Sugar – the Real Demon in the Diet
FOR THOSE OF YOU WHO LIKE TO CUT RIGHT TO THE CHASE, here’s this post’s take-home point: Sugar is a far greater danger to your heart than fat ever was.
The full story of sugar, and of its often ignored influence on heart disease, requires that we venture into a topic we like to call Endocrinology 101. We understand this sounds like something an evil high school biology teacher designed for the express purpose of making your life miserable, but we promise not to make your eyes glaze over. In fact, by the time you finish this post, you will know more than many doctors do about the common link among heart disease, diabetes, obesity, and hypertension—conditions that are not exactly of casual interest to most readers.
Once you understand the link that joins all of these modern degenerative diseases and its connection to heart disease, we believe you’ll come to the same conclusion we have: Our health gurus have tried and convicted the wrong man, your honor. Fat was innocent all the time.
It’s sugar that’s the true culprit in the American diet.
ENDOCRINOLOGY 101: THE HORMONAL EFFECT OF FOOD
Our journey starts with one simple premise: Hormones control almost every metabolic event that goes on in your body, and you control some of the most critical hormones through your lifestyle. Food—along with several key lifestyle factors such as stress—is the drug that stimulates hormones, and those hormones direct the body to store or burn fat, just as they direct the body to perform a gazillion other metabolic operations.
“Food may be the most powerful drug you will ever encounter because it causes dramatic changes in your hormones that are hundreds of times more powerful than any pharmaceutical,” said Barry Sears, Ph.D. Hormones are the air traffic controllers that determine the fate of whatever flies in (or in our case, “slides” in through the gullet!).
This fact has been conveniently ignored by many mainstream dietitians and doctors whose standard message to overweight people at increased risk for heart disease is to simply reduce calories and saturated fat. But all calories are not created equal. Some foods significantly boost levels of a hormone that stores fat, while other foods do not—even when the calories are the same. Not coincidentally, that fat-storing hormone also has some serious consequences for the heart.
The name of that fat-storing hormone? Insulin.
Insulin, a hormone first discovered in 1921, is the star actor in our little hormonal play. It is an anabolic hormone, which means it is responsible for building things up—putting compounds like glucose (sugar and amino acids) inside storage units (such as cells). Its sister hormone, glucagon, is responsible for breaking things down—opening those storage units and releasing their contents as needed. Insulin is responsible for saving; glucagon is responsible for spending. Together their main job is to maintain blood sugar levels within the tightly regulated range it needs to be to keep your metabolic machinery running smoothly.
Insulin is at the hub of a significant number of diseases of civilization. When you control insulin, you reduce the risk for not only heart disease but also hypertension, diabetes, polycystic ovary syndrome, inflammatory diseases, and even, possibly, cancer.
Both insulin and glucagon are essential to health. Without insulin, blood sugar would skyrocket, and the result would be coma and death, the fate of virtually every type 1 diabetic in the early part of the twentieth century prior to the discovery of insulin. However, without glucagon, blood sugar would plummet, and the result would be brain dysfunction, coma, and death.
So the body knows what it’s doing. This little dance between the force that keeps blood sugar from soaring too high (insulin) and the forces that prevent it from going too low (glucagon, for one) is essential for survival. It’s interesting to note that although insulin is the only hormone responsible for preventing blood sugar from rising too high, there are several other hormones besides glucagon—cortisol, adrenaline, noradrenaline, and human growth hormone—that prevent it from going too low. You could say that insulin is such a powerful hormone that it needs five other hormones just to counterbalance its effects!
To see how insulin is supposed to work in the body, let’s take a look at a metabolism that hasn’t been “screwed up” yet by years of bad diet and sedentary living. Let’s look at the metabolism of a mythical five-year-old child who’s been living on an organic ranch, eating nothing but whole foods, breathing clean air, and getting a vigorous amount of exercise on a daily basis. (We know, we know—we haven’t seen too many of these kids, either, but let’s just postulate one for the sake of our discussion.)
The kid comes home from school and eats an apple. His blood sugar goes up slightly, as it always does when you eat food. The pancreas responds to this slight elevation in blood sugar by secreting a little shot of insulin, and insulin promptly goes to work rounding up the excess sugar in the kid’s bloodstream and escorting it over to the muscle cells. Which is just dandy, because this boy is now going to go out and play, or ride a bike, or work on the ranch, or do some other physical activity for which those muscle cells of his require fuel.
So far, so good.
The muscle cells welcome the extra sugar, which they use for fuel, and eventually blood sugar drops back down to normal and even goes down a bit further because the muscles are eating it right up. Now the boy gets hungry again, comes home, and eats supper. All is right with the world.
However, this ideal metabolism is not your metabolism.
Your metabolism looks like this: You wake up late, stress hormones coursing through your body. (These stress hormones are an important factor in heart disease, and we’ll discuss them at greater length later.) One of the things stress hormones do is send a primitive signal to the brain that it’s time to fuel up for an emergency. So you run out the door and stop at Starbucks for a sweetened latte and a “low-fat” bran muffin that contains a gazillion calories. Your blood sugar takes off like the Challenger. The pancreas says, “Uh-oh, better send in the big guns this time, the guy’s gone mad, there’s sugar all over the place!” And it produces a bucketful of insulin to try to start bailing all that sugar out of your bloodstream and get it to the muscle cells pronto!
Except the muscle cells aren’t having it.
“What do we need all this sugar for?” they ask. “This guy’s just going to sit around all day pushing a computer mouse, and when he goes home, he’s going to sit on the couch and play with the clicker.”
So the muscle cells begin to resist the effects of insulin. “We’re good,” they say, “go somewhere else.” Insulin now has no choice but to take its sugar pay-load to another location, and guess where it winds up?
Your fat cells, which happily welcome it in.
For a while, your pancreas can manage to keep up with the added demand for more and more insulin, and your muscle cells may still absorb enough sugar to keep you from becoming officially diabetic. But those elevated levels of insulin produced by excess sugar (in the diet and in the bloodstream) are not without serious consequences, including ones that directly affect the heart.
For a stunning example of this phenomenon, all we need do is look at the effect of insulin on blood pressure.
WHAT YOU NEED TO KNOW
• The number one dietary contributor to heart disease is sugar, which is a far greater danger to your heart than fat.
• Sugar contributes to inflammation in the artery walls.
• Sugar is the missing link among diabetes, obesity, and heart disease.
• High sugar intakes drive up the hormone insulin, which raises blood pressure and increases cholesterol.
• Sugar and processed carbs raise triglycerides, which are an important and independent risk factor for heart disease.
• When sugar in the bloodstream sticks to proteins, it creates damaging and toxic molecules called advanced glycation end products, or AGEs.
• This same process also damages LDL, contributing to inflammation and ultimately to heart disease.
INSULIN RESISTANCE AND HIGH BLOOD PRESSURE
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.
And this is not just theoretical. Research from Wake Forest Baptist Medical Center 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.”
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!
THE INSULIN–CHOLESTEROL CONNECTION
Interesting factoid: Insulin has a profound effect on cholesterol as well. It turns up the cholesterol-making machinery by turbocharging the activity of the enzyme that actually controls the cholesterol-manufacturing machinery in your body. This enzyme—with the unwieldy name of HMG-CoA reductase—is the very same enzyme that’s shut down by cholesterol-lowering drugs! You could probably lower your cholesterol—if you still care about that—by simply lowering your insulin levels. And doing so would have none of the side effects of cholesterol-lowering medication, unless you call a longer life span and better health side effects!
By the way, we’re not kidding about the “longer life span and better health” part. A 1992 study examined the blood work of healthy centenarians in an effort to find out whether there were any commonalities among the members of this unusually long-lived demographic. It found three: low triglycerides, high HDL cholesterol, and—wait for it—low fasting insulin. Your diet affects two of these blood measures—triglycerides and fasting insulin—and both measures will fall like a rock when you reduce or eliminate sugar and processed carbs in your diet. Lowering triglycerides is one of the major health benefits of a diet lower in sugar, as high triglycerides are far more of a danger sign for heart disease than high cholesterol is.
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. “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.”
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. 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, and we suspect that the number is a bit higher.
Back in this post 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!
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).
SUGAR: CAUGHT AT THE SCENE OF THE CRIME
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 this previous post 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, on this website 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.
What does this have to do with cholesterol and heart disease? Actually, everything. You may recall our earlier discussion about LDL cholesterol in which we pointed out that LDL cholesterol is never a problem until it becomes damaged. (Remember, damaged LDL cholesterol of the BB gun pellet variety [pattern B] gets stuck to the artery walls, ultimately triggering the immune system reaction that causes inflammation.) We discussed one primary way in which LDL cholesterol gets damaged—through oxidative stress generated by free radicals.
Can you guess the other way it gets damaged?
So now you have sugar at the scene of several crimes, all related to heart disease. “High blood sugar causes the lining cells of the arteries to be inflamed, changes LDL cholesterol, and causes sugar to be attached to a variety of proteins, which changes their normal function,” says Dwight Lundell, M.D., author of The Cure for Heart Disease. High blood sugar, as we’ve seen, also sends insulin levels skyrocketing, and in most people that will lead to insulin resistance, the central player in every condition we’ve examined that is intimately connected to heart disease: diabetes, obesity, high blood pressure, and metabolic syndrome.
Is it any surprise that we think reducing sugar is far more important than reducing fat or cholesterol?
And by the way, we’re hardly the first people to say so.
The Voice of Dissent: Introducing John Yudkin
By 1970, Ancel Keys’s research had been published and was being picked up by the media; the low-or nocholesterol brigade was gearing up for an assault on the consciousness of the American public. Then in 1972, Robert Atkins published Diet Revolution, which became the de facto poster child for the low-carb movement two decades later. Atkins advocated an approach completely opposite to the one promoted by Keys: He said that insulin and carbohydrates, not fat and cholesterol, were the problem in the American diet.
Because his high-fat, high-protein, low-carb diet went so dramatically against the conventional wisdom of the times, Atkins was attacked mercilessly in the press and vilified by the medical mainstream, which turned him into a pariah in the medical community. But in the same year that Atkins published his book, an English doctor named John Yudkin was making waves by politely and reasonably suggesting to the medical establishment that perhaps its emperor, while indeed cholesterol-free and low-fat, was nonetheless naked as a jaybird.
A professor of nutrition at Queen Elizabeth College, University of London, Yudkin was a highly respected scientist and nutritionist who had dozens of published papers in such renowned peer-reviewed journals as The Lancet, the British Medical Journal, the Archives of Internal Medicine, the American Journal of Clinical Nutrition, and Nature.
Yudkin was typically portrayed by his detractors as a wild-eyed fanatic who blamed sugar as the cause of heart disease, but in fact he was nothing of the sort. In his 1972 book, Sweet and Dangerous, he was the embodiment of reason when he called for a reexamination of the data—which he considered highly flawed—that led to the hypothesis that fat causes heart disease.
In the 1960s, Yudkin did a series of animal experiments in which he fed sugar and starch to a variety of critters, including chickens, rabbits, pigs, and college students. Invariably he found that the levels of triglycerides in all these subjects were raised. (Remember, high triglycerides are a major risk factor for heart disease.) In Yudkin’s experiments, sugar also raised insulin, linking sugar to type 2 diabetes, which, as you now know, is intimately related to heart disease as well.
Yudkin was one of the many who pointed out that statistics for heart disease and fat consumption existed for many more countries than those referred to by Keys, and that these other figures didn’t fit into the “more fat, more heart disease” relationship that was evident when only the seven selected countries were considered. He pointed out that there was a better and truer relationship between sugar consumption and heart disease, and he said that “there is a sizable minority—of which I am one—that believes that coronary disease is not largely due to fat in the diet.” (Three decades later, Dr. George Mann, an associate director of the Framingham Heart Study, arrived at the same conclusion and assembled a distinguished group of scientists and doctors to study the evidence that fat and cholesterol cause heart disease, a concept he later called “the greatest health scam of the century.”)
In the same year that Atkins published the first edition of his book, an English doctor named John Yudkin was making waves by politely and reasonably suggesting to the medical establishment that perhaps its emperor, while indeed cholesterol-free and low-fat, was nonetheless naked as a jaybird.
Around the same time, the brilliant Danish scholar Uffe Ravnskov, M.D., Ph.D., reanalyzed the original Keys data and came to an identical conclusion. His exemplary scholarship is supported by hundreds of referenced citations and studies from prestigious peer-reviewed medical journals and can be found in his book, The Cholesterol Myths, or on his website (www.ravnskov .nu/cholesterol.htm).
Though Yudkin did not write a low-carb diet book per se, he was one of the most influential voices of the time to put forth the position that sugar was responsible for far more health problems than fat was. His book called attention to countries in which the correlation between heart disease and sugar intake was far more striking than the correlation between heart disease and fat. And he pointed to a number of studies—most dramatically of the Masai in Kenya and Tanzania—in which people consumed copious amounts of milk and fat and yet had virtually no heart disease. Interestingly, these people also consumed almost no sugar.
The Sweetening of America
To be clear, Yudkin never said that sugar causes the diseases of modern civilization, just that a case could easily be made that it deserved attention and study, certainly as much as, if not more than, fat consumption. Heart disease is associated with a number of indicators, including fat consumption, being overweight, cigarette smoking, a sedentary lifestyle, television viewing, and a high intake of sugar. (Yudkin himself did several interesting studies on sugar consumption and coronary heart disease. In one he found that the median sugar intake of a group of coronary patients was 147 g, twice as much as it was in two different groups of control subjects that didn’t have coronary disease; these groups consumed only 67 g and 74 g, respectively.)
“Many of the key observations cited to argue that dietary fat caused heart disease actually support the sugar theory as well,” Taubes wrote. “During the Korean War, pathologists doing autopsies on American soldiers killed in battle noticed that many had significant plaques in their arteries, even those who were still teenagers, while the Koreans killed in battle did not. The atherosclerotic plaques in the Americans were attributed to the fact that they ate high-fat diets and the Koreans ate low-fat. But the Americans were also eating high-sugar diets, while the Koreans, like the Japanese, were not.”
As Yudkin put it, “It may turn out that [many factors, including sugar] ultimately have the same effect on metabolism and so produce coronary disease by the same mechanism.” What is that mechanism? Fingers are beginning to point suspiciously to an overload of insulin as a common culprit at the root of at least some of these metabolic and negative health effects, such as heart disease; controlling insulin was the main purpose of the original Atkins diet and has become the raison d’être of the low-carb approach to living. Though the Atkins diet is certainly not the only way to control insulin, Atkins—who was after all a cardiologist—is to be commended for being prescient when it comes to identifying carbohydrates and insulin resistance as causative factors in diabetes, obesity, hypertension, and, you guessed it, heart disease.
Yudkin’s warnings against sugar and Atkins’s early low-carb approach to weight loss were mere whispers lost in the roar of anti-fat mania. By the mid-1980s, fat had been utterly and completely demonized, and fat phobia was in full bloom, with hundreds of cholesterol-free foods being foisted on a gullible public. In November 1985, the National Heart, Lung, and Blood Institute launched the National Cholesterol Education Program with the stated goal of “reducing illness and death from coronary heart disease in the United States by reducing the percent of Americans with high blood cholesterol [italics ours].”
In 1976, Nathan Pritikin opened his Pritikin Longevity Center in Santa Barbara, California, and for the next decade preached the super-low-fat dogma to all who would listen, which included most of the country. Pritikin died in 1985, but his mantle was quickly taken up by Dr. Dean Ornish. Ornish’s reputation—and much of the public’s faith in the low-fat diet approach—was fueled by his famous five-year intervention study, the Lifestyle Heart Trial, which demonstrated that intensive lifestyle changes may lead to regression of coronary heart disease. Ornish took forty-eight middle-aged white men with moderate to severe coronary heart disease and assigned them to two groups. One group received “usual care,” and the other group received a special, intensive, five-part lifestyle intervention consisting of (1) aerobic exercise, (2) stress-management training, (3) smoking cessation, (4) group psychological support, and (5) a strict vegetarian, high-fiber diet with 10 percent of the calories coming from fat.
When Ornish’s study showed some reversal of atherosclerosis and fewer cardiac events in the twenty men who completed the five-year study, the public perception—reinforced by Ornish himself—was that the results largely stemmed from the low-fat diet. This conclusion is an incredible leap that is in no way supported by his research. The fact is that there’s no way to know whether the results were because of the low-fat diet portion of the experiment (highly unlikely in our view), the high fiber, the whole foods, the lack of sugar, or some combination of the interventions. It is entirely possible that Ornish would have gotten the same or better results with a program of exercise, stress management, smoking cessation, and group therapy plus a whole foods diet high in protein and fiber and low in sugar.
Yet low-fat eating managed to remain the dietary prescription of every major mainstream health organization. This recommendation was built on a foundation of two basic beliefs: that low-fat diets will reduce cholesterol, and that reducing cholesterol will actually reduce heart disease and extend life.
Although some studies have shown that low-fat diets do reduce overall cholesterol, many have shown nothing of the sort. When you replace fat in the diet with carbohydrates, which is exactly what low-fat diets do, you wind up with higher triglycerides and lower HDL cholesterol.
Bad news indeed. Higher triglycerides are an independent risk factor for heart disease—and raising them while lowering HDL cholesterol at the same time is a double whammy, a really bad “side effect” of the supposedly heart-healthy low-fat diet. Not only do you raise one important independent risk factor for heart disease (triglycerides) while at the same time lowering one protective measure (HDL cholesterol), but you also change the all-important ratio of triglycerides to HDL cholesterol in the worst way possible. A higher triglycerides number and a lower HDL cholesterol number mean a much higherratio of triglycerides to HDL. As we’ve seen, you want your ratio to be low, not high; low-fat, high-carbohydrate diets make the ratio higher.
The Sugar Lobby in Action
So how did fat get demonized while sugar got a “get out of jail free” card?
Well, there’s no political lobby for “fat,” but there’s a powerful one for sugar.
In 2003, the World Health Organization (WHO)—not exactly a bunch of wide-eyed radicals—published a conservative, reasonable report called Diet, Nutrition and the Prevention of Chronic Diseases. In it, the WHO made the unexceptional statement that it would be a good idea for people to derive no more than 10 percent of their daily calories from added sugars. The report suggested that people could lower their risk of obesity, diabetes, and heart disease simply by curbing some of the sugar they were consuming. A completely mainstream, noncontroversial, “vanilla” recommendation if ever there was one. Who could possibly object, you might think?
WHAT YOU NEED TO KNOW
• Hypertension, high levels of triglycerides, and a high ratio of triglycerides to HDL are all better predictors of heart disease than cholesterol. Sugar, or more specifically fructose, raises every single one of these measures.
• Fat raises LDL cholesterol, but it raises the big, fluffy, harmless particles (producing the desirable pattern A profile) and lowers the nasty little BB gun–pellet LDLs that actually do cause heart disease. Sugar, in contrast, has the opposite effect, increasing the number of really bad LDL molecules (producing the harmful pattern B profile) and decreasing the number of harmless ones. On top of that, high levels of sugar and insulin damage those nasty little LDL particles, making them far more likely to start the process of inflammation.
• If you accept our theory that inflammation, not cholesterol, is at the “heart” of heart disease, it’s worth pointing out that the metabolic effects of sugar are highly inflammatory to your artery walls.
Well, the U.S. sugar industry, for one.
“Hoping to block the report . . . the Sugar Association threatened to lobby Congress to cut off the $406 million the United States gives annually to the WHO,” reported Juliet Eilperin in the Washington Post. The Post quoted an April 14, 2003, letter from the Sugar Association’s president, Andrew Briscoe, to the general director of WHO in which he stated, “We will exercise every avenue available to expose the dubious nature of the Diet, Nutrition and the Prevention of Chronic Diseases report.”
Two senators wrote a letter to then Health and Human Services Secretary Tommy G. Thompson, urging him to squelch the report. Not soon afterward, the U.S. Department of Health and Human Services submitted comments on the report, stating that “evidence that soft drinks are associated with obesity is not compelling.”
Oh, really? Shades of the tobacco industry’s defense of cigarettes.
In a 2005 report by the Institute of Medicine, the authors acknowledged that there was a ton of evidence suggesting that sugar consumption could increase the risk of heart disease and diabetes—and that it could even raise LDL (“bad”) cholesterol. The problem was they couldn’t say that the research was definitive. “There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much,” Taubes wrote.
This dovetailed nicely with the last assessment of sugar by the Food and Drug Administration (FDA) back in 1986 that basically said “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.”
“This is another way of saying that the evidence by no means refuted the [charges against sugar], just that it wasn’t definitive or unambiguous,” Taubes said. It’s also worth noting that at the time, we were consuming approximately 40 pounds per year of “added sugars,” meaning sugar beyond what we might naturally obtain from fruits and vegetables. (That comes to about two hundred extra sugar calories a day, about a can and a half of Coke.)
That doesn’t sound so bad, really, and if that were all the sugar we were consuming, most nutritionists in America would be pretty happy. The problem was it wasn’t 40 pounds a year. Even back then the Department of Agriculture said we were consuming 75 pounds a year, and by the early 2000s it was up to 90 pounds. As of late 2011, we’re up to 156 pounds a year. That’s the equivalent of thirty-one 5-pound bags for every man, woman, and child in America.
What’s So Bad about a Little Sugar?
The way in which sugar damages the heart can be directly related to insulin resistance.
Ordinary table sugar, known technically as sucrose, is actually composed of equal parts glucose and fructose, two simple sugars that are anything but metabolically equal. Glucose can be used by any cell in the body. Fructose, on the other hand, is metabolic poison. It’s the fructose in our sweetened foods that we should fear the most.
Before you point the finger of blame exclusively at high-fructose corn syrup (HFCS), an additive that’s made it into virtually every processed food on the market, consider the following:
• Regular sugar (sucrose) is 50 percent glucose and 50 percent fructose.
• High-fructose corn syrup is 55 percent fructose and 45 percent glucose, a difference that just doesn’t matter very much.
• So sugar and high-fructose corn syrup are essentially the same thing.
Because high-fructose corn syrup has gotten so much heat in the press, some food manufacturers now proudly advertise that their products contain none of it and are instead sweetened with “natural” sugar (meaning ordinary sucrose). Meanwhile, the Corn Refiners Association has claimed that high-fructose corn syrup is being unjustly targeted and is no worse than “regular” sugar.
Sadly, the association is technically right. Fructose is the damaging part of sugar, and whether you get that fructose from regular sugar or from HFCS doesn’t make a whit of difference. That doesn’t absolve HFCS at all; it just means that “regular” sugar is just as bad as HFCS. It’s the fructose in each of them that’s causing the damage, and here’s why.
Fructose and glucose are metabolized in the body in completely different ways. They are not identical. Glucose goes right into the bloodstream and then into the cells, but fructose goes right to the liver. Research has shown that fructose is seven times more likely to form the previously mentioned artery-damaging AGEs (advanced glycation end products). Fructose is metabolized by the body like fat, and it turns into fat (triglycerides) almost immediately. “When you consume fructose, you’re not consuming carbs,” says Robert Lustig, M.D., professor of pediatrics at the University of California, San Francisco. “You’re consuming fat.”
Fructose is the major cause of fat accumulation in the liver, a condition known technically as hepatic steatosis but which most of us know as fatty liver. And there is a direct link between fatty liver and our old friend, insulin resistance.
A top researcher in the field of insulin resistance, Varman Samuel of the Yale School of Medicine, told the New York Times that the correlation between fat in the liver (fatty liver) and insulin resistance is remarkably strong. “When you deposit fat in the liver, that’s when you become insulin resistant,” he said.
And all together now, class: What causes fat to accumulate in the liver? Fructose.
If you want to watch a bunch of lab animals become insulin resistant, all you have to do is feed them fructose. Feed them enough fructose and, sure enough, the liver converts it to fat, which then accumulates in the liver—with insulin resistance right behind it. This can take place in as little as a week if the animals are fed enough fructose, whereas it might take a few months at the levels we humans normally consume. Studies conducted by Luc Tappy, M.D., in Switzerland revealed that feeding human subjects a daily dose of fructose equal to the amount found in eight to ten cans of soda produced insulin resistance and elevated triglycerides within a few days.
Fructose found in whole foods such as fruits, however, is a different story. There’s not all that much fructose in, for example, an apple, and the apple comes with a hefty dose of fiber, which slows the rate of carbohydrate absorption and reduces insulin response. But fructose extracted from fruit, concentrated into a syrup, and then inserted into practically every food we buy at the supermarket—from bread and hamburger buns to pretzels and cereals—well, that’s a whole different animal.
High-fructose corn syrup was first invented in Japan in the 1960s and made it into the American food supply around the mid-1970s. It had two advantages over regular sugar, from the point of view of food manufacturers. Number one, it was sweeter, so theoretically you could use less of it. Number two, it was much cheaper than sugar. Low-fat products could be made “palatable” by the addition of HFCS, and before long, manufacturers were adding the stuff to everything. (Doubt us? Take a field trip to your local supermarket and start reading labels. See if you can find any processed foods that don’t contain it.)
The result is that our fructose consumption has skyrocketed. Twenty-five percent of adolescents today consume 15 percent of their calories from fructose alone! As Lustig points out in a brilliant lecture, “Sugar: The Bitter Truth” (available on YouTube), the percentage of calories from fat in the American diet has gone down at the same time that fructose consumption has skyrocketed, along with heart disease, diabetes, obesity, and hypertension. Coincidence? Lustig doesn’t think so, and neither do we.
Remember our mention of metabolic syndrome? It’s a collection of symptoms—high triglycerides, abdominal fat, hypertension, and insulin resistance—that seriously increases the risk for heart disease. Well, rodents consuming large amounts of fructose rapidly develop it. In humans, a high-fructose diet raises triglycerides almost instantly; the rest of the symptoms associated with metabolic syndrome take a little longer to develop in humans than they do in rats, but develop they do. Fructose also raises uric acid levels in the bloodstream. Excess uric acid is well known as the defining feature of gout, but did you know that it also predicts future obesity and high blood pressure?
Fructose and glucose behave very differently in the brain as well, as research from Johns Hopkins has suggested. Glucose decreases food intake while fructose increases it. If your appetite increases, you eat more, thus making obesity, and an increased risk for heart disease, far more likely. “Take a kid to McDonald’s and give him a Coke,” Lustig said. “Does he eat less? Or does he eat more?”
M. Daniel Lane, Ph.D., of the Johns Hopkins University School of Medicine stated, “We feel that [the findings on fructose and appetite] may have particular relevance to the massive increase in the use of high-fructose sweeteners (both high-fructose corn syrup and table sugar) in virtually all sweetened foods, most notably soft drinks. The per capita consumption of these sweeteners in the USA is about 145 lbs/year and is probably much higher in teenagers/youth that have a high level of consumption of soft drinks.”
All told, the case against fructose consumption as a key factor in the development of heart disease seems to us to be far more cogent than the case against fat. It’s also worth pointing out that every single bad thing that fructose does to increase our risk for heart disease—and it does a lot—has virtually nothing to do with elevated cholesterol.
The fact is that sugar is far more damaging to the heart than either fat or cholesterol are, but that has never stopped the diet establishment from continuing to stick to its story that fat and cholesterol are what we ought to be worried about.
As the old journalistic maxim goes, “Never let the facts get in the way of a good story.”
Unfortunately, this story is long past its expiration date. Sticking to it in the face of all evidence continues to make many people very sick indeed