Excessive sugar consumption could cause weight gain and obesity, which are precursors for diabetes, says study.
But now the results of a large epidemiological study have suggested sugar may also have a direct, independent link to diabetes.
Researchers from the Stanford University School of Medicine, the University of California-Berkeley and the University of California-San Francisco examined data on sugar availability and diabetes rates from 175 countries over the past decade.
After accounting for obesity and a large array of other factors, the researchers found that increased sugar in a population's food supply was linked to higher diabetes rates, independent of obesity rates.
The study provides the first large-scale, population-based evidence for the idea that not all calories are equal from a diabetes-risk standpoint, said Sanjay Basu, MD, PhD, an assistant professor of medicine at the Stanford Prevention Research Center and the study's lead author.
"We're not diminishing the importance of obesity at all, but these data suggest that at a population level there are additional factors that contribute to diabetes risk besides obesity and total calorie intake, and that sugar appears to play a prominent role," he noted.
Specifically, more sugar was correlated with more diabetes: For every additional 150 calories of sugar available per person per day, the prevalence of diabetes in the population rose 1 percent, even after controlling for obesity, physical activity, other types of calories and a number of economic and social variables. A 12-ounce can of soda contains about 150 calories of sugar. In contrast, an additional 150 calories of any type caused only a 0.1 percent increase in the population's diabetes rate.
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.
The researchers had to rely on food-availability data for this study instead of consumption data because no large-scale international databases exist to measure food consumption directly.
Basu said follow-up studies are needed to examine possible links between diabetes and specific sugar sources, such as high-fructose corn syrup or sucrose, and also to evaluate the influence of specific foods, such as soft drinks or processed foods.
Another important future step, he said, is to conduct randomized clinical trials that could affirm a cause-and-effect connection between sugar consumption and diabetes.
Their study has been published in PLOS ONE.