A controversial proposal would regulate sugar as a toxic substance, and not simply because it’s a calorie-rich enabler of obesity. Some researchers say it’s intrinsically dangerous, not unlike alcohol or tobacco, with unique properties that set off a hormonal cascade ending in higher risks of heart disease, stroke and type 2 diabetes.
It’s not a scientifically certain proposition, though a growing body of research suggests it may very well be true, and the implications are thorny. Even people sympathetic to public health-based regulations may balk at treating pastries as cigarettes, as University of California, San Francisco nutritionists suggested in a Feb. 2 Nature paper.
But to anyone looking to artificial sweeteners as an alternative, as pastel-packaged reassurances that regulators won’t ever need to pry donuts from their cold, dead and pudgy hands, science offers only more uncertainty. Some studies even suggest that fake sugar may cause the same problems as real sugar.
“That’s the $64,000 question,” said Susan Swithers of the Ingestive Behavior Research Center at Purdue University. “There are several epidemiological studies showing increased risk of metabolic syndrome in coincidence with the consumption of diet sodas” — a rich source of sweeteners. “But how they should be interpreted is not really clear right now. Because they’re correlational studies, they don’t tell us what caused what.”
Artificial sweeteners are a fast-growing, multi-billion dollar product, present in thousands of foodstuffs and synthesized by chemists as zealously as drug researchers pursue blockbuster drugs. But as described in a massive 2008 American Journal of Clinical Nutrition Review, the seemingly obvious health benefits expected of low-calorie sugar replacements have failed to materialize.
Even as Americans consumed more sweeteners, waistlines continued to expand. Cause and effect was ambiguous: Sweeteners might lead to weight gain, but maybe people most prone to gaining weight consume the most sweeteners. “This association may be coincidental or causal, and either mode of directionality is plausible,” concluded that study’s authors.
Other researchers, however, are more suspicious. When University of Texas Health Science Center epidemiologists conducted a 9-year-long study of 5,158 adult residents of San Antonio, Texas, they found a link between sweeteners and obesity. It persisted even after statistically accounting for gender, ethnicity, diet and beginning-of-diet body mass index. “These findings raise the question whether artificial sweetener use might be fueling — rather than fighting — our escalating obesity epidemic,” they wrote.
Another study of 6,184 adult Americans linked diet soda consumption with higher rates of metabolic syndrome, the umbrella term for a physiological disruption that leads to heart disease, stroke and type 2 diabetes. Once again, the link survived statistical adjustment for demographics, lifestyle and diet.
That’s precisely what’s expected from eating too much sugar, which at least in rats is converted in the liver to fat. That in turn provokes, via as-yet-unidentified mechanisms, resistance to insulin, a hormone used by cells to process glucose, better known as blood sugar. When insulin’s signals are ignored, blood sugar levels rise. Metabolic syndrome follows. But why should this happen when eating fake sugar, not real?
Swithers thinks she knows. In 2008, she and fellow Purdue researcher Terry Davidson fed rats a yogurt supplement sweetened either with glucose, a simple sugar, or zero-calorie saccharin. Apart from the supplement, both groups ate standard rat fare. Those that ate saccharin packed on more fat, gained more weight and consumed extra calories. A follow-up 2009 study reinforced the findings, and found that unusual weight gain persisted even when rats stopped eating sweeteners.
According to Swithers, two mechanisms may be responsible. When the rats’ bodies learned that sweetness didn’t predict an imminent caloric rush, as would naturally be produced by sugar-rich foods, their bodies may have automatically shifted into calorie-saving mode. At the same time, metabolic acceleration that normally occurs when eating high-calorie foods, and helps to process them, may have been slowed.
“All of our work has been in rats. We think similar processes happen in humans, but we haven’t tested them,” Swithers said.
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