The rise in America’s obesity rates parallel the rise in consumption of high-fructose corn syrup, which occurred as manufacturers replaced costlier cane sugar (sucrose) in drinks and snacks with high-fructose corn syrup (HFCS).
HFCS is produced by processing corn starch to yield glucose, and then processing the glucose to create a syrup that is usually about 45 percent fructose and 55 percent glucose.
Since sucrose (cane sugar) consists of one molecule of glucose and one molecule of fructose (i.e., 50 percent each), you'd think its effects would be similar to those of HFCS. But sucrose behaves very differently in the body, compared with glucose, fructose, or HFCS.
Conversely, the body’s digestion, absorption, and metabolism of fructose differ from the ways it digests, absorbs, and metabolizes glucose or sucrose.
The HFCS-obesity hypothesis
American’s consumption of HFCS increased by more than 1,000 percent between 1970 and 1990, far exceeding the changes in intake of any other food or food group (Bray GA et al 2004).
HFCS now represents more than 40 percent of caloric sweeteners added to foods and beverages and it is the sole caloric sweetener in soft drinks in the United States.
The increased use of HFCS in the United States mirrors the rapid increase in obesity, and the way in which the liver metabolizes fructose favors creation of new body fat.
In addition, unlike glucose, fructose does not stimulate secretion of insulin or leptin: hormones that act as key signals in the regulation of food intake and body weight (Teff KL et al 2004).
These epidemiological and experimental findings explain why many researchers believe that dietary fructose may promote increased calorie intake and weight gain.
The rise in HFCS intake also correlates with the rise in rates of metabolic syndrome: a condition linked to increased risks of type-2 diabetes and cardiovascular disease and characterized by abdominal obesity, hypertension, and impaired glucose (blood sugar), fat, and insulin metabolism.
Tellingly, HFCS produces signs of metabolic syndrome in animal and human studies: especially elevated triglycerides and altered fat metabolism.
Almost one in three Americans have symptoms of metabolic syndrome, and according to the World Health Organization (WHO), some 2.3 billion adults will be overweight by the year 2015 while more than 700 million people, many of them children, will suffer from obesity.
There are some problems with claims that HFCS is a major cause of obesity or metabolic syndrome:
- The rise in America’s obesity rates also parallels the rise in consumption of soybeans and soy oil, which are high in omega-6 fatty acids, which promote inflammation and other obesity-fueling effects.
- Obesity is also rising in countries where cane sugar still dominates.
- Most studies of the effects of fructose have been in rodents, and those in humans have produced mixed results with regard to insulin resistance: a key pre-diabetic, obesity-promoting condition.
Still, the evidence against HFCS seems to be mounting.
As researchers at Children's Hospital of Pittsburgh wrote recently, “High-fructose consumption is associated with insulin resistance and diabetic dyslipidemia [unhealthful blood-fat profiles]…” But, as they also said, “… the underlying mechanism is unclear.” (Qu S et al 2006)
New research from Spain may shed some light on the mystery.
Barcelona study details fructose effects on the liver
The authors of an animal study in Spain report some disturbing findings about the way in which fructose is metabolized: outcomes that may bolster the accusations made against HFCS, and increase calls to remove it from foods and beverages (Roglans N et al 2007).
Researchers from the University of Barcelona found that liquid fructose changes the way the livers in rats metabolize fat. Fructose affects a genetic switch called PPAR-alpha in ways that impair the liver's ability to break down the sweetener.
As the Spaniards noted, “Because PPAR-alpha activity is lower in human than in rodent livers, fructose ingestion in humans should cause even worse effects, which would partly explain the link between increased consumption of fructose and widening epidemics of obesity and metabolic syndrome.” (Roglans N et al 2007)
PPAR-alpha is believed to help regulate the burning of body fat (fatty acid oxidation).
Researchers led by Dr. Juan Carlos Laguna fed lab rats a fructose- or glucose-sweetened liquid (10 percent sugars by volume).
The livers of the animals drinking the fructose-sweetened liquid metabolized the syrup differently, yielding a calorie overload to which the animals’ bodies could not adapt.
Dr. Laguna’s team report that dietary fructose increased fat synthesis in the animals' livers and also acted on the PPAR-alpha receptor to reduce breakdown of the fructose.
As he said, “The most novel finding is that this molecular mechanism is related to an impairment in the leptin signal. Leptin is a hormone that plays a key role in the body's energy control; among its peripheral actions, it accelerates fat oxidation in the liver and reduces its synthesis.” (Roglans N et al 2007)
The Spaniards also observed that fructose decreased fat-burning in the animals' livers (thereby increasing levels of blood triglycerides and body fat) and activated the pro-inflammatory (hence, pro-obesity) genetic switch called NF-kappaB: two negative changes not observed in the glucose-fed rats
No weight differences seen: short study duration blamed
The Spanish scientists found no significant differences in weight between the rats drinking liquids with glucose or fructose, possibly because this study was too short for such changes to be measurable.
Even though manufacturers call fructose “fruit sugar” -- to mislead and lull consumers of added fructose -- most fruits have much more sucrose than fructose, and the implications of this study have no bearing on the fructose in fruit.
As Dr. Laguna said, “Fruit is healthy and its consumption is strongly recommended. Our study focuses on liquid fructose intake as an addition to the ordinary diet.”
Sources
- Roglans N, Vila L, Farre M, Alegret M, Sanchez RM, Vazquez-Carrera M, Laguna JC. Impairment of hepatic Stat-3 activation and reduction of PPARalpha activity in fructose-fed rats. Hepatology. 2007 Mar;45(3):778-88.
- Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004 Apr;79(4):537-43. Review. Erratum in: Am J Clin Nutr. 2004 Oct;80(4):1090.
- Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D'Alessio D, Havel PJ. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72.
- Qu S, Su D, Altomonte J, Kamagate A, He J, Perdomo G, Tse T, Jiang Y, Dong HH. PPAR{alpha} mediates the hypolipidemic action of fibrates by antagonizing FoxO1. Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E421-34. Epub 2006 Sep 19.
- Le KA, Faeh D, Stettler R, Ith M, Kreis R, Vermathen P, Boesch C, Ravussin E, Tappy L. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Am J Clin Nutr. 2006 Dec;84(6):1374-9.
- Wei Y, Wang D, Topczewski F, Pagliassotti MJ. Fructose-mediated stress signaling in the liver: implications for hepatic insulin resistance. J Nutr Biochem. 2007 Jan;18(1):1-9. Epub 2006 Jul 18. Review.
- Le KA, Tappy L. Metabolic effects of fructose. Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):469-75. Review.
