Fructose from added sugars linked to high blood pressure
Posted Jul 27 2010 1:39pm
The consumption of fructose has increased significantly since the 1970s, when high fructose corn syrup (HFCS) was introduced into the United States food supply. The use of HFCS now exceeds that of sucrose (table sugar) in sweetened foods in the U.S.
Absorption of fructose and glucose:
Sucrose is composed of one fructose molecule and one glucose molecule. There are differences between fructose and glucose metabolism. Fructose is absorbed in the small intestine, transported to the liver through the portal vein, and then metabolized via the same process that breaks down glucose to make energy – however, fructose is only broken down in the liver, whereas glucose can be used by any cell in the body. Ingesting glucose raises blood glucose levels, and ingesting fructose does not raise glucose as quickly or as much, but raises triglyceride levels much more.1
Fructose was once regarded as a “safe” sweetener for diabetics, because of its small effect on blood glucose levels. However, fructose is a reducing sugar, which means that it contributes to the formation of advanced glycation end products (AGEs), which contribute to diabetes and its complications, Alzheimer’s disease, and cardiovascular disease.2 Since fructose consumption also elevates triglycerides and diabetics are already at risk for cardiovascular disease, increasing triglycerides adds to this risk. Added fructose consumption has also been associated with non-alcoholic fatty liver disease, and elevated cholesterol and retinopathy in diabetics.1
Fructose in natural foods vs. fructose in HFCS:
Fructose makes up half of the sucrose molecule, and HFCS contains similar proportions of fructose and glucose as sucrose does (HFCS is 55% fructose). Fructose may be found alone (free) or complexed with glucose as sucrose. In most fruits, much of the fructose is bound to glucose. Fructose entry into blood is slowed when it is in sucrose form, because sucrose must be first split by enzymes in intestinal cells. Fructose molecules in HFCS, however, are free, and therefore absorbed more rapidly. It is thought that the enzymes in the liver responsible for breaking down fructose are overwhelmed by the large loads of fructose delivered by HFCS-sweetened beverages, allowing for large quantities of fructose to be released into the blood.1
Fructose and elevated blood pressure:
The current study examined data from 4528 adults, whose median fructose intake from added sugars was 74 grams per day. As a reference point, 74 grams of fructose is roughly the amount present in 2 ½ twenty-ounce soft drinks or 13 bananas.1,3 The researchers determined that fructose intake at or above the median 74 grams per day increased the risk of elevated blood pressure.
Subjects who consumed 74 grams or more of fructose each day in added sugar increased their risk of blood pressure elevated above 135/85 by 26%, above 140/90 by 30%, and above 160/100 by 77%.4
Essentially, the average fructose intake in the U.S. is a quantity that increases chronic disease risk – and not just risk of diabetes. Elevated blood pressure contributes to risk of heart attack, stroke, heart failure, and kidney disease.
There are no “safe” sweeteners - whole fruits and root vegetables are the only sweet-tasting foods that are health-promoting. Added sugar in any form is calorie-dense and deficient in nutrients, and therefore detrimental to health.
1. Teff KL, Grudziak J, Townsend RR, et al. Endocrine and metabolic effects of consuming fructose- and glucose-sweetened beverages with meals in obese men and women: influence of insulin resistance on plasma triglyceride responses. J Clin Endocrinol Metab. 2009 May;94(5):1562-9.
2. Glenn JV, Stitt AW. The role of advanced glycation end products in retinal ageing and disease. Biochim Biophys Acta. 2009 Oct;1790(10):1109-16.
Loy CT, Twigg SM. Growth factors, AGEing, and the diabetes link in Alzheimer's disease. J Alzheimers Dis. 2009 Apr;16(4):823-31.
Peppa M, Uribarri J, Vlassara H. Aging and glycoxidant stress. Hormones (Athens). 2008 Apr-Jun;7(2):123-32.
Peppa M, Stavroulakis P, Raptis SA. Advanced glycoxidation products and impaired diabetic wound healing. Wound Repair Regen. 2009 Jul-Aug;17(4):461-72.
Yamagishi S. Advanced glycation end products and receptor-oxidative stress system in diabetic vascular complications. Ther Apher Dial. 2009 Dec;13(6):534-9.
Barlovic DP, Thomas MC, Jandeleit-Dahm K. Cardiovascular disease: what's all the AGE/RAGE about? Cardiovasc Hematol Disord Drug Targets. 2010 Mar;10(1):7-15.