Cholesterol Confusion

Posted: May 28, 2014 in Anti-aging, Lifestyle, Nutrition

First off, this not intended to be an exhaustive review of cholesterol science. Peter Attia did a great job of that in his 10 part series here. The purpose of this article is just to shed a bit of light on a confusing topic to help get readers up to speed on the current understanding of cholesterol measurements and ultimately, relevance to your health and longevity. Very few nutrition or medical experts are making recommendations based on the most current data, some are quite a bit farther behind than others. The reasons for this discordance are numerous and will be touched upon later.

The information provided here should be taken as opinion, not medical advice. This opinion, however, is based on an extensive review of published scientific literature, books and blogs from a small number of true experts, as well as years of intricately analyzing lab tests from clients and watching how values change given specific dietary and lifestyle interventions. But the volume of blood work I have had the opportunity to review is a drop in the bucket compared to cardiologists that do this all day, every day, which is why I defer to their data when possible (and by possible, I mean the inclusion of only cardiologists who actually keep up with, and/or contribute, to current research).

Outdated concepts regarding cholesterol continue to permeate mainstream advice, like the existence of bad (LDL) and good (HDL) cholesterol, or that LDL and HDL are even cholesterol at all (they’re not, they’re vessels that transport cholesterol through the bloodstream, which it turns out, is a very important distinction). However, the more educated professionals have, for quite some time now, abandoned the unfounded and flat out dangerous Lipid Hypothesis theory of heart disease, which has prevailed in the medical community and therefore public consensus since the 1970’s. This theory basically states that serum cholesterol levels are a direct predictor of atherosclerosis and heart disease. Combine that with a similar and often mistakenly rolled-into-one hypothesis called The Diet Heart Hypothesis, which states that the more cholesterol and saturated fat we eat, the higher our cholesterol gets, and the more likely we are to get heart disease. These were not bad hypotheses at the time given the limited amount of information and the inadequate testing methods available. Instead of rigorously testing this hypothesis however, it was embraced prematurely and almost every public health organization hopped on board demonizing saturated fat and promoting an increase of grains. The way this played out in history is actually pretty interesting, you can read more about it here, and here, but I’m sure it won’t come as a major surprise that the whole thing has been motivated by money, confirmation bias, and a bit of “playing not to lose”.

Back to the abandonment of the Lipid Hypothesis and the Diet Heart Hypothesis by educated health professionals, taking the next steps beyond that level of understanding is where it starts to get interesting.

Enter the development of more sensitive blood lipid testing methods, like the Vertical Auto Profile (VAP). As of 2007 when Atherotec made the VAP publically available, we have been able to easily identify different subclasses of LDL particles, namely type-A (large/buoyant) and type-B (small/dense). Think of type-A as fluffy cotton balls and type-B as little marbles.

Quite a bit of recent research looked at these distinctions and it was preliminarily determined that only type-B (the marbles) were dangerous. The science savvy hopped on board with this right away (including myself) and started making this a major focus in the discussion of heart disease prevention.

As the field continues to progress, we now have even more accurate information and better testing available. One new type of testing is called an NMR panel (nuclear magnetic resonance), click here for a sample report. It turns out that even type-A LDL particles can be atherogenic, which doesn’t necessarily nullify the theory of type-B particles being a relevant risk factor, but it requires some re-evaluation.

With an NMR test, we can now look directly at the actual number of LDL particles (think of them as the number of boats carrying cargo through the bloodstream, known as LDL-P) instead of the current testing which just looks at LDL cholesterol (think of this as how much cargo the boats are carrying, known as LDL-C or just LDL). Current research demonstrates this (LDL-P measurement) is likely a far better predictor of heart disease risk and atherogenic potential than LDL-C or even particle size. The small/dense theory is not without merit, it just probably acts as a potential proxy for LDL-P values. The problem is, and I’ve seen this several times, that they don’t always match up as expected.

Here’s a comment on this particular matter on Peter Attia’s blog from one of my favorite cholesterol experts, Dr. Thomas Dayspring:

“If you have too many small LDLs or too many big LDLs you are at risk for CHD. If you have all small LDLs but total LDL-P is normal, there is no risk. If you have normal numbers of very large LDLs your LDL-C might be high but LDL-P will be fine and thus no risk exists. Peter nicely illustrates that if you have small LDLs, it will take 40-70% more LDLs to traffic a given mass of cholesterol, hence untreated folks with small LDLs always have a high LDL-P and that is what drives risk. Likewise if one’s LDLs are pathologically carrying TG instead of cholesterol (i.e. a cholesterol depleted LDL) it will take many more such cholesterol-depleted LDLs to carry a given cholesterol mass. Risk is related to particle number not to the amount of cholesterol within the LDL particles, because it is particle number that drives the LDLs into the artery.”

ApoB is another important reading to look at, as each LDL-P can have only one ApoB protein bound to its cell wall, so measuring ApoB can give us an idea of the LDL-P number, although it is not as exact as true LDL-P measurement.

From a nutrition perspective, carbohydrate intake directly relates to both triglyceride and HDL levels. Eat more carbs (with the exception of fibrous vegetables), and HDL goes down, triglycerides go up. Bad news. However, I’ve seen several people replace their starchy carb intake with good fats, and while their Triglyceride:HDL ratio improves, their small/dense LDL’s don’t budge, yet their LDL-P drops. This is likely uncommon, but it just tells us these proxies are not foolproof, just a guess with a decent probability. And in this case, going off of the LDL pattern type would be detrimental, as the HDL/Trig ratio and LDL-P values improved which is what is really important.

Research also demonstrates that reducing fat intake in the diet can often encourage a decrease in LDL-C, at the expense of shifting the particle size to the small/dense type, and actually raising LDL-P. Keeping lots of good fat (including saturated fat) in the diet while reducing carbohydrate intake typically has the exact opposite effect, LDL-C might go up a little, but the particle size shifts to large/buoyant type-A, and LDL-P goes down. So yes, a low fat diet can often make numbers look better on paper, if you’re looking at the wrong numbers in the first place.

To summarize, its better to have more data than not enough, and if LDL-P is above optimal, that should outweigh all other values on a lipid test. If you don’t have your LDL-P number, but you have a VAP test, you might be able to get a decent guess by looking at your LDL pattern size. If you just have the basic cholesterol test your doctor typically gives you, you might be able to get a decent guess at your heart disease risk by looking at your Triglyceride:HDL ratio (1:1 is optimal, 2:1 is passable, anything above that is likely trouble). But these proxy tests are still a guess, and NMR testing is inexpensive and easy to get, you can order the test here for $127 and go to a local lab to get it drawn.

From my experience, many physicians will tell their patients that more in-depth cholesterol testing like the VAP and NMR are unnecessary. This would be entirely true if the Lipid Hypothesis had any sort of validity, which it doesn’t. One doctor told a client of mine that there is no point in doing the NMR test because it wouldn’t change the treatment recommendations beyond what would be advised from the basic cholesterol test (either I’m going to prescribe you statins or I’m not), which is basically admitting a complete lack of understanding of the data. If your doctor tells you this, order the test yourself and find a qualified Registered Dietician or a different doctor to interpret it for you and give you recommendations. There’s lots of great, progressive physicians out there willing to help, see my resources at the end of the article for some ideas.

Obviously cholesterol and its relationship to heart disease is an emerging science, and we are learning more every year. We don’t know everything yet, but what we are rapidly learning is what we can rule out. At this point, we can confidently rule out total cholesterol (TC) and LDL-C as relevant information. However some doctors still consider extremely high LDL-C a reliable proxy for high LDL-P, stating that LDL-C is therefore not useless, but it’s still based on likelihood of what the LDL-P value would be, so why not test it in the first place? HDL particles being thought of as simply “good” cholesterol is outdated. Particle size (type-A or type-B) is interesting to look at, but again it is likely only a risk factor as it relates to predictability of LDL-P number.

Also, I should mention, that due to genetic makeup (specific ApoE genotypes in particular, which are actually easy to test for), or other factors, some people will notice a worsening of LDL-P on a lower carbohydrate, higher fat diet. So get your bloodwork done and work with a knowledgeable professional when making dietary changes, particularly if you’re doing it for the purpose of disease avoidance and life extension.

So how does this high LDL-P number act as a predictor for heart disease risk? That involves inflammation, oxidation, aggregation, and another article for another time.

Want to get more in depth? Depasi Fitness is currently hosting webinars on Lipidology for small gym owners. Shoot us an email for more info.

For more general information on the topic, see the following great resources:

Cholesterol and Saturated Fat Prevent Heart Disease- David Evans

Cholesterol Clarity- Jimmy Moore

The Great Cholesterol Myth- Stephen Sinatra

Ignore the Awkward- How Cholesterol Myths are Kept Alive- Uffe Ravnskov

The Great Cholesterol Con- Dr. Malcolm Kendrick

Cholesterol is Not the Enemy

Peter Attia’s cholesterol video:

  1. Anonymous says:

    Nice article Dr. Mcdougal.

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