The Obesity Code, page 15
In southwest England, six schools launched a program called “Ditch the Fizz.”15 The single goal was to reduce soda drinking in children aged seven to eleven years. The program succeeded in reducing daily consumption by about 5 ounces (150 milliliters), which resulted in a decrease in obesity by 0.2 percent. While it may seem trivial, obesity increased among the control group by a massive 7.5 percent. Reducing the use of sugar-sweetened beverages is a highly effective method of preventing childhood obesity.
This program was effective because it contained a very specific message: reduce soda consumption. Other programs are too ambitious and too vague, and often, multiple mixed messages repeat in an endless loop. The importance of reducing intake of sugar-sweetened beverages can get lost in the cacophony.
WHAT YOUR GRANDMA SAID
WHILE STUDY AFTER study showed the failure of conventional weight-loss strategies, we plunged ahead with national exercise programs. We spent money and energy promoting exercise or building playgrounds in a misguided attempt to curb childhood obesity. When I grew up in the 1970s in Ontario, Canada, we had the ParticipACTION program, which was revived in 2007 at a cost of $5 million. ParticipACTION’s explicit aim is increasing physical activity in children, with a tagline of “Bring Back Play.” (Having watched my own children play exuberantly everywhere, I somehow doubt that “play” is in danger of disappearing.) The original program that ran from the 1970s to the 1990s certainly failed to make a dent in the obesity crisis, but instead of burying these tired ideas, we resurrected them.
Michelle Obama launched the Let’s Move! campaign with the ambitious goal of ending childhood obesity. Her strategy? Eat Less, Move More. Does she believe that this advice will work now, after forty years of uninterrupted failure? Insulin, not calories, causes weight gain. It’s not (and never was) a matter of restricting calories. It’s a matter of reducing insulin.
Despite the blunders, the news on childhood obesity is good. Recently, an unexpected ray of hope shone through the darkness. In 2014, the Journal of the American Medical Association reported that obesity rates for the age group two to five years had dropped by 43 percent between 2003 and 2012.16 There was no change in youth or adult rates of obesity. However, since childhood obesity is strongly linked to adult obesity, this is indeed very good news.
Some groups wasted no time in congratulating themselves on a job well done. They believe that their campaign of physical activity and caloric reduction has played a key role in this success. I don’t buy it.
The answer is more straightforward. Consumption of added sugars steadily increased from 1977 along with obesity. By the late 1990s, increasing attention focused on the key role that sugar plays in weight gain. The irrefutable truth remained that sugar causes weight gain, with no redeeming nutritional qualities. Sugar intake began to fall in 2000, and after a five- to ten-year lag, so did obesity. We see this first in the youngest age group since they have had the least exposure to high insulin levels and therefore have less insulin resistance.
The most ironic part of this entire wretched episode is that we already knew the answers. The pediatrician Dr. Benjamin Spock wrote his classic bible of child rearing, Baby and Child Care, in 1946. For more than fifty years, it was the second-bestselling book in the world, after the Bible. Regarding childhood obesity, he writes, “Rich desserts can be omitted without risk, and should be, by anyone who is obese and trying to reduce. The amount of plain, starchy foods (cereals, breads, potatoes) taken is what determines . . . how much (weight) they gain or lose.”17
This, of course, was exactly what Grandma would say. “Cut back sugars and starchy foods. No snacking.” If only we had listened to Grandma instead of Big Brother.
PART FIVE
What’s Wrong with Our Diet?
( 14 )
THE DEADLY
EFFECTS OF FRUCTOSE
SUGAR IS FATTENING. This nutritional fact enjoys almost universal agreement. The 1977 Dietary Guidelines for Americans clearly warned against the dangers of excessive dietary sugar, but the message got lost in the anti-fat hysteria that followed. Dietary fat was the overwhelming concern of health-conscious shoppers, and the sugar content of food was ignored or forgotten. Bags of jellybeans and other candies were proudly proclaiming themselves to be fat free. The fact that they were virtually 100 percent sugar didn’t seem to bother anybody. Sugar consumption rose steadily from 1977 to 2000, paralleled by the rising obesity rates. Diabetes followed with a time lag of ten years.
IS SUGAR TOXIC?
THE WORST OFFENDER, by far, is the sugar-sweetened drink—soft drinks, sodas and, more recently, sweetened teas and juices. Soda is a $75 billion industry that had, until recently, seen nothing but good times. Per capita intake of sugar-sweetened drinks doubled in the 1970s. By the 1980s, sugar-sweetened drinks had become more popular than tap water. By 1998, Americans were drinking 56 gallons per year. By the year 2000, sugar-sweetened drinks provided 22 percent of the sugar found in the American diet, compared to 16 percent in 1970. No other food group even came close.1
Thereafter, sugar-sweetened drink relentlessly declined in popularity. From 2003 to 2013, soft-drink consumption in the United States dropped by close to 20 percent.2 Sweetened iced teas and sugary sports drinks have valiantly tried to take their place, but have been unable to block the winds of change. By 2014, Coca Cola had faced nine consecutive years of sales decline as health concerns about sugar mounted. Concerned with declining health and ballooning waistlines, people were less inclined to drink a toxic, sugary brew.
Sugar-sweetened drinks now face strong political opposition—from proposed soda taxes to the recent effort by New York mayor Michael Bloomberg to outlaw oversized beverages. Some of the problems, of course, are self-inflicted. Coca Cola spent decades convincing people to drink more soda. They were wildly successful, but at what cost? As the obesity crisis grew, the companies found themselves under increasing fire from all sides.
But the sugar pushers weren’t so easily defeated. Knowing that they were fighting a losing battle in much of North America and Europe, they took aim at Asia to make up for lost profits. Asian sugar consumption is rising at almost 5 percent per year,3 even as it has stabilized or fallen in North America.
The result has been a diabetes catastrophe. In 2013, an estimated 11.6 percent of Chinese adults have type 2 diabetes, eclipsing even the long-time champion: the U.S., at 11.3 percent.4 Since 2007, 22 million Chinese were newly diagnosed with diabetes—a number close to the population of Australia.5 Things are even more shocking when you consider that only 1 percent of Chinese had type 2 diabetes in 1980.6 In a single generation, the diabetes rate rose by a horrifying 1160 percent. Sugar, more than any other refined carbohydrate, seems to be particularly fattening and leads to type 2 diabetes.
Daily consumption of sugar-sweetened drinks not only carries a significant risk of weight gain, but also increases the risk of developing diabetes by 83 percent compared to drinking less than one sugar-sweetened drink per month.7 But is the culprit sugar or calories? Further research suggested that the prevalence of diabetes rose by 1.1 percent for every extra 150 calories per person per day of sugar.8 No other food group showed any significant relationship to diabetes. Diabetes correlates with sugar, not calories.
Sucrose, against all logic and common sense, had not been considered bad for diabetics. In 1983, Dr. J. Bantle, a prominent endocrinologist, asserted in the New York Times9 that “the message is that diabetics may eat foods containing ordinary sugar, if they keep the amount of calories at the same constant level.” The U.S. Food and Drug Administration (FDA) undertook a comprehensive review in 1986.10 Citing more than 1000 references, the Sugars Task Force declared, “there is no conclusive evidence on sugars that demonstrates a hazard.” In 1988, the FDA would reaffirm sugar as “Generally Recognized as Safe.” In 1989, the National Academy of Sciences’ report Diet and Health: Implications for Reducing Chronic Disease chimed in with the view that “sugar consumption (by those with an adequate diet) has not been established as a risk factor for any chronic disease other than dental caries in humans.”11
Yes, cavities. There seemed to be no concern that eating more sugar would raise blood sugar. Even in 2014, the American Diabetes Association website stated that “experts agree that you can substitute small amounts of sugar for other carbohydrate-containing foods into your meal plan.”12
Why is sugar so fattening? Sugar is sometimes considered “empty calories,” containing few nutrients. It is also thought to make food more “palatable” and “rewarding,” causing overconsumption and obesity. But perhaps the fattening effect of sugar is due to its nature as a highly refined carbohydrate. It stimulates the production of insulin, which causes weight gain. But then again, most refined carbohydrates, such as rice and potatoes, do so too.
What was it specifically about sugar that seems to be particularly toxic? The INTERMAP study compared Asian and Western diets in the 1990s.13 The Chinese, despite much higher intakes of refined carbohydrates, had far lower rates of diabetes. Part of reason for this advantage lies in the fact that their sugar consumption was much lower.
Sucrose differs from other carbohydrates in one important way. The problem? Fructose.
SUGAR BASICS
GLUCOSE, A SUGAR with the basic molecular structure of a six-sided ring, can be used by virtually every cell in the body. Glucose is the main sugar found in the blood and circulates throughout the body. In the brain, it is the preferred energy source. Muscle cells will greedily import glucose from the blood for a quick energy boost. Certain cells, such as red blood cells, can only use glucose for energy. Glucose can be stored in the body in various forms such as glycogen in the liver. If glucose stores run low, the liver can make new glucose via the gluconeogenesis process (literally meaning “making new glucose”).
Fructose, a sugar with the basic molecular structure of a five-sided ring, is found naturally in fruit. It is metabolized only in the liver and does not circulate in the blood. The brain, muscles and most other tissues cannot use fructose directly for energy. Eating fructose does not appreciably change the blood glucose level. Both glucose and fructose are single sugars, or monosaccharides.
Table sugar is called sucrose, and is composed of one molecule of glucose linked to one molecule of fructose. Sucrose is 50 percent glucose and 50 percent fructose. High-fructose corn syrup is composed of 55 percent fructose and 45 percent glucose. Carbohydrates are composed of sugars. When these carbohydrates contain a single sugar (monosaccharides) or two sugars (disaccharides), they are called simple carbohydrates. When many hundreds or even thousands of sugars are linked into long chains (polysaccharides), they are called complex carbohydrates.
However, it was recognized long ago that this classification provided little physiologically useful information, since it only differentiates based upon the chain length. It had previously been thought that complex carbohydrates were digested more slowly, causing less of a rise in blood sugar, but this is not true. For example, white bread, which is composed of complex carbohydrates, causes a very quick spike in blood sugar, almost as high as a sugar-sweetened drink.
Dr. David Jenkins reclassified foods according to their blood glucose effect in the early 1980s, which provided a useful comparison of the different carbohydrates. This pioneering work led to the development of the glycemic index. Glucose was given the value of 100, and all other foods are measured against this yardstick. Bread, both whole wheat and white, has a glycemic index of 73, comparable to Coca-Cola, which has a value of 63. Peanuts, on the other hand, have a very low value of 7.
There is an unspoken assumption that most of the negative effects of carbohydrates are due to their effect on blood glucose, but this idea is not necessarily true. Fructose, for example, has an extremely low glycemic index. Furthermore, it should be noted that the glycemic index measures blood glucose, not blood insulin levels.
FRUCTOSE: THE MOST DANGEROUS SUGAR
WHERE DOES FRUCTOSE fit in? Fructose does not raise the blood glucose appreciably, yet is even more strongly linked to obesity and diabetes than glucose. From a nutritional standpoint, neither fructose nor glucose contains essential nutrients. As a sweetener, both are similar. Yet fructose seems particularly malevolent to human health.
Fructose was previously considered a benign sweetener because of its low glycemic index. Fructose is found naturally in fruits, and is the sweetest naturally occurring carbohydrate. What could be wrong with that?
The problem, as often is the case, is a matter of scale. Natural fruit consumption contributed only small amounts of fructose to our diet, in the range of 15 to 20 grams per day. Things began to change with the development of high-fructose corn syrup. Fructose consumption steadily rose until the year 2000, when it peaked at 9 percent of total calories. Adolescents in particular were heavy users of fructose at 72.8 grams per day.14
High-fructose corn syrup was developed in the 1960s as a liquid equivalent of sucrose. Sucrose was processed from sugar cane and sugar beets. While not exactly expensive, it wasn’t exactly cheap. High-fructose corn syrup, however, could be processed from the river of cheap corn that was flowing out of the American midwest—and that was the decisive factor in favor of high-fructose corn syrup. It was cheap.
In processed food, high-fructose corn syrup found a natural partner. As a liquid, it could easily be incorporated into processed food. But its advantages didn’t stop there. Just consider that it
•is sweeter than glucose,
•prevents freezer burn,
•helps browning,
•mixes easily,
•extends shelf life,
•keeps breads soft and
•has a low glycemic index.
Soon, high-fructose corn syrup found its way into almost every processed food. Pizza sauce, soups, breads, cookies, cakes, ketchup, sauces—you name it, it probably contained high-fructose corn syrup. It was cheap, and big food companies cared about cost more than anything else in the world. Food manufacturers raced to use high-fructose corn syrup at every opportunity.
Fructose has an extremely low glycemic index. Sucrose and high-fructose corn syrup, with roughly 55 percent fructose, have significantly better glycemic-index measures than glucose. Furthermore, fructose produces only a mild rise in insulin levels compared to glucose, which led many people to regard fructose as a more benign form of sweetener. Fructose is also the main sugar in fruit, adding to its halo. An all-natural fruit sugar that doesn’t raise blood sugars? Sounded pretty healthy. A wolf in sheep’s clothing? You bet your life. The difference between glucose and fructose will very literally kill you.
The tide began to turn in 2004 when Dr. George Bray from the Pennington Biomedical Research Center of Louisiana State University showed that the increase in obesity closely mirrored the rise in use of high-fructose corn syrup. (See Figure 14.1.15) In the public consciousness, high-fructose corn syrup developed as a major health issue. Others correctly pointed out that high-fructose corn syrup use increased in proportion to the decreased use of sucrose. The rise in obesity really mirrored the increase in total fructose consumption, whether the fructose came from sucrose or from high-fructose corn syrup.
But why was fructose so bad?
Figure 14.1. Obesity rates have risen in proportion to high-fructose corn syrup intake.
FRUCTOSE METABOLISM
AS THE DANGERS of dietary fructose received increased scrutiny, researchers scrambled to investigate. Glucose and fructose differ in many significant ways. Whereas almost every cell in the body can use glucose for energy, no cell has the ability to use fructose. Where glucose requires insulin for maximal absorption, fructose does not. Once inside the body, only the liver can metabolize fructose. Where glucose can be dispersed throughout the body for use as energy, fructose is targeted like a guided missile to the liver.
Excessive fructose puts significant pressure on the liver since other organs cannot help. It is the difference between pressing down with a hammer and pressing down with a needlepoint: much less pressure is needed if it is all directed onto a single point.
At the liver, fructose is rapidly metabolized into glucose, lactose and glycogen. The body handles excess glucose consumption through several well-defined metabolic pathways, such as glycogen storage and de novo lipogenesis (creation of new fat). No such system is present for fructose. The more you eat, the more you metabolize. The bottom line is that excess fructose is changed into fat in the liver. High levels of fructose will cause fatty liver. Fatty liver is absolutely crucial to the development of insulin resistance in the liver.
That fructose directly causes insulin resistance was discovered long ago. As far back as 1980, experiments proved that fructose (but not glucose) caused the development of insulin resistance in humans.16 Healthy subjects were given an extra 1000 calories per day of either glucose or fructose. The glucose group showed no change in insulin sensitivity. The fructose group, however, showed a 25 percent worsening of their insulin sensitivity—after just seven days!
A 2009 study showed that pre-diabetes could be induced in healthy volunteers in only eight weeks. Healthy subjects ate 25 percent of their daily calories as Kool-Aid sweetened with either glucose or fructose. While this seems high, many people consume this high proportion of sugar in their diets.17 With its low glycemic index, fructose raised blood glucose much less.
The fructose, but not the glucose group, developed pre-diabetes by eight weeks. Insulin levels as well as measures of insulin resistance were significantly higher in the fructose group.
So only six days of excess fructose will cause insulin resistance. By eight weeks, pre-diabetes is establishing a beachhead. What happens after decades of high fructose consumption? Fructose overconsumption leads directly to insulin resistance.
