For years, research has supported a roundabout path from excess sugar intake to type 2 diabetes. Eat too much of anything, including sugar, and the resulting weight gain raises your diabetes risk, the theory goes. There’s lots of evidence to support this pattern, but also a big hitch: A small but noteworthy proportion of people with type 2 diabetes aren’t overweight or obese. And up to 40 percent of normal-weight people show signs of the metabolic syndrome, a constellation of metabolic disturbances that predisposes people to diabetes.
So what’s going on? New epidemiological evidence, published today in PLOS ONE, suggests that sugar intake may be directly associated with diabetes risk. This research doesn’t refute the sugar-to-obesity-to-diabetes pathway; instead, it suggests that eating too much sugar promotes diabetes in more than one way.
The researchers, who are from Stanford, UC-Berkeley and UC-San Francisco, analyzed a decade’s worth of data on sugar availability in the food supplies and diabetes rates in the populations of 175 countries. They used new statistical methods derived from the field of econometrics to control for several factors that could provide alternate explanations for the relationship between sugar intake and diabetes, including obesity, overweight, sedentary behavior, other calorie sources, and a long list of socioeconomic measures. The statistical controls were more sophisticated than those typically used in biomedical research, the study’s lead author, Sanjay Basu, MD, PhD, explained to me when I interviewed him about the findings. (And for those who want more information about the statistics, Basu has written an interesting post on his personal blog to explain the methods in detail.)
After all the statistical crunching was done, the research showed that every 150-calorie increase in available sugar was associated with a 1 percent increase in the population’s diabetes rate. A 12-oz soda contains about 150 calories of sugar.
From our press release on the study:
Not only was sugar availability correlated to diabetes risk, but the longer a population was exposed to excess sugar, the higher its diabetes rate after controlling for obesity and other factors. In addition, diabetes rates dropped over time when sugar availability dropped, independent of changes to consumption of other calories and physical activity or obesity rates.
The findings do not prove that sugar causes diabetes, Basu emphasized, but do provide real-world support for the body of previous laboratory and experimental trials that suggest sugar affects the liver and pancreas in ways that other types of foods or obesity do not. “We really put the data through a wringer in order to test it out,” Basu said.
“As far as I know, this is the first paper that has had data on the relationship of sugar consumption to diabetes,” said Marion Nestle, PhD, a professor of nutrition, food studies and public health at New York University who was not involved in the study. “This has been a source of controversy forever. It’s been very, very difficult to separate sugar from the calories it provides. This work is carefully done, it’s interesting and it deserves attention.”