Finishing Up Cholesterol

Most people say that it is the intellect which makes a great scientist. They are wrong: it is character.
–Albert Einstein
When I say “finish up” of course I don’t mean that there’s nothing more to say. There’s always more that someone can say. Hence the continued existence of the Internet. And Alex Baldwin.
In the last few posts we talked about what cholesterol is, why you need it, why LDL and total cholesterol levels are not reliable markers for heart health, why HDL and your ratio of HDL to triglycerides is important, and that the real culprit in heart issues is ultimately inflammation.

This brings us to some pretty important and obvious questions, then. What can we do to reduce inflammation, for one thing, which is implicated not only in heart attack issues, but causes us sadness in lots of areas of life?

For another, is there something we can do that will make us healthier in a way that manifests itself through higher HDL levels and lower triglycerides? (Remembering that it isn’t going to do us much good to just artificially raise/lower markers of health by artificial means.)

Finally, what happened when I’ve been eating well, I’ve got awesome HDL, great triglycerides but a pretty high LDL? Should I panic? Lady who called me from the testing place sure did…

Reducing chronic inflammation.

The first and simplest thing to do is avoid refined carbohydrates. Excessive sugar of any kind, and refined carbs in particular, will cause inflammation and oxidation. To be honest, of course, you’re going to your grave no matter what. Let’s not kid ourselves. But there’s no need for you to run at your grave as fast as you possibly can. You’ll only trip on something along the way and make getting there harder than it has to be. Now exercise (not endless “cardio” [there’s no such thing, actually]), proper sleep, and less stress will also help lower inflammation. The problem is that we can’t always control either our sleep or the stress to which we are exposed. But we can control what we eat and do.


Higher HDL and lower triglycerides.

You’ll never guess what I’m about to say, I know. Stop eating carbs and start eating plenty of healthy fat. No Omega-6 rich Frankenfats like seed oils and vegetable oils: saturated fat from animals, and fat from olive oil and coconuts. These simultaneously raise HDL and lower triglycerides. How do you lower triglycerides by eating more fat? Well, triglycerides appear in you from two possible sources. Some–a small minority–are from the fat you actually eat. This is such a small amount of your triglycerides that eating less fat hardly makes a dent in your triglyceride levels by itself.

Most of it is the byproduct of lipogenesis in your liver; which is when your liver converts sugars into fat. This hasn’t always been known–in the past we were measuring people’s triglycerides an hour or two after eating and blaming fat for the small increase that was seen. But it turns out that if you wait till four or six hours after eating you see a much, much larger increase after eating grains and sugars than you can after stuffing yourself with fat. The slight increase from eating fat goes away very quickly; the huge increase after eating carbs can last for weeks.

But my LDL!

If you are eating a very low carb and higher fat diet, you cannot trust your total LDL numbers at all, so don’t worry about it. LDL is not a measured value: it is calculated. It is based on the Friedewald calculation, a crude measurement based on several basic assumptions which no longer apply to you if you’re eating high fat, low carb. It assumes that your macro-nutrient composition is “average.” Since average is  high carb and low fat, you are hopefully eating nothing like “average.”

It also assumes that the amount of triglycerides in your LDL is the same as that in everyone else–but it has been proven that this varies significantly from person to person. Even the most basic medical definition of a lipoprotein now carries that piece of information.

Finally, when you eat low carb and high fat you tend to produce a different pattern size of LDL than grain and sugar eaters, but the Friedewald equation assumes you have the same size as everyone else and that everyone has the same size. It’s much better to find out your LDL particle size. Your total calculated number can tell you nothing important. For more detailed information on this whole process, I recommend the three podcasts available here. (Link is to the first one). I also recommend the book Cholesterol Clarity. For some faster blog resources, try Dr. Malcolm Kendrick.

In all of it, do be aware that there are going to be differences of opinion. There always are, which is what makes science so great. Scientists see problems with a working hypothesis, attack them and hopefully get at the truth. All the people I linked to above challenge the conventional wisdom of the United States dietary assumptions because it is obviously flawed–we have over-prescription of statins; low fat diets doing nothing to stem heart disease or obesity, which just keep getting worse; more than half the people with heart disease presenting with “normal” or “below-normal” serum or LDL cholesterol levels: something’s wrong with this hypothesis.

But just knowing that hypothesis A is clearly wrong doesn’t tell me which other hypothesis is right. What we need are honest researchers who are willing to look into these things, test them, and do it right. People like Jeff Voleck. Or the people who put together NuSI: doctors and researchers who don’t agree on everything but are determined to conduct the experiments necessary to figure out what’s really going on.

We get into trouble sometimes because we’ve come to expect that science and/or medicine can give us all the answers. We ourselves may be guilty of pressuring people in these fields to come up with a solution–hence the stereotype that both patients and doctors complain about, where the doctor prescribes an unneeded medication because the patient won’t be happy without one.

But the truth is science and medicine do not have all the answers, no matter how that latest health news article is worded. Science has always been faster and better at pointing out what isn’t right than at figuring out what is; but we want to know what is right. We want all the answers. Hence when doctors lined up out the doors in the 60s to tell George McGovern’s senate committee that the evidence did not warrant commanding all Americans to stop eating animal fat, he told them that senators “don’t have the luxury of waiting” to find out what we actually should eat. That’s what we all want.

Humans are extremely good at drawing patterns. We all look for patterns all the time, from the moment we wake up. We make inferences based on data we observe, and thank the Lord for making us that way because we’ve done some amazing things with that ability. But occasionally our ability to see these patterns messes with our perception of truth. That’s why the scientific method exists: humans were self-aware enough to realize this downside to the amazing pattern-drawing gift we have, and developed a method to help us overcome this limitation. Otherwise we can get distracted and misled by exceptions and anomalies.

What do I mean?

Any student in a class being graded on a bell curve can tell you how upset everyone is by that A++ student. Just one student who scores way above average, and the whole curve is blown off several degrees to the right. When we’re researching health and the heart, just one genetic anomaly, just one exception to the general rule, can throw our whole standard deviation out of whack.

As humans we’re also sometimes not very good at determining the relationship between cause and effect. We’re wired to make a judgment quickly: A caused B. I once got spectacular food poisoning. I assumed it was from a certain food: some chicken. I had eaten that food right before I got sick–case closed. It turned out to be a different food entirely. A vegetable in fact. I am aware of this intellectually, but gastronomically I still cannot even look at the restaurant where they sell this kind of chicken without getting a little queasy.

I recently read an example of this that really struck me. The discussion was on swimmers. The writer was pointing out that most people see that professional swimmers have a certain body type and then extrapolate that their swimming gave them that shaped body. We might have even been told that if we “want a swimmer’s body” we have to swim.

The reality is the exact opposite, as we can see if we go to a swim meet. The early matches include people of every possible body type, all of whom train with ferocity and determination. As the day goes on, the field narrows until we get to the semi-finals and then the finals. The body types start looking more and more similar till the final round shows us a group of people who–except for their faces and the color of their swimsuits–could all be twins. As John Little says:

It wasn’t the activity that produced the body type; it was the body type that did well in that activity…therefore if one desires to have the body type of, say, a champion swimmer, the best course is to start by having the same parents as that champion swimmer–rather than his or her training methods.

So what’s the point?

I’m trying to keep you from being dismayed if you see some differences of opinion about cholesterol among all the different links I gave you above. They’re taking the first steps–and that’s important because a lot of scientists and researchers won’t even do that. They’re saying: Hey, your theory that all dogs are white can’t be right, because these black dogs keep coming into my office… Some of them are even taking the second step and hunting for black dogs, or roan dogs, or blonde dogs or parti-colored ones.

The third step is to start trying to figure out exactly how many colors of dogs there might be, and then–once you’ve decided there are, say, 130 possible colors of dogs–try as hard as you can to find that 131st color.

But there’s one thing we can all be sure of: not all dogs are white.


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