How Essential Are the Essential Fatty Acids?

My 2008 Special Report, updated with some new reflections.

I wrote this Special Report in 2008.

This report is reserved for Masterpass members. Learn more about the Masterpass here.

I believe this knowledge is well worth taking in now, 14 years later. I have included updates and reflections below.

My original intention was to investigate the claims of physiologist Ray Peat that the essential fatty acids are not essential at all. I came away from my research believing that they are, in fact, essential, but that mainstream textbooks and reviews made several serious errors. One was that they grossly inflated the requirement. Another was that they missed the most important point, that the requirement is far lower when supplied by animal fats, especially liver.

My most stunning discovery was that the omega-3 fatty acid, EPA, might not even be a normal constituent of the mammalian body. I stand by this discovery and it has shaped my view of modern omega-3 research ever since.

That finding was overseen by Ralph Holman. When I was writing this report I called him to discuss the implications of it, but he unfortunately was in his 90s and didn’t remember the details of the experiments, conducted decades earlier.

I would now update my views from 2008 in several important ways:

• In the report, I make arguments about how we should define “essential.” Today, I would refine my language for greater clarity: something is physiologically essential if it needs to be in the body to prevent signs and symptoms of deficiency. Something is dietarily essential if it has to be present in the our food for the same reasons. In this framework, the physiologically essential fatty acids are the omega-6 arachidonic acid and the omega-3 DHA. These are conditionally dietarily essential depending on nutritional status, genetics, and other factors that can help or hurt our ability to synthesize them from the linoleic and alpha-linolenic acids found in plant oils. The latter, however, are not essential in either sense, unless we stipulate that arachidonic acid and DHA will not be present in the diet. That is, they become essential conditional on the choice to consume an un-supplemented vegan diet.
  

• In the report, I do refer to polyunsaturated fatty acids (PUFAs) as representing an oxidative liability, but I also refer to them repeatedly as contributors to oxidative stress. Today, I would refine my language by adopting the former exclusively and dropping the latter. In other words, PUFAs do not cause oxidative stress. Rather, in the presence of oxidative stress — caused by deficiencies of antioxidant nutrients, illness, toxic exposures, or aging — they pose an oxidative liability. Their presence in excess makes it more likely the oxidative stress will lead to a greater degree of oxidative damage. Lesson 2 of my Antioxidant Course is the best place to learn more about my framework for distinguishing between oxidative stress and oxidative damage.
  

• The distinction between causing oxidative stress and representing an oxidative liability provides a framework for reconciling short-term benefits of PUFAs with long-term harms. The best example of this is that PUFAs decrease the amount of fat stored in the liver in the short-term, but in the long-term they worsen the progression of simple fat accumulation to nonalcoholic steatohepatitis (NASH), which is the pathway for the progression to fibrosis, cirrhosis, and liver failure. For more on this, see my 2012 article, AJCN Publishes a New PUFA Study that Should Make Us Long for the Old Days as well as Lesson 9 in my Antioxidant Course.
  

• My analysis of the heart disease data in this report is honestly cherry-picked. I was trying to illustrate some important points and had not yet had the chance to make the comprehensive analysis of the data that I made later. My full analysis of the topic on vegetable oils and heart disease is found in Lesson 13 of my Antioxidant Course. The gist of this is that short-term well-controlled trials are neutral, but the only trial lasting 8 years suggested that the initial benefit to heart disease is lost with time as an aggravation of cancer risk emerges. That lesson does not cover fish oils, but the situation is similar: trials lasting lasting less than one year showed the bulk of the benefit and the only trial lasting more than four years found a 30% relative increase in heart disease mortality.
  

• I have since developed a much better-synthesized view of the interactions between biotin, vitamin B6, riboflavin, and essential fatty acids in the usually candida-infected skin lesions that are common to all of their deficiencies. This is found in my recent article, High Protein? You Need More Biotin.
  

• The report states that EPA can only be metabolized to compounds that resolve inflammation in the presence of aspirin. There is now evidence that bacteria can cause this conversion, so the ability of EPA to contribute to the resolution of inflammation probably depends on the person according to their microbiome and might interact with probiotics. I discuss and reference this on page 63 of my COVID Guide.
  

• The report states that one or two teaspoons of cod liver oil supplying one or two grams of the sum of EPA and DHA has some support for use during pregnancy, lactation, and childhood, but that otherwise these fatty acids should not be specifically sought out, because a whole-foods diet with a mix of animal products will provide everything needed. I would revise this in several ways:
  

  • First, I would not use one or two teaspoons of cod liver oil indefinitely, so this should be limited to the context of pregnancy and lactation, where it was originally studied. I would limit the childhood dose to 3/4 of a teaspoon, which was the dose Weston Price used. My rationale for cod liver oil dosing is explained in more detail in Nutrition and Immunity.
    

  • Second, some evidence has amassed to support one or two grams of the sum of EPA and DHA for psychiatric disorders, with higher doses of EPA being favored for depression, although the jury is still out on omega-3s and psychiatric disorders in general. If EPA is more effective than DHA, this suggests the effect is pharmacological rather than nutritional, and is a result of the EPA acting as an NSAID and lowering peak inflammation. As I covered in Nutrition and Immunity and in Good Fats, Bad Fats, this risks preventing the full resolution of inflammation. Whether these high doses are needed to replete levels of DHA in the nervous system in adulthood under some conditions needs more research. I am open to the use of high-dose omega-3s in this context, but I lean toward it being a pharmacological effect and I would not use it as a first resort.
    

  • Third, even higher doses of EPA on the order of 4 grams a day has pharmacologic benefit to reduce triglyceride levels. My suspicion is that this effect results from the disruption of carbohydrate signaling, and is mainly serving to disrupt the excessive synthesis of fat in people with underlying insulin resistance. This might have greater value in people with genetic hypertriglyceridemia, but if the problem is underlying insulin resistance I believe that is best addressed directly with nutritional support and body composition management.
    

• My discussion of essential fatty acid deficiency in this report could be broadened to include food intolerances and disruptions to all epithelial barriers, including the gut and the blood-brain barrier. It could also be broadened to include how NSAID use could be a widespread factor causing signs and symptoms of deficiency to arise even when dietary supply of arachidonic acid is adequate. I cover this in Nutrition and Immunity and in Good Fats, Bad Fats: Separating Fact From Fiction.
  

• Finally, in the report I say that outside the context of pre-conception diets, pregnancy, lactation, and early childhood, there is no particular reason to seek out omega-3s on a whole foods diet. While I still largely agree with this, I think that, besides the pharmacological uses covered above, consuming around one serving of fatty fish per week alongside pasture-raised liver and egg yolks is a good thing, as it would provide “reserve capacity” of omega-3s without going overboard.

Apart from those updates, I believe the information below remains as valuable as when I wrote it in 2008. You can listen to the audio, or simply keep scrolling to read the entire report in text format. Masterpass members can also download the PDF.