The first thing I’m going to say about cholesterol is that we don’t understand it well enough. On my first day of medical school back in the early 1990’s, Dr. Kirby, our Dean of Students, said that half of what we were about to learn over the next four years would turn out to be false. The problem was that no one knew which half! Here are some of the things I learned in medical school that have turned out to be false:

1) LDL cholesterol is bad cholesterol.

2) There is no reliable way to increase your good cholesterol (HDL).

3) We don’t really know how triglycerides fit in, but they probably don’t matter anyway.

Let’s discuss these statements one at a time.

LDL comes in two major types, either 1) small and dense or 2) big and fluffy. Small, dense LDL is bad, but large, fluffy LDL is okay. Small, dense LDL is highly atherogenic, which is a medical term meaning that it causes plaque formation, heart disease, hardening of the arteries (also known as atherosclerosis). It’s like sand. It gets stuck everywhere, which the body responds to by laying down plaque all around it. It reminds me of the grain of sand that irritates an oyster, who responds by coating that sand particle with layers of nacre, the shiny, luminescent stuff that creates pearls. Humans don’t get pearls. We get heart attacks and strokes.

Then there are the big, fluffy LDL particles that float through the blood stream without attaching to the walls of the blood vessels. This subtype of LDL is much better. If you want to know what kind of LDL you have, you can ask your doctor to run a special type of panel instead of a standard lipid profile. This will show how much of your LDL is small and dense, and how much is large and fluffy. You want large, fluffy LDL. If your LDL comes back slightly high but not exceedingly so, say 135, for example, finding out whether it’s small or large might influence your doctor’s decision about whether to start you on cholesterol-lowering medication. But there are other ways to infer whether your LDL is dense or fluffy.

HDL cholesterol is sometimes referred to as “good” cholesterol. H for healthy. There is an inverse relationship between HDL and risk of heart attack: the lower your HDL, the greater your risk of developing hardening of the arteries. A number of important research studies have shown low HDL to be a much more serious risk factor than high LDL (the small, dense kind as you now know). There are a number of reliable ways to increase your HDL, and all of them have one thing in common: All of them improve your insulin sensitivity, to make it work more efficiently, conserve your insulin supply, protect your insulin-production machinery. When I see very low HDL levels in patients, I can usually guess that they are eating large amounts of fast food, processed food, and/or stripped (refined) carbohydrates, along with little or no fruits, vegetables or legumes.

How do you raise your HDL? By improving the nutritional value of the foods you are choosing, by reducing the amount of fast and highly processed food you eat, and by getting more exercise. All of these strategies improve your insulin sensitivity. Skip the doughnuts, and eat foods that are rich in B vitamins, found in abundance in whole grains, fruits, vegetables, beans, and nutritional yeast.

What about triglycerides? If HDL is good cholesterol, and small, dense LDL is bad cholesterol, then triglycerides are ugly cholesterol. The goal, from a medical standpoint, is to keep triglycerides below 150, but the truth is that the lower, the better. Triglyceride molecules, which happen to be shaped like the capital letter “E,” are the chemical compound form in which we store fat. They consist of a single vertical sugar backbone (the glycerol) with three horizontal tails (the fatty acids). The more stripped carb you eat, the more glycerol molecules you make. The more glycerol molecules you make, the more triglyceride you can create. You cannot make triglyceride without glycerol, and glycerol comes straight from the sugar and starch that you eat.

Remember that the more stripped carb (white flour, corn starch, corn syrup, sugar) you eat, the more insulin you need to make. The more insulin that floats around in your blood stream, the more triglycerides you make. So high triglycerides are associated with the hyperinsulinemic (high insulin) state, and the higher your insulin levels, the higher your triglycerides. Generally, I see high triglycerides in folks whose diets contain large amounts of 1) stripped carbs, 2) fast food, and/or 3) alcohol. I can also predict, with a fair degree of reliability, whether a patient has an elevated triglyceride level with a quick glance at their waistline. Hyperinsulinemia causes fat deposition under the chin and in the abdomen — no surprise there; that’s where the gastrointestinal tract is — so that’s where the action is happening. Another name for this condition is a “beer belly.” Drinking beer is like eating grain without the fiber. That means it’s stripped carb. Drinking excessive amounts of beer can be a serious problem, and a great many people noticed this connection long before me.

Now, low HDL is bad, and high triglycerides are ugly, but the combination of low HDL and high triglycerides is downright scary. This combination is highly associated with high insulin levels and hardening of the arteries. Any time I see a patient with the combination of low HDL and high triglycerides, I know they are at high risk of becoming diabetic, that is, if they haven’t got it already. When I explain the data, I let them know I do not intend to wait around for them to develop the symptoms of diabetes; I already know how high their risk is. They deserve to know about it now, and they deserve to be able to fix it before it becomes a much bigger problem. And, yes, it is fixable.

I also know that a lipid panel showing a “low HDL/high triglyceride” pattern is strongly associated with the small, dense LDL subtype. This is not coincidental, but rather a predictable consequence of eating stripped, refined, processed and fast “food.” And that means it is not so hard to fix. Notice that I do not look at each measurement in the lipid profile as an individual entity, but rather at the overall pattern. And I also am not looking at the numbers as ends in themselves; I am much more interested in the person who is carrying those numbers.

This is a complex topic, and it raises at least as many questions as it answers. So please feel free to post your questions, and give me an opportunity to try to answer them. Do not worry that your questions are simple. I guarantee you that many people are wondering the same thing. I may even have attended medical school with some of them.