HFCS was developed in 1971 by food scientists in Japan as a way to economically produce a cheaper sweetener that retained stability, an advantage to convenience food producers. It is six times sweeter than cane sugar (sucrose) and made from corn, a cheap commodity product.

HFCS however has posed a troubling issue for those concerned about our growing obesity epidemic and the food industry in general. Fructose, unlike sucrose or dextrose, takes a decidedly different route during human metabolism. Sucrose travels in the human body through a complex breakdown process before arriving in the liver, but fructose bypasses the critical breakdown process and arrives almost completely intact in the liver where it is metabolized. This unique feature of fructose, which is intensified by the high concentrations found in HFCS, is known as “metabolic shunting”.

Once in the liver, scientists found fructose was being metabolized in the liver as a building block of triglycerides. This caused the liver to release fatty acids into the bloodstream increasing triglyceride levels. Bombarded by fatty acids, muscle tissue develops insulin resistance, often found to be an undetected precursor to pre-diabetes. According to the National Institute of Diabetes & Digestive & Kidney Diseases an estimated 18 million Americans have diabetes and another 41 million have pre-diabetes, and most don’t even know it.

Studies at the University of Minnesota compared a fructose diet (17% of total calories from fructose, typical “fast food diet”) to diet sweetened mainly with sucrose. The results were dramatic. The fructose diet produced significantly higher levels of triglycerides in the blood, in men about 32% higher, than the sucrose-sweetened diet. The fructose diets also made triglyceride levels peak faster, just after mealtime, when such fats can do most damage to artery walls.

Fructose consumption now comprises about 9% of the average individual’s daily energy intake, and up to 20% of the average child’s diet and is thought to have lead to the prevalence of obesity, not merely from increased caloric consumption, but through the mechanism it is metabolized within the human body.

In 1995 researchers from the University of California at Berkeley, studying how certain sugars alter how the body selects certain fuels to burn, concluded basically the same thing: long- term dietary changes involving simple sugars, as has happened in the past two decades with fructose, “contribute to overall changes in fat oxidation.” Overuse of fructose was skewing the national metabolism toward fat storage.

Obesity is a major epidemic, but its causes are still unclear. Scientists investigated the relationship between the intake of high-fructose corn syrup (HFCS) and the development of obesity. They analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 years of age, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/day.

The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis (translation: new origination of fats). In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, caloric sweetened beverages may enhance caloric over-consumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the over-consumption of HFCS in caloric sweetened beverages may play a role in the epidemic of obesity.

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