Is our use of cooking oils responsible for the insufficient conversion of Omega-3 to EPA and DHA?

Question

It is well known that the conversion rate of Omega-3 to EPA and DHA is too low to supply us with the required amounts. But this is nevertheless a strange situation, why would natural selection have led to a vulnerability where lack of seafood means that you're going to be deficient on EPA and DHA?

But if we dig deeper and consider someone who only eats natural foods, then we need to consider that such a person will not eat any refined fats and oils. Such a person would end up getting all the fats from vegetables, nuts and seeds, the fats contained in there are for a large part Omega-3 and Omega-6 fats. This doesn't seem to be relevant to the low conversion rate, however, when sticking to such a diet on the long term, a large fraction of the body fat would become the Omega-3 and Omega-6 fats that this person eats.

Then given that in a natural setting, the Omega-3 in the human body is present in high concentrations in fat tissue, it seems to me that it's there that the enzymes that convert Omega-3 to EPA and DHA should be present. The low conversion rate in our bodies is then due to having filled the fat cells with saturated fats an mono-unsaturated fats with only very small amounts of poly-unsaturated fats.

Answer 1

Reasoning with "evolution" and 'natural' settings is a good starting point in terms of human nutrition. But there are caveats in this:

• it tends to be armchair reasoning without archaeological or paleontological evidence
• evolution can be very quick, even for slowly reproducing and mutating humans: before the neolithic revolution humans did not eat so much starches or fats from grassy corns (that we transformed considerably by breeding in a very short time) and lactose tolerance in adults spread very quickly from anatolian cattle keepers to the north and west (mainly)
• evolution is still ongoing and not a finished process we have to live with. Epigenetics alone indicate that genetic adaptability is intergenerationally high
• humans are true omnivores and can and did survive in good health and into old age on a very broad spectrum of foods. And they did so in the past. This is not to be read as everyone in our supposedly golden past got quite old. Insects, game, fish, mollusks, birds, tubers, roots, grass seeds, nuts, vegetables and fruit, all on the menu but in very different ratios at differernt times.

For the vast majority of our history the main concern with food was always: getting more in order to ensure to get enough. More than enough food eaten was only a problem for a minute 'elite' of the past and starvation or malnutrition is still a big problem in some parts of this world. Starving to death is much quicker than eating to death.

It is very funny to read old recipes for "war-bread" in World War I Germany: when the (now so called) bad carbohydrates from grains were in short supply and bran, beets and potatoes were added to stretch out what was there. What today is sold as "health-food" was once one of the very sparse reasons for ordinary Germans to riot and rebel and make a revolution!

The conversion rate for EPA and DHA is usually low but not necessarily too low

If fed much omega-3 the conversion rate in rats can exceed the brain's uptake limit. And in humans this is quite similar.

The conversion efficiency of ALA to EPA varies between 0.2% and 21%, and that of ALA to DHA varies between 0% and 9% (Andrew et al. 2006; Williams and Burdge 2006). The conversion of ALA to EPA and DHA is affected by multiple factors such as sex and competitive inhibition of Δ6-desaturase by LA and ALA. […] Besides the amount of PUFA, the ratio of ω6/ω3 is known to be of nutritional importance as it is the key index for balanced synthesis of eicosanoids in the body (Steffens 1997). For optimal infant nutrition, the ratio of n-6/n-3 must be not higher than 10 (Gerster 1998). In Coastal states where mothers consumed high amounts of fish rich in n-3 PUFA, n-6/n-3 ratios were significantly lower than that of other countries (6.5 and 8.5, respectively) (Kneebone et al. 1985; Boersma et al. 1991). High consumption of plant oils rich in n-6 PUFA and consumption of relatively low marine foods (as source of n-3 PUFA) increases the n-6/n-3 ratio. When one has a diet rich in ALA and lower LA consumption levels, EPA and DHA in muscle tissue increased due to reduced competition for Δ6 desaturase. In most Indian consumers, the n-6/n-3 intake ratio is equal to 1/30-70, but the ideal ratio is 1/5-10 to protect human health. Japanese are the only people who take an ideal ratio of 1/2-4 and this is due to their consumption of seafood (Aleksandra et al. 2009). In communities in the west, consumption of ω6 is much higher than that of ω3; such that in the United States, consumption of ω6 is 10–30 times more than that of ω3. Nutritional scientists suggest the 2:1 to 4:1 n-6/n-3 ratio, which indicates a high consumption of seafood (Aleksandra et al. 2009). From: Long-chain polyunsaturated fatty acid sources and evaluation of their nutritional and functional properties

This is partially illustrated here:

As you can see, both pathways use the same enzymes, making them the limiting factor:

More specifically, most studies in humans have shown that whereas a certain, though restricted, conversion of high doses of ALA to EPA occurs, conversion to DHA is severely restricted. The use of ALA labelled with radioisotopes suggested that with a background diet high in saturated fat conversion to long-chain metabolites is approximately 6% for EPA and 3.8% for DHA. With a diet rich in n-6 PUFA, conversion is reduced by 40 to 50%. It is thus reasonable to observe an n-6/n-3 PUFA ratio not exceeding 4-6. From: Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)?

Omega-3: ALA intakes enough for EPA/DPA levels for non-fish eaters?
The conversion of the plant-based omega-3 ALA to the long-chain EPA and DHA may be increased in vegans and vegetarians who do not eat fish, suggest results from the European Prospective Investigation into Cancer and Nutrition (EPIC).

So while it is true that artificial transfats are really bad, and otherwise industrially damaged fats should be avoided at all cost it is not true that saturated fats have a bad influence on eicosanoid status. Total consumption of plant based alpha-linoleic acid (ALA) is one key, over abundance of omega-6 acids like arachidonic acid (AA) and linoleic acid (LA) is another. That is quite ironic because a vegetarian or vegan diet that is not well planned tends to increase this unhealthy ratio of fatty acids.

While the view that the ratio of all fatty acids to one another has come under attack, the rate of conversion is still dependent on dietary ALA in this view:

Conversion of α-linolenic acid in humans is influenced by the absolute amounts of α-linolenic acid and linoleic acid in the diet and not by their ratio

Too much PUFAs of the wrong kind is detrimental.

Beef from cows that are grass fed tends to be a much richer source of omega-3 acids than those fed soy and maize to fatten them and us up.

If you look at these sources of essential fatty acids:

Apart from leaving out sources of good fat, like the nutritious monkey brain that's full of DHA because that ape ate all the good stuff away from us: You see an important ingredient in our diet suspiciously absent from that picture. The same article, however, does list it partially elsewhere:

Food Sources of Linoleic Acid (18:2n-6) (157)
Food                         Serving         Linoleic Acid (g)
Safflower oil                1 tablespoon    10.1
Sunflower seeds, oil roasted 1 oz            9.7
Pine nuts                    1 oz            9.4
Sunflower oil                1 tablespoon    8.9
Corn oil                     1 tablespoon    7.3
Soybean oil                  1 tablespoon    6.9
Pecans, oil roasted          1 oz            6.4
Brazil nuts                  1 oz            5.8
Sesame oil                   1 tablespoon    5.6

Sunflower-fat and oils from grains are a major contributor of PUFAs in a suboptimal ratio, providing too much AA and LA. And this is one part of refining fat: feeding animals the wrong kind of fodder that then ends up damaging us. Only eating the plants with this ratio directly might be even more damaging. A vegan cooking his gluten-rich seitan-steak in sunflower oil is very likely on the wrong track.

That means from an evolutionary view it is perfectly reasonable to assume that humans evolved to eat what was/is found in the African savannah far from the coast. Only after the neolithic revolution when our western diet slowly came into the abysmal shape it is today did we decrease our ability to synthesise EPA and DHA so much that adding external i.e. marine sources for them is now almost mandatory. If one wants to keep the high amount of omega6 in the diet.

Parts of the reasoning in the question are perfectly valid. But the unqualified call for poly-unsaturated essential fatty acids is the culprit. Mono-unsaturated acids and saturated fats might raise concerns because of their energy density, not because of their effect on DHA/EPA conversion. While omega-6 acids are necessary, they have been present in western diets in much to high ratios. It is therefore unwise to call for an increase in all PUFAs across the board. It is not the use of cooking oil per se that brought us into this situation. It is industrialised agriculture and food preparation that favoured the very lopsided narrowing of our meal plans into the unhealthy category for way too many people.

1. Limit total fat intake, avoid trans fatty acids, and reduce saturated fats.
2. Make monounsaturated fatty acids the primary dietary fat
3. Include good sources of ALA (omega-3 fatty acids from plants) daily.
4. Reduce intake of omega-6 fatty acids, if excessive.
5. Consider a direct source of EPA and DHA.
   [from: Vegetarian’s Challenge — Optimizing Essential Fatty Acid Status]