CHAPTER 3

INFLAMMATION: THE TRUE CAUSE OF HEART DISEASE

SO IF CHOLESTEROL ISN’T THE CAUSE OF HEART DISEASE, what is?

We know you don’t want to wait any longer, so here’s the short answer: The primary cause of heart disease is inflammation.

The subject of inflammation will be a running theme throughout this book for reasons that will soon be made clear, but the first thing you need to know about inflammation is this: It comes in two flavors. You’re probably already familiar with one of them, but it’s the one you’re less familiar with that’s at the core of heart disease.

Let us explain.

Almost all of us have experience with acute inflammation. It happens every time you stub your toe, bang your knee, or get a splinter in your finger. When you complain about your aching back, an abscess in your mouth, or a rash on your skin, that’s acute inflammation. It’s visible and uncomfortable, if not downright painful. The redness on your skin is a result of blood that’s rushed to the affected area. The swelling you experience is the result of an army of specialized cells (with names like phagocytes and lymphocytes) dispatched by the immune system to mend the injured area. (The job of these immune system cells is to surround the site of the injury and neutralize nasty invaders such as microbes, preventing the spread of potential infection.) The swelling, redness, and soreness you experience as a result of acute inflammation are all natural accompaniments to the healing process.

So we all know about acute inflammation, most of us from personal experience. But the other flavor of inflammation, chronic inflammation, well, that’s a whole different ball game.

Acute inflammation hurts, but chronic inflammation kills.

WHY YOU SHOULD CARE ABOUT CHRONIC INFLAMMATION, NOT CHOLESTEROL

Chronic inflammation flies beneath the pain radar. Much like high blood pressure, it has no obvious symptoms. Yet chronic inflammation is a significant component of virtually every single degenerative condition, including Alzheimer’s, diabetes, obesity, arthritis, cancer, neurodegenerative diseases, chronic lower respiratory disease, influenza and pneumonia, chronic liver and kidney diseases, and, most especially, heart disease.

A BETTER WAY TO PREDICT HEART DISEASE

Want a much better way to tell whether you’re at risk? Look at these two line items on your blood test: triglycerides and HDL (the so-called “good” cholesterol).

Now if you’re not too freaked out about doing a bit of math, calculate the ratio of your triglycerides to your HDL. If, for example, your triglycerides are 150 mg/dL and your HDL is 50 mg/dL, you have a ratio of 3 (150:50). If your triglycerides are 100 mg/dL and your HDL is 50 mg/dL, you have a ratio of 2 (100:50).

This ratio is a far better predictor of heart disease than cholesterol ever was. In one study out of Harvard published in Circulation, a journal published by the American Heart Association, those who had the highest triglyceride-to-HDL ratios had a whopping sixteen times the risk of developing heart disease as those with the lowest ratios.1 If you have a ratio of around 2, you should be happy, indeed, regardless of your cholesterol levels. (A ratio of 5, however, is problematic.)

When chronic inflammation exists unchecked in the cardiovascular system, it usually spells big trouble for the heart.

And inflammation is rarely a local phenomenon. For instance, women with rheumatoid arthritis, a highly inflammatory condition that primarily affects the joints, wind up having double the risk of a heart attack when compared to women without it. Microbes that cause problems in one part of the body can easily migrate to other areas and cause inflammatory damage there. An infection that starts in the gums, for example, can easily leak bacteria into the bloodstream, bacteria that may then find fertile ground in a weakened arterial wall and fan the fires of inflammation there.

So how exactly does inflammation happen, and, more importantly, what can we do about it?

OXIDATION: THE INITIATOR OF INFLAMMATION

In The Most Effective Ways to Live Longer, Dr. Jonny introduced the concept of the “Four Horsemen of Aging.” These Four Horsemen all contribute mightily to heart disease, and we’ll go over all of them in the pages that follow. For those of you who just have to know right now what they are, here’s the list: oxidation, inflammation, sugar, and stress. In this chapter, we’ll concentrate on the first two.

One of the prime initiators of inflammation is oxidation. If you’ve ever seen rust on metal, you’re familiar with oxidation (also known as oxidative damage), even if you didn’t know the technical name for it. You’re also familiar with oxidation if you’ve ever left apple slices out on a picnic table where they were exposed to the air. They turned brown, didn’t they? That’s oxidative damage.

For those of you who don’t remember high school chemistry (or would understandably prefer to forget it), electrons travel in pairs and orbit around atoms. Every so often one of those electrons gets “loose,” and pandemonium ensues. The unpaired electron—known as a free radical—starts running around like a headless chicken trying to find its head. Free radicals are like college sophomores on spring break—temporarily free from the constraints of dormitory living, they basically go nuts and will “mate” with anyone! Free radicals “hit” on existing, stable pairs of electrons thousands of times a day, trying to find an electron they can pair-bond with and meanwhile, inflicting enormous damage upon your cells and DNA.

The free radicals that come from oxygen (known, not surprisingly, as oxygen free radicals) are the most deadly and damaging. (Now you know what the term “antioxidants” means—it’s a class of substances, including certain vitamins, minerals, and many plant chemicals, that helps neutralize free radicals, soaking them up like little sponges, thus limiting the damage they can do to your body. The reason cut apple slices don’t turn brown so quickly when you squirt lemon juice on them is because lemon juice contains a fair amount of vitamin C, a powerful antioxidant.)

Free radicals are so important that in the mid-1950s a scientist named Denham Harman, M.D., Ph.D., put forth a theory called the Free Radical Theory of Aging that remains popular to this day.2 In it he basically proposes that aging is a kind of “rusting from within,” largely due to the damage caused by oxygen free radicals.

Okay, hold that thought. We’re going to come back to it. But before we go any further, let’s look at the arteries, or more specifically the arterial walls, because that’s where the damage starts.

Ground Zero for Damage: Introducing the Endothelium

The arterial walls are anything but hard and firm. They’re composed of smooth muscle that expands and contracts like a mini accordion; they respond to the rhythm of the heart and accommodate the pulsing of the blood. These arteries—far from being a static system of tubes and pipes—are a living, breathing, very dynamic organ. And the innermost layer of the artery walls—the “interface,” if you will, between the blood inside the arteries and the walls that contain it—is a central player in our little drama. This layer is called the endothelium—and it’s the starting point for the damage that can ultimately lead to a heart attack.

Big word, endothelium, yes, not often bandied about in cocktail party chatter about heart disease, but it’s one of the most important places in the arteries for you to know about because that’s where the damage to your arteries starts. The endothelium is only one cell thick, but it’s where a tremendous amount of biochemical activity takes place. There’s even a name for the pathological state in which damage to that innermost layer exists—it’s called endothelial dysfunction, and it’s a key event in the development of heart disease.

WHAT YOU NEED TO KNOW

• Cholesterol is the parent molecule for sex hormones (estrogen, progesterone, and testosterone) as well as vitamin D and bile acids needed for digestion.

• The only time cholesterol is a problem is if it’s oxidized (damaged).

• Damaged or oxidized LDL cholesterol sticks to the lining of the arteries and begins the process of inflammation.

• The true cause of heart disease is inflammation.

• Inflammation is initiated by damage from free radicals (oxidative stress).

• The concept of “good” and “bad” cholesterol is outdated.

• There are several types of LDL (“bad”) cholesterol and several types of HDL (“good”) cholesterol.

• It is far more important to know whether you have a pattern A or pattern B LDL cholesterol profile than to know your total amount of LDLs.

• A cholesterol level of 160 mg/dL or less has been linked to depression, aggression, cerebral hemorrhages, and loss of sex drive.

FOR MEN ONLY

Note to the men reading this: Endothelial dysfunction has the same acronym (ED) as another condition you may be familiar with or concerned about: erectile dysfunction. They’re not unrelated. Our friend Mark Houston, M.D., director of the Hypertension Institute and an associate professor of medicine at Vanderbilt University, wryly commented, “I’ve never seen a case of ED (erectile dysfunction) that didn’t also have ED (endothelial dysfunction).”

Bottom line: A healthy functioning endothelium is essential for . . . more things than just the heart!

Okay, we’ve introduced two important concepts here—oxidative damage and inflammation—and one important structure—the endothelium. Now we need to take a look at what cholesterol is and see how it fits into the whole picture. Once we do, we will return to the interaction among oxidation, inflammation, and the arterial walls.

“GOOD” AND “BAD” CHOLESTEROL: A COMPLETELY OUTDATED CONCEPT

Contrary to cholesterol’s negative reputation, your body simply can’t function without it. It’s found in every single cell and is so essential that the lion’s share of the cholesterol in your body is actually made by your body, specifically by the liver, which produces this fatty, waxy substance precisely because it is so essential to the health of your cells.

The cholesterol you eat has a minimal effect on your blood levels of cholesterol, which is why the admonition to eat less of it and the prominent listing of cholesterol on food nutrition labels are not as significant as we are led to believe they are. If you eat less cholesterol, your liver will simply take up the slack and make more. If you eat more of it, the liver makes less. It is primarily, overwhelmingly made in the liver, though small amounts are made in other locations. For all intents and purposes, “manufacturing central” is the liver, and this is what responds to the “eat more/make less, eat less/make more” seesaw. The Framingham Heart Study found that there was virtually no difference in the amount of cholesterol consumed on a daily basis by those who went on to develop cardiovascular disease and those who did not. Egg-white omelet eaters, take note!

Cholesterol’s ability to fight toxins may be one reason why it’s found at the site of arterial injuries caused by inflammation. But blaming cholesterol for those injuries is a little like blaming firemen for fire.

As we said earlier, cholesterol is the basic raw material that your body makes into vitamin D; sex hormones such as estrogen, progesterone, and testosterone; and the bile acids needed for digestion. The emphasis on lowering cholesterol as much as possible is not only misguided but also dangerous. Studies show that those at the lowest end of the cholesterol spectrum have a significantly increased risk of death from myriad conditions and situations unrelated to heart disease, including, but not limited to, cancer, suicide, and accidents.

Accidents and suicides? Really? Yes. Here’s the connection: You need cholesterol to make brain cells. A cholesterol level too low (around 160 mg/dL) has, in fact, been linked to depression, aggression, and cerebral hemorrhages. (The connection to sex drive will be discussed later in chapter 6—it’s a doosey!)

The membranes of your cells contain a ton of cholesterol because it helps maintain their integrity and also facilitates cellular communication. The consistency of the cell membrane has to be just right—hard enough to act as a barrier to all sorts of molecular riff-raff but pliable and soft enough to allow access to the molecules that need to get inside. Essentially, you need cholesterol for memory. Lower cholesterol too much and it can easily promote a kind of global amnesia; with too little cholesterol in the cell membranes, nerve transmission can be affected. It’s no surprise to us that Duane Graveline, M.D.—a former flight surgeon and astronaut who received international recognition for his research on zero gravity deconditioning—gave his book about the memory loss he experienced after taking statin drugs the ominous title Lipitor: Thief of Memory.

Cholesterol is also one of the important weapons your body uses to fight infections. It helps neutralize toxins produced by bacteria that swarm into the bloodstream from the gut when the immune system is weakened. When you have an infection, the total blood level of cholesterol goes up, but HDL (which we’ll define in a moment) falls because it’s being used up in the fight. Cholesterol’s ability to fight toxins may be one reason why it’s found at the site of arterial injuries caused by inflammation. But blaming cholesterol for those injuries is a little like blaming firemen for the fire.

Now here’s an interesting fact of which you might not have been aware: It’s actually impossible to measure cholesterol directly in the bloodstream. Being a fatty substance, cholesterol is not soluble in water or blood. So how does it get in the bloodstream? Simple. Your liver coats it with a “protein wrapper” and bundles it with a few other substances (such as triglycerides); packaging it in this protective shell allows it to enter your circulatory system, much like stones would float in the ocean if they were contained in a buoyant, waterproof container. In our case, the protein wrapper acts like a passport, allowing cholesterol to travel throughout your bloodstream. It’s these packages, known as lipoproteins, that we actually measure when we measure our cholesterol levels.

We know these cholesterol–protein combinations as HDL (high-density lipoprotein) and LDL (low-density lipoprotein). Both contain cholesterol and triglycerides, but the percentages are different, and the two types of lipoproteins have different functions in the body. LDL, known as “bad” cholesterol, carries cholesterol to the cells that need it, while HDL, known as “good” cholesterol, picks up the excess and carries it back to the liver.

But this old idea of “good” and “bad” cholesterol is a wholly outdated concept.

We now know that there are many different “subtypes” of both HDL and LDL, and they do very different things. LDL, the imprecisely named “bad” cholesterol, has several different subtypes, and not all of them are bad at all—quite the contrary.

The most important subtypes of LDL are subtype A and subtype B. When most of your LDL is of the “A” type, you’re said to have a pattern A cholesterol profile. When most of your LDL is of the “B” type, you’re said to have a pattern B cholesterol profile. Simple, right? And absolutely essential to know for reasons soon to be made clear.

Subtype A is a big, fluffy molecule that looks like a cotton ball and does just about as much damage, which is to say none. Subtype B, however, is small, hard, and dense, like a BB gun pellet. It’s the real bad actor in the system, because it’s the one that becomes oxidized, sticks to the arterial walls, and starts the cascade of damage. Subtype B particles (what we might call the “bad” bad cholesterol) are atherogenic, meaning that they contribute significantly to heart disease. As we’ve already noted, big, fluffy LDL particles (the “good” bad cholesterol) are pretty much benign. Knowing you have a “high” LDL level is pretty much a useless piece of information unless you know how much of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least). Both of us would be totally comfortable having a high LDL number if the bulk of it was composed of the big, harmless, cotton ball–type molecules (the pattern A distribution). That’s much more preferable than having a lower LDL number mostly composed of the BB gun pellet–type molecules (the pattern B distribution).

Unfortunately, most doctors are behind the times on this one. They look at that total LDL number—not the size and type—and if that number is even slightly higher than the lab says it should be, out comes the prescription pad. Pharmaceutical companies love when advisory committees—which are often heavily stacked with doctors who have financial ties to the pharmaceutical companies—recommend that we maintain lower and lower LDL levels, because that means a bigger and bigger market for cholesterol-lowering drugs. Sadly, most doctors do not perform the easily available tests—often covered by insurance—that determine your LDL.

You may recall from the first chapter that present-day health recommendations to reduce cholesterol by any means possible started with the Framingham Heart Study. In 1948, when the study began, cholesterol was only measured as “total” cholesterol. If you knew what your cholesterol was, you knew one specific number (200 mg/dL or 220 mg/dL, for example). As recently as 1961 we didn’t have the technology to distinguish between “good” and “bad” cholesterol (HDL and LDL), much less the newer technology that allows us to zero in on different subtypes of the so-called “bad” cholesterol, which, as you can see, is far from being all “bad” after all.

Even HDL, the so-called “good” cholesterol, isn’t all good. A study published in the December 2008 issue of the FASEB Journal, produced by the Federation of American Societies for Experimental Biology, challenged the conventional wisdom that simply having high levels of good cholesterol (HDL) and low levels of bad cholesterol (LDL) is necessary for good health. The researchers showed that even good cholesterol has varying degrees of quality and that some HDL cholesterol is actually bad news.

“For many years, HDL has been viewed as good cholesterol and has generated a false perception that the more HDL in the blood, the better,” said the lead researcher, Angelo Scanu, M.D., of the University of Chicago.3 “It is now apparent that subjects with high HDL levels are not necessarily protected from heart problems and should ask their doctors to find out whether their HDL is good or bad.” Scanu’s study found that the HDL of people with chronic diseases such as rheumatoid arthritis and diabetes is very different than the HDL of healthy individuals, even when their blood levels of HDL are similar. Normal, “good” HDL cholesterol reduces inflammation; dysfunctional, “bad” HDL does not.

Knowing you have a “high” LDL level is pretty much a useless piece of information unless you know how much of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least).

THE GOOD, THE BAD, AND THE REALLY, REALLY UGLY!

This just in: As of this writing, new research funded by the British Heart Foundation has uncovered still another subtype of LDL cholesterol that is particularly bad. It’s called the MGmin-low-density lipoprotein, and it’s more common in people with type 2 diabetes and in the elderly. It’s “stickier” than normal LDL, which makes it much more likely to attach to the walls of the arteries.

This new “ultra-bad” boy is actually created by a process called glycation, which sharp-eyed readers will recall is one of the Four Horsemen of Aging. Glycation happens when there’s too much sugar hanging around in the bloodstream. The excess sugar starts gumming up the works, inserting itself in places where it doesn’t belong—in this case, the LDL molecule. (We’ll have a lot more to say about sugar and its role in heart disease later on in chapter 4. Preview: Sugar is way more of a threat to your heart than fat ever was!)

“This is yet one more line of research that explains why some people can have perfect cholesterol levels, but still develop cardiovascular disease,” said Gerald Weissmann, M.D., editor-in-chief of the FASEB Journal. “Just as the discovery of good and bad cholesterol rewrote the book on cholesterol management, the realization that some of the ‘good cholesterol’ is actually bad will do the same.”⁴

The point is that there is, indeed, “bad” cholesterol—even “ultra-bad” cholesterol—but simply using a shotgun pharmaceutical approach to lowering all cholesterol doesn’t accomplish anything and has significant unwanted side effects, as we will see in chapter 6.

Now that the four main characters in our drama have been introduced—oxidation, inflammation, cholesterol, and the arterial walls—let’s see how they interact in real life, and how they work together to create a dangerous situation for your heart.

WHEN LDL REALLY IS BAD FOR YOU: THE SMOKER’S PARADOX

Here’s a riddle for you: Why is it that smokers with normal LDL (the so-called “bad” cholesterol) levels have a much higher risk of heart disease than non-smokers with elevated LDL levels?

Sure, we all know how cigarette smoke damages the lungs, and that cigarette smoking significantly increases the odds of getting lung cancer. But, really, what’s the connection between smoking and heart disease, or, more specifically, between smoking and LDL cholesterol?

Glad you asked.

Besides the harsh smoke, cigarettes also graciously provide your body with myriad toxic chemicals, all at no extra charge, thank you very much. These chemicals and toxins both constrict the blood vessels and harm the arterial walls. Specifically, they cause your LDL to become oxidized—damaged by the free radicals that are found in abundance in cigarette smoke! (And, by the way, it’s not just cigarette smoke that can oxidize LDL. Heavy metals like mercury can do it, as can insecticides, radiation, and all manner of toxins in the environment, the air, and the food supply.)

And listen carefully now: LDL is never a problem in the body until it becomes oxidized. Only oxidized LDL sticks to the arterial walls, contributing to plaque and causing further inflammation and injury. Non-oxidized LDL is pretty much harmless. It’s oxidation that actually initiates the process that culminates in atherosclerosis.

So a smoker with a low amount of LDL, most of which has been damaged by oxidation, is at far greater risk for heart disease than a nonsmoker with a much higher level of LDL, only a tiny percentage of which has been damaged. It’s not the LDL that causes the problem—it’s damaged (oxidized) LDL.

So LDL floats around in the bloodstream, delivering cholesterol to the cells that need it, and some of this LDL, the LDL that’s damaged by oxidation, infiltrates the endothelium. Once the endothelium becomes infiltrated with this damaged LDL, the process of inflammation begins in earnest.

Remember our earlier discussion about harmless “bad” cholesterol (LDL pattern A) and dangerous “bad” cholesterol (LDL pattern B)? Well, one of the reasons why pattern B molecules (those BB gun–pellet types) are so bad is that they are the ones most likely to be damaged and most likely to be oxidized. On top of that, they’re small enough to penetrate the arterial walls in the first place. The smaller the particles (and pattern B particles are small indeed), the more inflammatory they are. Oxidized LDL is like “angry” LDL, and the smaller the particle, the angrier it is. So these nasty little damaged LDL particles stick to the endothelium and begin the process of inflammation. In the presence of oxidative damage—or in the presence of high blood sugar, which is such an important initiator of damage that we’ll examine it separately in chapter 4—this LDL experiences chemical changes that the immune system perceives as dangerous.

Once the immune system notices this damaged (oxidized) LDL, it sends in the heavy artillery. First, cells known as monocytes rush to the scene of the action, releasing chemicals called cytokines. Cytokines are essentially chemical messengers that help regulate the immune system response, but many of these cytokines are themselves highly inflammatory. In the presence of some of these cytokines, the lining of the blood vessels (the endothelium) secrete sticky little molecules called adhesion molecules that act like molecular glue, grabbing on to the monocytes that have rushed to the scene of the crime to help put out the fire. Heart surgeon Dwight Lundell, M.D., cleverly refers to this as the “Velcro effect.”

Monocytes now convert into a type of cell we like to call “Little Ms. Pac-Man.” They’re technically called macrophages, and their job, much like Ms. Pac-Man in the video game, is to eat up the enemy, in this case the damaged LDL particles and other molecular junk that have caused the problem in the first place. (The word macrophage literally means “big eater.”)

The macrophages are like sugar addicts at a pie-eating contest. They have no off button; they’ll keep eating, consuming oxidized LDL until they literally choke to death, leaving something called the lipid core of plaque. Once they reach a certain size they start to look like foam and actually become what pathologists call “foam cells,” living cells that will continue the work of the macrophages, fighting and consuming until the “invader” is gone.

But it isn’t an invader that sets them off. It’s just plain old LDL experiencing chemical changes from sugar, starches, or oxidation and thus initiating an inflammatory process that can easily become an out-of-control “fire” within your arterial walls. As we’ve said, without inflammation, it’s pretty irrelevant what your cholesterol levels are.

If inflammation isn’t halted and if macrophages continue to feast away until they bust, they’ll release a whole new set of toxins into the walls of the artery.

“We can see this in surgery as a yellow streak inside the artery wall,” said Lundell, who has performed more than five thousand heart surgeries. “It is called the ‘fatty streak,’ and it is the beginning of significant heart disease.”5

The body tries to contain this fatty streak by building a wall to hold it in—scarring is an example. But the immune system is now on full alert; it sends more soldiers to the front, and they try valiantly to break down the wall (the scar tissue), and the cycle continues—more scarring, more soldiers. Over time, if the body’s immune system defenses are good enough, they will weaken the wall of the artery and literally “chew through” the scar tissue. A rupture will occur, resulting in more inflammation, and the potentially deadly cycle continues.

Not good news.

If the cycle is not stopped, the fatty streak grows into what’s known as plaque. (Plaque is basically a big old collection of foam cells.) Some foam cells will die, and they will release a whole bunch of the accumulated fats (lipids), which in turn develop into the aforementioned lipid core, a soft, yellowy substance that resembles melted butter (but isn’t nearly as good for you).

Now if you stop the inflammation at this point in time, the artery heals itself with what’s called a fibrous cap. The fibrous cap is composed of fibrous scar tissue and will stay nice and stable. (Cardiologists like Steve call this “stable plaque.”) Of course, if there’s new inflammation, the cycle begins all over again.

So the more inflammation continues, the more foam cells accumulate. This means more macrophages (Ms. Pac-Man), which in turn means more oozy, slimy lipid core. This lipid core gets into the bloodstream, where the blood immediately puts out a signal saying, “What the heck is this? Foreign object! Foreign object!” And a blood clot is formed in an attempt to keep this foreign, gooey substance from spreading.

So the blood clot is actually a protective mechanism. It’s the blood’s—or the body’s, if you prefer—way of saying, “Let’s contain this threat and keep it from spreading!” But though this strategy makes sense, it has a big downside. That blood clot may block access to the heart muscle, preventing oxygen from getting through. Anytime you deprive cells of oxygen, the tissue they make begins to die.

And when that tissue is the muscle of the heart, you’re looking at—you guessed it—a heart attack.

So overall, LDL can be likened to trees in a forest. A forest that has tons of trees but gets plenty of rain isn’t likely to be the site of a wildfire, but a forest with far fewer trees can be a tinder box just waiting to ignite if all those trees are dried up (damaged) and there’s very little rainfall! Getting rid of the trees is surely one crude way to prevent forest fires, just as lowering cholesterol indiscriminately might theoretically decrease the risk of a “fire” in your artery walls, but at what cost? Those trees serve a lot of ecological purposes, and removing them is not without consequences, both to the environment and to the landscape.

Wouldn’t it be better to reduce the conditions under which a fire is likely to break out? That way we could have all the wonderful benefits of trees with none of the side effects of a compromised ecology.

We hope we’ve convinced you that inflammation is at the core of heart disease, and that it’s inflammation—and its main initiator, oxidation—we need to be concerned about, not cholesterol.

But oxidation is only one of the conditions—albeit a very important one—that causes inflammation.

Another cause of inflammation is so important we’re giving it its own chapter. It’s something you eat every day and something you already know is bad for you, but only because of its well-documented role in diabetes and obesity. What you’re about to learn is the connection between this common food and heart disease.

By the time you finish the next chapter, you’ll be convinced—as we are—that this food is a far, far greater danger to your overall health, and specifically to your heart, than fat ever was.

We’re talking about sugar.