Banting and Best where are you when we really need you? I am
always amazed by authors such as Basu et al who come out with a new discovery
regarding sugar and Diabetes. It is as if they have just gotten some clear
insight into the obvious. Obesity drives the suppression of the islet cells
which drives down the insulin production which drives up the glucose level. Get
the BMI below 22.5 and you drive out the main initiator of Type 2 Diabetes, the
inflammatory effects of weight.
Now the authors state[1]:
While experimental and observational studies suggest that
sugar intake is associated with the development of type 2 diabetes, independent
of its role in obesity, it is unclear whether alterations in sugar intake can
account for differences in diabetes prevalence among overall populations.
Using econometric models of repeated cross-sectional data
on diabetes and nutritional components of food from 175 countries, 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. …
In summary, population-level variations in diabetes
prevalence that are unexplained by other common variables appear to be statistically
explained by sugar. This finding lends credence to the notion that further
investigations into sugar availability and/or consumption are warranted to
further elucidate the pathogenesis of diabetes at an individual level and the
drivers of diabetes at a population level.
Well one would think that to be the case. Sugar, sucrose, is
a powerful carbohydrate and Diabetes is a carbohydrate disorder, and Type II
Diabetes is exacerbated by obesity and sugar has excess calories thus causing
obesity. It is logical causality. We have seen genes, billboards, environment,
sugar, and endless excuses for the fact that people eat too much.
Most physicians treating Type II Diabetes sees the patient
as obese, having a high carb diet, more than likely smoking and with no
exercise. Further if they examine the diet, they find tremendous amounts of
carbs, and if they look deeper they are dominated by various sugars. Thus this
conclusion is not only obvious but it faces physicians on a day by day basis.
The prototypical Type II Diabetic is a candy eating obese
person. Instead of a small candy bar, they get bags of them, cakes, cookies,
and the list continues. So what is new?
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