Content Library Articles Is High Fructose Corn Syrup Really that Bad for You?

Is High Fructose Corn Syrup Really that Bad for You?

Is High Fructose Corn Syrup Really that Bad for You?

High-fructose corn syrup (HFCS) is an insidious chemical that has crept into our food supply over the past few decades. Today HFCS represents1 more than 40 percent of caloric sweeteners added to foods and beverages.

HFCS can contain anywhere from 55 to 90 percent fructose and is derived from corn, a heavily subsidized (read: cheap) crop. Manufacturers love HFCS because, especially when compared to regular sugar, it’s cheaper, sweeter and produced in abundance.

Not surprisingly, HFCS’s ubiquity in the 1980s correlated with the beginning of the obesity epidemic. Other factors, including increased portion sizes, certainly play a role, but the inclusion of HFCS in soft drinks and other sweetened beverages merits serious consideration as an important cause of the obesity epidemic.

Public opinion about HCFS has radically shifted from a diabetic-friendly sweetener to a very harmful one. "Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index," researchers in the journal Physiological Reviews wrote.2 "However, chronically high consumption of fructose in rodents leads to [liver and systemic] insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure."

Realizing the public has a rather dismal view about this sweetener, manufacturers have gradually removed HFCS from processed foods. The United States Department of Agriculture (USDA) data show 3 decreased HFCS consumption since 2002, while other sugar consumption has held steady or increased.

Don’t be fooled. HFCS still lurks in many foods in numerous disguises, and you must carefully scrutinize labels to learn where it hides.

How Does Fructose Differ From Glucose?

Table sugar (sucrose) and other sugars break down into the simple sugars glucose and fructose in your body, but from there they behave far differently.

Nearly every cell can use glucose, which becomes the basic sugar your body uses for energy and metabolism. Glucose is one of the key building blocks of all carbohydrates and often found as part of other slowly absorbed sugars found in beans and whole grains.

Only your liver cells can process fructose, and that’s where the problems begin. Among the damning claims, recent studies conclude HFCS increases appetite4, promotes obesity5 more than regular sugar, and is more addictive than cocaine6. HFCS contributes to diabesity and inflammation.

High doses of fructose have been proven to literally punch holes in the intestinal lining7, allowing nasty by-products of toxic gut bacteria and partially digested food proteins to enter your bloodstream and trigger inflammation.

Because fructose goes straight to your liver and triggers lipogenesis (the production of fats like triglycerides and cholesterol), liver damage—called fatty liver— affects 70 million people in this country. Studies show fructose8 contributes to the development and severity of non-alcoholic fatty liver disease, increasing hepatic fat, inflammation, and possibly fibrosis.

Unlike glucose, fructose doesn’t trigger two key satiating hormones. “The digestion, absorption, and metabolism of fructose differ from those of glucose,” researchers in a review published in The American Journal of Clinical Nutrition wrote. “[U]nlike 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 [to control appetite], this suggests that dietary fructose may contribute to increased energy intake and weight gain.”5

In other words, your brain doesn't get the message to stop eating HFCS, making it easy to overeat and create hormonal and metabolic havoc. Even though it doesn’t raise insulin, studies show fructose contributes to insulin resistance9, leading to weight gain, elevated triglycerides10,Type 2 diabetes11, and even cancer12.

What Makes Fructose in Fruit Different Than HFCS?

Fruit is an exception to the fructose rule. Naturally occurring fructose in fruit is part of a complex web of nutrients and fiber and doesn’t exhibit the same biological effects as the high fructose found in corn sugar.

Unless you just eat massive amounts of fruit, fructose shouldn’t become a problem. When you eat fruit, the amount of fructose you ingest is significantly lower than in sweetened beverages, and the metabolic effects of it are different because the increased intake of fiber, vitamins, minerals, phytonutrients, and antioxidants helps slow absorption and improve metabolism.

When fructose is processed into high-fructose corn syrup (HFCS), it is absorbed more quickly than regular sugar and enters your cells without any help. It doesn’t require the help of insulin the way glucose does, nor do the fiber and nutrients help buffer out that fructose load. Fructose makes a beeline straight to your liver, where metabolic havoc ensues.

How Can I Eliminate HFCS From My Diet?

The easiest way to completely avoid HFCS is to eat real, whole, unprocessed foods. If you buy packaged foods, read food labels carefully to identify sugar in other disguises.

Sugar is sugar by any other name. Be wary about the numerous disguises manufacturers hide sugar as, and if you have any doubt put the package back. If you find “high-fructose corn syrup” or the new term “corn sugar” on the label, you can be sure it is not whole, real, fresh food full of fiber, vitamins, minerals, phytonutrients, and antioxidants. Stay away if you want to stay healthy.

Are you convinced? Ready to rid yourself of sugar? Join me for the 10-Day Detox Diet Challenge, starting very soon. Click here to find out how.

Additional References

1George A Bray, Samara Joy Nielsen, and Barry M Popkin, Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity1,2 - 2004 American Society for Clinical Nutrition
2Tappy L1, Lê KA., Metabolic effects of fructose and the worldwide increase in obesity - Physiol Rev. 2010 Jan;90(1):23-46. doi: 10.1152/physrev.00019.2009.
3USDA - Sugar and Sweeteners Yearbook Tables.
4Richard J Johnson, Mark S Segal, Yuri Sautin, Takahiko Nakagawa, Daniel I Feig, Duk-Hee Kang, Michael S Gersch, Steven Benner, and Laura G Sánchez-Lozada, Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease1,2,3 - 2007 American Society for Clinical Nutrition
5George A Bray, Samara Joy Nielsen, and Barry M Popki - Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity1,2 - Am J Clin Nutr April 2004 vol. 79 no. 4 537-543
6Magalie Lenoir equal contributor, Fuschia Serre equal contributor, Lauriane Cantin, Serge H. Ahmed, Intense Sweetness Surpasses Cocaine Reward - Published: August 01, 2007DOI: 10.1371/journal.pone.0000698
7Jean Robert RapinI,III and Nicolas WiernspergerII,II, Possible Links between Intestinal Permeablity and Food Processing: A Potential Therapeutic Niche for Glutamine -!po=5.00000
8Vos MB1, Lavine JE., Dietary fructose in nonalcoholic fatty liver disease. - Hepatology. 2013 Jun;57(6):2525-31. doi: 10.1002/hep.26299. Epub 2013 May 1.
9Basciano H1, Federico L, Adeli K., Fructose, insulin resistance, and metabolic dyslipidemia. - Nutr Metab (Lond). 2005 Feb 21;2(1):5.
10Elliott SS1, Keim NL, Stern JS, Teff K, Havel PJ., Fructose, weight gain, and the insulin resistance syndrome. - Am J Clin Nutr. 2002 Nov;76(5):911-22.
11Stanhope KL1, Havel PJ., Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup. - Am J Clin Nutr. 2008 Dec;88(6):1733S-1737S. doi: 10.3945/ajcn.2008.25825D.
12Port AM1, Ruth MR, Istfan NW. - Fructose consumption and cancer: is there a connection? - Curr Opin Endocrinol Diabetes Obes. 2012 Oct;19(5):367-74. doi: 10.1097/MED.0b013e328357f0cb.

Brownell KD, Horgen KB. Food fight: The inside story of America’s obesity crisis— and what we can do about it. New York: McGraw-Hill, 2003.

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