We’re Back!

After a brief hiatus, Theo and I have decided to keep on blogging for our Santa Clara folks on a twice-a-week basis. I’ll be posting on Tuesdays and Theo will post  on Fridays, and when I run across a post somewhere else that I think you’ll like, I’ll post that too! We’ll cover anything and everything you’re interested in, so please send us your questions and ideas!

Today, I’m going to share a post written by my friend and fellow Paleo-eater, Jonathan Allen (aka “Goat” on the CrossFit Main Page).  He originally posted this on his CrossFit Rising website.

Before you read Jonathan’s article, let me give you some links to additional articles on Cholesterol, which I hope will add to Goat’s fine piece and make a somewhat sticky subject a little more understandable.

Mark Sisson has several great posts, including his Definitive Guide to Cholesterol and  Eight Foods to Lower LDL Cholesterol, Boost HDL cholesterol, and Fight Inflammation.

Robb Wolf has a short but pithy post on Cardiovascular Disease (CVD) and Cholesterol. Dr. Loren Cordain has a lot of information about fats and cholesterol here. This British site has a wealth of information about “the compound that makes us different from plants.”

For a few personal anecdotes/testimony about the effect of Paleo nutrition on cholesterol, read Steve Parsoneault’s post, Ari Armstrong’s blog post or this one from Chet at CrossFit East Decatur. (I liked their picture so much I borrowed it 🙂 )

March 7th, 2010 – Cholesterol

(by Jonathan Allen, CrossFit Rising)

Having gone from a weak and flabby 250 pounds to a strong and lean 175 pounds, I am often asked for the details of how I did it. When I describe a diet moderate-to-high in protein, high in saturated and mono-unsaturated fats, made of real foods and excluding processed food-products, grains, added sugar (which technically is a processed food-product), and legumes, I almost invariably hear some variation on, “Saturated fats? Won’t that raise my cholesterol?”

This has to be the most common stumbling block I encounter when I try to encourage my clients to eat healthfully. Since at least the 1970’s, science has understood that total blood cholesterol levels are not a good predictor of heart disease. In fact, many people with very high cholesterol levels never develop heart disease, and many people who have died of heart disease had cholesterol levels only slightly above “normal”. Yet the medical establishment continues to push the idea that high cholesterol kills, and eating saturated fat will turn you into a cholesterol factory working overtime. Most men are so afraid of heart disease that they have serious reservations about a way of eating which can eliminate excess body fat, lower blood pressure, reduce cancer and Alzheimer’s risk, and practically eliminate dozens of auto-immune diseases, but which might raise cholesterol levels.

So today I would like to take a closer look at cholesterol, and it’s role in our health. I know this has already been done by other people, but maybe I will reach the three or four internet-savvy people they haven’t, and besides, I understand things better when I write about them, so here goes.

First, what exactly is cholesterol? According to wikipedia.com, “Cholesterol is a waxy steroid metabolite found in the cell membranes and transported in the blood plasma of all animals.[2] It is an essential structural component of mammalian cell membranes, where it is required to establish proper membrane permeability and fluidity. In addition, cholesterol is an important component for the manufacture of bile acids, steroid hormones, and several fat-soluble vitamins.” Well, I sure am glad I know that. I guess for my purposes, cholesterol is something found in animal cell membranes and blood plasma. Good enough.

What is cholesterol for? Well, it is required to build and maintain cell membranes, regulate membrane fluidity, intracellular transport, cell signaling and nerve conduction, forms the myelin sheaths on neurons. It forms bile, which is essential to intestinal absorption of fat molecules as well as the fat-soluble vitamins, Vitamin A, Vitamin D, Vitamin E, and Vitamin K, (ask me why I hate Olestra, sometime) and it is a precursor molecule in several biochemical pathways. That all sounds like it is pretty important to me. It seems that we humans need cholesterol in many, many ways to ensure our bodies actually function properly.

In fact, our bodies make most of our cholesterol, and carefully regulate the levels. If we increase or decrease our dietary levels of cholesterol, our bodies respond by making less or more of it to maintain balance. Today, it is fairly commonly known to doctors that reducing cholesterol intake will not do much to reduce blood cholesterol levels.

So why is everyone afraid of what is not only an essential part of our bodies, but also a product of those self-same bodies? The answer lies in something called the Diet-Heart Hypothesis. The Diet-Heart Hypothesis basically says that saturated fat elevates blood cholesterol levels, and that elevated blood cholesterol causes blood lipid accumulation in arterial walls (a.k.a. plaques or lesions), and that this is at the root of coronary artery disease. The hypothesis has been around in one form or another for over 100 years, but it really came into the public’s notice in the 1950’s, when Ancel Keys published his Seven Countries Study, which allegedly showed a direct correlation between fat intake and heart disease. Keys made it onto the cover of Time magazine, which failed to mention that he had reliable data from twenty-two countries, but didn’t publish it because the data as a whole showed very little correlation between fat intake and heart disease. Basically, he cherry-picked his data.

One part of this and subsequent studies which really caught the public eye was the super-low heart disease rate on the island of Crete. The people of Crete had a low saturated fat intake, and ate a great deal of fresh vegetables, and this is the basis of today’s “Mediterranean Diet”. What most people don’t hear about is the fact that the Cretans ate large amounts of meat, did not have a low total fat intake (and in fact ate copious amounts of olive oil, some going so far as to drink it straight up), had no electricity (an therefor didn’t stay up very long past dark, generally), walked everywhere, worked hard in the physical sense… and so on. Their lifestyles were, and probably are, entirely different than ours. Singling out not just diet, but one small component of diet, and saying that must be the difference which makes their heart disease rate so low is just sheer idiocy.

These ideas about cholesterol and heart disease have persisted to this day, despite the fact that high-quality studies to back them up are pretty hard to come by. So what is really going on inside of us? Let’s take a look.

Our bodies produce molecules called “lipoproteins”. There are many kinds, but the kinds which are important to us are high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very-low-density lipoproteins (VLDL). Many of you have probably heard of these, or at least the first two.

What lipoproteins do, in simple terms, is shuttle cholesterol and triglycerides (fat) around in our bloodstream. HDL’s collect cholesterol from the body’s tissues, and bring it back to the liver. LDL’s carry cholesterol from the liver to cells of the body, and VLDL’s carry (newly synthesized) triglycerides from the liver to adipose tissue. So when the tissues need cholesterol the LDL’s take it to them, when they are done with it the HDL’s take it back to the liver, and when the liver makes triglycerides the VLDL’s take them to the adipose tissue.

In the eyes of the general public and most General Practitioners, HDL is the good, LDL is the bad, and VLDL might count as the ugly if they have even heard of it. Yet each one of these has an important role to play inside of us. LDL is demonized because it is often found as part of arterial plaques (see, it isn’t really the cholesterol at all), yet it has long been known that LDL levels are only marginal risk factors for heart disease, and a much more reliable indicator is the ratio of the blood triglycerides to HDL cholesterol. But why?

Not all LDL particles are created equal. Some of them are large and fluffy, sometimes called “buoyant”, and some of them are small and dense. It is the small, dense ones which seem to be gathering in the arterial lesions which are associated with coronary artery disease; the large, fluffy ones are simply too big and buoyant to get stuck in the pile-up. On a standard lipid profile, the small, dense LDL and the large, fluffy LDL do not show up separately. This means that the lipid profile is not telling you which you have or whether you should be worried about them if your LDL actually is elevated. And if it is notelevated? You could still have the majority of your LDL as the small, dense kind, and be at a higher risk of heart disease than someone with a higher LDL level, but much lower small, dense particle levels. So much for total LDL levels telling you anything.

What increases the small, dense LDL particle levels? Is it really saturated fat? Let’s ask Gary Taubes: “This suggests that saturated fat elevates LDL-cholesterol in part by increasing theamount of cholesterol in the LDL, and so making larger and fluffier LDL to begin with, rather than by increasing the number of LDL particles or by increasing the number of small, dense LDL particles.” So if it isn’t the cholesterol itself which is the problem, but the LDL particle it is carried on, and it isn’t just any LDL particles, but the small, dense ones we need to worry about, then saturated fat is not going to cause heart disease.Nothing I have said leading up to that last statement is really considered controversial science. It is commonly known and accepted as fact, by both sides of the argument, that saturated fat raises large, fluffy LDL and that it is the small, dense LDL which is very strongly associated with heart disease. It makes me wonder why the Diet-Heart Hypothesis lives on.

Still the question remains, what increases the small, dense LDL particles? Taubes again, “After we eat a carbohydrate rich meal, the bloodstream is flooded with glucose, and the liver takes some of this glucose and transforms it into fat—i.e., triglycerides—for temporary storage… The triglycerides constitute the cargo that the lipo-proteins drop off at tissues throughout the body… The resulting lipo-protein has a very low density, and so is a VLDL particle.” As these VLDL particles go about their business of dropping the triglycerides off hither and yon, they slowly become the small, dense LDL particles we should fear. The more triglycerides which were originally packed into the VLDL particle, the smaller and denser the resulting LDL particle will be.

What this means is that eating a lot of carbohydrate, and in particular, highly refined carbohydrates such as flour and sugar, will increase the amount of small, dense LDL we produce. The more of it we eat, the more we produce, while at the same time making them smaller and denser. Sugar itself, and all things related to it (high-fructose corn syrup, anyone?), go one step further. The fructose portion of sucrose is processed exclusively in the liver. Unlike the glucose portion, none of it is burned by the cells as energy. The liver deals with what is effectively a toxin by converting it to triglycerides, and shipping it out for storage. Comparing glucose to fructose (all carbohydrate you eat, except fructose, becomes glucose in your body), you will get a much, much higher elevation in blood triglycerides from the fructose. The particles which carry the resulting triglycerides around are those same VLDL mentioned above. That is why knowing your ratio of blood triglycerides to HDL is a much better indicator of heart disease risk than just your LDL levels, or LDL to HDL ratio.

What is the take-away? We know that eating cholesterol will not affect our cholesterol very much, and that our cholesterol levels are not really the issue anyway. We understand that our bodies need lipoproteins to function, that LDL has an important role in our bodies, and that we cannot live without it. We have seen that it is the small, dense LDL we don’t want, and that the large, fluffy LDL is what we should be making. We have also seen that it is carbohydrates, especially refined carbohydrates, which result in the creation of the small, dense particles, and that it is saturated fat which helps to raise the levels of the large, fluffy LDL particles. Knowing all of this, it sure seems clear to me that replacing the refined carbs in our diets with fats, especially the saturated kind (and not those damned trans-fats), will greatly reduce the risk of developing heart disease. I would not be surprised to find that such a change could actually reduce the symptoms of heart disease where it already exists. The next time you start out making egg whites and oatmeal with honey for breakfast, throw out the oatmeal and eat the yolks instead.

One response to this post.

  1. Welcome back! And thanks for the article!


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