PUFAs (Omega-3/6 Fatty Acids)

I wrote this for myself as I deep-dived polyunsaturated fatty acids (PUFAs). I find that writing documentation for something helps me learn it, and to figure out what to learn. I'm sharing this in case others find it helpful, but please remember: I'm not a doctor, and any medical advice you see in this is me talking to myself (The “you”s are to me.), not me advising you or anyone else.

Also, fwiw, the source for a lot of this is me talking to ChatGPT. I wrote 100% of this myself, minus quotes (and I typed most of this on my phone (Greek letters included)), and I was pretty careful to call ChatGPT out on its BS and to ask it multiple times across fresh prompts for specifics. I also include data from my own research, which I link to where relevant. I also included some knowledge I already had, and ran a bunch of numbers on my own, and came up with all of my own conclusions from the mechanics and data I was seeing. So while I did use ChatGPT as an alternative to a search engine in developing this note, it was still very much my own endeavor. That said, some “facts” probably do need to be taken with a grain of salt, just because AIs are dumb. So please double-check things if you want! My logic is good though.

I wrote this over the span of two nights, and did a little editing on the third.

Worth noting: There are a lot of Greek letters in this; these are shorthands for the names of those letters: “α” as “alpha”, “γ” as “gamma”, “Δ” as “delta”, and “ω”as “omega”.

Chemistry

Makeup

A polyunsaturated fatty acid (PUFA) is a fatty acid that has a mixture of single and double bonds. There are two main PUFAs: ω3 and ω6; others are rare and largely irrelevant. Their nomenclatures refer to the number of carbons between their first double-bond and their methyl end, with this end referred-to as the molecule's “omega” (Omega (ωμέγα, literally “big O”) is the final letter (the end) of the Greek alphabet.). There are multiple kinds of ω3s and ω6s, with these subtypes differing in length (number of carbons in their spine) and the total number of double bonds they have, and where those double-bonds are located.

There are several kinds of ω3s that are relevant in humans: αLA (α-Linolenic Acid), SDA (SteariDonic Acid), ETA (EicosaTetraenoic Acid), EPA (EicosaPentaenoic Acid), DPA₃ (DocosaPentaenoic Acid), TPA (TetracosaPentaenoic Acid), THA (TetracosaHexaenoic Acid), DHA (DocosaHexaenoic Acid).

There are likewise several kinds of ω6s: LA (Linoleic Acid), γLA (γ-Linoleic Acid), DγLA (Dihomo-γ-Linoleic Acid), AA (Arachidonic Acid), AdA (Adrenic Acid), OA (Oxaenoic Acid), THA (TetracosaHexaenoic Acid), DPA₆ (DocosaPentaenoic Acid, also known as “Osbond Acid”).

Nomenclature

The acids whose names end in “-enoic” are IUPAC-style, which means that their names are just the Greek numbers for the length of the acid and the number of double bonds it possesses. For example, DHA, which is docosa-hexa-en-oic acid, can be literally translated into English as “twentytwo-six-doublebond-carboxyl” (with “carboxyl” meaning “carboxylic acid”, which is something that ends in COOH (Carbon-Oxygen-Oxygen-Hydrogen)); and it can also be notated as 22:6n-3. I stick to the initialisms in this document, for ease of reading.

(Note: αLA, γLA, and DγLA are more-commonly written as “ALA”, “GLA”, and “DGLA”; but my keyboard supports Greek letters, so I've been writing them more-exactly than this more-common convention. I've likewise written “ω3” and “ω6” instead of the longer “omega-3” and “omega-6”.)

Packaging

PUFAs typically come in one of three packages: Phospholipid (PL), Triglyceride (TG), Ethyl Ester (EE). I have listed these packages in order of bioavailability. PL is found in krill oil, TG in fish oil, and EE in synthetic supplements. PL is the form found in your cell membranes, and TG in your bloodstream.

In the body

Enzymes

Conversions

ω3:

• αLA→SDA (Δ6-desaturase)
• SDA→ETA (elongase-5)
• ETA→EPA (Δ5-desaturase)
• EPA→DPA₃ (elongase-2)
• DPA₃→TPA (elongase-2); DPA₃→EPA (peroxisomal β-oxidation)
• TPA→THA₃ (Δ6-desaturase)
• THA₃→DHA (peroxisomal β-oxidation)
• DHA→DPA₃ (peroxisomal β-oxidation)

ω6:

• LA→γLA (Δ6-desaturase)
• γLA→DγLA (elongase-5)
• DγLA→AA (Δ5-desaturase)
• AA→AdA (elongase-2)
• AdA→OA (elongase-2); AdA→AA (PLA₂ / peroxisomal β-oxidation)
• OA→THA₆ (Δ6-desaturase)
• THA₆→DPA₆ (peroxisomal β-oxidation)

Products

ω3:

• αLA: Nothing
• SDA: Nothing
• ETA: RvE₀ (weakly anti-inflammatory)
• EPA: RvE₁-₃, PGE₃, LTB₅, LXA₅, TXA₃ (anti-inflammatory, anti-thrombotic, neuroprotective)
• DPA₃: RvD₀ (mildly anti-inflammatory)
• TPA: Nothing
• THA₃: Nothing
• DHA: RvD₁-₆, NPD₁, MaR₁-₂ (highly anti-inflammatory, neuroprotective)

ω6:

• LA: 9-HODE, 13-HODE (neutral / slightly inflammatory)
• γLA: PGE₁, TXA₁, LXA₁ (anti-inflammatory, vasodilatory)
• DγLA: PGE₁, TXA₁, LXA₁ (anti-inflammatory)
• AA: PGD₂, PGE₂, LTB₄, LTC₄, LTD₄, TXA₂ (highly inflammatory); LXA₄, LXB₄ (mildly anti-inflammatory)
• AdA: 22-HDoHE (weakly inflammatory)
• OA: intermediate step (maybe weakly inflammatory)
• THA₆: Nothing
• DPA₆: PGD₆, PGE₆ (mildly inflammatory); LXA₆, LXB₆ (mildly anti-inflammatory)

Notes

Many PUFAs (ω3s and ω6s alike) compete for the same Δ-desaturase and elongase enzymes. (In practice, though, unless you are one of the few people able to get your ideal PUFA composition through αLA consumption, Δ5-desaturase experiences minimal competition.)

AA and its derivatives create pro-inflammatory eicosanoids; ETA and its derivatives create anti-inflammatory eicosanoids. The more of each (and their prodrugs) that you eat, the more of their byproducts you get. To increase inflammation, eat AA and its prodrugs; to decrease inflammation, eat ETA and its prodrugs.
Notably: γLA and DγLA, despite being ω6s, create anti-inflammatory products.

LA converts into γLA via Δ6-desaturase, then to DγLA via elongase-5, then to AA via Δ5-desaturase. This is why seed oils (which are overwhelmingly LA) ultimately cause inflammation. The extreme overuse of LA in industrial diets is essentially tantamount to putting a pro-inflammatory drug directly into the water supply. You do need AA for your body to work properly, but too much is too much (and it is very easy to get too much).

DHA downregulates elongase-2, which reduces how much AA gets stored as AdA, which can paradoxically elevate inflammation (if not for the fact that this requires a lot of DHA, which calms inflammation). This also helps EPA stay EPA. This feedback mechanism may exist to help EPA convert into DHA when DHA is low but not when it is high.

EPA downregulates elongase-5, which means that as EPA levels rise, αLA becomes progressively less-efficient at converting into EPA.

DPA₆ competes with DHA.

Multiple outcomes

As mentioned, DγLA converts to AA via Δ5-desaturase, which turns it from anti-inflammatory (good) to pro-inflammatory (bad).
Insulin upregulates Δ5-desaturase, EPA, DHA, and SDA downregulate it, and ETA competes for it.
Chronically-elevated insulin (from diabesity) and frequent/prolonged insulin spikes (from regular glucose intake) both therefore result in more AA, meaning higher ω6-mediated inflammation and higher uptake of AA and its derivatives into cell membranes.
Sufficient αLA/EPA intake and healthy insulin levels can prevent DγLA from turning into AA, which allows it to instead reduce inflammation. This means that LA is safer to eat when you're eating enough αLA/EPA, and can actually paradoxically further-reduce inflammation.

Likewise, LA converts to γLA via Δ6-desaturase. But this enzyme slows with age, insulin resistance, and higher αLA and DPA₃ levels. So healthy insulin levels and higher ω3 intake can actually reduce how much γLA and therefore DγLA you have.

AA is converted to AdA by elongase-2. AdA is primarily structural/storage (inert), and can be converted back into AA when needed via β-oxidation or the PLA₂ enzyme.

Topical use

The Δ-desaturases are not expressed in the skin, but the elongases are, meaning that you can apply γLA to the skin to yield DγLA without worrying about DγLA or LA converting to AA. This makes borage oil a potentially great way to treat skin inflammation. My mom suffers with some autoimmunity from a past mono infection, and doxycycline always clears up her skin. DγLA reduces inflammation in one of the same ways doxy does; I wonder if topical borage oil might clear her skin up without the downsides of doxy.

Also, on that note: you can apparently change the composition of your skin cell membranes by just putting lipids on them, which is kinda wild/crazy, but makes sense. Jojoba oil can apparently help with penetration. Vitamin E (an antioxidant) is probably important to add to any skin oils, to avoid rancidification. Failing to couple a PUFA oil with an antioxidant can actually end-up making inflammation worse by directly damaging and intoxicating cells. Also, the ease with which PUFAs oxidize should logically imply that applying PUFAs to your skin will increase your Sun sensitivity and cause you to photoage. So do not apply them without also applying antioxidants (like tocopherol (vitamin E)).

Transport

PUFAs all compete for the same transport lipoproteins. This means that having too much of one kind of PUFA will prevent the transport of another. So if you have a decent ω3 intake but your ω6 intake is astronomical, you make have effectively very little ω3 intake.

Ratios

As mentioned in earlier sections, most ω3s calm the immune system, while AA and its derivatives ultimately aggravate the immune system. Keeping a balance between them helps keep the immune system in-check. In pre-industrial times, the ratio of ω3:ω6 in diet was roughly 1:1–1:4. But nowadays, with the preponderance of seed oils (high in LA, an ω6) out there, it is common to have a ratio of 1:10–1:50. That's very much not what you want.

It's important to note though that this talk of an ω3:ω6 ratio in diet is an oversimplification/heuristic — what actually matters is the ETA/EPA/DPA₃/DHA:AA/AdA/DPA₆ ratio in the body after consumption, because the ratio is really one of anti-inflammatory:pro-inflammatory substrates. Also, because this “ω3:ω6 ratio” is dietary, the “ω6” in it refers pretty much exclusively to LA, which as we know from earlier sections results more in DγLA (anti-inflammatory) when ETA/EPA/DHA/SDA are high, and AA (pro-inflammatory) when they are low.

Limits

Ratio matters generally, but it especially matters when you have enough PUFA intake to where there are more PUFAs than enzymes to handle those PUFAs. At that point, your ratio determines what your body does, rather than raw quantity. Each enzyme has a different limit.

• Δ6-desaturase: 0.3–0.5 g/kg/day of LA, or up to 0.2 g/kg/day of αLA.
• Δ5-desaturase: 0.3–0.5 g/kg/day of DγLA or ETA.
• elongase-2: 0.1–0.2 g/kg/day of EPA or AA.
• elongase-5: 0.2–0.3 g/kg/day of γLA or SDA.

The exact amounts for you can vary a lot by genetics and intake. (Also these numbers are from ChatGPT, so take them with a big grain of salt!)

Eclipsing these limits isn't a great idea in general, since it will mean a backlog of unprocessed PUFAs, which are more-likely to then uncontrolledly oxidize, thus subtly poisoning you and worsening inflammation in that way. So unless you need to go above that limit for some reason and are eating plenty of antioxidants, maybe try to keep below these limits. Also, as mentioned earlier, the activity of some enzymes (like Δ5-desaturase) declines with age, so older people must be less-able to process PUFAs than younger people.

For me at about 111kg of bodyweight, I can handle about 44.4g of LA, 22.2g of αLA, and 16.7g of EPA per day. These are… pretty astronomically high; but, to be fair, I'm a big dude. Apparently, the average weight of Javanese women (random ethnicity I chose because they tend to be smaller than other ethnicities (homo floresiensis admixture)) is 52.5kg, which would make their limits 21 g/kg/day of LA, 10½ of αLA, and 7⅞g of EPA, the formest of which is achievable — it is actually quite easy to hit 30 g/kg/day on a diet when your diet includes seed oils. Because LA is upstream of everything, overdosing on it will overwhelm all of your PUFA enzymes, which will hurt you on the ω3s you consume. So it's paramount to keep your LA intake below your personal limit, because it's very hard to eat even 4g of ω3s per day, let alone anywhere even remotely enough to meaningfully compete with 30g of LA.

Ratio of EPA:DHA

It's not easy to control for EPA independently of DHA. Just eat stuff that has a relatively balanced (between 1:1 and 1:2/2:1) amount of each (most foods that have EPA will be relatively balanced), and you'll be fine. If for some reason you need to pump up DHA specifically, though, then algal oil is your best bet. αLA is effectively useless for most people. More on all this later.

Your body can convert EPA into DHA and DHA into EPA, and these conversions are downregulated by the levels of each; so your body will automagically correct moderate imbalances in eaten EPA/DHA.

Membranes

As mentioned a number of times, PUFAs incorporate into your cells' membranes. You need a certain amount of PUFAs or your cells are too stiff; too much, and your cells are too flexible. This is because your body's “native” fat, palmitic acid, is saturated, which is stable and thereby solid at room temperature. PUFAs, by contrast, are less-stable and thereby liquid at room temperature. Incorporating them into cell membranes destabilizes the membranes. Some instability is actually good — we wouldn't be alive if we were frozen solid, after-all. But too much is bad — we're not supposed to be liquids.

(Also, it's important to note that what matters is not just the total amount of PUFAs incorporated into your cell membranes, but the ratios of them, because different PUFAs have different stiffnesses. Also: saturated fat intake reduces the rate of PUFA turnover in membranes.)

Oxidation / Rancidification

Unfortunately, all PUFAs are prone to oxidation, and the result of that is that PUFAs will literally go rancid while they are part of your cells. This obviously hurts the affected cell, and causes inflammation — the immune system has to clean up this damage. Worse, the resulting rancid byproducts (termed “OXLAM”s in the case of LA, the easiest PUFA to get through diet) are directly toxic in myriad ways. So not only does your cell now have a hole in it, but that hole has a bunch of poisons in it that have wide-reaching negative everywhere in your body.
ω3s (being more-unsaturated) are even more-likely to go rancid than ω6s, though potentially with slightly less-bad byproducts.

So there is probably some compromise to be had somewhere between “enough PUFA intake at the right ratios to achieve optimal cell membrane fluidity” and “no more PUFAs than your body has the capacity to antioxidize”, because PUFAs are in a sense ticking time-bombs for our cells.

And so, in this way, PUFAs are paradoxical: your brain needs them for optimal function, but the very molecules it needs can at any time just randomly turn into a neurotoxin. The human body is full of paradoxes like this. It unavoidably produces toxins all day long from all manner of processes. You definitely want to avoid toxins where you can; but sometimes there are trade-offs there. Current medical consensus views the upsides of increased cell-flexibility as worth the trade-offs of oxidation risk. But this said, you can absolutely reduce the rate of oxidation by consuming more antioxidants. And so I think that, given the propensity of PUFAs (ω3s especially) to rancidify, it is probably unwise to suggest their consumption without also suggesting the consumption of a proportional amount of antioxidants.

Also: in general, it's bad for almost anything in your body to randomly oxidize — not just PUFAs. But PUFAs are particularly prone to it.

Genetics

From ChatGPT:

1. FADS1/FADS2 (Fatty Acid Desaturase 1 and 2)

These genes encode delta-5 and delta-6 desaturases, which are crucial for converting shorter-chain PUFAs (e.g., linoleic acid and alpha-linolenic acid) into longer-chain forms (e.g., arachidonic acid and EPA/DHA).

• rs174537 (G > T) [FADS1]

  • T allele: Reduced conversion of linoleic acid (LA) to arachidonic acid (AA), decreasing inflammation risk and potentially requiring more dietary long-chain PUFAs (EPA/DHA).
    
  • Strongest known SNP affecting PUFA metabolism.

• rs174545 (G > C) [FADS1]

  • C allele: Lower delta-5 desaturase activity, decreasing arachidonic acid (AA).
    

• rs174550 (T > C) [FADS1]

  • C allele: Lower conversion of linoleic acid to arachidonic acid, favoring lower inflammation.

• rs3834458 (Insertion/Deletion) [FADS2]

  • Insertion: Increased delta-6 desaturase activity, boosting PUFA synthesis.

• rs1535 (A > G) [FADS2]

  • G allele: Lower conversion of alpha-linolenic acid (αLA) to EPA, suggesting a greater need for preformed EPA/DHA.

2. ELOVL2/ELOVL5 (Elongases for PUFA Chains)

These genes help elongate long-chain PUFAs.

• rs953413 (G > A) [ELOVL2]

  • A allele: Less efficient conversion of EPA to DHA, potentially increasing DHA deficiency risk.

• rs2397142 (A > G) [ELOVL5]

  • G allele: Lower efficiency in elongating omega-3 and omega-6 PUFAs.

3. SCD (Stearoyl-CoA Desaturase)

SCD is involved in monounsaturated fatty acid (MUFA) synthesis but indirectly affects PUFA balance.

• rs508384 (C > T) [SCD]
  
  • T allele: Lower MUFA production, possibly increasing PUFA levels.

4. ALOX5 (Arachidonate 5-Lipoxygenase)

ALOX5 is involved in leukotriene synthesis from AA, impacting inflammation.

• rs2228065 (T > C) [ALOX5]
  
  • C allele: Lower leukotriene production, reducing inflammation risk.

5. CPT1A (Carnitine Palmitoyltransferase 1A)

CPT1A is involved in mitochondrial oxidation of PUFAs.

• rs80356779 (C > T) (P479L) [CPT1A]
  
  • T allele: Found in Arctic populations; associated with reduced PUFA oxidation, helping retain omega-3s. However, some studies suggest it may lead to higher triglycerides in modern diets.

6. PPARG (Peroxisome Proliferator-Activated Receptor Gamma)

PPARG regulates fatty acid metabolism and influences PUFA effects.

• rs1801282 (C > G) [PPARG]
  
  • G allele: Reduced response to dietary PUFAs and a slightly increased risk of metabolic disorders.

My results:

1. FADS1/FADS2
   • rs174537(T;G) — Somewhat reduced Δ5-desaturase activity. (Good)
   • rs174545(C;G) — Somewhat reduced Δ5-desaturase activity. (Good)
   • rs174550(T;C) — Somewhat reduced Δ5-desaturase activity. (Good)
   • rs3834458(?;?) — Untested
   • rs1535(A;G) — Somewhat reduced Δ6-desaturase activity. (Bad)
2. ELOVL2/ELOVL5
   • rs953413(C;C) — (forward strand reading; same as G;G in this context) Normal (Good)
   • rs2397142(?;?) — Untested
3. SCD
   • rs508384(?;?) — Untested
4. ALOX5
   • rs2228065(?;?) — Untested
5. CPT1A
   • rs80356779(G;G) — (reverse strand reading; same as C;C in this context) Normal (Good)
6. PPARG
   • rs1801282(C;C) — Normal (Good)

In summary, ceteris paribus (assuming no other genes impact this), compared to normal:

• I may be more-able to handle a semi-poor ω3:ω6 ratio.
• My αLA and γLA conversion may be lower.

Intake

The optimal ω3 index (the percent of your red blood cell (henceforth “RBC”) membranes composed of ω3s) appears to be 8–10%, with up to 12% sometimes targeted. Your current ω3 index is gradually (over 4 months — the lifespan of an RBC) adjusted up and down according to chronic ω3 (and antioxidant) intake. I generally do not like the idea of loading doses for things, after I experienced kidney paid from a common creatine monohydrate loading dose of 20g/day for the first week. As with many things, for supplementation it's generally best to go the slow-but-steady way.

To reach an 8–10–12% ω3 index on a 2000kcal diet, you need to consume 2–3–4g of ω3s. (ChatGPT spat out a bunch of papers I haven't read as citations for these figures.) I, being larger than the average person, have correspondingly higher needs. I had my BMR measured a year ago, and it was right about 2500kcal. Guidelines from various medical organizations suggest that PUFA intake should be proportional to caloric intake. So for me to reach the target ω3 index, I would need to eat 2.5–3.75–5g of ω3s; and if I were to be physically active again (3000kcal/day), I would need to eat 3g–4.5–6g of ω3s.

In-keeping with what was mentioned in the ratios section, your ω6 index should be kept similar to your ω3 index. That means the same amount of dietary ω6s as dietary ω3s. If your dietary ω6s are higher than your dietary ω3s, then consider targeting 12% instead of 8–10% for your ω3s.

Options

Given how hard it is to avoid ω6s in our postmodern world and given that I will likely burn a little more Calories than my BMR on any given day, I have decided to use 4g of EPA+DHA as the target for all the calculations in this section — this is rounded-up from the 3.75g that should give me 10% when sedentary.

αLA

αLA is… problematic, to say the least. Your body converts less than 5% of it into DHA and 5–15% into EPA, these being what our bodies actually use. The exact amount varies a lot by person, and is worsened by age, improved a lot by estrogen, worsened by LA intake, and worsened by insulin. The majority (80%–95%) of the αLA you consume is burned as energy, stored in fat cells, used in cell membranes, or peroxidized. So this is not a particularly useful lipid.

(Note that I am assuming that the DHA and EPA percentages are independent; but it might well be that the DHA percent is downstream of the EPA percent, which would make the numbers even worse than what you'll see below.)

The best options for αLA are perilla oil (60%ish), chia seed oil (59%ish), and flaxseed oil (55%ish), in that order; though all are great sources. However, what your body actually uses is not what you see in those numbers. The average human αLA → DHA+EPA conversion rate is 12.5%; and your actual conversion could be as low as 5% (with a near-total lack of DHA) or as high as 20% (if you're young, female, have low LA intake, and don't have bad genetics). The LA in these oils are 14%ish for perilla, 18%ish for chia seed, and 17%ish for flaxseed. Compare that to the DHA+EPA your body is making: about 3%–7%–12% for all of these. That is not a fantastic ratio. In the best-case scenario (perilla and great conversion), your ratio is ω3:ω6::12%:14%::1:1 (good) and your worst-case scenario (flaxseed and poor conversion), your ratio is ω3:ω6::3%:17%::1:6 and you are DHA-deficient (bad).

1tbsp of flaxseed oil has about 7640mg of αLA. That translates to 382–955–1528mg of EPA+DHA. For me to get enough EPA+DHA, I'd need 10.5–4.3–2.6tbsp of flaxseed oil per day. 1tbsp of flaxseed oil is about 122.5kcal. When multiplied by the number of tbsp needed, that yields 1283–513–321kcal. Unless I have peak conversion, that's a lot of calories for not a lot of DHA and potentially a lot of LA. I grant that I am a large person, and that the amount of flaxseed oil needed by the average Indonesian woman (who is half my mass), would be half this. If you are small, have high conversion efficiency, and are using perilla oil, you can probably get by on a pretty reasonable 150kcal of oil per day. But if you're not that ideal person, you're kind of SOL.

Perhaps the worst thing about αLA is how much of a black box your personal conversion is. To depend on αLA as your sole source of ω3s, you'd have to commit to the lowest regimen (2tbsp) for months, have your ω3 index checked, adjust accordingly, and repeat to confirm; then, you'd have to regularly check it as you age, and you'd have to go on ERT at menopause.

And even with high αLA conversion, your DHA will still be lower than it would be with fish oil. You must accordingly consume algal oil alongside perilla oil, to get yourself a more-even balance of EPA+DHA. Assuming the αLA→EPA and αLA→DHA conversion percents go up and down linearly to each other, you could have ratios of EPA:DHA::1:0–4:1–3:1. One particular fish oil product, for comparison, is EPA:DHA::4:3.
Let's do the math for myself. I'd need 2286mg of EPA and 1714mg of DHA to hit that 4:3 ratio. Assuming average αLA conversion, I'd need 3tbsp of flaxseed oil (which would also provide 191mg of DHA) and 0.5–0.85tbsp of algal oil (though it'd vary by oil). That's about 450kcal/day, all together. And the cost would be $1.86 for the flaxseed oil and $0.61 for the algal oil, so $2.47/day, and $74.16/mo.

So I just don't see αLA being viable as an ω3 source unless you're in a small minority of young women who are physically small and posses peak αLA conversion. Based on all the above, I'd argue that anyone who unironically encourages you to meet your ω3 needs with αLA does not actually know what they are talking about, because the numbers simply do not pan out.

It gets worse, though. 7640mg of αLA at 55% of the total fat means a total fat of 13891mg; and 17% of that total fat being LA means 2361.5mg of LA. This means that to get your ω3s via αLA, you must also consume 24.8–10.2–6.1g of LA. If you are not high on αLA efficiency, the amount of oil you need to get enough αLA to make your EPA/DHA will include so much LA that you completely overwhelm what your enzymes can actually process in a day.

It gets even worse: As mentioned much earlier in the document, EPA downregulates a crucial step in the αLA→EPA chain, meaning that αLA is self-limiting, and you may end-up being unable to get an optimal EPA level through αLA consumption, even if you somehow eliminate all that LA.

DHA

DHA comes principally from algae. You can easily add it to your diet with algal oil, but this is inherently deficient in EPA. Some oils are fortified with EPA, but typically not with enough to meet your needs. Also, algal oil is less-bioavailable than, say, krill oil.

At 1800–3000mg of DHA and 0–300mg of EPA per tablespoon of algal oil, I would need 1.25–2.25tbsp of algal oil per day to get enough ω3… and it would leave me with a serious EPA deficiency. At $0.72/tbsp, I'd be out $27–$48.6/mo.

Algal oil is simply unviable as an ω3 source unless paired with a lot of αLA, which is likewise fraught as a source. Accordingly, algal oil's only real use is to supplement DHA subsequent to a proper animal-based EPA+DHA supplement.

EPA+DHA

Afaik, all significant EPA sources come also with DHA; and EPA comes primarily from krill that eat algae. Krill oil is the healthiest, most-bioavailable even mixture of EPA/DHA. However, this is not really food, and I'd have to take like 8 capsules a day with a high-potency supplement, which at $0.11/capsule amounts to $26.4/mo. This is the most-affordable, most-absorbable, most-antioxidized, lowest-Calorie (99.2kcal) option, but I really don't like the idea of swallowing 8 of these capsules each day.

Caviar (salmon roe) is an actual food option, but it's not cheap. I'd need probably 4tbsp/day, and with cheap caviar ($44/lb), I'd be looking at $5.81/day. That's $174.45/mo. Unsurprisingly, this is quite expensive (though at least it counts as food, meaning less money spent on food). Surprisingly, however, this is not a lot more money per ω3 than fish. So it may be a good idea to alternate between caviar and fish to potentially halve my exposure to whatever pollutants are present in either.

Pasture-raised eggs, grass-fed beef, grass-fed cow's milk, and grass-fed pork lard all have ω3s, but none have anywhere near enough to meet your needs. You should still eat them if your income permits, though, because they have other health benefits over the factory-farmed alternatives.
The best option among these are ω3-enriched eggs, and they're almost viable (if you love 3-egg omelets and want to eat them for literally every single meal)… but not really.
Anyways, for the sake of completeness: it would take 10 very-high-EPA eggs per day to get enough EPA (a lot of specialty eggs, and a lot of money); and it would take 27–80 pasture-raised eggs per day. So… not a realistic option (unless you're Gaston).
The same can be said for any other “ω3-enriched” versions of the above.

Fish products

Past these are fish oil, which can take the form of a supplement, a bottle o' cod liver oil (bad option for ω3 supplementation because I would literally assuredly die from hypervitaminosis A at the amount of CLO I'd need to ingest), and fatty fish.

Fish and fish-derived products are problematic. Our oceans are polluted. Of particular note is methylmercury, which is exceptionally toxic, and which gets into the water via coal burned about 50 years ago (thanks, Boomers). Different waters are more or less polluted. Do not eat shit from the Baltic Sea — dioxins, PCBs, and other industrial horrors will lurk in food wrought therefrom.
The north Pacific tends to be among the least bad waters out there, but even it is polluted.

Fish Oil

Molecularly-distilled fish oil is a decent option. It should be devoid of methylmercury (which is stored in muscle) and it should have almost none of the fat-soluble pollutants in fish (methylmercury, PCBs, dioxins, PFAS, etc). A fish oil that is molecularly distilled and that states what fish it came from is best — you want it to come from the bottom of the food-chain: sardines, anchovies, mackerel, etc.

Unfortunately, it works out to a similar price to krill oil, even if you get it high potency or in a bottle. And at that point, krill oil is the better choice for numerous reasons.

Fish

Apparently two kippers of herring per day can provide enough ω3s for me, but even though it's pretty much at the bottom of the fish food chain, the sad truth is that most of the ocean toxins we don't want to eat are inherently drawn to the very fats and proteins we're eating fish for. There's little winning. I'm not interested in dailily microdosing methylmercury/etc. It gets even worse when you consider the plasticizers you're ingesting from fish stored in lined cans. And while you can find some fatty fish in glass jars, I'm not about to deal with the PITA that is deboning small fish all the time.

That said, just two kippers per day is a pretty winning proposition. It's affordable for what it is (meat), it's tasty, it's easy to find a large selection at stores and in a boneless form too. But it's just tricky to find them from sustainable fisheries in unpolluted waters and stored in cans without plasticizers. That said, I've never had a kipper brand I didn't like the taste of.

I can also eat sardines, which are basically just young herring, and are a little closer to the bottom of the food-chain. They don't typically come as smoked kippers though, and I like kippers.

Also, I like that two herring per day is not a weird thing to eat. My ancestors (mostly Norwegians, but also Saxon English, Scots, and Swedes) have been eating fish all the time since they first set foot in Scandinavia 60,000ish years ago (my mitochondrial haplogroup is from the first humans to ever go to Scandinavia). My grandpa ate and my uncle eats herring for lunch all the time. One of my most-important heuristics for food, is “did normal people eat this as a staple before industrialization?”, and a couple herrings a day seems to me to be a resounding “yes”.

All of this said, though, the way the fish is prepared matters — heat will oxidize ω3s in the fish. So the actual amount you end up with may be less than you set out for. It's probably best to eat the fish right out of the tin, such as by mixing it in to the rest of your meal after it has cooked.

Ideally, I'll be able to find frozen or glass-canned kippers that were sustainably fished from Hudson Bay, the Barents Sea, the northern Pacific (Alaska and British Columbia), or the northern Atlantic (Iceland, Norway, and Greenland).

Alright, that's enough of a foreword; lets get into my options:

• Polar was the best flavor and price, but it's Baltic, which is… not healthy to eat. It would have taken me 3 tins per day to get enough ω3s. That's $3. Dirt-cheap, but it's from shitty waters, so you're getting what you pay for. What you save now you'll more than make up for in medical costs if you get cancer from all that pollution in the Baltic Sea. Yes, the listing on Wal-Mart's website says “caught in the wild sea of the Norwegian North Sea and Northeastern Atlantic Sea”; but the actual cans say they're Baltic; more, the cans are lined with BPA-NI.

• I switched to this one once I realized Polar was typically Baltic. I don't know where in Canada this herring comes from, and that's not good. Also, it would have taken me 4 tins per day to get enough ω3s, which is 400g and $7.28 — quite a lot, on both counts.

• Bar Harbor makes a large tin of smoked, boneless sardines — it might as well be a tin of kippered herring. I used to eat a fair bit of this in the past, and I liked it. It doesn't list its ω3 contents, but MyFoodData says 190g of kippered herring should be 4225.6mg of ω3s, which is believable for this product given its fat totals. This is dead-center of what I need to achieve at 8%–12% ω3 index. This particular product is fished from the Bay of Maine, which is somewhat polluted, particularly with PFAS (I don't love this.); but it's also not the worst oceanwater out there, and the product is at least certified sustainable. My daily costs would be $4.625 for one can — high, but not obscene. Also, I can buy it at Publix (which is what I did in the past).

• Bar Harbor also makes a large tin of kippered herring for the same money. It's the same species and nutrition facts as the sardines. This, I cannot buy at Publix. Also, while the picture at this link says it's lined with BPA-NI, the overpriced ones for sale on Amazon say they're BPA-free. The only Bar Harbor stuff I've seen irl have all been BPA-free, so it's possible what's on their website is just an old picture. But, anyways, my point is: it seems to be basically the same product as their smoked sardines, just with different market segmentation.

• Another Sardine option (one that I've always really liked the idea of but never seen in stores) is Wild Planet. It costs a lot more than the competition, but you're getting sustainably-caught fish from safe waters. I'd need to eat four tins of this each day to hit my ω3 needs, which would amount to $14.24/day for 4g ω3s and 80g protein. That's… a lot of money. And while that's a decent chunk of my daily protein needs, it doesn't bring me to the 220g/day that beef and chicken can get me to for way less money. So it's really hard to justify getting this.

• Mackerel is another option, but I haven't looked into it yet.

• Salmon could also bear investigation, despite not being low on the food-chain.

• Shellfish also bears investigation.

Antioxidants

Eating a lot of PUFAs means needing to eat a lot of antioxidants. The easiest way to do this is berries. Eat some berries with your herring. Just like Scandinavians do and have done since time immemorial. Herring + lingonberries is a winning combination.

Or take mixed tocopherol (vitamin E) supplements.

Krill oil comes with antioxidants already: astaxanthin.

Also, NAC (a precursor to glutathione, a powerful antioxidant) can be helpful to supplement. Your body won't make more glutathione than it wants, so you can't overproduce it with NAC; but NAC will at least ensure you have enough precursors.

I've heard CoQ10 could also be a good add, but I've not looked into it yet.

Usage

Storage

As mentioned countless times: PUFAs are prone to oxidation. It is therefore paramount that you store them in total darkness with absolutely minimal oxygen exposure, and ideally at low temperatures. That means painted glass stored in a refrigerator or freezer.

Products that come in plastic bottles are typically exposed to oxygen through the plastic.
Products that come in clear bottles are exposed to light.

Capsules are less-susceptible to oxidation than bare oils. But if they have strong fishy tastes/smells, be aware that this can indicate rancidification. Rancidification means the creation of toxins. You don't want to be eating those. Throw away any PUFA supplements that have gone bad.

Canned fish should be refrigerated if possible.
Bulging cans are likely to have gone bad.

Cooking

PUFAs are best-eaten without cooking. If you must cook them, microwaving in a covered dish is best — you want to keep the temps low (at or below 100°C is a good rule-of-thumb), and you want to prevent oxygen from mixing in.

Result

I'm either going to have to start taking 8 krill oil capsules per day, or I'm going to need to re-start eating a couple kippers every day. The first step to the latter is finding a product I fully trust — after-all, we are what we eat, and I do not want to eat industrial pollution. And in either case, I need to add some jam on the side, too.
Down the road of this, I should get my ω3 index and my triglycerides checked, to gauge whether I need to make any changes.

And I'm going to continue to do everything I can to avoid seed oils. They're everywhere and inescapable and just outright bad for you at the quantities they are used nowadays. The easiest way to get a healthy amount of LA is to aim for 0 LA, and then the stuff that inevitably slips past that goal will likely put you where you need to be (or, at least I reckon so, anyway). But if you end-up finding you do need to deliberately eat some, it's easy to find.

Also, I'm going to stop eating peanuts. Their ω6 content is crazy-high. ¼ cup of peanuts is my entire day's worth of ω6s. I've been eating ⅓ cup with my breakfast for years and not been balancing it with sufficient ω3s. With how chock-full peanuts are with ω6s at such low volumes, I struggle to fathom any way that they can be reasonably incorporated into a human diet.
It's ironic how I've been avoiding seed oils only to sabotage myself right off the bat each day. And in retrospect, I wonder if my rapid weight gain in late 2019 after losing a ton of weight in the months prior didn't coincide with switching from sugar-sweetened oats to savory oats with peanuts.