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Fructose: How Sweet It Is?or Is It?

Weapons of mass destruction? Forget anthrax and smallpox. A far more immediate threat to the health and well-being of Americans lurks within our borders.

Weapons of mass destruction? Forget anthrax and smallpox. A far more immediate threat to the health and well-being of Americans lurks within our borders. The ‘weapon’ wasn’t secretly smuggled into the United States by such familiar foes as Saddam Hussein or Osama bin Laden but instead has been here for years, reaping slow destruction and death. At least, that’s what some recent articles and books say about a common sugar called fructose.

One fact cannot be denied: American are getting fatter. The usual explanation for that not-so-creeping obesity epidemic is the rise of processed-food intake, coupled with a decline in physical activity. Two food ingredients in particular are linked to the rise in obesity, cardiovascular disease and cancer. One of them has been discussed in past issues of IRONMAN’trans fats are a biochemical Frankenstein metamorphosed from natural fats. They’re popular with food companies because they add shelf life to foods, which equals greater profits’and a high public-health cost.

The other prime suspect in the obesity epidemic is fructose, especially in the form of high-fructose corn syrup (HFCS), the refined in refined sugar. As with trans fats, food companies favor it because it’s relatively cheap and stable in foods. Children are particularly high consumers of HFCS; it’s ubiquitous in all things sweet, such as candies and sodas. But fructose in one version or another also is commonly found in many foods targeted at bodybuilders and other active people, such as protein supplements, protein bars and energy drinks.

Some portray fructose as a nutritional devil with little or no redeeming qualities, but the attacks are just so much hyperbole. After all, some of the most healthful and protective foods on the planet’such as fruits and vegetables’naturally contain fructose. How could nature have made such a serious blunder?

The fructose content of fruits has inspired some self-styled nutrition experts to declare that fruit makes you fat. Forget all the protective phytonutrients in fruits, which, paradoxically, defend the body against diseases linked to excess fructose intake, such as cardiovascular disease. Avoid fruit like the proverbial plague, unless you want a physique with definition like the Michelin tire man’s. Or so say the antifructose fanatics.

Fructose Facts

Fructose is classified as a monosaccharide, along with glucose, galactose and maltose. These are the simplest of all simple sugars, but fructose differs from the others in one major respect: It doesn’t promote an immediate release of insulin. As you might expect, that gives fructose a low-glycemic-index number, 23. Compare that to what many people think of as a complex carbohydrate, potatoes, which has a glycemic-index number of 83. The lack of insulin release after fructose intake was recognized back in 1874, when diabetics appeared to tolerate fructose better than sucrose, or table sugar.

Such fruits as grapes, oranges and watermelon contain fructose. Vegetables contain 1 to 2 percent free fructose and up to 3 percent fructose as part of sucrose, which is a double sugar, or disaccharide, made of fructose and glucose. Honey has the highest natural concentration of fructose, which accounts for 42.4 percent of its total weight.

Fructose consumption has greatly increased over the past 20 years, most of it from the highly processed HFCS, which was introduced in 1967 and consists of 55 percent fructose blended with 45 percent glucose. Just two 12-ounce cans of soda (not diet soda) can supply up to 50 grams of fructose from HFCS. Most regular sodas contain 11 percent HFCS by weight.

Why use processed sugar like HFCS? Fructose is more soluble than sucrose or glucose and less likely to form crystals than sucrose, making it an ideal sweetener for drinks. Canned fruits and juices contain 4 to 8 percent fructose. Recent statistics indicate that the average person takes in 60 pounds of fructose a year.

Small doses of fructose help with the uptake of glucose into the liver, and the liver uses it for glycogen synthesis. Conversely, glucose enhances the absorption of fructose. Recent evidence shows that many people cannot tolerate fructose in significant amounts. That leads to symptoms that look like irritable bowel syndrome’gas, abdominal pain, bloating, diarrhea and constipation. Lactose intolerance produces some of the same symptoms, and some people who complain of lactose problems may actually be feeling the effects of fructose. ALL Features of Fructose

Much confusion over the effects of fructose is linked to how much of the sugar the body actually takes in. Large concentrations of fructose have a greater tendency than other sugars to be converted into triglycerides, or fat’particularly in the case of HFCS, the processed form of the substance that so many people are eating. That’s particularly true when the process form is consumed in excess, which is precisely what many people are doing. The glucose portion of the HFCS compound produces a whopping release of insulin into the blood, which, in turn, promotes triglyceride, or fat, synthesis.

A recent experiment put two groups of healthy people on separate diets for six weeks.1 The diets, which contained the same number of total calories, differed only in their fructose contents, with the fructose diet providing 17 percent of energy as fructose. The other diet contained glucose but no fructose. The men on the fructose diet had average blood triglyceride levels 32 percent higher than those on the glucose diet, although none of the women showed that effect. No other blood lipids, such as cholesterol or HDL, were affected.

Another study showed that what many would consider a beneficial effect of fructose’lack of insulin secretion’can actually lead to overeating and obesity.2 According to the study, fructose doesn’t stimulate the release of insulin and leptin, which signal the central nervous system and brain to indicate satiety. When they aren’t secreted, the body thinks it hasn’t been fed and sets into motion processes that result in increased hunger, thereby initiating a vicious cycle.

Despite not promoting an insulin release, high intake of free fructose, such as in HFCS, paradoxically leads to insulin resistance. That happens because when fructose is eaten in large amounts, the liver upgrades triglyceride production, which interferes with insulin activity and fosters resistance.

Another interesting aspect of fructose metabolism is that it may accelerate the aging process. This has to do with the production of advanced glycation end products (AGE), which leads to sugar accumulation in protein structures and a stiffness and hardening of connective tissue. That’s the process thought to produce the rapid aging effects of uncontrolled diabetes, a disease of poor sugar metabolism by way of insulin defects. Fructose is thought to increase AGE through what chemists call the Maillard reaction’a cross-linking of proteins, or a browning effect, resulting from abnormal accumulation of sugar in protein structures. Many scientists consider this reaction a primary cause of the aging process, and fructose is particularly efficient at promoting it, working seven times faster than glucose.

In a study that compared the level of AGE in vegetarians and meat eaters, the veggie eaters had higher levels of AGE than the meat eaters.3 That seems odd; you’d think that because vegetarians eat more of their food raw, they’d show lower levels of AGE, which is triggered by cooking. Since vegetarians eat more fruit, and thus fructose, could that be the cause? Not according to the study authors, who note that the fructose intake of the vegetarians was not considered excessive.

Studies in rats do, however, show that long-term high intake of fructose does lead to increased AGE and apparent increased aging effects.4 Of all the organs in the body, the kidneys are the most susceptible to the ravages of aging. Most older people have only about 40 percent of their total kidney function remaining. A recent rat-based study suggests that one reason for kidney malfunction with age may be long-term high intake of fructose promoting a Maillard reaction in the kidneys.5

Other studies show that eating large amounts of sucrose, or table sugar, has a pro-oxidant effect6 because of excess production of unpaired electrons, or free radicals, that wreak havoc on various cellular structures and organs of the body. Another theory of aging is that we age because of long-term oxidative damage that may lead to problems in cellular replication. The study cited here hints that the fructose portion of the sucrose molecule causes the pro-oxidant effect.

There may be a way to prevent both the oxidative and triglyceride-raising effects of fructose, according to a recent study.7 It found that when rats on a high-fructose diet got oligofructose’the name given to long chains, or a sort of complex-carbohydrate version, of fructose’the oxidative effects and increase in triglyceride levels were nullified. An example of this is inulin, found in chicory. While that type of carb can’t be digested, it can be fermented by bacteria in the intestine. A form of oligofructose called FOS is sold as a probiotic supplement to promote the growth of beneficial bacteria in the intestine. FOS consists of three to five units of D-fructose and D-glucose, both of which cannot be digested as sugars (the body can only use L forms of sugars).

Fructose, which increases the absorption rates of iron, zinc and magnesium, affects mineral metabolism for both good and ill.8 It shows a potent chelating activity with minerals, leading to greater absorption’significant because minerals are far harder for the body to absorb than vitamins. One study, however, connected low intake of magnesium to fructose’s promotion of increased kidney calcium deposits and loss of phosphorus in male and female rats.9 Copper is a vital mineral nutrient. The body needs it in order to use iron; it’s an essential part of superoxide dismutase, a primary antioxidant enzyme in the body; and it’s needed for collagen and connective-tissue synthesis. Recent studies link colon cancer to decreased copper intake. Too little copper also lowers levels of high-density lipoprotein (HDL), a cholesterol carrier that protects against cardiovascular disease onset. Animal studies show that a high fructose intake dramatically promotes copper excretion. But a study of humans who got 20 percent of their energy intake from fructose showed a minimal effect on copper metabolism. On the other hand, both zinc and vitamin C promote copper excretion and in combination with high fructose intake could lead to real problems with that essential mineral.

Fructose and Exercise

Most of the published studies comparing the intake of fructose and glucose before exercise clearly show that glucose is superior. The longer assimilation time of fructose is a disadvantage before exercise, with one notable exception. If taken 45 minutes before extended exercise sessions, fructose supplements can extend existing glucose stores, thus preventing fatigue.

You’d think fructose would be an ideal energy source before training because it doesn’t promote an insulin release, which can lead to hypoglycemia, or low blood sugar, in some people. Unfortunately, fructose tends to cause gastrointestinal distress because its longer absorption time enables water to enter the gut and dilute the concentration of fructose. On the other hand, a study presented at the 2003 meeting of the American College of Sports Medicine found that a combination of fructose and glucose led to a level of carbohydrate oxidation greater than that of glucose alone.

Another problem with taking in fructose either before or during exercise is that the body can absorb only a limited amount of it. In addition, exercise reduces intestinal transit time, which can lead to the fructose’s not being completely absorbed and thus to indigestion.10 Another study found that, during exercise to exhaustion, fructose may offer some benefit if combined with glucose.11

You may also want to think twice about taking in large amounts of fructose following a workout. Since you want to promote an insulin surge after training to increase muscle glycogen synthesis and amino acid uptake, fructose is no help there. In addition, exercise lowers the induction of liver fat-synthesizing enzymes, an effect that fructose blocks.12

On the other hand, you can take advantage of fructose’s slow absorption to delay the absorption of higher-glycemic-index carbs, such as baked potatoes. Just take in fructose 30 to 60 minutes before eating a starchy carb.13 Lowering absorption times of high-glycemic-index carbs leads to decreased insulin release, less chance of bodyfat synthesis and a more stable blood glucose level for more energy and appetite control.

Fructose and the Future

Most of the negative effects of fructose are linked to either an excessively large intake or too many processed foods containing high-fructose corn syrup. The notion that eating fruits and vegetables will make you fat is just plain wrong. Fruits and veggies contain significant levels of fiber, which itself offers considerable health benefits and slows down the absorption of fruit sugars. Vegetarians and semivegetarians, who generally eat much more fruit than others, don’t show any of the negative health effects associated with high fructose intake.

Nor is fruit as high in fructose as many antisugar fanatics would have you believe. It accounts for 5 to 7.7 percent of the wet weight of cherries, pears, bananas, grapes and apples. If you still think that’s too much, then opt for other fruits, such as strawberries, blackberries, blueberries, oranges and grapefruit. They contain only 2 to 3 percent fructose, or 2 to 3 teaspoons per pound. Studies show that the average intake of fructose from fruit amounts to only 15 grams a day, not nearly enough to cause any of the problems linked to fructose overdose.

By eating fruits and veggies you’ll be getting all their protective nutrients and none of the fructose negatives. Forget what the antifructose advocates allege about the ‘dangers’ of eating fruit. Indeed, based on the benefits of fruits and vegetables, you’d have to conclude that their critics are simply bananas.


1 Bantle, J.P., et al. (2000). Effects of dietary fructose on plasma lipids in healthy subjects. Am J Clin Nutr. 72:1128-34.
2 Elliot, S.S., et al. (2002). Fructose, weight gain and insulin resistance syndrome. Am J Clin Nutr. 76:911-22.
3 Sebekova, K., et al. (2001). Plasma levels of advanced glycation end products in healthy, long-term vegetarians and subjects on a Western mixed diet. Eur J Nutr. 40:275-81.
4 Levi, B., et al. (1998). Long-term fructose consumption accelerates glycation and several age-related variables in male rats. J Nutr. 126:1442-1449.
5 Kizhner, T., et al. (2002). Long-term fructose intake: Biochemical consequences and altered renal histology in the male rat. Metabolism. 51:1538-1547.
6 Busserolles, J., et al. (2002). Short-term consumption of a high-sucrose diet has a pro-oxidant effect in rats. Brit J Nutr. 87:337-42.
7 Busserolles, J., et al. (2003). Oligofructose protects against the hypertriglyceridemic and pro-oxidant effects of a high fructose diet in rats. J Nutr. 133:1903-08.
8 O’Dell, B. (1993). Fructose and mineral metabolism. Am J Clin Nutr. 58(suppl):771S-778S.
9 Milne, D.B., et al. (2000). The interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men. J Am Coll Nutr. 19:31-37.
10 Fujisawa, F., et al. (1993). The effect of exercise on fructose absorption. Am J Clin Nutr. 58:75-79.
11 Brundle, S., et al. (2000). Comparison of fructose and glucose ingestion before and during endurance cycling to exhaustion. J Sports Med Phys Fitness. 40:343-349.
12 Fiebig, R., et al. (1998). Exercise training downregulates hepatic lipogenic enzymes in meal-fed rats: fructose vs. complex carbohydrate diets. J Nutr. 128:810-817.
13 Heacock, P., et al. (2002). Fructose prefeeding reduces the glycemic response to a high glycemic index, starchy food in humans. J Nutr. 132:2601-2604. IM

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