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Excess energy intake causally increases the blood pressure and hypertension risk: A two sample Mendelian randomization analysis
Journal article   Peer reviewed

Excess energy intake causally increases the blood pressure and hypertension risk: A two sample Mendelian randomization analysis

Farshad Teymoori, Mahdi Akbarzadeh, Niloufar Saber, Mitra Kazemi Jahromi, Danial Habibi, Hossein Farhadnejad, Maryam Zarkesh, Parvin Mirmiran, Mohammadreza Vafa and Maryam S. Daneshpour
Clinical nutrition ESPEN, Vol.70, pp.386-393
12/2025
DOI: https://doi.org/10.1016/j.clnesp.2025.10.001
PMID: 41077126
Appears in  Recent Faculty of Health Publications

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Abstract

energy intake blood pressure hypertension Mendelian randomization causal association
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(beta) 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 (beta = 0.093, 95%CI:0.027-0.160, P = 0.006) and DBP(beta = 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 (beta = 0.096, 95%CI:0.032-0.169, P = 0.012) and DBP (beta = 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:1.002-1.0 06, 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. (c) 2025 Published by Elsevier Ltd on behalf of European Society for Clinical Nutrition and Metabolism.

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