Written by Angeline A. De Leon, Staff Writer. Using a mouse model, researchers demonstrated that aspartame (known as NutraSweet and Equal) impaired glucose metabolism by altering gut composition and promoting hyperglycemia and insulin resistance.

health hazards - artificial sweetenersAspartame (APM) is one of the most popular artificial sweeteners on the market today. Commercially known as NutraSweet and Equal, this sugar substitute is reportedly present in over 6000 food products 1 and is perhaps most commonly associated with diet soft drinks. Dietary intake of artificially sweetened foods and beverages has been linked to cardiometabolic disorders such as high blood pressure, obesity, and insulin resistance 2,3. In fact, daily consumption of APM-sweetened diet soda has been found to increase risk of type 2 diabetes by nearly 75% 4, although findings in general have been somewhat mixed. Emerging evidence now suggests that the onset of metabolic disease can be traced to alterations in the gut microbiome 5, referring to the population of microorganisms living in the human intestine. Approximately comprised of tens of trillions of bacterial species, gut microbiota play a key role in metabolism and caloric extraction, with compositional changes in the microbiome correlating to changes in metabolite concentrations in the blood 6. To explore the potential mechanisms through which APM may affect metabolism and gut microbiota profile, Canadian researchers at the University of Calgary carried out an investigation 7 looking at the impact of low-dose APM (equivalent to 2-3 cans of diet soda daily for the average American) on the gut flora of diet-induced obese rats.

A total of 44 male Sprague-Dawley rats were randomized into two dietary groups (standard chow with 12% kcal fat or high fat with 60% kcal fat) for two weeks and then randomly assigned to fluid treatment (water or low-dose APM at 5-7 g/kg/d), resulting in four treatment groups: chow water (CHW), high-fat water (HFW), chow aspartame (CHA), and high-fat aspartame (HFA). Access to food and fluid was ad libitum for 8 weeks prior to sacrifice. Animals were weighed weekly for 10 weeks, measured for food and fluid intake at Week 7, and given oral glucose and insulin tolerance tests at Week 8. Fecal samples were collected at Week 10 and analyzed for gut bacterial composition.

Results indicated that while CHA and HFA groups consumed less calories, compared to their control groups (17% and 25%, respectively, p < 0.05), fasting blood glucose levels were elevated in both APM groups (p < 0.05, respectively). The insulin tolerance test also showed that aspartame was associated with impaired insulin-stimulated glucose disposal in both CHA and HFA groups, relative to water controls, independent of body composition (p < 0.05, respectively). Furthermore, APM was found to increase total bacteria and elevate circulating levels of the short chain fatty acid propionate (a bacterial end product reported to contribute to reduced glucose and insulin tolerance 8) by about 2.5-fold in both CHA and HFA, relative to controls (p < 0.05, respectively).

General findings suggest that APM has a differential influence on aspects of metabolic disease: although a beneficial effect of APM was apparent in terms of caloric consumption and total gut bacteria count, it was also found to result in hyperglycemia and an impaired ability to reduce to insulin, as well as higher levels of a microbial metabolite associated with altered insulin resistance. Overall, findings appear consistent with the controversial profile currently associated with aspartame in the field of dietetics. 

Source: Palmnas MSA, Cowan TE, Bomhof MR, et al. Low-dose aspartame consumption differentially affects gut microbiota-host metabolic interactions in the diet-induced obese rat. PLoS ONE. 2014; 9(10): e109841. DOI: 10.1371/journal.pone.0109841.

© 2014 Palmnas et al. Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Posted April 3, 2018.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

  1. Magnuson B, Burdock G, Doull J, et al. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. Critical reviews in toxicology. 2007;37(8):629-727.
  2. Dhingra R, Sullivan L, Jacques PF, et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007;116(5):480-488.
  3. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2008;117(6):754-761.
  4. Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes care. 2009;32(4):688-694.
  5. Ley RE, Bäckhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proceedings of the National Academy of Sciences of the United States of America. 2005;102(31):11070-11075.
  6. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006;444(7122):1022.
  7. Palmnäs MS, Cowan TE, Bomhof MR, et al. Low-dose aspartame consumption differentially affects gut microbiota-host metabolic interactions in the diet-induced obese rat. PloS one. 2014;9(10):e109841.
  8. Tremaroli V, Bäckhed F. Functional interactions between the gut microbiota and host metabolism. Nature. 2012;489(7415):242.