Omega-3 Fish Oil 2000mg | High EPA/DHA | Cardiovascular & Brain Longevity

2000 mg of wild-caught fish oil per softgel, standardized to deliver 720 mg EPA + 480 mg DHA in the clinically-studied 3:2 ratio. Triglyceride-form (rTG), molecularly distilled, third-party tested for heavy metals and PCBs, in a small enteric-coated softgel — no fishy reflux, no aftertaste. The single nutrient with more peer-reviewed cardiovascular and brain-longevity research behind it than anything else in this catalog.

The 30-second answer

• Why people take it: long-chain omega-3s (EPA + DHA) lower triglycerides 20–30% (Skulas-Ray 2019, AHA Science Advisory), reduce systemic inflammation (Calder 2017), and physically build the phospholipid membranes of every neuron, retinal cell, and cardiomyocyte you own.
• What it’s NOT: not flaxseed oil. ALA-to-EPA conversion in humans is 1–10% (Burdge 2002), and ALA-to-DHA is closer to 0.5%. If your goal is a measurable Omega-3 Index, fish oil is the only practical route — or algal oil for vegans.
• The form matters: triglyceride (TG / re-esterified TG) is absorbed roughly 70% better than ethyl-ester (EE) over 6 months (Dyerberg 2010, Neubronner 2011). Most pharmacy fish oil is EE because it’s cheaper to concentrate. Ours is rTG.
• Dose: 2 softgels = 1,440 mg EPA + 960 mg DHA. The dose used in REDUCE-IT (Bhatt 2019, NEJM) was 4 g/day icosapent ethyl, but every dose-response analysis (Skulas-Ray 2019, Mozaffarian 2011) shows clear cardiovascular signal starting at ≈1 g/day combined EPA+DHA.
• Timeline: Omega-3 Index moves measurably in 8–12 weeks. Triglycerides move in 4–6 weeks. Joint and mood signal in 8–16 weeks. Cardiovascular event reduction is a multi-year endpoint.
• Where it sits in this catalog: alongside Vitamin D3 5000 IU + K2 MK-7 100mcg and Magnesium Glycinate 400mg TRAACS, this is one of the three foundational supplements that earn their place in essentially every healthspan protocol — the always-on layer underneath your NAD+ stack.

Why omega-3s sit at the foundational layer

Most longevity stacks chase mechanisms — sirtuins, mitophagy, NAD+ precursors, senolytics. Omega-3s are different: they are a structural intervention. Every cell membrane in your body is built from a phospholipid bilayer, and the fatty acids on the “sn-2” position of those phospholipids dictate how the membrane behaves — how fluid it is, how it folds, how its receptors signal, and what eicosanoids it releases when injured.

EPA and DHA compete with arachidonic acid (the omega-6 you get from seed oils, conventional poultry, and processed food) for incorporation into those membranes. When dietary EPA/DHA is low and arachidonic acid is high — the default modern Western pattern — cells generate predominantly pro-inflammatory eicosanoids: 2-series prostaglandins, 4-series leukotrienes, thromboxane A2. When EPA/DHA replace arachidonic acid in the membrane, the same enzymes (COX, LOX) instead generate 3-series prostaglandins, 5-series leukotrienes, and the entire Specialized Pro-resolving Mediator (SPM) family — resolvin E1/E2, resolvin D1-D6, protectin D1, maresin 1 — which actively terminate inflammation rather than amplify it (Serhan 2014, Nature; Calder 2017).

This is why omega-3 supplementation has measurable effects across 12+ unrelated organ systems: it’s not a drug acting on one receptor — it’s a building material that changes the resolution capacity of every membrane in the body.

The Omega-3 Index — the only blood marker that matters here

The Omega-3 Index (Harris & von Schacky 2004, Prev Med) is the percentage of EPA + DHA in red blood cell membrane phospholipids. It’s the cleanest single biomarker for omega-3 status because RBC membranes turn over slowly (≈120 days) and reflect long-term incorporation rather than the previous meal.

• < 4% — high cardiovascular risk zone. The U.S. average sits in this range. Sudden cardiac death risk roughly 10x vs >8% (Albert 2002, NEJM, n=22,071 male physicians).
• 4–8% — intermediate.
• > 8% — cardioprotective range. This is the level epidemiologically associated with the lowest all-cause mortality in the Framingham Offspring follow-up (Harris 2018, J Clin Lipidol, n=2,500, 11-year follow-up: each 1% Omega-3 Index increase associated with 13% lower all-cause mortality).

2 softgels/day of this product (1.44 g EPA + 0.96 g DHA) typically moves the Omega-3 Index from the 3–5% Western baseline into the 8–10% range over 12–16 weeks (Flock 2013, J Lipid Res — dose-response curve). 3–4 softgels move it faster but plateau in the same range.

Triglyceride vs ethyl ester — why the form on the label is non-negotiable

Native fish oil is in triglyceride (TG) form — three fatty acids attached to a glycerol backbone, just as they exist in fish flesh. To concentrate EPA and DHA above the ≈30% native ratio (most fish oil starts there), manufacturers add ethanol, releasing fatty acids as ethyl esters (EE). EE allows molecular distillation up to >90% EPA+DHA but produces a synthetic form that the gut absorbs differently:

• Lipase activity: pancreatic lipase hydrolyzes TG roughly 10–50x faster than EE (Yang 1990, Biochim Biophys Acta).
• 6-month bioavailability: rTG produces 70% higher RBC incorporation than EE at the same dose (Dyerberg 2010, Prostaglandins Leukot Essent Fatty Acids; Neubronner 2011 same-design replication).
• Reflux/burping: EE generates ethanol on hydrolysis and tends to produce more “fish-oil reflux.”
• Stability: rTG is more oxidation-resistant than free fatty acid (FFA) form, less so than EE.

Re-esterified TG (rTG) is EE that has been enzymatically converted back to TG form — you get the concentration of EE plus the absorption of native TG. Most premium fish oil is rTG. Ours is rTG. Most U.S. pharmacy and big-box brands are EE because the regulatory pathway and unit cost are cheaper. Read the label; if it doesn’t specifically say “triglyceride form” or “rTG,” assume EE.

The clinical evidence — six domains, not just heart

1. Cardiovascular

The cardiovascular evidence is the largest and most contentious in nutrition science. The high-level synthesis:

• GISSI-Prevenzione (Marchioli 1999, Lancet): 11,324 post-MI patients, 850 mg/day EPA+DHA, 3.5 years — 20% all-cause mortality reduction, 45% sudden cardiac death reduction. The trial that put fish oil on every cardiology guideline.
• JELIS (Yokoyama 2007, Lancet): 18,645 Japanese hypercholesterolemics, 1.8 g/day EPA-only on top of statins, 4.6 years — 19% major coronary event reduction.
• REDUCE-IT (Bhatt 2019, NEJM): 8,179 high-risk patients with elevated triglycerides, 4 g/day icosapent ethyl (high-purity EPA), 4.9 years — 25% reduction in composite cardiovascular events. The strongest modern signal, and the basis for the FDA approval of icosapent ethyl as an Rx drug.
• VITAL (Manson 2019, NEJM): 25,871 healthy U.S. adults, 1 g/day EPA+DHA, 5.3 years — no change in primary composite, but a 28% reduction in MI in the “low fish intake” subgroup, suggesting baseline status matters.
• STRENGTH (Nicholls 2020, JAMA): EPA+DHA carboxylic acid form failed to reduce CV events vs corn oil placebo. The negative trial that complicates the EPA-only narrative.
• Triglyceride lowering: meta-analyzed across 70+ RCTs, 2–4 g/day EPA+DHA lowers TG 20–30% in normolipidemic and up to 45% in hypertriglyceridemic patients (Skulas-Ray 2019, AHA Science Advisory).

The honest read: the evidence for triglyceride-lowering and Omega-3 Index improvement is unambiguous; the evidence for hard cardiovascular outcomes is dose-, form-, and population-dependent. The dose used in REDUCE-IT (4 g/day high-purity EPA) is what produced the strongest signal. Your 2-softgel dose here is the foundational maintenance dose, not the pharmacological-event-reduction dose.

2. Brain & cognition

DHA is ≈30% of all gray matter fatty acids (Bradbury 2011, Nutrients) and is concentrated in synaptic membranes. Adult brain DHA turnover is slow but real, and dietary supply matters because de novo synthesis from ALA is <0.5%.

• MIDAS (Yurko-Mauro 2010, Alzheimers Dement): 485 healthy older adults, 900 mg DHA/day, 24 weeks — episodic memory improved equivalent to roughly 3 years of cognitive aging reversal.
• Smith 2010, PLoS One: B-vitamin trial in MCI showed brain atrophy slowed only in subjects with high baseline omega-3 status — a treatment-effect-modifier signal that’s been replicated in the OmegAD and AlphaOmega trials.
• Pottala 2014, Neurology: Omega-3 Index correlated with total brain volume and hippocampal volume in 1,111 women in the WHIMS-MRI cohort.
• BDNF / synaptic plasticity: DHA upregulates BDNF and supports LTP in hippocampal preparations (Wu 2008, Neuroscience). The mechanistic story behind the cognitive trial signal.

3. Mood & mental health

EPA — not DHA — carries the depression signal. Meta-analyses repeatedly show that EPA-predominant formulations (>60% EPA) reduce depressive symptoms while DHA-predominant ones do not (Sublette 2011, J Clin Psychiatry; Mocking 2016 meta-analysis, Transl Psychiatry, n=1,233 patients across 13 RCTs — effect size SMD −0.40 with EPA-predominant). Our 3:2 EPA:DHA ratio is on the EPA-predominant side.

4. Eye health

The retina has the highest DHA concentration of any tissue in the body — outer-segment photoreceptor membranes are ≈50% DHA. The AREDS2 trial (NIH-funded, n=4,203, 5 years) tested DHA + EPA on AMD progression and found no significant primary effect, but multiple smaller trials show benefit on dry eye symptoms (Bhargava 2013), tear film stability, and Meibomian gland function.

5. Joints & inflammation

Omega-3s are the most-studied non-NSAID joint intervention.

• Maroon & Bost 2006, Surg Neurol: 1,200 mg EPA+DHA/day, 250 patients with chronic neck/back pain — 60% reduced or eliminated NSAIDs at 75 days.
• Goldberg & Katz 2007 meta-analysis, Pain: 17 RCTs, omega-3s reduced morning stiffness, joint swelling, and NSAID consumption in inflammatory joint pain.
• Mechanism: resolvins and protectins actively terminate the inflammatory phase rather than just blocking COX. This is why the effect builds over months rather than within hours like NSAIDs.

6. Metabolic / liver

Omega-3s lower hepatic triglyceride content via SREBP-1c suppression and PPAR-α activation. Multiple meta-analyses show 2–4 g/day EPA+DHA reduces liver fat 20–40% in NAFLD (Parker 2012, J Hepatol meta-analysis of 9 RCTs, n=355). HDL typically rises slightly; LDL rises modestly in some patients (the so-called “LDL paradox”), driven by a shift toward larger, less atherogenic LDL particles.

EPA vs DHA — what each one actually does

The 3:2 EPA:DHA ratio in this product (720 mg : 480 mg) is the ratio used in the largest cardiovascular trials including GISSI-Prevenzione — a balanced foundational profile that captures both the EPA-driven inflammation/triglyceride/mood story and the DHA-driven neural/retinal/membrane story. If your goal is purely depression-targeting you’d want pure EPA; if it’s purely pregnancy/infant brain you’d want pure DHA; if it’s general healthspan, balanced is correct.

What’s in each softgel

• Wild-caught fish oil concentrate: 2,000 mg, sourced from anchovy, sardine, and mackerel (low-trophic-level species — minimum bioaccumulation of mercury and PCBs).
• EPA (eicosapentaenoic acid): 720 mg, in re-esterified triglyceride (rTG) form.
• DHA (docosahexaenoic acid): 480 mg, rTG form.
• Other omega-3s: ≈100 mg DPA (docosapentaenoic acid), the “forgotten” intermediate omega-3 with its own resolvin pathway.
• Antioxidant package: mixed natural tocopherols (vitamin E) to prevent in-bottle oxidation. No synthetic BHT/BHA.
• Enteric coating: the softgel is enteric-coated so it dissolves in the small intestine, not the stomach — the single most effective fix for the “fishy reflux” problem.
• What’s NOT in it: no titanium dioxide, no artificial colors, no soybean oil filler (a common label trick in budget fish oil), no proprietary blends.

Quality, sourcing, and oxidation

Fish oil is a peroxidation-vulnerable product. The clinical-grade signals to look for:

• Molecular distillation — multi-stage vacuum process that removes mercury, PCBs, dioxins, and PFAS to below the most stringent international standards (CRN, GOED Voluntary Monograph, IFOS 5-star).
• Peroxide value (PV) < 5 meq/kg and p-Anisidine value (p-AV) < 20 — both measures of oxidation. Industry-grade rancidity is – at minimum — PV > 5 or p-AV > 20. Multiple supermarket brands fail this on independent testing.
• TOTOX (total oxidation) < 26 — the combined freshness metric.
• Heavy metals: Hg, Pb, As, Cd all under USP <232> limits, third-party verified per batch.
• Marine-traceable sourcing: small forage fish (anchovy, sardine, mackerel) — not large predators (tuna, swordfish, shark) where mercury and PCBs concentrate.
• Nitrogen-flushed fill and UV-protected amber bottle — both reduce in-bottle oxidation.
• cGMP-manufactured, FDA-registered facility — per-batch certificate of analysis available on request.

How to take it

• Standard dose: 2 softgels daily with the largest meal of the day. Fat-meal absorption > light/empty-stomach absorption (Lawson 1988, Biochem Biophys Res Commun — the original observation; Davidson 2012 NEJM letter on the same effect with prescription EPA).
• Higher-dose protocol: 3–4 softgels daily for elevated triglycerides, active inflammatory pain, or aggressive Omega-3 Index targeting. Monitor with a finger-prick Omega-3 Index test at week 12 (DHL OmegaQuant or equivalent).
• Timing: any consistent timing works; with-food matters more than morning vs evening. The 24-hour pharmacokinetic curve is flat at steady state.
• If you take a blood thinner (warfarin, apixaban, rivaroxaban, clopidogrel): omega-3 prolongs bleeding time modestly at high doses (>3 g/day). The clinical evidence for actual bleeding events at maintenance doses is weak (Wachira 2014 meta-analysis, Mayo Clin Proc; ACC/AHA 2019 guidelines explicitly do not recommend stopping fish oil pre-procedure for <3 g/day). Talk to your prescriber.
• Surgery: some surgeons request a 7–14 day stop pre-op out of caution. Follow your surgical team’s protocol.
• Storage: cool, dark, dry. Refrigeration extends shelf life beyond the printed expiration. If a softgel ever tastes overtly fishy or rancid, throw out the bottle — it’s oxidized.

What it pairs with — the foundational layer

What to expect — realistic timeline

• Week 1–2: usually no felt change. Some people notice softer stools (mild lipid laxation) or a one-week period of mild fish-oil reflux that resolves once the enteric coating is acclimated. Triglycerides start to decline but you wouldn’t lab-detect it yet.
• Weeks 4–6: measurable triglyceride drop (lab a fasting lipid panel at week 6 if you want a number). Some users notice less morning joint stiffness. Mood signal — if any — starts here in the EPA-responsive subgroup.
• Weeks 8–12: Omega-3 Index moves measurably (re-test at week 12 with a finger-prick kit). Joint, skin barrier, and dry-eye signals consolidate. Cognitive signal — if any — starts here.
• Months 3–6: the membrane composition is now fully turned over. This is the steady-state phase — omega-3 is doing what it does for you, whatever that turns out to be in your particular biology.
• Year 1+: the cardiovascular and cognitive endpoints in the long-term cohorts (Framingham Offspring, AlphaOmega, MIDAS open-label extension) are measured in years, not weeks. Maintenance is the strategy, not pulse-dosing.
• What NOT to expect: not a stimulant, not a quick fix, not a weight-loss agent (modest at best), not a substitute for omega-6 reduction (vegetable oils still matter), not a substitute for blood pressure or lipid medication if your numbers are deep into clinical-treatment range.

Who this is for

• Anyone whose dietary fish intake is <2 servings/week of fatty fish — which is most adults outside coastal Asia and the Mediterranean.
• Anyone running an NAD+ stack, sirtuin stack, or longevity protocol — omega-3 is the foundational substrate underneath those interventions.
• Adults 40+ thinking about cardiovascular and cognitive trajectory.
• Postmenopausal women: omega-3 status correlates with hippocampal and total brain volume in WHIMS-MRI; the period of most-rapid bone and brain aging.
• Athletes and high-training-load individuals managing chronic low-grade inflammation.
• People with elevated triglycerides (>150 mg/dL) for whom dietary change alone hasn’t moved the number.
• Anyone with a family history of premature cardiovascular disease — the highest-leverage intervention category in the entire VITAL/REDUCE-IT/JELIS literature.
• People with chronic joint pain or low-grade inflammation looking to reduce NSAID load.

Who this is NOT for

• Fish allergy: this is a fish-derived product. A vegan algal-DHA product is the alternative.
• Active anticoagulation at high doses: 1–2 g/day combined EPA+DHA appears safe in the meta-analyzed evidence even on warfarin/DOAC; doses >3 g/day in this context warrant prescriber discussion.
• Pre-surgery (< 7–14 days): follow your surgical team’s instructions. Most current cardiology guidance does not require a stop, but practice varies by surgeon.
• Pregnancy: DHA is critical for fetal brain development — but pregnancy supplementation should be guided by your OB, ideally with a low-mercury algal DHA product or a doctor-supervised fish oil protocol. This product is not labeled for pregnancy.
• Atrial fibrillation history: very-high-dose icosapent ethyl in REDUCE-IT modestly increased AF events. Standard 1–2 g/day combined EPA+DHA carries no comparable signal in maintenance trials, but if you have known AF, raise it with your cardiologist before going to 3–4 g/day.
• Chronic GI fat malabsorption (severe pancreatic insufficiency, advanced IBD with steatorrhea): rTG fish oil still requires lipase. Speak with your GI team about phospholipid-form omega-3 (krill, herring roe) which is partially absorbed without lipase.

FAQ

Is this triglyceride form (TG/rTG) or ethyl ester (EE)?
Re-esterified triglyceride (rTG). The form with the best long-term bioavailability data (Dyerberg 2010, Neubronner 2011) and the form most premium fish oil brands use. If you’ve compared labels and seen the EE/TG distinction, this is on the rTG side.

Why is the dose 1,200 mg EPA+DHA at 2 softgels rather than 4 g like REDUCE-IT?
REDUCE-IT used 4 g/day icosapent ethyl (high-purity EPA) in patients with elevated triglycerides on statins as a pharmacologic intervention. The 1,200 mg combined EPA+DHA dose (or 2,400 mg at 4 softgels) is the maintenance dose used in the foundational Omega-3 Index literature and in GISSI-Prevenzione. If your goal is post-MI cardioprotection or aggressive triglyceride lowering, 4 softgels/day = 2,880 mg combined EPA+DHA is closer to the trial-equivalent dose. For general healthspan, 2 softgels.

How does this compare to flaxseed oil or chia?
Flax/chia provide ALA, the short-chain plant omega-3. ALA-to-EPA conversion in humans is 1–10%; ALA-to-DHA is 0.5% or less (Burdge 2002, Br J Nutr). If your goal is moving the Omega-3 Index, flax does it inefficiently. Algal oil (DHA-only or DHA+EPA) is the legitimate vegan alternative.

How does this compare to krill oil?
Krill provides phospholipid-form omega-3 plus astaxanthin, both at lower per-capsule EPA+DHA than fish oil. Phospholipid form has a small absorption advantage in some studies (Schuchardt 2011); the per-mg cost is higher; the krill stocks are managed but ecologically debated. For matched EPA+DHA delivery, fish oil is more cost-efficient. The classical “fish oil + standalone astaxanthin” pair gives you both in measured doses.

Will this raise my LDL?
In some individuals, particularly with high baseline triglycerides, omega-3 raises LDL-C modestly. This is largely a particle-size shift (fewer small dense LDL, more large buoyant LDL) which is metabolically favorable, not a true atherogenic burden increase. ApoB and LDL-P are the better markers. Re-test ApoB at week 12 if this question matters to you.

What about “burping fish”?
Three causes: oxidized oil (the bottle is rancid — throw it out), gastric-dissolution softgels (no enteric coating), and large dose on empty stomach. Enteric coating on this product addresses #2; with-food dosing addresses #3; cool-dark storage addresses #1.

How much mercury / heavy metal is in fish oil?
In a properly molecularly-distilled product, all heavy metals are below detection limits per USP <232>. Mercury bioaccumulates in fish flesh, not fish oil — the distillation process strips it almost entirely. Anchovy/sardine/mackerel are low-trophic-level forage fish that don’t accumulate much to begin with; molecular distillation removes the residual.

Should I take this with or without food?
With food — particularly with a meal containing some fat — absorption is meaningfully better than empty-stomach (Lawson 1988; Davidson 2012 NEJM letter). Same fat meal as your Vitamin D3+K2, your CoQ10, and your astaxanthin if you take them.

Can I take this with my statin?
Yes. The cardiovascular evidence for omega-3 is largely on top of statin therapy (JELIS, REDUCE-IT). No pharmacokinetic interaction. Many cardiologists actively co-prescribe.

Does fish oil thin the blood — should I stop before surgery?
Modest effect on bleeding time at high doses; weak evidence for actual bleeding events at maintenance doses. ACC/AHA 2019 guidelines explicitly do not require pre-procedure cessation at standard doses. Your surgical team may have local policy — follow theirs.

Why DPA on the label?
Docosapentaenoic acid (22:5 ω-3) is the “forgotten” intermediate omega-3 between EPA and DHA. It’s a precursor to its own resolvin family (Rv-DPA series) and has independent triglyceride and platelet effects (Byelashov 2015). It’s naturally present in marine oils (the ≈100 mg here is native, not added) and is generally not concentrated out of premium products.

How do I know if it’s working?
Three options: (1) lab a fasting lipid panel at week 6 and look for triglyceride decline; (2) order a finger-prick Omega-3 Index test at week 12; (3) track subjective endpoints — morning joint stiffness, dry eye, mood, sleep — against a baseline diary. Option 2 is the only truly objective single-data-point readout because the Omega-3 Index reflects the membrane-level intervention you’re actually buying.

Vegan / vegetarian alternative?
Algal oil (Schizochytrium-derived DHA, sometimes with EPA) is the legitimate plant-based EPA/DHA source. Same molecules, different organism, lower aftertaste. We don’t currently stock an algal product but it’s on the catalog roadmap.

Can I take this if I have an iodine sensitivity?
Fish oil contains negligible iodine — iodine concentrates in fish flesh and thyroid, not the oil fraction. Generally compatible with low-iodine diets.

What’s the difference between this and prescription fish oil (Vascepa, Lovaza)?
Vascepa is icosapent ethyl — pure EPA in ethyl ester form, FDA-approved as a drug. Lovaza is mixed EPA/DHA in ethyl ester form, FDA-approved. Both are EE not rTG; both are dosed at 2–4 g/day; both are insurance-billable for triglyceride lowering or for the REDUCE-IT indication. This is not a drug, and the FDA disclaimer below applies. The active fatty acid molecules are the same.

Why enteric coating?
A standard softgel dissolves in the stomach. If the contents oxidize there or the user is sensitive to fish-oil reflux, “fish burps” happen. An enteric-coated softgel passes intact through the stomach and dissolves in the duodenum, where the oil meets bile acids and lipase under physiological conditions. The reflux/burp problem largely disappears.

Where this sits in the True Health Protocol catalog

Omega-3 Fish Oil 2000mg is one of the four foundational always-on supplements in the catalog — alongside Vitamin D3 + K2, Magnesium Glycinate TRAACS, and the NAC+Glycine GlyNAC pair. These are the supplements that do not chase a specific pathway but instead supply the structural and cofactor inputs that every other intervention assumes. Without them, an aggressive NMN/sirtuin/senolytic stack is being deployed onto a substrate-deficient cellular environment.

The supplementary anti-inflammatory and joint pairings — Curcumin + BioPerine, Quercetin, Multi Collagen Complex, Marine Collagen Peptides — sit on top of the omega-3 substrate. The cardiovascular pairings (CoQ10, Taurine) similarly assume omega-3 as the membrane-quality baseline.

The NAD+ family (NMN 1000, NMN 500, Liposomal NAD+ Ultimate, NAD+ Daily Boost) and the senolytic/sirtuin family (Fisetin, Quercetin, Apigenin, Resveratrol, Pterostilbene) layer above this. None of those pathways function correctly with stiff arachidonic-acid-dominated membranes.

The science (selected references)

1. Marchioli R et al. GISSI-Prevenzione. Lancet 1999;354(9177):447-455. (Post-MI all-cause mortality reduction.)
2. Yokoyama M et al. JELIS. Lancet 2007;369(9567):1090-1098. (EPA on statins, Japanese hyperlipidemic cohort.)
3. Bhatt DL et al. REDUCE-IT. N Engl J Med 2019;380:11-22. (4 g/day icosapent ethyl, 25% CV event reduction.)
4. Manson JE et al. VITAL. N Engl J Med 2019;380:23-32. (1 g/day EPA+DHA in healthy U.S. adults, subgroup signal in low-fish-intake stratum.)
5. Nicholls SJ et al. STRENGTH. JAMA 2020;324(22):2268-2280. (EPA+DHA carboxylic acid, negative primary trial — the complicating result.)
6. Albert CM et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 2002;346(15):1113-1118.
7. Skulas-Ray AC et al. AHA Science Advisory: omega-3 fatty acids for the management of hypertriglyceridemia. Circulation 2019;140:e673-e691.
8. Harris WS, von Schacky C. The Omega-3 Index: a new risk factor for death from coronary heart disease? Prev Med 2004;39(1):212-220.
9. Harris WS et al. Omega-3 blood levels and total and cause-specific mortality — the Framingham Offspring Cohort. J Clin Lipidol 2018;12(3):718-727.
10. Dyerberg J et al. Bioavailability of marine n-3 fatty acid formulations. Prostaglandins Leukot Essent Fatty Acids 2010;83(3):137-141. (rTG vs EE absorption.)
11. Neubronner J et al. Enhanced increase of Omega-3 Index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters. Eur J Clin Nutr 2011;65(2):247-254.
12. Yurko-Mauro K et al. MIDAS: Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimers Dement 2010;6(6):456-464.
13. Pottala JV et al. Higher RBC EPA + DHA corresponds with larger total brain and hippocampal volumes — WHIMS-MRI study. Neurology 2014;82(5):435-442.
14. Smith AD et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. PLoS One 2010;5(9):e12244. (Omega-3 baseline as treatment-effect modifier.)
15. Mocking RJT et al. Meta-analysis and meta-regression of omega-3 polyunsaturated fatty acid supplementation for major depressive disorder. Transl Psychiatry 2016;6:e756.
16. Maroon JC, Bost JW. Omega-3 fatty acids (fish oil) as an anti-inflammatory: an alternative to non-steroidal anti-inflammatory drugs for discogenic pain. Surg Neurol 2006;65(4):326-331.
17. Calder PC. Omega-3 fatty acids and inflammatory processes. Biochem Soc Trans 2017;45(5):1105-1115.
18. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature 2014;510:92-101.
19. Burdge GC. Conversion of α-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. Br J Nutr 2002;88(4):411-420.
20. Parker HM et al. Omega-3 supplementation and non-alcoholic fatty liver disease: a systematic review and meta-analysis. J Hepatol 2012;56(4):944-951.
21. Wachira JK et al. Fish oils, omega-3 fatty acids, and bleeding: a systematic review and meta-analysis. Mayo Clin Proc 2014.

Reading on this catalog’s blog

• The Foundational Four: omega-3, vitamin D, magnesium, and the GlyNAC pair
• The Omega-3 Index — the only blood marker that actually measures fish oil status
• Triglyceride vs ethyl ester: why the form on the label is non-negotiable
• The cardiovascular pairing stack — omega-3, CoQ10, magnesium, taurine, vitamin K2
• Membrane fluidity and aging: why every NAD+ stack assumes omega-3 substrate

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Speak with a qualified healthcare professional before adding fish oil to your protocol if you take blood thinners, are scheduled for surgery, or have a known atrial fibrillation history. The information here is educational and reflects published research as of 2025.