DATA FROM MORE than 175 nations links sugar intake inextricably to diabetes, independent of obesity.
For example, Asian sugar consumption is rising at almost 5 percent per year, even as it has stabilized or fallen in North America.
The result has been a tsunami of diabetes.
In 2013, an estimated 11.6 percent of Chinese adults had type 2 diabetes.11 Yet the Chinese being diagnosed with diabetes have an average body mass index of only 23.7, which is considered in the ideal range.
By contrast, American diabetics average a body mass index of 28.7, well within the overweight category.
Consider that in 1980 only 1 percent of Chinese had type 2 diabetes.
This situation presents an apparent paradox since the Chinese diet has traditionally been based upon white rice.
Yet, despite such a high intake of refined carbohydrates, the Chinese have suffered little obesity or type 2 diabetes.
The reason for this apparent protection is that they ate almost no sugar, as Figure 8.2 shows.
Refined carbohydrates, such as white rice, are composed of long chains of glucose, whereas table sugar contains equal parts of glucose and fructose.
In the late 1990s, the INTERMAP study compared the diets of the U.K., U.S., Japan, and China.12 Chinese sugar consumption has steadily
increased since the time of that study, and diabetes rates have moved in lockstep. Combined with their original high-carbohydrate intake, the Chinese are facing their current diabetes disaster.
Figure 8.2. The traditional Chinese diet: High carbs, low sugar, no diabetes13
To a lesser extent, the same story has played out in the United States.
Americans gradually switched from consuming their carbohydrates as grains to eating them as sugar in the form of corn syrup.14 Consider Figure 8.3; when both grain and fructose intake began to rise in the late 1970s, the result was the start of an epidemic of obesity and type 2 diabetes.
Sugar is more fattening than any other refined carbohydrate, and leads specifically to type 2 diabetes.
The prevalence of diabetes climbs 1.1 percent for every extra 150 sugar calories per person per day.15 Each additional daily 12-oz serving of soda increases the risk of diabetes by 25 percent and the risk of metabolic syndrome by 20 percent.16 No other food group, not dietary fat, not protein, shows any significant relationship to diabetes.
Diabetes correlates strongly to sugar, not other sources of calories.
Fructose overconsumption directly stimulates fatty liver and leads directly to insulin resistance.
Consumption of high-fructose corn syrup, which is
chemically almost identical to sugar, also shows the same tight correlation to diabetes.17
Figure 8.3. Replacement of whole grain carbs with HFCS in the U.S.18
There is something sinister about overconsumption of fructose. What distinguishes sugar from other highly refined carbohydrates? What is the common link to disease? Fructose. Yes, Dr. Robert Lustig had it right. The dose makes the poison, and in the doses we are currently eating it, sugar is a toxin.
FRUCTOSE TOXICITY
FRUCTOSE IS PARTICULARLY toxic for several reasons. First, as we’ve seen, only the liver can metabolize it, so virtually all ingested fructose is stored as newly created fat. This excessive liver fat directly causes insulin
resistance.
Second, the liver metabolizes fructose without limits.
More ingested fructose leads to more hepatic DNL and more liver fat, independent of insulin.
Fructose does little to activate natural satiety pathways that limit food intake, and no natural brakes exist to slow down the overproduction of new fat.
This explains why you can still eat sweet desserts even after a full meal.
Third, fructose has no alternative runoff pathway.
The liver stores excess glucose safely and easily as glycogen, breaking it back down into glucose when the body needs access to energy.
On the other hand, the body cannot store fructose directly.
When the body has enough energy to meet its actual needs, the liver metabolizes fructose into fat through a process that cannot be easily reversed.
Therefore, the body can handle only small amounts of fructose.
Remember, the dose makes the poison.
But this toxicity is not easily recognized.
In the short term, fructose has few obvious health risks since it affects neither blood glucose nor insulin levels.
Instead, it exerts its toxicity mainly through long-term effects on fatty liver and insulin resistance, which may take decades to manifest.
Short-term studies, often focusing on insulin, blood glucose, and calories, miss this long-term effect, just as short-term studies of cigarette smoking miss the long-term cancer risk.
So sucrose or high-fructose corn syrup, both of which are roughly equal parts glucose and fructose, play a dual role in obesity and type 2 diabetes.
More than simply empty calories, glucose is a refined carbohydrate that stimulates insulin production and, when consumed in large amounts, leads to fatty liver.
Overconsuming fructose, on the other hand, produces fatty liver and insulin resistance directly, without noticeably disturbing blood glucose or insulin.
Fructose is many times more likely than glucose to cause fatty liver, setting off a vicious cycle.
Insulin resistance leads to hyperinsulinemia, leading back to more insulin resistance.
Sugar, as both glucose and fructose, therefore stimulates insulin production in both the short term and the long term.
In this way, sucrose is far more menacing than starches that contain only glucose, such as the amylopectin in flour.
However, while the glycemic index makes the effect of glucose obvious, the effect of fructose is completely hidden, which has long led scientists to downplay the role of sugar in obesity.
A seemingly obvious solution is to replace fructose in the diet with artificial sweeteners.
While the biochemistry of these compounds is far beyond the scope of this book, these agents are not a satisfactory solution to the fructose overload.
The proof of the pudding is in the eating: we have used large and increasing amounts of these sweeteners in our diets and diabetes has not gone away.
So we can debate why artificial sweeteners should work, but the bottom line is that they do not.
So when Dr.
Lustig stepped onto that lonely stage in 2009 and declared that sugar was toxic, the world listened with rapt attention.
This professor of endocrinology was telling us something we already, instinctively, knew to be true despite all the platitudes and the reassurances that sugar was not a problem: in sufficiently large amounts, sugar in any form is a toxin.
The dose makes the poison.
THE METABOLIC SYNDROME CONNECTION
THE IDENTIFICATION OF metabolic syndrome (MetS), originally termed Syndrome X, is one of the great medical advances of the past thirty years. The 2005 National Cholesterol Education Program (NCEP) Adult Treatment Program III (ATP III) defines metabolic syndrome as three of the following five conditions1: