Many of us may know that the omega 3 ALA (aplha-linolenic acid) is not readily converted into EPA. Even less is converted to DHA. Apparently conversion is slightly better in woman, than for men.
DHA (and EPA), ALA (omega 3) and arachidonic acid (omega 6) are main precursors for eicosanoids.
(Now I may not understand all of this, but I am no stranger to science either, so feel free to point out any errors, or point to a study)
Being that ALA is poorly converted, and little ends up being DHA, and DHA and arachidonic acid is readily converted as bases for eicosanoids generally (and DHA can easily be converted to EPA), it would appear the best eicosanoid precursors are mainly DHA (and perhaps EPA), and arachidonic acid which are preformed and occur in meats - which makes sense logically- we eat meat partly because the chemicals are preformed, because its less work chemically for us.
DHA (EPA) is of course high in fish, and arachidonic acid is high in some fish, and red meat, and occurs to some degree in all meats, eggs and dairy.
Like with omega 3's, and ALA, a similar story can be told of linoleic acid, and AA. AA is far further down the metabolism chain compared to LA.
Now omega-6's have a reputation for being inflammatory, and AA is metabolised into mainly inflammatory compounds such as prostaglandins - but it is also end metabolised into anti-inflammatory compounds, such as the endocannabinoids anandamide, and the powerful tissue anti-inflammatory palmitoylethanolamide - which is a basic part of the tissue inflammatory response. Such endocannabinoids are also required for regulation of responses like pregnancy, excercise, mood and the pain response.
Of course omega 3's, in the form of EPA and DHA provide the missing elements of inflammatory regulation, making the pro-inflammatory parts of the AA cascade less inflammatory with their anti-inflammatory. We need these two (or three if you count the less efficient ALA) precursors in order to provide proper function in our brains and bodies. The two cascades, primarily the EPA, and AA need to be in balance for the inflammatory response not to go too far either way (we also need the inflammatory response, its part of th healing response)
Of course there seems to be a prevaling thought in paleo that we should limit our omega 6 intake severely for its inflammatory effects. But this is in fact a balance with our omega 3 intake. And that we should limit our overall levels because of oxidization. However animals containing animal based PUFAs also contain high levels of Coenzyme Q10, which is shown to reduce such oxidation.
High sources of q10 include organ meats, and a range of fish. Arguably a decent intake of multiple anti-oxidants will also help mitigate this effect. So one could argue that rather than limit PUFAs severely (seeing as we need them), we should eat q10 containing organ meats, fish and anti-oxidant rich leafy greens and coloured berries.
It IMO would be a mistake to overly limit omega 6 in the form of AA, because despite its cascade being pro-inflammatory, PEA is the fundamental anti-inflammatory in skin tissue and endocannabinoids have a raft of vital functions. Of course cooking comes into this cooking reduces q10 and increases oxidation - although not nearly as much as plant oils get oxidised.
It also should be apparent that we will need far less omega 3, or 6 to meet our needs - if we are getting them primarily from meat sources, because ALA is poorly converted, and so is linoeic acid (vs AA). Meat sources of omegas are at least partly preformed, so we need less.
So...(sorry for the ramble)...
I have been thinking, that if high omega 3 is unhealthy, and high omega 6 is unhealthy, yet they are essential for proper function, perhaps the problem with these various studies is the lack of differentiation between animal and plant sourced omegas.
Presumably, a large amount of ALA just remains unused, if you have alot. Perhaps the same is true too of linoleic acid, as it certainly requires a load of work to turn into anything useful. Anyone chime in on these two elements?
Preformed omegas on the other hand, dont need to be ingested in massive amounts, and get put straight to use, efficiently..this would mean less oxidation. It would also mean there would be less direct effect from unusable, or hard to process intermediaries. Its hard to know without alot of research what LA, and ALA and their less useful metabolites actually do in the body when they are not converted into useful substances
Now this is all very much speculation (apart from the few points I am sure of), and I have to also admit that most AA also comes with other omega 6s, and most DHA also comes with ALA, at least in land animals. But that doesnt change that these substances are far more readily usable, and thus really quite incomparable to their less preformed counterparts.
Thus - Is it really right to talk of "omega 3" health effects and risks, and "omega 6" health effects and risks and "omega 3/6 ratios", when in fact some of these omegas are needed in much smaller quantities, are used more efficiently and are much further down the metabolistic chain?
(Or even more fine in detail, when they themselves have their own chemical properties before they are utilitized etc)
I mean to use an easy example, less than 1/10 of ALA becomes EPA. A smaller fraction becomes DHA (virtually none).
If your omega 6:3 ratio is 2:1, but your 3's are all ALA
Your ratio is 20:1, or even maybe 30:1 but most of your 3s are EPA/DHA
- it would seem like the later situation is still more favourable, making this ratio next to useless.
I am not sure about LA conversion rates to AA, but at least vaguely similarly, AA will be more potent than LA. Making the omega 6 side of the equation also out of balance...
Novel done :P
Any thoughts/criticisms/info/studies/reflections on my theories and musings? This isnt my university thesis and I havent studied all year, so no doubt I have some things wrong....and would be interesting to see what people generally think regardless of the heavy details!
asked byJamie_14 (5381)
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on June 10, 2012
at 10:05 AM
In reference to your point about differentiating between plant and animal source omegas I wanted to bring up this study: Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids David Despain's blog does a good job of summarizing the findings.
In my understanding most people are adapted to efficiently convert ALA and LA, perhaps an adaptation to make up for a lack of long-chain PUFAs in the environment of our earliest ancestors. This helped us to grow bigger brains as I understand it. However, perhaps due to their diets; nearly all Native Americans and half of Polynesians and East Asians are dependent on animal sources for DHA especially. They may be protected to some degree from excess LA in plants and seeds but in my opinion that only increases chances that O3 will be dangerously low if one doesn't supplement or make dietary adjustments. I'm beginning to think we need to approach these things with our genetic heritage in mind.
on June 10, 2012
at 07:34 AM
Lots to consider in here. I would like to sit on the sidelines while Erasmus & Peat debate the points you raise.
It has been contended that ALA conversion gets upregulated in vegans - sorry can't find a ref, but seems reasonable if one steps back and reflects on just how adaptable the human organism is, ie successful.
However, I'm with you on getting my omegas from animal sources, and shying from veg sources. No sense in overloading with short chain omega while it gets debated whether they truly get stored, and that slow conversion rates aren't the issue we think.
Stay with the KISS paradigm (Keep it Simple) - and avoid seeds/limit nuts - feast on animal fats to your heart's content.
on June 10, 2012
at 12:48 PM
Is it really preferable to bypass ALA (which would be present at rather high levels in natural diets) in preference to longer chain o3s? Are there no heath benefits to ALA consumption? I think such reductionist thinking ultimately bites you in the ass.