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The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number

Published on May 9, 2013,

We recently featured an article by Chris Kresser which set out to bust a common diet and heart myth that suggests eating cholesterol and saturated fat raises cholesterol levels in the blood. Chris has now produced a second article in the series busting the follow-up myth – that high cholesterol is the cause of heart disease. This is from ChrisKresser.com…

English: Love heart

(Photo credit: Wikipedia)

Part of the confusion about cholesterol and its role in heart disease is caused by imprecise terminology. So, before I explain why high cholesterol is not the underlying cause of heart disease, we have to cover some basics.

Cholesterol is not technically a fat; rather, it’s classified as a sterol, which is a combination of a steroid and alcohol. It’s crucial to understand that you don’t have a cholesterol level in your blood. Cholesterol is fat-soluble, and blood is mostly water. In order for cholesterol to be transported around the body in the blood, it has to be carried by special proteins called lipoproteins. These lipoproteins are classified according to their density; two of the most important in cardiovascular disease are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

I know this can get confusing quickly, so let me use an analogy to make this more clear. Imagine your bloodstream is like a highway. The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.

Coronary arteries are essentially hollow tubes, and the endothelium (lining) of the artery is very thin—only one cell deep. The blood, which carries lipoproteins like LDL, is in constant contact with the endothelial lining. So why does the LDL particle leave the blood, penetrate the endothelium and enter the artery wall? The answer is that it’s a gradient-driven process. Going back to our analogy, the more cars there are on the road at one time, the more likely it is that some of them will “crash” into the fragile lining of the artery. It’s not the number of passengers (cholesterol) the cars are carrying that is the determining factor, but the number of cars on the highway.

The significance of this in terms of determining your risk of heart disease is profound. When you go to the doctor to get your cholesterol tested, chances are he or she will measure your total, LDL and HDL cholesterol. This tells you the concentration of cholesterol (passengers) inside of the lipoproteins (cars), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood.

LDL cholesterol levels and LDL particle number are often concordant (i.e. when one is high, the other is high, and vice versa), and this is probably why there is an association between LDL cholesterol and heart disease in observational studies. The elevated LDL cholesterol was more of a proxy marker for elevated LDL particle number in these cases. But here’s the kicker: they can also be discordant. In layperson’s terms, it’s possible to have normal or even lowcholesterol, but a high number of LDL particles. If this person only has their cholesterol measured, and not their particle number, they will be falsely led to believe they’re at low risk for heart disease. Even worse, the patients that are the most likely to present with this pattern are among the highest risk patients: those with metabolic syndrome or full-fledged type 2 diabetes. The more components of the metabolic syndrome that are present—such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL—the more likely it is that LDL particle number will be elevated.

On the other hand, patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease. In fact, studies suggest they’re at even lower risk than patients with low LDL-C and low LDL-P. Yet they will often be treated with statin drugs or other cholesterol lowering medications, because the clinician only looked at LDL-C and failed to measure LDL particle number. This is a concern for two reasons. First, statin drugs aren’t harmless. (I’ll go into more detail on this in the third post of the series.) Second, studies suggest that lowcholesterol can increase the risk of death, especially in women and the elderly…

The article concludes…

Heart disease is a complex, multifactorial process. The likelihood that we’ll have a heart attack depends on numerous factors, including genetics, diet, lifestyle and living environment. The purpose of this article is not to suggest that LDL-P is the only risk factor that matters, or that other risk factors shouldn’t be taken into consideration. It is simply to point out that existing evidence suggests that LDL-P is a much better predictor of heart disease risk than LDL or total cholesterol, and that it appears to be one of the better markers available to us now.

More (including references) at:  The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number

Chris Kessler has a special follow up article here: What Causes Elevated LDL Particle Number?

The Diet-Heart Myth: Cholesterol and Saturated Fat Are Not the Enemy

Published on April 25, 2013,

Health and wellness writer and therapist Chris Kresser has embarked on a series of three posts looking at the devastating impact of heart disease in the US and the consistent efforts of the medical establishment to keep treating it with approaches based on science that was outdated decades ago. In particular, he sets out to debunk three common myths about heart disease, starting with the idea that eating cholesterol and saturated fat raises cholesterol levels in the blood, then moving on to the myths that high cholesterol in the blood is the cause of heart disease and Statins save lives in healthy people without heart disease. Here are some extracts from the first of these articles from Chris Kesser…

Romantic Heart from Love Seeds

(Photo credit: epSos.de)

It’s hard to overstate the impact that cardiovascular disease (CVD) has in the U.S.. Consider the following:

  • Cardiovascular disease affects 65 million Americans.
  • Close to one million Americans have a heart attack each year.
  • In the U.S., one person dies every 39 seconds of cardiovascular disease.
  • 1 of 3 deaths that occurs in the U.S. is caused by cardiovascular disease.
  • 1 in 3 Americans have metabolic syndrome, a cluster of major cardiovascular risk factors related to overweight/obesity and insulin resistance.
  • The total cost of cardiovascular disease in 2008 was estimated at $300 billion…

Unfortunately, cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. We’ve learned a tremendous amount about what causes heart disease over the past decade, but the medical establishment is still operating on outdated science from 40-50 years ago.

Most of us grew up being told that foods like red meat, eggs and bacon raise our cholesterol levels. This idea is so deeply ingrained in our cultural psyche that few people even question it. But is it really true?

The diet-heart hypothesis—which holds that eating cholesterol and saturated fat raises cholesterol in our blood—originated with studies in both animals and humans more than half a century ago. However, more recent (and higher quality) evidence doesn’t support it.

On any given day, we have between 1,100 and 1,700 milligrams of cholesterol in our body. 25% of that comes from our diet, and 75% is produced inside of our bodies by the liver. Much of the cholesterol that’s found in food can’t be absorbed by our bodies, and most of the cholesterol in our gut was first synthesized in body cells and ended up in the gut via the liver and gall bladder. The body tightly regulates the amount of cholesterol in the blood by controlling internal production; when cholesterol intake in the diet goes down, the body makes more. When cholesterol intake in the diet goes up, the body makes less.

This explains why well-designed cholesterol feeding studies (where they feed volunteers 2-4 eggs a day and measure their cholesterol) show that dietary cholesterol has very little impact on blood cholesterol levels in about 75% of the population. The remaining 25% of the population are referred to as “hyper-responders”. In this group, dietary cholesterol does modestly increase both LDL (“bad cholesterol” and HDL (“good cholesterol”), but it does not affect the ratio of LDL to HDL or increase the risk of heart disease.

In other words, eating cholesterol isn’t going to give you a heart attack. You can ditch the egg-white omelettes and start eating yolks again…

What about saturated fat? It’s true that some studies show that saturated fat intake raises blood cholesterol levels. But these studies are almost always short-term, lasting only a few weeks. Longer-term studies have not shown an association between saturated fat intake and blood cholesterol levels. In fact, of all of the long-term studies examining this issue, only one of them showed a clear association between saturated fat intake and cholesterol levels, and even that association was weak.

Moreover, studies on low-carbohydrate diets (which tend to be high in saturated fat) suggest that they not only don’t raise blood cholesterol, they have several beneficial impacts on cardiovascular disease risk markers. For example, a meta-analysis of 17 low-carb diet trials covering 1,140 obese patients published in the journal Obesity Reviews found that low-carb diets neither increased nor decreased LDL cholesterol. However, they did find that low-carb diets were associated with significant decreases is body weight as well as improvements in several CV risk factors, including decreases in triglycerides, fasting glucose, blood pressure, body mass index, abdominal circumference, plasma insulin and c-reactive protein, as well as an increase in HDL cholesterol…

See the full article and all references at: The Diet-Heart Myth: Cholesterol and Saturated Fat Are Not the Enemy

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