If the story of diet-soda consumption had a tagline, it might be "The best intentions can result in unintended consequences." Diet soda was created to fill a gap in the market for diabetics seeking sugar-free drinks, and it was also an opportunity to satisfy the soda cravings of people trying to lose weight.
The development of diet soda was marked by the search for a noncaloric artificial sweetener (NAS). Over the decades, NAS have been commonly introduced into foods ranging from cereal to dessert. NAS were popularized as a "healthier" alternative, and their consumption has skyrocketed over the past few decades.
A study published earlier this month in Nature suggested, controversially, that NAS could induce glucose intolerance. Glucose intolerance is the inability to tolerate glucose (natural sugar), typified by conditions such as pre-diabetes and diabetes. In other words, the chemicals we developed to cater to a diabetic market may in fact be causing diabetes.
With such a provocative claim, it's important to examine what we know through this new paper.
The authors first tested varying concentrations of three different NAS (saccharin, sucralose and aspartame), glucose and sucrose in the drinking water of lean mice. They found that glucose tolerance was significantly decreased in mice consuming NAS. In particular, saccharin had the most pronounced effect. They then looked at saccharin and glucose in obese mice. As seen in the lean state, the saccharin-consuming mice showed glucose intolerance after as few as five weeks of exposure. The saccharin quantity that the mice ingested corresponded to the FDA-recommended acceptable daily intake. It is of note that in general, it is likely that consumers exceed the acceptable daily intake, given the saccharin quantities in widely used foods.
The authors then went on to explore the changes within the biological system that may have led to this change. It is widely believed that the benefits of losing weight and gaining better control of diabetes following gastric bypass surgery are at least partly due to beneficial changes in the kinds of microbes we have in our gut (gut microbiota) following surgery. The authors tested the effect of saccharin in the presence of antibiotics that will eliminate the gut microbes. It is understood that the gut microbiota is controlled by diet and in turn has a profound impact on physiology and metabolism. In the presence of antibiotics, the difference in glucose intolerance between NAS-drinking mice and controls was abolished in both lean and obese mice. To further test whether the link between gut microbiota and glucose intolerance was causal, transplantation experiments were conducted. The authors investigated this link fully, proving a connection between gut microbiota and glucose intolerance in both in vivo and in vitro conditions. Small-scale human studies were also performed -- while preliminary, early data do not dispute the hypothesis.
At this point, all evidence suggests that the ingestion of noncaloric artificial sweeteners is accompanied by a change in gut microbiota that decreases the body's natural glucose tolerance. In other words, that diet soda we drink in an attempt to avoid diabetes may really be triggering the onset of diabetes.
While there are more data to collect, the evidence at this point is compelling and logical. It is enough for me, as a longtime Diet Coke aficionado, to step away from my daily consumption habits.
Unfortunately, influencing public opinion with catchy jingles and a smart marketing opportunity is easy, but changing it in the face of new scientific evidence is an uphill battle. In the few weeks since the article appeared, the conclusion has raised far less of an outcry than it should have. We should be demanding answers, questioning why it has taken decades for us to figure out that we unwittingly created a bigger problem for ourselves in search of a simpler solution. We should be questioning why research like this wasn't funded much sooner, and we should be pushing for research on the latest trends to occur sooner.
After all, what if gluten-free food contains a substitute that causes gluten sensitivity? What if soy milk perpetuates lactose intolerance? We need to investigate and fund research to discover the answers before we introduce unknown artificial products into our diets as staples.