Nutrition, metabolism, and cardiovascular diseases : NMCD · 2025
Novel insights into the causal effects of triglycerides to high density lipoprotein cholesterol ratio on blood pressure.
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Wan Aihong, Han Yuqin, Wu Lingling, Wei Yuanhao, Xiang Xiqiao, Chen Yi, Chen Jinquan, Song Aihua, Zhao Kun
Аннотация
BACKGROUND AND AIMS: Previous studies have suggested links between the triglycerides to high-density lipoprotein cholesterol (TG:HDL-C) ratio on blood pressure (BP) traits and hypertension (HTN) risk. However, the causal relationships remain unclear.
METHODS AND RESULTS: We conducted genome-wide linkage disequilibrium score regression (LDSC), two-sample Mendelian randomization (MR), colocalization, reverse, and multivariable MR (MVMR) analyses to evaluate the causal relationships between the TG:HDL-C ratio and BP traits. BP traits (systolic BP [SBP], diastolic BP [DBP], and pulse pressure [PP]) were obtained from the International Consortium for Blood Pressure and UK Biobank. HTN data were from GWAS meta-analyses. The primary analysis used the inverse variance method (IVW), with sensitivity analyses for MR. Significant genetic correlations were found between the TG:HDL-C ratio and BP traits (all P values < 0.05). Genetically predicted TG:HDL-C ratio was associated with increased SBP (β = 1.194, 95 % CI: 1.007-1.382), DBP (β = 0.680, 95 % CI: 0.553-0.807), and PP (β = 0.469, 95 % CI: 0.359-0.579). It also increased HTN risk (OR = 1.030, 95 % CI: 1.025-1.036, discovery; OR = 1.169, 95 % CI: 1.138-1.200, replication; OR = 1.089, 95 % CI: 1.049-1.131, meta-analysis). MVMR showed persistent causal relationships with DBP (β = 0.219, 95 % CI: 0.072-0.366) and HTN (OR = 1.010, 95 % CI: 1.005-1.015, discovery; OR = 1.055, 95 % CI: 1.024-1.086, replication). Colocalization analysis supported shared genetic architecture. Sensitivity analyses confirmed robustness.
CONCLUSIONS: Our study provides genetic evidence that the TG:HDL-C ratio is causally related to DBP and HTN. These findings were consistent across robust MR methods. However, no independent causal relationship was observed between the TG:HDL-C ratio and SBP or PP after lipid adjustment in MVMR. Further interventional studies are needed.
METHODS AND RESULTS: We conducted genome-wide linkage disequilibrium score regression (LDSC), two-sample Mendelian randomization (MR), colocalization, reverse, and multivariable MR (MVMR) analyses to evaluate the causal relationships between the TG:HDL-C ratio and BP traits. BP traits (systolic BP [SBP], diastolic BP [DBP], and pulse pressure [PP]) were obtained from the International Consortium for Blood Pressure and UK Biobank. HTN data were from GWAS meta-analyses. The primary analysis used the inverse variance method (IVW), with sensitivity analyses for MR. Significant genetic correlations were found between the TG:HDL-C ratio and BP traits (all P values < 0.05). Genetically predicted TG:HDL-C ratio was associated with increased SBP (β = 1.194, 95 % CI: 1.007-1.382), DBP (β = 0.680, 95 % CI: 0.553-0.807), and PP (β = 0.469, 95 % CI: 0.359-0.579). It also increased HTN risk (OR = 1.030, 95 % CI: 1.025-1.036, discovery; OR = 1.169, 95 % CI: 1.138-1.200, replication; OR = 1.089, 95 % CI: 1.049-1.131, meta-analysis). MVMR showed persistent causal relationships with DBP (β = 0.219, 95 % CI: 0.072-0.366) and HTN (OR = 1.010, 95 % CI: 1.005-1.015, discovery; OR = 1.055, 95 % CI: 1.024-1.086, replication). Colocalization analysis supported shared genetic architecture. Sensitivity analyses confirmed robustness.
CONCLUSIONS: Our study provides genetic evidence that the TG:HDL-C ratio is causally related to DBP and HTN. These findings were consistent across robust MR methods. However, no independent causal relationship was observed between the TG:HDL-C ratio and SBP or PP after lipid adjustment in MVMR. Further interventional studies are needed.