Gastrointestinal Issues and the Gut Microbiome

By the Calorie Control Editorial Team

Many of the questions asked about a possible association between aspartame consumption and gastrointestinal (GI) symptoms can be answered by reviewing its composition and what happens to it after ingestion. The key point is that it has the same destiny as many nutritious foods people eat every day.

How Aspartame is Digested

Aspartame is made up of the amino acids aspartic acid and phenylalanine. The dipeptide is completely broken down in the small intestines by the same digestive enzymes that break down the proteins in foods such as eggs, milk and lentils. Methanol is also a byproduct of aspartame digestion similar to the production of methanol from digestion of other foods. All three of these end products of aspartame digestion – aspartic acid, phenylalanine and methanol – are indistinguishable from those derived from a mixed diet and are absorbed and utilized by the body in the same way as those from foods. Aspartame is digested quickly and never enters the blood stream.

Claims of gastrointestinal issues from aspartame not scientifically confirmed

Subjective reports of digestive disturbances after consuming aspartame sweetened foods or beverages include loose stools, diarrhea, constipation, less frequent stools, nausea, stomach cramps, bloating and gastroenteritis. These symptoms are common after ingesting many other foods and beverages and can also be caused by medications, illnesses and psychological and emotional problems.

The reported GI symptoms associated with aspartame have not been confirmed in double-blind placebo controlled clinical trials using capsules containing varying doses of aspartame compared to identical appearing placebo capsules for periods lasting up to six months.
The reported GI symptoms associated with aspartame have not been confirmed in double-blind placebo-controlled clinical trials using capsules containing varying doses of aspartame compared to identical appearing placebo capsules for periods lasting up to six months. (Nehrling et al., Leon et al.) Symptoms were reported by both the aspartame and placebo groups, all mild to moderate, with no statistically significant differences between groups in the number of subjects experiencing symptoms or in the number of symptoms per subject. Researchers suggest the high incidence of symptoms reported by subjects in both groups may have been due to the power of suggestibility over the duration of the studies, but also state lack of differences in complaints between the groups does not rule out the possibility of idiosyncratic responses to aspartame.

The question also arises whether aspartame has an effect on individuals with gastrointestinal diseases, such as celiac disease, cystic fibrosis and tropical sprue. A 2007 review by Magnuson et al., found no studies in the scientific literature that evaluated plasma levels of amino acids following aspartame ingestion in these populations, but other studies indicate these individuals display impaired absorption of amino acids and peptides. Based on these studies, they suggest plasma amino acids levels of aspartic acid and phenylalanine would be similar or lower following consumption of aspartame compared to levels seen in normal individuals.

 A Look at the Gut Microbiome

Dietary recommendations to modify the microbiome may be premature.
Our gastrointestinal tract contains thousands of different bacteria, particularly in the intestine. These bacteria and other microbes are collectively called the gut microbiome. Studies investigating the role of the gut microbiome in health and disease have expanded worldwide in recent years. Areas of interest include obesity, metabolic syndrome, type 2 diabetes, systemic inflammation, autism, multiple sclerosis and autoimmune disorders (Shanahan -Murphy., Jumpertz et al, Kotzampassi et al.). Current research indicates the human gut microbiota is unique to each individual and made up of as many as 100 trillion cells. Over 50 phyla have been identified, with Firmicutes and Bacteroidetes accounting for more 90% of the human microbiome. Available evidence shows a low Bacteroidetes to Firmicutes ratio is associated with obesity and it is thought that the bacteria are able to extract more calories from the diet for their host. What remains unknown is whether the alterations in the microbiota are the cause or consequence of obesity. It’s also important to note that while the National Institutes of Health (NIH) Common Fund Human Microbiome Project (HMP) will allow for the characterization of the human microbiome and analysis of its role in human health and disease, dietary recommendations to modify the microbiome may be premature.

Aspartame Not Reaching Colon at Odds with Two Microbiota Impact Studies

Changes in the composition of gut microbiota have been reported as a result of changes in diet, exercise, circadian rhythm, gastric bypass surgery and the use of antibiotics, prebiotics and probiotics. Schnorr et al., proposed that the ability of the microbiota to rapidly change is an evolutionary trait that enhanced survival for hunter-gatherers experiencing a continuously changing food supply.

Before taking a look at two studies on this subject, it is worth noting here that the most recent review of the safety of aspartame released by the European Food Safety Authority (2013) stated that neither aspartame nor its digestion products ever reach the colon, so aspartame itself cannot affect the gut microbiota.

Studies by Suez et al. and Palmnas et al. suggest the gut microbiota may be altered by the consumption of low-calorie sweeteners (LCS). Given the very different chemical composition of the LCS currently in use and their very different metabolic fates once ingested by humans, it is highly unlikely they would all have the same effect on the gut microbiota. So the first question that must be raised when such studies are published is, “Which low-calorie sweeteners were used?”

First we’ll look at the series of studies by Suez et al., conducted with various protocols and experimental conditions. Seven involve mice and three have human subjects. Aspartame and sucralose were utilized in only one experiment. There are no data to support the allegations that either sweetener affects the microbiome or glycemic response. Instead, the data presented show no difference between these two LCS and controls. There were several other limitations in the study that greatly affect the interpretation of the findings, including small sample sizes, non-representative sample, lack of control group, lack of baseline data, limited testing episodes and recall bias. The results also contradict the large body of evidence showing long-term consumption of aspartame does not affect blood glucose, even in individuals with diabetes. (Leon et al., Nehrling et al.)

The objective of a study by Palmnas et al., was to examine the association between long-term low-dose aspartame consumption on the metabolic and microbial profiles in rats. The paper states they randomized 44 diet-induced obese Sprague-Dawley rats into two dietary groups, standard chow and high fat chow, for two weeks and then randomly assigned them water or water sweetened with aspartame for another 8 weeks. This should have resulted in four treatment groups, but the results show the data from two of the groups were part of a shared control group from a previously published study. The results also say a glucose tolerance test was administered at 8 weeks and weight, fecal and blood samples were taken at 10 weeks, but these measurements were not taken before the fluid treatment was started to use as a reference point.

Outcomes from the aspartame groups in this study included lower net energy consumption, body mass, body fat percentage and plasma insulin levels along with fasting hyperglycemia, impaired insulin tolerance, changes in gut microbiota and increased serum propionate, a short-chain fatty acid of bacterial origin. The authors conclude their results show aspartame mitigates many of the effects of high-fat feeding, yet produces hyperglycemia and impaired insulin tolerance and further investigation is needed to explain the mechanism. The limitations of this study and conflicting findings do not provide evidence of the proposed association stated in their objective for either rats or humans.

Cited References

Items of Interest

February 13, 2017 Claims & Myths