In step #1, we talked about what not to eat. In this article, we’ll talk about what to eat.

Most of the calories we get from food come from protein, carbohydrates and fat. These are referred to as macronutrients. We also get other important nutrients from food, such as vitamins and minerals. These don’t constitute a significant source of calories, so they’re called micronutrients.

For the last 50 years we’ve been told to follow a diet low in this or that macronutrient. From the 1950s up until the present day the American Heart Association and other similarly misguided and pharmaceutically-financed “consumer organizations” have advocated a low-fat diet. More recently, low-carbohydrate diets are all the rage.

Not all macronutrients are created equal

The problem with these approaches is that they ignore the fact that not all macronutrients are created equal. There’s a tremendous variation in how different fats and carbohydrates affect the body, and thus in their suitability for human consumption. Grouping them all together in a single category is shortsighted – to say the least.

What many advocates of low-fat or low-carbohydrate diets conveniently ignore is that there are entire groups of people around the world, both past and present, that defy their ideas of what constitutes a healthy diet.

For example, the low-fat crowd will tell you that eating too much fat – especially of the saturated variety – will make you fat and give you a heart attack. Tell that to the traditional Inuit, who get about 90% of calories from fat, and were almost entirely free of obesity and modern degenerative disease. The same is true for the Masai tribe in Africa, who get about 60-70% of calories from fat (almost entirely from meat, milk or blood.) And then there’s the modern French, who have the lowest rate of heart disease of any industrialized country in the world – despite the highest intake of saturated fat.

The low-carb crowd is very much aware of these statistics, which are often used in defense of low-carb diets as the best choice. Tell that to the Kitavans in Melanesia, who get about 70% of calories from carbohydrate and, like the Inuit and Masai, are almost entirely free of obesity, heart disease and other chronic, degenerative diseases that are so common in industrialized societies. We see a similar absence of modern diseases in the Kuna indians in Panama and the Okinawans of Japan, two other healthy indigenous populations that get about 65% of calories from carbohydrate.

These rather inconvenient exceptions to the low-fat and low-carb dogma vigorously promoted by advocates of both approaches show us that humans can in fact thrive on a wide range of macronutrient ratios, ranging from extremely high fat (Inuit, Masai) to very high carb (Kitavans, Kuna & Okinawans). They also hint at the idea that perhaps not all carbohydrates are the same in terms of their effects on human health.

Human fuel: food that nourishes the body

We need to shift away from the idea of macronutrients – as Dr. Kurt Harris of PaleoNu recently suggested – and move towards the idea of nourishment or fuel. This means we classify foods not based on their macronutrient ratios, but on their ability to provide the energy and nutrition the body needs to function optimally.

Gasoline and diesel are both fuel that cars can run on. If you put gasoline in a diesel engine, or vice versa, the engine may run but it won’t run well – or for very long. In a similar way, the human body can run on the entire range of fats, carbohydrates and proteins. But it runs much better on the ones it was designed to run on, and if you put too much of the others in, the body will eventually break down.

With this classification in mind, let’s look primarily at how the different types of fat and carbohydrate (our primary sources of energy) affect us, and which of them we should choose as our preferred “human fuel”.

Know your fats

LONG-CHAIN SATURATED FAT
We’ll begin with long-chain, saturated fats (LCSFA): myristic, palmitic and stearic acid. These fats are found mostly in the milk and meat of ruminant animals like cattle and sheep. They form the core structural fats in the body, comprising 75-80% of fatty acids in most cells, and they’re the primary storage form of energy for humans. In other words, when the body stores excess energy from food for later use, it stores it primarily as long-chain saturated fat.

Unlike polyunsaturated fats (PUFA) and carbohydrates like glucose and fructose, saturated fats have no known toxicity – even at very high doses – presuming insulin levels are in a normal range. Long-chain saturated fats are more easily burned as energy than PUFA. The process of converting saturated fat into energy the body can use leaves no toxic byproducts. In fact, it leaves nothing but carbon dioxide and water.

This means that, assuming you are metabolically healthy, you can eat as much saturated fat as you’d like without adverse consequences. I’m sure this will come as a surprise to many of you, since we’ve been collectively brainwashed for 50 years to believe that saturated fat makes us fat and causes heart disease. If you still believe this is true, watch these two videos and read all of the articles in my special report on cholesterol, fat and heart disease.

Verdict: eat as much as you’d like. The majority of the fats you consume should be LCSFA.

MEDIUM-CHAIN TRIGLYCERIDES
Medium-chain triglycerides (MCT) are another type of saturated fat. They’re found in coconut and in mother’s milk, and they have unusual properties. They’re metabolized differently than long-chain saturated fats; they don’t require bile acids for digestion and they pass directly to the liver via the portal vein. This makes MCTs a great source of easily digestible energy. They’re so easy to digest, in fact, that they’re used in the liquid hospital formulas fed to patients that have had sections of their intestine removed and aren’t able to digest solid food.

In addition to being a good energy source, MCTs have therapeutic properties. They’re high in lauric acid, a fat found in mother’s milk that has anti-bacterial, anti-viral and antioxidant properties.

Verdict: eat as much as you’d like. Coconut oil is an especially good cooking fat, because it is not vulnerable to the oxidative damage that occurs with high-heat cooking using other fats.

MONOUNSATURATED FAT
Monounsaturated fat (MFA), or oleic acid, is found primarily in beef, olive oil, avocados, lard and certain nuts like macadamias. Like saturated fats, MFA form the core structural fats of the body and are non-toxic even at high doses. Interestingly, monounsaturated fats seem to be the only fats that typically fat-phobic groups like the AHA and fat-friendly groups like Atkins and other low-carbers can agree are completely healthy.

Verdict: eat as much as you’d like. But be aware that certain foods that are high in monounsaturated fats, like nuts and avocados, can contain significant amounts of the dreaded omega-6 polyunsaturated fats, which we’ll discuss below. Exercise caution.

These three fats – long-chain saturated, medium chain triglycerides and monounsaturated – should form the bulk of your fat intake. In addition to their lack of toxicity, eating these fats will:

• Reduce your risk of heart disease by raising your HDL, lowering your triglycerides and reducing levels of small, dense LDL (a type of LDL associated with a higher risk of heart disease). If you don’t believe me, read this.
• Increase muscle mass. Muscle is composed of equal weights of fat and protein.
• Stabilize your energy and mood. Fat provides a steadier supply of energy throughout the day than carbohydrate, which can cause fluctuations in blood sugar.

POLYUNSATURATED FAT: OMEGA-6 & OMEGA-3
Polyunsaturated fat (PUFA) can be subdivided into omega-6 and omega-3. PUFA are fragile and vulnerable to oxidative damage, a process that creates free radicals in the body and raises our risk for everything from heart disease to cancer. As I pointed out in Step #1: Don’t Eat Toxins, both anthropological and modern research suggest that for optimal health we should consume roughly the same amount of omega-6 and omega-3 fat (1:1 ratio), and that our total intake of PUFA should be no more than 4% of calories.

But Americans’ omega-6:omega-3 ratio today ranges from 10:1 to 20:1, with a ratio as high as 25:1 in some individuals! This means some people are eating as much as 25 times the recommended amount of omega-6 fat. And it is this excess consumption of omega-6 PUFA – not cholesterol and saturated fat – that is responsible for the modern epidemics of cardiovascular disease, type 2 diabetes, obesity, metabolic syndrome, autoimmune disease and more.

Omega-6 PUFA (linoleic acid, or LA) is found in small or moderate amounts of a wide variety of foods including fruits, vegetables, cereal grains and meat. But it is found in very large amounts in industrial processed and refined oils, like soybean, cottonseed, corn, safflower and sunflower. These oils are ubiquitous in the modern diet, present in everything from salad dressing to chips and crackers to restaurant food. LA is also relatively high in most nuts and in all poultry, especially in dark meat with skin.

Linoleic acid is an essential fatty acid. This means it is required for proper function but cannot be produced in the body, and thus must be obtained from the diet. However, the amount of omega-6 that is needed is exceedingly small: less than 0.5 percent of calories when supplied by most animal fats and less than 0.12 percent of calories when supplied by liver. When consumed in excess amounts – as is almost always the case in industrialized countries like the U.S. – omega-6 contributes to all of the diseases mentioned above.

Omega-3 PUFA can be further subdivided into short-chain (alpha-linolenic acid, or ALA) and long-chain (EPA & DHA). ALA is found in plant foods like walnut and flax, whereas EPA & DHA is found in seafood and to a lesser extent the meat and fat of ruminant animals.

While ALA is considered essential, the long-chain EPA & DHA are responsible for the benefits we get from eating omega-3 fats, and they form the denominator of the omega-6:omega-3 ratio. A common misconception is that we can meet our omega-3 needs by taking flax oil or eating plant foods containing ALA. It’s true that the body can convert some ALA to EPA & DHA. But that conversion is extremely inefficient in most people. On average, less than 0.5% of ALA gets converted into the long-chain EPA & DHA, and that number is even worse in people that are chronically ill or have nutrient deficiencies (common in vegans and vegetarians).

This means that it is probably EPA & DHA that are essential, in the sense that they are crucial for proper function but cannot be produced in adequate amounts in the body, and thus must be obtained from the diet. Of the two, evidence suggests that DHA plays the more important role.

Verdict: for optimal health, eat no more than 4% of calories (about 9g/d for a 2,000 calorie diet) of polyunsaturated fat, with an equal amount of omega-6 and omega-3. Make sure the omega-3 you eat is long-chain EPA & DHA (from seafood and animal sources) rather than short-chain ALA from plant sources like flax. It is very difficult to limit omega-6 to 4.5g/day. See this article for tips.

TRANS-FATS
There are two types of trans-fats: natural (NTF), and artificial (ATF). The primary natural trans-fat, conjugated linoleic acid (CLA) is found in small amounts (about 2%) in the meat, fat and dairy fat of ruminant animals. CLA does not have the harmful effects of ATFs, and may have anti-cancer properties and other benefits.

Artificial trans-fats have been linked with a variety of diseases. I think most people are aware of this, so I’m not going to belabor the point. We’ve still got carbs to talk about.

Verdict: avoid artificial trans-fats like the plague. Natural trans-fats like CLA are harmless and probably even beneficial, but as long as you’re eating long-chain saturated fats, you’ll get CLA. You don’t have to go out of your way to find it.

SUMMARY OF FATS
Long-chain saturated fat, monounsaturated fat and medium chain triglycerides should form the bulk of your fat intake. Long-chain omega-3 fats (EPA & DHA) should be consumed regularly, while omega-6 LA should be dramatically reduced. Click on the fat pyramid below for a graphic representation.

Know your carbs

Carbohydrates are broken down into either indigestible fiber, glucose or fructose. Let’s discuss the suitability of each of these as human fuel.

Glucose
Glucose is a simple sugar (monosaccharide) found mostly in plant foods like fruits, vegetables, starchy tubers and grains. It has three main uses in the body:

• It forms structural molecules call glycoproteins;
• Like fat, it is a source of energy for cells (especially in the brain); and,
• it’s a precursor to compounds that play an important role in the immune system.

Glucose preceded fatty acids as a fuel source for living organisms by a very long time, and it is the building block of foods that have the longest evolutionary history of use by mammals like us. The fact that glucose can be produced in the body from protein is often used as an argument that we don’t need to eat it in the diet. But I agree with Dr. Harris’s interpretation that, rather than viewing this as evidence that that glucose isn’t important, we should view it as evidence that glucose is so metabolically essential that we evolved a mechanism to produce it even in its absence in the diet.

One of the few differences between our digestive tract and that of a true carnivore, like a lion, is that we produce an enzyme called amylase. Amylase allows us to digest starch – a long-chain polymer of glucose molecules we can’t absorb – into single molecules of glucose that easily pass through the gut wall into the bloodstream.

Presuming we are metabolically healthy, the glucose and starch we eat is digested and rapidly cleared by the liver and muscle cells. It is only when the metabolism is damaged – usually by years of eating toxins like refined cereal grains, industrial seed oils and fructose – that excess glucose is not properly cleared and leads to insulin resistance and diabetes.

Verdict: the range of glucose that is tolerated varies widely across populations and individuals. Assuming no metabolic problems and an active lifestyle, glucose may be consumed relatively freely. However, many people today do have some form of metabolic dysfunction, and live a sedentary lifestyle. If you fall into this category, glucose should probably be limited to 400 calories (about 100g) of glucose per day.

Fructose
Fructose is another simple sugar found primarily in fruits and vegetables. While it has the same chemical formula and caloric content as glucose, it has an entirely different effect on the body.

As I pointed out in Step #1: Don’t Eat Toxins, fructose is toxic at high doses. It damages proteins in a process called fructation, which disrupts metabolic function and causes inflammation and oxidative damage. To prevent this, fructose is shunted directly to the liver for conversion into glucose or innocuous fats. But this process damages the liver over time, leading to non-alcoholic fatty liver disease (which one in three Americans now suffer from) and metabolic syndrome.

Another issue is that excess fructose is not well absorbed in the gut, which in turn leads to its rapid fermentation by bacteria in the colon or abnormal overgrowth of bacteria in the small intestine. Small-bowel bacterial overgrowth, or SIBO, is now believed to be the major cause of irritable bowel syndrome (IBS), a common functional bowel disorder that is the second-leading cause of people missing work behind only the common cold.

Most people without metabolic dysfunction can handle small amounts of fructose (as found in a few servings of fruit per day) without problems. But on the scale that fructose is consumed in the U.S. – including 64 pounds of high-fructose corn syrup per person each year on average – fructose wreaks havoc on the body. It should therefore be limited as a source of carbohydrate.

Verdict: 3-4 servings a day of fruit is fine for people without metabolic problems. Those with fatty liver, insulin resistance or other issues should further limit fructose intake, and everyone should avoid high-fructose corn syrup and other concentrated sources like agave syrup.

Fiber
Fiber is plant matter that is indigestible to humans. But although we can’t digest it, some of the 100 trillion bacteria that live in our gut can. In fact, up to 10% of the body’s caloric needs can be met by the conversion of glucose into short-chain fats like butyrate, propionate and acetate by intestinal bacteria. These short-chain fats are the primary energy source for intestinal cells in the colon, and butyrate in particular has been associated with several benefits. These are outlined in The Perfect Health Diet, by Paul & Shou-Ching Jaminet. Butyrate:

• Prevents obesity.
• Heals the intestine.
• Improves gut barrier integrity.
• Relieves constipation.
• Improves cardiovascular markers.
• Reduces inflammation.
• Stabilizes blood sugar.

The evidence clearly suggests that vegetable fiber is beneficial. However, just as not all fats are created equal, not all fiber is created equal. Grain fiber – which the AHA and other so-called “heart healthy” organizations have been promoting for decades – is toxic for two reasons: it contains toxic proteins like gluten, and it is prone to injure the intestinal wall.

We’ve been bullied into believing that grain fiber prevents heart disease and provides numerous health benefits. But this claim has only been tested in a single clinical trial, and the results were less than spectacular. The Diet and Reinfarction Trial, published in 1989, included 2,033 British men who had suffered a heart attack, and compared a high-fiber group with a control group. The high-fiber group ate whole grains and doubled their grain fiber intake from 9 to 17 grams per day.

How did that work out for them? Not too well. Deaths in the high fiber group were 22% higher over the two year study. 9.9% of the control group died vs. 12.1% of the high fiber group.

There are other reasons to limit all types of fiber. Fiber isn’t essential. Human breast milk doesn’t have any, and traditional people like the Masai – who are free of modern, degenerative disease – eat almost no fiber at all (subsisting on a diet of meat, blood and milk). And while fiber can feed the good bacteria in our gut and increase the production of beneficial short-chain fats like butyrate, it can also feed pathogenic and opportunistic bacteria in the gut.

Verdict: vegetable (but not grain) fiber is beneficial in moderate amounts – about one-half pound of vegetables per day. But think about vegetables and fiber as accompaniments or flavorful condiments to fat and protein, which should form the bulk of calories consumed, rather than the other way around.

SUMMARY OF CARBOHYDRATES
Assuming a healthy metabolism (which isn’t necessarily a safe assumption these days), glucose and starch can be eaten relatively freely, which fructose should be limited to 2-3 servings of fruit per day. Vegetable fiber is beneficial but should also be limited, to about one-half pound of vegetables per day. See the carb pyramid below for a graphic representation.

Know your protein

What about protein? As it turns out, eating the right type of protein is easy if you simply follow Step #1 (don’t eat toxins) and base your diet on the healthy fats I listed above.

Protein is mostly found in animal products, seafood, nuts, legumes and grains. Legumes and grains have toxic compounds that can damage the gut. These toxins can be partially and in some cases completely neutralized by traditional preparation methods like soaking, sprouting and fermenting. But the vast majority of people in modern industrial societies don’t do this and aren’t willing to do it, so I generally recommend that people avoid them altogether.

As I explained above, nuts are often high in omega-6 LA, which we get far too much of as it is. So nuts should not constitute a significant source of protein. Walnuts are especially high. Just 100g of walnuts a day amounts to a whopping 266g of omega-6 per week. Keeping in mind that we want a 1:1 ratio of omega-6 to omega-3, you’d have to eat 34 pounds of salmon a week to achieve a balance. Good luck with that.

Poultry, especially dark meat with the skin on, can also be very high in omega-6 and should also be limited. For example, chicken skin has about 14 times more omega-6 than even grain-finished beef, and 10 times more than grain-finished pork.

That leaves the meat and milk (including butter, cream and cheese) of ruminant animals (beef & lamb), pork, and seafood as the most suitable sources of protein. Animal protein is easy to absorb, is not toxic and is rich in beneficial long-chain saturated fats and natural trans-fats like CLA. Seafood is similarly easy to absorb, and is the primary dietary source of long-chain omega-3 fats DHA & EPA, as well as micronutrients like vitamin D and selenium.

We don’t need a pyramid for protein; you can simply follow the fat pyramid and you’ll naturally get the right type and amount of protein.

I hope you all had happy holidays and are off to a great start this year. I thought I’d share a few thoughts that have been bouncing around my head lately, stimulated most recently by two articles written by fellow health bloggers.

Don Matesz over at Primal Wisdom wrote a thought-provoking piece on the hormone composition of grass-fed and factory-farmed meat. In it he argues (convincingly, I might add) that meat from CAFO (confined animal feeding operations) does not have dangerously high levels of hormones, in spite of claims to the contrary made by advocates of eating grass-fed meat.

Got testicles?

I recommend reading the entire article, I’ll summarize it briefly here. Before CAFO came into being, humans predominantly ate bulls, since eating female animals (cows) was taboo. The taboo made perfect sense in a hunter-gatherer culture, since killing the female could eliminate potential offspring, while killing a few bulls would have no effect on the fecundity of the herd.

Today, CAFO use steer, which are neutered bulls. One reason for this is that steer are a lot easier to manage than bulls. Why? Because hormone levels in bulls (with intact sex organs) are significantly higher than in steer. In fact, bull meat has between 34 and 105 times more testosterone than steer meat. No wonder bulls are harder to manage!

Even when hormones are added to steer in CAFO, the levels are nowhere close to what they are in intact bulls. In fact, studies have found no significant difference in hormone levels between meat from hormone-treated and untreated animals.

This means that Paleo Pete was eating meat with a lot more hormones in it a million years ago than American Andy is when he gets a cheeseburger at McDonalds today.

Hormones in meat are bad – if you eat 200 pounds of meat a day

Studies have also shown that the hormones ingested from food, including CAFO meat, have a negligible effect on human health. From Don’s article:

For example, a prepubertal boy, most vulnerable to adverse effects of excess dietary estrogens, produces about 100 micrograms of estrogen daily. Beef muscle meat contains less than 0.02 micrograms of estrogens per kilogram. To get from beef an intake of estrogens equal to just one percent of his endogenous estrogen production, i.e. 1 microgram, he would have to consume 50 kilograms–110 pounds– of beef in a day!

Another common claim is that adding hormones to meat has increased the rates of cancer and other modern, degenerative diseases. But if that were true, we would have seen these diseases in hunter-gatherer populations that were eating large amounts of bull meat, which has on average 50 times more hormones than the CAFO steer meat eaten today.

So it would seem that there isn’t much difference between grass-fed and CAFO meat when it comes to hormones. So should we all just save some money and eat conventional meat?

It’s not all about hormones. Don’t forget omega-3s!

Not so fast. Mark Sisson published an article earlier this week reporting on a study comparing the effects of eating grass-fed and CAFO meat on omega-3 and omega-6 concentration in human plasma and platelets.

Turns out those that ate the grass-fed meat had significantly higher levels of omega-3 in their plasma and platelets than those that ate CAFO meat, despite the fact that the amount of omega-3 fatty acids in the two types of meat were not hugely different.

The folks consuming grass-finished meat ate, on average, 65 mg/d of long chain omega-3s, while those eating concentrate-finished meat ate about 44 mg/d of long chain omega-6s, yet the lab results – the big improvements in plasma and platelet fatty acid numbers – were lopsided.

What’s happening here? I suspect the answer lies with the difference in omega-6 content in the diets of both groups. Those who ate the CAFO meat had an average intake of 8.5g/d of omega-6 fats, while those that ate grass-fed meat had an average intake of 5.5g/d. In a previous article about how too much omega-6 is making us sick, I explained that omega-6 and omega-3 fatty acids compete for the same conversion enzymes.

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 works the other way, too. The more omega-6 is consumed, the less omega-3 is available to the tissues. So if two people eat a diet identical in omega-3 content, but one person’s diet is high in omega-6, and the other person’s is low, guess who will end up with more omega-3 in their tissues? That’s right – the one with a low omega-6 intake. This is why I constantly tell people that the most important step they can take in normalizing their omega-3:omega-6 ratio is not boosting omega-3 intake, but reducing omega-6. And this is likely what explains the higher levels of omega-3 in the grass-fed meat eaters in the study, even though grass-fed meat doesn’t have a lot more omega-3 than CAFO meat.

This is important, because the ratio of omega-3 to omega-6 in our tissue is crucial to health. Too much omega-6 in relation to omega-3 has been shown to be a factor in everything from depression and arthritis to heart disease and diabetes. There isn’t a modern disease out there that isn’t influenced by this ratio.

Black, white & shades of grey

So here we have one study suggesting there isn’t much difference between CAFO and grass-fed meat, and another suggesting the opposite. What do we make of this?

As much as we’d all like things to be simple when it comes to food and health, they often aren’t. We have to use our brains to sift through the available information and make intelligent choices based on several different factors.

In the case of grass-fed vs. CAFO meat, there’s a lot more to consider than hormones and fatty acids. There’s also antibiotic use in CAFO cattle and the increased risk of foodborne illness in CAFO meat, and there are several economic and social issues as well. Grass-fed animals are generally treated in a more humane way than CAFO animals. If you’ve ever visited a CAFO you will know what I mean. It’s shocking and disgusting. I personally prefer to support local farmers that use traditional methods of animal husbandry, that pay attention to how the animals are treated and slaughtered, and who care about every phase of the process. I like the money I spend on food to stay in my local community whenever possible.

Clearly this is not a black and white issue, and there’s a lot to take into account when choosing between grass-fed and CAFO meat. As usual, I’d love to hear your thoughts.

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.

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.

In 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:

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 overestimated.

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:

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:

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.

I 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!

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.

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.