Artificial Sweeteners Raise Blood Sugar via Changes in Gut Bacteria

Artificial sweeteners—the likes of saccharine (the pink packets), aspartame (the blue packets), and sucralose (the yellow packets)—were created as an alternative to caloric sweeteners like sugar and honey, which contribute to raised blood sugar and the development of metabolic syndrome and type 2 diabetes. Artificial sweeteners are added to a wide range of commonly consumed foods such as diet sodas, cereals, and sugar-free desserts, which are often recommended for people with, or at risk of, type 2 diabetes.

Artificial sweeteners are not absorbed by the body, but are instead passed through the digestive tract largely intact. Due to the 100 trillion bacteria inhabiting the gut, however, they may have more of an effect on metabolism than experts previously realized. In a recent study published in the journal Nature, researchers found that artificial sweeteners trigger an imbalance of gut bacteria that leads to an increase in glucose intolerance (an inability of the body to deal with excess sugar in the bloodstream—in other words, high blood sugar and insulin resistance).

In an elegant collection of experiments, the scientists found that artificial sweeteners are likely not the safe sugar alternative that we are led to believe.

“Together with other major shifts that occurred in human nutrition, this increase in non-caloric artificial sweetener (NAS) consumption coincides with the dramatic increase in the obesity and diabetes epidemics,” noted the researchers. “Our findings suggest that NAS may have directly contributed to enhancing the exact epidemic that they themselves were intended to fight.”

The scientists began by adding saccharine, sucralose, aspartame, sucrose (table sugar), glucose (the basic sugar molecule that makes up table sugar and is found in the bloodstream), or nothing to the drinking water of mice. Those mice drinking water with an added artificial sweetener were found to have increased glucose intolerance when compared to mice given sugar or plain water. Of the three artificial sweeteners tested, saccharine had the most pronounced effect.

Next, the mice were given antibiotics while continuing to consume the saccharine, sugar, or plain water. The antibiotic treatment induced a reversal of the glucose intolerance in those mice consuming artificial sweeteners, a finding that suggests that gut bacteria play a role in the alterations of glucose tolerance. When the gut bacteria were diminished by antibiotics, the glucose intolerance disappeared, so we know the bacteria were involved. In addition, the stool of mice consuming saccharine (before antibiotics) was tested and found to exhibit dysbiosis, or bacterial imbalance when compared to the control groups consuming sugar or plain water. This also implicates the bacteria as playing a role.

To test the idea that gut bacteria might be the cause of the glucose intolerance, the researchers transplanted stool from the saccharine-consuming mice into germ-free mice, or mice without gut bacteria. After only six days, the germ-free mice began to exhibit impaired glucose tolerance. This demonstrates that not only is saccharine responsible for triggering gut bacteria imbalance, but that the imbalance is directly responsible for impairing glucose tolerance after consumption of saccharine.

Think about that. Bacteria inside the gut are altered by saccharine, and they trigger the body to have a faulty response to dietary sugar, leading to increases in blood sugar. I don’t know about you, but I’ll hold off on the pink stuff (and all artificial sweeteners, for that matter.)

“Collectively, these results demonstrate that saccharine directly modulates the composition and function of the microbiome and induces dysbiosis, accounting for the downstream glucose intolerance…” noted the scientists.

Next the researchers took their investigation to the next level by studying these effects in humans. They first found a link between consumption of artificial sweeteners and several parameters related to the metabolic syndrome, including increased weight and waist-to-hip ratio, higher fasting blood sugar and glucose intolerance as well as elevated levels of HbA1C (a measure of long-term blood sugar control).

To determine whether these links may be more than a coincidence—that is, that consumption of artificial sweeteners causes these abnormalities rather than occurring alongside them—the scientists followed seven healthy individuals who do not normally consume artificial sweeteners. For six days, the participants consumed saccharine at the highest allowable daily intake level, and for even this short period of time, four of the seven participants developed glucose intolerance. Stool tests of these individuals showed that their gut bacteria differed from those who did not have an abnormal glucose response, showing that an imbalance of gut bacteria plays a role in the abnormal blood sugar response to saccharine in humans, as well.

To test this idea out and determine whether gut bacteria causes the glucose intolerance rather than occurs alongside it, they transplanted stool from two people who exhibited abnormal blood sugar response after consuming saccharine and two people who did not into germ-free mice. As predicted, those mice who received stool from people who exhibited abnormal glucose response went on to exhibit the same abnormal glucose response as well as a gut bacterial imbalance.

This is quite an impressive and eye-opening study. If you regularly consume artificial sweeteners, you may want to think twice. While more studies will be needed to replicate these results and to determine whether the other artificial sweeteners sucralose and aspartame have the same effects in humans, taking the precautionary measure and avoiding these sweeteners is a good idea. Even the study’s lead author, Eran Elinav, MD, PhD, has made the personal decision to stop using them. I, myself do not eat them, and I have recommended against them for many years now. Opt instead for natural non-caloric sweeteners like stevia, lo han (monkfruit), erythritol, or xylitol.

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