Clinical nutrition ESPEN · 2025
Excess energy intake causally increases the blood pressure and hypertension risk: A two sample Mendelian randomization analysis.
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Teymoori Farshad, Akbarzadeh Mahdi, Saber Niloufar, Jahromi Mitra Kazemi, Habibi Danial, Farhadnejad Hossein, Zarkesh Maryam, Mirmiran Parvin, Vafa Mohammadreza, Daneshpour Maryam S
Аннотация
BACKGROUND/AIM: The impact of excess energy intake on blood pressure (BP) and hypertension (HTN) has not been extensively studied. This study aimed to evaluate the causal link between energy intake and systolic and diastolic BP (SBP and DBP) and HTN, using a Mendelian randomization (MR) approach.
METHODS: We conducted an MR analysis using summary statistics from large-scale genome-wide association studies (GWAS) datasets of European ancestry. Several MR methods were applied, including inverse-variance weighted (IVW), weighted median and mode, and MR-Egger regression. Genetic variants associated with energy intake were obtained from a published GWAS of the UK Biobank (N = 64,979). GWAS datasets for SBP, DBP, and HTN included 436,419; 436,424; and 361,194 individuals (1237 cases and 359,957 controls), respectively, all from the UK Biobank. Effect estimates were reported as beta coefficients(β) with 95 % confidence intervals (CIs) for continuous outcomes and odds ratios (ORs) with 95 % CIs for binary outcomes.
RESULTS: The IVW analyses indicated that each SD increase in energy intake was causally associated with one SD increase in SBP (β = 0.093, 95%CI:0.027-0.160, P = 0.006) and DBP(β = 0.070, 95%CI:0.014-0.126, P = 0.014), based on 10 and 8 included SNPs, respectively. These significant associations were confirmed by the weighted median MR method for SBP (β = 0.096, 95%CI:0.032-0.169, P = 0.012) and DBP (β = 0.077, 95 %CI:0.006-0.148, P = 0.044). Furthermore, a causal relationship between energy intake and HTN was observed using the IVW (OR = 1.004, 95 %CI:1.002-1.006, P = 0.012) and the MR Egger method (OR = 1.012, 95%CI:1.004-1.020, P = 0.045), based on 9 included SNPs. No evidence of weak instrument bias, heterogeneity, or horizontal pleiotropy was detected. The significant findings were consistent across most applied MR methods.
CONCLUSIONS: Our findings support a direct causal relationship between excess energy intake and both BP and HTN.
METHODS: We conducted an MR analysis using summary statistics from large-scale genome-wide association studies (GWAS) datasets of European ancestry. Several MR methods were applied, including inverse-variance weighted (IVW), weighted median and mode, and MR-Egger regression. Genetic variants associated with energy intake were obtained from a published GWAS of the UK Biobank (N = 64,979). GWAS datasets for SBP, DBP, and HTN included 436,419; 436,424; and 361,194 individuals (1237 cases and 359,957 controls), respectively, all from the UK Biobank. Effect estimates were reported as beta coefficients(β) with 95 % confidence intervals (CIs) for continuous outcomes and odds ratios (ORs) with 95 % CIs for binary outcomes.
RESULTS: The IVW analyses indicated that each SD increase in energy intake was causally associated with one SD increase in SBP (β = 0.093, 95%CI:0.027-0.160, P = 0.006) and DBP(β = 0.070, 95%CI:0.014-0.126, P = 0.014), based on 10 and 8 included SNPs, respectively. These significant associations were confirmed by the weighted median MR method for SBP (β = 0.096, 95%CI:0.032-0.169, P = 0.012) and DBP (β = 0.077, 95 %CI:0.006-0.148, P = 0.044). Furthermore, a causal relationship between energy intake and HTN was observed using the IVW (OR = 1.004, 95 %CI:1.002-1.006, P = 0.012) and the MR Egger method (OR = 1.012, 95%CI:1.004-1.020, P = 0.045), based on 9 included SNPs. No evidence of weak instrument bias, heterogeneity, or horizontal pleiotropy was detected. The significant findings were consistent across most applied MR methods.
CONCLUSIONS: Our findings support a direct causal relationship between excess energy intake and both BP and HTN.