Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health (22 page)

For years, this simple fact eluded nutrition scientists. After all, dietary fats, maligned and feared, are composed of triglycerides. Logically, increased intake of fatty foods, such as greasy meats and butter, should increase blood levels of triglycerides. This proved true—but only transiently and to a small degree.

More recently, it has become clear that, while increased intake of fats does indeed deliver greater quantities of triglycerides into the liver and bloodstream, it also shuts down the body’s own production of triglycerides. Because the body is able to produce large quantities of triglycerides that handily overwhelm the modest amount taken in during a meal, the net effect of high fat intake is little or no change in triglyceride levels.
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Carbohydrates, on the other hand, contain virtually no triglycerides. Two slices of whole grain bread, an onion bagel, or sourdough pretzel contain negligible triglycerides. But carbohydrates possess the unique capacity to stimulate insulin, which in turn triggers fatty acid synthesis in the liver, a process that floods the bloodstream with triglycerides.
¹⁶
Depending on genetic susceptibility to the effect, carbohydrates can send triglycerides into the hundreds or even thousands of mg/dl range. The body is so efficient at producing triglycerides that high levels, e.g., 300 mg/dl, 500 mg/dl, even 1,000 mg/dl or more, can be sustained twenty-four hours a day, seven days a week for years—provided the flow of carbohydrates continues.

In fact, the recent discovery of the process of de novo lipogen-esis, the liver alchemy that converts sugars into triglycerides, has revolutionized the way nutritionists view food and its effects on lipoproteins and metabolism. One of the crucial phenomena required to begin this metabolic cascade is high levels of insulin in the bloodstream.
^17,
18
High insulin levels stimulate the machinery for de novo lipogenesis in the liver, efficiently transforming carbohydrates into triglycerides, which are then packaged into VLDL particles.

Today, approximately half of all calories consumed by most Americans come from carbohydrates.
¹⁹
The early twenty-first century will go down in history as The Age of Carbohydrate Consumption. Such a dietary pattern means that de novo lipogenesis can proceed to such extreme degrees that the excess fat created infiltrates the liver. That’s why so-called nonalcoholic fatty liver disease, NAFLD, and nonalcoholic steatosis, NAS, have reached such epidemic proportions that gastroenterologists have their own convenient abbreviations for them. NAFLD and NAS lead to liver cirrhosis, an irreversible disease similar to that experienced by alcoholics, thus the nonalcoholic disclaimer.
²⁰

Ducks and geese are also capable of packing their livers full of fat, an adaptation that allows them to fly long distances without sustenance, drawing on stored liver fat for energy during annual migration. For fowl, it’s part of an evolutionary adaptation. Farmers take advantage of this fact when they produce geese and duck livers full of fat: Feed the birds carbohydrates from grains, yielding foie gras and the fatty paté you spread on whole wheat crackers. But for humans, fatty liver is a perverse, unphysiologic consequence of being told to consume more carbohydrates. Unless you’re dining with Hannibal Lecter, you don’t want a foie gras-like liver in your abdomen.

This makes sense: Carbohydrates are the foods that encourage fat storage, a means of preserving the bounty from times of plenty. If you were a primitive human, satiated from your meal of freshly
killed boar topped off with some wild berries and fruit, you would store the excess calories in case you failed to catch another boar or other prey in the coming days or even weeks. Insulin helps store the excess energy as fat, transforming it into triglycerides that pack the liver and spill over into the bloodstream, energy stores to be drawn from when the hunt fails. But in our bountiful modern times, the flow of calories, especially those from carbohydrates such as grains, never stops, but flows endlessly. Today,
every
day is a day of plenty.

The situation is worsened when excess visceral fat accumulates. Visceral fat acts as a triglyceride repository, but one that causes a constant flow of triglycerides into and out of fat cells, triglycerides that enter the bloodstream.
²¹
This results in liver exposure to higher blood levels of triglycerides, which further drives VLDL production.

Diabetes provides a convenient testing ground for the effects of high-carbohydrate eating, such as a diet rich in “healthy whole grains.” The majority of adult (type 2) diabetes is brought on by excessive carbohydrate consumption; high blood sugars and diabetes itself are reversed in many, if not most, cases by reduction of carbohydrates.
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Diabetes is associated with a characteristic “lipid triad” of low HDL, high triglycerides, and small LDL, the very same pattern created by excessive carbohydrate consumption.
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Dietary fats therefore make only a modest contribution to VLDL production, while carbohydrates make a much larger contribution. This is why low-fat diets rich in “healthy whole grains” have become notorious for increasing triglyceride levels, a fact often glossed over as harmless by advocates of such diets. (My personal low-fat adventure many years ago, in which I restricted intake of all fats, animal and otherwise, to less than 10 percent of calories—a very strict diet, a la Ornish and others—gave me a triglyceride level of 350 mg/dl due to the plentiful “healthy whole grains” I substituted for the reduced fats and meats.) Low-fat diets
typically send triglycerides up to the 150, 200, or 300 mg/dl range. In genetically susceptible people who struggle with triglyceride metabolism, low-fat diets can cause triglycerides to skyrocket to the
thousands
of mg/dl range, sufficient to cause fatty liver NAFLD and NAS, as well as damage to the pancreas.

Low-fat diets are not benign. The high-carbohydrate, plentiful whole grain intake that unavoidably results when fat calories are reduced triggers higher blood glucose, higher insulin, greater deposition of visceral fat, and more VLDL and triglycerides, all of which cascades into greater proportions of small LDL particles.

If carbohydrates such as wheat trigger the entire domino effect of VLDL/triglycerides/small LDL particles, then reducing carbohydrates should do the opposite, particularly reducing the dominant dietary carbohydrate: wheat.

And if thy right eye offend thee, pluck it out, and cast it from thee: for it is profitable for thee that one of thy members should perish, and not that thy whole body should be cast into hell.

Matthew 5:29

Dr. Ronald Krauss and his colleagues at the University of California-Berkeley were pioneers in drawing the connection between carbohydrate intake and small LDL particles.
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In a series of studies, they demonstrated that, as carbohydrates as a percentage of diet increased from 20 to 65 percent and fat content decreased, there was an explosion of small LDL particles. Even people who start with
zero
small LDL particles can be forced to develop them by increasing the carbohydrate content of their diet. Conversely, people with plenty of small LDL particles will show marked reductions (approximately 25 percent) with reduction in carbohydrates and an increase in fat intake over just several weeks.

Dr. Jeff Volek and his colleagues at the University of Connecticut have also published a number of studies demonstrating the lipoprotein effects of reduced carbohydrates. In one such study, carbohydrates, including wheat flour products, sugared soft drinks, foods made of cornstarch or cornmeal, potatoes, and rice were eliminated, reducing carbohydrates to 10 percent of total calories. Subjects were instructed to consume unlimited beef, poultry, fish, eggs, cheese, nuts and seeds, and low-carbohydrate vegetables and salad dressings. Over twelve weeks, small LDL particles were reduced by 26 percent.
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From the standpoint of small LDL particles, it is nearly impossible to tease out the effects of wheat versus other carbohydrates, such as candy, soft drinks, and chips, since all of these foods trigger small LDL formation to varying degrees. We can safely predict, however, that foods that increase blood sugar the most also trigger insulin the most, followed by the most vigorous stimulation of
de novo lipogenesis in the liver and greater visceral fat deposition, followed by increased VLDL/triglycerides and small LDL. Wheat, of course, fits that description perfectly, triggering greater spikes in blood sugar than nearly all other foods.

Accordingly, reduction or elimination of wheat yields unexpectedly vigorous reductions in small LDL, provided the lost calories are replaced with those from vegetables, proteins, and fats.

Who doesn’t love a Mission Impossible double agent story, where the trusted companion or lover suddenly double-crosses the secret agent, having worked for the enemy all along?

How about the nefarious side of wheat? It’s a food that has been painted as your savior in the battle against heart disease, yet the most current research shows it is anything but. (Angelina Jolie made a movie about multiple layers of espionage and betrayal called
Salt.
How about a similar movie starring Russell Crowe called
Wheat,
about a middle-aged businessman who thinks he’s eating healthy foods, only to find out … ? Okay, maybe not.)

While Wonder Bread claims to “build strong bodies 12 ways,” the many “heart healthy” varieties of bread and other wheat products come in a range of disguises. But whether stone-ground, sprouted grain, or sourdough, organic, “fair trade,” “hand-crafted,” or “home-baked,” it’s still wheat. It is still a combination of gluten proteins, glutenins, and amylopectin, triggering wheat’s unique panel of inflammatory effects, neurologically active exorphins, and excessive glucose levels.

Don’t be misled by other health claims attached to a wheat product. It may be “vitamin-enriched” with synthetic B vitamins, but it’s still wheat. It could be organic stone-ground, whole grain bread with added omega-3 from flax oil, but it’s still wheat. It could help you have regular bowel movements and emerge from the ladies’ room
with a satisfied smile, but it’s still wheat. It could be taken as the sacrament and blessed by the pope, but—holy or not—it’s still wheat.

I think you’re probably getting the idea. I hammer this point home because it exposes a common ploy used by the food industry: Add “heart healthy” ingredient(s) to a food and call it a “heart healthy” muffin, cracker, or bread. Fiber, for instance, does indeed have modest health benefits. So does the linolenic acid of flaxseed and flaxseed oil. But no “heart healthy” ingredient will erase the adverse health effects of the wheat. “Heart healthy” bread packed with fiber and omega-3 fats will still trigger high blood sugar, glycation, visceral fat deposition, small LDL particles, exorphin release, and inflammatory responses.

Foods that increase blood glucose to a greater degree therefore trigger VLDL production by the liver. Greater VLDL availability, through interaction with LDL particles, favors formation of small LDL particles that linger for longer periods of time in the bloodstream. High blood glucose encourages glycation of LDL particles, particularly those that are already oxidized.

LDL particle longevity, oxidation, glycation … it all adds up to heightened potential to trigger the formation and growth of atherosclerotic plaque in arteries. Who’s the head honcho, the top dog, the master at creating VLDL, small LDL, and glycation? Wheat, of course.

There’s a silver lining to this dark wheat cloud: If wheat consumption causes marked increase in small LDL and all its associated phenomena, then elimination of wheat should reverse it. Indeed, that is what happens.

Dramatic reductions in small LDL particles can be accomplished by eliminating wheat products, provided your diet is otherwise healthy and you don’t replace lost wheat calories with other foods that contain sugar or readily convert to sugar on consumption.