Key result
Omega-3 supplementation lowers daytime SBP by ~7 mmHg vs placebo at 12 weeks.
Why the study?
Omega-3 fatty acids exert anti-inflammatory and hemodynamic effects, but their concurrent effects on inflammatory biomarkers, central and ambulatory blood pressure, and vascular function in patients treated for hypertension and dyslipidemia remained incompletely characterized.
Does 12 weeks of supplementation with omega-3 ethyl esters (2 g/day) improve inflammatory biomarkers, ambulatory and central blood pressure, and vascular function in adults treated for hypertension and dyslipidemia?
RCT (n=100)
Double-blind
Randomized
Does 12 weeks of supplementation with omega-3 ethyl esters (2 g/day) improve inflammatory biomarkers, ambulatory and central blood pressure, and vascular function in adults treated for hypertension and dyslipidemia?
In an exploratory pilot trial of patients treated for hypertension and dyslipidemia, 2 g/day of omega-3 ethyl esters for 12 weeks showed preliminary reductions in inflammatory markers (NLR, ferritin), ambulatory and central blood pressure, and estimated pulse wave velocity compared to placebo.
Answers are grounded in this paper and cite their sources.
May reduce ambulatory and central BP plus inflammation in treated patients; leaves open confirmation in larger outcome trials.
Background: Omega-3 fatty acids exert anti-inflammatory and hemodynamic effects; however, their concurrent effects in patients receiving treatment for hypertension and dyslipidemia remain incompletely characterized. Objective: To evaluate the effects of 12 weeks of supplementation with pharmaceutical-grade omega-3 fatty acids on inflammatory biomarkers, central and brachial blood pressure including office and 24 h ambulatory measurements, and vascular function in this population. Methods: In this exploratory, randomized, double-blind, placebo-controlled pilot trial, 100 adults received omega-3 ethyl esters at a capsule dose of 2 g/day or a matching placebo for 12 weeks, in addition to stable usual pharmacological treatment. Treatment effects were estimated using linear mixed-effects models. p-values were nominal, and 95% confidence intervals were not adjusted for multiplicity. Results: Compared with placebo, omega-3 supplementation was associated with greater reductions in the neutrophil-to-lymphocyte ratio (NLR; −0.43; 95% CI, −0.73 to −0.13; p = 0.005), ferritin (−47.32 ng/mL; 95% CI, −77.55 to −17.08; p = 0.003), daytime systolic blood pressure (−6.52 mmHg; 95% CI, −10.66 to −2.39; p = 0.002), nighttime diastolic blood pressure (−5.55 mmHg; 95% CI, −9.87 to −1.22; p = 0.013), central systolic blood pressure (−6.71 mmHg; 95% CI, −12.22 to −1.20; p = 0.019), and estimated pulse wave velocity (−0.77 m/s; 95% CI, −1.19 to −0.36; p < 0.001). Conclusions: The trial identified exploratory signals involving NLR, ferritin, selected ambulatory blood-pressure measures, central systolic blood pressure, and algorithm-derived ePWV. Multiplicity, limited sample size, and incomplete outcome availability preclude confirmatory interpretation. Independent replication in larger, prospectively registered trials with clearly specified endpoints and reproducible sample-size calculations is required.
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Kotliar et al. (2026) conducted an RCT in Treated hypertension and dyslipidemia (n=100). Pharmaceutical-grade omega-3 ethyl esters vs. Matching placebo was evaluated on Daytime systolic blood pressure (exploratory endpoint alongside inflammatory biomarkers, central/ambulatory blood pressure, and vascular function) (MD -6.52 mmHg, 95% CI -10.66 to -2.39, p=0.002). Omega-3 supplementation (2 g/day) reduced daytime SBP (−6.52 mmHg; 95% CI −10.66 to −2.39; P=0.002) and NLR (−0.43; P=0.005) vs placebo at 12 weeks.
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