We agree with Vasankari that dietary fat and inactivity are likely environmental factors contributing to the marked worldwide increase in the prevalence of obesity, and this was noted in our review on the metabolic effects of fructose (1). However, we believe that an increase in fructose consumption also deserves attention as a potential third factor contributing to the escalation of obesity. Because we are not aware of quantitative data regarding the relative contributions of the 3 factors, we consider it premature to conclude that dietary fat and reduced physical activity are "much more probable contributors" to the obesity epidemic. As we and Bray (2) have pointed out, fructose consumption has increased concurrently with the obesity epidemic. Furthermore, because fructose--similarly to dietary fat--does not stimulate insulin secretion, leads to decreased leptin production, and does not suppress the orexigenic gastric hormone ghrelin (3), the lack of effects of long-term fructose consumption on these endocrine systems involved in the regulation of energy homeostasis could lead to increased energy intake, weight gain, and obesity. We therefore regard increased fructose consumption to be a likely contributor to the increased prevalence of obesity in the past 2-3 decades.
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