The Sugar Smart Diet: Stop Cravings and Lose Weight While Still Enjoying the Sweets You Love (7 page)

Insulin resistance promotes fat storage everywhere. Fructose, on the other hand, contributes to belly fat specifically, according to some studies. It’s found naturally in fruits and some veggies that are packaged with vitamins, minerals, phytochemicals, and fiber. As any nutrition expert would tell you, though, fruit salad isn’t the problem.

The real issue: The amounts of fructose we’re consuming in added sugars, such as table sugar (cane or white sugar) and HFCS, are swelling our bellies and menacing our health. Our bodies were designed to handle fructose in small amounts (i.e., in a few servings of fruit or a little honey a day), not the 60 pounds of HFCS a year the average American consumes, often unknowingly. And in this form, you aren’t getting any of the good stuff along with it.

Too much fructose takes a toll on even the youngest hearts, according to a study published in the
Journal of Nutrition
. The study found that teens who consumed the most fructose had higher blood pressure and blood sugar levels than those who ate the least, and it linked high-fructose diets to increases in visceral fat.

My son and I were in the supermarket recently. As we rolled our cart down the cookie aisle, he asked me why his friend gets to have
seven
chocolate chip cookies in his lunch, while he and my other kids get two a day, max (
after
they’ve done the dishes and their homework). I said, “Well, let me tell you about nonalcoholic fatty liver disease.” I’ll tell you what I told him: When you overdo the cookies or other sugary foods, your liver takes the fructose hit.

Located on the right side of your abdomen, tucked behind your lower ribs, your liver is the body’s alchemist. One of its most critical jobs is to turn toxins—both formed naturally in the body and man-made, such as from prescription
or over-the-counter medications, street drugs, and alcohol—into harmless substances. This hardworking organ uses about 20 percent of the calories you take in to fuel itself and its critical work, which also includes converting proteins and sugars from food into energy for your body, aided by insulin.

Recent research suggests that calories from different types of food are metabolized differently in the body. Every single one of your body’s 10 trillion cells can metabolize glucose. But only the liver can metabolize fructose. Sucrose, or table sugar, is half fructose, so it puts some burden on the liver; the glucose it contains is processed by the rest of the body. HFCS contains about 10 percent more fructose than sucrose, making the liver’s job that much harder. Worse, these sugars are found in foods that sound healthy. Let’s say your standard breakfast is a 16-ounce, 250-calorie strawberry-banana smoothie, which you pick up every morning at the local drive-thru. Strawberries. Banana. Only 250 calories. Sounds healthy. Sweet.

You have no idea. That wholesome-sounding smoothie packs 54 grams of sugar, almost all of it added, and the yogurt base contains straight-up fructose. The added sugars are coming from the “strawberry banana fruit base,” which implies whole fruit but is not. The ingredients list reveals “puree” of both strawberry and banana, along with grape juice concentrate, something called clarified demineralized pineapple juice concentrate, and plain old sugar (sucrose).

Your liver must work much harder to break down all that fructose than if you ate a 250-calorie bowl of, say, steel-cut oatmeal topped with half a sliced banana—because these foods contain much less total sugar, and the fiber in the oatmeal slows the absorption of sugar into the bloodstream. Since the smoothie’s sugars come in liquid form, they reach your liver fast. Imagine wading in the ocean, and out of nowhere a huge wave smashes into you, knocking you off your feet. Figuratively speaking, that’s how a large influx of fructose hits your liver.

Consume a high-fructose diet for long enough, and globules of fat begin to form in the cells of the liver. Before 1980, doctors rarely saw this fatty buildup, known as nonalcoholic fatty liver disease (NAFLD). Now, it affects 30 percent of US adults. It’s worth noting that the rise in the incidence of NAFLD parallels the increase in obesity and diabetes, and that the condition affects between
70 and 90 percent of those who are obese or have type 2 diabetes. In fact, experts consider NAFLD a hallmark of a condition characterized by the cluster of obesity-related conditions known as metabolic syndrome. (More on that condition in a bit.)

This buildup of fat in the liver isn’t necessarily obvious on your thighs, either. A 2012 study in the
American Journal of Clinical Nutrition
found that people who ate 1,000 extra calories of sugary foods for 3 weeks saw just a 2 percent increase in body weight, but a 27 percent increase in liver fat.

When you lose weight, liver fat returns to normal levels. But if NAFLD isn’t caught in time, the liver can become inflamed, which can lead to a more severe liver condition known as nonalcoholic steatohepatitis (
steato
means fat, and hepatitis is liver inflammation). If the inflammation becomes severe enough, scar tissue replaces healthy tissue, impairing the liver’s ability to perform its many crucial functions. When that happens, it’s called cirrhosis. (Cirrhosis only happens with really severe alcoholism, right? At least that’s what I always thought. Now, it appears, an excessively sugary diet could play a role, too. Amazing.) A fat-riddled liver may become resistant to the action of insulin. As the pancreas churns out more and more of this fat-storage hormone to prod the liver into doing its job, insulin levels increase—and so does body fat.

As you’ll recall, one of the liver’s jobs is to convert the sugars in food into fuel for the body. It’s also tasked with turning excess energy into body fat. This process is called lipogenesis, and at least theoretically, research suggests, the body may turn fructose into body fat more efficiently compared to sucrose and glucose.

An early study that looked for a link between fructose consumption and body fat was conducted on mice. German researchers allowed them to freely drink either plain water or fructose-sweetened water—the rodent version of soft drinks—for 10 weeks. Though the fructose-sipping mice regularly ate fewer calories from solid food, they gained weight and ended up with 27 percent more body fat than the mice that drank plain water. Because fructose doesn’t need insulin to enter the cells, it floods the body and is quickly stored as fat, the study found.

Another study, this one on people, addressed the question of whether fructose really does cause the body to pack on fat. Researchers at the University of Texas Southwestern Medical Center fed “breakfast” to six volunteers—four men and two women. That morning meal was actually 8 ounces of lemonade that contained three different combinations of sugar—100 percent glucose, an equal mix of glucose and fructose, and 25 percent glucose and 75 percent fructose.

Immediately after the volunteers had breakfast, the team measured the conversion of the sugars to fat in the liver. Four hours later, the volunteers ate lunch—turkey sandwiches, salty snacks, and cookies. Each volunteer’s lunch contained different amounts of sugars based on body weight. Then the researchers measured how the food was metabolized.

The results: Lipogenesis rose 17 percent when the volunteers had the fructose-containing drinks, compared to 8 percent for the glucose drink. Simply put, their bodies made fat more efficiently. Further, after metabolizing fructose in the morning, the liver increased the storage of fats eaten at lunch. As the study’s lead researcher, Elizabeth Parks, PhD, put it: “The carbohydrates came into the body as sugars, the liver took the molecules apart like Tinkertoys, and put them back together to build fats. All this happened within 4 hours after the fructose drink. As a result, when the next meal was eaten, the lunch fat was more likely to be stored than burned.” Although this research is preliminary, it certainly raises important questions about starting your day with a fructose-filled sugary drink.

Most likely, these results underestimated the effect of fructose because the test subjects consumed the sugar drinks while fasting and because they were healthy and lean, and could presumably process the fructose quickly, according to Dr. Parks. So the fat-packing potential of fructose may be worse if you’re overweight, because this process may be already revved up.

As you may know, carrying extra pounds sets the stage for a host of metabolic diseases. You’re familiar with the BOGO sales at stores? With metabolic
syndrome, you “buy” the extra pounds, and you’re likely to get all the nasty freebies—belly fat, high blood pressure, high fasting blood sugar, low HDL (“good”) cholesterol, and high triglycerides (fatty substances in the blood).

You don’t have to be overweight to have metabolic syndrome, which is the name for the bundle of risk factors listed above that raise your odds for heart disease, diabetes, and stroke. Up to 40 percent of normal-weight adults have it. But weight—healthy or no—isn’t the defining characteristic of metabolic syndrome. Insulin resistance is.

A team of researchers, including Robert Lustig, MD, author of
Fat Chance
, advanced a theory of exactly how metabolic syndrome—and its disastrous, system-wide consequences—might occur. The process, described in an article published in
Pediatrics
, is extraordinarily complex. But it begins with the body being forced to store excess fat in the liver, as well as in the tissue around the internal organs. This excess fat makes the liver resist the action of insulin. In response, the pancreas produces more insulin to prod the liver into doing its job. Insulin levels rise even higher and cause even more energy to be stored in subcutaneous fat tissue (like your thighs or butt). This is the fat you see in the mirror, the kind you moan over.

The liver tries to export the excess fat that is damaging it in the form of a specific type of blood fat called triglycerides. But too many triglycerides floating around in your bloodstream can be just as problematic. High triglycerides may raise your risk of coronary artery disease, especially if you’re a woman.

There’s more to this insidious progression of system-wide havoc. But the bottom line is, high insulin levels affect every part of the body—including your belly. In a study published in the
Journal of Clinical Investigation
, 32 overweight men and women drank either glucose- or fructose-sweetened drinks three times a day, along with following a standard diet for 10 weeks. The drinks totaled 25 percent of their daily calories.

At the end of the study, all the participants had gained weight. But CT scans showed that the fructose group mostly gained belly fat. They were actually growing sugar bellies! On the other hand, most of the glucose group’s fat gain was subcutaneous. Compared to the glucose group, the fructose group
also had higher total cholesterol and LDL (“bad”) cholesterol, plus greater insulin resistance—consistent with metabolic syndrome.

So if a sugary diet appears to promote the storage of this deep and dangerous belly fat, it’s reasonable to conclude that type 2 diabetes can’t be far behind. Indeed, research already links sugar intake to the development of type 2 diabetes, independent of its role in obesity. In other words, it’s possible that people develop diabetes because they’re overweight or obese. But it may
also
be possible that they develop it because they’re consuming added sugars to excess.

One recent study found a smoking gun: an independent, direct link between sugar in the food supply and risk of developing type 2 diabetes. The findings give weight to the still-controversial hypothesis that it’s not obesity that’s driving this now global pandemic, but the rising consumption of sugar worldwide.

In this study, published in
PLoS ONE,
researchers from the Stanford University School of Medicine, the University of California, Berkeley, and the University of California, San Francisco, analyzed a decade’s worth of health data from the United Nations, including diabetes rates and sugar availability, across 175 countries. After controlling for factors like obesity, aging, income, and total calories, the link between sugar and diabetes remained significant. For every extra 150 calories from sugar available per person each day, diabetes prevalence rises by 1.1 percent, the study found. (By the way, 150 calories is just a little more than the number of sugar calories in a 12-ounce can of soda.) Conversely, reduced exposure to sugar was linked to a drop in diabetes prevalence.

This relationship was unique among food types. Categories like protein, fat, and fiber didn’t show a significant link to diabetes. Neither did total caloric intake.

While the findings don’t prove that sugar causes type 2 diabetes, they do support the ever-expanding body of research—in test tubes, animals, and humans—that suggests sugar affects the liver and pancreas in ways that other
types of foods don’t. Another study, published in
Global Public Health
, found that as a nation’s fructose intake rises, so do levels of type 2 diabetes. Again, the study didn’t prove a direct cause-and-effect link, but did conclude that the prevalence of type 2 is about 20 percent higher in countries where use of HFCS is high, compared to nations where consumption is lower.