This week we’re glad to welcome Chris Masterjohn to the show. Chris is currently pursuing a PhD in Nutritional Sciences with a concentration in Biochemical and Molecular Nutrition at the University of Connecticut. He writes a blog called The Daily Lipid and is also a frequent contributor on the Weston A. Price Foundation’s blog.

I consider Chris to be one of the foremost experts on the topic of cholesterol and its relationship to heart disease. In this episode, we discuss (among other things):

• the history of the cholesterol-heart disease connection
• misconceptions around diet vs. lipid hypothesis
• finding middle ground between cholesterol skeptics and proponents of the lipid hypothesis
• the LDL receptor and familial hypercholesterolemia and what they can tell us about cholesterol and CHD in normal populations

We didn’t get to any questions this time around, but Chris has graciously offered to come back and do an entire episode devoted to Q&A in the future – so look out for that!

I do a lot of public speaking. As you might suspect, regardless of the specific topic I’m presenting the dietary recommendations I make are always essentially the same: high-fat, nutrient-dense and low in toxins. Since omega-6 vegetable oils are toxins, when I say high fat I’m talking about saturated and monounsaturated fat. You know this.

But a lot of people I speak to don’t. They fully steeped in 50 years of mainstream propaganda perpetuating the idea that saturated fats cause heart disease – primarily by raising blood cholesterol. So, inevitably, when I stand up in front of a group of people and tell them all to eat lots of saturated fat, I get a question that goes something like this:

But won’t that raise my cholesterol? And won’t high cholesterol give me a heart attack?

I haven’t yet perfected an answer that can dismantle a half century of cultural brainwashing about fat and cholesterol in less than 3 minutes. But I’m working on it.

In the meantime, I usually explain some variation of the following:

Point #1: Eating saturated fat doesn’t raise cholesterol levels in the blood

There’s no convincing evidence that eating saturated fat raises blood cholesterol. Stephan Guyenet spanked that old yarn to the curb in this recent blog post. In short, of all of the studies examining the relationship between saturated fat intake and serum cholesterol, only one found a clear relationship between the two and even that association was weak. The rest found no association at all.

Point #2: Eating cholesterol doesn’t (usually) raise cholesterol levels in the blood

Nor is there evidence that eating cholesterol in the diet raises cholesterol levels in your blood. 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.

An increase of HDL is a good thing. And as it turns out, so is a boost of the type of LDL that eating saturated fat and cholesterol increases. We now know there are two different types of LDL: small, dense LDL, and large, buoyant LDL. Small, dense LDL is a significant risk factor for heart disease because it’s more likely to oxidize and cause inflammation. Large, buoyant LDL is not a risk factor for heart disease. And guess what? Eating eggs not only increases the benign large, buoyant LDL, but it also decreases the harmful small, dense LDL by 20%. I’ve written more about this here and here, and you can also watch some videos on this topic here.

Point #3: Even if eating saturated fat and cholesterol did raise cholesterol levels in your blood, it wouldn’t matter because “high cholesterol” isn’t a strong risk factor for heart disease.

This is the one that really spins people out. Even if they follow me on the first two points, their eyes tend to glaze over when I mention this one. As Mark Twain used to say:

The history of our race, and each individual’s experience, are sown thick with evidence that a truth is not hard to kill and that a lie told well is immortal.

Nowhere is that more true than with the lie that high cholesterol causes heart disease. It’s so deeply ingrained in our collective consciousness that it’s become an almost unassailable article of faith. That’s why people are so surprised to learn that there’s very little evidence to support the idea.

This point is the current bottleneck in my “3-minute” explanation, because it takes a while to explain why it’s not true. I’ve written about it extensively here, here and here. For the purposes of this brief article, we’ll have to leave it at this: both total and LDL cholesterol – which are the numbers your doctor, the media and everyone else seems to be concerned with – are only weakly associated with heart disease.

If “high cholesterol” were the cause of heart disease, you’d expect it to be a risk factor in:

1. All populations around the world.
2. In both men and women.
3. In people of all ages.

And you’d also expect that lowering cholesterol should prevent heart disease.

Makes sense, right?

Unfortunately for the lipophobes, the cholesterol hypothesis fails on all fronts.

1. High cholesterol is not a risk factor in all populations. The French have among the highest cholesterol levels in the world, and among the lowest rates of heart disease of any industrialized nation. The Austrians and other European nations are similar.
2. Women on average have 300% lower rates of heart disease than men, despite higher average cholesterol levels.
3. The rate of heart disease in 65 year-old men is 10 times that of 45-year old men. Yet high cholesterol is not a risk factor in men over 65. (In fact, men over 65 with low cholesterol (<150 mg/dL) are twice as likely to die from heart disease as those with normal or even "high" cholesterol.)

Finally, more than 40 trials have been performed to see if lowering cholesterol prevents heart disease. In some trials more people got heart disease, in others fewer. But when all the results were taken together, just as many people died in the treatment groups (those who took cholesterol-lowering drugs) as the control groups (those who did not).

Point #4: If you want to worry about your cholesterol numbers, forget about total cholesterol and LDL and pay attention to the ratio of triglycerides to HDL.

In general I’m not a fan of people worrying about their lipid panel numbers at all. Like Dr. Kurt Harris, I think this compulsive testing and re-testing of lipids that has become common in the Paleo community not only isn’t necessary, but may even be harmful. There’s still a lot we don’t know about how these numbers change on a day-to-day basis. What’s more, it’s not always easy to distinguish between cause and effect. Researchers made the mistake of assuming high cholesterol was the cause of heart disease, when in reality it’s much more likely that high cholesterol is a consequence of it.

But for crying out loud, if you’re going to get your lipds tested at least pay attention to the right numbers. And the most important number on a conventional lipid panel is the relationship between triglycerides and HDL. (Divide triglyercids by HDL to get it.) If that number is less than 2, this suggests you have mostly large, buoyant LDL – which is not a risk factor for heart disease. If that number is higher than 3, it suggests you have mostly small, dense LDL – which most certainly is a risk factor for heart disease.

Point #5: Eat good food and don’t worry about the numbers.

But in the end, even that ratio doesn’t matter so much. Why? Because the treatment is always the same! If your TG:HDL ratio is high (bad), what should you do? Eat a high-fat (saturated, of course) diet. This will reduce your triglycerides and small, dense LDL, and increase your HDL. Triple win. And if your TG:HDL ratio is low (good), what should you do? The exact same thing: eat a high-fat diet.

Conversely, replacing saturated fat with carbs, as we’ve been told to do for 50 years to protect ourselves from heart disease, actually contributes to it in three ways: it increases triglycerides and small, dense LDL, and decreases HDL.

Finally, I often get emails from people who’ve switched to a high-fat / Paleo-type diet expressing concern that their LDL and total cholesterol levels have gone up. My response usually has three parts: 1) don’t worry about it, because high total and LDL cholesterol do not cause heart disease; 2) the increase is usually temporary, and may be the result of the body curing itself of fatty liver (a good thing!); 3) don’t worry about it. Doesn’t hurt to remind them.

**Note: if your total cholesterol levels are very high (i.e. above 300 mg/dL), this may be an indicator of a metabolic abnormality or inflammatory process that needs to be addressed. Cholesterol is a repair substance in the body, and persistent elevations beyond a certain threshold may point to an underlying problem that hasn’t been identified.

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!

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.

The persistent myth that cholesterol causes heart disease has scared many of us away from eating eggs on a regular basis. But there is absolutely no research that links egg consumption to heart disease.

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.

You’ve probably been conditioned to believe that anything that raises LDL cholesterol (so-called “bad” cholesterol) should be avoided like the plague. But even the medical mainstream has come to recognize that all LDL cholesterol is not the same. It’s true that small, dense LDL particles have been linked to heart disease. This is primarily due to the fact that they are much more susceptible to oxidative damage than normal LDL cholesterol particles.

However, egg consumption increases the proportion of large, buoyant LDL particles that have been shown to be protective against heart disease. Egg consumption also shifts individuals from the LDL pattern B to pattern A. Pattern B indicates a preponderance of small, dense LDL particles (risk factors for heart disease), while pattern A indicates a preponderance of large, buoyant LDL particles (which protect us from heart disease). This is a good thing.

Eggs one of the most nutrient-dense foods available. One egg provides 13 essential nutrients, all in the yolk (contrary to popular belief, the yolk is far higher in nutrients than the white).

Eggs are an excellent source of B vitamins, which are needed for vital functions in the body, and also provide good quantities of vitamin A, essential for normal growth and development.

The vitamin E in eggs protects against heart disease and some cancers; eggs also contain vitamin D, which promotes mineral absorption and good bone health.

Eggs are rich in iodine, for making thyroid hormones, and phosphorus, essential for healthy bones and teeth.

Eggs are also good sources of antioxidants known to protect the eye. Therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts.

There’s absolutely no reason to limit your consumption of eggs to three to four per week, as recommended by “heart-healthy” nutritional guidelines. In fact, consuming two to three eggs per day would provide a better boost to your health and protection against disease than a multivitamin supplement. Eggs truly are one of nature’s superfoods.

It’s important, however, to make sure that you buy organic, pasture-raised eggs. Studies show that commercially-raised eggs are up to 19 times higher in pro-inflammatory omega-6 fatty acids. Unfortunately, almost all eggs sold in supermarkets – even the organic eggs sold at chains such as Whole Foods and Wild Oats – are not truly pasture-raised. To find these eggs, check your local farmer’s market or visit the Eat Wild website to locate a source in your area.