In a recent paper, Le et al. (1) reported finding differences between the two most commonly used sweeteners in the US, concluding that “compared with sucrose, HFCS [high fructose corn syrup] leads to greater fructose systemic exposure and significantly different acute metabolic effects.” Evidence in support of this conclusion was unconvincing, however, due to significant deficiencies in the experimental design.
First, this was not a comparison of HFCS and sucrose as advertised, but rather a comparison of HFCS and an inconsistent mix of sugars that ranged from 20% sucrose at the start of the study to 0% sucrose at the end (Table 1). Furthermore, the 16% and 12% loss of total sugars over the course of the study in the sucrose and HFCS soft drink variables, respectively, was both significant and not addressed by the authors (Table 1). This variability in sugars composition and concentration over the course of the study could well account for the reported differences in metabolic effects, and effectively nullifies the study conclusions.
Second, the experimental design did not reflect how humans typically consume soft drinks and sugars, and served to exaggerate any existing effects. Soft drinks were administered in large bolus form (24-oz; 300 kcal) to subjects fasted a minimum of 8-h overnight and given no other caloric intake over the course of the 6-h study. While soft drinks are occasionally consumed alone, they are frequently accompanied by foods containing nutrients that can appreciably influence human metabolism.
Third, despite these experimental irregularities, the fasting response parameters in Table 3 from HFCS and sucrose variables were all within the normal human range (2). The small differences observed were, therefore, of questionable clinical significance.
And fourth, the authors’ claim that the increasing frequency of a number of important health disorders is correlated with increased fructose use ignores current consumption trends. In fact, there has been no correlation for more than a decade, since use of HFCS (with sucrose, one of the major sources of added fructose) began to decline in 1999.
The methodological inconsistencies and irregularities in this study invalidate the authors’ conclusion about differences between HFCS and sucrose, and fail to challenge recent literature that supports metabolic similarities between HFCS and sucrose (3-5) and a rational role for fructose at typical human exposures (6-8).