Role of Fructose and Low-Calorie Sweeteners on Gut Microflora is Speculation

An article “Gut Microbial Adaptation to Dietary Consumption of Fructose Artificial Sweeteners and Sugar Alcohols: Implications for host-microbe interactions contributing to obesity,” fails to show that fructose and low-calorie sweeteners contribute to obesity. The authors hypothesized that consuming fructose or low-calorie sweeteners could disrupt the environment where food is digested and that could lead to metabolic disorders and obesity.  However, this hypothesis is a theory that has not been proven scientifically, and is not supported by the current body of scientific research.

The Calorie Control Council cites the following as serious limitations of this study:

  • The hypothesis presented in this paper does not reflect the extensive body of literature on low-calorie sweeteners (LCS) and fructose.  Numerous studies have shown that low-calorie sweeteners may assist individuals in losing weight, maintaining weight loss or reducing energy intake.1 Two recent reviews concluded that fructose does not cause changes in bodyweight.2 Further, leading health groups such as the American Heart Association, Academy of Nutrition and Dietetics and American Diabetes Association support the safe use of low-calorie sweeteners in healthy weight management.  Thus, the theory that low-calorie sweeteners and fructose could lead to weight gain is counter to the robust scientific research that has already been established on low-calorie sweeteners and weight.
  • The authors alleged that consuming low-calorie sweeteners leads to spikes in insulin production which causes blood sugar levels to drop. However, a 2010 review by Renwick and Molinary concluded that, “There is no consistent evidence that LCS increase appetite or subsequent food intake, cause insulin release… in normal subjects.”3
  • Payne et al also asserted that fructose does not cause satiety, which delays eating after a meal and may also contribute to obesity. However, the research on fructose and satiety has been inconsistent. For example, in a paper published in the Journal of Nutrition, Moran suggests that the relationship between fructose and satiety may be influenced by a number of external factors such as the time of consumption and the composition of fructose (pure vs. mixed).4

Obesity is a multi-faceted issue.  Weight maintenance and health involve many factors, such as healthful eating habits (including balance and moderation), exercise and long-term commitment.  There is no scientific evidence that one component of the diet, such as fructose or low-calorie sweeteners, is responsible for obesity or metabolic disorders.

References
  • Alternative Sweeteners; Edited by Lyn O’Brien Nabors; 4th edition; 2012
  • Dolan LC PS, Burdock GA. Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals. Crit Rev Food Sci Nutr. 2010;50(1):53-84.
  • Renwick, A.G., and Molinary, S.V. 2010. Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release. British Journal of Nutrition 104(10): 1415-1420.
  • Moran, T.H. 2009. Fructose and Satiety. Journal of Nutrition 139: 1S-4S.
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