Consuming as little as 40-50 grams or slightly over 1.5-ounce fructose over a 10 hour period may increase blood pressure, blood triglycerides, reduced insulin binding & insulin sensitivity, and increase fat weight gain. The disturbing fact is that the general population has been consuming more than that amount every day for the past 34 years. Total fructose consumed per person from combined consumption of sucrose and high-fructose corn syrup has increased by +26%, from 64 g/d in 1970 to 81 g/d in 1997. As Body Mass Index increases (fat weight gain), the increased risk of insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension may occur. Fructose consumption as reported from animal studies (1) has been associated with:


Insulin and leptin are hormones that influence the central nervous system withregars to regulation of energy homeostasis. Unlike the sugar glucose, fructose does not stimulate insulin secretion from pancreatic ß cells. Foods and beverages containing fructose produce smaller insulin excursions than can be expected following the consumption of glucose-containing carbohydrates.

Leptin production is regulated by insulin response to food. Because fructose does not stimulate the secretion of insulin, fructose consumption reduces circulating leptin levels.

Low circulating leptin and insulin in diets high in fructose, results in weight gain. Further, fructose, metabolized to lipid in the liver, to a far greater degree than is seen with ingested glucose.

————————————-edit, below Hepatic fructose metabolism begins with phosphorylation by fructokinase. Fructose carbon enters the glycolytic pathway at the triose phosphate level (dihydroxyacetone phosphate and glyceraldehyde-3-phosphate). Thus, fructose bypasses the major control point by which glucose carbon enters glycolysis (phosphofructokinase), where glucose metabolism is limited by feedback inhibition by citrate and ATP. This allows fructose to serve as an unregulated source of both glycerol-3-phosphate and acetyl-CoA for hepatic lipogenesis. P, phosphate. The hepatic metabolism of fructose has important effects on both glucose and lipid metabolism. Absorbed fructose is delivered to the liver via the portal vein. Fructose is phosphorylated in the liver by adenosine triphosphate to form fructose-1-phosphate. The reaction is catalyzed by the enzyme fructokinase. Fructose-1-phosphate is split by aldolase B into glyceraldehyde and dihydroxyacetone phosphate. Both can be converted to glyceraldehyde-3-phosphate. Thus, the fructose molecule is metabolized into 2 triose phosphates that bypass the main rate-controlling step in glycolysis, 6-phosphofructokinase. By contrast, hepatic glucose metabolism is limited by the capacity to store glucose as glycogen and, more importantly, by the inhibition of glycolysis and further glucose uptake resulting from the effects of citrate and ATP to inhibit phosphofructokinase. The products of fructose metabolism in the glycolytic pathway of the liver are glucose, glycogen, lactate, and pyruvate. Because fructose uptake by the liver is not inhibited at the level of phosphofructokinase, fructose consumption results in LARGER INCREASES OF CIRCULATING LACTATE than does consumption of a comparable amount of glucose.

Elliott et al., (1) hallmark review of the literature reported several harmful effects from habitual consuming of processed fructose-containing sweetener agents. They report that regular consumption of processed fructose negatively impacts blood pressure, blood lipid triglycerides, insulin resistance and glucose metabolism, with fat weight gain proportionate to time and total dose:


Only a modest amount of processed fructose sugar is associated with harmful consequences to human subjects and more precarious interventions imposed in animal research. Healthy normal athletes should NOT therefore impose a known health risk during exercise or during sedentary mealtimes by consuming a processed fructose-sugar sweetener.

(1) Fructose, weight gain, and the insulin resistance syndrome, Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff, Peter J Havel, American Journal of Clinical Nutrition, Vol. 76, No. 5, 9 11-922, November 2002.

(2) Storlien LH, Oakes ND, Pan DA, Kusunoki M, Jenkins AB. Syndromes of insulin resistance in the rat. Inducement by diet and amelioration with benfluorex. Diabetes 1993;42:457-62.

(3) Cavadini C, Siega-Riz AM, Popkin BM. US adolescent food intake trends from 1965 to 1996. Arch Dis Child 2000;83:18-24.

(4) Takagawa Y, Berger ME, Hori MT, Tuck ML, Golub MS. Long-term fructose feeding impairs vascular relaxation in rat mesenteric arteries. Am J Hypertens 2001;14:811-7.

(5) Martinez FJ, Rizza RA, Romero JC. High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs. Hypertension 1994;23:456-63.




David S. Klein

Stages of Life Medical Institute

1917 Boothe Circle

Longwood, FL 32750