If we ever want to settle the good-fat/bad-fat debate, we need to listen to the lipid scientists.
Lipid scientists have been trying to tell us for decades that saturated fat and cholesterol are not the problem.
Oxidized polyunsaturated fat (PUFA) is dangerous because it is chemically unstable.
Eliminating toxic fats can make you virtually heart-attack proof.
Your lipoprotein particle size is the best gauge of your risk of heart attack.
When I was fresh out of medical school, if you had asked me what causes heart disease, I would have answered, “Fat and cholesterol, of course.” I felt confident in this advice not only because it was what I had been taught, but because it seemed to make intuitive sense; I could picture fat accumulating inside a person’s artery, gradually choking it closed like cooking grease in a pipe. Moreover, the American Medical Association, the American Heart Association, the American Diabetes Association, the American Cancer Society, the American College of Cardiologists, and other organizations endorsed this cholesterol theory of heart disease.
But as I started practicing medicine, one thing about this theory nagged me: Why, if cholesterol is so deadly, were so many of my oldest patients enjoying excellent health after a lifetime of consuming butter, eggs, and red meat?
Not long ago, physicians and scientists at the center of establishment medicine started asking similar questions in light of increasing evidence that the cholesterol issue warranted revisiting. In 2001, a few nutrition scientists at the Harvard School of Public Health went so far as to suggest that “the low-fat campaign has been based on little scientific evidence and may have caused unintended health consequences.”225 Further, they contended that the low-fat, anti-cholesterol campaign might not only be a flop as far as fighting obesity and diabetes were concerned, it could be making both epidemics worse.
Thanks to Michael Pollan and authors of several recent books, who cite this article and others like it, the reading public has witnessed cracks forming in the foundation of modern nutritional thought.226, 227, 228 As more researchers discover all manner of evidence that animal fat has health-promoting effects (such data has now been published in dozens of academic journals), the pressure is building toward a sea of change in organized medicine.229 Until that change comes, however, your doctor is unlikely to contradict the official guidelines. Only when current guidelines change to reflect better science will the average doctor’s advice on nutrition cease to put patients at risk for those “unintended health consequences.”
By the end of this chapter, you may be convinced that there is little reason to fear cholesterol. My hope is that, at the very least, you will recognize that the cholesterol theory of heart disease is far from unassailable and that when your doctor admonishes you to “get your numbers down,” you need not accept this advice without objection.
The other thing I want you to understand is that a necessary outgrowth of the indictment of cholesterol is a rejection of the traditional, natural fats that have sustained humankind for thousands of generations. It’s a little like the idea Nestle successfully used in the 1940s to sell infant formula to my grandmother and many other women, claiming it was “more perfect than breastmilk.”230 Those who mean to replace natural, traditional foods with modern-day food-like products in the name of health are championing the position that nature doesn’t know best; a corporation does. This is an extraordinary claim requiring extraordinary evidence—a burden they have failed to meet.
So why do we fall for it?
To understand how easy it is to sell us completely bogus ideas, to get us begging for products that we barely know anything about, we will begin with the most successful sales pitch in the history of medicine, delivered by a man regarded by many as the hero of modern nutritional thought.
It’s 1958. A fit and handsome Ancel Keys stands before a laboratory chalkboard on a CBS documentary entitled The Search to warn us of “the new American plague.”231 Onscreen, we see a row of ten little wooden men standing on Keys’s desk. He flicks five of them with his finger, knocking them over as he speaks. “The chief killer of Americans is cardiovascular disease…. It strikes without warning. Of ten men we can expect five to get it.” From that moment forward, America would turn to Keys for advice on preventing heart disease.
The camera reveals Keys in front of a small but attentive group of men dressed in white coats, staged to make it appear as though he were delivering a speech to a cadre of enraptured physicians. Though he never claims outright to be a heart specialist, he wears a doctor’s jacket and talks confidently about heart health, looking every bit the part of the reassuring physician as he soberly enunciates just the right words for maximum impact. Delivered with a newscaster’s sense of gravitas and the suave confidence of Madmen’s ad exec character Don Draper, Keys’s charisma catapulted him to the front page of Time magazine. But unlike Draper, who sold household products using catchy slogans delivered by attractive spokespeople, Keys sold himself as the go-to expert on all manner of heart disease using bad science, covert deception, and fear.
In reality, the father of the “diet-heart hypothesis” was not a cardiologist or even an M.D. Keys had earned his Ph.D. in the 1930s studying salt-water eels. His nutritional credentialing rested on the fact that, during WWII, the military assigned him to design the ready-to-eat meal that could be stored for years and shipped to millions of soldiers. Dr. Keys named his pocket-sized meal the K-ration, after himself. When the war was over, the Minnesota public health department hired Keys to study the problem of rising rates of heart attacks. But ego got the better of him.
At his first scientific meeting he presented the idea that in countries where people ate more animal fat, people died of heart disease more often, suggesting a possible causal relationship. But his statistical work was so sloppy (see figure on the following page) that he was lambasted by his peers. Rather than cleaning up his act, Keys vowed vengeance: “I’ll show those guys.”232 More than anything else, it seems, Keys wanted folks to think he had single-handedly discovered the cause of heart disease. And so did the country’s margarine producers, who in Keys had found the perfect spokesperson. Though Keys’s work failed to convince professional scientists (at least for the first decade or two), the margarine industry knew he still had a shot at convincing the man on the street. If the public thought butter and other animal fats would “clog their arteries,” they could be persuaded to buy margarine instead.
It wasn’t long before the American Heart Association, which depends on large donations of cash from the vegetable oil industry, jumped on the bandwagon with Keys. They took his sloppy statistics and ran with it, eventually convincing most doctors that steak is a “heart attack on a plate” and that margarine made from hydrogenated vegetable oils (full of trans fat) was healthy. Within a decade, grocery store shelves were loaded with ready-to-eat foods, and Americans were buying. No longer insisting on fresh food from small farmers right in our neighborhoods, we’d been convinced that products made in distant factories were safer, healthier, and better. And they were also cheaper. But even Keys had his doubts about eating them.
HOW KEYS FAKED IT
Lies, damn lies, and statistics. Keys blamed natural fat consumption for heart attacks. But the United States, England, Canada, and Australia had the highest levels of margarine consumption. Keys never mentions margarine in his famous “Six-Countries Study” and the deception was never exposed. Keys is still considered to be a hero of modern medicine.
By 1961, under increasing scientific scrutiny, Keys began to waver in his support for his own (now publicly accepted) diet-heart hypothesis.233 Scientists had pointed out Dr. Keys’s misleading use of scientific terms. In public, he fingered animal fat as the culprit behind the rising rates of heart attacks. But in his laboratory and human experiments, he didn’t use animal fat.234 His subjects were fed margarine made from partially hydrogenated vegetable oil. And what was in the margarine? Trans fat—a full 48 percent!
Trans fats are the infamous artery-hardening molecules that have been banned from restaurants in New York City and elsewhere due to their now well-known associations with heart disease. These fats do not exist in foods that nature makes. (Trans describes a chemical bond between two molecules, not a molecule per se. More on this below.) While nature makes healthy versions of trans-containing fats, the trans fat that’s been banned is the byproduct of an industrial process called hydrogenation. And so, for Keys to conclude from studies that used hydrogenated vegetable oil that animal fat causes heart disease is utterly nonsensical.
Unfortunately, the public never heard the straight story. Because margarine also contains saturated fat (made during the same hydrogenation process that generates trans fat), the food industry was handed the opening they needed to put an anti-saturated-fat spin on Keys’s findings. Ignoring the presence of trans fat (and other distorted fats in margarine), spokesmen simply blamed saturated fat. And on TV, Keys equated saturated fat with animal fat, completing the deception.235 This ingenious spin on the facts is akin to poisoning rats with strychnine-laced milk and then blaming the deaths on the milk.
The anti-saturated fat, anti-cholesterol ball was rolling along nicely, and there was so much money being made selling “healthy” low-cholesterol, low-fat processed foods, that the rolling ball wasn’t going to be easy to stop. All the news reports you’ve heard on the hazards of saturated fat and cholesterol are supported in large part by studies that evaluated the effects of hydrogenated vegetable oil, which is full of unnatural molecules that aren’t found in butter, steak, or any natural food.236
With so much junk science saturating the media, professionals who give nutritional advice need to go beyond the sound bites to discover the truth for themselves. While it’s easy to go with the flow and tell patients to “cut out animal fat,” doing so turns well-meaning healthcare practitioners into unwitting participants in an ongoing campaign to sell high profit-margin manmade substitutes for natural foods—substitutes which, in turn, make people sick.
In an earlier chapter, I suggested that our health took a turn for the worse when we stopped talking about food the way farmers and chefs do and adapted the language of scientists. The scientists are not the problem. The problem arises when we use scientific terms without a true understanding of what we’re saying. Case in point: the story I just told you about the media scaring us away from saturated fat coming from foods like butter and cream when the food in the studies actually was margarine and was, therefore, loaded with trans fats that only recently—fifty years down the road—we’ve learned are bad for our health.
These days we so frequently hear such terms as trans and polyunsaturated it’s easy to forget that those are chemical descriptions of compounds with specific types of molecular bonds and conformations—details most non-chemists wouldn’t be able to describe. So when the young man restocking salad dressing on grocery store shelves insists the dressing is healthy because it’s high in polyunsaturates, or your server at the local restaurant extols the merits of omega-3 in canola, it’s best to take this nutritional advice with a grain of salt. In 1961, when Ancel Keys brought national attention to lipids and their role in human health, he was hailed as Time magazine’s Man of the Year. In the sixty-plus years since the lipid discussion took center stage of the nutrition conversation, the heart-health cover stories have reflected a consistent fascination with fats, but they have delivered a completely inconsistent message: “Cholesterol: And Now the Bad News” was a cover story in 1984, arguing that eating cholesterol is bad for you.237 But by 2014, Time reported, in an article entitled “Ending the War on Fat,” that doctors were now suggesting butter is okay.238 What—or who—are we supposed to believe?
In my view we should only listen to the group of people who actually spend their careers studying fat: lipid scientists, who focus solely on learning more about various lipids (fats) and their respective roles in human health. In the decades we’ve been trying out different kinds of fats in different combinations—from Rip Essylstein’s near-zero fat, Engine 2 Diet, to the South Beach Diet (only fish and plant-based dietary fats), to Atkins’s emphasis on animal fats—the American public has never heard from a single lipid scientist. That’s a real shame, because lipid scientists have plenty to say on the matter. And because they know more on this topic than anyone else, what they have to tell you could save your life.
If there’s such a thing as a lipid science rock star, then I would consider Gerhard Spiteller to be something like Elvis Presley, Jim Morrison, and Mick Jagger rolled into one. This brilliant Austrian scientist has been quietly getting to the bottom of the role of fats in heart attacks for nearly half a century. A superstar among super-geeks whose resume includes teaching and research positions at MIT, Innsbruck, and other prestigious universities, he is lead author of over 130 published scientific articles. While other members of the lipid research community have studied and written extensively about lipid peroxidation and its potential role in arteriosclerosis, it was Dr. Spiteller, who, in his 2000 article, “Oxidation of Linoleic Acid in Low-Density Lipoprotein: An Important Event in Atherogenesis,” definitively points us in the right direction.239 In this meticulously researched article, Dr. Spiteller makes the case that it is processed polyunsaturated fats, not saturated fat or cholesterol, that deserve the blame for the stiffening of arteries throughout the body. (We’ll learn more about what polyunsaturated fats are, and where they come from, later in this chapter.)
I’m going to guess that until now you’d never heard of Dr. Spiteller. Lipid scientists, as a rule, don’t land their own TV shows. They are not asked to comment on the latest medical story on morning news programs. They do not wind up on the cover of Time or in any other mainstream magazine. Unlike living the life of a heart surgeon, or a brain surgeon, or a cardiologist, spending your career in a windowless lab studying fats isn’t likely to impress people at a dinner party. Let’s face it: for most us, “lipid scientist” is hardly synonymous with “sexy.”
This explains why the general public—even those who study nutrition and health—don’t usually get to hear what lipid scientists have to add to the nutrition dialogue, a conversation that, at least lately, largely concerns itself with the good-fat/bad-fat question. But what about other researchers and medical professionals? Surely, even the jocks of the medical world would take the time to acquaint themselves with the latest findings coming from those lipid researchers who know far more about how fats behave in the body than anyone else, right?
Wrong. By and large, the guy driving the Porsche Carrera to the surgical suite to thread another stent into another artery of another patient is almost guaranteed to be thirty years, or more, behind in his knowledge of nutrition and its role in the etiology of the arterial disease that, indirectly, paid for his house, his upcoming trip to Italy, and his children’s Ivy League college educations. In fact, by the time you’ve finished reading this chapter, it’s likely that you’ll know far more about the causes of heart disease than your local heart surgeon or cardiologist. You’ll understand what lipid scientists have been telling us—and what the research has supported for years—cholesterol and saturated fat are not your heart’s enemy; industrial fat products, the vegetable oils, are.
Industrial fat products like vegetable oils are toxic to your arteries because they contain delicate polyunsaturated fatty acids (PUFAs) that are particularly prone to oxidative damage, especially when exposed to heat and when separated from the antioxidants that would otherwise help protect them from that oxidative damage. I know, that’s nowhere near as catchy as “cholesterol clogs your arteries.” But it is what the research evidence supports.
So, as lipid scientists have long argued, I submit that natural fats and cholesterol have been a part of the human diet for millennia and are not the problem. The historically recent rise in arteriosclerosis and heart disease is the result of an historically recent invention of the food industry—refined, bleached, and deodorized vegetable oils. By revealing how certain fatty acids are changed by heating and processing, Dr. Spiteller offers us a chemically indisputable definition of good fats versus bad.
Over the rest of this chapter, I’ll discuss these concepts and show how eating heat-damaged fatty acids leads to plaque building up in your arteries. But first I want to show you the consequences of Keys’s pet theory, and why anyone who villifies saturated fat is helping to support both the sickness and the junk-food industries.
In the 1950s, Ancel Keys and others popularized the idea that fat clogs our arteries the way grease clogs the pipe under a kitchen sink. And although the vast majority of all available research tells us that this concept is no longer tenable, the medical community, by and large, insists on sticking to that story. True, over the years we’ve modified this model a bit, but the central idea is that somehow the body is flawed and unable to deal with natural fats. All of this comes from failing to appreciate the chemical sleight of hand that Dr. Keys pulled off when he described his experiments using the term saturated fat while referring to margarine—but everyone thought he was talking about butter.
Let’s take a moment to look at some of the ongoing consequences of this single misdirection.
Prior to Keys’s campaign, people ate far more saturated fat and cholesterol-rich foods than we do today, but heart attacks were so rare they were almost unheard of.240, 241 Over the past century, as butter consumption dropped to less than one quarter of what it was (from eighteen pounds per person per year to four), vegetable oil consumption went up five-fold (from eleven pounds per person per year to fifty-nine).242, 243 In 1900, heart disease was rare.244 By 1950, heart problems were killing more men than any other disease.245 Now, at the dawn of the second millennium, heart disease is the number-one cause of death in both men and women.246
Natural fat consumption: down. Processed fat consumption: up. Heart disease: up—way up. Forget for a moment what the “experts” are saying, and ask yourself what these trends suggest to your inner statistician. The next time you go to the grocery store, see how many foods you can find that don’t contain vegetable oil as an ingredient. What do you make of the fact that while watching TV at home, you catch a sixty-second health spot espousing the benefits of some low-cholesterol spread, followed by a commercial for a cholesterol drug, then another one for erectile dysfunction? What does this scenario say to the critical thinker in you?
What’s been dropping us like flies is not any upsurge in saturated fat consumption, but an upsurge in consumption of two major categories of pro-inflammatory foods: vegetable oils (a.k.a. unnatural fats) and sugar. Cutting both from your diet will not only protect your heart, it will help protect you from all chronic diseases.
To help you understand why it’s completely unscientific to blame natural fat for heart disease, I will appeal to your inner chemist, showing you why natural fats are beneficial. But first, I want to give you just a little bit of the history of these oils and tell you why vegetable oil has managed to work its way into nearly every product the majority of Americans eat every day. Food manufacturers use vegetable oils for the same reasons other manufacturers use plastic: it is easy to manipulate chemically, the public can be taught to ignore the consequences of its use, and best of all, it’s cheap.
In the late 1800s, Emperor Napoleon III offered a prize for a butter substitute to feed his army and “the lower classes.”247 The goal was a product that cost very little and wouldn’t rot on extended sea voyages. After some experimentation, a chemist named Hippolyte Mege-Mourie found that squeezing slabs of tallow under pressure extracted oily elements that fused into a solid when churned together with skim milk. The dull gray material had a pearly sheen and so Mege-Mourie called it margarine, after the Greek margarites, meaning “pearl.” It didn’t taste good, but it was cheap.
Not cheap enough for America, however. Raising, housing, feeding, breeding, and milking cows is an expensive enterprise compared to growing plants. By the turn of the century, chemists had found a way to reinvent the reinvented butter by starting with material nearer the bottom of the food chain: cottonseeds. There were sacks and sacks of them lying around without much use. In fact, the tiny black seeds were hard to store because, if left alone, they would ferment and make a terrible stink. Chemists recognized that odoriferous volatiles meant the oil was reacting with oxygen, and they smelled opportunity. The reactive nature of the oil meant that it had the potential to be chemically modified for a variety of purposes and, soon enough, they found a way to spin this worthless byproduct of the textile industry into solid gold. Thus began a happy relationship between chemists, farmers, and petroleum companies that continues to this day.
To make the liquid cottonseed oil more like butter, they needed to thicken it into a solid paste. Chemistry offered two options: either tangling bunches of oil molecules together or making the individual molecules less flexible and more stackable. The first option creates a primordial form of plastic, too inedible to pass off as food. So they chose the second option. They engineered a transformation of the fatty acids in the oil, ironing them almost flat with heat, pressure, hydrogen gas, and a nickel catalyst. The key to making the product appear edible was the catalyst, which prevented the molecules from tangling up into plastic. When the oils get squashed flat in this process, their double bonds change from the natural bent and flexible configuration to something stiffer. And thus, trans fat was born.
PARTIAL HYDROGENATION SQUASHES FATS FLAT
The chemical process of partially hydrogenating an unsaturated fatty acid may turn cis-shaped fatty acids into trans or convert the unsaturated bond into a saturated bond. Either outcome leads to a flatter shaped molecule with less fluid characteristics than the original cis-configuration, unsaturated fatty acid. Food manufacturers exploit this to make butter substitutes.
We call partially hydrogenated fatty acids trans fat after the type of bond that holds the carbon atoms together. Naturally occurring fatty acids contain bonds in a cis configuration. In this configuration, fatty acids are highly flexible, which prevents crystallization (solidification), and so the molecules behave as liquids. Partial hydrogenation does two things: it irons some cis-configuration bonds completely flat (by saturating the bond with hydrogen) and switches others around to trans. Converting a cis fatty acid to saturated or trans makes it a stiffer and more stackable molecule. This is why partially hydrogenated vegetable oils solidify like butter (which contains naturally stiff and stackable saturated fats). Cottolene was the first major brand to be successfully marketed in the United States, over a century ago. It didn’t taste quite like butter, but it was cheap. This process is still used to make “butter” for the “lower classes” today.
Now, most experts agree that consumption of inexpensive butter substitutes such as margarine and shortening is bad for our health. Nevertheless doctors are generally loathe to recommend butter to their patients. So what do people use instead? Some of the most dangerous food products in the store.
One of the fundamental concepts of this book is that physical beauty isn’t, as it turns out, in the eye of the beholder. Beautiful living things are the manifestations of the immutable laws of natural growth, rules grounded in mathematics. These rules apply everywhere, even at the molecular level.
Biomolecules, including fatty acids, cholesterol, and DNA, typically twist into either hexagonal or pentagonal configurations to facilitate their interaction with each other and with water. Processing distorts the fatty acids in vegetable oil so they can no longer assume the typical five- or six-sided geometry. Like Chinese finger traps, our enzymes pick up these distorted fatty acids and then can’t let them go, which hampers cellular function so profoundly it can kill your cells. And if you eat enough trans fats, cellular dysfunction will impair so many cells in so many tissues that the cumulative effects will disrupt basic functions (like blood circulation or your body’s ability to fight infection) and eventually kill you. Vegetable oils rarely kill children, but they can disrupt normal metabolism so profoundly that a child’s dynamic symmetry is lost, and their skeletal proportions become imbalanced.
No food represents such a full spectrum of molecules—from healthy to distorted and extremely toxic—as fat. Good fats are some of the best foods you can eat. And some of the healthiest, most robust people on the planet live in cultures whose diets are highly dependent on natural fats, like animal fat. But take those good-fat foods away and replace them with foods high in refined carbohydrates and distorted fats, and the same problems we have in our country begin to crop up around the world: weight gain, heart troubles, mood disorders, other chronic diseases, newborn children exhibiting organ and facial deformation, and other hallmarks of physical degeneration. So far, establishment medicine blames milk and meat. But I blame toxic, distorted fats (and sugar). Fortunately, the principle behind avoiding toxic, distorted fats is easy to remember: Eat natural fats and avoid processed ones. This formula works because nature doesn’t make bad fats; factories do.
| GOOD FATS AND BAD | |
| Good Fats These traditional fats can handle the heat involved in processing or cooking.
|
Bad Fats These industrial-era fats cannot handle the heat involved in processing or cooking.
|
The seductive flavors of fat-rich foods tempt us for good reason. Unlike sugar—which offers no nutrition—a meal complete with animal fat actually helps us absorb and taste other nutrients. This is why butter makes other foods taste so delicious.248, 249, 250, 251 And because animal fats contain cholesterol—a natural appetite suppressant—they satisfy in a way that little else can.252, 253, 254 In contrast, vegetable oils impair vitamin absorption and do little to suppress appetite, so you eat more and get less nutrition.255
When you worry about chemicals hidden in modern food, you might first think of monosodium glutamate (MSG), pesticide residues, and contaminants, like mercury. But compared to bad fats, those are small potatoes. Of all the dietary changes attending modernization, nothing compares to what we’ve done with fats and oils. Over the past one hundred years in the United States, our fat intake has gone from largely animal-based and natural to plant-based and so unnatural that our bodies can’t adapt. Thanks to Dr. Keys and his associates in industry, and also in the AMA, we have been tricked into questioning our own senses, convinced that our health depends on staying away from these once-prized sources of sustenance and allowing ourselves to be herded into buying tasteless, processed, “neutral” vegetable oils instead. Without even realizing it, we’ve traded in healthy fats for toxic ones, and now it’s making us sick.256
What do you suppose would have happened if, several decades ago, an unknown lipid scientist conclusively proved that an artificial fat molecule present in margarine, as well as all kinds of other products for sale in every grocery store in the country, was deadly, and was very likely causing disease, growth defects, and premature mortality? And what if that scientist had had the opportunity to present this public health information to Congress? Would Congress have responded? Would their corporate supporters—companies as powerful as Unilever, Monsanto, and ADM—have recalled the millions of products containing the toxin this scientist had discovered? Would they have halted their production lines, given up their subsidies and, if necessary, torn up millions of acres of corn which (no longer devoted to the production of margarine) would no longer be needed? Would they have abandoned margarine production and gone back to making real butter, trading in the cash cow of margarine products for actual, milk-producing cows? Or rather, would the corn product freight train roar straight through the scientist’s warnings, and even pick up speed as agribusiness marketing engineers frantically shoveled disinformation into the firebox?
We don’t have to guess at the answer, because there was such a scientist, and her findings were brought to Congress—way back in 1988—to warn of the dangers of trans fat, present in hydrogenated oils.257 We can only presume that the politicians who learned of Dr. Mary Enig’s research had little personal experience with cheap butter substitutes or the convenience foods that contain them. But the rest of us were eating plenty of the stuff and we continued to do so decades after Enig’s warnings because we had never heard them. Only after European countries outlawed trans fat did we finally hear that it might be bad for our health.
Why did it take the United States so long to take trans fat seriously? Earlier, I mentioned that scientific discoveries that are incompatible with commercial interests have a tough time making it to the papers. Trans is just one example. Cigarette smoking, another. Asbestos, another still. And I’m guessing that if there’s something you and your family might be eating every day that scientists already know is deadly, you’d like to know about it now, not thirty years from now. That’s why I’d like to tell you the truth about vegetable oil.
Vegetable oils contain mostly heat-sensitive polyunsaturated fats. When heated, these fragile fats turn into toxic compounds including trans fat.258 The heat sensitivity issue means that all processed vegetable oils, and all products that contain vegetable oil, necessarily contain trans fat. Canola oil degrades so rapidly that a testing company, needing to find the purest canola oil to use as a standard against which other oils could be compared, couldn’t locate any canola oil even from pharmaceutical-grade manufacturers with a trans fat content lower than 1.2 percent.259
This means that vegetable oil, and products made from vegetable oil, contain trans fat—even when the label seems to guarantee them trans free. But because heat so readily distorts their fatty acids, vegetable oil and products made from vegetable oil also contain something that is worse for us than trans. Before we get to that, I’d like to take a moment to compare and contrast the various fatty acids and their ability to handle heat.
FAT VERSUS OIL: WHAT’S THE DIFFERENCE?
Lipid is a generic term for both fats and oils. If the lipid is solid at room temperature, it’s called fat. If it’s liquid, it’s oil. Butter is solid, so it’s called a fat. In general, lipids made of stiff, inflexible saturated fats are solid and those made of fluid, flexible unsaturated fats are liquid. However, to describe butter (and other animal fat) as “saturated fat” is not strictly correct, because many fatty acids in butter are not saturated.
All storage fats (as opposed to fats in cell membranes and other actively functioning fats) exist in a chemical assemblage called a triglyceride. A triglyceride is made with three fatty acids that dangle like keys from a chain made out of glycerol, a short molecule to which each of the fatty acids is bound. The fatty acids can be any combination of saturated, monounsaturated, and polyunsaturated. Butter carries more saturated fatty acids in its triglyceride chains than vegetable oil, but not all are saturated fat. If they were, butter would be as stiff and solid as wax. Vegetable oil actually contains saturated fatty acids, but nowhere near as many as butter. The different blends of saturated and unsaturated combine to generate the final melting point of the fat.
WHY VEGETABLE OILS ARE PRONE TO OXIDATION
Polyunsaturated fats (PUFAs) have two or more double bonds, hence the “poly.” The two molecules shown here are the two most common PUFAs found in canola and other vegetable oils, linoleic and linolenic acid. If a fatty acid has two double bonds near one another, the molecule becomes highly susceptible to attack by oxygen, particularly when heated as in processing and cooking. If it has three double bonds near one another, as does linolenic acid, it’s even more vulnerable to an attack by oxygen. The products of these oxidation reactions are the damaged, distorted molecules that make vegetable oils so toxic.
For the purposes of cooking, we want to pick the kinds of fats that can take heat. On that count, saturated fats (present in butter, coconut oil, lard, and traditional fats) win hands down. Why? Because they can resist a kind of heat-related damage called oxidation. Thanks to their shape, saturated fats have no room for oxygen to squeeze in, and even high heat can’t force these tough molecules to be more accommodating. Monounsaturated fats have room for just one oxygen molecule to sneak in. But it’s not easy, so monounsaturated fat-rich olive oil resists the harmful oxygen-induced molecular rearrangements and is still okay to cook with. Polyunsaturated fat—now that’s another story. Polyunsaturated fat has two places where oxygen can chemically react, which makes oxygen not twice as likely to bind with the fat molecule, but billions of times more likely. This exponential increase in reactivity with oxygen is true of molecules generally, not just fats. TNT (trinitrotoluene) has six places where oxygen can react, making it so reactive it’s literally explosive! But we’re not cooking with explosives in our frying pans, are we? Actually, in a sense, we are, though on a slightly less dramatic scale. And it is those explosive oxidative reactions that we need to avoid.
The oils extracted from seeds that get processed into vegetable oils are composed primarily of polyunsaturated fatty acids, or PUFAs. If you want to remember which type of fatty acid most readily reacts with oxygen, just remember this: “PUFAs go Poof!”
Biology makes use of this reactivity. Enzymes in plants and animals fuse oxygen to polyunsaturated fats on purpose to change them from one shape to another. For example, fish oil isn’t anti-inflammatory per se. Enzymes in the human body oxidize the PUFAs in fish oil to convert them into specific compounds that turn off pro-inflammatory enzymes. But this mutability also means polyunsaturated fats are more capable of being accidentally altered, and thus heat is a threat to their utility.
Vegetable oil is the lipid extracted from corn, canola, soy, sunflower, cottonseed, safflower, rice bran, and grapeseed. Vegetable oil doesn’t come from broccoli, and it doesn’t equate to a serving of greens. It is found in almost all ready-made foods, from granola and squishy-soft baked goods, to rice milk and soy milk, to vegetarian cheese and meat substitutes, to frozen meals and side dishes, even salad dressings that say olive oil on the front label. I once purchased a package of dried cranberries only to discover, after I brought it home and read the label, that they were coated with vegetable oil.
There’s a reason these oils are particularly temperature sensitive. Seeds stay dormant over the cold winter. But come spring thaw, the heat-sensitive PUFAs wake up in response to warming, facilitating germination.260 To protect the PUFAs from damage as the ground warms and the sun’s rays beat down on them, the plant has loaded its seeds with antioxidants. Unfortunately, refining these oils ultimately destroys both healthy PUFAs and their complementary antioxidants, converting them into distorted, unhealthy molecules. So what was once healthy in the seed isn’t healthy in the bottle.
When I advise my patients to avoid vegetable oils, they often tell me that they only use canola oil, as if it were somehow exempt. I can’t blame them for thinking this; the canola industry goes to great lengths to present their product as heart healthy, and the American Heart Association plays right along. They claim that canola oil is rich in anti-inflammatory omega-3 essential fats. And there’s a grain—I should say seed—of truth to that claim. There’s just one problem: omega-3 is a PUFA, which means it is easily distorted when exposed to heat. And since the omega-3 in canola seeds has three places for oxygen to react, it’s really, really reactive. Canola oil still in the seed may indeed be full of omega-3, but factory-processed canola oil, even organic-expeller-pressed, contains mutated, oxidized, heat-damaged versions of once-healthy fats.261 Canola consumption has been shown to cause the same health problems as the rest of the vegetable oils.262, 263 If we could somehow get canola oil out of the seed without exposing it to heat, it would be good for us. But nobody can.
Well, that’s not entirely true. In the old days, flax and rapeseed (a relative of canola) were gently extracted in the home using a small wedge press. Over the course of a day, the wedge would be tapped into the press a little further until, ever so slowly, the golden oil would start to drip, fresh and full of natural antioxidants and vitamins. These oils were not used to fry food, and therefore never exposed to damaging heat. If you aren’t up for installing a wedge press in your kitchen, a few small enterprises can provide flax, hemp, and other healthy omega-3 rich oils—none of which should ever be used for cooking.
If we took a stethoscope and placed it to the side of a giant factory press as it applied more and more intense heat and pressure to a batch of tiny oil seeds, we might very well hear muffled cries indicating that, rather than being treated like little ambassadors of a heart-healthy diet, the seeds were being processed and refined like so much machine oil. In fact, one of the initial steps in making vegetable oil involves the use of hexane, a component of gasoline. If you were to get up close and catch the stench of the initial extract, you might never imagine it could be cleaned up. Making these stinky oils palatable requires a degree in chemical engineering; it takes twenty or so additional stages to bleach and deodorize the dark, gunky muck. And don’t be fooled by so-called health products containing “expeller-pressed” oil; that only means the manufacturer didn’t use solvents to maximize extraction. Organic, expeller-pressed oil has gone through all the usual hazardous steps in the process of being “refined.”
Olive oil, palm oil, and other oils that are good for us (see here) have mostly saturated and monounsaturated fatty acids, which are not so fragile. They are also easily extracted at low temperatures. Vegetable oils come out less readily, and are more prone to side reactions that polymerize and mutate the fat molecules. So getting them out creates a witch’s brew of toxic lipids, only some of which will be removed. The rest, you eat.
Chemical analysis shows that even bottles of organic, expeller-pressed canola oil contain as much as 5 percent trans fats, plus cyclic hydrocarbons (carcinogens) and oxyphytosterols (highly damaging to arteries).264 Of course, natural fats are all okay before they’re processed and refined, so there’s no harm in eating corn, soybeans, sunflower, and other tasty seeds.
Maybe 5 percent trans (and other mutant fats) doesn’t sound that scary. The real trouble is not so much that there’s bad fat in the bottles (and other products). The real trouble has to do with the fact that after you eat these distorted, mutated fatty acids, they can reproduce inside you.
Imagine a zombie movie, filmed at the molecular level, except the mutant fatties don’t stumble through your bloodstream in slow motion. Using free radicals (defined in the next section), mutated PUFAs convert normal fatty acids into fellow ghouls at the rate of billions per second.265 I call this conversion-on-contact the zombie effect because, as every horror-movie connoisseur knows, when a zombie bites you, you become one of them. When a throng of molecular miscreants starts hacking away at your cells, things can really get scary. Their ability to damage normal PUFAs makes this class of oxidized PUFAs more dangerous than the trans fat we’ve all heard about on the news. Since they’re a lot like trans, only worse, I call them MegaTrans.
There are many technical names for MegaTrans, including peroxidized fats, lipoxygenases, oxidized fat, lipid peroxides, lipid hydroperoxides, and a few others. Think of them all as different gangs of bad fats. While some of these toxic fats are in the trans configuration and others aren’t, that’s not the point. The point is these toxic fats are all gangsters with one thing in common: they’re really bad for you. They contaminate all foods with trans fat and, in fact, all foods made from vegetable oils. They’re bad because they lead to the formation of free radicals, which not only turn normal polyunsaturated fatty acids into mutants, but can also damage almost any part of your body: cell membranes, chromosomes, other fats—you name it.
Free radicals are high-energy electrons that are involved in every known disease. They cause disease by restructuring nearly every molecule they come into contact with, converting biologically functional molecules into dysfunctional or even toxic molecules. Why would they do this? After all, the human body sometimes employs free radicals in order to perform basic physiologic functions like killing bacteria. It all boils down to a kind of loneliness—at the atomic level.
Imagine a set of neighboring molecules in your cell membranes as a village of polyamorous communes in the middle of a forest in Upstate New York. The electrons who are the members of these communes agree on one rule: we must always maintain an even number of members so that no one electron will ever feel left out; everyone should have a partner. Now imagine a circumstance where one electron decides to pursue an acting career and clears out one night without notice. Immediately, the unpaired electron it left behind goes berserk, racing through the halls of the commune, busting down doors, breaking walls, and completely disturbing the commune’s essential structure as it desperately seeks out a new lover. The unpaired electron has been (free) radicalized—turned into a free radical. This commune now has two serious problems. One, it’s no longer the commune that it once was; it’s been beaten up and rendered entirely unrecognizable. And two, because it’s breaking the cardinal even-number rule it has to do something about it. It chooses to solve the problem by passing the abandoned lover electron to another commune, and letting them deal with the consequences.
FRENCH-FRIED HEART
This dissected artery shows some fatty deposits, but of far greater concern is the effect MegaTrans has had on the arterial wall as free radical cascades have literally fried the arterial tissue. The artery and surrounding heart muscle are greasy and fragile, much like crispy fried food. When that fragile tissue tears and bleeds into the artery, it creates a clot. That’s a heart attack.
HOW FREE RADICALS DAMAGE MEMBRANES
This is a closeup view of a cell membrane under attack. This particular section of membrane is composed of PUFAs. (The insert in the upper right is a cross-section of the same membrane.) Once the radical strips an electron from one of the PUFAs, it initiates a cascade reaction across the membrane, releasing more damaging unpaired electrons. In addition to mangling and distortion membrane PUFAs, the cascade reaction can damage hormone receptors, nutrient channels, and other proteins in the membrane, disrupting membrane function and putting the entire cell at risk.
Those consequences are predictable. Whether the newly introduced electron ousts another lover from his bed or fails to find anyone willing to partner with him, in no time commune number two will have to deal with a lonely electron knocking down walls and wreaking havoc and forcing the commune members to hold an emergency meeting. Until such time that a patchouli-wearing therapist antioxidant, such as the totally groovy vitamin E, shows up to say, “Whoa, dudes. I’ll take your extra lover … it’s all good … I’ve got another therapist friend I work with called vitamin C and, like, the whole even-number lovers thing will be, like, totally restored,” this chaotic process will continue, leaving each and every affected commune permanently changed—and not for the better.
Chemists call this series of reactions a free radical cascade. Free radical cascades damage normal PUFAs, turning them into ugly molecular ghouls (the zombie effect). Just a little MegaTrans in the bottle of canola oil can become a lot of MegaTrans after you—or the cereal/donut/frozen dinner manufacturers—cook with it. On the plus side, free radical cascades make your food extremely crispy. (Free radical cascades also happen to play a role in the polymerization reactions that make plastic solid. This is probably the origin of the well-intentioned, but not strictly scientific, assertion that “margarine is one molecule away from plastic.”) On the minus side, free radical cascades make your arteries extremely crispy. They will also damage other bodily tissues, which can generate inflammation, a kind of chemical chaos that interferes with normal metabolic function.
In the frying pan, MegaTrans reacts with oxygen to generate one free radical after another. Frying in vegetable oils doesn’t so much cook your foods as blast them with free radicals—fusing molecules together to make the material stiff and inflexible.
WHY MEN GET HEART ATTACKS BEFORE WOMEN
Men get heart attacks ten to fifteen years on average before women. Why would that be? The only explanation cardiologists offer is that “women are just more perfect organisms.”266 While I tend to agree, I also believe there’s more to the story. The real reason is that men have more testosterone, which makes them produce more red blood cells, so that men also have more iron in their blood.267
Iron acts as an accelerant, activating oxygen in ways that make it more likely to damage the linoleic acid and other fragile PUFAs traveling in lipoproteins right alongside iron-rich red blood cells.268 Does this mean men are doomed to get heart attacks? Of course not! Aside from cutting vegetable oil, eating plenty of antioxidant-rich fresh vegetables will slow the reaction between iron and PUFA fats, rendering them less explosive and preventing the process of lipid deposition inside a person’s arteries.269, 270
HOW CAN SOMETHING SO BAD TASTE SO GOOD?
If fast food fries and other crispy treats are so awful, why would nature allow them to tempt our tongues so tantalizingly?
Fast-food flavors are not real. Were they not doped with MSG, sugar, and other chemicals, you’d realize how flat those curly fries and meat nuggets taste. They’re crispy, yes, but they lack flavor complexity. What happened? Processing and cooking with vegetable oil destroys complex nutrients and deadens flavors. (Flavor ligands become fused, rendering them either unrecognizable or too large to fit into your taste bud receptors.) You can get all the tangy, zesty, savoriness that you love in fast food from traditional cooking methods that enhance food flavors naturally by making nutrients more bioavailable.
Traditional cooking methods often make nutrients more bioavailable and are, for that reason, anti-inflammatory. Cooking with vegetable oil, on the other hand, destroys complex nutrients. So aside from the fact that foods cooked in vegetable oil will deposit loads of “zombie” fats into your tissues where they can, with little provocation, blast your tissues with free radicals, foods cooked with vegetable oils will also carry fewer vitamins and antioxidants than foods cooked using traditional methods and better oils.271
Free radicals can fry your cell membranes, damaging your arteries and, as I suggested earlier, eating foods fried in vegetable oil may very well precipitate a heart attack. But something happens before you have a full-blown heart attack: your arteries stop responding to normal body stresses. It’s called abnormal endothelial function. And there’s a test for it.
In 1999, a team of lipid scientists in New Zealand wanted to see what eating deep-fried food does to our arteries in the short term. They planned to feed subjects french fries and then test them to see if their blood vessels were still able to regulate blood flow normally (this ability is called endothelial function). The test is performed by slipping the patient’s arm into a blood pressure cuff, then squeezing it to cut off the blood flow for a few minutes. Normally, on releasing the cuff again, the oxygen-starved arteries open wider so blood can come rushing back in, just like you would suck in more air after holding your breath for a while. This dilation response depends on the endothelial cells lining the blood vessels which have to be healthy enough to generate the nitric oxide that makes arteries dilate. If endothelial cells can’t make nitric oxide, or if the nitric oxide they make gets destroyed too soon, a person’s circulatory system can’t work correctly.
Male sexual function depends on healthy endothelial function, for reasons that pertain to arterial dilation and the obvious tissue expansion facilitated by such dilation. What may be less obvious is, if a person has erectile dysfunction (ED), they (most likely) have endothelial dysfunction, meaning their health problems extend beyond the bedroom. Specialized centers can perform an endothelial function test on anyone. This easy test tells your doctor how healthy your arteries are and how readily they can deliver blood in response to exercise or other activities.
The scientists in New Zealand acquired week-old frying oil (rich in MegaTrans) from a typical restaurant and made a batch of fries. Four hours after study subjects ate the fries, they slipped their arms into blood pressure cuffs to test their endothelial function. The effect of the oil was unmistakable. Before the fries, the subjects’ arteries had dilated normally, opening 7 percent wider. Afterward, there was almost no dilation—barely one percent.272
(You might be wondering if the results were affected because the scientists used week-old frying oil. Well, the truth is, although law requires that fryer oil be replaced weekly, lots of restaurants use the same oil for more than a week. One restaurant owner told me of a new oil that extends this time to two weeks or even longer.273 So we have to believe that the week-old oil used in the study was, like it or not, a good example of what our fries are cooked in when we order them at a restaurant.)
What this test tells us is that after eating food fried in vegetable oil, your blood vessels won’t work right. You may feel lethargic. Men may suffer from temporary ED. As the authors point out, exercising after a fast food meal will also stress your heart.274 Why? MegaTrans free radicals attack the nitric oxide signal that arteries send when they sense oxygen levels are low. Without that signal, your muscles don’t get the oxygen they need. The most active muscles will be the most affected—and your heart is always active.
Men with ED have sick endothelial cells that can’t generate normal amounts of nitric oxide. Viagra works by helping sick endothelial cells in the penile arteries generate nitric oxide as if they were healthy. Nasty frying oil temporarily inhibits that ability. You could call it anti-Viagra. But listen up, boys: if you keep eating foods made with vegetable oil (especially if you also eat too much sugar), you’ll damage those endothelial cells so much that even Viagra won’t work anymore.
The New Zealand study was performed on young people with healthy arteries, but what might happen to a person whose arteries are older, or already damaged? After reading the study, I started asking patients admitted to the hospital for heart attacks what they’d eaten last. So far, everyone has told me they ate something fried in vegetable oil. One Japanese man had eaten fried fish, which goes to show you: the use of vegetable oil can turn an otherwise healthy meal into a 911 emergency. That winded feeling you get when you try to exercise may be a sign that you are just out of shape. But it may mean that MegaTrans has already damaged your arteries.
An endothelial function test will tell you something about the health of your arteries. But there’s an easier way to determine whether or not they’ve been damaged. If you’ve been eating vegetable oil and sugar-rich foods, you can be certain they have. Some people want proof, of course. It’s like spending money: some of us know when we’ve been spending more cash than we’re bringing in, and others of us have to look at that bank statement to confirm the bad news. So if you can’t get an endothelial function test, but you still want to test the condition of your blood vessels, there are several other things you can do.
One is to have your doctor check your fasting blood sugar level. If it’s 89 or higher, you may have prediabetes, a condition in which your cell membranes have become too rigid to take in glucose as fast as they normally could. (This often leads to insulin resistance and full-blown diabetes.) And what makes cell membranes stiff? MegaTrans-instigated free radical damage, nutrient deficiency, and sugar. It’s also not a bad idea to check your blood pressure. Normal levels range from 80 to 120 over 50 to 75. Higher than 130/80 (while relaxed) can indicate abnormal endothelial function. You can also get a test of your liver enzymes. Elevated liver enzymes occur when MegaTrans explosions damage liver cells. Finally, you can get a cholesterol test. But ordering the right test and then interpreting the test correctly requires some knowledge of the way fats circulate through your body, a physiologic function I call the lipid cycle.
The lipid cycle describes the process by which fats are packaged into particles that travel through your bloodstream in order to be delivered to various body tissues that either make immediate use of them or store them for later.
Your body needs to control and regulate every nutrient in your diet. For example, regulating calcium involves vitamins D, K2, and A and hormones estrogen, testosterone, and calcitriol, among others. To keep your blood sugar in range, the body requires insulin, glucagon, growth hormone, and leptin, among others. And to keep your sodium balanced, the body requires hormones aldosterone, renin, and angiotensin, among others. Meanwhile, your body also needs to regulate things like oxygen and carbon dioxide levels, temperature, pH, and hydration. And this is just the tip of the iceberg. Your body is the ultimate multitasking expert, and, to keep everything coordinated, your cells are designed to be absolute control freaks.
Doctors go to school to learn about these and other precision control systems that enable our body’s cells to work together and put nutrients to best use. But for some reason, it doesn’t dawn on most of us that the body would have systems in place for controlling fat and cholesterol utilization as well. Instead, we allow ourselves to be led to believe that keeping fat and cholesterol out of our bloodstream almost entirely, using extremely restrictive diets or drugs, is the best way to prevent heart attacks.
I prefer to understand the methods by which the body controls where fats and cholesterol go. To that end, I’d like to show you the model I’ve created from the best currently available evidence that shows how the body safely ferries dietary fat (from natural sources) through the bloodstream, just as it does with every other nutrient. And I’d like to help you avoid those elements of a modern diet that disrupt your body’s ability to control these nutrients, thus increasing your risk for arterial disease.
If you eat like the average American, somewhere around 30 percent of your dietary calories probably come from fats.275 After your food is broken down by enzymes in the intestine, the fat and most other nutrients get absorbed into intestinal cells (called enterocytes). Here, fat and fat-soluble nutrients are prepared for circulation through the bloodstream. You can eat all the fat and cholesterol you want, and none of it will get into your arteries without first being wrapped inside a special layer of protein. When they’re working as designed, the special proteins suspend all the fats inside them in the solution of our bloodstream, and this is what prevents dietary fat from clogging our arteries. The resulting little blobs of fat wrapped in protein are called lipoproteins.
Lipoproteins are designed rather like microscopic M&Ms. Just as the candy’s coating prevents the chocolate inside it from getting all over your hands, the protein coat enables lipoproteins to circulate throughout your body without getting their messy insides smeared on your arterial walls. Of course, lipoproteins don’t carry chocolate. If your diet is healthy, your lipoproteins are full of essential nutrients—all kinds of good stuff.
LIPOPROTEINS: SUPERHEROES OF LIPID CIRCULATION
Lipoproteins have two essential parts, like an M&M: an outer coating (made of proteins called apoproteins), and soft, yummy insides (made of fat, called the lipid core). The apoproteins serve a little like address labels on a parcel, directing the lipoprotein to deliver its goods to the tissues that need them the most.
When intestinal cells are preparing the lipids from your last meal for entry into the bloodstream, they don’t throw just any old kind of protein over the fats, kick the little particle out into circulation, and say, “Good luck!” The cells of our bodies must be able to recognize lipoproteins as sources of fatty nutrients. So the protein coating (called an apoprotein) also serves as a kind of barcode describing the particle’s origin and contents.
Lipoproteins made in the intestine are called chylomicrons. They contain some cholesterol, but mostly they contain triglycerides, other fatty nutrients (like lecithin, choline, omega-3 and omega-6, and phospholipids), varying amounts of fat-soluble vitamins, and antioxidants. Other tissues that participate in the lipid cycle make other types of lipoproteins, all with the same general design: a blob of fat wrapped in protein.276
LIPOPROTEINS: THE GOOD AND BAD
The LDL and HDL your doctor talks to you about refers to two types of lipoproteins: low-density lipoprotein and high-density lipoprotein. During such discussions, you’ll typically hear that LDL is “bad” and too much will damage your arteries, and that HDL is “good” and cleans your arteries. These characterizations are inaccurate. LDL, HDL and other lipoproteins (chylomicrons, VLDL and IDL) each play important roles in making sure the fat-soluble nutrition from your food gets distributed correctly.
As with any package delivery service, the accuracy of this labeling system is critical to the success of the whole delivery process. If anything were to damage the label (we’ll return to this idea soon), the lipoprotein would fail to carry out its function, and the whole system would be thrown out of whack.
After the packaged lipoprotein leaves an intestinal cell, it travels through the bloodstream for several hours, completing many circuits. As it floats along, it deposits its fatty nutrients into the tissues that need them most.
Hungry tissues get fed by signaling endothelial cells lining their smallest blood vessels to place special proteins on their surface, which act like tiny fishing rods set to snag lipoproteins as they float by. Once snagged, the particle may unload some of its payload into the endothelial cell or, alternatively, the endothelial cell may open up a tunnel-like structure right through its center to allow the lipoprotein to pass from the bloodstream, through the endothelial cell, and directly into the hungry tissues.
Hours after a meal, the amount of fat in circulation drops as lipoproteins either exit circulation or give up their fat and shrink (gradually decreasing in size and increasing in density as they travel). Eventually, the liver picks up the shrunken, high-density remnants and sorts through the contents to recycle anything useful while discarding any waste. Unwanted or damaged fats exit by way of the liver’s bile system back into the intestinal tract for disposal.
The lipid cycle can take any of several different routes. Fats can enter the circulation by way of the intestine (as lipoproteins called chylomicrons) or by way of the liver, or even by way of the fat under your skin. There are actually multiple points of entry, and even the brain may participate. The fats can exit the cycle by being transported into a hungry cell anywhere in the body, or by being exported out of the body through the liver’s bile system. The liver is like a transfer station. It sorts through the incoming lipoproteins to separate the good fats from the bad. When it has collected enough good fats, the liver fashions its own lipoproteins (called VLDL, for “very low density lipoprotein”), complete with new identifying labels, and sends them back into the bloodstream again. These particles go through another arm of the cycle, following the same series of steps, delivering cargo piecemeal or transporting it to a final destination intact. Those particles that deliver cargo piecemeal eventually get small enough to be picked up by the liver again, where they will be disassembled and their fats either discarded or recycled once more.
One loop of the lipid cycle starts in the intestine and distributes lipids you just ate. Another starts in the liver and distributes lipoproteins your liver made. And a third loop starts in the periphery—that is, the rest of the body—and distributes lipoproteins made by the skin, brain, and other organs. Each of the three sources (intestine, liver, and periphery) manufactures its own brand of lipoproteins complete with its own proprietary labels.
The lipid cycle is an amazingly efficient system that allows cells to order up the delivery of fatty nutrients. It functions a little like Uber, the on-demand transportation service.
Here’s how. Say, for example, a brain cell (named Fred) needs more omega-3 fatty acid. No problem! Like a passenger using the Uber app to request a nearby driver, Fred the brain cell makes a request that one of the circulating lipoproteins stop by and deliver omega-3. Fred does this by releasing a stream of a specific type of apoprotein called APO E into the bloodstream. Soon enough, one or more of the APO Es Fred released will encounter one or more of the body’s fat-rich lipoproteins. When they meet, APO E inserts itself into a lipoprotein particle (one APO E per particle) and can now serve to direct the particle back to Fred, waiting patiently in the brain.
The APO E need not give the nutrient-carrying lipoprotein specific directions on how to find Fred in order to serve its purpose. Instead, because the APO E acts as a little handle sticking out of the lipoprotein it’s riding in, it simply waits to circulate through the brain, where Fred, waiting with open arms (a receptor for APO E on his surface) will be able to grab the lipoprotein particle by its inserted APO E as it floats by.
Once Fred the brain cell has retrieved the APO E, he can help himself to all the omega-3 and whatever other fats might be on offer in the particle, and then release the lipoprotein back into circulation.
Of course, other cells in the brain (or elsewhere) may be requesting omega-3 (or other fatty nutrients) at the same time using the system. Unlike Uber, where a driver is assigned to you specifically, this is a first-come first-serve system, and other cells can poach Fred’s APO E before it ever gets back to him. But the body works as a cooperative unit and eventually another APO E containing particle (with APO E perhaps made by another cell) will float by Fred to deliver the omega-3 he ordered.
As efficient as this system is, it has one important vulnerability. The APO E lacks the ability to distinguish good fats from bad. So if a person’s diet is loaded with MegaTrans fat, their lipoproteins will be too—and that’s what Fred will get delivered to him, whether he likes it or not.
Obviously, this intricate and ancient internal fat-distribution system is amazing and complex. And I don’t mean to imply, by describing it to you, that I know everything about the way it works. I don’t. But let me tell you a secret: neither do the drug manufacturers who tell us we need to get our LDL numbers down, and they have just the pill to do it.
When everything works properly, when all the connections are made without a hitch, your arteries stay wide open, pretty, pink, and clean. But when the system breaks down and the connections can’t be made, the lipoproteins can’t exit the bloodstream, your cholesterol numbers may climb, and the particles eventually break apart, dumping their contents into the bloodstream, where they damage epithelial cells. Repeat this process over and over, and the accumulating lipids give your arteries a yellowish, irregular, lumpy appearance that is conspicuously unhealthy (see the illustration). This is the disease we call atherosclerosis.
Atherosclerosis refers to hardening of the arteries. It is the diagnosis doctors give you when you’ve got plaque building up in your circulatory system. When your diet disrupts your lipid cycle and fats don’t get where they need to go, your cholesterol numbers will often start to go out of whack. Your LDL can go up, and your HDL can go down. Neither is good, as they are both warning signs that damaged lipoproteins may be damaging your blood vessels.
The key concept here is that the underlying problem—the reason your numbers go out of whack—is not eating too much cholesterol or saturated fat. It’s eating foods that disrupt the lipid cycle. So the real secret to preventing (and reversing) heart disease is avoiding foods that disrupt the lipid cycle.
What are those cycle-disrupting foods? You guessed it: foods rich in vegetable oils (and sugary foods as well). These foods disrupt the lipid cycle by damaging the very fragile proteins on their surfaces, the apolipoproteins, which serve to help direct the particles during their journey through the lipid cycle.
HOW I INTERPRET A STANDARD LIPID PANEL
The best test available to gauge the health of your lipid cycle is a properly interpreted particle size test (see here). If you can’t afford this test, you can still get a lot of information from a standard test. Here’s how I interpret the results:
Your cholesterol profile contains four different numbers: total cholesterol, LDL, HDL, and a triglyceride value. The two numbers I’m most interested in are the triglyceride and HDL levels. HDL should be over 45 in men and over 50 in women (I’ve seen it as high as 108). I like to see LDL less than three times the HDL value. This ratio, together with triglyceride levels less than 150, tell me a person’s fat-distribution system, lipoproteins, and diet are healthy. I don’t worry about a high total cholesterol number if the ratio of LDL to HDL is within an acceptable range. On the other hand, if triglycerides are above 150 and/or the HDL level is below 40, it’s very likely that your lipoprotein cycle is disrupted.
Let’s take a closer look.
As we saw in the figure here entitled “Lipoproteins: Superheroes of Lipid Circulation,” the apoprotein, the protein layer encasing the round lipoprotein shown in the picture, serves as a kind of address label that helps to ensure that the particle’s contents end up someplace useful in the body. I believe the key to preventing and reversing heart diseases lies in this idea: damage to those lipoproteins’ labels disrupts the lipid cycle, which, ultimately, leads to atherosclerosis.
HOW DYSFUNCTIONAL LIPOPROTEINS CAUSE ATHEROSCLEROSIS
The endothelial cell on the right is worried because naked oxidized fats from degraded lipoproteins are landing on him and oxidizing his membrane PUFAs. PUFA oxidation can disrupt cell metabolism or even kill the cell (see “How Free Radicals Damage Cell Membranes”). When this kind of damage affects many endothelial cells, it can lead to the first state of atherosclerosis, called “The Fatty Streak.”
To better understand how damaged lipoprotein labels can cause such disruption, imagine a six-year-old girl traveling back and forth across the country by plane between the homes of her divorced mom and dad. Suppose that this young child is traveling unchaperoned and carries an identification tag on a string around her neck displaying her name, the addresses of both parents, and contact information. If the receiving parent wasn’t at the airport, this tag would enable airport officials to know who she was, where she was coming from, and where she needed to go. But if the tag were to get damaged so that the words became unintelligible, she’d be lost.
If your lipoprotein particles have their labels damaged, they can get lost, too. Like vagrant children hopelessly tugging the shirtsleeves of every stranger they see, lipoproteins missing proper identification are given the cold shoulder from cells unable to recognize them. These orphaned lipoproteins float aimlessly through the bloodstream, begin to disintegrate, and ultimately collect onto the lining of your arteries (see illustration on the opposite page), where they cause problems.
What damages lipoprotein labels? One of the most important factors appears to be vegetable oil. Since 1977, lipid scientists have been writing about linoleic acid oxidation in lipoproteins. Citing articles published that year and in the 1980s by himself and by others, Dr. Spiteller, the Austrian lipid scientist, writes, “Oxidatively modified LDL is no longer recognized by the LDL receptor.”277 And how does LDL get oxidatively modified? MegaTrans fat generates free radicals that char the lipoprotein’s surface, rendering it unrecognizable by the LDL receptor. The more MegaTrans-rich vegetable oil you eat, and the worse your diet in general—low in antioxidants and particularly low in naturally occurring vitamin E—the faster the LDL label (the apoprotein coat by which each LDL particle is identified) gets oxidized.278, 279
Another factor that damages lipoprotein labels is sugar. As I’ll discuss in Chapter 9, sugar adheres to things by a process called glycation. Over time, this stiffens cell membranes, leading to prediabetes and consistently elevated blood sugar levels. Whenever blood sugar levels are high, it creates an opportunity for sugar to gum up the protein labels on your lipoprotein particles. And that’s a problem.
In 1988, researchers working in Lyon, France, discovered that when the labels on HDL particles got jammed up with sugar, they simply fell off.280 The study was done in a test tube, where the denuded HDL particles adhered to the glass. In your body, the naked fat would be exposed to blood. That’s no good, and I’ll explain why below. First let me point out that one of the common findings in diabetic patients is a low HDL level. One possible explanation is that the excessive sugar in their blood has knocked the coats off their HDL, and the naked particles have fallen out of circulation.
EATING MORE FAT CAN MAKE LDL CHOLESTEROL GO UP, AND WHAT TO DO IF IT DOES
You might be thinking, “You had me at butter.” However, the reality is, eating more fat can sometimes make LDL cholesterol go up, whether it’s healthy fat or not. How your body responds to adding fats into your diet depends on many factors, including activity, age, sex, hormones like insulin, leptin, thyroid, cortisol, and whether or not you’re simply eating too much. So it’s difficult to predict what will happen to your LDL until you run the experiment.
I don’t see LDL as a bad thing. What I worry about is whether or not your body is able to control where fats and cholesterol in LDL will end up, and thus successfully prevent the particle and its contents from depositing inside your arteries. However, when most doctors see LDL cholesterol going up they consider this a red flag indicating that their patient either needs to change his diet or needs to take a cholesterol pill, or both. If your doctor thinks your diet is a problem and you disagree, then the conversation around your LDL can cause you unnecessary stress. I’d like to help prepare you for that conversation beforehand by teaching you about the test I use to determine if your body has lost control of its lipoproteins (see here).
And what does sugar do to LDL? In 1990, another experiment investigated just that. This time, the labels didn’t fall off, but rather became so deranged as to be illegible and unrecognizable to hungry cells.281 As a result, these sugar-encrusted (glycated) LDL particles stayed in circulation too long, which would explain why some diabetics have high LDL levels: with so many undeliverable LDL packages floating around, they just start adding up.282, 283 (When LDL levels are high because of glycation, then high LDL is a problem, as we’ll see.)
Most prediabetics and diabetics have high triglyceride levels. High triglycerides suggest a serious problem with all the lipoproteins in your body. Triglyceride is not a lipoprotein, it is a component of all lipoproteins. Triglycerides are carried in both LDL and HDL particles. But the vast majority of triglyceride is carried by chylomicrons (the lipoprotein particles your gut makes right after a meal) and very low-density lipoproteins (VLDL), which your liver makes from recycled fats. These plump nutrient carriers want to deliver their cargo into your hungry cells. But, like all lipoproteins, they can’t do the job all alone. They need a special enzyme—think of it as a dock worker—to pick the fatty acids up and carry them into the cell. A study done in 1990 showed that sugar interferes with the function of this enzyme.284 So if you have high blood sugar, that sugar may shred the lipoprotein coats beyond recognition, or simply rip them off the particles’ backs. If the particles ever do make it to a cellular dock, sugar keeps them from completing the delivery. With so many barriers to getting nutrition into hungry cells, it’s no wonder people with diabetes feel hungry all the time.
WHY LOWERING LDL DOESN’T DO MUCH TO PREVENT HEART DISEASE: IT’S NOT THE TRUCK—IT’S THE CARGO
Getting your LDL down well below average—to, say, 70—still leaves you with very nearly the same risk of heart attack you’d have at an LDL of 150.285 Your risk goes down, but very little. For example, if your risk of heart attack is 20 percent when your LDL is 150, cutting that number to under 70 will drop your risk down to roughly 15 percent. Meanwhile, your risk of cancer,286 infections,287 depression,288 anxiety,289 hemorrhagic stroke (bleeding in the brain)290 and dying (if you have severe kidney disease)291 all go up significantly. In the decades before pharmaceutical companies created the blockbuster class of cholesterol lowering drugs called statins, doctors didn’t pay much attention to LDL.
What they looked at was HDL, the so-called “good” cholesterol, because statistical evidence showed high HDL correlated with a very low risk of heart attack.292 Get your HDL up to 60, and even if your risk of heart disease was previously a whopping 20 percent, you’ve just slashed your risk to less than 2 percent. Meanwhile, your risk of those above named diseases also goes down. Pretty good deal, huh? (By the way, if your HDL is low and you follow the Human Diet outlined in Chapter 13, you will almost certainly see your HDL climb within three months.)
The online risk calculators cardiologists use (and you can use, too) to determine your chances of heart attack don’t even ask for your LDL level.293 So why do we talk about LDL at all? You probably already know the answer. There’s no drug to raise HDL but there are drugs to lower LDL: the statins (Lipitor, Zocor, Crestor, Vytorin, and their generic equivalents). If you sell one of these drugs, and you can use statistics and sleight of hand to convince people that getting LDL down is the strategy for living a longer life, you’re spinning straw into gold.
While researchers funded by pharmaceutical corporations have been busy trying to produce evidence condemning LDL, a particle that’s been with us for as long as we’ve been human, lipid scientists like our “rock star” scientist Dr. Spiteller have been performing a chemical inspection of the cargo carried inside LDL and other nutrient-carrying lipoproteins. This investigation has enabled us to gain insights into what’s really causing heart attacks.
As an analogy, you could say that the researchers for pharmaceutical corporations are like investigators who, following a terrorist attack in which a government building was blown up, focused all their attention on the truck that blew everything up: Are yellow trucks somehow uniquely explosive? Is it the size of the truck that made it detonate? Dr. Spiteller chose a different avenue of inquiry: What if we consider what the vehicle is carrying? Maybe it’s not the vehicle itself but, rather, its cargo. Maybe it’s not the truck that’s so dangerous but the hundreds of pounds of explosive petrochemical fertilizer and diesel fuel inside it!
Dr. Spiteller focused his investigation on the most prevalent PUFA in all vegetable oils—linoleic acid, a kind of omega-6.294 His interest in linoleic acid was piqued because, as a lipid scientist, he understood how easily linoleic acid oxidizes and how damaging it can be. His research suggests that the total amount of LDL in a person’s bloodstream is practically irrelevant. What matters to our health, and particularly to our risk of heart attack, is how much oxidized linoleic acid is present in LDL.
And I would agree. Over the years, I’ve found that people who eat foods fried in vegetable oil can have very low LDL, particularly when they’re taking one of the statin drugs, but still often suffer one or more heart attacks. I’ve also learned that the best indicator of oxidized linoleic acid is low HDL and high particle counts. (For more on particle counts see “The Best Cholesterol Test”.)
As you can see, there is plenty of evidence that sugar can gum up, jam, or simply confuse the otherwise perfectly orchestrated choreography of fat and nutrient delivery that is the lipid cycle. Inevitably, this leads to a lot of misdirected—and, as far as the body is concerned, missing—cargo. How much of a problem is this? That depends on what kind of material has gone missing. If a shipping company misplaced a truckload of paper towels, the authorities could tell the HazMat units to stay home. If, on the other hand, they lost a couple pounds of high-grade uranium, there would be cause for concern. In your body, one of the most dangerous things a lipoprotein can carry is oxidized, pro-inflammatory fat—MegaTrans. When that gets spilled inside your arteries, your body calls on its own HazMat unit.295 But in pre-diabetics and diabetics, so much bad fat is released (either all at once or over time) that the cleanup crews can’t keep up, and arteries wind up getting injured by free radical cascades and, literally, fried (see illustration).
THE BEST CHOLESTEROL TEST: WHEN IT COMES TO LDL CHOLESTEROL, SIZE MATTERS
If your LDL number is high, say 160, that may or may not be a problem. Likewise, if your LDL is low, say 70, that may or may not indicate you’re in good metabolic shape. What matters more than these numbers is the size of your LDL particles, because that’s the best proxy we have to assess how well the LDL particles function. Bigger LDL particles are healthier LDL particles. Why? For the simple reason that healthy LDL particles can deliver the fat they’re carrying efficiently. They enter the bloodstream, do a delivery job or two (which reduces their size), and are then easily recognized by the liver, which plucks the little particles out of circulation and refills them with more cholesterol and lipid supplies, making them big again.
But what happens when the liver can’t recognize the smaller, partially empty lipoprotein (what lipidologists call a “remnant” particle) because the particle’s protein coat (which displays vital information identifying the particle and it’s cargo) has been damaged by oxidation? These smaller, orphan particles are now forced to wander through the bloodstream looking for a home until the same oxidative process that damaged their coats forces them to precipitate out of circulation and onto the delicate surfaces of your arterial walls. A regular cholesterol test can’t tell you how many of these little, wayward particles are floating around destined to cause damage, but a particle-size test can! (See Chapter 14 to learn how to talk to your doctor about ordering one of these tests.)
The diet/heart disease story is a fairly simple one. Sugar and vegetable oil combine forces to destroy lipoproteins. First, the one-two punch of oxidation and glycation reactions rusts and sugar encrusts the delicate equipment on the surface of the lipoprotein (the apoproteins), which function as a kind of navigation system, preventing lipoprotein particles of all kinds from getting to their destination. Eventually, like damaged sputniks falling out of orbit, they crash land on the insides of your arteries.
When a single lipoprotein lands in your arteries, it does not automatically cause a heart attack or stroke. However, if your diet is high in vegetable oil, then the fallen lipoprotein particles pile up like so much useless debris, polluting every avenue, side street, and back alley of your circulatory system.
The damage wrought by MegaTrans is nothing as peaceful as litter quietly blowing through the streets. At a molecular level, it’s more like Darth Vader’s evil forces strafing the surface of Yoda’s home planet with white-hot streams of free radicals. Large swaths of the cell membrane are scorched as “zombie” fats spawn and free radicals propagate across the surface, incinerating everything they touch—ion channels, sugar transporters, hormone receptors (see illustration). This disables, and ultimately destroys, functional cells. This is how free radicals fry arteries. Over the years, the damage can become so advanced that during open heart surgery it is visible to the naked eye. It looks a lot like fried chicken skin.
And it’s about as crispy and weak as fried chicken skin, too, and tears more easily than the unfried version. Free radical chain reactions weaken the underlying collagen scaffolding and fuse molecules together, polymerizing the arterial walls into a kind of crunchy protein plastic. Now the artery can easily rupture and bleed.296 If blood ever contacts collagen directly it will clot, plugging up the artery. And that’s how you get a heart attack or a stroke. So it’s a blood clot, not fat, that shuts off the flow of blood. That’s why ER doctors treat heart attacks and strokes with clot busters, not fat busters.
What does plaque have to do with any of this? Think like your body. Your arteries are under continued attack from MegaTrans and sugar. Although your entire vascular tree is being damaged, some sections are getting fried so badly they are in danger of rupture. Your body tries to patch these badly damaged sections with matrices of protein, calcium, and cholesterol. Most of these patches do just fine, holding the arterial section together for the rest of your life. These sturdy, calcium-reinforced plaques are called stable plaques.
The image of a clogged artery cutting off blood to your heart is scary. In reality, however, that’s almost never what causes a heart attack or stroke. In fact, if the arterial plaques that the body has built to repair damaged arterial surfaces were perfect—permanent fixes that would remain forever stable—they would pose little threat at all. Your body has a way of responding to arterial narrowing by growing more arteries elsewhere, what doctors call collaterals. As we age this process of rerouting arterial pathways goes on all the time. Your heart muscle and other tissues are perfectly fine with this solution, as long as they continue to get a sufficient, uninterrupted supply of blood.
Stable plaques only cause problems when continued inflammation weakens the plaque material so that within the stable plaque, small patches develop that are more prone to spontaneous rupture. These weakened areas are called unstable plaque. Unstable plaques can also form over broad areas of an artery but are not as thick or as hard; cardiologists call them buttery plaque. Whether the unstable areas are large or small, they are dangerous because they can burst open, bleed, and clot.
Plaque can grow so thick that it will narrow a section of an artery enough to be visible on an angiogram. A cardiologist will typically point a finger at a picture of the narrowed section, tell you how you are a ticking time bomb, and schedule you for bypass surgery or stenting. But that one thick plaque is not the real problem. If you have such a thick, stable plaque that it’s visible on an angiogram, it’s a sure thing that your entire vascular tree has been damaged, and there’s really no way to tell where you might develop a clot. If I had my way, instead of hearing, “You need surgery to save your life,” people would hear, “You need to get off vegetable oil and sugar immediately. But if you’re unwilling to do that, then I’ll need to crack your chest open and replace as many of these damaged arteries as I can with cleaner blood vessels from somewhere else in your body.”
Eating vegetable oil doesn’t just mess up your arteries. Those disruptive free radicals can interfere with nearly everything a cell might need to do, leading to almost any disease you can name.297, 298
At no point in our life cycle is this disruption more devastating than while we’re developing in the womb. In 2006, when researchers tested the blood of mothers whose babies were born with congenital spinal and heart defects, they found evidence of oxidative stress,299, 300 exactly what you would expect to find in someone eating lots of vegetable oil. In 2007, an article in Genes to Cells showed how oxidative stress can disrupt hormone production and interfere with hormonal responses, suggesting that women who consume vegetable oil while pregnant are increasing their child’s risk of all kinds of growth deformities and disease.301 So if you are pregnant or plan on getting pregnant, banish vegetable oil and foods containing vegetable oil from your kitchen, and get the stuff out of your life.
A PLAY-BY-PLAY PICTORIAL OF A HEART ATTACK (OR STROKE)
The story of a heart attack, illustrated here, begins with degraded lipoproteins dropping out of circulation, landing on the lining of your blood vessels, where they attract a cleanup crew of white blood cells. But sometimes, during the cleanup procedure, oxygen ignites a free radical reaction so large that the underlying collagen is exposed to flowing blood. Whenever collagen contacts blood, clots form. If the clot is large enough to disrupt arterial flow, it may cause a heart attack, stroke, or venous thrombosis (a blood clot in your leg).
You may have noticed the various cut-off levels over the years to identify people at “high risk” of a heart attack. Years ago, if your total cholesterol was 300 or less, your doctor would have said you were fine. Soon, that number was lowered to 200. Now people also watch their LDL, “safe” levels of which have been lowered from 200 to 160, to 130, to 100, and now 80. Currently, the average person’s LDL level is still about what it’s always been, around 120 to 130.302 The controversial 2013 revision of the cholesterol guidelines means nearly half of the United States population between the ages of forty and seventy-five can now be labeled “high risk.”303 And drug companies are raking it in. According to Harvard’s Dr. John Abramson and former New England Journal of Medicine editor Dr. Jerome Kassirer, the reason our medical leadership plays along, unflinchingly insisting that there’s no potential harm from pushing these numbers so low, may stem from financial conflicts of interest.304, 305
So what’s a good number? As I’ve said, I like to see LDL less than three times the HDL value. If it’s higher, you may have prediabetes and fat-encrusted arteries. Keep in mind the really important number is your fasting blood sugar level—and we’ll learn more about that in the next chapter.
The war against cholesterol is not without casualties. Women with the lowest cholesterol levels have five times more premature births than women with higher levels.306 Even when carried to term, babies of mothers with low cholesterol are often born smaller, with abnormally small brains. Remember, epigenetic alterations can accumulate over generations. So when these small-brained babies have babies of their own while on low-cholesterol diets themselves, it’s anybody’s guess what the outcome of this ongoing experiment will be.
And it’s not just baby’s developing brain we need to worry about. In the next chapter you’ll learn of the mounting evidence that, due in large part to the fact that it is such a fatty organ, our own brains are uniquely susceptible to the damaging effects of vegetable oil.
