In this “Grab Bag Q&A” episode of the podcast, I discuss the role of nutrition in healing, obstacles to optimal health, macronutrient ratios and more.

Questions include:

• Do you feel with the right nutrition the body is capable of healing itself?
• In your practice, what do you find to be the biggest barrier stopping people from reaching their optimal health?
• Should I eat low-carb, low-fat, or do macronutrient ratios not matter?
• Do you have anything you could teach on the problem of developing gastritis AFTER going paleo?
• Does the food combining theory have any scientific merit?

As part of the recent re-branding of the site from The Healthy Skeptic toward Chris Kresser, I will also be changing the name of the podcast soon. I haven’t settled on a name yet, but keep an eye out for the change.

The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
- Peter @Hyperlipid

I don’t think there are too many people out there familiar with the mechanisms of diabetes and insulin resistance that would disagree with that statement.

But just because a low-carb diet causes fat loss in this population, that doesn’t mean that carbs caused the fat gain or damaged metabolism in the first place.

I wrote about this in a previous article, There is No Single Cause of (or Treatment or) Obesity, but based on some of the comments and discussion I’ve been seeing online recently, I think it bears repeating: in order to properly frame this debate, it’s essential to separate the causes and treatment of obesity. If we don’t do this, we might as well not even have a debate at all because we won’t be talking about the same thing.

We know without a doubt that statins lower cholesterol. But does that mean high cholesterol is caused by a statin deficiency? If you break your arm, your doctor will probably put a cast on to help it heal. Does that mean we should all wear casts on our arms to make sure they don’t break?

Metabolically damaged vs. healthy: apples & oranges

Another important distinction that should be made – but often isn’t – is the difference between how people that are metabolically healthy and metabolically damaged respond to food. Of course excess carbohydrates are more likely to cause problems in someone with leptin and insulin resistance and impaired glucose tolerance. But it doesn’t follow that the same will be true in someone without metabolic problems.

People without gall bladders don’t digest fat very well. Does that mean fat causes indigestion? I have patients with iron overload due to a genetic condition called hemachromatosis. They need to limit their red meat intake because of this. Does this mean we should all avoid red meat to prevent iron overload?

We’re not robot clones. We have different genes, lifestyles, gut flora, immune fitness and exposures to toxins, stress and infections, as well as different emotional and psychological relationships with food. All of these factors play a role in weight regulation.

This explains why two people can react to the same diet in entirely different ways. And it also explains why it’s so ridiculous to extrapolate something that you experience personally to everyone else. (If I read another comment from someone saying that a low-carb diet worked for them, so the insulin-carb theory must be correct, I’m going to lose it. And it takes a lot to make me lose it!)

My unified theory of obesity

For what it’s worth, here’s my “unified theory” on what causes obesity.

Modern lifestyle + genetic predisposition = obesity.

It really is that simple.

Modern lifestyle includes processed, refined and highly rewarding and palatable foods, excess fructose, unprepared grains (especially flour), industrial seed oils, environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.

But the modern lifestyle doesn’t cause obesity in all people. I’m sure we all know someone who eats a horrible diet, doesn’t exercise, is under tons of stress and lives a shockingly unhealthy lifestyle – but doesn’t gain a single pound.

That’s where genetics come in.

Human evolution didn’t stop in the Paleolithic

A commonly held belief in the Paleo-sphere (I held it myself, until fairly recently) is that our genes haven’t changed much since the Paleolithic era. But recent evidence suggests a much more rapid pace of genetic change in humans than was previously estimated.

The birth of agriculture introduced significant selection pressure, and thus mutation, because humans were not well-adapted to this new way of life. And the evolutionary response to agricultural diet differs because different peoples adopted agriculture at different times and in different places.

Agriculture began in the Middle East 10,000 years ago, but it was never adopted by Aboriginal Australians. Might we expect the descendants of people from these two regions to have different responses when exposed to agricultural diets?

Absolutely. Researchers in Iceland have discovered a gene that regulates blood sugar tolerance. (I discussed the role of genetics in obesity and diabetes in a previous article, Are You At Risk For Diabetes and Obesity?) And we know that Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.

Lactase persistence is another example. During Paleolithic times, humans stopped producing lactase (the enzyme required to digest lactose, the sugar in milk) shortly after weaning. There was no need for it, since Paleo people didn’t raise cattle or drink milk. Skeletal remains from northern Europeans 8,000 – 9,000 years ago confirm that there was no lactose tolerance at that time.

However, skeletal remains from northern Europeans living in the Bronze Age 3,000 years ago show roughly 25% of adults produced lactase. And today, in certain Scandanavian countries, more than 95% of adults are now lactose tolerant. ¹

All of these genetic changes happened within the last 8,000 years, after the advent of agriculture.

The hand you were dealt: life isn’t always fair

What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet.

But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.

Does it even matter what causes obesity? I just want to lose weight!

Some might argue that this discussion is irrelevant, since once someone become obese it’s clear their metabolism is damaged. There are two main problems with that argument.

First, not all obese people have deranged metabolisms. Research over the past several years has defined a subset of “metabolically healthy obese” (MHO) people with normal fasting glucose, triglycerides, insulin sensitivity and other markers. I wrote about this in my article Not All Fat People Get Diabetes, and Not All Diabetics Are Fat.

Second, separating the cause and treatment of obesity is necessary to prevent confusion. Something I see all the time in my practice and in the blogosphere is normal or even underweight people following zero- or very-low-carb diets. Why? Because they’ve absorbed the notion that “carbs are bad” from the “carbs-insulin-fat gain” theory, and they avoid them in a misguided attempt to promote health. While this may work for some people, it doesn’t for many others. I know because they end up coming to me with complaints like low energy, hair loss, bad breath, constipation and more.

Food reward vs. the carbohydrate hypothesis: setting the ground rules

I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation.

Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.

Over the last couple of years, as the popularity of the Paleo diet has expanded, a lot of controversy has emerged over exactly what a Paleo diet is.

Part of the problem is that there are now a number of authors and bloggers – from Mark Sisson to Kurt Harris to Robb Wolf to Paul Jaminet to myself – that advocate what might generally be called a Paleo diet, but with slight variations in each case. This has unfortunately led to some confusion for people new to the “Paleo diet”.

It has also spawned new terminology in an effort by each author/blogger to clarify the differences in their approach, such as Mark Sisson’s “Primal diet”, Paul Jaminet’s “Perfect Health Diet”, and Kurt Harris’ former “PaNu or Paleo 2.0″ and current “Archevore” concepts.

So what’s the controversy or confusion all about? It usually revolves around the following questions:

• Is the Paleo diet low-carb or low-fat? Is saturated fat permitted? If so, how much?
• How much protein should someone eat on a Paleo diet?
• Does the Paleo diet include dairy products – or not? Which kinds of dairy?
• Are any grains at all permitted?

In the early days, following Loren Cordain’s book, The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat, the Paleo diet was considered to be moderate in carbohydrate and low in saturated fat (though monounsaturated fat wasn’t restricted).

Then, as low-carb diets rose in popularity and many low-carbers switched over to Paleo, it seemed that the lines between low-carb and Paleo began to blur. For these folks, the Paleo diet is high in fat – especially saturated fat – and low in carbohydrates, with a moderate amount of protein.

More recently, some authors/bloggers have advocated a diet based roughly on Paleo principles but that also may include dairy products and even certain grains like white rice and buckwheat, depending on individual tolerance. Still others have suggested that a high carb, lower fat diet – provided the carbs come from starchy vegetables and not grains – may be optimal.

So what is a Paleo diet? Is it low-carb? Low-fat? Does it include dairy? Grains?

We’re not robots: variation amongst groups and individuals

The answer to that question depends on several factors. First, are we asking what our Paleolithic ancestors ate, or are we asking what an optimal diet for modern humans is? While hard-core Paleo adherents will argue that there’s no difference, others (including me) would suggest that the absence of a food during the Paleolithic era does not necessarily mean that it’s not nutritious or beneficial. Dairy products are a good example.

Second, as recent studies have revealed, we can’t really know what our ancestors ate with 100% certainty, and there is undoubtedly a huge variation amongst different populations. For example, we have the traditional Inuit and the Masai who ate a diet high in fat (60-70% of calories for the Masai and up to 90% of calories for the Inuit), but we also have traditional peoples like the Okinawans and Kitavans that obtained a majority (60-70% or more) of their calories from carbohydrate. So it’s impossible to say that the diet of our ancestors was either “low-carb” or “low-fat”, without specifying which ancestors we’re talking about.

Third, if we are indeed asking what the optimal diet is for modern humans (rather than simply speculating about what our Paleolithic ancestors ate), there’s no way to answer that question definitively. Why? Because just as there is tremendous variation amongst populations with diet, there is also tremendous individual variation. Some people clearly do better with no dairy products. Yet others seem to thrive on them. Some feel better with a low-carb approach, while others feel better eating more carbohydrate. Some seem to require a higher protein intake (up to 20-25% of calories), but others do well when they eat a smaller amount (10-15%).

The Paleo diet vs. the Paleo template

I suggest we stop trying to define the “Paleo diet” and start thinking about it instead as a “Paleo template”.

What’s the difference? A Paleo diet implies a particular approach with clearly defined parameters that all people should follow. There’s little room for individual variation or experimentation.

A Paleo template implies a more flexible and individualized approach. A template contains a basic format or set of general guidelines that can then be customized based on the unique needs and experience of each person.

But here’s the key difference between a Paleo diet and a Paleo template: following a diet doesn’t encourage the participant to think, experiment or consider his or her specific circumstances, while following a template does.

In my 9 Steps to Perfect Health series, I attempted to define the general dietary guidelines that constitute the Paleo template:

• Don’t eat toxins: avoid industrial seed oils, improperly prepared cereal grains and legumes and excess sugar (especially fructose)
• Nourish your body: emphasize saturated and monounsaturated fat while reducing intake of polyunsaturated fat, favor glucose/starch over fructose, and favor ruminant animal protein and seafood over poultry
• Eat real food: eat grass-fed, organic meat and wild fish, and local, organic produce when possible. Avoid processed, refined and packaged food.

Within these guidelines, however, there’s a lot of room for individual differences. When people ask me whether dairy products are healthy, I always say “it depends”. I give the same answer when I’m asked about nightshades, caffeine, alcohol and carbohydrate intake.

The only way to figure out what an optimal diet is for you is to experiment and observe. The best way to do that is to remove the “grey area” foods you suspect you might have trouble with, like dairy, nightshades, eggs, etc. for a period of time (usually 30 days is sufficient), and add them back in one at a time and observe your reactions. This “30-day challenge” or elimination diet is what folks like Robb Wolf have recommended for a long time.

As human beings we’re both similar and different. We share the same basic physiology, which is why a Paleo template makes sense. There are certain foods that, because of their chemical structure, adversely affect all of us regardless of our individual differences. These are the foods I mentioned in my “Don’t Eat Toxins” article.

On the other hand, each of us is unique. We grew up in different families, with different dietary habits, life experiences, exposures to environmental toxins and lifestyles. Many of our genes are the same, but some are different and the way those genes have been triggered or expressed can also differ.

For someone with an autoimmune disease, dairy products, nightshades and eggs may be problematic. Yet for others, these foods are often well-tolerated. This variation merely underscores the importance of discovering your own optimal diet rather than blindly following someone else’s prescription.

I think it’s a complete waste of time and energy to argue about what a Paleo diet is, because the question is essentially unanswerable. The more important question is, what is your optimal diet?

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 got an email from Pamela Schoenfeld, R.D. the other day. She wanted to make me aware of a paper she and her colleagues (Hite, et al)published on Friday in the journal Nutrition. It’s a critique of the Report of the 2010 Dietary Guidelines Committee (DGAC) that recommended that we all go on eating the same low-fat, high-carb diet that has contributed to the epidemics of obesity, diabetes and heart disease (among others).

The paper is open-access, which means you can read the full text for free (PDF). Here’s the gist: the new dietary guidelines proposed by the DGAC aren’t based on scientific evidence. The authors criticize the DGAC for excluding recent research that contradicts their low-fat propaganda, and for conveniently ignoring the fact that disease rates have skyrocketed over the past 30 years in spite of Americans eating less fat and more carbs.

The DGAC report essentially said, “Hey Americans! You’re fat and sick because you haven’t done a good enough job following our advice. What you need to do is eat even less fat (and by extension more carbs), and then you’ll finally lose weight and maybe not die of a heart attack.

Obviously the DGAC has never heard Einstein’s definition of insanity, which is to do the same thing over and over again and expect a different result.

Hite et al start the paper off with this gem of a quote:

What is required is less advice and more information. – Gerald M. Reaven

Amen to that! There’s no doubt we’re in the midst of a serious nutritional crisis, but the DGAC is dead wrong about what’s causing it. Hite et al continue:

Nutritional health covers a wide range of concerns but first and foremost in the mind of the public are whether the standing recommendations for lowering fat intake and increasing carbohydrate intake were ever appropriate for the prevention of obesity, diabetes, and cardiovascular disease;

You took the words right out of my mouth!

The authors go on to dismantle the DGAC dietary recommendations by reviewing all of the available evidence (imagine that!), rather than just focusing on the studies that support their viewpoint. Real science! What a breath of fresh air.

If you’re interested in learning more about how we’ve been collectively duped into the idea that fat is bad and carbs are good, read the paper. It’s not highly technical and is intended, to some degree I think, for a lay audience. But for those of you who don’t have time to read it, I’m going to list a few of the section headings to give you the idea:

“Strong recommendations, weak evidence”

“Animal versus plant protein: Recommendations do not reflect limitations and uncertainties of the science”

This is an important paper. It’s one of the most comprehensive critiques of the mainstream dietary recommendations I’ve seen, and it’s all in one place. So please, share this with as many people as you can. Post it to Facebook. Tweet it. Print it and take it to your doctor. Send it to your Mom & Dad, who might still think butter is bad for them. Tape it on your refrigerator. Get the word out!

Still think saturated fat is bad for you? Still think eating eggs raises cholesterol? Still think high cholesterol causes heart disease?

If you answered yes to any of those questions, you really need to watch these videos. (But hey, you might learn something even if you answered “no”.)

In this presentation I:

• debunk the myth that eating saturated fat and cholesterol causes heart disease.
• explain why LDL and total cholesterol are not useful markers for heart disease.
• present three markers that are useful markers for heart disease.
• demonstrate that low-fat, high carb diets promote – rather than protect against – heart disease.
• show you how eating saturated fat and cholesterol can prevent heart attacks
• tell you how to order a test that more accurately predicts your risk of heart disease

At the end of these two videos, you’ll be heading to the fridge for some extra butter or cheese on those veggies or a little extra cream in your coffee!

From the documentary Fat Head

This is the second article in a series on heartburn and GERD. If you haven’t read the first one, I’d suggest doing that first.

The idea that heartburn is caused by too much stomach acid is still popular in the media and the public. But as Daniel pointed out in the comments section of the last post, anyone familiar with the scientific literature could tell you that heartburn and GERD are not considered to be diseases of excess stomach acid.

Instead, the prevailing scientific theory is that GERD is caused by a dysfunction of the muscular valve (sphincter) that separates the lower end of the esophagus and the stomach. This is known as the lower esophageal valve, or LES.

The LES normally opens wide to permit swallowed food and liquids to pass easily into the stomach. Except for belching, this is the only time the LES should open.

If the LES is working properly, it doesn’t matter how much acid we have in our stomachs. It’s not going to make it back up into the esophagus. But if the LES is malfunctioning, as it is in GERD, acid from the stomach gets back into the esophagus and damages its delicate lining.

Here’s the key point. It doesn’t matter how much acid there is in the stomach. Even a small amount can cause serious damage. Unlike the stomach, the lining of the esophagus has no protection against acid.

We’ve been asking the wrong question

In a recent editorial published in the journal Gastroenterology, the author remarked:

Treating gastroesophageal reflux disease with profound acid inhibition will never be ideal because acid secretion is not the primary underlying defect.

I couldn’t agree more. For decades the medical establishment has been directing its attention at how to reduce stomach acid secretion in people suffering from heartburn and GERD, even though it’s well-known that these conditions are not caused by excess stomach acid.

Instead, the question researchers should have been asking is, “what is causing the LES to malfunction?” Since it is universally agreed upon that this is the underlying mechanism producing the symptoms of GERD, wouldn’t it make sense to focus our efforts here?

That’s exactly what we’re going to do in this article.

GERD is caused by increased intra-abdominal pressure

It is well accepted in the literature that GERD is caused by an increase in intra-abdominal pressure (IAP). Acid reflux occurs when pressure causes gastric distention (stomach bloating) that pushes the stomach contents, including acid, through the LES into the esophagus.

According to current thought, factors contributing to this include overeating, obesity, bending over after eating, lying down after eating, and consuming spicy or fatty foods.

For example, several studies have indicated an association between obesity and GERD, and this recent paper in Gastroenterology concluded that increased intra-abdominal pressure was the causative mechanism.

But while I agree that all of the currently accepted factors play a role, I do not think they are the primary causes of the increased IAP seen in GERD.

The two primary causes of increased intra-abdominal pressure

Instead, I believe the primary causes of IAP (and thus heartburn and GERD) are bacterial overgrowth and maldigestion of carbohydrates – both of which are caused at least in part by low stomach acid.

In a nutshell, the process looks like this:

Let’s look at each step in turn.

Low stomach acid causes bacterial overgrowth

As I will explain in the next article, one of the chief roles of stomach acid is to inhibit bacterial overgrowth. At a pH of 3 or less (the normal pH of the stomach), most bacteria can’t survive for more than 15 minutes. But when stomach acid is insufficient and the pH of the stomach rises above 5, bacteria begin to thrive.

The gastrin knockout mouse, which is incapable of producing stomach acid, suffers from bacterial overgrowth – as well as inflammation, damage and precancerous polyps in its intestines. It is also well documented that acid-suppressing drugs promote bacterial overgrowth. Long-term use of Prilosec, one of the most potent acid suppressing drugs, reduces the secretion of hydrochloric acid (HCL) in the stomach to near zero. In one trial, 30 people with GERD were treated with a high dose of Prilosec (40g/day) for at least 3 months. 11 of the 30 Prilosec-treated people had developed significant bacterial overgrowth, compared with only one of the ten people in the control group.

Low stomach acid causes maldigestion of carbohydrates

Stomach acid (HCL) supports the digestion and absorption of carbohydrates by stimulating the release of pancreatic enzymes into the small intestine. If the pH of the stomach is too high (due to insufficient stomach acid), the pancreatic enzymes will not be secreted and the carbohydrates will not be broken down properly.

Bacterial overgrowth + maldigested carbohydrates = GAS!

Though microbes are able to metabolize proteins and even fats, their preferred energy source is carbohydrate. The fermentation of carbohydrates that haven’t been digested properly produces gas. The resulting gas increases intra-abdominal pressure, which is the driving force behind acid reflux and GERD.

When stomach acid is sufficient and carbohydrates are consumed in moderation, they are properly broken down into glucose and rapidly absorbed in the small intestine before they can be fermented by microbes. However, if stomach acid is insufficient and/or carbohydrates are consumed in excess, some of the carbs will escape absorption and become available for intestinal microbes to ferment.

A nasty vicious cycle: the role of hydrogen gas

Hydrogen (H2) is one of the gases produced by bacterial fermentation of carbohydrates. In fact, there have been explosions during intestinal surgery due to the high amounts of hydrogen gas production in the gut. This is significant because a recent landmark study demonstrated that pathogenic bacteria feed on hydrogen gas.

So, the more undigested carbohydrate you have in your gut, the more hydrogen gas bacteria will produce. The more hydrogen gas is produced, the more bacterial overgrowth will occur. And the more bacteria you have in your gut, the more gas will be produced by fermentation of undigested carbohydrate. This becomes a nasty vicious cycle.

There is significant evidence that the carbohydrates consumed in the “standard American diet” contribute to this phenomenon. Fructose is a particular problem. In one study researchers fed fructose to 15 normal adults. They found that more than half of the 15 adults showed evidence of fructose malabsorption after just 25g of fructose, and greater than two-thirds showed malabsorption after 50g of fructose. To put this in perspective, one 12 oz. can of Coca-Cola contains 30g of fructose.

One of the measures of malabsorption used in the study was a hydrogen breath test. Both the 25g and the 50g doses caused a large increase in H2, especially the 50g dose (a 5-fold increase). Bacterial fermentation of carbohydrate is the only source of hydrogen in the human body. This means that the hydrogen measured in the study indeed came from the undigested fructose in the gut.

Certain type of fiber and starch also promote hydrogen production. Almost all of the fiber and approximately 15-20% of the starch we consume escape absorption. The amount of gas that can be produced by undigested carbohydrates is almost hard to believe. According to Suarez and Levitt, just 30g of carbohydrate (equivalent to 1/2 of a small muffin) that escapes absorption in a day could produce more than 10,000 mL of hydrogen gas. That’s equivalent to ten large one-liter water bottles full of intestinal gas!

Finally, a recent study showed that ingestion of lactose (the carbohydrate found in milk) results in an increased number of transient lower esophageal sphincter relaxations (TSELRs), increased reflux episodes, higher esophageal acid exposures, and more severe GERD symptoms. Another study showed that oral administration of fructo-oligosaccharides (FOS) produces similar findings. Together these studies suggest that colonic fermentation of malabsorbed carbohydrates contributes to the pathogenesis of GERD.

Other supporting evidence

If gas produced by microbial fermentation of carbohydrates causes acid reflux, we might expect that reflux could be treated by either 1) reducing bacterial overgrowth or 2) reducing carbohydrate intake.

In fact, that’s exactly what we see. In a study by Pehl, administration of erythromycin (an antibiotic) significantly decreased esophageal reflux. In another study by Pennathur, erythromycin strengthened the defective lower esophageal sphincter in patients with acid reflux.

To my knowledge there have only been two small trials performed to test the effects of carbohydrate restriction on GERD. Both had positive results. A small case series showed a significant, almost immediate resolution of GERD symptoms in obese individuals initiating a very low-carb diet. A more recent study found that a very low-carb diet decreased distal esophagus acid exposure and improved the symptoms of GERD. Perhaps most importantly, the magnitude of the improvement was similar to what has been reported with treatment with proton-pump inhibitors (acid suppressing drugs).

Many researchers now believe that Irritable Bowel Syndrome (IBS) is caused by bacterial overgrowth in the small intestine (SIBO). A study performed at the GI Motility Center in Los Angeles in 2002 found that 71% of GERD patients tested positive for IBS – double the percentage seen in non-GERD patients being examined.

The high prevalence of IBS in GERD patients combined with the recognition that bacterial overgrowth causes IBS is yet another line of evidence suggesting that bacterial overgrowth is also a causative factor in GERD.

A unified theory

To summarize, GERD is caused by increased pressure in the stomach resulting in a malfunction of the lower esophageal sphincter (LES). The increase in pressure is caused by bacterial overgrowth and malabsorption of carbohydrates, both of which are precipitated by low stomach acid. Reducing bacteria loads and limiting carbohydrate intake have both been shown to greatly improve, and in some cases completely cure, acid reflux and GERD.

In the Part III of the series I discuss the connection between GERD and H. pylori, and further evidence supporting the theory that GERD is caused by bacterial overgrowth. Read on!

Summary:

• The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
• Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
• Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
• Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
• The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.

Not all cholesterol is created equal

By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.

But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”

Words to live by.

The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.

But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.

In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.

You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).

Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.

It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.

The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.

In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.

On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.

Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.

Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.

I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.

Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol

Here’s where the story gets even more interesting. And tragic.

Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.

It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.

Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.

In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.

Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.

Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.

Here’s what the authors said about their results:

Translation: following the advice of the American Heart Association is hazardous to your health.

Eating cholesterol reduces small LDL

The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.

Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.

If you’re confused right now I certainly don’t blame you.

Let’s review what we’ve been told for more than 50 years:

1. Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
2. Reducing intake or saturated fat and cholesterol protects us against heart disease.

Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:

1. Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
2. Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.

Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”

In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.

I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.

We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.

Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?

Really?

Sometimes it seems like everything is backwards.

How to reduce small LDL

Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.

Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.

As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.

In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.

Testing your small LDL level

I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.

If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.

However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.

First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.

The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.

Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.

If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:

1. LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
2. The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.

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!