Dataset Information

Mood swings are causally associated with intracranial aneurysm subarachnoid hemorrhage: A Mendelian randomization study.

ABSTRACT:

Background

Mood swings have been observed in patients with intracranial aneurysm (IA), but it is still unknown whether mood swings can affect IA.

Aim

To explore the causal association between mood swings or experiencing mood swings and IA through a two-sample Mendelian randomization (MR) study.

Methods

Summary-level statistics of mood swings, experiencing mood swings, IA, aneurysm-associated subarachnoid hemorrhage (aSAH), and non-ruptured IA (uIA) were collected from the genome-wide association study. Two-sample MR and various sensitivity analyses were employed to explore the causal association between mood swings or experiencing mood swings and IA, or aSAH, or uIA. The inverse-variance weighted method was used as the primary method.

Results

Genetically determined mood swings (odds ratio [OR] = 5.23, 95% confidence interval (95%CI): 1.65-16.64, p = .005) and experiencing mood swings (OR = 2.50, 95%CI: 1.37-4.57, p = .003) were causally associated with an increased risk of IA. Mood swings (OR = 5.67, 95%CI: 1.40-23.04, p = .015) and experiencing mood swings were causally associated with the risk of aSAH (OR = 2.91, 95%CI: 1.47-5.75, p = .002). Neither mood swings (OR = 1.95, 95%CI: .31-12.29, p = .478) nor experiencing mood swings (OR = 1.20, 95%CI: .48-3.03, p = .693) were associated with uIA.

Conclusions

Mood swings and experiencing mood swings increased the risk of IA and aSAH incidence. These results suggest that alleviating mood swings may reduce IA rupture incidence and aSAH incidence.

SUBMITTER: Peng K

PROVIDER: S-EPMC10636415 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature

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Publications

Mood swings are causally associated with intracranial aneurysm subarachnoid hemorrhage: A Mendelian randomization study.

Peng Kang K Li Yanwen Y Adegboro Abraham Ayodeji AA Wanggou Siyi S Li Xuejun X

Brain and behavior 20230825 11

<h4>Background</h4>Mood swings have been observed in patients with intracranial aneurysm (IA), but it is still unknown whether mood swings can affect IA.<h4>Aim</h4>To explore the causal association between mood swings or experiencing mood swings and IA through a two-sample Mendelian randomization (MR) study.<h4>Methods</h4>Summary-level statistics of mood swings, experiencing mood swings, IA, aneurysm-associated subarachnoid hemorrhage (aSAH), and non-ruptured IA (uIA) were collected from the g ...[more]

PMID: 37632147

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Project description:IntroductionObservational studies suggest that different classes of antihypertensive drugs may have different effects on the occurrence of intracranial aneurysms (IA) and subarachnoid hemorrhage (SAH). However, the reported results in previous studies are inconsistent, and randomized data are absent. We performed a two-sample Mendelian randomization (MR) analysis to study the causal effects of genetically determined blood pressure (BP) and genetic proxies for antihypertensive drug classes on the risk of IA and SAH.Materials and methodsGenetic instruments and outcome data were obtained from independent genome-wide association studies (GWAS) or published data, which were exclusively restricted to European ancestry. Causal relationships were identified using inverse-variance weighted MR analyses and a series of statistical sensitivity analyses. The FinnGen consortium was used for repeated analysis to verify results obtained from the above GWAS.ResultsTwo-sample MR analysis showed that genetically determined Systolic BP, Dystolic BP, and Pulse Pressure were related to a higher risk of IA and SAH. Based on identified single nucleotide polymorphisms (SNPs) that influence the effect of calcium channel blockers (CCB, 42 SNPs), beta-blockers (BB, 8 SNPs), angiotensin-converting enzyme inhibitors (ACEI, 2 SNPs), angiotensin receptor blockers (ARB, 1 SNPs), and thiazides (5 SNPs), genetically determined effect of CCBs was associated with a higher risk of IA (OR, 1.07 [95% CI, 1.03-1.10], p = 5.02 × 10-5) and SAH (OR, 1.06 [95% CI, 1.03-1.09], p = 1.84 × 10-3). No associations were found between other antihypertensive drugs and the risk of IA or SAH. The effect of CCBs on SAH was confirmed in FinnGenconsortium samples (OR, 1.04 [95% CI, 1.00-1.08], p = 0.042).Discussion and conclusionThis MR analysis supports the role of elevated blood pressure in the occurrence of intracranial aneurysms and subarachnoid hemorrhage. However, genetic proxies for calcium channel blockers were associated with an increased risk of intracranial aneurysms and subarachnoid hemorrhage. Further studies are required to confirm these findings and investigate the underlying mechanisms.

Project description:Recent studies have explored the impact of personality traits, including mood swings, on physical health. However, it remains unclear whether there is a direct cause-and-effect link between mood swings and cardiovascular diseases (CVDs). A STROBE-compliant cross-sectional observational study was conducted and analyzed using a two-sample Mendelian randomization (MR) approach to examine the potential causal relationship between mood swings and a range of CVDs, such as arrhythmia, artery aneurysm, coronary heart disease (CHD), heart failure, hypertension, stroke, ischemic stroke, and peripheral artery disease. We sourced genome-wide association studies (GWAS) summary data for mood swings from the UK Biobank, and for CVDs from the GWAS Catalog and FinnGen databases. We excluded single-nucleotide polymorphisms (SNPs) linked to potential confounders such as obesity, smoking, sex, diabetes, as well as SNPs suspected of horizontal pleiotropy, as identified by MR-PRESSO and the MR-pleiotropy method, prior to the final analysis. Sensitivity analyses were conducted using the MR-Egger, inverse variance weighted, and leave-one-out methods. After screening, 57 SNPs were identified as instrumental variables for mood swings, and 9 SNPs related to confounding factors were excluded. An increase in mood swing frequency is correlated with a significant increase in the likelihood of various conditions. Notably, arrhythmia in the FinnGen dataset showed an odds ratio (OR: 2.28, 95% confidence interval [CI]: 1.44-3.61, P < .001), and atrial fibrillation had an OR (OR: 2.25, 95% CI: 1.23-4.11, P = .01). CHD risk was elevated in both the IEU OpenGWAS project (OR: 2.05, 95% CI: 1.30-3.21, P < .001) and GWAS Catalog (OR: 4.45, 95% CI: 1.75-11.33, P < .001). Increased risks were also noted for heart failure (GWAS Catalog: OR: 1.75, 95% CI: 1.09-2.83, P = .02) and hypertension (FinnGen: OR, 2.17; 95% CI: 1.47-3.19, P < .001). However, no significant associations were found for conditions such as arterial aneurysms or ischemic stroke. In combined analyses, mood swings were associated with a higher risk of CHD (OR: 2.21, 95% CI: 1.64-2.97, P < .01), heart failure (OR: 1.74, 95% CI: 1.21-2.50, P < .01), and other CVDs. This study revealed a causal link between mood swings and various CVDs, highlighting intriguing findings. This suggests that implementing proper psychological interventions to stabilize mood may be beneficial for preventing negative cardiovascular events.

Project description:Ruptured intracranial aneurysm (IA)‑induced subarachnoid hemorrhage (SAH) triggers a series of immune responses and inflammation in the brain and body. The present study was conducted to identify additional circulating biomarkers that may serve as potential therapeutic targets for SAH‑induced inflammation. Differentially expressed (DE) long non‑coding RNAs (lncRNAs; DElncRNAs) and genes (DEGs) in the peripheral blood mononuclear cells between patients with IA rupture‑induced SAH and healthy controls were identified in the GSE36791 dataset. DEGs were used for weighted gene co‑expression network analysis (WGCNA), and SAH‑associated WGCNA modules were identified. Subsequently, an lncRNA‑mRNA regulatory network was constructed using the DEGs in SAH‑associated WGCNA modules. A total of 25 DElncRNAs and 1,979 DEGs were screened from patients with IA‑induced SAH in the GSE36791 dataset compared with the controls. A total of 11 WGCNA modules, including four upregulated modules significantly associated with IA rupture‑induced SAH were obtained. The DEGs in the SAH‑associated modules were associated with Gene Ontology biological processes such as 'regulation of programmed cell death', 'apoptosis' and 'immune response'. The subsequent lncRNA‑mRNA regulatory network included seven upregulated lncRNAs [HCG27, ZNFX1 antisense RNA 1, long intergenic non‑protein coding RNA (LINC)00265, murine retrovirus integration site 1 homolog‑antisense RNA 1, cytochrome P450 1B1‑AS1, LINC01347 and LINC02193] and 375 DEGs. Functional enrichment analysis and screening in the Comparative Toxicogenomics Database demonstrated that SAH‑associated DEGs, including neutrophil cytosolic factor (NCF)2 and NCF4, were enriched in 'chemokine signaling pathway' (hsa04062), 'leukocyte transendothelial migration' (hsa04670) and 'Fc gamma R‑mediated phagocytosis' (hsa04666). The upregulated lncRNAs and genes, including NCF2 and NCF4, in patients with IA rupture‑induced SAH indicated their respective potentials as anti‑inflammatory therapeutic targets.

Dataset Information

Mood swings are causally associated with intracranial aneurysm subarachnoid hemorrhage: A Mendelian randomization study.

Background

Aim

Methods

Results

Conclusions

Publications

Mood swings are causally associated with intracranial aneurysm subarachnoid hemorrhage: A Mendelian randomization study.

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