The Great Cholesterol Myth (10 page)

High levels of insulin will increase your blood pressure in a couple of ways. For one thing, insulin can narrow the artery walls. Narrower walls translate into higher blood pressure because a harder pumping action is required to get the blood through the narrower passageways.

But there’s an even more insidious way in which insulin raises blood pressure.

It talks to the kidneys.

Insulin’s message to the kidneys is this:
Hold on to salt
. Insulin makes the kidneys do this even if the kidneys would much prefer not to. Because the body controls sodium within a tight range, as it does sugar, the kidneys figure, “Listen, if we have to hold on to all this salt, we’d better bring on more water to dilute it so that it stays in the safe range.” And that’s exactly what they do. Increased sodium retention results in increased water retention. More water means more blood volume, and more blood volume means higher blood pressure. Fully 70 percent of people with hypertension (high blood pressure) have insulin resistance.
¹

And this is not just theoretical. Research from Wake Forest Baptist Medical Center
²
demonstrates that insulin resistance is
directly
related to high blood pressure. “We found you can predict who’s at higher risk for developing high blood pressure based on their insulin resistance,” said lead researcher David Goff Jr., Ph.D., M.D. “The one-third of participants [in our study] with the highest levels of insulin resistance had rates of hypertension that were 35 percent higher than the one-third with the least resistance. These findings point out that reducing the body’s resistance to insulin may help prevent hypertension and cardiovascular disease.”
³

Back to our story.

After a while, under the constant assault of more and more sugar and more and more insulin—all produced, mind you, by a sugar-heavy, high-carb diet—the fat cells start to say, “Enough, already!” They become somewhat resistant to the effects of insulin (a condition known, not surprisingly, as
insulin resistance
). Now your blood sugar is high (as it’s got nowhere left to go!), your insulin is high, and you’re on the way to full-blown diabetes.

A side note to those of you who are concerned about weight: Not only does insulin load up your cells with sugar, making you fatter, it also locks the doors
to the fat cells, making it fiendishly difficult to lose weight. And one reason being overweight significantly increases the risk of heart disease is that all those fat cells are loaded with chemicals that contribute mightily to inflammation!

Beginning to connect the dots?

“Normally, insulin has some fairly positive effects on the body, such as being anti-inflammatory,” says Jeff Volek, Ph.D., R.D., one of the top researchers in the field of diet and health.
⁵
“But if you’re insulin resistant, chronically high insulin levels have the opposite effect. They actually promote inflammation and cardiovascular problems. That’s not generally appreciated yet; what is well accepted is that high glucose (blood sugar) will cause problems over time.”
⁶

So insulin is
anti-
inflammatory in people with normal insulin sensitivity, but it is
highly
inflammatory in those with insulin resistance. Having insulin resistance is a double whammy when it comes to developing heart disease. Insulin resistance makes it more likely you’ll have hypertension and puts you at significantly greater risk for diabetes and obesity—all major risk factors for cardiovascular disease. But to add insult to injury, that excess insulin has an inflammatory effect on your system as well. As we’ve seen, inflammation is a major player in the development of plaque, and a far more important risk factor for heart disease than cholesterol is.

The collection of diseases strongly influenced by insulin resistance has been given the acronym CHAOS: coronary disease, hypertension, adult onset diabetes, obesity, and stroke. They’re all related, and what they have in common is insulin resistance. If you have any degree of insulin resistance, controlling your insulin by dietary means may be one of the most effective strategies for reducing the risk of coronary disease. It certainly beats the fairly irrelevant strategy of lowering cholesterol!

“[H]aving chronically elevated insulin levels has harmful effects of its own—heart disease for one,” Gary Taubes wrote in the
New York Times
.
⁷
Elevated insulin increases triglycerides, raises blood pressure, and lowers HDL cholesterol—all making insulin resistance even worse and substantially upping the risk for heart disease.

At this point you may be wondering, “How do I know if I have insulin resistance?” Good question. Though there are blood measures to determine this, there’s also a nice, simple, low-tech way to do it. Stand in front of a wall and walk toward it. If your belly touches the wall before the rest of your body, there’s an excellent chance that you’re insulin resistant. Men with waist sizes of 40 inches or more are almost
certainly insulin resistant, as are women with waist sizes of 35 inches or more. (Although there are, indeed, people with insulin resistance who are rail thin, the vast majority of people with insulin resistance are not.)

Not only does insulin load up your cells with sugar, making you fatter, it also locks the doors to the fat cells, making it fiendishly difficult to lose weight.

Stand in front of a wall and walk toward it. If your belly touches the wall before the rest of your body, there’s an excellent chance that you’re insulin resistant.

Insulin resistance
is
reversible. And it’s hardly a rare phenomenon. The prevalence of insulin resistance has skyrocketed 61 percent in the past decade alone, according to Daniel Einhorn, M.D., cochair of the AACE Insulin Resistance Syndrome Task Force and medical director of the Scripps Whittier Diabetes Institute in California.
⁸
The prevalence of insulin resistance has probably been underestimated from the beginning. Gerald Reaven of Stanford University did the original work on insulin resistance in the 1980s. Here’s how he approximated the number of people who were insulin resistant. He divided his test population—nondiabetic, healthy adults—into quartiles and tested their ability to metabolize sugar and carbohydrates. He found that while the top 25 percent of the population could handle sugar just fine, the bottom 25 percent could not—they had insulin resistance (or, in the parlance of researchers, impaired glucose metabolism). So for a long time, it was thought that the number of people with insulin resistance was one in four (25 percent).

But there’s a problem.

What happened to the 50 percent of people
between
those two extremes? It turns out they had neither the terrific glucose metabolism of the top 25 percent nor the full-blown insulin resistance of the bottom 25 percent; instead, they fell somewhere in between. One could easily argue that because only 25 percent of the population had flawless glucose metabolism, the rest of us—up to 75 percent of the population—had
some
degree of insulin resistance! Also, Reaven used young, healthy adults as subjects, and their numbers were definitely not representative of the population as a whole—the fact is, sensitivity to insulin actually
decreases
(and insulin resistance
increases
) as you get older. The take-home point: Insulin resistance isn’t just something that happens to other people. The American Association of Clinical Endocrinologists has estimated that one in three Americans is insulin resistant,
⁹
and we suspect that the number is a bit higher.

Back in
chapter 3
we mentioned that calculating your ratio of triglycerides to HDL cholesterol is a much better way to predict heart disease than by assessing cholesterol levels. (Just so you don’t have to go back and look it up, you calculate your ratio by simply looking at two line items on your blood test—triglycerides and HDL cholesterol. If, for example, your
triglycerides are 150 mg/dL and your HDL cholesterol is 30 mg/dL, your ratio is 150:30, or five.) As it turns out, this same ratio is an excellent predictor of insulin resistance. In one study, a ratio of three or greater was a reliable predictor of insulin resistance.
¹⁰

That same triglyceride-to-HDL ratio gives us other important information as well. As noted previously, only the small, dense, BB gun pellet–type LDL molecules are the ones that cause damage (the “bad” bad cholesterol). There are several blood tests your doctor can order that will tell you just how much of your LDL cholesterol is “bad” bad cholesterol (the BB gun pellets) and how much of your LDL cholesterol is “good” bad cholesterol (the cotton ball molecules). (Tests for particle size include the widely used NMR test; the Lipoprotein Particle Profile test, or LPP; the Berkeley cholesterol test from Berkeley HeartLab; and the Vertical Auto Profile test, or VAP.)

But the triglyceride-to-HDL ratio is also a great indicator of the kind of LDL you’re packing. Those with high ratios have more of the BB gun pellet–type LDL (which is atherogenic), while those with low ratios have more of the cotton ball molecules (harmless). Triglyceride levels higher than 120 mg/dL and HDL levels below normal (less than 40 mg/dL in men and less than 50 mg/dL in women) are usually associated with the small, dense, atherogenic LDL particles you don’t want!
¹¹

In fact, if you prefer not to do any math, one single number on your blood test will tell you whether your LDL cholesterol is primarily the big, fluffy, harmless kind (pattern A) or the mean, angry, small, dense kind (pattern B). Just look at your triglyceride levels.

High triglycerides in general correlate strongly with high levels of those dangerous LDL-B particles.
Low
levels of triglycerides correlate with
higher
levels of the harmless LDL-A particles. In other words, the higher your triglycerides, the greater the chance that your LDL cholesterol is made up of the kind of particles that are way more likely to lead to heart disease. And the higher your triglycerides, the greater the chance that you’re insulin resistant, which in turn means that insulin is contributing mightily to the very inflammation that damages LDL cholesterol in the first place and starts the whole cycle of plaque formation. The take-home point: Reduce your triglycerides (and raise your HDL), and you reduce your risk of heart disease.

Lowering your sugar intake probably won’t affect your HDL level, but it will dramatically affect two of the other three indicators of a long and healthy life: triglycerides and fasting insulin, both of which will certainly drop when you lower the amount of sugar and processed carbs you’re eating (or drinking).

We’re pretty sure that if you asked a random sampling of ordinary people what part of their diet is most dangerous to their heart, the majority of them would say “fat.”

They’d be wrong.

The number one dietary contributor to heart disease is sugar.

Diets that are lower in sugar and processed carbs will reduce inflammation, blood sugar, insulin, insulin
resistance,
and
triglycerides. And lowering triglycerides automatically improves that all-important ratio of triglycerides to HDL. (If your triglycerides were 150 mg/dL and your HDL was 50 mg/dL, you’d have a ratio of three, but if you brought your triglycerides down to 100 mg/dL, the ratio would automatically drop to two, or 100:50. Neat, huh?)

You may remember from
chapter 3
a concept called the “Four Horsemen of Aging.” We’ve already covered two of those horsemen—oxidation and inflammation—and seen how oxidation initiates the inflammation that ultimately leads to plaque formation and heart disease. Now it’s time to tie up some loose ends and introduce the third horseman of aging: sugar.

Sugar is directly responsible for one of the most damaging processes in the body, something called
glycation
. (Previously, Dr. Jonny originally named glycation as one of the Four Horsemen of Aging, but because glycation is impossible without sugar, and because sugar affects heart disease in other ways as well, in this book we’re going to be talking about the heart-damaging effects of sugar in general.)

Here’s how it works.

Glycation is what happens when sticky sugar molecules glom onto structures and get stuck where they don’t belong, essentially gumming up the works.

You see, sugar is sticky (think cotton candy and maple syrup). Proteins, on the other hand, are smooth and slippery (think oysters, which are pure protein). The slippery nature of proteins lets them slide around easily in the cells and do their jobs effectively. But when you’ve got a lot of excess sugar in your system, it keeps bumping into proteins, ultimately getting stuck onto the protein molecules. Such proteins are now said to have become
glycated
. The glycated proteins are too big and sticky to get through small blood vessels and capillaries, including the small vessels in the kidneys, eyes, and feet, which is why so many diabetics are at risk for kidney disease, vision problems, and amputations of toes, feet, and even legs. The sugar-coated proteins become toxic and make the cell machinery run less efficiently. They damage the body and exhaust the immune system. Scientists have given these sticky proteins the acronym AGEs—which stands for
advanced glycation end products
—partially because these proteins are so involved in aging the body.