In 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.

## 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.

## 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:

- Making no changes to n-6 intake and increasing intake of EPA & DHA to
**3.67g/d**(11-oz. of oily fish every day!) - 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. - 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.

Check out my Update on Omega-6 PUFAs here.

Hi Chris,

Interesting stuff.

That said, I what I never see addressed in such articles is the fact that, say, 1g of LA from veg sources isn’t comparable to 1g of EPA/DHA from oily fish – they’re at different stages in PUFA metabolism.

It’s my understanding that the body’s ability to convert LA and ALA into AA and EPA/DHA respectively is very poor. So, in an omnivorous diet, doesn’t this muddy the waters when it comes to calculating one’s ratios?

Theoretically, if LA to AA conversion is poor, I could envision someone taking EPA/DHA in order to ‘balance’ things gram for gram actually pushing AA levels into deficit.

Cheers,

Rob

Chris,

I have had a “battle” with fats, for a few years now. I get dizzy when I consume them. I eat mostly vegan diet. It would be great to talk to you “one on one” and get more in-depth.

Basically, I lost significant body weight due to stress and have cold extremities. It seems I may not get enough. No sex drive at all and I’m not even 40. Lost majority of hair on my legs. Acidic foods make me irritable, trembling in legs. And I do have some parasites according to Genova tests. Doctors here are useless.

To add more fish oil to my diet means unbearable dizziness.

Any general advice? And any possibility of consults with you?