Is sugar a ‘fundamental cause of diabetes’ beyond adding empty calories, BMJ author asks

By Elizabeth Crawford contact

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Is sugar a ‘fundamental cause of diabetes’ BMJ author asks
While the jury is still out on what role, if any, sugar plays in the development of diabetes, recommendations to restrict consumption should be strengthened and research should be redoubled until a clear determination is found, according to an essay in The BMJ today.

Gary Taubes, cofounder of the non-profit Nutrition Science Initiative, argues in the essay​ that for more than 100 years doctors have suspected that refined sugar – namely sucrose – is a likely cause of the ongoing diabetes epidemic, as illustrated by early trends data that tracked the rise and fall of the disease with consumption levels of the nutrient.

He notes, this data was bolstered by additional research that hypothesized “sugar has deleterious effects on the human body independent of its calorific content,”​ in the form of a “distinct causal pathway” ​revealed in the metabolism of fructose primarily in the liver, which could lead to increased hepatic fat. From there, he added, it contributed “to the insulin resistance that is the fundamental biochemical disturbance in type 2 diabetes.”

However, Taubes points out,“the idea that sugar could be a fundamental cause of diabetes, not just a source of empty calories, fell out of fashion over the years,”​ as the health community instead focused on the role of fat and overconsumption of calories in the development of obesity, for which diabetes was considered “a penalty.”

While this led to recommendations to strictly limit the consumption of sugar to reduce the intake of “empty”​ calories and the development of dental caries, Taubes says this is not enough to balance the potential health dangers of the nutrient.

Pointing to the “present dire situation”​ with diabetes impacting one in 11 people in the US and costing the American healthcare system as much as $1 billion a day, Taubes argues that the idea that sugar could fundamentally lead to diabetes – as well as obesity – “should be considered seriously again.”

Taubes acknowledges that the evidence connecting sugar to diabetes is “far from definitive,”​ but, he also says it is growing. He points to animal studies that connect high-sugar diets with metabolic syndrome and insulin resistance.

The only way to know for sure whether sugar is connected to diabetes development is to fund additional research, including randomized controlled studies looking at hard endpoints such as mortality and cardiovascular events – similar to the research looking at the relationship between dietary fat consumption, blood cholesterol levels and chronic disease development.

“Given the scale of the obesity and diabetes epidemics … a concerted program of research to establish reliable knowledge on this subject should be among our highest priorities,”​ Taubes said. At the same time, he concluded, “we can acknowledge the uncertainties while still recommending strongly against consumption.”

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