Knowledge, Not Numbers

A good decision is based on knowledge, not numbers.


In the previous post we discussed some important foundational ideas when talking about cholesterol. Today we’ll start going into all this just a bit deeper, starting with what all those numbers mean and why I say that your total cholesterol number is meaningless for you, personally.

What sadly happens to way too many people is this:

First, they get a cholesterol test.

Second, they get an ominous call that their test results are in. They are given their total cholesterol number–something over 200, which it should be unless they’re sick–with a warning that they ought to talk to their doctor about this immediately. There are some other numbers thrown around, perhaps. Maybe. Some talk of HDL, or LDL, or triglycerides. But a lot of times those are kind of ignored, and sometimes you may even have to specifically ask them to tell you the breakdown, so focused are they on that scary total number.

Perhaps the most disturbing thing in all is how many in the health care profession have taken to looking at these surrogate markers–because that’s all cholesterol testing does–and become obsessed with making the marker levels change instead of dealing with the underlying health issues involved. This is as if your white blood cell count were abnormally high and instead of your doctor looking to see if you might have a serious disease or infection, he instead prescribed you a drug that lowered white blood cell count and told you to come back in a month.

So what is cholesterol? In terms of heart health, here’s what you need to know:

In the beginning, you get inflammation in your arteries. This could be for a vast variety of reasons, from lack of sleep, to smoking, to stress, to eating inflammatory foods–particularly grains and sugars–to just generally having poor glycemic control, too much iron in your blood, or too much Omega-6 and/or not enough Omega-3 fats.

Your body responds to these inflammations and damaged arteries the way God designed it to: lipoproteins start carrying cholesterol around. LDL (or low density lipoprotein) carries the cholesterol to the damaged area to repair it. LDL does not damage arteries in any way, nor does it trigger an inflammatory state. If you didn’t have plenty of LDL available to do this chore, you wouldn’t die of an arterial plaque rupture at 50–instead you’d get to die from arterial failure in your 20s. Maybe earlier.

HDL (high density lipoprotein) then carries the used cholesterol away. Obviously this is important. You can’t have the LDL just laying around there building up all the time. Having enough HDL is far more important to your heart health than your LDL or total cholesterol levels. But neither LDL and HDL are “bad” or “good.” You need both.

You should also know that LDL comes in different sizes. The smaller LDL (sometimes known as VLDL, or very low density lipoproteins) is easily oxidized, so that’s something you don’t want too much of. That’s because while there is no link between LDL levels and heart disease, there is a link between oxidized LDL and heart disease.

Oxidize is a fancy name for “rust.” It’s what happens when an oxygen atom combines with anything, and whether it’s the inside of your boat or the inside of you, oxidizing causes deleterious effects.

OOH OOH CLASS! Here’s a question…if you don’t want your LDL oxidizing…HOW CAN YOU STOP IT FROM HAPPENING?

Well, according to modern statin-pushing theory, the best thing to do is just make sure you don’t have any LDL in your blood. Or at least as little as possible. Take a statin or don’t eat any butter and your LDL will drop below 130 or so (we think) and you’ll be fine! No LDL to oxidate, no oxidised LDL.

This is a brilliant solution!

I’m going to apply this solution to my moped and my bike. The reason I’m getting all that rust is because I’ve got all that metal in them. The answer isn’t for me to keep them covered, or in any way protect the metal so it isn’t exposed to oxygen. The answer is for me to just cut all that metal off! No metal to rust, no rusted metal.

Ok, obviously I’m jesting. Obviously that solution is…say it with me now..STUPID.

Instead of lowering your total LDL, why not stop doing things that cause you oxidative stress? Then your LDL won’t be oxidizing at enormous rates no matter how much of it there is.

SO what can we do to lower oxidative stress? The number one, first, most important, easiest, simplest, most straightforward way to do this is to keep your blood sugar low. Chronically high blood sugar is what is causing your diabetic friend to age faster than you–he is literally rusting away at a faster rate. If you looked at that last link I posted, the one showing that it is oxidized LDL and not LDL total levels that are linked to heart disease, you’ll see that those with “metabolic syndrome” were twice as likely to have high oxidized LDL levels. What is metabolic syndrome? Put simply, you can consider it the precursor to diabetes and something one in five Americans have: the inability to properly control blood sugar.

How do you lower your blood sugar? Very, very, very, very simple. (At least simple for those who haven’t yet gone into full-blown diabetes). Stop eating stuff that spikes it. Don’t drink sodas and fruit juices, or eat candies and sweet things, potato products and starches. Don’t whirl up enormous amounts of fruit into smoothies and suck down three times as much fruit as you would normally eat in the form in which God made it for you to enjoy. Enjoy your vegetables in moderation and with plenty of healthy fat to go with them. Do not eat salads the size of your own head, especially on an empty stomach, with sugary low-fat dressings. Don’t eat that ice milk garbage or that low-fat frozen yogurt nonsense. Stop downing granola bars, Special K, and low-fat milk.


Here’s another reason to put down the pizza–remember I mentioned that LDL comes in different sizes? Well that VLDL kind is easily oxidized, unlike the large, fluffy LDL. It also tends to stick around your arteries longer, seemingly for two reasons: First, it’s harder for HDL to carry away in the first place. Second, it’s inversely proportional to HDL, meaning that whatever is causing you to produce VLDL is also lowering your HDL.

Changing the makeup of your LDL from tiny and dense to big and fluffy is much more important than lowering your total LDL level. (Or it might be more proper to say, producing large fluffy LDL instead of VLDL. I don’t believe you can actually change the size pattern of an already existing lipoprotein). And whatever you do to change your LDL size pattern production also tends to change the level of your HDL, for good or bad. So what can you do?

Stop eating carbs.

I’m noticing a pattern here. Are you?

In case you’re too busy to read that link I just gave, I’ll summarize for you. Researchers took a bunch of fat, middle-aged men, took away almost all their carbs, and put them on a high fat diet. One low carb diet included added fiber, one did not. They were eating 10% carbs, 65% fat, and the rest protein. They did this for 12 weeks.

So first, these guys lost an average of 16 1/2 pounds in those 12 weeks. (“Water weight!” Can you hear them screaming it at us? “It was all water weight! That’s why low carb diets give such great results!”) Well, sadly for all those people whose brains have been damaged by eating low fat, these guys also reduced their measurable abdominal fat by 20%.

For our current purposes, though, what’s really important is that these men saw their LDL and triglyceride levels drop, their HDL levels skyrocket, and their LDL changed in pattern from small and dense to big and fluffy and happy.

Just if you’re curious, what these guys ate was:

Unlimited amounts of beef, poultry, fish, and eggs, moderate amounts of cheese, low-carbohydrate vegetables, low-carbohydrate salad dressing, and small amounts of nuts and seeds.

And, by the way, the fiber that half the guys were drinking didn’t make one lick of difference in any way, shape or form to any health marker of any sort.

Let’s get back on track.

I said that there’s no link between your LDL levels and heart disease risk. Or between your total cholesterol level and heart disease risk. That’s because there isn’t.

Look here. This writer summarizes for you a bunch of different studies, all of which he cites and you can check for yourself. Just a few of them include:

1. One showing that half, HALF, of the people who get coronary heart disease have normal or low LDL levels.

2. “Among elderly Belgians, higher levels of oxidized LDL were accompanied by  significantly increased risk of heart attack, regardless of total LDL levels.”

3. ” In Japanese patients undergoing surgery to remove plaque from their carotid arteries, blood levels of oxidized LDL were significantly higher than those measured in healthy controls. Elevated oxidized LDL was also associated with an increased susceptibility of plaque rupture. However, there was no association between oxidized LDL concentrations and total LDL levels.”

4. A two-year double blind study with fish oil in people with heart disease, which found that taking fish oil every day caused arteries to stop distending and plaques to get smaller and the people themselves to experience fewer “cardiovascular events.” But…their LDL cholesterol levels were higher!!!! Oh no! Give them statins, quick!

5. Two studies in which plaques were measured in the arteries. Both groups were treated with statins to lower their LDL, but one group was also given niacin to lower it even further. They succeeded–the statin/niacin group had much lower LDL. But sadly, they didn’t experience any fewer or any smaller plaques than the others, leading the researchers to conclude that “with respect to LDL cholesterol lowering, ‘lower is better’ is not supported by changes in calcified plaque progression.”

6. And finally, two groups with calcified aorta were treated, one with a statin, the other with a placebo. The ones with the placebo kept their perfectly normal, if not slightly low, 130 mg/dL level of LDL. The ones on the statin got down to 63! What an achievement! Unfortunately, it didn’t make the slightest difference to their arterial health.

And here’s another. From the very first study of its kind in 1957, all the way to today, no study has ever shown any benefit to mortality rates by lowering cholesterol. In fact, that first study was totally successful in getting cholesterol levels to drop, yet the ones eating the cholesterol-lowering, low fat diet got more heart disease and more of them died than the control group eating a normal, fatty diet.

And here. 100 guys from heart-disease rampant Lithuania and 100 from heart-disease free Sweden. (Relatively speaking, of course). The guys from Lithuania had lower total cholesterol and lower LDL than the Swedes. Their triglycerides were similar, and smoking rates and general health were similar.  Shockingly, the Lithuanians had higher blood pressure, more LDL oxidation, and more heart attacks.

And here. Another summary of some studies, among them my favorite being the MR-FIT study, which got a huge number of men to reduce their cholesterol consumption by 42% and their saturated fat consumption by 28% and their total calorie consumption by 21% and yet saw 0% change in heart disease. Researchers referred to these results as “disappointing.”

And here. A study designed to be longer-term and measure not just whether a statin and successful cholesterol lowering stopped people from having heart attacks, but whether they actually improved all-cause mortality. As we mentioned last time, no one will be happy that you didn’t get a heart attack as they are burying you after you die of cancer or kill yourself in a depressive fit. The study, again, found that while the drug was super successful at lowering cholesterol, it didn’t stop people from dying any faster than anyone else, and it didn’t do much to stop them having heart attacks.

And here: This one is kind of sad. This one was with at-risk elderly people. Again they succeeded in getting a drug to lower their cholesterol. If you just read the abstract you’d think this was a study that proved how great it is to take this drug. But keep reading and look at the numbers.

Math’ll get ya in the end, folks. That’s why I don’t do it…

Anyway, go down past all the stuff and look at the numbers. In the end, it made almost no difference at all whether you took the placebo or the drug, as far as your likelihood to die. 306 placebo patients died; 298 taking the drug died. And there were 22 more patients taking the placebo than the drug, anyway. Since we’re talking about elderly people (70+ years old), we really have to wonder if the side effects of this powerful drug were really worth the infinitesimally lower risk of death.

Don’t worry, there’s more coming…


Plato says he’s hungry

Help us keep paying for this site and feeding the dogs.


Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s