The first zero-calorie sweetener, saccharin, was invented 135 years ago. The first campaign against its use took off not long after. When the original commissioner of the FDA proposed to ban the additive, it took a fiat from the president to stop him. “Anybody who says that saccharin is injurious to health is an idiot,” said Teddy Roosevelt, who used diet drinks to lose weight.
The debate over artificial sweeteners has seesawed back and forth since then. On one side, science optimists say that substituting artificial sugar for the real thing can stave off excess fat. On the other, sweetener skeptics say it does more harm than good.
The supposed risks of saccharin, like those of other sweeteners, have a way of glomming on to whatever other fears happen to be in the public mind. In Roosevelt’s day, we worried over fraud in manufacturing—flour cut with sawdust, coffee mixed with powdered acorns—and saccharin was decried as a cheapo surrogate for sugar. By the time Richard Nixon declared a war on cancer, the sweeteners were seen as dangerous carcinogens. These days we’re more concerned with diabetes and obesity, and so the putative effects of drinking diet soda have shifted once again. Now they’re blamed for bringing on the very thing they’re meant to counter: a growing scientific literature hints that artificial sweeteners could make us fat.
The latest, and most high-profile, study to support this claim turned up Wednesday, in the latest issue of the journal Nature. Many others have tried to suss out sweeteners’ effects in human populations, and measured their behavior in the mouth and stomach. But the Weizman Institute’s Jotham Suez, Eran Segal, and Eran Elinav, the lead authors of the new paper, approached the question from the other end: How might a sweetener affect the bottom of our digestive tracts, in the piping near the rectum? Could these sugar substitutes be messing with our gut bacteria in a way that changes our digestion?
The Israeli researchers began with inbred Black-6 mice treated in the lab, finding that artificial sweeteners impaired the animals’ response to glucose—it made them pre-diabetic. Then the researchers fed some mice with saccharin, and transferred samples of their feces to another set of mice. The latter suffered from the same defects in metabolism. A careful look at the bacteria living in that transferred poop revealed the reason why: The sweetener had reshaped the mouse’s ecosystem of microbes, and made it more hospitable to strains that harvest energy from carbohydrates. (The effect was reversible as well: When they dosed affected mice with antibiotics, and killed off all the microbes in their guts, the sugar sensitivity went away.) Finally, the group tested their hypothesis on humans. Four of seven volunteers showed intolerance to glucose after taking hefty slugs of saccharin. When those people’s feces were transplanted back into the mice, the effect transferred once more.
The paper is a tour de force, with a clever design that zeroes in on causal linkage, and one that shows a curious effect. But Suez, Segal, and Elinav make a further claim: “Our findings suggest that [artificial sweeteners] may have directly contributed to enhancing the exact epidemic that they themselves were intended to fight,” they write. 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.
Among the misleading aspects of this coverage has been its emphasis on “artificial” additives, as if these were especially dangerous to health. That fits with at least 100 years of consumer intuition, but it’s not consistent with the facts. The Israeli group did look at a few standard lab-made sweeteners—saccharin (Sweet’N Low), aspartame (Equal), and sucralose (Splenda)—but there’s no reason to think that so-called “natural” sugar substitutes, such as stevia and monk fruit, would have a different effect. Though the latter are untested in this regard, one of the Israeli authors, Eran Elinav, told me that plant-based products might impair glucose tolerance just as much as the chemicals they tested.
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.
It’s true that the prevalence of obesity and diabetes started shooting upward in the early 1980s, along with skyrocketing consumption of diet soda (brought on by the introduction of aspartame-sweetened Diet Coke). The researchers cite this overlap to support the claim that fake sugar makes us fat. More recent data suggest the opposite, however. The last decade has seen a leveling off of obesity rates, at least in terms of BMI, while the use of non-caloric sweeteners has dramatically increased over the same period, especially among children and adolescents. Meanwhile, white people—both adults and children—consume, on average, twice the volume of diet beverages as black people, though obesity rates are much higher among the latter.
Perhaps more to the point, researchers have tested the effects of diet soda on people trying to lose weight, and gotten positive results. A randomized, controlled trial published in May compared the efficacy of artificially sweetened beverages and water in a 12-week weight-loss program. Both treatment groups ended up with smaller waists, and the people taking diet drinks appeared to lose more weight. That study’s lead authors are consultants for Coca-Cola, so perhaps we shouldn’t take this as the final word. But another randomized trial from 2012, this one funded by a bottled-water company, came to a similar conclusion. When overweight and obese adults switched to diet beverages or water for a six-month stretch, both groups shed 1 inch of girth, on average, and 5 pounds.
There’s plenty of evidence that full-sugared beverages contribute to weight gain, but even the new Israeli study didn’t find evidence that artificial sweeteners might do the same. The experimental mice showed a change only in their response to glucose—a physiological risk factor that happens to be strongly associated with obesity. Perhaps diet soda doesn’t make us fat (at least at first), but only messes with our metabolism. Yet neither study described above came to this conclusion. Drinking artificially sweetened beverages and drinking water appeared to have the same effect on glucose tolerance.
In fact, 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. The main thing that these additives have in common is their tendency to bind sweet receptors in the mouth—but even that may be a quirk of human evolution. Black-6 mice, the kind used in the Israeli experiment, don’t have much taste for aspartame at all. So why should their guts respond the same to every artificial sweetener? And why should they respond the same as ours?
The best science papers are often those that create an unexpected puzzle, rather than solving one we knew about before. We may soon find out what, exactly, non-caloric sweeteners are doing to our microbiomes, and whether it affects our health. But for the time being, the conventional wisdom remains the same: To the extent that artificial sweeteners help us wean off sugared drinks, they’re a boon to public health.