CARBOHYDRATES ARE SUGARS, either as single molecules (also called simple sugars or monosaccharides) or as chains of sugars (also called complex sugars or polysaccharides).
Glucose and fructose are examples of single-sugar carbohydrates.
Table sugar, known as sucrose, is a two- chain carbohydrate since it contains one molecule each of glucose and fructose.
Naturally occurring carbohydrates are said to be unrefined, or unprocessed.
These include sugars found in fruit, vegetables, and raw grains.
Refined carbohydrates have been processed: for example, wheat milled into flour; rice polished and hulled for easier steaming and boiling; corn treated with acids and enzymes to turn it into syrup.
As we saw in chapter 5, glucose is the primary sugar found in the blood.
The terms blood sugar and blood glucose are used interchangeably.
Every cell in the body can use glucose, and it circulates freely throughout the body.
Muscle cells greedily import glucose from the blood for a quick energy boost.
Certain cells, such as red blood cells, can only use glucose for energy.
Fructose is the sugar naturally found in fruit, and it is the sweetest- tasting naturally occurring carbohydrate.
Only the liver can metabolize fructose, and this sugar does not circulate freely in the blood.
The brain, muscles, and other tissues cannot use fructose directly for energy.
Eating fructose does not appreciably change the body’s blood glucose level,
since they are different sugar molecules.
Neither does fructose produce much insulin response directly.
Sucrose is composed of one molecule of glucose linked to one molecule of fructose, making it half glucose and half fructose.
Chemically, high-fructose corn syrup is similar to sucrose, being composed of 55 percent fructose and 45 percent glucose.
Pure fructose is generally not consumed directly, although it can be found as an ingredient in some processed foods.
Starches, the main carbohydrates in potatoes, wheat, corn, and rice, are long chains of glucose.
Produced by plants, starches function as a store of energy.
Sometimes they grow underground, as in root vegetables, and other times above ground, as in corn and wheat.
By weight, starches are approximately 70 percent amylopectin and 30 percent amylose (both are types of glucose chains).
Animals, including humans, chain glucose molecules together as glycogen instead of starch.
Once eaten, the chains of glucose in starches are broken down into individual glucose molecules and absorbed into the intestines.
Refined carbohydrates, such as flour, are quickly digested, whereas unprocessed carbohydrates, such as beans, take much longer.
As explained in chapter 4, the glycemic index reflects how much various carbohydrates raise blood glucose.
Pure glucose causes the largest rise in blood glucose and is therefore given the maximal reference value of 100.
All other foods are measured against this yardstick.
Other dietary sugars, like fructose or lactose (the sugar found in milk), do not raise blood glucose levels appreciably and therefore have correspondingly low glycemic index values.
Since sucrose is half glucose and half fructose, it has an intermediate glycemic index.
Only the glucose portion of sucrose raises blood glucose appreciably.
Fructose, which raises neither blood glucose nor insulin, was considered more benign than other sweeteners for many years.
An all- natural sweetener found in fruit that didn’t raise the glycemic index sure sounded healthy.
But it had a hidden dark side that was not obvious for many decades.
The toxicity of fructose was invisible when looking at the blood glucose; it only became apparent by looking at the slow accumulation of fat in the liver.
THE DOSE MAKES THE POISON
PARACELSUS (1493, 1541), a Swiss-German physician who is considered the founder of modern toxicology, neatly summarized one of its most basic principles as “the dose makes the poison.” That is, anything can be harmful in excessive amounts, even if it is typically considered beneficial.
Oxygen can be toxic at high levels.
Water, too, can be toxic at high levels.
Fructose is no different.
Before the year 1900, the average person consumed 15 to 20 grams of fructose per day.
All of it would have come from raw fruit, which contributes little fructose to our diet.
An apple, for example, contains 7.6 grams of sugar per 100 grams; a grapefruit, just 1.2 grams.
By World War II, sugar cane and sugar beets were farmed on large plantations, which made sucrose, the sugar processed from these plants, cheaper and more available than it had ever been.
Yearly per capita consumption of fructose rose to 24 grams per day after the war and reached 37 grams per day by 1977.
In the 1960s, the development of high-fructose corn syrup (HFCS), a liquid-sugar equivalent of sucrose, became a game-changer.
Processed from the river of cheap corn flowing out of the American Midwest, HFCS was much less expensive to produce than other forms of sugar.
To increase profits, big food companies raced to replace sucrose with this cheaper substitute.
Soon HFCS had found its way into almost every processed food imaginable: pizza sauces, soups, breads, cookies, cakes, ketchup, spreads.
Fructose intake skyrocketed.
By 1994, the average person consumed 55 grams per day, or 10 percent of their calories.
Fructose consumption finally peaked in the year 2000, by which time it had increased fivefold within the space of 100 years.
Adolescents, in particular, were eating as much as 25 percent of their calories as added sugars, at 72.8 grams per day.
Between the late 1970s and 2006, the per capita intake of sugar- sweetened beverages almost doubled to 141.7 kcal per day.
Countries that use large amounts of HFCS have suffered a 20 percent increase in the prevalence of diabetes compared to those that do not.
The United States, by the way, is the undisputed heavyweight champion of HFCS, with a per capita consumption of almost 55 pounds.4 The dose makes the poison.
FRUCTOSE AND FATTY LIVER
FRUCTOSE IS EVEN more strongly linked to obesity and diabetes than glucose is.
From a nutritional standpoint, neither fructose nor glucose contains essential nutrients.
As a sweetener, both are similar.
Yet fructose is particularly malevolent to human health compared to glucose due to the unique way the body metabolizes it.
Whereas every cell in the body can use glucose for energy, none can use fructose.
Only the liver metabolizes fructose.
Whereas excess glucose can be dispersed throughout the body for use as energy, fructose targets the liver like a guided missile.
When we eat large quantities of glucose, such as starches, these sugars circulate to every cell, helping disperse the load.
Cells other than the liver metabolize 80 percent of the ingested glucose.
At mealtimes, the heart, lungs, muscles, brain, and kidneys help themselves to this all-you- can-eat glucose buffet, leaving only 20 percent of it for the liver to mop up5 and convert into glycogen for storage.
When we eat large quantities of fructose, on the other hand, it heads straight to the liver, since no other cells can use or metabolize it.
Consider what this means for an average person weighing 170 pounds.
Sucrose provides equal amounts of glucose and fructose.
Whereas all 170 pounds of the body metabolize the glucose, the 5-pound liver must valiantly metabolize the equivalent amount of fructose all on its own.
Moreover, the liver metabolizes fructose into glucose, lactose, and glycogen without limitations, so the more you eat, the more you metabolize.
And because the refining process removes the protein, fiber, and fat naturally found in carbohydrates, the satiating effect of these constituents is lost.
For example, 1000 calories of baked potato will make you quite full, but the same 1000 calories of sugary cola will not, despite that fact that both are mostly carbohydrate.
However, one is unprocessed and the other is highly processed.
As a result, we digest refined carbohydrates such as HFCS faster, and because we don’t feel full, we eat more of them and our blood glucose increases.
When the limited glycogen stores are full, DNL changes the excess fructose directly into liver fat.
Fructose overfeeding can increase DNL fivefold,6 and replacing glucose with a calorically equal amount of fructose increases liver fat by a massive 38 percent within only eight days.
This fatty liver plays a crucial role in the development of insulin resistance.
Fructose’s propensity to
cause fatty liver is unique among carbohydrates.
Furthermore, this harmful effect of fructose does not require high blood glucose or blood insulin levels to wreak its havoc.
Fructose functions as efficiently as a bullet train in causing fatty liver disease, which is only a short step away from insulin resistance.
Since fatty liver and the resultant insulin resistance is a key contributor to hyperinsulinemia and obesity, this means that fructose is far more dangerous than glucose.
A back-of-the-envelope calculation shows that, for an average 170-pound person, fructose would be approximately 34 times (170 divided by 5) more likely to cause fatty liver and thus obesity and insulin resistance.
The way the body metabolizes ethanol (alcohol) is quite similar.
Once ingested, tissues can only metabolize 20 percent of the alcohol, leaving 80 percent targeted straight to the liver.7 The liver metabolizes it to acetaldehyde, which stimulates de novo lipogenesis, so alcohol, like fructose, easily becomes liver fat.8 This explains the well-known effect of alcohol consumption in producing fatty liver disease.
Figure 8.1.
Hormonal obesity V: Fructose, fatty liver, and insulin resistance
FRUCTOSE AND INSULIN RESISTANCE
THAT FRUCTOSE OVERFEEDING could experimentally provoke insulin resistance has been known since as far back as 1980. Healthy subjects overfed 1000 calories per day of fructose showed a 25 percent worsening of their insulin sensitivity after just seven days. Glucose overfeeding of
subjects, by contrast, did not show any similar deterioration.9 A more recent study (2009) reinforced how easily fructose induces insulin resistance in healthy volunteers.10 Subjects consumed 25 percent of their daily calories as Kool-Aid sweetened with either glucose or fructose.
While this amount seems extreme, many people do consume this high a proportion of sugar in their diets.
The fructose group, but not the glucose group, increased their insulin resistance so much that they would be clinically classified as prediabetics, a development that required only eight weeks of fructose overconsumption.
Remarkably, it only takes one week of excess fructose to cause insulin resistance.
It only takes eight weeks to allow prediabetes to establish a beachhead.
What happens after decades of high fructose consumption?
The result is a diabetes disaster, precisely the one we are experiencing right now.