No plausible mechanism to explain allegations that aspartame may prevent weight loss in humans
24 November 2016
ISA response to mice study by researchers at Massachusetts General Hospital
The mechanism suggested by researchers at Massachusetts General Hospital claiming that aspartame might not promote weight loss is simply not biologically plausible. On the contrary, strong evidence from clinical studies in humans supports the helpful role of low calorie sweeteners, such as aspartame, in reduced energy intake and weight loss, when used in place of sugar as part of a weight loss programme.
The new publication in Applied Physiology, Nutrition, and Metabolism1 claims that the aspartame breakdown product phenylalanine interferes with the action of an enzyme previously shown to prevent metabolic syndrome. However, what the authors fail to mention in a Press Release2 issued by Massachusetts General Hospital is that phenylalanine is actually a common amino acid naturally occurring in meat, fish, eggs, legumes, dairy products, nuts and other food products.
Aspartame is a molecule whose structure is quite simple, being composed of a dipeptide containing 2 amino acids, aspartic acid and phenylalanine3. After ingestion, aspartame is quickly digested into its main components and a small amount of methanol4. It is well documented that both aspartic acid and phenylalanine are in the same form as when absorbed into the body from natural food sources such as meat or dairy products5. Importantly, the amounts of phenylalanine from aspartame breakdown is much lower than those obtained from many other natural dietary sources. For example, specifically for phenylalanine, 100 g of chicken provide a 12.5 greater intake of phenylalanine than a diet soda.6
Therefore, the claims in this paper based on research in mice simply do not apply to humans, who consume a variety of foods that contain much higher amounts of the amino acid phenylalanine.
Scientific evidence shows that use of low calorie sweeteners in place of sugar, in both children and adults, actually leads to reduced energy intake and body weight.
- Gul SS, Hamilton ARL, Munoz AR, et al. Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice. Applied Physiology, Nutrition, and Metabolism, 2016; DOI: 10.1139/apnm-2016-0346
- European Food Safety Authority. Scientific Opinion on the re-evaluation of aspartame (E 951) as a food additive. EFSA J. 2013;11:3496. doi:10.2903/ j.efsa.2013.3496.
- Magnuson BA, Burdock GA, Doull J, et al. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. CRC Crit Rev Toxicol. 2007;37:629–727.
- Butchko HH, Stargel WW, Comer CP, et al. Aspartame: review of safety. Regul Toxicol Pharmacol. 2002;35:S1–S93
- Magnuson BA, Carakostas MC, Moore NH, et al. Biological fate of low-calorie sweeteners. Nutrition Reviews 2016; 74(11): 670-689
- Rogers PJ, Hogenkamp PS, de Graaf K, et al. Does low-energy sweetener consumption affect energy intake and body weight? A systematic review, including meta-analyses, of the evidence from human and animal studies. Int J Obes 2016; 40(3): 381-94