Coronary heart disease is a major cause of morbidity and mortality in Western societies. The metabolic syndrome, characterized by obesity, insulin resistance, elevated blood pressure, elevated triglycerides, and low levels of high-density lipoprotein cholesterol, confers substantial risk of coronary heart disease. Current pathogenetic models suggest that postprandial hyperlipidemia is one specific metabolic abnormality that is typically associated with increased morbidity. In this issue of the JCI, Stanhope and colleagues demonstrate that consumption of fructose-sweetened but not glucose-sweetened beverages for 10 weeks increases de novo lipid synthesis, promotes dyslipidemia, impairs insulin sensitivity, and increases visceral adiposity in overweight or obese adults (see the related article beginning on page 1322).
Susanna M. Hofmann, Matthias H. Tschöp
Submitter: John White | email@example.com
White Technical Research
Published March 10, 2010
In their commentary accompanying the recent mechanistic paper from Peter Havel’s group (1), Hoffman & Tschöp (2) do not show the same restraint Havel does in extrapolating his admittedly unphysiologic results to typical human diets.
Their focus on added sugars disregards the importance of looking at all caloric sources. Energy intake over the past 35 years from added sugars, flour/cereal and fats increased 50, 190 and 300 cal/d, respectively (3). We are not just taking in more fructose sweetener; we are eating more of everything.
The authors confuse two commercial products. Pure (crystalline) fructose is a specialty ingredient used for specific functional reasons comprising <1% of the sweetener market (4). High fructose corn syrup (HFCS) is nearly equal parts fructose and glucose; it is now generally agreed to be metabolically equivalent to sucrose (5-8).
Hoffman & Tschöp fail to put Havel’s work into proper perspective—there are no reliable data that fructose poses a specific health risk at typical intake levels (9.1% of energy) (9). The fructose diet used by Havel at 25% of energy is a poor model for the typical human diet on two counts: it tests pure sugars in isolation, whereas fructose and glucose are nearly always taken together in fruits/vegetable/nuts or added sugars (sucrose, HFCS, fruit juice concentrates, honey); and it uses levels 2.5-fold higher than mean consumption levels and 50% greater than even the highest consumers of fructose (95th percentile <18% of energy).
It is precisely because of the lack of perspective offered by Hoffman & Tschöp and others that the public is now convinced fructose poses a health risk, when in reality none has been demonstrated in humans at typical intake levels.
Conflict of interest statement: The author is a consultant to the food and beverage industry in the area of nutritive sweeteners. His clients include research institutes, food industry councils, trade organizations and individual companies.