The prevalence of obesity is Western nations closely matches the rise in the consumption of sugar sweetened beverages. Sugar is an interesting molecule, because it is a natural part of many fruits and vegetables and as a result can be said to have formed part of the human diet for millennia. However, only recently has the sugar from plants been processed into a crystalline form on an industrial scale, making it cheap enough for mass consumption, and therefore only recently have humans been exposed to the deleterious metabolic changes associated with refined crystalline sugar. Sugar is chemically called sucrose, and is composed of a fructose moiety bonded through a glycosidic bond to a glucose moiety. This disaccharide sugar is digested in humans by the enzyme sucrase, to form both glucose and fructose. The glucose is absorbed to the blood and contributes to a rise in blood sugar, and this can be used as a source of energy for metabolic purpose, particularly by skeletal muscle and the central nervous system. However, the fructose can only be processed by the liver, and here it has one of two fates.
Upon entry to the liver, fructose can enter the gluconeogenic pathway to form glucose-6-phosphate. This phosphorylated form of glucose is trapped in the liver and so is used to synthesise liver glycogen stores. These stores are high molecular weight branched polymers of glucose that are used as a source of fuel during the postprandial period. However, the liver only has a finite capacity to synthesise glycogen, and after the liver stores of glycogen are full, excess fructose spills over to enter the de novo lipogenesis pathway, a pathways that is used to synthesise new fatty acids. In this regard fructose can feed into the glycolytic pathway, resulting in the formation of acetyl-CoA, and this can be used as a substrate for fatty acid synthesis. The liver has an infinite capacity to produce fatty acids given adequate substrate, and so high intakes of fructose cause a massive increase in fatty acid production. These fatty acids can then accumulate in skeletal muscle and liver tissue where they cause insulin resistance.
It is insulin resistance that drives obesity, and sugar sweetened beverages are increasingly being seen as a primary driver of this process. A number of animal studies have investigated the role of fructose at causing obesity and found that high fructose diets induce insulin resistance in just a few short weeks in otherwise healthy animals (here, here and here). The association between consumption of sugar and deleterious changes to glucose metabolism have also been investigated in human observational studies. For example, in one study1 researchers assessed the amount of liquid sugar in the diets of children aged 8 to 10 years. The results showed that a higher consumption (10 grams per day) of added sugar in a liquid form (soft drinks, flavoured milk and fruit drinks) was associated with a 0.04 mmol/L higher fasting blood glucose level, a 2.3 pmol.L higher fasting insulin level, a 0.1 unit higher homeostasis model assessment of insulin resistance (HOMA-IR) and a 0.4 unit lower Matsuda-insulin sensitivity index (Matsuda-ISI).
Dr Robert Barrington’s Nutritional Recommendation: These results support other data showing that sugar sweetened soft drinks, fruit juice and other sources of liquid sugar cause detrimental changes to the metabolic regulation of glucose. As shown in this study, this likely occurs through a decrease in insulin sensitivity (a decreased Matsuda-ISI score) and an increase in insulin resistance (an increased HOMA-IR score). Consuming sugar sweetened beverages are therefore a risk factor for Western disease including obesity, type 2 diabetes, and cardiovascular disease because they are likely drivers of the metabolic syndrome.
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