A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases
Abstract Experiencing a traumatic event may lead to Posttraumatic Stress Disorder (PTSD), including symptoms such as flashbacks and hyperarousal. Individuals suffering from PTSD are at increased risk of cardiovascular disease (CVD), but it is unclear why. This study assesses shared genetic liability...
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2025-01-01
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| Series: | Translational Psychiatry |
| Online Access: | https://doi.org/10.1038/s41398-024-03197-z |
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| author | Eva Lukas Rada R. Veeneman Dirk J. A. Smit Tarunveer S. Ahluwalia Jentien M. Vermeulen Gita A. Pathak Renato Polimanti Karin J. H. Verweij Jorien L. Treur |
| author_facet | Eva Lukas Rada R. Veeneman Dirk J. A. Smit Tarunveer S. Ahluwalia Jentien M. Vermeulen Gita A. Pathak Renato Polimanti Karin J. H. Verweij Jorien L. Treur |
| author_sort | Eva Lukas |
| collection | DOAJ |
| description | Abstract Experiencing a traumatic event may lead to Posttraumatic Stress Disorder (PTSD), including symptoms such as flashbacks and hyperarousal. Individuals suffering from PTSD are at increased risk of cardiovascular disease (CVD), but it is unclear why. This study assesses shared genetic liability and potential causal pathways between PTSD and CVD. We leveraged summary-level data of genome-wide association studies (PTSD: N = 1,222,882; atrial fibrillation (AF): N = 482,409; coronary artery disease (CAD): N = 1,165,690; hypertension (HT): N = 458,554; heart failure (HF): N = 977,323). First, we estimated genetic correlations and utilized genomic structural equation modeling to identify a common genetic factor for PTSD and CVD. Next, we assessed biological, behavioural, and psychosocial factors as potential mediators. Finally, we employed multivariable Mendelian randomization to examine causal pathways between PTSD and CVD, incorporating the same potential mediators. Significant genetic correlations were found between PTSD and CAD, HT, and HF (r g = 0.21-0.32, p ≤ 3.08 · 10−16), but not between PTSD and AF. Insomnia, smoking, alcohol dependence, waist-to-hip ratio, and inflammation (IL6, C-reactive protein) partly mediated these associations. Mendelian randomization indicated that PTSD causally increases CAD (IVW OR = 1.53, 95% CIs = 1.19-1.96, p = 0.001), HF (OR = 1.44, CIs = 1.08-1.92, p = 0.012), and to a lesser degree HT (OR = 1.25, CIs = 1.05-1.49, p = 0.012). While insomnia, smoking, alcohol, and inflammation were important mediators, independent causal effects also remained. In addition to shared genetic liability between PTSD and CVD, we present strong evidence for causal effects of PTSD on CVD. Crucially, we implicate specific lifestyle and biological mediators (insomnia, substance use, inflammation) which has important implications for interventions to prevent CVD in PTSD patients. |
| format | Article |
| id | doaj-art-52f85f0670e1436b8666e4aa52b206f6 |
| institution | Kabale University |
| issn | 2158-3188 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Translational Psychiatry |
| spelling | doaj-art-52f85f0670e1436b8666e4aa52b206f62025-01-05T12:47:16ZengNature Publishing GroupTranslational Psychiatry2158-31882025-01-0115111110.1038/s41398-024-03197-zA genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseasesEva Lukas0Rada R. Veeneman1Dirk J. A. Smit2Tarunveer S. Ahluwalia3Jentien M. Vermeulen4Gita A. Pathak5Renato Polimanti6Karin J. H. Verweij7Jorien L. Treur8Genetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of AmsterdamGenetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of AmsterdamGenetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of AmsterdamSteno Diabetes Center CopenhagenDepartment of Psychiatry, Amsterdam UMC, University of AmsterdamDepartment of Psychiatry, Yale University School of Medicine, 60 Temple, Suite 7ADepartment of Psychiatry, Yale University School of Medicine, 60 Temple, Suite 7AGenetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of AmsterdamGenetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of AmsterdamAbstract Experiencing a traumatic event may lead to Posttraumatic Stress Disorder (PTSD), including symptoms such as flashbacks and hyperarousal. Individuals suffering from PTSD are at increased risk of cardiovascular disease (CVD), but it is unclear why. This study assesses shared genetic liability and potential causal pathways between PTSD and CVD. We leveraged summary-level data of genome-wide association studies (PTSD: N = 1,222,882; atrial fibrillation (AF): N = 482,409; coronary artery disease (CAD): N = 1,165,690; hypertension (HT): N = 458,554; heart failure (HF): N = 977,323). First, we estimated genetic correlations and utilized genomic structural equation modeling to identify a common genetic factor for PTSD and CVD. Next, we assessed biological, behavioural, and psychosocial factors as potential mediators. Finally, we employed multivariable Mendelian randomization to examine causal pathways between PTSD and CVD, incorporating the same potential mediators. Significant genetic correlations were found between PTSD and CAD, HT, and HF (r g = 0.21-0.32, p ≤ 3.08 · 10−16), but not between PTSD and AF. Insomnia, smoking, alcohol dependence, waist-to-hip ratio, and inflammation (IL6, C-reactive protein) partly mediated these associations. Mendelian randomization indicated that PTSD causally increases CAD (IVW OR = 1.53, 95% CIs = 1.19-1.96, p = 0.001), HF (OR = 1.44, CIs = 1.08-1.92, p = 0.012), and to a lesser degree HT (OR = 1.25, CIs = 1.05-1.49, p = 0.012). While insomnia, smoking, alcohol, and inflammation were important mediators, independent causal effects also remained. In addition to shared genetic liability between PTSD and CVD, we present strong evidence for causal effects of PTSD on CVD. Crucially, we implicate specific lifestyle and biological mediators (insomnia, substance use, inflammation) which has important implications for interventions to prevent CVD in PTSD patients.https://doi.org/10.1038/s41398-024-03197-z |
| spellingShingle | Eva Lukas Rada R. Veeneman Dirk J. A. Smit Tarunveer S. Ahluwalia Jentien M. Vermeulen Gita A. Pathak Renato Polimanti Karin J. H. Verweij Jorien L. Treur A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases Translational Psychiatry |
| title | A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| title_full | A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| title_fullStr | A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| title_full_unstemmed | A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| title_short | A genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| title_sort | genetic exploration of the relationship between posttraumatic stress disorder and cardiovascular diseases |
| url | https://doi.org/10.1038/s41398-024-03197-z |
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