Dr Mercola Doesn’t Like Seed Oils

I’ve learned a great deal from Dr Mercola over the years. His orientation toward natural approaches to long-term health, using diet and lifestyle in preference to pharmaceuticals, aligns with my own. I agree with most of what he has to say.

So, when he launched a campaign vilifying seed oils in the diet, I stood up and paid attention. “Linoleic acid found in vegetables and seed oils may be the biggest contributor to chronic disease in the Western world.” [from Dr Mercola’s Censored Library]

Last spring, he published a review article on health hazards from Ω 6 fatty acids in general and linoleic acid (LA) in particular. He makes a multi-pronged theoretical case linking LA to defective cell membranes, leading to diabetes, cognitive impairment, heart disease, and cancer. At the end, he tries to tie these concerns to real life results with epidemiological studies. To me, it seems that the theoretical arguments are strong, but epidemiology doesn’t seem to support his fears. In particular, most nuts are abundant sources of LA, and yet nut consumption is robustly linked to good health and long life.

Chemistry background

Petroleum oil consists of chains of carbon atoms surrounded by hydrogen. These have no biological presence. Saturated fats (biological oils) in biology are similar chains with COOH at one end — essentially petroleum-like molecules with vinegar at one end. Unsaturated fats have a double bond between carbons, which is a place where there are missing hydrogens, and an angle or kink in the chain.



Saturated fat: 

Unsaturated fat:


For omega 3s, the kink is close to the end opposite the vinegar end. For omega 6s, the kink is closer to the vinegar end.


(The pictures are alpha linoleic acid, ALA, an omega 3 (left), and and gamma linoleic acid, GLA, an omega 6 (right).)


Petroleum oils are biologically inert because there are no enzymes that can attack the carbon-carbon and carbon-hydrogen bonds. But the vinegar end of a fatty acid is a biochemically active site, and each double bond in the fatty acid is another active site. 

Food Chemistry

Animal fats tend to be saturated (no double bonds). They are more viscous. Vegetable oils end to be unsaturated, less viscous, more chemically active.

The double bonds make it easier for the body to work with a fat and put it to use. But each double bond is also a place where oxygen can attack the molecule and turn it into a useless and harmful product. OXLAM means “oxidated linoleic acid metabolite”, and it is not a single chemical, but a class of chemical byproducts which, Mercola says, can cause disease.

Even before it enters the body, unsaturated fats are prone to being oxidized in high-temperature frying. Saturated fats are theoretically better for frying because the double bonds in unsaturated fats are target sites for oxidation. So, for home-fried foods, it is safer to use coconut oil, ghee, butter, or lard. Restaurant and commercially fried foods are often made with unsaturated seed oils, which are likely to be oxidized by the time we ingest them.

The benefits of maintaining the proper omega 3:6 ratio are well-established. Bodily tissues consist primarily of saturated and monounsaturated fats, which are a readily utilized source of nutrients that support the development and maintenance of cells. The primary PUFAs are omega-3 and omega-6 fats, which the body needs in relatively small quantities [ref].

It is important to consume sufficient amounts of omega 3 fatty acids to sustain optimal health, with the recommended daily serving being between 500 and 1000 milligrams of omega 3 [ref, ref]. Contrary to previous perceptions, however, consuming larger servings of omega 3 fatty acids does not support an ideal ratio. Instead, excessive quantities of omega 3s may cause additional metabolic damage—similar to that which occurs due to the conversion of elevated LA levels. [from Mercola & D’Adamo]

It is well accepted that omega 3 fatty acids have benefits for reducing inflammation. Mercola claims that animal-derived omega 3’s are better in this regard, on the authority of this review. DHA and EPA are long-chain omega 3s, and are converted by our bodies into resolvins that cool inflammation. They come from either fish or ocean algae sources. ALA is a short-chain omega 3 that comes from walnuts, chia seeds, flax seeds and other vegetarian sources. ALA can be converted to DHA in the body, but slowly and inefficiently.

Examine.com  agrees

Omega 3 fatty acids in flax seed (as well as in Hemp Protein) are found in the form of Alpha-Linolenic Acid (ALA). Not only is ALA not sufficient to supplement on its own[1], but ALA has to be converted by the body into a usable form, and the ratio of conversion from unusable form to usable is rather poor, somewhere in the range of 5-15%[2]. Omega 3 supplements in the form of EPA and DHA are what the body tends to use for many of the benefits associated with fish oil.

For vegetarians and vegans, supplementing with DHA from algae can “markedly enhance the DHA status (of serum and platelets)” and “provide for the formation of substantial EPA”[3]. Supplementation of ALA and/or GLA is not enough[4].


Mercola fingers inadvertent oxidation as the process that turns LA into toxic OXLAMs. LA becomes incorporated into cell membranes, where it can remain for years. The membranes are then more fragile, and oxidation of LA in the membranes makes them porous, not functioning as the cell needs them to function. A particular OXLAM called 4-hydroxynonenal (4-HNE) accumulates, and high levels can trigger programmed cell death in the same way that peroxide is designed to do. 

Cardiolipin, created from four fatty acids, is essential for the efficient operation of mitochondria. Mitochondria are particularly vulnerable to oxidative damage, and incorporation of LA into cardiolipin is problematic for the mitochondria. Misformed cardiolipin distorts the convoluted shape of mitochondria, impairing their function

Health statistics

The epidemiological evidence for Mercola’s worries is weak, and he admits as much. There are conflicting studies, associating LA level positively and negatively with CV risk. Mercola claims the same is true of LA and diabetes, but the beneficial effects are documented by epidemiology, while the paper he cites for detrimental effects is theoretical. The effect of LA on cancer is mixed, and too small to measure

In this study, higher levels of circulating LA were associated with slightly lower all-cause mortality. In this study, addition of safflower oil to the diet was associated with slightly higher all-cause mortality.

Nuts — a counter-example

Nuts generally have high fat content, with 80% or more of the total calories coming from fat. Most of that fat is unsaturated (87% in peanuts, 95% in almonds, 80% in cashews), so Dr Mercola recommends limiting nuts to a small part of the diet. But many epidemiological studies have associated nuts in the diet with modest but significant benefits for CV risk, insulin resistance, and all-cause mortality,. [meta-analysis, review]


This recent review highlighted the benefits of omega 3s for brain health. The focus is on long-chain omega 3s, derived from either fish or algae. Plasmalogens are singled out as a promising supplement for preventing and even reversing dementia. Plasmalogens are ether phospholipids constructed by the body out of ingested fatty acids including ALA. Plasmalogens are essential components of cell membranes, especially in the nervous system. Levels decline after age 40, and declining plasmalogen levels are associated with cognitive decline. 

Confusingly, the word plasmalogen in the singular is sometimes used to denote a particular short-chain polyunsaturated species, AKA plasmenyl-phosphatidylethanolamine. Dietary supplements of plasmalogen are derived from cow milk or soy, and have been applied successfully in dementia trials. 

Dietary implications

Though there are many things that Mercola gets right, he has never understood aging as internally signaled self-destruction, so he is more fearful of accumulated damage than I think is appropriate. Oxidized lipids fits well with his damage model of aging. I understand the theory, but I think the real-world evidence of epidemiology is more compelling, and epidemiology tells us that nuts and even olive oil are pro-longevity. 

I agree with Mercola that the story about saturated fats ⇒ cholesterol ⇒ cardiovascular risk is discredited. Nevertheless, I’m a vegetarian for 50 years now. There is some evidence that vegetarians live longer, but my personal motivation is more empathetic than scientific [newer ref].  

I continue to eat a lot of nuts in the context of a low-carb vegetarian diet. I make salad dressing from olive oil and avocados, and cook with coconut oil. In the past, I have gone out of my way to include chia seeds and flax seeds, both for fiber and for Ω3s. Having learned what I did in writing this piece, I will back off the chia and flax seeds because their short chain Ω3s do not offer significant value. I don’t eat fish, so I will continue to supplement generously with fish oil and krill oil. It’s possible to get Ω3s from vegetarian ocean sources, but it’s expensive.

I’ve followed this diet for decades and it works for me, but your metabolism is different from mine, and diets are individual by nature. There is no one optimal diet.

12 thoughts on “Dr Mercola Doesn’t Like Seed Oils

  1. The late Ray Peat wrote for many years about the dangers of polyunsaturated fats from seed oils and their detrimental effects on metabolism and mitochondrial function. He was of course derided by nutritionists and doctors as an eccentric quack. He recommended lots of coconut oil, orange juice, coffee, gelatin, carrot salads and aspirin. Anyhow, it seems like the science is slowly catching up to him.

    • Yea I used to read some of Rays stuff and a lot of it made sense but his diet always seemed very restrictive. Maybe worth trying if you’re ill. Didn’t he advocate eating lots of sugar? Personally now I bicycle everyday I need more carbs and my metabolism is on fire.

  2. I’m a fan of Peter Dobromylski’s (Hyperlipid blog) hypothesis for why seed oils are bad for you. This would not be in contradiction to your description of Merocola’s position, they would be complementary, but Peter offers a mechanism over and above oxidative damage.

    Per Peter, cells have a homeostatic mechanism to ensure that they turn off their insulin receptors and stop importing FFAs and glucose once the cell is replete. This happens because the electron transport chain starts to leak backwards once the potential difference across the mitochondrial membrane gets too high, and that creates ROS which in this case act as signalling molecules.

    Those ROS should do their job and then be sanitized by glutathione before they do too much damage. In the presence of levels of PUFA beyond the evolutionary milieu, the ROS are instead spent oxidising fats. The cell may have converted all available ADP to ATP, but continues nonetheless to import glucose and pump up the membrane potential. Eventually this will break the cell permanently. An adipocyte, for example, will be permanently insulin resistant but will constantly leak FFAs.

    I hope I’m describing this OK, most of Peter’s blog these days is at a level which goes right over my head.

    Anyway, what I wanted to argue is this:

    I think you’re saying that epidemiological studies are equivocal and the effects are not large, so it can’t be much of a problem.

    By Peter’s hypothesis, I would not expect to see anything useful from such studies, but there would be a serious problem. Firstly, there’s a threshold effect (PUFA beyond evolutionary levels), which causes a range limit effect in any study on western populations. Secondly, there’s a temporal effect. If you exceed the threshold, you will slowly but inexorably get metabolic syndrome. I gather that some stunning proportion of the US population are already there (do I remember 60% or some such). Once broken, modulating your PUFA will have no further effect, the only amelioration is to control your glucose levels manually (low carb diet).

    To run a useful study, you’d have to start with a population on a diet with a baseline PUFA level an order of magnitude below anything you could achieve with a standard American diet, and who were not already metabolically broken. Then, you’d feed a little extra corn oil to some participants, and watch for twenty years…

    I know this sounds a little like a true believer carefully crafting an unfalsifiable hypothesis, but I think it’s just how it is.

  3. I have been listening to a lot of Georgie Dinkov’s interviews lately who I know Dr Mercola has been influenced by regarding PUFA’s etc. I must admit, I’ve found some of his theories and observations extremely interesting and it has caused me to re-think my position on the low sugar diet I’ve been following and I have started to become more concious of the PUFA’s I have been eating. Have also added in more aspirin, caffeine and niacinamide as per his recommendations, in the hope of increasing my middle age metabolism. So far so good…let’s see.

  4. Artemis Simopoulos wrote the book on oils. In fact she wrote several books on the subject. Her research indicated that we should keep our dietary ratio of omega 6 to omega 3 oils at one-to-one for optimal health. I’ve done this on a vegan diet by avoiding all vegetable and plant oils and eating flaxseed, chia, hemp hearts and walnuts. I eat no other seed or nut because of their unfavorable ratio. I don’t supplement with EPA or DHA. Instead, I find plant sources of ALA to be adequate and enough of them convert into long-chain omega-3s to give me a normal amount in my blood tests, along with excellent health. Generally I have an ounce of walnuts and 1 1/2 tablespoons of flaxseed a day.

  5. It seems like these sorts of theories don’t usually account for the different molecular forms of ostensibly similar nutrients. Maybe his research is better, but I think that would account for a lot of the conflicting nutrition advice.

  6. I’ve suspected that GLA (evening primrose oil) is far more important to the diet than people think. It’s been shown in at least mice to extend the health span. It’s a fatty acid tied to the chaperone mediated autophagy, which is one possible reason for the benefits of having your blood diluted with albumin or younger blood, there is less junk in it due to a functioning CMA because the body can still produce a lot of GLA on its own. On an unrelated note though: I’ve always dismissed Mercola as a fraudulent quack. He’s up there with Dr. Oz in my list of people not to listen to. I dunno why he’s being given more credibility here.

  7. Your article is misleading as you hardly make a difference between mono unsaturated and polyunsaturated fatty acids and you lump them together in a category of “unsaturated fats” versus saturated fats. Animals do not synthesize polyunsaturated fatty acids (pufa) but do produce mono unsaturated fatty acids in abundance. Pufa oxidize at temperatures over 20°C and are very unstable in an environment of 37°C breaking down into toxic and inflammatory molecules. There’s a lot of evidence that high consumption of Pufa correlates with higher occurrence of cancer, diabetes, cardiovascular diseases and chronic diseases while mono unsaturated fatty acids are stable at 37°C and consequently do not correlate with an increase in aforementioned diseases. Obviously lumping together polyunsaturated fatty acids and mono unsaturated fatty acids into one category of unsaturated fats makes “epidemiological evidence” very weak.

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