High-fructose corn syrup (HFCS) is a liquid sweetener similar to sucrose
(table sugar) first introduced in the 1970s. Chemically it is similar
to other sweeteners like agave, honey, and fruit juice concentrates which
also contain Fructose and Glucose. But unlike table sugar, which has a
1:1 ratio of glucose to fructose, the ratio in HFCS is often modified
to 42-55% fructose. When combined with other ingredients, popular beverages
made with HFCS can have even higher total fructose-to-glucose ratios.
Fruit juices can have twice as much fructose as glucose. To metabolize
sucrose, stomach acids have to break apart the bonds between glucose and
fructose but, in HFCS, there are no bonds to break, effectively bypassing
this important digestion step. The result of this bypass appears to be
that fructose in HFCS is absorbed much faster into the blood stream than
for sucrose. Likely the small amounts of fructose present in natural foods
(such as fruit) are slowly absorbed and then completely or almost completely
metabolized by the intestines and liver, therefore little or no fructose
would pass into the blood stream. So, even though fructose is present
in natural foods, it is contained in a way that it was perhaps never destined
to reach our blood stream intact.
To make HFCS, corn starch (glucose) is modified by acids and enzymes to
convert some of it into fructose. The mixture of glucose and fructose
is HFCS, and different formulations are created by changing the amounts
of fructose. HFCS also goes by other names such as Maize syrup, Glucose
syrup, Tapioca syrup, Dahlia syrup, Fruit fructose, Fruit sugar, and Crystalline
fructose, so identifying it on a food label is not always easy. The
Corn Refiners Association recently petitioned the FDA to change the name
to "corn sugar."  Their petition was ultimately rejected.
Look at the first ingredient listed for the popular children's drink
From 1970 to 2000 there was a 25% increase in “added sugars”
in the U.S., and HFCS replaced sucrose as the main sweetener of soft drinks.[7,
8] During this same time, obesity rates in the US increased, leading many
to question if the two are related. It is to be noted that the consumption
of flour, cereal products, and added fats also increased.[1, 8] The European
Union did not experience this massive switch to this corn-based, chemically
modified sweetener, where it is known as Fructose-Glucose Syrup (GFS)
or Isoglucose. In the EU, GFS is limited to only 5% of the total sugar
production and, soft drinks continue to be sweetened mostly with sucrose.
In the US, they are sweetened with HFCS. Obesity rates have also risen
in the EU without a rise in GFS intake. Therefore the increase in obesity
does not seem to be related entirely to GFS/HFCS consumption.
HFCS makes up 40 percent of caloric sweeteners added to foods and beverages.
(Non-caloric sweeteners include Aspartame, Saccharin, and Sucralose, although
they are not necessarily healthier than HFCS.) The use of HFCS in
our food chain is not likely to decrease any time soon. Government subsidies
for corn keep HFCS cheaper to use than table sugar. Still, there are some
signs of change. Recently Kraft foods decided to remove HFCS from Capri
Sun 12 but Pepsi Co. is not willing to follow suit, despite Panera's
Since HFCS is so ubiquitous in the US foods, what is the big deal? For
starters, a study from Columbia University demonstrated more than one
HFCS soda per day was associated with increased risk of having gout, kidney
stones, and chronic kidney disease.[14, 15, 16, 17] Consumption of sweetened
beverages (containing either sucrose or HFCS) is associated with obesity,
diabetes, heart disease, accelerated aging, non-alcoholic fatty liver
disease, high cholesterol and lipids, and irritable bowel syndrome, just
to name a few.[1, 3] To explore further, we should look at how our body
processes fructose and glucose.
Fructose is rapidly metabolized almost exclusively in the liver, whereas
glucose is metabolized in many other organs. In the liver, fructose metabolism
leads to a transient depletion of phosphate and results in the production
of an acid called lactic acid, which is released into the systemic circulation.
(Lactic acid is more typically produced in muscle cells and red blood
cells during intense exercise.) This fructose-induced hyperlactatemia
may contribute to the suppression of breakdown of fat cells, providing
an additional mechanism for causing obesity.
Fructose is also converted into glucose and fatty acids. A substantial
portion of fructose-derived glucose is stored in the liver as glycogen.
Glycogen is typically used during times of fasting to maintain normal
blood glucose levels. More glycogen is stored from fructose than from
an equivalent dose of glucose. But fructose also decreases sensitivity
to insulin and it does not require insulin for transport, unlike glucose.
When someone is less sensitive to insulin, glucose production remains
activated and does not receive the signal (insulin) to turn off. This
is especially a problem for diabetic patients who have shown a markedly
enhanced insulin response to fructose compared with nondiabetic people,
potentially dropping their blood glucose levels to dangerously low levels. [20, 21]
A high-fructose diet leads to elevated fatty acid and lipid levels, especially
two components of cholesterol: triglycerides (TGs) and Very Low Density
Lipoproteins (VLDLs), and was shown to occur in healthy people after just
one week of a high-fructose diet, through increased lipid production in
the liver and decreased clearance. [22,23] For unclear reasons, this effect
occurs to a greater extent in obese people and to a lesser degree in premenopausal,
healthy females.[24, 25] High VLDL and TG levels are associated with increased
risk of heart disease and stroke. When lipids are stored in the liver,
this can lead to
nonalcoholic fatty liver disease (NAFLD), which is also is tightly linked to insulin resistance. Thankfully, these
effects can be reversed. In some studies, the effect of fructose on lipid
levels can be ameliorated with fish oil supplementation, using honey for
sweetener instead of corn syrup, and changing the bacteria in the intestines.[26, 27, 28]
Changing the types and amounts of bacteria in the intestinal tract can
be accomplished through the use of prebiotics and probiotics. Sometimes
in severe cases, a short course of antibiotics are given initially, especially for
Small Intestine Bacterial Overgrowth (SIBO). In our experience, the amounts of probiotics necessary to see clinical
improvement often exceed what are sold in health-food stores, groceries,
and retail pharmacies.
In addition to its effects on the chronic diseases like diabetes and hyperlipidemia
described above, fructose causes an increase in blood pressure, which
is not seen with glucose.
There is evidence to suggest that fructose decreases a person's sensation
of fullness after a meal, called satiety, which typically signals to the
brain to stop eating. After eating a meal high in fructose, the rise in
blood glucose is blunted since its glycemic index is about fivefold lower
than that of glucose. A rise in glucose level and resultant release of
insulin is one way the brain knows it is time to stop eating. A high fructose
meal also blunts the suppression of the appetite-stimulating hormone ghrelin,
compared to a meal containing an equivalent amount of glucose. Leptin
is a hormone released from fat cells which signals to the brain to decrease
the overall appetite. Obese people often have increased leptin levels
but are resistant to its effects. In addition to producing a lesser secretion
of leptin compared with equivalent doses of glucose, it has been observed
that high fructose intake impairs leptin’s actions, suggesting fructose-induced
leptin resistance.[30, 31] Leptin resistance may also contribute to causing
In summary, HFCS contains the same fructose and glucose molecules as "natural"
table sugar (sucrose) but they are manufactured in varying ratios and
are not bound together. The increase in obesity does not seem to be related
entirely to HFCS consumption, but HFCS is present in many processed foods
in the US. Consumption of sweetened beverages is associated with increased
rates of gout, kidney stones, chronic kidney disease, obesity, diabetes,
heart disease, accelerated aging, non-alcoholic fatty liver disease, high
cholesterol and lipids, and irritable bowel syndrome. The fructose is
of particular concern for several reasons. It increases lactic acid production,
which may cause obesity. A substantial portion of fructose-derived glucose
is stored in the liver as glycogen and fatty acids. Over time these can
build up and cause NAFLD. Fructose decreases sensitivity to insulin, keeping
glucose production going even when there is an abundance of sugars. A
high-fructose diet leads to increased lipid production and decreased clearance
fatty acids and lipids, including cholesterol, which is associated with
increased risk of heart disease and stroke. These effects can be reversed
with fish oil, honey, and changing the intestinal tract flora. Fructose
causes an increase in blood pressure and increases appetite.
Finally, many are familiar with one of the most socially undesirable effects
of fructose. When it is incompletely absorbed from the gut and is fermented
by intestinal bacteria, gas is produced. And we all know how much fun
gas is, when you are a kid, and how much not fun it is when you grow up.
For more information or for assistance with modifying your diet, give our
office a call at 480-240-2600. We are happy to schedule a free 15-minute
phone consultation with one of our practitioners, to help you determine
whether we are the best medical office for you.
 Luc Tappy, Kim-Anne Lê.
Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiological Reviews Jan 2010, 90 (1) 23-46.
 Walker RW, Dumke KA, Goran MI.
Fructose content in popular beverages made with and without high-fructose
corn syrup. Nutrition. Volume 30, Issues 7-8, July-August 2014, Pages 928-935.
 Gaby AR.
Adverse effects of dietary fructose. Altern Med Rev. 2005 Dec;10(4):294-306.
 Marshall RO, Kooi ER.
Enzymatic conversion of D-glucose to D-fructose. Science 125: 648-649, 1957.
 High Fructose Corn Syrup: Questions and Answers. FDA.
 Parker-Pope T. A New Name for High-Fructose Corn Syrup. New York Times
Blogs. SEPTEMBER 14, 2010.
 Leeper HA, Jones E (October 2007).
How bad is fructose?
Am J Clin Nutr 86 (4): 895-896.
 White JS.
Straight talk about high-fructose corn syrup: what it is and what it ain’t. Am J Clin Nutr. 2008 Dec;88(6):1716S-1721S.
 European Food Information Council.
 Mohr CR. The Dangers of High Fructose Corn Syrup. Diabetes Health.
 Suez J., et al.
Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 514, 181-186, 2014.
 Hogan B. Kraft’s Capri Sun drinks to drop high-fructose corn
syrup. Chicago Tribune. Feb. 10, 2015.
 Unglesbee B. Panera head chef to PepsiCo: High-fructose corn syrup
going off menu. St. Louis Business Journal. Jul 6, 2015.
 Bomback AS.
Sugar-sweetened soda consumption, hyperuricemia, and kidney disease. Kidney International (2010) 77, 609-616.
 Choi HK, Curhan G.
Soft drinks, fructose consumption, and the risk of gout in men: prospective
cohort study. BMJ 336: 309-312, 2008.
 Taylor EN, Curhan GC.
Fructose consumption and the risk of kidney stones. Kidney Int 73: 207-212, 2008.
 Reiser S.
Effect of dietary sugars on metabolic risk factors associated with heart disease. Nutr Health 3: 203-216, 1985.
 Abdel-Sayed A, Binnert C, Le KA, Bortolotti M, Schneiter P,Tappy L.
A high-fructose diet impairs basal and stress-mediated lipid metabolism
in healthy male subjects. Br J Nutr 1-7, 2008.
 Nilsson LH, Hultman E.
Liver and muscle glycogen in man after glucose and fructose infusion. Scand J Clin Lab Invest 33: 5-10, 1974.
 Crapo PA, Insel JI, Sperling M, Kolterman OG.
Comparison of serum glucose, insulin and glycogen responses to different
types of complex carbohydrates in non insulin dependent diabetic patients. Am J Clin Nutr 34: 184-190, 1981.
 Crapo PA, Kolterman OG, Olefsky JM.
Effects of oral fructose in normal, diabetic, and impaired glucose tolerance subjects. Diabetes Care 3: 575-582, 1980.
 Livesey G, Taylor R.
Fructose consumption and consequences for glycation, plasma triacylglycerol,
and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr 88: 1419-1437, 2008.
 Tappya L and Lê KA.
Does fructose consumption contribute to non-alcoholic fatty liver disease?
Clinics and Research in Hepatology and Gastroenterology. Volume 36, Issue
6, December 2012, Pages 554-560.
 Teff KL, 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 94: 1562-1569, 2009.
 Ashley JM, St Jeor ST, Perumean-Chaney S, Schrage J, Bovee V.
Meal replacements in weight intervention. Obes Res 9 Suppl 4:312S-320S, 2001.
 Faeh D, Minehira K, Schwarz J, Periasami R, Seongus P, Tappy L.
Effect of fructose overfeeding and fish oil administration on hepatic de
novo lipogenesis and insulin sensitivity in healthy males. Diabetes 54: 1907-1913, 2005.
 Busserolles J, et al.
Substituting honey for refined carbohydrates protects rats from hypertriglyceridemic
and prooxidative effects of fructose. J Nutr 132: 3379-3382, 2002.
 Bergheim I, et al.
Antibiotics protect against fructose induced hepatic lipid accumulation
in mice: role of endotoxin. J Hepatol 48: 983-992, 2008.
 Brown CM, Dulloo AG, Yepuri G, Montani JP.
Fructose ingestion acutely elevates blood pressure in healthy young humans. Am J Physiol Regul Integr Comp Physiol 294: R730-R737, 2008.
 Teff KL, et al.
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial
suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 89: 2963-2972, 2004.
 Le KA, et al.
A 4-wk high-fructose diet alters lipid metabolism without affecting insulin
sensitivity or ectopic lipids in healthy humans. Am J Clin Nutr 84: 1374-1379, 2006.
 Vila L, et al.
Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine
(Ser/Thr) phosphoproteins involved in leptin transduction mediate the
effect of fructose on rat liver lipid metabolism. Hepatology 48: 1506-1516, 2008.