Dataset Information

Genetically Predicted Obesity Causally Increased the Risk of Hypertension Disorders in Pregnancy.

ABSTRACT:

Aims

This study aimed to evaluate the causal association between obesity and hypertension disorders in pregnancy.

Methods

Two-sample Mendelian randomization (MR) study was conducted based on the data obtained from the GIANT (n = 98,697 participants) consortium and FinnGen (n = 96,449 participants) consortium to determine the causal effect of obesity on the risk of hypertension disorders in pregnancy. Based on a genome-wide significance, 14 single-nucleotide polymorphisms (SNPs) associated with obesity-related databases were used as instrumental variables. The random-effects inverse-variance weighted (IVW) method was adopted as the main analysis with a supplemented sensitive analysis of the MR-Egger and weighted median approaches.

Results

All three MR methods showed that genetically predicted obesity causally increased the risk of hypertension disorders in pregnancy. IVW analysis provided obesity as a risk factor for hypertension disorders in pregnancy with an odds ratio (OR) of 1.39 [95% confidence interval (CI) 1.21-1.59; P = 2.46 × 10^-6]. Weighted median and MR Egger regression also showed directionally similar results [weighted median OR = 1.49 (95% CI, 1.24-1.79), P = 2.45 × 10^-5; MR-Egger OR = 1.95 (95% CI, 1.35-2.82), P = 3.84 × 10^-3]. No directional pleiotropic effects were found between obesity and hypertension disorders in pregnancy with both MR-Egger intercepts and funnel plots.

Conclusions

Our findings provided directed evidence that obesity was causally associated with a higher risk of hypertension disorders in pregnancy. Taking measures to reduce the proportion of obesity may help reduce the incidence of hypertension disorders in pregnancy.

SUBMITTER: Wang W

PROVIDER: S-EPMC9175023 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Publications

Genetically Predicted Obesity Causally Increased the Risk of Hypertension Disorders in Pregnancy.

Wang Wenting W Tan Jiang-Shan JS Hua Lu L Zhu Shengsong S Lin Hongyun H Wu Yan Y Liu Jinping J

Frontiers in cardiovascular medicine 20220525

<h4>Aims</h4>This study aimed to evaluate the causal association between obesity and hypertension disorders in pregnancy.<h4>Methods</h4>Two-sample Mendelian randomization (MR) study was conducted based on the data obtained from the GIANT (<i>n</i> = 98,697 participants) consortium and FinnGen (<i>n</i> = 96,449 participants) consortium to determine the causal effect of obesity on the risk of hypertension disorders in pregnancy. Based on a genome-wide significance, 14 single-nucleotide polymorph ...[more]

PMID: 35694671

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Project description:Background: It is not clarified whether the elevation of adiponectin is the results of kidney damage, or the cause of kidney function injury. To explore the causal association of adiponectin on estimated glomerular filtration rate (eGFR) and chronic kidney disease (CKD), this study was performed. Materials and methods: The genetic association of adiponectin were retrieved from one genome-wide association studies with 39,883 participants. The summary-level statistics regarding the eGFR (133,413 participants) and CKD (12,385 CKD cases and 104,780 controls) were retrieved from the CKDGen consortium in the European ancestry. Single-variable Mendelian randomization (MR), bilateral and multivariable MR analyses were used to verify the causal association between adiponectin, eGFR, and CKD. Results: Genetically predicted adiponectin reduces the risk of CKD (OR = 0.71, 95% CI = 0.57-0.89, p = 0.002) and increases the eGFR (β = 0.014, 95% CI = 0.001-0.026, p = 0.034) by the inverse variance weighting (IVW) estimator. These findings remain consistent in the sensitivity analyses. No heterogeneity and pleiotropy were detected in this study (P for MR-Egger 0.617, P for global test > 0.05, and P for Cochran's Q statistics = 0.617). The bilateral MR identified no causal association of CKD on adiponectin (OR = 1.01, 95% CI = 0.96-1.07, p = 0.658), nor did it support the association of eGFR on adiponectin (OR = 0.86, 95% CI = 0.68-1.09, p = 0.207) by the IVW estimator. All the sensitivity analyses reported similar findings (p > 0.05). Additionally, after adjusting for cigarette consumption, alcohol consumption, body mass index, low density lipoprotein, and total cholesterol, the ORs for CKD are 0.70 (95% CI = 0.55-0.90, p = 0.005), 0.75 (95% CI = 0.58-0.97, p = 0.027), 0.82 (95% CI = 0.68-0.99, p = 0.039), 0.74 (95% CI = 0.59-0.93, p = 0.011), and 0.79 (95% CI = 0.61-0.95, p = 0.018), respectively. Conclusion: Using genetic data, this study provides novel causal evidence that adiponectin can protect the kidney function and further reduce the risk of CKD.

Project description:Background The causal relationship between hypertension, antihypertensive drugs and the risk of erectile dysfunction is still uncertain. We performed a univariable and multivariable Mendelian randomization study to investigate whether they are causally related to erectile dysfunction. Methods Genetic variants associated with blood pressure were derived from the genome-wide association study meta-analysis of the UK Biobank and International Consortium of Blood Pressure (N = 757,601). Summary association data for hypertension were obtained from the UK Biobank (N = 463,010) and the FinnGen study (N = 356,077). The summary statistics of erectile dysfunction were obtained from the European ancestry with 223,805 subjects. The SNP instruments used to assess the effect of the protein targets of antihypertensive drugs on erectile dysfunction were obtained from previous studys. Causal effects were estimated using the univariate Mendelian randomization method (inverse variance weighted, MR-Egger, weighted median, MR-PRESSO and Wald ratios) and the multivariate Mendelian randomization method. Sensitivity analyses were implemented with the Cochran's Q-test, MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis. Results Univariate MR found that elevated diastolic blood pressure may increase the occurrence of erectile dysfunction (odds ratio [OR] = 1.012; 95% confidence interval [CI]: 1.000–1.024; P = 0.047). Genetically predicted hypertension is also associated with ED (For the FinnGen, OR = 1.106; 95% CI: 1.027–1.191; P = 0.008. For the UK Biobank, OR = 3.832; 95% CI: 1.410–10.414; P = 0.008). However, after adjusting for systolic blood pressure, diastolic blood pressure and hypertension using multivariate Mendelian randomization, only hypertension was causally associated with ED occurrence (For the FinnGen, OR = 1.103; 95% CI: 1.018–1.195; P = 0.017. For the UK Biobank, OR = 5.037; 95% CI: 1.601–15.846; P = 0.006). We found no evidence that the use of angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and thiazide diuretic increased the risk of erectile dysfunction. Conclusions Genetically predicted hypertension increases the risk of erectile dysfunction, but we found no causal relationship between elevated systolic/diastolic blood pressure and erectile dysfunction. We speculate that the relationship between elevated blood pressure and erectile dysfunction risk may be nonlinear. We found little evidence that antihypertensive drugs increase the risk of erectile dysfunction.

Dataset Information

Genetically Predicted Obesity Causally Increased the Risk of Hypertension Disorders in Pregnancy.

Aims

Methods

Results

Conclusions

Publications

Genetically Predicted Obesity Causally Increased the Risk of Hypertension Disorders in Pregnancy.

Similar Datasets

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