to determine the function of identified genes and their relationship to putative pathological processes. For example, in SCZ the MHC locus is now thought to influence risk, in part, through pruning of synapses using immune machinery rather than through classical immune pathways Third, our results also illustrate that there may be genetic contributions to the well-documented association between PTSD and dysregulation in inflammatory and immune processes It has been widely recognized that PTSD is associated with a broad range of adverse physical health conditions over the life course ranging from typediabetes and cardiovascular disease to dementia and rheumatoid arthritis 46 , Less is known about the biological mechanisms driving the relationship between PTSD and these outcomes.

Our genetic correlation analyses may provide some initial clues for further investigation. Our subsequent gene-set and pathway analyses provide some clues further implicating the immune system. Of note, these genetic results converge with evidence from epidemiologic cohort studies documenting the role of stress-related disorders such as PTSD in autoimmune diseases 48 , case-control studies showing elevations of immune-related biomarkers in women with PTSD 49 , and epigenetic studies pointing to the role of the immune system in PTSD etiology 50 , Further work is needed to determine whether PTSD has genetic overlap with immune disorders broadly and the causal direction between disorders.

At minimum, the emerging genetic evidence presented here suggests that association between PTSD and health conditions may, in some cases, have some genetic origin.

Fourth, PGC-PTSD is distinct in relation to current genomics consortia due to its high proportion of data from participants of diverse ancestries. For example, a recent review found that only three percent of all samples in genetic studies were from African ancestry Our GWAS in subjects of African ancestry indicated at least one ancestry-specific locus using local ancestry methods developed for this analysis.

We note the sample size in the AFA analysis has only about 15, participants, which is small and under-powered, increasing the chance for false positives. However, other work has shown that genetic studies of underrepresented populations afford the opportunity to discover novel loci that are invariant in European populations As others have noted, there are major limitations in our knowledge of the genetic and environmental risk architecture of psychiatric disorders in persons of African descent Our findings provide further evidence of the need to invest in research that includes diverse ancestral populations, to expand reference data, and to continue to develop methods to analyze data from such populations.

Until such an investment is made, we are limited in our ability to understand biological mechanisms, predict genetic risk 55 , and produce optimal treatments for non-European populations. African genomes are characterized by shorter haplotype blocks and contain many millions more variants per individual than populations outside Africa Further, including data from African populations in genetic studies of PTSD and other neuropsychiatric disorders may accelerate genetic discovery and could be useful for fine mapping disease causing alleles Fifth, although PTSD heritability remained relatively stable across methods, studies, and ancestries, sex differences in heritability were observed in the overall cohort analyses as well as in the AFA analyses It is of note that the sex differences in heritability were not evident in the UK Biobank data, which we hypothesize is due to differences between the PGC1.

PTSD is conditional on trauma exposure, which is also highly heterogeneous across individuals and populations Unlike PGC1. In contrast, a substantial proportion of men in the PGC1.

The environmental experiences e. In future work, we aim to investigate this empirically by pooling detailed trauma and PTSD phenotypic information on both males and females and by modeling the effects of measurement variability on heritability estimates.

Future work could also aim to increase samples of civilian men and military women to allow for analyses stratified by military trauma and sex. Lastly, we report a significant polygenic risk score for PTSD, which also significantly predicts re-experiencing symptoms in independent data from the MVP 9.

However, larger sample sizes are needed to achieve sensitivity and specificity at levels of clinical utility In the future, polygenic risk may eventually be useful in algorithms developed to identify vulnerable persons after exposure to trauma. PTSD is one of the most theoretically preventable mental disorders, as many people exposed to trauma come to clinical attention in first response settings such as emergency rooms, intensive care units, and trauma centers.

Controlled clinical trials show that PTSD risk can be significantly reduced by early preventive interventions 59 , However, these interventions have nontrivial costs, making it infeasible to offer them to all persons exposed to trauma, given that only a small minority goes on to develop PTSD 61 , They are also unnecessary for many survivors who recover spontaneously To be cost-effective, risk prediction rules are needed to identify which exposed persons are at high risk of PTSD.

Such risk prediction tools have been developed 63 , 64 , but none to date has included polygenic risk as a predictor. PTSD is similar to major depression in both prevalence among trauma-exposed persons and in heritability.

There are now genome-wide significant signals for major depression; notably, that level of discovery required , cases and , controls Other limitations include the treatment of PTSD as a binary disorder in our analysis. Extensive epidemiologic work has shown that subthreshold PTSD is highly prevalent and debilitating 65 , In our analysis, persons with subthreshold PTSD are classified as controls, which would likely reduce our power to find genetic associations.

Of note, Gelernter et al. Finally, we used mostly unscreened controls, but controls carefully screened for trauma may increase power since trauma is required for a PTSD diagnosis.

In addition to increasing sample size, we aim in the future to also pool item-level phenotypic data from our cohorts in order to address these limitations. Advances in understanding the genomic architecture of PTSD are critical for understanding the pathophysiology of this debilitating syndrome and to developing novel biologically-based treatment approaches.

Of these, 12 were already included in Freeze 1 The majority of controls was trauma-exposed. A detailed description of the studies included is presented in Supplementary Methods. We have complied with relevant ethical regulations for work with human subjects. Subjects were genotyped on a range of Illumina genotyping arrays exception: UKB was genotyped on the Affymetrix Axiom array. At the time of analysis, direct access to individual-level genotypes was permitted for 65, subjects.

Such studies then shared summary results for meta-analyses. Pre-QC genotypes were used for these analyses. Supplementary Fig. The ancestry pipeline was shared with external sites in order to ensure consistency in ancestry calling across cohorts.

In the modified pipeline, each dataset was processed separately, including subjects of all ancestries.

Imputation was based on the Genomes phase 3 data 1KGP phase 3 Analyses were performed separately for each study and ancestry group, unless otherwise indicated. The minimum number of subjects per analysis unit was set at 50 cases and 50 controls, or a total of at least subjects, and subsets of smaller size were excluded. Smaller studies of similar composition were genotyped jointly in preparation for joint analyses e. In addition, all GWAS analyses were also performed stratified by sex.

Summary statistics on the linear scale from GEMMA and BGenie were converted to a logistic scale prior to meta-analysis for formula see Meta-analyses across studies were performed within each of the three ancestry groups and across all ancestry groups. March25 In PM-plots, M-values are plotted against -log 10 P -values.

Regional association plots were generated using LocusZoom 79 with KB windows around the index variant and compared to the corresponding windows in the other ancestry groups, including the Genomes Nov. To test for sex-specific effects, a z-test was performed on the difference of the effect estimates from male and female sex-stratified analyses. Unconstrained regression intercepts were used to account for potential inclusion of related subjects and residual population stratification, and precomputed LD scores from 1KGP EUR populations were used.

Sample prevalence was set to the actual proportion of cases in each set of data. To estimate h 2 SNP in admixed individuals and compare h 2 SNP across different ancestries, individual-level genotype data was analyzed using an unweighted linear mixed model 81 as implemented in the LDAK software To prevent bias of h 2 SNP due to cryptic relatedness, strict relatedness filters were applied.

To reduce standard error given this relatively small sample, we estimated heritability with the LDSC intercept constrained to 1, after first testing that the intercept was not significantly different from 1.

Participants reported here completed the PCL-C that asked respondents to report how much they have been bothered in the past 30 days by symptoms in response to stressful experiences i. The symptom cluster most distinctive for PTSD, re-experiencing symptoms range 5—25 , was analyzed.

After accounting for missing phenotype data, the final sample for European Americans was ,, of whom Imputation was performed with Minimac 3 83 and the Genomes Phase 3 reference panel. Individuals from the cohort and reference panel were then separated and exported as harmonized sample and reference panel VCFs to be fed into RFMix All reference populations were taken from 1KGP phase 3 data We used the HapMap b37 recombination map 86 to inform switches.

The -n 5 flag terminal node size for random forest trees was included to account for an unequal number of reference individuals per reference population. We additionally used the --reanalyze-reference flag, which recalculates admixture in the reference samples for improved ability to distinguish ancestries.

Local ancestry of genome-wide significant variants : Haplotypes of the genomic regions around genome-wide significant associations were aligned to the local ancestry calls according to genomic position. To compare MAF of top hits on different ancestral backgrounds within a specific admixed population AFA or AMA , subjects were grouped according to the number of copies 1 or 2 of a specific ancestry European, African, and Native American, respectively at that position.

Finally, to compare if effects of the minor allele depend on a specific ancestral background European, African, and Native American , for each SNP, we coded variables that counted the number of copies of the minor allele per ancestral background.

Annotations are based on human genome assembly GRCh37 hg FUMA was used with default settings unless stated otherwise. Chromatin interaction mapping was performed using built-in chromatin interaction data from the dorsolateral prefrontal cortex, hippocampus and neuronal progenitor cell line. SNPs were mapped to 18, protein-coding genes. To test if tissue-specific gene expression was associated with PTSD, gene-set-based analysis was also used with expression data from GTEx v7 RNA-seq and BrainSpan RNA-seq, where the expression of genes within specific tissues were used to define the gene properties used in the gene-set analysis model.

All experiments were run in duplicates. T1 images were processed in Freesurfer version 5. Regional volumes that were visually confirmed to contain a segmentation error were discarded. Startle data were collected by recording the eyeblink muscle contraction using the electromyography EMG module of the Biopac system. A common ground electrode was placed on the palm.

Impedance levels were less than 6 kilo-ohms for each participant. PRS prediction plots were based on quintiles of PRS, with odds ratios calculated in reference to the lowest quintile. P -values for PRS were derived from a likelihood ratio test comparing the two models. Summary statistics for PTSD studies were restricted to the EUA meta-analysis, including UKB subjects 23, cases, , controls and significance was evaluated based on a conservative Bonferroni correction for phenotypes i.

Due to substantial overlap with other traits, two education, four anthropometric and two cancer phenotypes were omitted. Publicly available summary statistics were supplied as program inputs: Bipolar cases vs.

All other data that support the findings of this study are available from the corresponding authors upon request. Ben Barnes, J. The structure of co-occurring PTSD and depression symptoms in a cohort of Marines pre- and post-deployment.

Psychiatry Res. Koenen, K. Post-traumatic stress disorder and cardiometabolic disease: improving causal inference to inform practice. Pollard, H. Howlett, J. Prevention of trauma and stressor-related disorders: a review. Neuropsychopharmacology 41 , — Shalev, A. Post-traumatic stress disorder. Kremen, W. Twin studies of posttraumatic stress disorder: differentiating vulnerability factors from sequelae.

Neuropharmacology 62 , — Wolf, E. A classical twin study of PTSD symptoms and resilience: evidence for a single spectrum of vulnerability to traumatic stress. Nievergelt, C. Genomic approaches to posttraumatic stress disorder: the psychiatric genomic consortium initiative. Psychiatry 83 , — Gelernter, J. Duncan, L. Interventions yielded positive effects across populations and in all the domains studied.

Turn recording back on. National Center for Biotechnology Information , U. Search term. Sexual health interventions: a meta-analysis Review published: Similar articles in PubMed. Review A systematic review of sexual health interventions for adults: narrative evidence.

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sex meta

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we meeta you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Help us improve our products. Sign up to take part. A Nature Research Journal.

The risk of posttraumatic stress disorder PTSD following trauma is heritable, but robust common variants have yet to be identified. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses.

Analyses stratified by sex implicate 3 additional loci in men. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations.

PTSD is frequently associated with the meta of comorbid mental disorders such as major depression 1 and other adverse health sequelae including type 2 diabetes and cardiovascular disease 23.

Given this high prevalence and impact, PTSD is a serious public health problem. An understanding of the biological mechanisms of risk for PTSD is therefore an important goal of research ultimately aimed at its prevention and mitigation 45. Exposure to traumatic stress ssex, meta definition, requisite for the development of PTSD, but individual susceptibility to PTSD conditioned on trauma exposure varies widely.

Twin studies over the past two decades provide persuasive evidence for at least some genetic influence on PTSD risk 67and the last decade has witnessed the meta of a concerted effort to detect specific genetic susceptibility variants for PTSD 89. With this limited sample size, no individual variants exceeded genome-wide significance; however, significant estimates of SNP heritability and genetic correlations between PTSD and other mental disorders such as schizophrenia were demonstrated for the first time.

Sex is apparent from previous PGC work on other mental disorders that sample size is paramount for GWAS to discern common genome-wide significant variants of small effect that are replicable Subsequent to the publication of data from the first freeze 10the PGC-PTSD has continued to acquire additional PTSD cases and controls through partnerships with an expanding network of investigators, such that we now have accrued sex sample size that has enabled us to turn the corner on genome-wide risk discovery.

Presented here are the results of our latest GWA studies that include over 23, European and over African ancestry PTSD cases, now involving a total trans-ethnic sample of overindividuals. In achieving this sample size, we identify sex- and ancestry-specific findings. GWAS and gene-based analyses across our cohorts indicate genome-wide significant associations, involving genes related to dopamine and immune pathways.

We show high genetic correlations between PTSD and related psychiatric disorders such as major depressive disorder, but meya evidence that some of the identified loci are likely specific to PTSD.

First ancestry groups were consistently defined across studies Supplementary Fig. Given the previously observed differences between male and female heritability estimates in PGC-PTSD Freeze 1 10we also performed sex-stratified analyses. Quantile-quantile plots showed low inflation across analyses Supplementary Fig. A comparison of heritability estimates in subsets of PGC2 studies stratified by sex, ancestry, and characteristics of study i. This is with the notable exception of PGC1.

As numerous small studies contribute to PGC1. Subsetting PGC1. Next, focusing on PGC1. Sex-stratified analyses for women were not significant Supplementary Fig. Regional plots of the six genomic regions can be found in Supplementary Figs.

The six leading markers show odds ratios of 1. This is supported by PM-plots posterior probability that a SNP effect exists in a given study showing a high consistency of effects among the studies predicted to have an effect 13 Supplementary Figs.

No evidence of replication was found by directly comparing the six leading markers, nor by investigating the larger genomic regions harboring the signal Supplementary Figs. Gene-based analyses in AFA did not result in genome-wide significant loci.

We show evidence that the African-ancestry-specific SNP rs seems to capture a genomic region that may influence the expression of non-coding RNAs from this PTSD risk locus in response to increased glucocorticoid receptor signaling, thus linking this African-specific genetic variant to stress response and non-coding RNA expression Supplementary Fig.

PRS generated from well-powered GWAS have recently become a tool of high relevance for polygenic disorders and traits e. Analyses include only subjects of European ancestry.

Analysis of shared heritability across common disorders metq the brain 17 and specific genetic correlations of psychiatric disorders with cognitive, anthropomorphic and behavioural measures 10181920 has been facilitated greatly by the development of a centralized database of GWAS results including a web interface for LDSC LD Hub Genetic variation associated with PTSD was positively correlated with PRS from other psychiatric traits including depressive symptoms, schizophrenia and neuroticism, as well as epidemiologically comorbid traits such as insomnia, smoking behavior, asthma, hip-waist ratio and coronary artery disease.

Significant positive correlations were also found for reproductive traits such as the number of children ever born, and, as previously reported for women 22PTSD was negatively correlated with age at first birth. Only traits with at least one significant correlation with the 5 psychiatric disorders are shown.

Solid points indicate significant correlation after Bonferroni correction. These findings are not surprising, as pleiotropic effects i.

SNPs impacting multiple traits have been widely reported for psychiatric disorders. In sex to test ssx what degree genome-wide significant findings from our GWAS meta-analyses were specific metaa PTSD rather than driven by correlated traits as identified above, we adjusted the top hits from our analyses for the effects of genetically correlated psychiatric traits.

These findings indicate that the genetic variants identified here are specific to Meta when tested in the context of the three psychiatric disorders genetically most significantly correlated with PTSD.

PTSD is a common and debilitating condition influenced by genetic factors, yet common genetic risk variants for PTSD have not been robustly identified. These results show this is also true of PTSD. This increased power has led us to draw neta major conclusions.

First, our genetic findings squarely place PTSD among the other psychiatric disorders in terms of heritability and genetic relationship with other disorders. While this statement may seem obvious to some, there remains debate about whether PTSD is entirely a social construction We found substantial SNP-based heritability i. The heritability results and pattern of genetic correlations are also consistent with our initial findings 10 and with those from twin studies.

PTSD shares common variant risk with other psychiatric disorders, which show substantial sharing of common variant risk with one another PTSD was most significantly genetically correlated with major depression, but also with schizophrenia, both of which have genome-wide significant loci implicated msta brain function. These loci pointed to a number of different target genes that merit further investigation. The dopaminergic system has a critical role in fear conditioning which is important in the development and maintenance of PTSD Finally, the HLA-B complex may be related through the known role of meta and inflammation in stress-related disorders 42 However, preliminary sex from our group mwta imaging and psychophysiology highlights the value of deep phenotyping in conducting functional investigations into the meaning of GWAS findings 8.

Extensive follow-up meta is needed to replicate our findings and to determine the function of identified ,eta and their relationship to putative pathological processes.

For example, in SCZ the MHC locus is now thought to influence risk, in part, through pruning of synapses using immune machinery rather than through classical immune pathways Third, our results also illustrate that there may be genetic contributions to seex well-documented sex between PTSD and dysregulation in inflammatory and immune processes It has been widely recognized that PTSD is associated with a broad range of adverse physical health conditions over the life course ranging from typediabetes and cardiovascular disease to dementia and rheumatoid arthritis 46 Less is known about the biological mechanisms driving the relationship between PTSD and these outcomes.

Our genetic correlation analyses may provide some initial clues for mets investigation. Our subsequent gene-set and pathway analyses provide some clues further implicating the immune system. Of note, these genetic results converge with evidence from epidemiologic cohort sex documenting the role of stress-related disorders such as PTSD in autoimmune diseases 48case-control studies showing elevations of immune-related biomarkers in women with PTSD 49and epigenetic studies pointing to the role of the immune system in PTSD etiology 50 Further sx is needed to sex whether PTSD has genetic overlap with immune disorders broadly and the causal direction between disorders.

At minimum, the emerging genetic evidence presented here suggests that association between PTSD and health conditions may, in some cases, have some genetic origin. Fourth, PGC-PTSD is distinct in relation to current genomics consortia due to its high proportion of data from participants of diverse ancestries.

For example, a recent review found that only three percent of all samples in genetic studies were from African ancestry Our GWAS in subjects of African ancestry indicated at least one ancestry-specific locus using local ancestry methods developed for this analysis. We note the sample size in the AFA analysis has only about 15, participants, meta is small and under-powered, increasing the chance for false positives.

However, other work has shown that genetic studies of underrepresented populations afford the opportunity to discover novel loci that are invariant in European populations As others have noted, there are major limitations in our knowledge of the genetic and environmental risk architecture of psychiatric disorders in persons of African descent Our findings provide further evidence of the need mea invest in research metq includes diverse ancestral populations, to expand reference data, and to continue to develop methods to analyze data from such populations.

Until such an investment is made, we are limited in our ability to understand biological mechanisms, predict genetic risk 55and produce optimal treatments for non-European populations. African genomes are characterized by shorter haplotype blocks and contain many millions more variants per sec than mtea outside Africa Further, including data from African populations in genetic studies of PTSD and other neuropsychiatric disorders mmeta accelerate genetic discovery and could be useful for fine mapping disease causing alleles Fifth, although PTSD heritability remained relatively stable across methods, studies, and ancestries, sex differences in heritability were observed in the overall sex analyses as well as in the AFA analyses It is of note that the sex differences in heritability were not evident in the UK Biobank data, which we hypothesize is due to differences between the PGC1.

PTSD is conditional on trauma exposure, which is also highly heterogeneous across individuals meta populations Unlike PGC1. In contrast, a substantial proportion of men in the PGC1. The environmental experiences e. In future work, we aim to investigate this empirically by pooling detailed trauma and PTSD phenotypic information on both males and females sfx by modeling the effects of measurement variability on heritability estimates. Future work could also aim to increase samples of civilian men and military women meta allow for analyses stratified by military trauma and sex.

Lastly, we report a significant polygenic risk score for PTSD, which also significantly predicts re-experiencing symptoms in independent data from the MVP 9.

However, larger sample sizes are needed to achieve sensitivity and specificity at levels of clinical utility In the future, polygenic risk may eventually be useful in algorithms developed to identify vulnerable persons after exposure to trauma.

PTSD is one of the most theoretically preventable mental disorders, as many people exposed to trauma come to clinical attention in first response settings such as emergency rooms, intensive care units, and trauma centers. Controlled clinical trials show that PTSD risk can be significantly reduced by early preventive interventions 59 However, these interventions have nontrivial costs, making it infeasible to offer sexx to all persons exposed to trauma, given that only a small minority goes on to develop PTSD 61 They mefa also unnecessary for many survivors who recover spontaneously To be cost-effective, sex prediction rules are needed to identify which exposed persons are at high risk of PTSD.

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In the second of two companion papers, we conducted a meta-analysis of sexual health interventions in three domains. The interventions chosen for the. Couples' Sexual Communication and Dimensions of Sexual Function: A Meta-​Analysis. Mallory AB(1)(2), Stanton AM(3), Handy AB(3).

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