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The dangers of fructose (fruit sugar)

Fructose is a simple sugar found in honey, fruit, table sugar (sucrose), and high-fructose corn syrup (HFCS). Worldwide fructose intake has quadrupled over the last century,(1) with the last 30 years witnessing the most rapid acceleration. This increase has been paralleled by a similar rise in obesity, diabetes, hypertension, and kidney disease. (1-2). While such associations don’t mean that the one necessarily caused the other, animal experiments have shown such causal relationships, with increases in diseases associated with the metabolic syndrome - insulin resistance, high levels of triglycerides in the bloodstream, high blood pressure, abdominal obesity, inflammation, arterial damage, kidney disease, and fatty liver - much higher in animals fed fructose than in those fed glucose or starches.(3)

Fructose is unique amongst sugars, in that it up-regulates its own transporter (Glut5) and metabolism (fructokinase) (4). Because of this, the more fructose one eats, the more sensitive one becomes to its effects. This explains why obese persons appear to be more sensitive to the harmful effects of fructose than are non-obese persons.(5)

Fructose consumption has been associated with weight gain in past studies. This may be because fructose doesn’t appear to trigger the hormonal signals involved in the long-term control of energy use in the way that glucose does.(6) A glucose diet stimulates the pancreas to secrete insulin. This results in the release of leptin by fat cells (adipocytes) and the inhibition of ghrelin secretion from the gastrointestinal tract. These alterations stimulate centres in the brain that regulate satiety and energy balance. As fructose doesn’t stimulate insulin, leptin and ghrelin responses are not generated (7). Study has shown that people fed fructose had a greater appetite the following day than those fed glucose-fed.(7) This could well result in leptin resistance.

Because fructose does not raise blood glucose levels, it has a lower glycaemic index than other sugars and starches. For this reason, it is a recommended sweetener for diabetics - plus, of course, ‘five portions of fruit’, etc; and in a few studies, HbA1c was lowered in diabetics using fructose. However, while low doses of fructose may improve glucose control in diabetics, the role of fructose in the metabolic syndrome, stimulating the production of advanced glycation end-products (AGEs) and in causing cataracts in diabetic animals means that fructose is a poor choice for any diabetic. This conclusion is also held by the American Diabetes Association, (8) - although they still promote ‘5-portions’ advice. Indeed, as far as heart disease is concerned, a ‘fructose index’ based on the percentage and amount of fructose in various foods might be a better indicator than the glycaemic index.(2)

So, are high doses of fructose safe? A recent study concluded that fructose intake up to 90 grams per day may actually be beneficial because of its effects of lowering HbA1c concentrations,(9) despite the potential countering effects of increases in blood triglycerides. But it may be misleading to conclude that this amount of fructose is safe by examining only the effects of fructose on triglycerides, weight, and HbA1c. Taking into consideration the increasing evidence that high fructose intake can also raise blood pressure, decrease insulin sensitivity, lower glucose tolerance, increase apolipoprotein-B concentrations, and cause microvascular disease, glomerular hypertension, kidney damage, fatty liver, and more, (10-12) there are some important questions about the safety of high doses of fructose in humans.


1.Johnson RJ, Segal MS, Sautin Y, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007; 86(4): 899-906.

2.Segal MS, Gollub E, Johnson RJ. Is the fructose index more relevant with regards to cardiovascular disease than the glycemic index? Eur J Nutr 2007; 46(7): 406-17.

3.Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol 2006; 290(3): F625-31.

4.Ouyang X, Cirillo P, Sautin Y, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol 2008; 48(6): 993-9.

5.Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr 2008; 87: 1194-203.

6.Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005; 63(5): 133-57.

7.Teff KL, Elliott SS, Tschop M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 2004; 89(6): 2963-72.

8.Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2002; 25(1): 202-12.

9.Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasmid triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr 2008; 88: 1419-37.

10.Brown CM, Dulloo AG, Yepuri G, Montani JP. Fructose ingestion acutely elevates blood pressure in healthy young humans. Am J Physiol 2008; 294(3): R730-7.

11.Swarbrick MM, Stanhope KL, Elliott SS, et al. Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women. Br J Nutr 2008; Apr 3: 1-6 (Epub ahead of print).

12.Glushakova O, Kosugi T, Roncal C, et al. Fructose induces the inflammatory molecule ICAM-1 in endothelial cells. J Am Soc Nephrol 2008 May 28 (Epub ahead of print).

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