The Problems With Sugar

Evidence Suggests that sugar is partly responsible for the obesity epidemic in Western countries. Sugar, chemically sucrose, and its synthetic cousin high fructose corn syrup, have nutritional properties that may allow them to contribute to obesity. In particular, both sugar and high fructose corn syrup can supply high amounts of fructose, and this may negatively disrupt certain metabolic pathways. Fructose for example, can stimulate the synthesis of fatty acids in the liver. Although glucose is also present in sugar and high fructose corn syrup, glucose does not stimulate tatty and synthesis in the same way. This is important nutritionally because it is the increase in fatty acids that may be the diver of insulin resistance that leads to weight gain and obesity. Understanding the role that fructose plays in fatty acid synthesis is therefore pivotal to understanding obesity. However, the mechanisms for fructose induced obesity are not clear, although a number of suggestions have been made.

One possibility is that high fructose intakes lead to the activation or expression of enzymes that cause certain metabolic pathways to increase their flux. Activation of the de novo lipogenesis pathway for example, by fructose, may lead to the accumulation of fatty acid synthesis in the liver and the development of nonalcoholic fatty liver. As fatty acids accumulate in the liver, metabolic pathways become disrupted and this can be a cause of central insulin resistance. High amounts of fructose may be required to cause these effects because fruit does not have such detrimental metabolic consequences. However, fruit juice which is a more concentrated source of fructose may be as detrimental as sugar and high fructose sweetened soft drinks in this respect. Studies attest to the weight gain and insulin resistance causing effects of fruit juice. The concentration as well as the rate of absorption therefore appear to be important considerations when assessing the metabolic effects of fructose.

The increase in the consumption of fructose in recent decades therefore mirrors the increased obesity rates in Western countries. In particular, the consumption of soft drinks may be a driver of obesity through their detrimental effects on insulin resistance. Although an increase in sugar and high fructose corn syrup will increase both glucose and fructose, animals are well able to dispose on glucose and it appears to have few detrimental effects on insulin resistance. The release of insulin by glucose may be pivotal in understanding why it is less able to cause weight gain compared to fructose. Insulin is a key appetite regulating hormone and glucose consumption results in energy absorption that can trigger satiety and allow regulation of body weight. Fructose in contrast does not cause the release of insulin and as a result may bypass these regulatory mechanisms thus increasing the risk of over consuming energy. The metabolic differences in the fate of fructose and glucose illustrates the fallacy of the paradigm that a calorie is a calorie.

RdB

Samuel. V. T. 2011. Fructose induced lipogenesis: from sugar to fat to insulin resistance. Trends In Endocrinology And Metabolism. 22 (2): 60-65

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
This entry was posted in de Novo Lipogenesis, Fructose, High Fructose Corn Syrup, Insulin Resistance, Non-alcoholic Fatty Liver Disease, Obesity, Soft Drinks, Sucrose, Sugar, Weight Loss. Bookmark the permalink.