When it comes to omega-6 fats, the quick and dirty soundbite resonating throughout the ancestral health community has been “omega-6 fats are inflammatory, omega-3s are anti-inflammatory.” Years ago, I wrote a post saying essentially the same thing – that an excessive intake of omega-6s and inadequate intake of omega-3s predispose us to an exaggerated inflammatory response. This sounds right. And the huge discrepancy between the estimated ratio of omega-3 to omega-6 fats in ancestral human diets – 1:3, 1:2, or even 1:1 – and the ratio in modern diets – ranging from 1:25 to 1:10 – just looks pathological. Then, bringing up the rear, you’ve got Bill Lands’ work showing that human populations with low levels of omega-3s and higher levels of omega-6s in their tissues are at greater risk for many diseases like heart disease. It all seems clear cut, no?
Well, kinda. While my general recommendation remains to limit omega-6 fats from vegetable oils, there’s more to the omega-6 story. First, let’s examine the main argument for the importance of the omega-3/omega-6 ratio.
The main argument for the importance of the balanced dietary ratio is that too much linoleic acid (the primary omega-6 fat) increases inflammatory precursors above and beyond the physiological norm, leading to an exacerbated inflammatory response, a general state of systemic inflammation, and the development of the various diseases with an inflammatory root.
Here’s how it’s supposed to work:
Linoleic acid converts to arachidonic acid (AA), a precursor for inflammatory cytokines.
Alpha linolenic acid (ALA; plant omega-3) converts to the anti-inflammatory precursors EPA and DHA, the omega-3 fatty acids we usually associate with fish oil.
Both of these conversions occur along the same rate-limited enzymatic pathway, which means they “compete” for a spot.
If we eat too much linoleic acid, the story goes, our tissue levels of AA will spike and predispose us to excessive inflammation and all the disease fallout that entails. Actually, increasing dietary linoleic acid doesn’t really increase the tissue level of arachidonic acid. Instead, since both linoleic acid and ALA use the same conversion pathway, an excess of linoleic acid does inhibit the conversion of ALA into EPA and DHA, leading to potential deficiencies in the latter nutrients and promoting an inflammatory environment – if you don’t eat preformed EPA and DHA in the form of seafood, pastured animal products, and/or supplements to make up for it.
That’s right: people for whom a fish dinner means battered and fried tilapia sticks are at risk of an inflammatory omega-3/omega-6 ratio, but people following a Primal way of eating are probably safe. Just eating some salmon, sardines, mussels, and pastured eggs can undo a lot of the damage caused when linoleic acid hogs the conversion pathway. Linoleic acid, however, is not directly increasing tissue omega-6 levels.
It appears as if the problem with low ratios of omega-3 to omega-6 is the lack of omega-3, not so much the omega-6. In studies that replace saturated fats with omega-6 fats, the only ones that show benefit are those that also include omega-3s with the omega-6s, while those that replace SFA with just omega-6 increase the risk of death. As long as you’re eating enough fish and other seafood, pastured animals and their fat (and eggs), and/or high quality fish oil supplements, whole food sources of omega-6 shouldn’t increase inflammation. The ratio is a helpful way to monitor your omega-3 and omega-6 intake, but it’s not a physiological law.
That’s not our only issue with linoleic acid, though. Where do we get our omega-6 fats?
No, not you reading this. Not the guy who asks that his eggs be cooked in butter or olive oil at the diner. Not the lady who shudders at the sight of one of those three gallon Costco jugs of corn oil. Where do most people living in industrialized nations get their omega-6s? You know, “normal” people.
Americans get almost 70% of their PUFA (mostly omega-6) from oils, shortening, and margarine and just 6% from beans, seeds, and nuts, 1% from eggs, and 13% from meat, poultry, and fish as of 2004 (PDF). So when we talk about omega-6 intake, we’re really talking about french fries (cooked in vegetable oil), packaged pastries (made with shortening), and processed, high-sugar, high-(vegetable)fat junk food intake.
If most of our omega-6 is coming from the linoleic acid found in cooking oils and processed baked goods, most of the omega-6 we’re eating is highly oxidized, rancid, and maybe even worse.
In one study, just 20 frying sessions were enough to drastically alter sunflower oil, oxidizing the fats and creating cyclic fatty acid monomers which – when eaten – affect fatty acid oxidation, carbohydrate metabolism, and liver enzymes. Dietary linoleic acid that has been oxidized via heat has been shown to directly lead to atherosclerosis. To determine how often most restaurants actually change their frying oil our for new oil, I looked at a topic called “How often do you clean your deep fryer?” in a popular online forum for diner owners. Responses varied from “every day” to “weekly,” with some topping off their oil as they went or relying mostly on filtration of solids. Either way, it’s not very reassuring.
The susceptibility to oxidation may be why diets high in linoleic acid have also been linked to increased oxidized LDL, while diets high in monounsaturated fat – like the traditional Greek diet, rich in extra virgin olive oil – produce considerably lower levels of oxidized LDL.
Omega-6 fat is thus “bad” because the most abundant source of it in our diet is heated vegetable oil, because it’s so susceptible to oxidation, because excessive heating can even create trans-fats out of it, because it’s a proxy for processed junk food, and because it contributes to oxidized lipids in our blood.
But what about whole foods that contain linoleic acid? Are they to be avoided?
Well, let’s look at a few and see what the research says.
Both reviled for its linoleic acid and beloved for its easy metamorphosis into low-carb baking meal, the almond assumes a precarious position in the Primal community. But it’s much more than the bag of linoleic acid. An almond contains vitamin E, magnesium, prebiotic fiber, and protective polyphenols. Why does this matter, and how does it relate to the claimed health effects of excess linoleic acid?
- Magnesium deficiency is strongly related to lipid peroxidation in vivo – the very same thing we’re trying to avoid by limiting omega-6 fats.
- Vitamin E protects the linoleic acid from oxidation (that’s why vitamin E tends to come packaged with linoleic acid in nature, because plants don’t like their fats oxidizing, either).
- The polyphenols found in almond skins protect LDL from oxidation, too, especially when combined with the vitamin E found in almond meat.
- Almond prebiotics are also beneficial, leading to a healthier, more diverse intestinal microbiota.
Or the Brazil nut, famous repository of “so much omega-6!” Yeah, okay, but it’s also a good source of magnesium, vitamin E, and selenium. We’ve already covered how magnesium and vitamin E can counter any potential negative effects of the linoleic acid they come packaged with, so let’s discuss the selenium in Brazil nuts.
One common complaint about linoleic acid is that it depresses the metabolism by interfering with thyroid function; the Ray Peat fans are fairly adamant about this one in particular. However, selenium is one of the most important pro-thyroid minerals in existence. It allows the conversion of the storage thyroid hormone (T4) into the active thyroid hormone (T3). T3 is what increases metabolism, improves LDL clearance by increasing LDL receptor activity, and generally does most of the positive stuff we associate with the thyroid. And arguably the best, and certainly the easiest, way to get enough selenium is by eating a couple Brazil nuts (a slab of sockeye salmon ain’t too shabby a selenium source, either).
It’s no surprise, then, that a single bout of acute Brazil nut ingestion results in long term depression of inflammatory markers.
Conventional wisdom says walnuts are healthy. Primals worry about linoleic acid intake, and walnuts are loaded with it (along with some ALA). How do they fare in the literature?
- Walnut meals (as in a plate of food that’s 75% walnut) reduce the propensity of blood lipids to oxidize (almond meals had similar effects).
- Walnuts increase Apo-A1 (a good lipid marker) and adiponectin (an anti-inflammatory hormone).
- Walnuts lower Apo-B, a rough surrogate for LDL particle number.
Seems they fare pretty well.
Then you’ve got pistachios which, despite their linoleic acid content (13.5g/100g), manage to lower the level of oxidized LDL particles in pistachio-eaters by improving lipids and increasing antioxidant status. They’re also excellent sources of prebiotics, improving the gut microbiota by a greater degree than even almonds.
Hazelnuts, which aren’t that high in linoleic acid compared to some other nuts, are quite good at reducing LDL oxidation and inflammatory markers in patients with elevated cholesterol.
The avocado is rather rich in linoleic acid (though most of the fat is monounsaturated), leading some among us to avoid or severely limit its consumption. But research in actual avocado-eating humans paints a different story. An avocado eaten with your meal lowers the postprandial inflammatory response, triglyceride increase, and endothelial dysfunction normally associated with meals. Avocados also lower the number of LDL particles in your blood, a significant (and probably real/causative) risk factor for heart disease. I mean, c’mon. No guacamole? No diced avocado in your salad? That’s not living.
It’s tough to reconcile this notion of linoleic acid being wholly bad with the overwhelming evidence for the health benefits of nuts and avocados, and I’ve never really bought into it. Omega-6 intake is strongly associated with age-related macular degeneration, for example, but nut intake is not. And I’m not just talking about epidemiological studies, since those are confounded by the fact that nuts and avocados are generally considered to be healthy foods, and people who eat a lot of them are more likely to do other healthy things, like exercise regularly, drink moderately rather than to excess, eat lots of vegetables, and maintain a healthy weight. The above studies are largely well-controlled, with live human subjects – just like you.
I’m not saying you should eat a cup of almonds every day, or forsake all vegetables save the avocado. I’m simply saying you needn’t fear these foods, for they are undoubtedly healthy foods in reasonable amounts (like most others). Foods. See that word? Fear the isolated, super-heated, burnt fatty acids, if you like. I don’t blame you. But nuts? These are complex nutrient matrices teeming with as-yet undiscovered bioactive compounds. Yeah, maybe one day some enterprising biohacker will identify, isolate, and quantify the effects of every last micronutrient in every food and then create the final perfect iteration of Soylent. Until then, the best option we have is to eat food – whole foods that make us feel and look good, help us perform well, and have solid scientific backing. I’d say that’s a pretty good option.
Linoleic acid in the form of refined vegetable oils is still to be avoided. But I’m just not convinced whole food sources of linoleic acid have the same effect on us. We call out other researchers when they demonize a food we like because of a single component, for good reason. We should be careful not to practice nutritional reductionism to justify demonizing a nutrient we don’t like.
Don’t you think?
Thanks for reading, everyone. Let me know what you think about all this. Did you fear avocados before reading this? Do you still?
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