High concentrations of fructose are detrimental because fructose in excess is converted to fatty acids which accumulate in the liver and cause insulin resistance. In nature fructose is found in two main repositories, fruit and honey. The fructose in fruit is contained in a watery medium encased by tough and fibrous cell walls, and eating whole fruit involves the swallowing of intact or semi-intact cells. This fibrous encasement of the fructose hinders the release of the sugar to the chyme in the gut and delays, or in some cases prevents, its absorption. In addition, the bulk of the whole fruit prevent overeating, and this reduces the risk of overloading the liver with nutrients. As we know too well, honey is protected by angry bees and this also slows the digestion rate somewhat. Eating fructose in the foods that nature provides is therefore not problematic. It is true that eating large amounts of fruit, or consumption of honey in excess, will cause liver overload and insulin resistance, but in reality this is unlikely as long as natural laws of consumption are followed.
However, the Western diet now contains sources of fructose that are not encapsulated in fibre and are not protected by angry bees. Food manufacturers have learned to crystallise sugar, a compound that contains both fructose and glucose in equal proportions, and put it in products to improve their appeal to consumers. High fructose corn syrup has been artificially created for the purpose of sweetening soft drinks and similar products, and is made by chemical isomerisation glucose to fructose. Whereas in Europe sugar is now infiltrating our food supply through its use in soft drinks, in the United States and Japan they prefer high fructose corn syrup. However, whatever the poison, the effects on health are the same. The high intake of fructose in the Western diet overloads the liver with energy, and is subsequently converted to fatty acids. These are deposited in tissues where they interfere with the insulin signal cascade and cause insulin resistance, metabolic syndrome, cardiovascular disease and premature death.
The effects of fructose on metabolic regulation have been well studied in rats (here, here, here and here). Human studies also show the rapid development of metabolic disorder when exposed to high concentrations of fructose (here). The use of rats is interesting, because although rats are not humans and extrapolation of results between the two is problematic, at the same time the ability to control the diet of rats and show the poisonous effect of fructose, sometimes over short durations, highlights the problems associated with its intake. For example, in one study, researchers investigated the effects of fructose, glucose or starch on the risk of copper deficiency in rats1. For 8 weeks, rats received a copper deficient diet supplemented with either 62 % starch, glucose or fructose as an energy source. Regardless of the diet, all rats exhibited metabolic changes that included increased liver and heart weights, increase liver lipid accumulation, increased hepatic iron concentrations as well as decreased serum copper, ceruloplasmin and haemocrit concentrations.
However, those rats fed the fructose exhibited more severe copper deficiency symptoms, compared to the starch and glucose fed rats. The fructose fed rats had lower body weights, lower liver glycogen, lower haemocrit levels, lower serum copper and lower albumin levels, but higher liver and heart weights, higher blood urea nitrogen levels and higher glutamic oxaloacetic transaminase concentrations. Plasma cholesterol also increased in the glucose and fructose fed rats, but not the starch fed rats, suggesting that the fibre in the starch was protective of rises in plasma cholesterol. Of the 40 rats initial rats, 17 died during the course of the study. Breaking down the deaths to carbohydrate type showed that 66 % of the fructose rats died compared to 26 % of the glucose rats, and 30% of the starch rats. The authors concluded that the fructose moiety of sugar is responsible for increasing the severity of copper deficiency. This likely results from the added metabolic stress associated with high fructose diets.
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