The dangers of fructose (fruit sugar)
Fructose is a simple sugar found in honey, fruit, table sugar
(sucrose), and high-fructose corn syrup (HFCS). Worldwide fructose
intake has quadrupled over the last century,(1) with the last 30 years
witnessing the most rapid acceleration. This increase has been
paralleled by a similar rise in obesity, diabetes, hypertension, and
kidney disease. (1-2). While such associations don’t mean that the
one necessarily caused the other, animal experiments have shown such
causal relationships, with increases in diseases associated with the
metabolic syndrome - insulin resistance, high levels of triglycerides
in the bloodstream, high blood pressure, abdominal obesity,
inflammation, arterial damage, kidney disease, and fatty liver - much
higher in animals fed fructose than in those fed glucose or
Fructose is unique amongst sugars, in that it up-regulates its own
transporter (Glut5) and metabolism (fructokinase)
(4). Because of this, the more fructose one eats, the more sensitive
one becomes to its effects. This explains why obese persons appear to
be more sensitive to the harmful effects of fructose than are non-obese
Fructose consumption has been associated with weight gain in past
studies. This may be because fructose doesn’t appear to trigger the
hormonal signals involved in the long-term control of energy use in the
way that glucose does.(6) A glucose diet stimulates the pancreas to
secrete insulin. This results in the release of leptin by fat cells
(adipocytes) and the inhibition of ghrelin secretion from the
gastrointestinal tract. These alterations stimulate centres in the
brain that regulate satiety and energy balance. As fructose doesn’t
stimulate insulin, leptin and ghrelin responses are not generated (7).
Study has shown that people fed fructose had a greater appetite the
following day than those fed glucose-fed.(7) This could well result in
Because fructose does not raise blood glucose levels, it has a lower
glycaemic index than other sugars and starches. For this reason, it is
a recommended sweetener for diabetics - plus, of course, ‘five
portions of fruit’, etc; and in a few studies, HbA1c was lowered in
diabetics using fructose. However, while low doses of fructose may
improve glucose control in diabetics, the role of fructose in the
metabolic syndrome, stimulating the production of advanced glycation
end-products (AGEs) and in causing cataracts in diabetic animals means
that fructose is a poor choice for any diabetic. This conclusion is
also held by the American Diabetes Association, (8) - although they
still promote ‘5-portions’ advice. Indeed, as far as heart disease
is concerned, a ‘fructose index’ based on the percentage and amount
of fructose in various foods might be a better indicator than the
So, are high doses of fructose safe? A recent study concluded that
fructose intake up to 90 grams per day may actually be beneficial
because of its effects of lowering HbA1c concentrations,(9) despite the
potential countering effects of increases in blood triglycerides. But
it may be misleading to conclude that this amount of fructose is safe
by examining only the effects of fructose on triglycerides, weight, and
HbA1c. Taking into consideration the increasing evidence that high
fructose intake can also raise blood pressure, decrease insulin
sensitivity, lower glucose tolerance, increase apolipoprotein-B
concentrations, and cause microvascular disease, glomerular
hypertension, kidney damage, fatty liver, and more, (10-12) there are
some important questions about the safety of high doses of fructose in
1.Johnson RJ, Segal MS, Sautin Y, et al. Potential role of sugar
(fructose) in the epidemic of hypertension, obesity and the metabolic
syndrome, diabetes, kidney disease, and cardiovascular disease. Am
J Clin Nutr 2007; 86(4): 899-906.
2.Segal MS, Gollub E, Johnson RJ. Is the fructose index more
relevant with regards to cardiovascular disease than the glycemic
index? Eur J Nutr 2007; 46(7): 406-17.
3.Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid
in fructose-induced metabolic syndrome. Am J Physiol 2006;
4.Ouyang X, Cirillo P, Sautin Y, et al. Fructose consumption as a
risk factor for non-alcoholic fatty liver disease. J Hepatol
2008; 48(6): 993-9.
5.Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ.
Twenty-four-hour endocrine and metabolic profiles following
consumption of high-fructose corn syrup-, sucrose-, fructose-, and
glucose-sweetened beverages with meals. Am J Clin Nutr 2008;
6.Havel PJ. Dietary fructose: implications for dysregulation of
energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev
2005; 63(5): 133-57.
7.Teff KL, Elliott SS, Tschop M, et al. Dietary fructose reduces
circulating insulin and leptin, attenuates postprandial suppression of
ghrelin, and increases triglycerides in women. J Clin Endocrinol
Metab 2004; 89(6): 2963-72.
8.Evidence-based nutrition principles and recommendations for the
treatment and prevention of diabetes and related complications.
Diabetes Care 2002; 25(1): 202-12.
9.Livesey G, Taylor R. Fructose consumption and consequences for
glycation, plasmid triacylglycerol, and body weight: meta-analyses and
meta-regression models of intervention studies. Am J Clin Nutr
2008; 88: 1419-37.
10.Brown CM, Dulloo AG, Yepuri G, Montani JP. Fructose ingestion
acutely elevates blood pressure in healthy young humans. Am J
Physiol 2008; 294(3): R730-7.
11.Swarbrick MM, Stanhope KL, Elliott SS, et al. Consumption of
fructose-sweetened beverages for 10 weeks increases postprandial
triacylglycerol and apolipoprotein-B concentrations in overweight and
obese women. Br J Nutr 2008; Apr 3: 1-6 (Epub ahead of
12.Glushakova O, Kosugi T, Roncal C, et al. Fructose induces the
inflammatory molecule ICAM-1 in endothelial cells. J Am Soc
Nephrol 2008 May 28 (Epub ahead of print).