omega-6

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How much omega-3 is enough? That depends on omega-6.

May 11, 2010 in Food & Nutrition | 28 comments


sardinesIn the first article of this series, 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. In the second article, we discussed how excess omega-6 (n-6) in the diet can block absorption of omega-3, and showed that the modern, Western diet contains between 10 and 25 times the optimal level of n-6.

In this article we’ll discuss strategies for bringing the n-6 to n-3 ratio back into balance. There are two obvious ways to to do this: increase intake of n-3, and decrease intake of n-6.

Many recommendations have been made for increasing n-3 intake. The important thing to remember is that any recommendation for n-3 intake that does not take the background n-6 intake into account is completely inadequate.

It’s likely that the success and failure of different clinical trials using similar doses of EPA and DHA were influenced by differing background intakes of the n-6 fatty acids. In the case of the Lyon Diet Heart Study, for example, positive outcomes attributed to ALA may be related in part to a lower n-6 intake (which would enhance conversion of ALA to EPA and DHA).

This explains why simply increasing intake of n-3 without simultaneously decreasing intake of n-6 is not enough.

Bringing n-3 and n-6 back into balance: easier said than done!

Let’s examine what would happen if we followed the proposed recommendation of increasing EPA & DHA intake from 0.1 to 0.65g/d. This represents going from eating virtually no fish to eating a 4-oz. serving of oily fish like salmon or mackerel three times a week.

The average intake of fatty acids (not including EPA & DHA) in the U.S. has been estimated as follows:

  • N-6 linoleic acid (LA): 8.91%
  • N-6 arachidonic acid (AA): 0.08%
  • N-3 alpha-linolenic acid (ALA): 1.06%

Keep in mind from the last article that the optimal ratio of omega-6 to omega-3 is estimated to be between 1:1 and 2.3:1. Assuming a median intake of n-6 (ALA + LA) at 8.99% of total calories in a 2,000 calorie diet, that would mean a daily intake of 19.9g of n-6. If we also assume the recommended intake of 0.65g/d of EPA and DHA, plus an average of 2.35g/d of ALA (1.06% of calories), that’s a total of 3g/d of n-3 fatty acid intake.

This yields an n-6:n-3 ratio of 6.6:1, which although improved, is still more than six times higher than the historical ratio (i.e. 1:1), and three times higher than the ratio recently recommended as optimal (i.e. 2.3:1).

On the other hand, if we increased our intake of EPA and DHA to the recommended 0.65g/d (0.3% of total calories) and maintained ALA intake at 2.35g/d, but reduced our intake of LA to roughly 7g/d (3.2% of total calories), the ratio would be 2.3:1 – identical to the optimal ratio.

Further reducing intake of n-6 to less than 2% of calories would in turn further reduce the requirement for n-3. But limiting n-6 to less than 2% of calories is difficult to do even when vegetable oils are eliminated entirely. Poultry, pork, nuts, avocados and eggs are all significant sources of n-6. I’ve listed the n-6 content per 100g of these foods below:

  • Walnuts: 38.1g
  • Chicken, with skin: 2.9g
  • Avocado: 1.7g
  • Pork, with fat: 1.3g
  • Eggs: 1.3g

It’s not too hard to imagine a day where you eat 200g of chicken (5.8g n-6), half an avocado (1.1g n-6) and a handful of walnuts (10g of n-6). Without a drop of industrial seed oils (like safflower, sunflower, cottonseed, soybean, corn, etc.) you’ve consumed 16.9g of n-6, which is 7.6% of calories and far above the limit needed to maintain an optimal n:6 to n:3 ratio.

Check the chart below for a listing of the n-6 and n-3 content of several common foods.

Click the thumbnail for a larger version

Ditch the processed foods and cut back on eating out

Of course, if you’re eating any industrial seed oils you’ll be way, way over the optimal ratio in no time at all. Check out these n-6 numbers (again, per 100g):

  • Sunflower oil: 65.7g
  • Cottonseed oil: 51.5g
  • Soybean oil: 51g
  • Sesame oil: 41.3g
  • Canola oil: 20.3g

Holy moly! The good news is that few people these days still cook with corn, cottonseed or soybean oil at home. The bad news is that nearly all processed and packaged foods contain these oils. And you can bet that most restaurant foods are cooked in them as well, because they’re so cheap.

So chances are, if you’re eating foods that come out of a package or box on a regular basis, and you eat out at restaurants a few times a week, you are most likely significantly exceeding the recommended intake of n-6.

Two other methods of determining healthy n-3 intakes

Tissue concentration of EPA & DHA

Hibbeln et al have proposed another method of determining healthy intakes of n-6 and n-3. Studies show that the risk of coronary heart disease (CHD) is 87% lower in Japan than it is in the U.S, despite much higher rates of smoking and high blood pressure.

When researchers examined the concentration of n-3 fatty acids in the tissues of Japanese subjects, they found n-3 tissue compositions of approximately 60%. Further modeling of available data suggests that a 60% tissue concentration of n-3 fatty acid would protect 98.6% of the worldwide risk of cardiovascular mortality potentially attributable to n-3 deficiency.

Of course, as I’ve described above, the amount of n-3 needed to attain 60% tissue concentration is dependent upon the amount of n-6 in the diet. In the Phillipines, where n-6 intake is less than 1% of total calories, only 278mg/d of EPA & DHA (0.125% of calories) is needed to achieve 60% tissue concentration.

In the U.S., where n-6 intake is 9% of calories, a whopping 3.67g/d of EPA & DHA would be needed to achieve 60% tissue concentration. To put that in perspective, you’d have to eat 11 ounces of salmon or take 1 tablespoon (yuk!) of a high-potency fish oil every day to get that much EPA & DHA.

This amount could be reduced 10 times if intake of n-6 were limited to 2% of calories. At n-6 intake of 4% of calories, roughly 2g/d of EPA and DHA would be needed to achieve 60% tissue concentration.

The Omega-3 Index

Finally, Harris and von Schacky have proposed a method of determining healthy intakes called the omega-3 index. The omega-3 index measures red blood cell EPA and DHA as a percentage of total red blood cell fatty acids.

Values of >8% are associated with greater decreases in cardiovascular disease risk. (Note that n-6 intake was not considered in Harris and von Shacky’s analysis.) However, 60% tissue concentration of EPA & DHA in tissue is associated with an omega-3 index of between 12-15% in Japan, so that is the number we should likely be shooting for to achieve the greatest reduction in CVD mortality.

The omega-3 index is a relatively new test and is not commonly ordered by doctors. But if you want to get this test, you can order a finger stick testing kit from Dr. William Davis’ Track Your Plaque website here. It’ll cost you $150 bucks, though.

What does it all mean to you?

These targets for reducing n-6 and increasing n-3 may seem excessive to you, given current dietary intakes in the U.S.. Consider, however, that these targets may not be high enough. Morbidity and mortality rates for nearly all diseases are even lower for Iceland and Greenland, populations with greater intakes of EPA & DHA than in Japan.

All three methods of calculating healthy n-3 and n-6 intakes (targeting an n-6:n-3 ratio of 2.3:1, 60% EPA & DHA tissue concentration, or 12-15% omega-3 index) lead to the same conclusion: for most people, reducing n-6 intake and increasing EPA & DHA intake is necessary to achieved the desired result.

To summarize, for someone who eats approximately 2,000 calories a day, the proper n-6 to n-3 ratio could be achieved by:

  1. Making no changes to n-6 intake and increasing intake of EPA & DHA to 3.67g/d (11-oz. of oily fish every day!)
  2. Reducing n-6 intake to approximately 3% of calories, and following the current recommendation of consuming 0.65g/d (three 4-oz. portions of oily fish per week) of EPA & DHA.
  3. Limiting n-6 intake to less than 2% of calories, and consuming approximately 0.35g/d of EPA & DHA (two 4-oz. portions of oily fish per week).

Although option #1 yields 60% tissue concentration of EPA & DHA, I don’t recommend it as a strategy. All polyunsaturated fat, whether n-6 or n-3, is susceptible to oxidative damage. Oxidative damage is a risk factor for several modern diseases, including heart disease. Increasing n-3 intake while making no reduction in n-6 intake raises the total amount of polyunsaturated fat in the diet, thus increasing the risk of oxidative damage.

This is why the best approach is to limit n-6 intake as much as possible, ideally to less than 2% of calories, and moderately increase n-3 intake. 0.35g/d of DHA and EPA can easily be obtained by eating a 4 oz. portion of salmon twice a week.

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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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Research update: carbs raise cholesterol & veggie oil associated with IBS & IBD

December 9, 2009 in Health Conditions | 10 comments


microscopeI recently came across two articles that I think you should read.

The first is over on Dr. William Davis’s blog, The Heart Scan. Dr. Davis reviews a study demonstrating that consumption of excess carbohydrate can raise cholesterol.

Now, if you’ve been reading my blog for a while you know that normal LDL cholesterol isn’t a risk factor for heart disease, right? So I am generally not concerned with what does or doesn’t raise cholesterol. However, there is a type of cholesterol that is a significant risk factor for heart disease: small, dense LDL cholesterol.

Small, dense LDL particles are more likely to become oxidized, and as I have explained in How to Increase Your Risk of Heart Disease, oxidized LDL is one of the strongest risk factors for heart disease we know of.

Dr. Davis clearly explains how eating too many carbs can increase your levels of small, dense LDL and he also explains why so many doctors and researchers don’t make this crucial connection. Check out the full article here.

The second article is on Dr. Barry Groves’ Second Opinions blog. He reviews a study which links consumption of linoleic acid to Inflammatory Bowel Disease (such as Crohn’s and Ulcerative Colitis) and Irritable Bowel Syndrome (IBS).

Linoleic acid is an omega-6 (n-6) essential fatty acid. “Essential” in this context means that humans can’t make it internally and need to eat it in the diet. However, we only need a tiny amount – about a teaspoonful per day – and eating too much of it can cause serious problems. Eating too much linoleic acid dramatically increases oxidized LDL cholesterol levels, which as I just explained in the last section significantly elevates our risk of heart disease. Linoleic acid is also pro-inflammatory, and inflammation is a major contributor to modern diseases like cancer, diabetes, heart disease and, you guessed it, Inflammatory Bowel Disease and Irritable Bowel Syndrome.

Tragically, linoleic acid has become one of the primary sources of calories in the American diet. Vegetable oils containing linoleic acid (such as soybean, corn, safflower, sunflower, cottonseed) are found in nearly all packaged and processed foods and all foods cooked in a restaurant. Almost all fried foods are extremely high in linoleic acid.

Is it any wonder, then, that Irritable Bowel Syndrome has reached such epidemic proportions? It is now the #2 leading cause for people missing work, behind only the common cold. It affects millions of people in the U.S. and abroad. There is no known “cure”, and the medications prescribed for it are largely ineffective.

This is yet another example of how toxic and harmful our modern diets are. If you want to avoid these conditions, eat traditional, saturated fats like butter, lard and coconut oil instead of industrially-processed vegetable oils. You’ll feel better, and you’ll enjoy your food a lot more too!

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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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