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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!

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bread and other high carbohydrate foodsThis 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:

diagram of what causes gerd

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!

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important

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:

The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.

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.

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

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

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

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

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

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

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

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

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

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

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