Aspartame has no effect on blood glucose levels

Aspartame has no effect on blood glucose levels: products with aspartame are effective tools in weight management.

17 September 2014: Allegations about foods and drinks with low calorie sweeteners, published in a paper by Suez et al and based largely on experiments in mice using saccharin, ignore the large body of science which demonstrates that low calorie alternatives help people to control their weight.

A thorough review and meta-analysis published by Miller & Perez earlier this year concludes that substituting "LCS (low calorie sweetened) options for the regular calorie versions results in modest weight loss and may be a useful dietary tool to improve compliance with weight-loss and weight management plans."

Furthermore, an earlier meta-analysis, undertaken by de la Hunty, Gibson & Ashwell, showed that replacing one regular soft drink per day with a low calorie soft drink sweetened with aspartame will lead to a weight loss of about 11 pounds over the course of one year.

There are a series of flaws in the paper by Suez et al:

  • Comments throughout the paper suggest that the authors are unfamiliar with the science which supports the safety and benefits of low calorie sweeteners.
  • The authors seem to be unaware that different sweeteners are metabolized differently or that aspartame, one of the most popular sweeteners globally, is broken down to common dietary components in the upper GI tract, just like other protein foods. Aspartame is not available to the gut microflora studied. It is reactions of the gut microflora that appear to form the primary basis of the authors' statements and conclusions. Aspartame cannot have the adverse effects that Suez et al allege.
  • Two experiments were reported. Several different low calorie sweeteners were used at the start, but the focus then moved to saccharin only. The conclusions, however, were generalized back to all low calorie sweeteners.
  • There were two human analyses, but they are not well described. One involved 7 people (which were then broken down into two groups, one of four and one of three, depending on whether or not a response was observed).
  • Clinical trials in humans (versus mice, the primary subjects in this study) show that low calorie sweeteners do not elicit a glycemic (blood glucose) response or other indicators of metabolic syndrome.

Overweight and obesity are major challenges to health and to the public purse. Scaremongering about safe and beneficial ingredients, which can help people to manage their weight, is not without consequences. Providing publicity for these allegations, and ignoring major reviews of gold-standard, randomly controlled trials, like those by Miller & Perez or de la Hunty, Gibson & Ashwell, does the public a disservice.

A Credulous Response to an Iffy Sweetener Study
Read what the International Food Information Council has to say about this paper

References:

  • Suez et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature (2014)

Weight Control:

  • Miller & Perez. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. American Journal of Clinical Nutrition (2014)
  • de la Hunty, Gibson & Ashwell. A review of the effectiveness of aspartame in helping with weight control. Nutrition Bulletin (2006)

Low calorie sweeteners do not elicit a glycemic (blood glucose) response:

  • Maerks (American Journal of Clinical Nutrition 2012)
  • Bryant (European Journal of Clinical Nutrition, 2014)
  • Renwick and Molinary (2010 review): "No consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects."
  • Carlson & Shah (1989): "No effect of aspartame on serum glucose or insulin…"
  • Horowitz et al (1988):"[I]ngestion of aspartame- or saccharin-sweetened beverages by fasting subjects, with or without diabetes, did not affect blood glucose homeostasis."
  • Also (on lack of cephalic phase insulin production): Abdallah et al. (American Journal of Clinical Nutrition, 1997); Bruce et al. (Metabolism, 1987); Coulston and Gori (Regulatory Toxicology and Pharmacology, 2002, review).