alpha-linolenic

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How too much omega-6 and not enough omega-3 is making us sick

May 8, 2010 in Food & Nutrition, Myths & Truths | 24 comments

vegetable oil poisonIn the last article we discussed the problems humans have converting omega-3 (n-3) fats from plant sources, such as flax seeds and walnuts, to the longer chain derivatives EPA and DHA. Since EPA and DHA (especially DHA) are responsible for the benefits omega-3 fats provide, and since EPA and DHA are only available in significant amounts in seafood, it follows that we should be consuming seafood on a regular basis.

But how much is enough? What does the research literature tell us about the levels of EPA and DHA needed to prevent disease and ensure proper physiological function?

I’m going to answer this question in detail in the next article. But before I do that, I need to make a crucial point: the question of how much omega-3 to eat depends in large part on how much omega-6 we eat.

Over the course of human evolution there has been a dramatic change in the ratio of omega-6 and omega-3 fats consumed in the diet. This change, perhaps more than any other dietary factor, has contributed to the epidemic of modern disease.

The historical ratio of omega-6 to omega-3

Throughout 4-5 million years of hominid evolution, diets were abundant in seafood and other sources of omega-3 long chain fatty acids (EPA & DHA), but relatively low in omega-6 seed oils.

Anthropological research suggests that our hunter-gatherer ancestors consumed omega-6 and omega-3 fats in a ratio of roughly 1:1. It also indicates that both ancient and modern hunter-gatherers were free of the modern inflammatory diseases, like heart disease, cancer, and diabetes, that are the primary causes of death and morbidity today.

At the onset of the industrial revolution (about 140 years ago), there was a marked shift in the ratio of n-6 to n-3 fatty acids in the diet. Consumption of n-6 fats increased at the expense of n-3 fats. This change was due to both the advent of the modern vegetable oil industry and the increased use of cereal grains as feed for domestic livestock (which in turn altered the fatty acid profile of meat that humans consumed).

The following chart lists the omega-6 and omega-3 content of various vegetable oils and foods:

efa content of oils

Vegetable oil consumption rose dramatically between the beginning and end of the 20th century, and this had an entirely predictable effect on the ratio of omega-6 to omega-3 fats in the American diet. Between 1935 and 1939, the ratio of n-6 to n-3 fatty acids was reported to be 8.4:1. From 1935 to 1985, this ratio increased to 10.3:1 (a 23% increase). Other calculations put the ratio as high as 12.4:1 in 1985. Today, estimates of the ratio range from an average of 10:1 to 20:1, with a ratio as high as 25:1 in some individuals.

In fact, Americans now get almost 20% of their calories from a single food source – soybean oil – with almost 9% of all calories from the omega-6 fat linoleic acid (LA) alone! (PDF)

This reveals that our average intake of n-6 fatty acids is between 10 and 25 times higher than evolutionary norms. The consequences of this dramatic shift cannot be underestimated.

Omega-6 competes with omega-3, and vice versa

As you may recall from the last article, n-6 and n-3 fatty acids compete for the same conversion enzymes. This means that the quantity of n-6 in the diet directly affects the conversion of n-3 ALA, found in plant foods, to long-chain n-3 EPA and DHA, which protect us from disease.

Several studies have shown that the biological availability and activity of n-6 fatty acids are inversely related to the concentration of of n-3 fatty acids in tissue. Studies have also shown that greater composition of EPA & DHA in membranes reduces the availability of AA for eicosanoid production. This is illustrated on the following graph, from a 1992 paper by Dr. William Landis:

percentage of n-6 and n-3 in tissue associated with

The graph shows the predicted concentration of n-6 in the tissue based on dietary intake of n-3. In the U.S. the average person’s tissue concentration of highly unsaturated n-6 fat is 75%. Since we get close to 10% of our calories from n-6, our tissue contains about as much n-6 as it possibly could. This creates a very inflammatory environment and goes a long way towards explaining why 4 in 10 people who die in the U.S. each year die of heart disease. (Note: the ratio of omega-6 to omega-3 matters, but so does the total amount of each.)

In plain english, what this means is that the more omega-3 fat you eat, the less omega-6 will be available to the tissues to produce inflammation. Omega-6 is pro-inflammatory, while omega-3 is neutral. A diet with a lot of omega-6 and not much omega-3 will increase inflammation. A diet of a lot of omega-3 and not much omega-6 will reduce inflammation.

Big Pharma is well aware of the effect of n-6 on inflammation. In fact, the way over-the-counter and prescription NSAIDs (ibuprofen, aspirin, Celebres, etc.) work is by reducing the formation of inflammatory compounds derived from n-6 fatty acids. (The same effect could be achieved by simply limiting dietary intake of n-6, as we will discuss below, but of course the drug companies don’t want you to know that. Less profit for them.)

As we discussed in the previous article, conversion of the short-chain n-3 alpha-linolenic acid (ALA), found in plant foods like flax and walnut, to DHA is extremely poor in most people. Part of the reason for that is that diets high in n-6 LA inhibit conversion of ALA to DHA. For example, one study demonstrated that an increase of LA consumption from 15g/d to 30g/d decreases ALA to DHA conversion by 40%.

Death by vegetable oil

So what are the consequences to human health of an n-6:n-3 ratio that is up to 25 times higher than it should be?

The short answer is that elevated n-6 intakes are associated with an increase in all inflammatory diseases – which is to say virtually all diseases. The list includes (but isn’t limited to):

  • cardiovascular disease
  • type 2 diabetes
  • obesity
  • metabolic syndrome
  • irritable bowel syndrome & inflammatory bowel disease
  • macular degeneration
  • rheumatoid arthritis
  • asthma
  • cancer
  • psychiatric disorders
  • autoimmune diseases

The relationship between intake n-6 fats and cardiovascular mortality is particularly striking. The following chart, from an article entitled Eicosanoids and Ischemic Heart Disease by Stephan Guyenet, clearly illustrates the correlation between a rising intake of n-6 and increased mortality from heart disease:

landis graph of hufa and mortality

As you can see, the USA is right up there at the top with the highest intake of n-6 fat and the greatest risk of death from heart disease.

On the other hand, several clinical studies have shown that decreasing the n-6:n-3 ratio protects against chronic, degenerative diseases. One study showed that replacing corn oil with olive oil and canola oil to reach an n-6:n-3 ratio of 4:1 led to a 70% decrease in total mortality. That is no small difference.

Joseph Hibbeln, a researcher at the National Institute of Health (NIH) who has published several papers on n-3 and n-6 intakes, didn’t mince words when he commented on the rising intake of n-6 in a recent paper:

The increases in world LA consumption over the past century may be considered a very large uncontrolled experiment that may have contributed to increased societal burdens of aggression, depression and cardiovascular mortality.

And those are just the conditions we have the strongest evidence for. It’s likely that the increase in n-6 consumption has played an equally significant role in the rise of nearly every inflammatory disease. Since it is now known that inflammation is involved in nearly all diseases, including obesity and metabolic syndrome, it’s hard to overstate the negative effects of too much omega-6 fat.

In the next article we’ll discuss three different methods for determining healthy intakes of n-3 that take background intake of n-6 into account.

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Why fish stomps flax as a source of omega-3

May 5, 2010 in Food & Nutrition, Myths & Truths | 32 comments

salmon on plateI want to thank everyone for sending in their questions and voting on the next topic. The good news is that there’s a lot of interest in all of the topics I’m researching right now. The bad news is that there was no clear winner.

I’ve decided to go ahead with the series on fish and fish oil, but I may write about thyroid and diabetes simultaneously. I’m also going to experiment with shorter (although I’m clearly breaking that rule here), but more frequent, articles. Hopefully these will be easier for me to write and for you to read.

Finally, stay tuned for the first episode of The Healthy Skeptic audio podcast, coming up next week. I’ll be interviewing Stephan Guyenet, Ph.D, on the subject of obesity and weight regulation. Stephan is a senior fellow at the University of Washington studying the neurobiology of body fat regulation. He’s also the author of Whole Health Source, which is one of my favorite health related blogs.

Before we get into talking about the benefits of fish consumption, or how how much fish or fish oil you should eat, it’s probably a good idea to start with a basic review of the omega-3 fatty acids.

Essential Fatty Acids 101

A fatty acid is a chain of carbon, oxygen and hydrogen atoms with a carboxyl group on one end. Fatty acids are classified on the basis of how many carbon atoms are in the chain, as well as how many double bonds exist within the molecule.

Fish contain a variety of fatty acids, but the ones that are believed to confer the majority of the benefits are the long-chain omega-3 fats eicosapentanaenoic acid (EPA) and docosahexaenoic acid (DHA). These omega-3 fats are found exclusively in seafood and marine algae.

As you can see from the chart below, it is also possible for the body to synthesize EPA and DHA from the short-chain omega-3 alpha-linolenic acid (ALA). ALA is found in plant foods such as flax, hemp and pumpkin seeds and walnuts.

Click thumbnail for a larger version

However, research clearly indicates that the conversion of ALA to EPA and DHA is extremely limited. Less than 5% of ALA gets converted to EPA, and less than 0.5% (one-half of one percent) of ALA is converted to DHA.

A common misconception, especially amongst vegetarians and vegans, is that our need for EPA and DHA can be met by consuming flax oil and other plant sources of ALA. But the conversion numbers above clearly indicate that this isn’t the case.

Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline. (ref) So unless they are supplementing with an algae-derived source of DHA, it is likely that most vegetarians and vegans are deficient.

This is significant because researchers now believe that the majority of the health benefits we get from dietary omega-3 fats come from the longer chain derivatives (especially DHA, as I will explain below).

Is DHA essential?

In fact, some researchers have proposed that DHA is essential. When scientists label a nutrient as “essential”, they they’re not just saying that it’s “very important”. In the context of nutrition essential means that the nutrient cannot be synthesized in the human body, and must be derived from dietary sources.

According to today’s nutrition textbooks, there are only two essential fatty acids, omega-6 linoleic acid (LA) and omega-3 alpha-linolenic acid (ALA). It is believed that as long as these fats are present in the diet, all of the longer-chain omega-3 and omega-6 derivatives can be synthesized in the body.

As I pointed out above, while this is theoretically possible, in reality the conversion doesn’t work well. This is true even for healthy people, but it’s especially true for those with nutrient deficiencies, because the conversion of ALA to DHA depends on zinc, iron and pyridoxine.

The bioavailability of iron in plant sources is poor compared to animal sources, so iron deficiency is common in vegans and vegetarians. This is another reason why they tend to be poor converters of ALA to DHA.

Several other observations support the hypothesis that DHA is essential:

  • DHA content in the tissues of all mammals is very similar despite widely varying intakes of omega-3 fatty acids. 1
  • DHA and AA, but not other omega-3 or omega-6 fatty acids, are selectively transferred across the placenta (PDF).
  • 60% of the dry matter of the brain is lipid, and DHA and AA are the most abundant fatty acids of brain phospholipids (PDF)
  • DHA status in newborns is much lower in those receiving formula with LA and ALA, than in those receiving milk or formula with pre-formed DHA (PDF)

It is possible that the primarily carnivorous diet of our ancestors, which ensured a consistently high dietary intake of DHA and AA, precluded the need to evolve efficient conversion mechanisms.

In other words, since we were eating a lot of meat and fish with pre-formed DHA and AA, our bodies didn’t need to be experts at converting ALA and LA in plants to DHA and AA. It is far easier for the body to assimilate pre-formed DHA and AA than it is to synthesize them from precursors.

What about EPA? Isn’t it essential too?

EPA is another long-chain omega-3 fatty acid that is conventionally believed to be responsible for the benefits of fish consumption.

EPA is often referred to as “anti-inflammatory”. However, according to this report on essential fatty acids by Masterjohn, EPA’s effect seems to be more of an interference with the metabolism of omega-6 arachidonic acid (AA) than the performance of any essential role itself.

Take a look at the chart again that I linked to in the beginning of the post. The fatty acids in blue boxes are less inflammatory, and those in pink boxes are more inflammatory. The chart shows that AA is used to synthesize prostaglandins that cause inflammation (indicated by the pink box on the chart). Because it has the same number of carbon atoms, EPA competes with AA for the enzymes that metabolize it. Since the prostaglandins made by EPA are less inflammatory than those made by AA (indicated by the blue box).

So while EPA is less inflammatory than AA, it doesn’t make sense that the body would require an essential fatty acid just to block the inflammatory effects of of another fatty acid.

By contrast, DHA is used to synthesize compounds that play an active role in resolving inflammation. EPA only makes these compounds in the presence of aspirin (PDF). EPA is thus likely to simply be a byproduct of compromised DHA synthesis.

What does this mean to you?

Putting all of this information together yields the following conclusions:

  1. DHA is the most important of the omega-3 fatty acids, and is primarily responsible for the benefits we get from consuming them.
  2. DHA is likely to be essential, which means that you must consume it in the diet to prevent disease and ensure optimal function.
  3. The conversion of plant sources of ALA, such as flax seed oil, to DHA is poor in healthy people and even worse in people deficient in certain nutrients. Vegans and vegetarians are especially prone to be poor converters of ALA to DHA.
  4. If you’ve been buying flax oil in the hopes that it will help, you’d be far better off putting that money towards some fish or fish oil capsules.

Dietary changes over the past century have lowered the DHA status to a state of subclinical deficiency in many people. Countless studies show that this deficiency is at least in part to blame for the rising incidence of cardiovascular disease, inflammatory disease, mental and psychiatric disorders and suboptimal neurodevelopment.

DHA is not the only reason to eat fish, which is also rich in selenium and vitamin D. However, DHA is likely to be the primary reason why populations that eat fish on a regular basis have consistently been shown to healthier than those that don’t. We’ll discuss this further in the next article.

  1. Jones PJH, Kubow S. Lipids, Sterols, and their Metabolites. In: Shils ME, et al., eds. Modern Nutrition in Health and Disease: Tenth Edition. Baltimore, MD; Philadelphia, PA: Lippincott Williams & Wilkins (2006) pp. 92-122. ↩

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Essential fatty acids: not so essential after all

April 15, 2008 in Food & Nutrition | 4 comments

Most health-conscious folks have heard of essential fatty acids (EFAs) by now. It isn’t unusual for a health food store to sell several different brands of fish oils, flax oil and other blends of “essential fatty acids”. We’ve been told that consuming these oils will keep us healthy and protect us from disease.

Today’s nutrition textbooks refer to omega-6 (linoleic) acid and omega-3 (alpha-linolenic) acid as essential components of the human diet, and cite the requirement as something between one and four percent of total caloric intake. When scientists say a nutrient is “essential”, they mean it cannot be synthesized within our bodies from other components by any known mechanism – and therefore must be obtained from the diet.

But are “essential fatty acids” truly essential?

Chris Masterjohn, a PhD candidate in Nutritional Science at the University of Connecticut, has just published a paper which directly challenges the belief that omega-6 linoleic acid and omega-3 alpha-linolenic acid are essential.

His review of the scientific research suggests that omega-6 arachidonic acid (AA) and the omega-3 docosahexaenoic acid (DHA) are the only fatty acids that are truly essential – and thus necessary in the diet – for humans. Further, the true requirement for EFA during growth and development (during childhood, pregnancy or recovery from injury and illness) is less than one-half of one percent of calories when supplied by most animal fats, and even less (0.12 percent) when supplied by liver. In healthy adults, the requirement is “infinitesimal if it exists at all.”

So why is this a concern? Excess consumption of linoleate (omega-6 fatty acid) from vegetable oil will interfere with the production of DHA , while an excess of EPA from fish oil will interfere with the production and utilization of AA. So, by consuming an abundance of the oils which are today heavily promoted as “essential” – vegetable oil and fish oil – we are actually reducing the amount of the fatty acids that are truly essential – DHA & AA.

Finally, it must be pointed out that EFAs of all types, even the health promoting DHA & AA, are polyunsaturated fatty acids (PUFAs). PUFAs are widely known to contribute to oxidative stress, and oxidative stress directly contributes to many diseases including cancer and heart disease. This is why it is important to restrict our intake of EFAs to as close to the minimum requirement as possible.
Most people are far above this requirement, since vegetable oil is pervasive in the American diet. It’s in just about all processed foods (even the “healthy” ones), fried foods and everything cooked in a restaurant. And many people cook with it at home, without knowing what the dangers are.

The best sources of EFA in the diet are liver, egg yolk and butter from grass-fed animals. Obtaining these foods from pasture-raised animals is important, as they contain significantly higher concentrations of DHA and AA (the truly essential EFAs) and fat-soluble vitamins than their commercial feedlot counterparts.

THS recommendations:

  • Gradually replace all vegetable oils in your diet with healthy traditional fats (which are protected from oxidative stress) such as butter, virgin (unrefined) coconut oil, palm oil, lard and beef tallow.
  • Eliminate (or at least dramatically reduce) consumption of processed and fried foods.
  • Do not take flax oil or fish oil supplements on a regular basis. Cod liver oil is recommended during pregnancy, lactation and childhood to provide extra DHA and to obtain fat-soluble vitamins.

Following these recommendations, along with a nutrient-dense, whole foods based diet low in sugar and rich in essential minerals, should reduce your intake of PUFA to closer to the recommended 0.5 (one-half of one) percent of calories, and ensure adequate intake of the truly essential DHA & AA.

Women who are pregnant or lactating, and perhaps attempting to become pregnant, children, and adults recovering from injury and suffering from chronic, degenerative disease can safely consume up to one percent of calories as PUFA. Studies have suggested that a subset of patients with pre-existing cardiovascular disease also benefit from a moderate dose of fish oil (up to one gram per day); however, in those same studies people with stable angina and with no heart disease at all, fish oil actually increased their risk of heart attack.

Check back here for a future post on what the research has to say about using omega-3 fatty acids (fish oil) in the treatment of heart disease.

Make sure to visit Chris Masterjohn’s website, where you can purchase the excellent full report for $15. It’s a worthwhile investment, in my opinion, if you want to get the straight scoop about EFAs and their role in our diet.

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