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As levels of diabetes, obesity, and other dietary issues increase (diabetes alone has increased 763% from 1935 to 1996 in the united states (Gross et al 2004)) studies have been conducted to investigate whether the 1,000% rise in the use of High Fructose Corn Syrup (HFCS) from 1967 to 2000 in the American food industry is a major contributor (Bray et al 2004).^{1  2} In this article, we will examine whether or not HFCS is truly a factor in this significant increase.

Early studies found that there were possible clinical explanations for metabolic differences derived from HFCS ingestion and other sweeteners; primarily that it did not trigger insulin creation and thereby was thought to not trigger satiety signals (Reiser et al 1989) (Elliott et al 2002) (Bray et al 2004) (Teff et al 2004) .^3 4 5 6  However, more recent studies have found no difference in resulting satiety in men or women resulting from HFCS, sucrose, or milk, (Soenen and Westerterp-Plantenga 2007) (Melanson et al 2008) (Akhavan and Anderson 2007),^7 8 9 and that HFCS yields similar metabolic responses to other caloric sweeteners. (Angelopoulos et al 2009),¹⁰ Stanhope et al 2008 and Melanson  et al 2007 determined that sucrose and HFCS do not have significantly different short-term metabolic effects,^11 12 and moderate levels (~1.5 grams of fructose per kilogram of body mass) of HFCS intake  does not cause ectopic lipid deposition or insulin resistance in healthy humans (Le et al 2006).¹³

Although HFCS is not itself responsible for the increase in dietary and metabolic disorders, other studies have demonstrated that increasing levels of excess energy consumption in general is a cause (Gross et al 2004).¹⁴  For thousands of years humans consumed fructose amounting to 16–20 grams per day, largely from fresh fruits (Gross et al 2004). ¹⁵ Westernization of diets has resulted in significant increases in food with added fructose, leading to typical daily consumptions amounting to 85–100 grams of fructose per day (Gross et al 2004). ¹⁶  For example, a 12 ounce Coke contains 39 grams of fructose and the USDA Recommended Daily Allowance allots for 32 grams of carbohydrates in a 2,000 calorie diet.¹⁷  A single 12 ounce Coke therefore contains significantly more than an individual’s entire excess dietary energy allowance for a day.  Raben et al 2002 found that people have a very difficult time compensating for increased levels of calories associated with increased sugar intake by lowering caloric intake elsewhere.¹⁸  While moderate ingestion of HFCS will not specifically cause harm to oneself, it is advisable to monitor and limit consumption as much as possible.

1. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
2. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
3. Fructose, weight gain, and the insulin resistance syndrome [↩]
4. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
5. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women [↩]
6. Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch [↩]
7. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads [↩]
8. High-fructose corn syrup, energy intake, and appetite regulation [↩]
9. Effects of glucose-to-fructose ratios in solutions on subjective satiety, food intake, and satiety hormones in young men [↩]
10. The Effect of High-Fructose Corn Syrup Consumption on Triglycerides and Uric Acid [↩]
11. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals [↩]
12. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women [↩]
13. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans [↩]
14. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment [↩]
15. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
16. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
17. Carbohydrates [↩]
18. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects [↩]