Sugar calories are worse for diabetes and obesity than others

Attentive clinicians who have been exhorting their patients for years to avoid excessively stimulating insulin production with sugar are heartily welcoming the superb research just published in PLoS One (Public Library of Science) that drives a stake through the heart of the mistaken notions that calories from sugar have the same effect as others, and that obesity causes diabetes. The authors observe:

"Global diabetes prevalence has more than doubled over the last three decades, with prevalence rates far exceeding modeled projections, even after allowing for improved surveillance...Most of the worldwide rise is thought to be type 2 diabetes linked to the “metabolic syndrome” – the cluster of metabolic perturbations that includes dyslipidemia, hypertension, and insulin resistance. Obesity associated with economic development — particularly from lack of exercise and increased consumption of calories — is thought to be the strongest risk factor for metabolic syndrome and type 2 diabetes..."

But as the data from a number of studies shows...

"...several countries with high diabetes prevalence rates have low obesity rates, and vice versa. High diabetes yet low obesity prevalence are observed in countries with different ethnic compositions...Trends in diabetes and obesity are also dyssynchronous within some nations..."

Moreover...

"This population-level puzzle is accompanied by individual-level data. About 20% of obese individuals appear to have normal insulin regulation and normal metabolic indices (no indication of diabetes) and normal longevity, while up to 40% of normal weight people in some populations manifest aspects of the “metabolic syndrome”.

It's been known for some time that sugars do a lot more damage than just contribute to obesity:

One controversial hypothesis is that excessive sugar intake may be a primary and independent driver of rising diabetes rates. Sugars added to processed food, in particular the monosaccharide fructose, can contribute to obesity, but also appear to have properties that increase diabetes risk independently from obesity. For example, liver fructose metabolism in the fed state generates lipogenic substrates in an unregulated fashion, which drives hepatic de novo lipogenesis and reduced fatty acid oxidation, forming excessive liver fat and inflammation that inactivates the insulin signaling pathway, leading to hepatic insulin resistance. Sugary foods have been significantly associated with the development of insulin resistance in laboratory-based studies. Reactive oxygen species are produced by the Maillard reaction, damaging pancreatic beta cells, and leading to a subcellular stress response (the “unfolded protein response” in the endoplasmic reticulum) that drives insulin inadequacy. In concert, insulin resistance and reduced insulin secretion lead to overt diabetes."

To determine whether added sugars or obesity are the primary driver of the world-wide diabetes pandemic, the authors...

"...conducted a statistical assessment of panel data (repeated multi-variate data from multiple countries over a time period) to empirically evaluate whether changes in sugar availability, irrespective of changes in other foodstuffs, can in part account for the divergence in diabetes prevalence rates worldwide."

To do so they used repeated cross-sectional data on diabetes and nutritional components of food from 175 countries over ten years, correlating with the prevalence overweight and obesity and the incidence of diabetes. Their exhaustive and detailed data accumulation and rigorous, multifaceted statistical analyses are the very model of superlative research. Their data provides the evidence to fuel important changes in public health policy:

"...we found that every 150 kcal/person/day increase in sugar availability (about one can of soda/day) was associated with increased diabetes prevalence by 1.1% (p <0.001) after testing for potential selection biases and controlling for other food types (including fibers, meats, fruits, oils, cereals), total calories, overweight and obesity, period-effects, and several socioeconomic variables such as aging, urbanization and income. No other food types yielded significant individual associations with diabetes prevalence after controlling for obesity and other confounders. The impact of sugar on diabetes was independent of sedentary behavior and alcohol use, and the effect was modified but not confounded by obesity or overweight. Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. Differences in sugar availability statistically explain variations in diabetes prevalence rates at a population level that are not explained by physical activity, overweight or obesity."

There are, of course, mutiple factors that can contribute to diabetes and metabolic syndrome. The rising tide of autoimmunity (as readers here are likely aware) and inflammation supported by other causes including adipokines generated in visceral fat are notable. But the importance of this study is to reverse the mistaken notion that obesity is the primary cause of insulin resistance diabetes; it is, for the most part, the other way around, with the excessive rise in insulin compensatory for receptor resistance that forces the storage of calories as fat.

"The worldwide secular trend of increased diabetes prevalence likely has multiple etiologies, which may act through multiple mechanisms. Our results show that sugar availability is a significant statistical determinant of diabetes prevalence rates worldwide. By statistically studying variation in diabetes rates, food availability data and associated socioeconomic and demographic variables across countries and time, we identified that sugar availability appears to be uniquely correlated to diabetes prevalence independent of overweight and obesity prevalence rates, unlike other food types and total consumption, and independent of other changes in economic and social change such as urbanization, aging, changes to household income, sedentary lifestyles and tobacco or alcohol use. We found that obesity appeared to exacerbate, but not confound, the impact of sugar availability on diabetes prevalence, strengthening the argument for targeted public health approaches to excessive sugar consumption. We also noted that longer exposure to high sugar was associated with accentuated diabetes prevalence, while reduced sugar exposure was associated with decline in diabetes prevalence, and that the sugar-diabetes relationship appeared to meet criteria for temporal causality without being the result of selection biases or the effect of secular trends that may be artifacts of economic development or changes in surveillance...In summary, population-level variations in diabetes prevalence that are unexplained by other common variables appear to be statistically explained by sugar."

Considering the massive dimensions of the diabetes pandemic and its grievous depredations, reducing sugar consumption is one of the leading public health issues of our time.