Abstract
The epidemic of obesity and related metabolic diseases continues to extract an enormous health toll. Multiple potential causes for obesity have been suggested, including increased fat consumption, increased carbohydrate consumption, decreased physical activity, and, most recently, increased fructose consumption. Most literature cited in support of arguments suggesting a link between obesity and fructose consumption is epidemiologic and does not establish cause and effect. The causes of obesity are well-known and involve the overconsumption of calories from all sources. Research employing a pure fructose model distorts the real-world situation of fructose consumption, which predominantly comes from sweeteners containing roughly equal proportions of glucose and fructose. The fructose hypothesis has the potential to distract us from further exploration and amelioration of known causes of obesity. Randomized prospective trials of metabolic consequences of fructose consumption at normal population levels and from sources typically found in the human diet such as sucrose and high-fructose corn syrup are urgently needed.