A new study out of Israel on the possible effects of artificial sweeteners is making a lot of headlines this week. Unfortunately (and as usual) members of the media from Forbes to NPR’s Diane Rehm are reporting on the study without taking into consideration the growing criticism of its methodology, conclusions, and prior research on the topic. As Stephen O’Rahilly, endocrinologist and head of Cambridge’s metabolic research lab put it, “It would be unfortunate if this data were to influence public policy.”
Jotham Suez, a graduate student in the Department of Immunology at the Weizmann institute of Science, led the study. Suez et al. gave doses of water laced with saccharin, sucralose, and aspartame to mice and observed that the mice then developed a glucose intolerance. When they looked at the effects of artificial sweeteners on humans, four out of the seven subjects displayed “significantly poorer glycaemic responses” after consuming the maximum recommended daily limit of saccharin for a week. None of the subjects were regular users of artificial sweeteners prior to the study.
While the results are certainly interesting, the researchers make quite a leap from their results to the assertion that artificial sweeteners “contributed to enhancing the exact epidemic that they themselves were intended to fight.” That is, they are suggesting a link between the consumption of non-caloric sweeteners, obesity, and type 2 diabetes. Yet, this link is dubious. The study may be the start of a significant investigation into how human gut bacteria is affected by artificial sweeteners, but it is preliminary and just one study among a number on the topic—many of which come to wildly different conclusions. Of course, you would never know that from the media coverage.
As Slate’s Daniel Engber put it, “[t]he paper is a tour de force, with a clever design that zeroes in on causal linkage, and one that shows a curious effect.” But as for their assertion that the study demonstrates a link between non-calorie sweeteners and obesity, “That’s how the new study has been presented to the public, too, with headlines screaming of a hidden link between artificial sugar and obesity. But that grand conclusion doesn’t gibe with common sense, nor does it match other research in the field.” He continues that “the closer you look at this week’s Nature study, the more peculiar its findings seem. Suez, Segal, and Elinav propose that at least three different non-caloric sweeteners (saccharin, aspartame, and sucralose) affect the body in matching ways, despite the chemicals’ fundamental differences.” This sentiment has been repeated by numerous researchers in the field.
According to Dr. Josh Bloom of the American Council on Science and Health, a watchdog on scientific research, “The basic premise is so flawed chemically that these flaws jump off page...that artificial sweeteners affect the microbial composition in the gut—makes absolutely no sense chemically, physiologically, or pharmacologically. The authors are taking chemicals that have exactly one thing in common—sweetness—and trying to correlate this with changes in gut bacteria that may be responsible for raising blood sugar…”
Michael Blaut, microbiologist at the German Institute of Human Nutrition had a similar thought, saying that he has a hard time imagining a mechanism that would account for three compounds as chemically different as aspartame, saccharin, and sucralose leading to the same changes in the gut microbiome.
Other scientists have criticized that mice are not particularly good stand-ins for human beings in this scenario. In a Science magazine article on the study, author Kai Kupferschmidt quotes Catherine Collins, a dietitian at St. George’s Hospital in London, saying, “On this evidence, I'd agree that lab mice shouldn't have lots of sweeteners in their drinking water,” and that lab mice get a lower portion of calories from carbohydrates than humans, noting, “Our naturally higher carbohydrate intake has generated bowel bacteria happily digesting whatever we swallow, and their symbiotic relationship with our bowel cells and beyond is testimony to this.”
Furthermore, as Engber pointed out, the Israeli study focused on saccharine—which had the most significant effect of all three of the non-caloric sweeteners.
The problem with the artificial-sweeteners-make-us-fat conclusion runs deeper, though. Suez, Elinav, and Segal considered three non-caloric sweeteners, but their study focused only on the one that’s least relevant to public health. Saccharin had the most acute effect on their laboratory animals—it provoked the most severe intolerance to glucose—so that’s the drug they chose to test with fecal transplants, and in human subjects. But saccharin is the oldest and most neglected of the major sugar substitutes: As of 2012, it makes up just 13 percent of the market for sweetener packets, and it’s all but disappeared from packaged foods. To blame obesity on saccharin is to say we’ve all been drinking too much Tab cola.
So, while the paper is certainly fascinating and deserving of follow-up and repeat studies, it shouldn’t be the basis for drawing grand conclusions about the effect non-caloric sweeteners may have on something as complex as obesity or type II diabetes which are the result of a lifetime of choices. As Mike Gibney, professor of food and health at University College Dublin, put it, in terms of the complexity of understanding a disease, heart disease gets a score of one, cancer a 10, and obesity gets a score of 100. Anyone arguing that obesity is caused by food alone isn’t being intellectually serious. We should also be skeptical of the seriousness of any journalist using this study to make the claim that non-caloric sweeteners cause obesity or diabetes.