Monday, November 19, 2007

Why Low-Carb Diets Work

In other fields, when bridges do not stand, when aircraft do not fly, when machines do not work, when treatments do not cure, despite all the conscientious efforts on the part of many persons to make them do so, one begins to question the basic assumptions, principles, theories, and hypotheses that guide one’s efforts.

—Arthur R. Jensen, Ph.D.

Professor of psychology at the University of

California at Berkeley, in Harvard Educational Review, winter 1969







On November 1, 1999, Woody Merrell—the Muhammad Ali of doctors, loved, respected, and admired across the entire political spectrum of medicine and nutrition—wrote an article in Time magazine about weight loss. This is how it started: “In my 25 years of medical training and practice in Manhattan, I’ve seen a wide range of diets come and go. Virtually none of them work.”

A few paragraphs later, Merrell wrote, “For most of my professional career, I adhered to the generally recognized dictum of weight management. I advised my patients to count their calories and follow a low-fat diet.”

He then talks about his experience with a few patients who weren’t getting anywhere no matter what they tried. Skeptically, he put them on a low-carb diet.

Finally he wrote, “I have become a convert. Carbohydrates . . . are often prime saboteurs of our weight. [O]f all the diets I’ve seen over the past few decades, the moderate-fat, lower-carbohydrate ones are the most successful. They stress not how much food you eat but what kinds. Calorie counting is not as important as carbo counting.” (All emphases mine.)

The article is titled “How I Became a Low-Carb Believer.”1

What convinced Merrell—and what is convincing more and more of his colleagues—is the fact that lower-carbohydrate diets really work for many, many people. The evidence of the senses is hard to argue with. People lose weight, feel better, and, equally important, have major improvements in their health. Chronic complaints and ailments have been known to disappear. Some of these people had tried every possible diet, had adhered to every conventional cholesterol-lowering, fat-reducing program, and wound up in exactly the same place as when they started—and sometimes were even worse. Yet on lower-carb diets, they do great.

How can something that is so counterintuitive work? (And it is counterintuitive for most of us—after all, even Gary Taubes, in his seminal article “What If It’s All Been a Big Fat Lie?”,2 said he couldn’t quite get over the feeling that the bacon and eggs on his plate were going to somehow jump up and kill him.) We need to remember that low-carb eating is counterintuitive precisely because we have all been taught a number of “truths” that we have internalized as nutritional gospel but which may in fact be nutritional hogwash.

We “know” low-carb diets can’t work because they are often high in fat or cholesterol (which we “know” causes heart disease), are often high in protein (which we “know” causes heart disease, bone loss, and possibly cancer), and may be higher in calories (which we “know” causes weight gain). Yet people eating the low-carb way are losing weight and lowering their risk for heart disease, hypertension, diabetes, and obesity. There is even some indication that they may be lowering their risk for some cancers.3, 4 How do we explain this? It is as though all three of Christopher Columbus’ ships returned home with great bounty from the New World, but the people back in Spain shook their heads in disbelief, saying, “How can this be? It must be a trick. The ships had to have fallen off the earth because we know the earth is flat!”

I’ve got news for you: low-fat is the flat-earth theory of human nutrition.

See, all theories of weight loss fit into one of two major categories of thought—all of them. There is no exception to this rule. If you understand the two categories, you’re immediately better informed than half the population on the subject of dieting and weight loss.

Let’s call category one the Thermodynamic View. It comes from the first law of thermodynamics, which basically says that what goes in must come out. Applied to weight loss, it means simply this: you eat a certain number of calories, and you burn up a certain number of calories. If you eat more than what you need, you gain weight. If you eat less than what you need, you lose weight. I call this the checkbook theory. If I deposit more money than I write checks for, I have some extra cash (i.e., I gain weight). If I spend more than I take in, I have to dip into that cash (i.e., I lose weight). If what I deposit exactly equals what I spend, I have a zero balance (i.e., my weight stays the same).

Let’s call category two the Telephone Theory of weight loss, based on the game of Telephone you may have played as a child. You line ten people up, then whisper something in the ear of the first person. That person whispers it to the second person, and so on down the line, until the words are repeated to the last person, who then says them out loud. What usually happens is that you start out with something like “A rose is a rose is a rose” and you wind up with “Gardenias don’t grow on the planet Mars.” Applied to weight loss, the theory goes something like this: the stuff that goes on in between the calories coming in and the calories going out is much more important than the actual number of calories involved. There are so many enzymes, cofactors, energy cycles, hormones, neurotransmitters, eicosanoids, genes, and other variables in the human body that determine the fate of the food coming in that it is impossible to predict what’s going to happen to someone’s weight just by knowing the number of calories that go in. It would be like predicting the outcome of Telephone simply by knowing the phrase that was originally said. Sure, if everything goes perfectly, “A rose is a rose is a rose” comes out as “A rose is a rose is a rose.” More often, though, it comes out as “Madonna’s latest movie stinks.”

The Thermodynamic View, known as the energy balance theory, has been the dominant theory of weight loss for years. The entire low-fat movement has been built on it: take in fewer calories and burn more, and you will lose weight. You have probably been hearing this advice for years. While this view is not entirely without merit, it’s so far from the whole picture as to almost constitute dietary malpractice.

The thinking behind low-carbing belongs to the second category of theories about weight loss, the Telephone Theory. This view asks a critical question: what goes on inside the body once those calories are taken in? Why do some people store everything as fat and others don’t? What determines whether what you eat goes on your hips or is burned up as energy and disappears as heat into the atmosphere?

The answer is one word: hormones.

Hormones control just about every metabolic event that goes on in your body, and you control hormones via your lifestyle. Food—along with several key lifestyle factors such as stress—is the drug that stimulates hormones, and those hormones direct the body to store or burn fat, just as they direct the body to perform a gazillion other metabolic operations. (Dr. Barry Sears has said that “food may be the most powerful drug you will ever encounter because it causes dramatic changes in your hormones that are hundreds of times more powerful than any pharmaceutical.”) Hormones are the air traffic controllers determining the fate of whatever flies in. If your food is stimulating the wrong hormones or creating a hormonally unbalanced state, you will find it extremely difficult, if not impossible, to lose weight and keep it off.

In this chapter you will learn why it is so vitally important to balance your hormones if you want to lose weight. It is probably as important or more important than counting calories, and it is certainly more important than reducing dietary fat. But managing our hormones has even bigger consequences. Insulin—the hormone most targeted by the low-carb diet plans discussed in this book—is at the hub of a significant number of diseases of civilization. When you control insulin, you hugely increase the odds that you will be able to control your weight. But, as you will see, you also reduce the risks for heart disease, hypertension, diabetes, polycystic ovary syndrome, inflammatory diseases, and even, possibly, cancer.

So let’s get to know the players in our hormonal dance. If I’ve done my job, at the end of this chapter you’ll have a much better understanding of what has now come to be popularly known as “endocrinology 101”: how the body makes fat, stores fat, and, finally, says goodbye to fat. You’ll also understand why the same eating plan that helps you lose weight also has the positive “side effect” of preventing you from becoming a medical statistic.





The Good, the Bad, and the Ugly: Insulin and Its Discontents



Insulin, a hormone first discovered in 1921, is the star actor in our little hormonal play. It is an anabolic hormone, which means it is responsible for building things up—putting compounds (like glucose and amino acids) inside storage units (like cells). Its sister hormone, glucagon, is responsible for breaking things down—opening those storage units and releasing their contents as needed. Insulin is responsible for saving; glucagon is responsible for spending. Together their main job is to maintain blood sugar within the tightly regulated range it needs to be to keep your metabolic machinery running smoothly.

And to keep you from dying. Without insulin, blood sugar would skyrocket and the result would be metabolic acidosis, coma, and death, the fate of virtually every type 1 diabetic in the early part of the twentieth century prior to the discovery of insulin. On the other hand, without glucagon, blood sugar would plummet and the result would be brain dysfunction, coma, and death. So the body knows what it’s doing. This little dance between the forces that keep blood sugar from soaring too high and those that prevent it from going too low is essential for survival. It’s interesting to note that while insulin is the only hormone responsible for preventing blood sugar from rising too high, there are several other hormones besides glucagon—cortisol, adrenaline, noradrenaline, and human growth hormone—that prevent it from going too low. Insulin is such a powerful hormone that five other hormones counterbalance its effects.





How a High-Carbohydrate Diet Raises Both Cholesterol and Triglycerides



Let’s follow the nutrients you eat on their journey through the body. When you eat food—any food—it mixes with acids and enzymes from the stomach, pancreas, and liver that break it down into smaller molecules. The nutrients are then absorbed through the intestinal walls, while the indigestible parts of the food pass through the digestive system as waste. Proteins break down into amino acids, carbohydrates into glucose, and fats into fatty acids. These pass through the intestinal walls into the portal vein, which is like their private passageway into the liver, the central processing plant of the body. After the liver works its magic, often repackaging these compounds into different forms, the new forms are released into the general circulation of the bloodstream, where they are transported to cells and tissues to be either used or saved for a rainy day.

As these smaller units pass through the portal vein en route to the liver, the pancreas immediately takes notice of the parade and responds by secreting our star player, insulin. It secretes some insulin in response to protein, but when it sees carbohydrates in the passageway, its eyes light up, and it brings out the big guns and goes to town. (Fat doesn’t even rate a “hello” from the pancreas and has no impact on insulin.)

Under the influence of this incoming insulin, the liver does a number of things. First, it decides how much of the sugar coming in is excess. It makes that decision based largely on how much insulin the pancreas has decided to send along to accompany the payload. If there’s a lot of insulin, the liver says, “Woo hoo, we’ve got a truckload of sugar on our hands; let’s get busy.” Some of the incoming sugar will pass right through (as glucose) to the bloodstream to be transported to muscle cells—which can use a hit of sugar now and then for energy—and to the brain, which needs sugar (or ketones, which we’ll discuss in detail later) to think and do all the other good things that brains like to do. Part of the excess sugar will be converted to the storage form of glucose, called glycogen, much of which will stay right there in the liver. (Glycogen is also stored in the muscles, but muscle glycogen is like a private bank account that can be used only by the muscle in which it is stored.) The liver doesn’t hold a lot of glycogen, so if there is still excess sugar, which there almost always is after a high-carbohydrate meal, it is packaged into triglycerides (fats found in the blood and in the tissues). The high level of insulin accompanying the high-carbohydrate meal stimulates the cholesterol-making machinery: the body starts churning out more cholesterol, which it then packages (together with triglycerides) into little containers called VLDLs (very low-density lipoproteins), most of which eventually become LDLs (low-density lipoproteins), or “bad” cholesterol. This is how a high-carbohydrate diet raises both triglycerides and cholesterol.





Which Is Worse, Sugar or Fat? No Contest!

Why, you may ask, does the liver feel this compelling need to get rid of the excess sugar, anyway? Why doesn’t it just give it a pass and let it go into the bloodstream as is? Why create all this work for itself? Why bother to turn it into triglycerides in the first place?

That’s a very good question, and the answer is central to understanding the health effects of a lower-carbohydrate diet: sugar is far more damaging to the body than fat. In a very real sense, what the liver is doing is detoxifying sugar into triglycerides.

As you just read, eating high-carb foods usually makes your cholesterol go up. Here’s why: insulin turbocharges the activity of a particular enzyme—with the unwieldy name of HMG-coenzyme A reductase, or HMG-CoA reductase—that runs the cholesterol-making machinery in the body. (Glucagon inhibits the HMG-CoA reductase enzyme, so your body makes less cholesterol.) So high levels of insulin basically signal the liver to ramp up the production lines on cholesterol, and high levels of sugar signal it to ramp up the production of triglycerides. (Interestingly enough, if you ate a diet of almost 90 percent fat, your cholesterol numbers would probably drop, because there would not be enough insulin around to power the cholesterol-making machinery.) However, the American diet—high-fat and high-carbohydrate—virtually guarantees both high cholesterol and high triglycerides. Your Honor, the body had motive, means, and opportunity. Motive—to get rid of the excess sugar. Means—fat and sugar. Opportunity—tons of insulin to drive the works. Case closed: when there’s plenty of excess sugar and insulin around, triglycerides skyrocket and so does cholesterol.

At this point, it may start to occur to you that since sugar is made into triglycerides, then maybe one of the reasons that blood levels of triglycerides are lowered on a low-carb diet is because there’s less excess sugar coming in to require packaging into triglycerides in the first place. And you’d be absolutely, 100 percent right. (Cholesterol usually comes down as well, but as you’ll see later, that doesn’t matter nearly as much.) This lowering of triglycerides is one of the major health benefits of a low-carb diet—high triglycerides are far more of a danger sign for heart disease than high cholesterol ever was.

You may also be thinking that the higher levels of fat that are frequently (though not always) part of low-carb diet plans may not be so bad after all if they’re not accompanied by the high insulin levels that go with high-carb diets. You’d be right on that count as well.





Insulin Prevents You From Losing Fat



An important thing to remember just from a weight loss point of view is that insulin isn’t only responsible for getting sugar into the cells and out of the bloodstream. It’s also responsible for getting fat into the fat cells and keeping it there. Insulin actually prevents fat burning. That’s why a low-carb diet usually produces more weight loss than a high-carb, low-fat diet with the same calorie count. By lowering insulin, you open the doors of the fat cells and allow the body to release fat.

One of the ways insulin interferes with fat burning is by inhibiting carnitine, an amino acid–like compound in the body that is responsible for escorting fatty acids into the little central processing units of the muscle cells, where those fats can be burned for energy. By inhibiting carnitine, insulin inhibits fat burning. That’s one reason you shouldn’t eat a big meal before going to bed—the resulting high levels of insulin virtually ensure that your body will not be breaking down fat as you sleep but instead will be busy storing whatever is around in the bloodstream. (A side note: many years ago, an American health magazine decided to do a weight loss story on sumo wrestlers. The writers reasoned that the wrestlers knew everything there was to know about putting on weight, so if we could just learn what it was they did, we’d know what not to do if we wanted to slim down. One of the major rituals of the sumo wrestlers was eating a huge meal and then going right to bed.)

So on a high-carbohydrate diet, you’ve got all this sugar coming into your system—because all carbs eventually break down into sugar—and your liver can basically do one of three things with it:



1. Pass it right through and send it into the bloodstream.

2. Transform it into glycogen and store it (in the liver or the muscles).

3. Use it to make triglycerides.



Remember, as far as your body is concerned, the most important thing is to prevent blood sugar from getting too high. Your insulin may very well be able to keep your blood sugar in the normal range, but the high level of insulin needed to do the job—plus the high levels of triglycerides and VLDLs being created at the same time—are silently laying the foundation for future damage: you are slowly on your way to becoming overweight and/or insulin-resistant.





Insulin Resistance: The Worst Enemy of a Lean Body



Insulin resistance makes losing weight incredibly difficult and is a risk factor for heart disease and diabetes. It is not something you want, and you can do something about it. Here’s how insulin resistance develops: the muscle cells don’t want to accept any more sugar (this is especially true if you have been living a sedentary life). They say, “Sorry, pal, we’re full, we don’t need any more, we gave at the office, see ya.” Muscle cells become resistant to the effects of insulin. But the fat cells are still listening to insulin’s song. They hear it knocking on their doors and they say, “Come on in; the water’s fine!” The fat cells fill up and you begin to put on weight.

Meanwhile, back in the bloodstream, those little packages called VLDLs that we talked about earlier are carrying triglycerides around trying to dump them. After the VLDL molecules drop off their triglyceride passengers to the tissues and the ever-expanding fat cells, most of them turn into LDL (“bad”) cholesterol.

Now you’re overweight, with high triglycerides, high LDL cholesterol, and definitely high levels of insulin, which the pancreas keeps valiantly pumping out in order to get that sugar out of the bloodstream. From here, two scenarios are possible, neither of them good.

In one scenario, your hardworking pancreas will somehow be able to keep up with the workload and keep your blood sugar from getting high enough for you to be classified as diabetic. But you will be paying the price for that with high levels of insulin and the increased risk factors for heart disease that go with them. In the other scenario, your poor pancreas will eventually become exhausted—even its most valiant efforts to shoot enough insulin into the system won’t be adequate for the job. The sugar will run out of places to go, so it will stay in the blood and your blood sugar levels will rise. Now you’ll have elevated insulin and elevated blood sugar, plus, of course, high triglycerides and abdominal obesity. If your blood sugar continues to rise even more, beyond the capacity of your insulin to reduce it, you’ll eventually have full-blown type 2 diabetes.

Welcome to fast-food nation.





What’s So Bad About a Little Sugar?



Obviously, the body knows how important it is to protect the tissues, the brain, and the bloodstream from excess sugar. So what exactly does sugar do that’s so damaging to the body that the body is willing to risk the effects of large amounts of insulin and dangerously high levels of triglycerides just to prevent it?

Well, for one thing, excess sugar is sticky (think cotton candy and maple syrup). Proteins, on the other hand, are smooth and slippery (think oysters, which are pure protein). The slippery nature of proteins lets them slide around easily in the cells and do their jobs effectively. But when excess sugar keeps bumping into proteins, the sugar eventually gums up the works and gets stuck onto the protein molecules. Such proteins are now said to have become glycolated. The glycolated proteins are too big and sticky to get through small blood vessels and capillaries, including the small vessels in the kidneys, eyes, and feet, which is why so many diabetics are at risk for kidney disease, vision problems, and amputations of toes, feet, and even legs. The sugar-coated proteins become toxic, make the cell machinery run less efficiently, damage the body, and exhaust the immune system.5 Scientists gave these sticky proteins the acronym AGES—which stands for advanced glycolated end-products—partially because these proteins are so involved in aging the body.

For another thing, high blood sugar is also a risk factor for cancer—cancer cells consume more glucose than normal cells do.6,7 Researchers at Harvard Medical School suggested in the early 1990s that high levels of a sugar called galactose, which is released by the digestion of lactose in milk, might damage the ovaries and even lead to ovarian cancer. While further study is necessary to definitively establish this link, Walter Willett, M.D.—chairman of the department of nutrition at the Harvard School of Public Health and one of the most respected researchers in the world—says, “I believe that a positive link between galactose and ovarian cancer shows up too many times to ignore the possibility that it may be harmful.”8

Sugar depresses the immune system. It makes the blood acidic, and certain white blood cells (lymphocytes) that are part of our immune system don’t work as well in an acidic environment.9–11 A blood sugar level of 120 reduces the phagocytic index—a measure of how well immune system cells gobble up bacteria—by 75 percent.12 Since refined sugar comes with no nutrients of its own, it uses up certain mineral reserves of the body that are needed to metabolize it, which in turn throws off mineral balances and results in nutrient depletions.13 (One of the minerals that refined sugar depletes is chromium, which is needed for insulin to do its job effectively!) Since minerals are needed for dozens of metabolic operations, these mineral deficiencies can wind up slowing down your metabolism and creating havoc with your energy level. Finally, sugar reduces HDL, the helpful, “good” cholesterol, adding yet another risk factor for heart disease to its résumé.14

Is it any wonder people drastically improve their health when they switch to a diet lower in sugar?

Excerpted from

Living the Low Carb Life: From Atkins to The Zone
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