1. Scope

What this covers:

• Long-chain marine omega-3 polyunsaturated fatty acids (LCn3 PUFA) — eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) — as dietary intake, over-the-counter supplements, and prescription-grade products (e.g. icosapent ethyl, EPA/DHA ethyl esters).
• Use in a UK private longevity/preventive-medicine setting, adjunctive to conventional primary and secondary care.
• Outcomes of interest to longevity practice: all-cause and cardiovascular mortality, cardiovascular events, cognitive decline/dementia, sarcopenia/frailty/physical function, and validated ageing biomarkers (telomere length, epigenetic clocks).

What this does NOT cover:

• Plant-derived alpha-linolenic acid (ALA) as a primary therapeutic strategy (referenced only where it informs ageing-biomarker data).
• Severe hypertriglyceridaemia management as a lipidology topic in its own right (covered only as it overlaps with omega-3 prescribing).
• Paediatric use, and use in pregnancy beyond brief safety notes.
• Any claim that surrogate biomarker change equates to a hard clinical benefit — such linkages are flagged explicitly and are NOT endorsed where robust outcome data are absent.

Regulatory anchor: NICE currently advises against offering omega-3 supplements for primary or secondary prevention of cardiovascular disease, while encouraging oily fish intake (as summarised in Abdelhamid et al., Cochrane Database of Systematic Reviews, 2020). Most longevity uses below are therefore off-label or not guideline-endorsed and should proceed as adjunctive care with informed consent.

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2. Background and pathophysiology

Biological rationale relevant to ageing:

• EPA and DHA are incorporated into membrane phospholipids, altering membrane fluidity, lipid-raft signalling and ion-channel behaviour (Marcus and Link, Circulation, 2024).
• They are substrates for specialised pro-resolving mediators (resolvins, protectins), which actively resolve inflammation — mechanistically relevant to “inflammaging.”
• Downstream effects with the most robust human support are triglyceride lowering and, at dietary doses, anti-arrhythmic/reduced sudden cardiac death signals (Mozaffarian and Wu, Journal of the American College of Cardiology, 2011).

Key mechanisms proposed for longevity (with candour on evidence level):

• Anti-inflammatory / pro-resolution — supported by human biomarker RCT data (e.g. reduced stress-related inflammatory reactivity; Madison et al., Molecular Psychiatry, 2021). Human mechanistic evidence: moderate.
• Muscle protein synthesis via anabolic signalling and reduced anabolic resistance — human acute metabolic data are limited and mixed (Therdyothin et al., Marine Drugs, 2023). Mechanistic plausibility with partial human support.
• Telomere/epigenetic ageing modulation — associations only; see below.

Preclinical / lower-certainty subsection (interpret with caution):

• Animal and mechanistic models describe DHA/EPA effects on neurogenesis, synaptic protein expression and microglial function. Animal data — not directly translatable.
• In-vitro effects on antioxidant response and telomerase are described but bidirectional across cell types (context discussed in Farzaneh-Far et al., JAMA, 2010). In-vitro/hypothesis-generating only.
• Observational and machine-learning analyses associate higher omega-3/ALA intake with lower epigenetic age and longer telomeres (Yan et al., Journal of Food Science, 2025). Cross-sectional/observational — no causal clinical inference.

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3. Evidence base and grading

Types of evidence available: Multiple large RCTs (REDUCE-IT, VITAL, ASCEND, STRENGTH, OMEMI), a comprehensive Cochrane systematic review (>140,000 participants), numerous meta-analyses, and large prospective cohorts. This is an unusually mature evidence base for a “longevity” intervention.

GRADE-style certainty by outcome:

Outcome	Evidence statement	Certainty	Key limitations	Strength of recommendation	Key source
All-cause mortality	High-certainty evidence (>143,000 participants) shows little or no effect (RR 0.97, 95% CI 0.93–1.01)	High	None major; minor small-study bias	Recommend against using omega-3 for the purpose of extending lifespan	Abdelhamid et al., Cochrane, 2020
CVD/CHD death and MI (supplement, ~1 g/d)	Meta-analyses suggest modest reductions in CHD death, fatal MI and total MI, larger with purified EPA; largest primary-prevention RCTs (VITAL, ASCEND) were negative for composite endpoints	Moderate	Inconsistency across trials; effect concentrated in secondary analyses	Conditional (consider in low-fish consumers/high-risk)	Abdelhamid et al., Cochrane, 2020; Weinberg et al., JACC, 2021
Major CV events, high-dose EPA + statin + high triglycerides	1 large RCT (REDUCE-IT, n=8179): 25% relative reduction in primary composite; CV death reduced	Moderate–High (single pivotal trial; mineral-oil comparator debate)	Single trial; comparator controversy	Strong in the specific REDUCE-IT phenotype	Bhatt et al., NEJM, 2019; Boden et al., European Heart Journal, 2020
Cognitive decline/dementia	Cohort/meta-analytic data suggest lower risk with higher dietary DHA; RCTs of supplementation largely null in established disease	Low (for supplementation)	Indirectness, cohort confounding, null RCTs	Only in research / conditional in early MCI	Wei et al., American Journal of Clinical Nutrition, 2023
Sarcopenia — muscle strength/mass	Meta-analyses of RCTs show small but clinically relevant strength gains at >2 g/d, best combined with resistance training; monotherapy trials null	Low–Moderate	Heterogeneity, small trials, indirect outcomes	Conditional (adjunct to resistance exercise)	Therdyothin et al., Marine Drugs, 2023; Varamini et al., Int J Environ Res Public Health, 2026
Ageing biomarkers (telomere, epigenetic clocks)	RCT biomarker signals (telomerase stress-reactivity) and observational associations only	Very low (for clinical benefit)	Surrogate endpoints, no hard-outcome linkage	Only in research	Madison et al., Molecular Psychiatry, 2021; Farzaneh-Far et al., JAMA, 2010

Publication bias: Funnel-plot analysis in the Cochrane review suggested minor small-study bias that, if corrected, would move estimates further toward the null (Abdelhamid et al., Cochrane, 2020). Positive supplement literature is prone to selective secondary-endpoint emphasis.

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4. Patient selection and indications

Who may benefit (candidate groups):

• Middle-aged adults with high cardiometabolic risk and elevated triglycerides already on optimised statin therapy — the strongest evidence base (REDUCE-IT phenotype: established ASCVD or diabetes + risk factors, triglycerides 1.52–5.63 mmol/L, controlled LDL-C; Bhatt et al., NEJM, 2019).
• Low or non-fish consumers (<1.5–2 oily fish portions/week) seeking cardiovascular risk reduction — modest signal and dietary-guideline rationale (Weinberg et al., JACC, 2021).
• Older adults with early sarcopenia/frailty — as an adjunct to resistance training, not monotherapy (Therdyothin et al., Marine Drugs, 2023; Varamini et al., Int J Environ Res Public Health, 2026).
• Adults with early subjective cognitive complaints or family history of dementia / APOE ε4 carriers — counselling on fish intake reasonable; supplementation only in research or shared-decision adjunct given null RCTs (Wei et al., American Journal of Clinical Nutrition, 2023).

Exclusion / high-risk groups:

• Active or high bleeding risk, or anticipated surgery — caution at high doses.
• High cardiovascular-risk patients considered for high-dose (>1.5 g/d) EPA/DHA — weigh atrial fibrillation risk (see §7; Abuknesha et al., Circulation: Arrhythmia and Electrophysiology, 2026).
• Genuine fish/seafood allergy — highly purified products are generally tolerated but use under supervision.

Regulatory/ethical status:

• Dietary oily fish intake: guideline-endorsed (NICE, AHA) — on-label lifestyle advice.
• OTC supplements for longevity/prevention: off-label / not NICE-endorsed — adjunctive care with informed consent.
• Icosapent ethyl 4 g/d for CV risk reduction in the REDUCE-IT phenotype: licensed indication (on-label) in appropriate patients (Bhatt et al., NEJM, 2019).
• Use for telomere/epigenetic-age modification: only in research — no validated clinical benefit.

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5. Assessment and baseline work-up

History and examination:

• Cardiovascular risk profiling (ASCVD history, diabetes, smoking, family history); use QRISK3 for UK primary prevention.
• Dietary oily fish frequency (drives expected benefit).
• Bleeding history, anticoagulant/antiplatelet use, planned procedures.
• Frailty/functional assessment where relevant (grip strength, gait speed, SPPB, Timed Up-and-Go).

Baseline investigations:

• Fasting lipid profile including triglycerides (defines the REDUCE-IT-type indication; Bhatt et al., NEJM, 2019).
• HbA1c, renal and liver function, FBC.
• Optional/emerging: Omega-3 Index (erythrocyte EPA+DHA %), commonly cited target range 8–11%; note inter-laboratory variability and lack of outcome-validated treat-to-target RCTs — use as a monitoring adjunct, not a proven surrogate.

Risk stratification (benefit vs harm):

• Higher expected benefit: established ASCVD/diabetes + elevated triglycerides on statin; low baseline fish intake/low Omega-3 Index.
• Higher potential harm: high CV-risk patient considered for >1.5 g/d (AF risk); bleeding risk; peri-operative.

Baseline documentation: triglycerides and full lipid panel, fish intake, concomitant antithrombotics, baseline functional measures (if frailty indication), and Omega-3 Index if used — to allow meaningful follow-up.

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6. Dosing regimens and practical implementation

Regimens supported by robust human data:

• Dietary: 1–2 portions oily fish/week (~250 mg/day EPA+DHA) for CHD/sudden-death risk reduction — guideline-endorsed, first-line (Mozaffarian and Wu, JACC, 2011).
• High-dose secondary prevention (REDUCE-IT phenotype): icosapent ethyl 2 g twice daily (4 g/day total), added to a statin, in patients with established ASCVD or diabetes + risk factors and triglycerides 1.52–5.63 mmol/L (Bhatt et al., NEJM, 2019).
• Hypertriglyceridaemia: prescription omega-3 (EPA/DHA or EPA-only) 4 g/day lowers triglycerides (Weinberg et al., JACC, 2021).

Regimens with weaker / adjunctive support (use with caution, off-label):

• General primary prevention in low-fish consumers: ~1 g/day EPA+DHA — modest, inconsistent evidence (Abdelhamid et al., Cochrane, 2020; Weinberg et al., JACC, 2021).
• Sarcopenia adjunct: >2 g/day combined EPA+DHA for ≥6 months, combined with resistance training; monotherapy is likely ineffective (Therdyothin et al., Marine Drugs, 2023).

Dose–response and formulation notes:

• Triglyceride-lowering and metabolic effects require higher (pharmacological, 3–4 g/day) doses; anti-arrhythmic/sudden-death signals appear at lower dietary doses (Mozaffarian and Wu, JACC, 2011).
• Triglyceride-based formulations raise the Omega-3 Index somewhat more than ethyl-ester products gram-for-gram; roughly 1,100–1,300 mg/day EPA+DHA is typically needed to reach an Omega-3 Index of ~8% in non-fish eaters (Omega-3 Index literature; not outcome-validated).
• No titration/loading is required; steady-state Omega-3 Index is reached over ~8–12 weeks.

Practical: take with a fat-containing meal to reduce reflux/”fishy burp” and improve absorption; choose third-party-purified products.

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7. Monitoring, safety and follow-up

Monitoring plan:

• Clinical: GI tolerability, dysgeusia, bruising/bleeding; new palpitations (AF).
• Laboratory: repeat lipids at 8–12 weeks if treating hypertriglyceridaemia; watch for LDL-C rise (more with DHA). Optional Omega-3 Index at ~12 weeks if used to guide dosing.
• Functional (frailty indication): grip strength/gait speed at 3–6 months.

Timepoints: baseline → 8–12 weeks (tolerability, lipids ± Omega-3 Index) → 6–12 months → annually.

Adverse effects and safety profile:

• Generally well tolerated; side effects typically in <5% (Weinberg et al., JACC, 2021).
• Common: dysgeusia/fishy burp, mild GI upset, diarrhoea (meta-analysis: significantly increased odds of diarrhoea, dysgeusia and bleeding tendency; Chang et al., Advances in Nutrition, 2023).
• Bleeding: small increase in bleeding tendency; no clinically significant bleeding excess demonstrated up to ~7 g/day even with antiplatelets/warfarin in earlier reviews, though high-dose EPA showed a numerical serious-bleeding increase in REDUCE-IT (2.7% vs 2.1%, P=0.06; Bhatt et al., NEJM, 2019).
• Atrial fibrillation (key dose-dependent harm): meta-analysis of 35 RCTs (n=114,592) found a significant AF increase only in high-CV-risk patients on >1500 mg/day EPA/DHA (OR 1.43, 95% CI 1.14–1.79; absolute risk difference ~0.8%); low-dose supplementation did not increase AF even in high-risk groups (Abuknesha et al., Circulation: Arrhythmia and Electrophysiology, 2026). REDUCE-IT and STRENGTH both showed increased AF hospitalisation at 4 g/day (Bhatt et al., NEJM, 2019).
• Serious AEs: no definite omega-3-related serious adverse events identified in the large safety meta-analysis (Chang et al., Advances in Nutrition, 2023).

Actions for abnormal findings: new/symptomatic AF → stop high-dose omega-3 and manage per AF pathway; clinically significant bleeding or pre-operative period → hold; significant LDL-C rise → reassess formulation/lipid strategy.

Interactions and comorbidities: additive bleeding risk with anticoagulants/antiplatelets (monitor, usually continue with vigilance); consider AF-predisposed patients before high dose.

Special populations:

• Pregnancy/breastfeeding: dietary fish beneficial for neurodevelopment; avoid high-mercury species; supplement use should be product-verified.
• Renal/hepatic impairment, frailty, extremes of age: no specific dose adjustment established; apply general caution and monitor.

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8. Contraindications and cautions

Absolute contraindications:

• Known hypersensitivity to a specific omega-3 product excipient.

Relative contraindications / specialist input advised:

• History of atrial fibrillation or high AF risk — avoid high-dose (>1.5 g/day) EPA/DHA (Abuknesha et al., Circulation: Arrhythmia and Electrophysiology, 2026).
• Active clinically significant bleeding, high bleeding risk, or imminent surgery — hold high doses.
• Concomitant full anticoagulation — use with monitoring.

Harm likely to outweigh benefit with current evidence:

• Use specifically to extend lifespan / lower all-cause mortality — high-certainty evidence shows no effect (Abdelhamid et al., Cochrane, 2020).
• High-dose use in high-CV-risk patients solely for prevention where triglycerides are normal — AF risk without a clear offsetting benefit (Abuknesha et al., Circulation: Arrhythmia and Electrophysiology, 2026).

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9. Practical management scenarios

Scenario A — Middle-aged patient, multiple cardiometabolic risk factors, elevated triglycerides on a statin.

• Recommendation: Offer icosapent ethyl 4 g/day if the patient matches the REDUCE-IT phenotype (established ASCVD or diabetes + risk factors, triglycerides 1.52–5.63 mmol/L, controlled LDL-C on a statin) — Strong in this phenotype (Bhatt et al., NEJM, 2019).
• Assessment: confirm statin optimisation, fasting triglycerides/LDL-C, AF and bleeding history.
• Shared decision-making: discuss ~25% relative CV event reduction vs increased AF and minor bleeding risk.
• Initiation: 2 g twice daily with food.
• Monitoring: lipids at 8–12 weeks; review for AF/bleeding; annual review.
• Escalate/stop: new AF or significant bleeding → stop and reassess.

Scenario B — Older, frail patient with multimorbidity.

• Recommendation: Consider EPA+DHA >2 g/day as an adjunct to resistance training for sarcopenia — Conditional (small, clinically relevant strength benefit; monotherapy likely ineffective; Therdyothin et al., Marine Drugs, 2023; Varamini et al., Int J Environ Res Public Health, 2026). Do not offer for mortality benefit.
• Assessment: baseline grip strength/gait speed/SPPB; AF and bleeding risk (frail elderly are often high CV risk — favour moderate rather than very high doses).
• Shared decision-making: set expectations (modest functional gains, exercise is the core intervention).
• Initiation: combine with a structured resistance programme.
• Monitoring: functional measures at 3–6 months; tolerability; AF.
• Escalate/stop: no functional benefit by 6 months, or new AF → stop.

Scenario C — Patient already under specialist care (e.g. cardiology/lipidology) wanting omega-3 as an adjunct.

• Recommendation: Restrict to coordinated adjunctive care — align with the treating specialist; avoid duplicating or exceeding prescribed omega-3, and avoid adding high-dose OTC product on top of prescription EPA.
• Assessment: reconcile current prescriptions (icosapent ethyl, anticoagulants, statin).
• Consent: clarify off-label status of any longevity-specific goals.
• Initiation/monitoring: defer dosing decisions to the specialist pathway; monitor AF/bleeding jointly.
• Escalate/refer: any new arrhythmia or bleeding back to the specialist team.

Scenario D — Healthy low-fish consumer seeking general prevention/”longevity.”

• Recommendation: Offer dietary advice first (1–2 oily fish portions/week); consider ~1 g/day EPA+DHA if intake remains low — Conditional, off-label (Weinberg et al., JACC, 2021). Be explicit that all-cause mortality benefit is not expected (Abdelhamid et al., Cochrane, 2020).

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10. Research gaps and future directions

• Formulation and dose: why purified high-dose EPA (REDUCE-IT) succeeded while mixed EPA/DHA trials (STRENGTH, VITAL, ASCEND) were largely negative — comparator (mineral oil) controversy remains unresolved (Abdelhamid et al., Cochrane, 2020; Bhatt et al., NEJM, 2019).
• AF risk-benefit: clarifying which doses, formulations and subgroups drive the dose-dependent AF signal (>1500 mg/day in high-risk patients) (Abuknesha et al., Circulation: Arrhythmia and Electrophysiology, 2026).
• Treat-to-target Omega-3 Index: no RCT has shown that titrating to an 8–11% index improves hard outcomes — this remains a hypothesis.
• Sarcopenia: optimal dose, sex-specific responses, and the omega-3 × resistance-exercise interaction need adequately powered trials (Varamini et al., Int J Environ Res Public Health, 2026).
• Cognition: RCTs targeting early MCI/APOE ε4 carriers before decline, using DHA-predominant regimens (Wei et al., American Journal of Clinical Nutrition, 2023).
• Ageing biomarkers: whether omega-3-associated changes in epigenetic clocks/telomeres translate into any clinical benefit is unproven — should remain confined to well-designed trials/registries (Madison et al., Molecular Psychiatry, 2021; Yan et al., Journal of Food Science, 2025).

Bottom line for practice: Omega-3 does not extend lifespan on current high-certainty evidence. Its clearest role in a longevity clinic is targeted cardiovascular risk reduction (high-dose EPA in the REDUCE-IT phenotype; dietary oily fish for low consumers) and as an exercise adjunct for early sarcopenia. All other longevity applications are off-label, experimental, or research-only and require explicit informed consent.

Footnote

The summary is deliberately conservative on the central longevity claim: high-certainty Cochrane evidence (>143,000 participants) shows omega-3 has little or no effect on all-cause mortality (RR 0.97, 95% CI 0.93–1.01), so it should not be offered as a life-extension intervention.[1] The strongest positive signal is confined to the REDUCE-IT phenotype, where icosapent ethyl 4 g/day cut major cardiovascular events by ~25% in statin-treated patients with elevated triglycerides.[2][14] Primary-prevention supplement trials (VITAL, ASCEND) were negative for their composite endpoints, with benefit largely limited to secondary analyses and low-fish consumers.[3][4]

Safety emphasis is on the dose-dependent atrial fibrillation signal — a recent 35-RCT meta-analysis (n=114,592) found increased AF only with >1500 mg/day in high-CV-risk patients (OR 1.43), plus minor bleeding and GI/dysgeusia effects.[6][7][3][5] Surrogate ageing biomarkers (telomere, epigenetic clocks) are explicitly graded very-low certainty and flagged as research-only, since no robust data link omega-3-associated biomarker changes to hard clinical outcomes.[13][11][12] The document notes NICE’s position against supplementation for CVD prevention, so most longevity uses are framed as off-label adjunctive care requiring informed consent.[1]

 

Figure 1.5 Comparison 1 Higher polyunsaturated fatty acids (PUFA) vs lower PUFA intake ‐ primary outcomes, Outcome 5 All‐cause mortality ‐ subgroup by duration. Abdelhamid AS, Martin N, Bridges C, et al. Polyunsaturated Fatty Acids for the Primary and Secondary Prevention of Cardiovascular Disease. The Cochrane Database of Systematic Reviews. 2018;11:CD012345. doi:10.1002/14651858.CD012345.pub3.

 

Figure 6 Figure 6. Mozaffarian D, Wu JH. Omega-3 Fatty Acids and Cardiovascular Disease: Effects on Risk Factors, Molecular Pathways, and Clinical Events. Journal of the American College of Cardiology. 2011;58(20):2047-67. doi:10.1016/j.jacc.2011.06.063.

 

Figure 5 Figure 5. Lavie CJ, Milani RV, Mehra MR, Ventura HO. Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Diseases. Journal of the American College of Cardiology. 2009;54(7):585-94. doi:10.1016/j.jacc.2009.02.084.

 

Figure 2 Figure 2. Bhatt DL, Steg PG, Miller M, et al. Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT. Journal of the American College of Cardiology. 2019;73(22):2791-2802. doi:10.1016/j.jacc.2019.02.032.

 

Figure 4 Forest Plot of Investigator-Reported Primary, Key Secondary, and Other Secondary Efficacy Endpoints Gaba P, Bhatt DL, Giugliano RP, et al. Comparative Reductions in Investigator-Reported and Adjudicated Ischemic Events in REDUCE-IT. Journal of the American College of Cardiology. 2021;78(15):1525-1537. doi:10.1016/j.jacc.2021.08.009.

 

Figure 3 Effect of Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) on the Primary End Point in Prespecified Subgroups Albert CM, Cook NR, Pester J, et al. Effect of Marine Omega-3 Fatty Acid and Vitamin D Supplementation on Incident Atrial Fibrillation: A Randomized Clinical Trial. Jama. 2021;325(11):1061-1073. doi:10.1001/jama.2021.1489.

 

References

1. Omega-3 Fatty Acids for the Primary and Secondary Prevention of Cardiovascular Disease. Abdelhamid AS, Brown TJ, Brainard JS, et al. The Cochrane Database of Systematic Reviews. 2020;3:CD003177. doi:10.1002/14651858.CD003177.pub5.
2. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. Bhatt DL, Steg PG, Miller M, et al. The New England Journal of Medicine. 2019;380(1):11-22. doi:10.1056/NEJMoa1812792.
3. Cardiovascular Impact of Nutritional Supplementation With Omega-3 Fatty Acids: JACC Focus Seminar. Weinberg RL, Brook RD, Rubenfire M, Eagle KA. Journal of the American College of Cardiology. 2021;77(5):593-608. doi:10.1016/j.jacc.2020.11.060.
4. 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia: A Report of the American College of Cardiology Solution Set Oversight Committee. Virani SS, Morris PB, Agarwala A, et al. Journal of the American College of Cardiology. 2021;78(9):960-993. doi:10.1016/j.jacc.2021.06.011.
5. Safety of Supplementation of Omega-3 Polyunsaturated Fatty Acids: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Chang JP, Tseng PT, Zeng BS, et al. Advances in Nutrition (Bethesda, Md.). 2023;14(6):1326-1336. doi:10.1016/j.advnut.2023.08.003.
6. Effects of Omega-3 Fatty Acid Treatment on Risk for Atrial Fibrillation: An Updated Meta-Analysis of 35 Trials Including 114 592 Individuals. Abuknesha NR, O’Keefe JH, Qian F, et al. Circulation. Arrhythmia and Electrophysiology. 2026;19(8):e014785. doi:10.1161/CIRCEP.125.014785.
7. Omega-3 Fatty Acids and Arrhythmias. Marcus MD, Link MS. Circulation. 2024;150(6):488-503. doi:10.1161/CIRCULATIONAHA.123.065769.
8. The Role of Omega-3 Polyunsaturated Fatty Acids on Sarcopenia and Aging Muscle. Varamini B, Yang JO, Merry BJ, Dau DJ. International Journal of Environmental Research and Public Health. 2026;23(3):355. doi:10.3390/ijerph23030355.
9. The Effect of Omega-3 Fatty Acids on Sarcopenia: Mechanism of Action and Potential Efficacy. Therdyothin A, Phiphopthatsanee N, Isanejad M. Marine Drugs. 2023;21(7):399. doi:10.3390/md21070399.
10. The Relationship of Omega-3 Fatty Acids With Dementia and Cognitive Decline: Evidence From Prospective Cohort Studies of Supplementation, Dietary Intake, and Blood Markers. Wei BZ, Li L, Dong CW, Tan CC, Xu W. The American Journal of Clinical Nutrition. 2023;117(6):1096-1109. doi:10.1016/j.ajcnut.2023.04.001.
11. Omega-3 Supplementation and Stress Reactivity of Cellular Aging Biomarkers: An Ancillary Substudy of a Randomized, Controlled Trial in Midlife Adults. Madison AA, Belury MA, Andridge R, et al. Molecular Psychiatry. 2021;26(7):3034-3042. doi:10.1038/s41380-021-01077-2.
12. Association of Marine Omega-3 Fatty Acid Levels With Telomeric Aging in Patients With Coronary Heart Disease. Farzaneh-Far R, Lin J, Epel ES, et al. JAMA. 2010;303(3):250-7. doi:10.1001/jama.2009.2008.
13. A Clinical Prediction Model Integrated With Machine Learning Algorithms Uncovers the Associations Between Dietary Omega-3, Its Components, and Aging Biomarkers. Yan Z, Xu Y, Peng T, Du X. Journal of Food Science. 2025;90(7):e70334. doi:10.1111/1750-3841.70334.
14. Profound Reductions in First and Total Cardiovascular Events With Icosapent Ethyl in the REDUCE-IT Trial: Why These Results Usher in a New Era in Dyslipidaemia Therapeutics. Boden WE, Bhatt DL, Toth PP, et al. European Heart Journal. 2020;41(24):2304-2312. doi:10.1093/eurheartj/ehz778.
15. Polyunsaturated fatty acids for the primary and secondary prevention of cardiovascular disease. Abdelhamid AS, Martin N, Bridges C, et al. The Cochrane Database of Systematic Reviews. 2018;11:CD012345. doi:10.1002/14651858.CD012345.pub3.
16. Omega-3 Fatty Acids and Cardiovascular Disease: Effects on Risk Factors, Molecular Pathways, and Clinical Events. Mozaffarian D, Wu JH. Journal of the American College of Cardiology. 2011;58(20):2047-67. doi:10.1016/j.jacc.2011.06.063.
17. Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Diseases. Lavie CJ, Milani RV, Mehra MR, Ventura HO. Journal of the American College of Cardiology. 2009;54(7):585-94. doi:10.1016/j.jacc.2009.02.084.
18. Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT. Bhatt DL, Steg PG, Miller M, et al. Journal of the American College of Cardiology. 2019;73(22):2791-2802. doi:10.1016/j.jacc.2019.02.032.
19. Comparative Reductions in Investigator-Reported and Adjudicated Ischemic Events in REDUCE-IT. Gaba P, Bhatt DL, Giugliano RP, et al. Journal of the American College of Cardiology. 2021;78(15):1525-1537. doi:10.1016/j.jacc.2021.08.009.
20. Effect of Marine Omega-3 Fatty Acid and Vitamin D Supplementation on Incident Atrial Fibrillation: A Randomized Clinical Trial. Albert CM, Cook NR, Pester J, et al. JAMA. 2021;325(11):1061-1073. doi:10.1001/jama.2021.1489.