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Background and objective <p>Hypertension is influenced by both genetic and dietary factors. Understanding gene-diet interactions across populations is key to precision prevention. Objectives: To identify genetic variants associated with hypertension in KoGES and UK Biobank (UKBB), and evaluate their interactions with nutrient intake.</p> Subjects/Methods <p>Genome-wide association analyses were conducted for hypertension (HTN: SBP ≥ 140 mmHg, DBP ≥ 90 mmHg or taking hypotensive medication) in KoGES (Non-HTN, <i>n</i> = 39,387; HTN, <i>n</i> = 13,727) and replicated in UKBB (Non-HTN, <i>n</i> = 334,785; HTN, <i>n</i> = 132,140). Genetic risk scores (GRS) were constructed from seven common SNPs. Genetic variant or GRS-diet interactions were analyzed via logistic regression.</p> Results <p>Common SNPs in genes such as <i>FGF5, CYP17A1, CNNM2, AS3MT, ATP2B1, BORCS7-ASMT, NT5C2</i>, and <i>RGL3</i> were significantly linked to hypertension in both cohorts (<i>P</i> &lt; 5 × 10⁻⁸). In KoGES, the associated genes were enriched in lipid metabolism pathways. In UKBB, vascular signaling pathways, including <i>AKT1, MAPK</i>, and <i>TGF-β</i> signaling, were predominant based on the selected genetic variants. Despite common variants, distinct biological mechanisms were implicated in Koreans and Caucasians. The GRS of the 6-SNP model, including <i>FGF5, CYP17A1, CNNM2, ATP2B1, BORCS7-ASMT</i>, and <i>RGL3</i>, was associated with hypertension risk. However, this effect was attenuated with high tea and coffee intake only in the low-GRS individuals in both cohorts (<i>P</i> &lt; 0.05). The <i>RGL3</i> rs167479 variant showed significant interactions with vitamins C, D, B12, and flavonoids in KoGES (<i>P</i> = 0.02–0.002).</p> Conclusions <p>Common genetic variants contribute to hypertension across populations but act through divergent molecular pathways. Targeted nutrient intake appears to mitigate genetic risk, underscoring the promise of gene-informed dietary strategies for hypertension prevention.</p>

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Precision nutrition for hypertension: tea, coffee, antioxidant vitamins interactions with polygenic risk in multi-ethnic populations

  • 期刊论文

  • 发表日期：

    2026年1月8日

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  • Haeng Jeon Hur,
  • Hye Jeong Yang,
  • Min Jung Kim,
  • Hyun-Jun Jang,
  • Myung-Sunny Kim,
  • Sunmin Park

摘要

Background and objective

Hypertension is influenced by both genetic and dietary factors. Understanding gene-diet interactions across populations is key to precision prevention. Objectives: To identify genetic variants associated with hypertension in KoGES and UK Biobank (UKBB), and evaluate their interactions with nutrient intake.

Subjects/Methods

Genome-wide association analyses were conducted for hypertension (HTN: SBP ≥ 140 mmHg, DBP ≥ 90 mmHg or taking hypotensive medication) in KoGES (Non-HTN, n = 39,387; HTN, n = 13,727) and replicated in UKBB (Non-HTN, n = 334,785; HTN, n = 132,140). Genetic risk scores (GRS) were constructed from seven common SNPs. Genetic variant or GRS-diet interactions were analyzed via logistic regression.

Results

Common SNPs in genes such as FGF5, CYP17A1, CNNM2, AS3MT, ATP2B1, BORCS7-ASMT, NT5C2, and RGL3 were significantly linked to hypertension in both cohorts (P < 5 × 10⁻⁸). In KoGES, the associated genes were enriched in lipid metabolism pathways. In UKBB, vascular signaling pathways, including AKT1, MAPK, and TGF-β signaling, were predominant based on the selected genetic variants. Despite common variants, distinct biological mechanisms were implicated in Koreans and Caucasians. The GRS of the 6-SNP model, including FGF5, CYP17A1, CNNM2, ATP2B1, BORCS7-ASMT, and RGL3, was associated with hypertension risk. However, this effect was attenuated with high tea and coffee intake only in the low-GRS individuals in both cohorts (P < 0.05). The RGL3 rs167479 variant showed significant interactions with vitamins C, D, B12, and flavonoids in KoGES (P = 0.02–0.002).

Conclusions

Common genetic variants contribute to hypertension across populations but act through divergent molecular pathways. Targeted nutrient intake appears to mitigate genetic risk, underscoring the promise of gene-informed dietary strategies for hypertension prevention.