News - Chiropractic
High Fructose Corn Syrup = Weight Gain
October, 2009
Prepared by: Dr. Shane Lynch, D.C.
Elliott SS, Klein NL, Stern JS, Teff K et al. Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr 2002;76:911-22.
The above review article explores whether consumption of fructose, specifically high-fructose corn syrup (HFCS) and sucrose (table sugar=fructose-glucose linked together), significantly contributes to the onset of obesity and metabolic abnormalities observed in the insulin resistance syndrome. The insulin resistance syndrome includes such metabolic abnormalities as insulin resistance, glucose intolerance, high blood insulin concentrations and increased blood pressure. Also included with this syndrome are central obesity and high triacylglycerol (fat) and low HDL (“good” cholesterol) blood concentrations.
Fructose naturally occurs in such foods as fruits and vegetables, and because these foods typically provide us with ~15 g of fructose per/day compared with 27g/day in processed foods sweetened with HFCS and sucrose, their consumption is not likely to contribute to metabolic abnormalities. High-fructose corn syrup is created in the laboratory via enzymatic isomerization of dextrose/glucose (a sugar) and has served as a popular sweetener is a wide range of products since the 1970’s. Metabolism of fructose and HFCS in particular involve different enzymes than glucose and other sugars such as lactose. In particular fructose metabolism does not activate specific enzymes that are responsible for decreasing appetite and limiting fat production in the body.
Key points from the article:
“In contrast with low doses of fructose, when much larger amounts of fructose are consumed (eg, in sucrose and HFCS-sweetened beverages), fructose continues to enter the glycolytic pathway distal to phosphofructokinase, and hepatic triacylglycerol production is facilitated”.
In other words, with metabolism of fructose the enzyme phosphofructokinase is not activated and this in turn allows for excess fat (triacylglcerol) production in the liver (hepatic).
“Fructose ingestion is more lipogenic (fat producing) than is glucose, an effect that might be exacerbated in subjects with existing hyperlidemia (high blood fat concentrations) or insulin resistance or type 2 diabetes”.
“...fructose does not stimulate the production of 2 key hormones, insulin and leptin, which are involved in the long-term regulation of energy homeostasis. Therefore, the decrease in insulin responses to meals and leptin production associated with chronic consumption of diets high in fructose may have delertious long-term effects on the regulation of energy intake and body adiposity (fat)”.
Insulin and leptin provide a sense of satiety or fullness by activating specific areas of the brain. Thus when these hormones are not present, such as with the consumption of HFCS, the brain does not receive feedback telling it that enough calories have been consumed and consequently you continue to eat more than you should.
Conclusion:
The metabolism of HFCS does not activate specific enzymes that limit excess fat production in the liver.
The metabolism of HFCS does not stimulate the production of important hormones that activate the brain telling it that enough food/calories have been consumed.
The consumption of foods containing naturally occurring fructose, such as in fruits and vegetables, do not raise the same concerns as those sweetened with HFCS because these natural foods provide micronutrients, fiber and antioxidants.
