#81

Maybe or maybe not. The issue is your Omega 6:Omega 3 ratio. If you have have a less than 4:1 ratio, the enzyme, delta-6-desaturase (which Omega 6 and 3’s compete for) that converts omega 3’s in walnuts (alpha-linolenic acid) and other plant based foods into DHA/EPA isn’t sufficiently active. So formally checking an Omega 3 index is necessary to know. Direct supplementation of EPA/DHA is often necessary as vegans run ~3.5, vegetarians ~4%, and Standard American Diet ~4.5% - with goal being 8-12%.

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#82

Do we know anything about what impact being above 12% has? I saw a video from the OmegaQuant people, and they said something like there are not enough people with measured levels that high for studies to have incidentally included enough of them to be able to have much existing observational evidence about the consequences.

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#83

High doses risk atrial fibrillation, and excess stroke. I do mine with goal of 8-9% personally as there is a sweet spot, which is why one needs to measure.

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#84

I just received my Omega test this morning. I was surprised that my Omega 3 level was only 5.1%. I eat fish 2-3 times per week and take 1.25 grams of fish oil (EPA 750mg, DHA 285mg, DPA 50mg) a day. Going to up the fish oil to 2.5 grams and see what that does.

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#85

What “low” means

Most labs now use the Omega-3 Index (O3I) — the percentage of EPA + DHA in red-blood-cell membranes.

  • < 4 % = clearly deficient (higher CVD and all-cause mortality risk)
  • 4–8 % = intermediate
  • 8–12 % = the “optimal” band seen in Japan, coastal Korea, and most RCTs showing benefit

How much does 500 mg/day move the needle?

Daily EPA + DHA dose Typical 4- to 5-month change in O3I Chance of hitting ≥ 8 %
300 mg ≈ +0.3 – 0.6 % Essentially 0 %
500 mg ≈ +0.5 – 1.0 % (large inter-individual spread) Rare unless you started at 7 %
600 mg Mean endpoint ≈ 6 % in an RCT 0 % of participants reached 8 % (GrassrootsHealth)
900 mg Mean endpoint 7.5 % ~25 % reached 8 % (GrassrootsHealth)
1 000 – 1 500 mg +2 – 5 % in 3–6 mo Often crosses 8 % if baseline > 4 % (PubMed Central)
2 000 mg Modelled to lift 5.4 % → 8 % in 20 wk Very likely for most adults (Mayo Clinic Proceedings)

Key point: 500 mg/day is the minimum many guidelines cite for general health (Office of Dietary Supplements), but dose-response data show it usually nudges a truly low O3I upward only modestly. It is seldom enough to exit the high-risk < 4 % zone, let alone reach ≥ 8 %.

Why responses differ

  1. Baseline status – the lower you start, the bigger (in absolute %) each gram produces.

  2. Body size & adiposity – larger lipid pool dilutes incorporation.

  3. Chemical form & timing

    • Re-esterified triglyceride or phospholipid (krill/algal) > ethyl-ester on an empty stomach.
    • Always take with a fat-containing meal; splitting BID slightly improves retention.

  4. Dietary ω-6 load – high linoleic acid competes for the same membrane slots.

  5. Genetics (FADS cluster) – “slow desaturators” need 15-30 % more intake to hit the same O3I.

Practical roadmap for an ovo-vegetarian who minimises calories

Step Rationale Calorie cost
1. Measure baseline O3I (finger-prick kits are <$50). Individual variation is huge; testing beats guessing. 0 kcal
2. Start at 1 000 mg EPA + DHA/day via algal oil (e.g., two 500 mg capsules). Likely to raise O3I by ~2 % in 3 mo; still only ~9 kcal. ≈ 9 kcal
3. Re-test after 12-16 weeks. Full RBC turnover is ~120 d. —
4. If still < 8 %, double to 2 g/day or cut dietary ω-6 (seed oils, commercial snacks). Dose–response and ω-6 reduction are synergistic. ≈ 18 kcal
5. Maintain vitamin E (mixed tocopherols 100–200 IU) & selenium 55 µg to protect the newly enriched membranes from peroxidation. Prevents paradoxical oxidative stress. negligible

When 500 mg is enough

  • You already sit in the 6–7 % band and just want maintenance.
  • You eat ≥ 2 portions/week of oily fish (not applicable here).
  • Your goal is minimal support for pregnancy (many obstetric bodies set 300–500 mg/d).

When you need much more

  • Triglyceride lowering: Rx preparations use 2–4 g/d EPA ± DHA.
  • Post-MI cardioprotection: AHA guideline is 1 g/d, often titrated higher if O3I < 8 %.
  • Anti-inflammatory or neuropsychiatric protocols (e.g., depression with high CRP) routinely test 2–4 g/d.

Bottom line

A steady 500 mg/day of EPA + DHA will usually move a deficient Omega-3 Index upward, but only by about half a percentage point – rarely enough to leave the “low” category. For a robust, evidence-based correction, plan on 1–2 g/day for 3–4 months, then adjust based on a repeat blood test. The extra calories (≈ 9–18 kcal) are trivial compared with the cardiovascular and cognitive dividends of reaching ≥ 8 %.

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#86

What the evidence actually shows — and what it doesn’t

Red-cell Omega-3 Index (EPA + DHA % of total RBC fatty acids) Typical daily intake needed Effect on in-vivo lipid-peroxidation markers (MDA, F₂-isoprostanes, 4-HNE) Key data
< 4 % ≤ 250 mg Highest baseline levels of MDA/F₂-Iso; correcting ω-3 deficiency lowers them. Large meta-analysis of 47 trials of ω-3 dosing < 1 g reduced MDA by −0.38 μmol/L vs control (ScienceDirect)
4 – 8 % 0.5 – 1 g Neutral to ↓ lipid-peroxidation; most RCTs report either no change or small decreases. Review of 20 human studies found zero increase in 4-HNE or TBARS at intakes ≤ 2 g/d (Wiley Online Library)
8 – 12 % (Japanese “coastal” range) 1 – 2 g Consistently lower MDA and urinary F₂-Iso; shift from 9-HNE (ω-6-derived) toward the milder 4-HHE (ω-3-derived). Mori et al. GC-MS F₂-Iso study (1.8 g/d, O3I ≈ 10 %) (Frontiers)
12 – 15 % 2 – 4 g Data sparse; most trials still show no rise provided vitamin E ≥ 10 IU per g fish-oil is present. Hypertensive-diabetic cohort on 4 g/d: F₂-Iso fell 22 % despite O3I ≈ 13 % (PMC)
> 15 – 16 % > 4 g for months Isolated reports of mild uptick in MDA or conjugated dienes when antioxidants are low; also where bleeding and atrial-fib risk starts to climb. Review of high-dose CV trials notes safety concerns appearing at O3I > 16 % (research.rug.nl)

Bottom line: No reproducible threshold exists inside the commonly targeted 8–12 % band at which ω-3 PUFA start driving oxidative damage. Most real-world signals of acrolein, 9-HNE or F₂-isoprostanes fall, not rise, as the Omega-3 Index climbs from deficient to optimal.

Why higher ω-3 does not automatically mean more 9-HNE or acrolein

  1. Origin of the aldehydes matters.
    9-/4-HNE and acrolein are largely downstream of ω-6 arachidonic or linoleic acid oxidation. Raising EPA/DHA lowers the ω-6 : ω-3 ratio and crowds AA out of membranes, so the very precursors of 9-HNE drop. (PubMed )

  2. Different aldehydes, different potency.
    DHA peroxidation yields 4-hydroxy-2-hexenal (4-HHE), which is 3- to 10-fold less electrophilic than 4-HNE and can even activate the Nrf2 antioxidant program. (PMC)

  3. Antioxidant buffering.
    Trials that did report a blip in peroxidation at very high ω-3 intakes used oils with < 2 IU vitamin E per g and subjects with low Se/α-tocopherol status. Adding 100–200 IU of mixed tocopherols or co-ingesting fruit/vegetable polyphenols abolished the rise. (Cambridge University Press & Assessment)

  4. Ex-vivo vs in-vivo confusion.
    Yes, poorly stored fish oil oxidises readily and can generate acrolein—even at room temperature. (J-STAGE) That has little to do with the peroxide load inside your red-cell membranes, which are enzymatically protected and constantly repaired.

Practical guidance

Goal Target Omega-3 Index Daily EPA + DHA (re-esterified TG or algal) Antioxidant pairing
Correct deficiency 8 % 1 g for 12 weeks, then re-test 100 IU mixed tocopherols + 55 µg Se
Sustain optimal 8–12 % 0.8–1.5 g, or 2 oily-fish meals / wk Diet rich in carotenoids/polyphenols
High-dose therapy (TG lowering, inflammation) 12–14 % 3–4 g under supervision ≥ 400 IU vitamin E/day & monitor MDA or F₂-Iso
Do not exceed† ≈ 16 % > 5 g chronically benefits plateau; bleeding & AF risk edge upward

†The European Food Safety Authority flags > 5 g/d long-chain ω-3 as the point where safety monitoring is prudent; this corresponds to an Omega-3 Index in the mid-to-high teens for most adults. (research.rug.nl)

Take-aways for someone worried about oxidative damage

  1. Stay in the 8–12 % “sweet spot.” It maximises cardiovascular and cognitive benefit while keeping oxidative markers flat or lower.
  2. Use fresh, N₂-sealed products. Smell the oil: a paint-like, fishy odour signals pre-formed aldehydes—you’re swallowing the oxidation instead of making it.
  3. Always feed the antioxidant network. The rule of thumb is ~10 IU of mixed tocopherols per gram of EPA + DHA plus selenium-dependent GPx cofactors.
  4. If you must push >3 g/day, measure both sides of the ledger. An at-home finger-prick Omega-3 Index kit plus urinary F₂-isoprostanes or plasma MDA every 3–6 months will tell you whether your antioxidant capacity is keeping up.

Summary

Current human data show no meaningful rise in acrolein, 9-HNE, 4-HNE, MDA, or F₂-isoprostanes until the Omega-3 Index approaches the mid-teens, a zone reached only with pharmacological fish-oil dosing and inadequate antioxidant cover. For everyday health optimisation, aim for 8–12 %, pair ω-3s with ample tocopherols-plus-polyphenols, and rancid-oil worries become a non-issue.

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#87

This seems to be low-quality BS that you copied-pasted from ChatGPT @AlexKChen. DHA supplementation is detrimental, meanwhile EPA supplementation might have cardiovascular benefits: Vitamin O (Omega 3) for athletes - #4 by adssx

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