Assessing the causal effects of type 2 diabetes and obesity-related traits on COVID-19 severity DOI Creative Commons

Ji-Eun Seo,

Gaeun Kim, Seunghwan Park

et al.

Human Genomics, Journal Year: 2025, Volume and Issue: 19(1)

Published: April 22, 2025

Type 2 diabetes (T2D) and obesity-related traits are highly comorbid with coronavirus disease 2019 (COVID-19), but their causal relationships severity remain unclear. While recent Mendelian randomization (MR) studies suggest a link between COVID-19 severity, findings regarding T2D inconsistent, particularly when adjusting for body mass index (BMI). This study aims to clarify these relationships. We applied various MR methods assess the effects of BMI-adjusted (T2DadjBMI) (BMI, waist circumference, waist-hip ratio) on severity. Genetic instruments were obtained from large-scale genome-wide association (GWAS), including 898K participants 2M To address potential bias sample overlap, we conducted simulations comparing results overlapping independent samples. Our analysis identified significant relationship T2DadjBMI increased (OR = 1.057, 95% CI 1.012-1.105). Obesity-related also causally associated Simulations confirmed that remained robust demonstrating consistency datasets. These highlight role in emphasizing need targeted prevention management strategies high-risk populations. The robustness our analysis, even presence strengthens reliability inferences.

Language: Английский

Unraveling the genetic links between depression and type 2 diabetes DOI
Ancha Baranova, Dongming Liu,

Vikas Chandhoke

et al.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Journal Year: 2025, Volume and Issue: 137, P. 111258 - 111258

Published: Jan. 19, 2025

Language: Английский

Citations

4
Causal effects of COVID‐19 on cancer risk: A Mendelian randomization study DOI Creative Commons
Jia Li,

Haocheng Bai,

Qiao Hao

et al.

Journal of Medical Virology, Journal Year: 2023, Volume and Issue: 95(4)

Published: April 1, 2023

Abstract In contemporary literature, little attention has been paid to the association between coronavirus disease‐2019 (COVID‐19) and cancer risk. We performed Mendelian randomization (MR) investigate causal associations three types of COVID‐19 exposures (critically ill COVID‐19, hospitalized respiratory syndrome 2 (SARS‐CoV‐2) infection) 33 different cancers European population. The results inverse‐variance‐weighted model indicated that genetic liabilities critically had suggestive with increased risk for HER2‐positive breast (odds ratio [OR] = 1.0924; p ‐value 0.0116), esophageal (OR 1.0004; 0.0226), colorectal 1.0010; 0.0242), stomach 1.2394; 0.0331), colon 1.0006; 0.0453). 1.1096; 0.0458), 1.0005; 0.0440) as well 1.3043; 0.0476). SARS‐CoV‐2 infection 2.8563; 0.0019) but decreasing head neck 0.9986, 0.0426). above combinations were robust through test heterogeneity pleiotropy. Together, our study effects on

Language: Английский

Citations

29
Shared genetics and bidirectional causal relationships between type 2 diabetes and attention-deficit/hyperactivity disorder DOI Creative Commons
Ancha Baranova,

Vikas Chandhoke,

Hongbao Cao

et al.

General Psychiatry, Journal Year: 2023, Volume and Issue: 36(2), P. e100996 - e100996

Published: March 1, 2023

Type 2 diabetes (T2D) is a chronic metabolic disorder with high comorbidity mental disorders. The genetic links between attention-deficit/hyperactivity (ADHD) and T2D have yet to be elucidated.We aim assess shared genetics potential associations ADHD T2D.We performed correlation, two-sample Mendelian randomisation polygenic overlap analyses T2D. genome-wide association study (GWAS) summary results of (80 154 cases 853 816 controls), ADHD2019 (20 183 35 191 controls from the 2019 GWAS dataset) ADHD2022 (38 691 275 986 2022 were used for analyses. dataset was obtained DIAGRAM Consortium. datasets Psychiatric Genomics We compared signals reveal variation using larger dataset. Moreover, molecular pathways constructed based on large-scale literature data understand connection T2D.T2D has positive correlations (rg=0.33) (rg=0.31). Genetic liability associated an increased risk (odds ratio (OR): 1.30, p<0.001), while had suggestive causal effect (OR: p=0.086). higher 1.05, p=0.001) 1.03, p<0.001). analysis showed that most variants are ADHD2022. three overlapping loci. Molecular pathway suggests could promote each other through inflammatory pathways.Our demonstrates substantial bidirectional

Language: Английский

Citations

28
Causal associations between major depressive disorder and COVID-19 DOI Creative Commons
Ancha Baranova, Yi Zhao, Hongbao Cao

et al.

General Psychiatry, Journal Year: 2023, Volume and Issue: 36(2), P. e101006 - e101006

Published: April 1, 2023

We aimed to evaluate whether major depressive disorder (MDD) could aggravate the outcomes of coronavirus disease 2019 (COVID-19) or genetic liability COVID-19 trigger MDD.We assess bidirectional causal associations between MDD and COVID-19.We performed correlation Mendelian randomisation (MR) analyses potential three outcomes. Literature-based network analysis was conducted construct molecular pathways connecting found that has positive correlations with (rg: 0.10-0.15). Our MR indicated is associated increased risks infection (odds ratio (OR)=1.05, 95% confidence interval (CI): 1.00 1.10, p=0.039). However, did not confer any effects on MDD. Pathway identified a panel immunity-related genes may mediate links COVID-19.Our study suggests increase susceptibility COVID-19. findings emphasise need social support improve mental health intervention networks for people mood disorders during pandemic.

Language: Английский

Citations

27
Causal associations and shared genetics between hypertension and COVID‐19 DOI
Ancha Baranova, Hongbao Cao, Fuquan Zhang

et al.

Journal of Medical Virology, Journal Year: 2023, Volume and Issue: 95(4)

Published: March 23, 2023

To evaluate the genetic relationship between hypertension and COVID-19 explore molecular pathways linking to COVID-19. We performed correlation Mendelian randomization (MR) analyses assess potential associations hospitalized compared genome-wide association signals reveal shared variation Moreover, hypertension-driven were constructed based on large-scale literature data understand influence of at level. Hypertension has a positive with (rg = 0.19). The MR indicate that liability confers causal effect (odds ratio [OR]: 1.05, confidence interval [CI]: 1.00-1.09, p 0.030). have three overlapping loci share eight protein-coding risk genes, including ABO, CSF2, FUT2, IZUMO1, MAMSTR, NPNT, RASIP1, WNT3. Molecular pathway analysis suggests may promote development through induction inflammatory pathways. Our study genetically determined increase for severe connecting underline links

Language: Английский

Citations

20
Evaluating the effects of circulating inflammatory proteins as drivers and therapeutic targets for severe COVID-19 DOI Creative Commons
Ancha Baranova,

Jing Luo,

Li Fu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 22, 2024

Objective The relationships between circulating inflammatory proteins and COVID-19 have been observed in previous cohorts. However, it is not unclear which may boost the risk of or protect against COVID-19. Methods We performed Mendelian randomization (MR) analysis using GWAS summary result 91 inflammation-related (N = 14,824) to assess their causal impact on severe phenotypes encompassed both hospitalized 2,095,324) critical 1,086,211). Moreover, sensitivity analyses were conducted evaluate robustness reliability. Results found that seven confer positive effects Among them, serum levels IL-10RB, FGF-19, CCL-2 positively contributed conditions (OR: 1.10~1.16), while other 4 conferred only 1.07~1.16), including EIF4EBP1, IL-7, NTF3, LIF. Meanwhile, five exert protective hospitalization progression 0.85~0.95), CXCL11, CDCP1, CCL4/MIP, IFNG, LIFR. Sensitivity did support presence heterogeneity majority MR analyses. Conclusions Our study revealed for COVID-19, vital implications treatment disease.

Language: Английский

Citations

8
COVID-19 is associated with changes in brain function and structure: a multimodal meta-analysis of neuroimaging studies DOI
Zixuan Guo, Shilin Sun,

Shu Xiao

et al.

Neuroscience & Biobehavioral Reviews, Journal Year: 2024, Volume and Issue: 164, P. 105792 - 105792

Published: July 3, 2024

Language: Английский

Citations

8
Metformin Alters mRNA Expression of FOXP3, RORC, and TBX21 and Modulates Gut Microbiota in COVID-19 Patients with Type 2 Diabetes DOI Creative Commons
Pavlo Petakh, Iryna Kamyshna, Valentyn Oksenych

et al.

Viruses, Journal Year: 2024, Volume and Issue: 16(2), P. 281 - 281

Published: Feb. 11, 2024

COVID-19 remains a significant global concern, particularly for individuals with type 2 diabetes who face an elevated risk of hospitalization and mortality. Metformin, primary treatment diabetes, demonstrates promising pleiotropic properties that may substantially mitigate disease severity expedite recovery. Our study the gut microbiota mRNA expression pro-inflammatory anti-inflammatory T-lymphocyte subpopulations showed metformin increases bacterial diversity while modulating gene related to T-lymphocytes. This found people did not take had downregulated FOXP3 by 6.62-fold, upregulated RORC 29.0-fold, TBX21 1.78-fold, compared control group. On other hand, patients 1.96-fold upregulation in group, along 1.84-fold downregulation 11.4-fold expression. Additionally, we correlation (F/B ratio alpha-diversity index) biomarkers. novel observation metformin’s impact on T-cells opens new horizons further exploration through clinical trials validate confirm our data. The potential modulate immune responses enhance suggests avenue therapeutic interventions facing increased severe outcomes from COVID-19.

Language: Английский

Citations

7
Shared genetics and causal associations between COVID‐19 and multiple sclerosis DOI
Ancha Baranova, Hongbao Cao, Shaolei Teng

et al.

Journal of Medical Virology, Journal Year: 2022, Volume and Issue: 95(1)

Published: Dec. 26, 2022

Neuroinflammation caused by COVID-19 negatively impacts brain metabolism and function, while pre-existing pathology may contribute to individuals' vulnerability the adverse consequences of COVID-19. We used summary statistics from genome-wide association studies (GWAS) perform Mendelian randomization (MR) analyses, thus assessing potential associations between multiple sclerosis (MS) two outcomes (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] infection hospitalization). Genome-wide risk genes were compared GWAS datasets on hospitalized MS. Literature-based analysis was conducted construct molecular pathways connecting MS found that genetic liability confers a causal effect (odd ratio [OR]: 1.09, 95% confidence interval: 1.03-1.16) but not SARS-CoV-2 (1.03, 1.00-1.05). Genetic (1.15, 1.02-1.30). Hospitalized share five within loci, including TNFAIP8, HSD17B4, CDC37, PDE4A, KEAP1. Pathway identified panel immunity-related mediate links Our study suggests associated with 9% increased for hospitalization, 15% Immunity-related underlie link

Language: Английский

Citations

25
Causal associations and genetic overlap between COVID-19 and intelligence DOI Creative Commons
Hongbao Cao, Ancha Baranova, Yuqing Song

et al.

QJM, Journal Year: 2023, Volume and Issue: 116(9), P. 766 - 773

Published: June 7, 2023

COVID-19 might cause neuroinflammation in the brain, which could decrease neurocognitive function. We aimed to evaluate causal associations and genetic overlap between intelligence.We performed Mendelian randomization (MR) analyses assess potential three outcomes intelligence (N = 269 867). The COVID phenotypes included severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection 501 486), hospitalized 1 965 329) critical 743 167). Genome-wide risk genes were compared genome-wide association study (GWAS) datasets on intelligence. In addition, functional pathways constructed explore molecular connections intelligence.The MR indicated that liabilities SARS-CoV-2 (odds ratio [OR]: 0.965, 95% confidence interval [CI]: 0.939-0.993) (OR: 0.989, CI: 0.979-0.999) confer effects There was suggestive evidence supporting effect of 0.988, 0.972-1.003). Hospitalized share 10 within genomic loci, including MAPT WNT3. Enrichment analysis showed these are functionally connected distinct subnetworks 30 linked cognitive decline. pathway revealed COVID-19-driven pathological changes brain multiple peripheral systems may lead impairment.Our suggests exert a detrimental tau protein Wnt signaling mediate influence

Language: Английский

Citations

14