OUT OF ALL THE FOOD PYRAMID’S VICTIMS, the most brutally slaughtered was fat—particularly the saturated form. Stuffed into the use-sparingly tip alongside sugar, fat became immortalized as a wasteland of empty calories, appropriate only for a rare and guilt-laden indulgence. Even the pyramid’s 2011 upgrade, the circular MyPlate, continues the ultra-lean legacy: nowhere is the existence of fat even acknowledged.
While attitudes about fat are beginning to change—evidenced by the ever-growing selection of olive oils available at the supermarket—saturated fat still remains firmly blacklisted. Its image as a thief of health is so widespread, in fact, that we rarely stop and question what crimes it actually committed—or, for that matter, examine the evidence that handed down the guilty verdict in the first place. The term “saturated fat” is virtually wed to its descriptor “artery clogging,” reinforcing the thought of a deadly (albeit delicious) substance sludging through our veins like grease through a pipe. Each bite supposedly lands us a little closer to a heart attack. And it works its black magic, we’re told, through an equally frightful avenue: cholesterol in our blood.
It might come as a surprise, then, that the case against saturated fat was never a foregone conclusion. Rather, it was cobbled together with pieces of observational data, short-term trials, animal studies, and guesswork, resulting in a theory that—even today—generates paradoxes and contradictions rather than adequately explaining the state of human health.
In this chapter, we’ll trace the evolution of the nation’s grudge against fat (and its partner in crime, cholesterol), and explore how its saturated form shifted from nourishment to nemesis. We’ll learn about two of the nutrition world’s most game-changing postulates—the lipid hypothesis and diet-heart hypothesis—as well as the studies and masterminds that ushered them into being. It’s a saga that starts in the arteries of some unfortunate bunnies and ends in a battlefield of bad science.
In 1913, Russian researcher Nikolai Anichkov sealed one of the first links in the chain that bound cholesterol to heart disease—a connection that would later lure fat into a federal food fight that continues to rage today. Like other scientists of his time, Anichkov had been sleuthing out the cause of atherosclerosis, a term dubbed in 1904 to describe the mysterious, waxy plaque accumulation found on the walls of arteries.1
It was a time when rabbit studies were en vogue, and one of Anichkov’s contemporaries, Russian scientist Alexander Ignatovski, managed to induce plaque in the arteries of rabbits by swapping their vegetarian diet with a more carnivorous meat-and-egg-based menu. Yet neither Ignatovski nor other researchers had figured out what in the carnivore diet, exactly, caused arteries to fill with plaque. (Many suspected it might be protein, believed at the time to accelerate the aging process.2)
Anichkov famously solved the mystery. Through a series of progressively honed experiments, feeding rabbits various foods and then their isolated components, he pinpointed dietary cholesterol (or cholesterin, as it was called back then) as the culprit. For the first time, he showed that feeding rabbits pure cholesterol was enough to induce atherosclerosis similar to that found in humans. His early studies, for the record, employed diets with 5 percent cholesterol by weight—the equivalent of a human gorging on about a hundred eggs per day.3
But here’s the interesting thing: Anichkov was never fully convinced that the results of his rabbit studies translated to humans. For one, rabbits, unlike humans, are hardcore herbivores—equipped with labyrinth-like digestive systems, a fondness for all things fiber, and a complete lack of predatory skills. So it’s no real surprise that stuffing them with foods foreign to their species would create unfavorable results. They don’t have the anatomy to digest cholesterol any more than we humans have the anatomy to digest nylon stockings or BB pellets.
So Anichkov and his colleagues, to clarify the effects of cholesterol on different creatures, conducted similar experiments using rats and guinea pigs—only to discover that the same dietary cholesterol that injured the arteries of one species often did nada to another.
With conflicting evidence at his fingertips, Anichkov cautioned against jumping to conclusions about whether dietary cholesterol was a threat for humans. In a 1913 paper titled, “On experimental cholesterin steatosis and its significance in the origin of some pathological processes,” he explained it as follows:
On the basis of the rat experiments described above, we conclude that the harmful effect of cholesterin-rich nourishment is not expressed equally in all types of animals…. The fact that cholesterin has different effects on different animals, even closely related ones, raises the question as to what degree the results described above are valid for human pathology.4
Indeed, if you’ll recall from our Hitchhiker’s Guide chapter, one of the caveats with animal studies is the difference—often vast—between humans and critters, particularly when it comes to physiology and metabolism. Just as one man’s trash is another man’s treasure, one species’ poison may be another’s healthy breakfast. Animal models, whether rabbit or rat or housefly, are best used to tweeze apart biological processes, pinpoint the roles of various genes, and help shape the direction of more sophisticated human studies. But when it comes to how we should fuel our bodies, they offer little to no real guidance.
From that perspective, Anichkov’s studies showed pretty clearly that rabbits can’t handle cholesterol from food: it’s promptly dumped into their bloodstream and deposited in unfortunate places around their bodies, including their livers and kidneys and eyelids. But whereas egg-eating rabbits are universally headed toward a future of disease, the same can’t be said of egg-eating humans. We might learn more about how that process works by reviewing the case of the eighty-eight-year-old Colorado man, who—after at least fifteen years of eating two-dozen eggs per day—had normal cholesterol levels and zero signs of heart disease.5 For most humans, the experience would be the same. Although genetic factors can influence how we respond to dietary cholesterol (and do include a good deal of individual variation), the effects, in general, range from minor to naught.
Nonetheless, Anichkov’s experiments weren’t entirely irrelevant to our two-legged, opposable-thumbed species. They may not have proven anything about the effect of dietary cholesterol on humans, but they did set the framework for a later—more momentous—breakthrough: the role of blood cholesterol in heart disease.
Before we continue, let’s take a quick pit stop at Cholesterol Central to catch our bearings.
Cholesterol is one of those terms we’ve all heard at some point—whether from a monotone biology teacher or a statin commercial or our own doctor. But most of us have an oversimplified, somewhat cartoonish understanding of the role this substance plays in our bodies, especially when it comes to heart disease.
For starters, the terms “good cholesterol” and “bad cholesterol” are woefully misleading. In reality, there’s really only one kind of cholesterol. When we talk about “good cholesterol” and “bad cholesterol,” we actually mean lipoproteins—high density lipoprotein (HDL) and low density lipoprotein (LDL), respectively—which shuttle cholesterol (and other lipids) around our bodies through the bloodstream. In other words, the stuff we call cholesterol is often referring to cholesterol’s vehicles—the lipoproteins—rather than the cholesterol itself. Kind of misleading, right?
And rather than your body’s perverted attempt to convert its innards into a self-made poison, cholesterol is actually quite a rock star substance. It’s crucial for synthesizing vitamin D and sex hormones like estrogen and testosterone, building cell membranes, and making bile acids to help you digest food. If you somehow managed to eradicate cholesterol from your body, you would be very much dead.
Where the problem comes in is when your body’s fabulous balance of cholesterol transportation and cleanup goes awry. Think of LDL particles as taxis—driving little cholesterol passengers out from your liver to wherever it is they need to go in the body. Your cells have LDL receptors to pull those particles in and unload the cholesterol.
By contrast, HDL comes along dump-truck style and whisks excess cholesterol away, returning it to the liver for your body to recycle or eliminate. (Maybe that’s not the nicest way to treat former taxi passengers, but frankly, your body is a pretty brutal place to live.)
Now imagine what happens when those LDL taxis get stuck in traffic and spend ages driving around in your bloodstream. We’d end up with some cranky cholesterol passengers, right? Just like cars on a congested highway, LDL particles can spend far too long circulating in your blood, becoming unruly road-rage terrors as a result.
This basically describes the process known as oxidation. You see, when cholesterol leaves your liver, it’s packaged with some helpful antioxidant goodies to sustain it for the journey, as well as protect it from reacting with unstable molecules hanging out in your blood.
But once the store of antioxidants are depleted, all bets are off: the LDL becomes subject to damage and attack, leading to molecular changes that render it invisible to the LDL receptors that usually reel it in. What’s more, once LDL oxidizes, your body sees it as a foreign invader, and unleashes its immunesystem army to wage war. And that sets off a cascade of other processes ultimately leading to what we know as atherosclerotic heart disease.
Although there’s a host of additional steps involved in plaque buildup and heart attacks, for now, it’s just worth noting that LDL becomes the biggest threat when it gets oxidized (or damaged in other ways, including through the effects of infection). Ultimately, high levels of LDL are a problem insofar as more LDL means more “traffic” and slower clearance from your blood, both of which increase its risk of oxidation.
So what turns your bloodstream into the LDL equivalent of Seattle’s rush hour? As we’ll see in the next chapter, saturated fat often gets the blame due to its cholesterol-raising abilities: it tends to reduce the activity of your LDL receptors, allowing more LDL particles to swim through your bloodstream at once—though the extent of that varies from person to person and depends on the type of saturated fat consumed. (Saturated fat also bestows other qualities that actually reduce LDL oxidation, too, so its effect may be a wash in some sense.)
Obesity, smoking, sedentary living, stress, and certain diseases and drugs can also increase circulating LDL levels. And apart from that, some conditions like familial hypercholesterolemia—a genetic defect that slashes LDL receptor activity—can cause cholesterol levels to skyrocket well beyond what most people could normally achieve, with extreme LDL oxidation and early heart disease often on its heels.
What’s more, contrary to the portrayal most of us are familiar with, our arteries aren’t some sort of simple plumbing system, subject to gumming up with all that cholesterol floating around. And the solution isn’t a massive Roto-Rooter in the form of a quadruple bypass to scrape it all out, either. Quite the contrary!
Arterial plaque actually builds up beneath the walls of your arteries, and is full of calcium, bloated immune cells, and oxidized LDL. If you’re curious about the full story of arterial plaque and how heart disease develops, check out Chris Masterjohn’s website The Daily Lipid (http://blog.cholesterol-and-health.com/). He offers one of the most integrative and intelligent explanations of cholesterol’s role in heart disease that I have thus far encountered.
Now, as you read on, bear in mind that the earliest forays into heart disease research didn’t have the luxury of our current cholesterol knowledge. Total cholesterol—without distinguishing between different types of lipoproteins or the oxidation process—was typically the only measurement available or understood. Heart disease, while still imperfectly grasped today, was even more of a mystery back then. The discovery process very much launched from intellectual scratch. So it’s hard to judge our early heart disease trailblazers for not knowing what we know today.
Let’s now return briefly to our Russian scientist, Anichkov. Differences between bunny and man aside, his research gave the world of science the lipid hypothesis, which states that deranged blood lipids—particularly elevated cholesterol—play a central role in heart disease.
It wasn’t until the 1970s that the term lipid hypothesis appeared verbatim in any literature. But once it did, it began to drive the mammoth industry of statin drugs, various interventions to reduce cholesterol levels, and even the cost of your life insurance.
Bear in mind that the lipid hypothesis, per its true definition, concerns itself only with the makeup of the blood. It doesn’t directly comment on what factors—for example, diet, smoking, stress levels, and exercise (or lack thereof)—drive those blood lipids into disarray. This is the clear distinction between the lipid hypothesis and the diet-heart hypothesis that we’ll expand on shortly.
And despite the eventual clout that Anichkov’s hypothesis gained, it lay dormant for decades—lost as an unconnected dot in the heart disease saga until one man brought it back to the fore: a researcher named Ancel Keys.