Sally-Ann Creed

Dangers Exposed

FRUCTOSE: DANGERS OF FRUCTOSE EXPOSED!
- BY DR NANCY APPLETON

The delusion that fructose is an acceptable form of sugar is quite prevalent in many nutritional circles. Studies done by Dr Appleton and others are important contributions to the scientific literature that confirms that it is not. Nearly all simple sugars are metabolized quickly and disrupt insulin levels, which contributes to most chronic illness. So don't be fooled - avoid fructose - it does the same, and much worse. This doesn't mean that one should avoid fruit, however. Eating small amounts of whole fruit will not provide tremendous amounts of fructose and should not be a problem for most people, unless diabetes, Syndrome X or obesity is an issue. However, fruit juices, sodas, and other beverages sweetened with fructose should be avoided at all costs.

On the basis of the available data regarding the endocrine and metabolic effects of consuming large quantities of fructose, and the potential to exacerbate components of insulin resistance syndrome, it is preferable to primarily consume dietary carbohydrates in the form of glucose (free glucose and starch). This is particularly important for those with existing high cholesterol levels or insulin resistance who could be more susceptible to the negative metabolic effects of fructose.
(American Journal of Clinical Nutrition)
November 2002 Vol. 76, No. 5, 911-922)

The consumption of fructose (corn syrup) has risen considerably in the general population within recent years. In 1980 the average person ate 39 pounds of fructose and 84 pounds of sucrose. In 1994 the average person ate 66 pounds of sucrose and 83 pounds of fructose. 153 pounds is approximately 20% of the average person's diet. This increase is due to several factors. There was a decreased use of cane and beet sugar (sucrose) in processed foods and a wide spread use of corn syrup due to economics. Corn is much cheaper, and is twice as sweet as table sugar. It is absorbed only 40% as quickly as glucose and causes a modest rise in blood sugar.

A few years ago the medical community revealed that there was good news for diabetics. Many people had previously known that table sugar (sucrose) was not a healthy food for diabetics because it raised their blood sugar levels above normal. The new 'revelation' was that diabetics could eat fructose because fructose did not raise their blood sugar level extremely high. The medical community recommended fructose because of a low increase in glucose in the blood. The scientists did not look at other factors in the body when a person eats sugar.

Let's look at some of these factors now.

Fructose has no enzymes, vitamins, and minerals and robs the body of its micronutrient treasures in order to assimilate itself for physiological use. Fructose browns food more readily (Maillard reaction) than with glucose. This may seem like a good idea, but it is not. The Maillard reaction, a browning reaction, happens with any sugar. With fructose it happens seven times faster with than glucose, results in a decrease in protein quality and a toxicity of protein in the body. This is due to the loss of amino acid residues and decreased protein digestibility. Maillard products can inhibit the uptake and metabolism of free amino acids and other nutrients such as zinc and some advanced Maillard products have mutagenic and/or carcinogenic properties. The Maillard reactions between proteins and fructose, glucose, and other sugars may play a role in ageing and in some clinical complications of diabetes.
Research showed that in subjects that had healthy glucose tolerance and those that had unhealthy glucose tolerance, fructose caused a general increase in both the total serum cholesterol and in the low density lipoproteins (LDL) in most of the subjects. This puts a person at risk for heart disease. Another study showed that the very low density lipoproteins (VLDL) increased without an apparent change in high density lipoproteins (HDL). The VLDL and the LDL should be as low as possible and the HDL should be as high as possible.
There is a significant increase in the concentration of uric acid that is dependent on the amount of fructose digested. After glucose no significant change occurs. An increase in uric acid can be an indicator of heart disease.
Fructose ingestion in humans results in increases in blood lactic acid, especially in patients with pre-existing acidotic conditions such as diabetes, postoperative stress, or uremia. The significance to human health is that extreme elevations cause metabolic acidosis and can result in death.
Fructose is absorbed primarily in the jejunum and metabolized in the liver. Fructose is converted to fatty acids by the liver at a greater rate than is glucose. When consumed in excess of dietary glucose, the liver cannot convert all of the excess of fructose in the system and it may be malabsorbed. What escapes conversion and being absorbed into the cells may be thrown out in the urine. Diarrhea can be a consequence.
Fructose interacts with oral contraceptives and elevates insulin levels in women on "the pill."
Fructose consistently produced higher kidney calcium concentrations than did glucose in a study with rats. Fructose generally induced greater urinary concentrations of phosphorus and magnesium and lowered urinary pH compared with glucose. The balance of minerals in the body is very important for the function of vitamins, enzymes and other body function. When the minerals are out of the right relationship, the body chemistry suffers. The presence of diarrhoea might be the cause of decreased absorption of minerals.
Fructose-fed subjects lose minerals. They had higher fecal excretions of iron and magnesium than did subjects fed sucrose. Apparent iron, magnesium, calcium, and zinc balances tended to be more negative during the fructose feeding period as compared to balances during the sucrose feeding period.
A study of 25 patients with functional bowel disease showed that pronounced gastrointestinal distress may be provoked by malabsorption of small amounts of fructose.
Many times fructose and sorbitol are substituted for glucose in parenteral nutrition (intervenious feeding, IV). This can have severe consequences with people with hereditary fructose intolerance, a congenital disorder affecting one in 21,000. A European doctor declared: "Fructose and sorbitol containing infusion fluids have no further place in our hospital pharmacies."
There is significant evidence that high sucrose diets may alter intracellular metabolism, which in turn facilitates accelerated aging through oxidative damage. Scientists found that the rats given fructose had more undesirable cross-linking changes in the collagen of their skin than in the other groups. These changes are also thought to be markers for ageing. The scientists say that it is the fructose molecule in the sucrose, not the glucose, which presents the larger problem.
Fructose is not metabolized the same as other sugars. Instead of being converted to glucose which the body uses, it is removed by the liver. Because it is metabolized by the liver, fructose does not cause the pancreas to release insulin the way it normally does. Fructose converts to fat more than any other sugar. This may be one of the reasons Americans continue to get fatter. Fructose raises serum triglycerides significantly. As a left-handed sugar, fructose digestion is very low. For complete internal conversion of fructose into glucose and acetates, it must rob ATP energy stores from the liver.
Fructose inhibits copper metabolism. A deficiency in copper leads to bone fragility, anaemia, defects of the connective tissue, arteries, and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks, and an inability to control blood sugar levels."
Nancy Appleton, Ph.D. is a Clinical Nutritionist, researcher, lecturer, and author of Lick the Sugar Habit, Healthy Bones, Heal Yourself With Natural Foods and the Curse Of Louis Pasteur, and her book Lick the Sugar Habit Sugar Counter.

Dr Appleton's website is www.NancyAppleton.com

Feed a lab rat fructose, at levels comparable to those in human diets, and it develops insulin resistance, even if it stays lean. Researchers at the University of Toronto in Canada fed a high-fructose diet to Syrian golden hamsters, which have a fat metabolism remarkably similar to humans'. In a matter of weeks, the hamsters developed Syndrome X - including high triglyceride levels and insulin resistance. A powerful study of fructose's effects on humans was published last year. Clinical Nutritionist, John Bantle and his colleagues at the University of Minnesota at Minneapolis fed a diet containing 17 per cent of the total energy as fructose to two dozen healthy volunteers for six weeks. It sounds like a lot of fructose, but Bantle reckons that at least 27 million Americans eat this much in their diet.

They then fed the volunteers a diet sweetened with glucose and nearly devoid of fructose. The results were dramatic, particularly in the men, who proved to be more sensitive than women to fructose. Why this should be so is not yet clear. "The fructose diet produced significantly higher triglyceride concentrations in the blood, compared to the glucose diet," says Bantle . In men, levels were 32 per cent higher. More importantly, on the fructose diet, the triglyceride levels peaked just after meals when these fats can do the most damage to our arteries. He'd like to see a marked reduction in the amount of fructose added to beverages and food in the Western diet. "It's a wake-up call for the food industry," Zammit agrees. "Food manufacturers are good at labeling processed foods as '99 per cent fat free'. What they don't say is that they are 15 per cent sugars, which is probably worse than some fats." His concern is that "people may deliberately select low-fat processed foods, thinking they are making a healthy choice, and yet the product could be very high in fructose."

The dangers of fructose are not yet widely known, and the amounts consumed in the average Western diet have shot up since the 1970s. The sucrose molecule is half fructose and half glucose, so eating anything with ordinary sugar in it gives you a dose of the stuff. Worse still, food manufacturers in the late 1960s started to use a cheap sweetener, corn (maize) syrup, which is virtually pure fructose. It's now added to all sorts of food, including breakfast cereals & a vast range of processed foods.

"Metabolic effects on the population from this rapid change may not be apparent for some time," reckons Judith Hallfrisch of the National Institute of Ageing in Baltimore. But give fructose a few decades to wreak its metabolic havoc, and the next generation of epidemiologists may be picking up the pieces. Of course, it's tempting to think you might be one of the lucky ones who will never develop insulin resistance. People differ in their susceptibility to Syndrome X, no doubt partly as a result of their genetic makeup - though the key susceptibility genes have yet to be tracked down.

Foetal nutrition and diet in early infancy may be equally important, as David Barker of the University of Southampton argues. Babies who are undernourished in the womb and shortly after birth seem to be particularly susceptible to Syndrome X, especially if they are well fed in later life and become overweight. Even if the genetic cards are stacked against you, there's intriguing evidence that diet can still make a difference. Consider the Pima, Native Americans of southern Arizona, nearly all of whom are cursed with a "thrifty genotype". Their metabolism is especially geared to laying down fat in preparation for times of famine. By old age, nearly all have developed type 2 Diabetes. Even by age eight, most are already insulin resistant. But this plague only struck after the Pima people were introduced to Western foods.

Pima Indians who ate a typical Western diet were found to be two and a half times as likely to develop diabetes as those who ate a somewhat more traditional diet over the 10 years of the study. Genes are not necessarily destiny. But scientists acknowledge that to change our ways, we need help - if only to resist all those tempting convenience foods now filling our supermarket shelves. If the food industry is reluctant to take the new health messages on board, it could be "strongly regulated" to produce a tasty but healthy diet, argues editor Waldhaus. Such a change might even be in food producers' own interests. Perhaps, says Waldhaus, the industry will one day be forced to pay damages "similar in scale to those awarded against the tobacco industry today" to consumers made fatally ill by eating their products.

How Much Fructose Is In Our Food?

The message from the latest nutritional research is that if you feel like something sweet, reach for a piece of fruit. Fructose is found in fruit and vegetables, but unlike processed foods it's present in vanishingly small amounts and is bound up with complex plant fibre and other nutrients that offer many health benefits.

But it's not just sugars we need to watch. The kinds of fats we eat also have an enormous impact on our long-term health, says Len Storlien, director of metabolic research at the Astra Zeneca. Instead of struggling to eat far less fat overall, he argues that people should reduce their consumption of saturated fat by switching to olive oil and especially marine fish oils. These can suppress the liver's release of harmful triglycerides. A diet high in these polyunsaturated fatty acids combats Syndrome X.

Dr Gerry Reaven of Stanford University, who coined the term Syndrome X, couldn't agree more. But he's also convinced that the "low-fat" message has encouraged people to eat more insulin-stimulating carbohydrate instead, fuelling the epidemic of insulin resistance. There's a third, albeit controversial strategy to avoid Syndrome X: eating "slow-release" carbohydrates that arguably don't provoke the same rush of insulin. These are complex carbohydrates with lots of plant fibre-such as barley, millet and brown rice - and those that the body can digest only slowly, such as pasta, beans and lentils.
(New Scientist Magazine, Volume 171 Issue 2306, January 9, 2001,
page 26. The Journal of Nutrition, Vol. 131:2001 p 2074)

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