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. 2010 Nov 4;7:82.
doi: 10.1186/1743-7075-7-82.

Health Implications of Fructose Consumption: A Review of Recent Data

Free PMC article

Health Implications of Fructose Consumption: A Review of Recent Data

Salwa W Rizkalla. Nutr Metab (Lond). .
Free PMC article


This paper reviews evidence in the context of current research linking dietary fructose to health risk markers.Fructose intake has recently received considerable media attention, most of which has been negative. The assertion has been that dietary fructose is less satiating and more lipogenic than other sugars. However, no fully relevant data have been presented to account for a direct link between dietary fructose intake and health risk markers such as obesity, triglyceride accumulation and insulin resistance in humans. First: a re-evaluation of published epidemiological studies concerning the consumption of dietary fructose or mainly high fructose corn syrup shows that most of such studies have been cross-sectional or based on passive inaccurate surveillance, especially in children and adolescents, and thus have not established direct causal links. Second: research evidence of the short or acute term satiating power or increasing food intake after fructose consumption as compared to that resulting from normal patterns of sugar consumption, such as sucrose, remains inconclusive. Third: the results of longer-term intervention studies depend mainly on the type of sugar used for comparison. Typically aspartame, glucose, or sucrose is used and no negative effects are found when sucrose is used as a control group.Negative conclusions have been drawn from studies in rodents or in humans attempting to elucidate the mechanisms and biological pathways underlying fructose consumption by using unrealistically high fructose amounts.The issue of dietary fructose and health is linked to the quantity consumed, which is the same issue for any macro- or micro nutrients. It has been considered that moderate fructose consumption of ≤50g/day or ~10% of energy has no deleterious effect on lipid and glucose control and of ≤100g/day does not influence body weight. No fully relevant data account for a direct link between moderate dietary fructose intake and health risk markers.


Figure 1
Figure 1
Fructose and glucose metabolism in liver cells: After several steps glucose is converted into fructose1,6-bi-phosphate. A reaction regulated by the rate-limiting enzyme phosphofructokinase, which is inhibited by ATP and citrate. Altogether the conversion of glucose to pyruvate is regulated by insulin. On the other hand, fructose, is massively taken by the liver, and converted rapidly to triose-phosphate independently of insulin control and without a feedback by ATP or citrate. A large portion of fructose is converted into glucose which can be released in the blood or stored as glycogen. A part is converted into lactate. A small portion is converted into fatty acids, which may play an important role in the development of hypertriglyceridemia and fatty liver.
Figure 2
Figure 2
Postprandial TG responses to fructose- and glucose sweetened beverage consumption. A. Changes of the area under the curve over 14 h sampling periods before and after 2 and 10 weeks of consuming fructose sweetened beverages at 25% of daily energy in 7 overweight or obese postmenopausal women, values are means ± SE, * :p < 0.05 vs 0wk (figure adapted from Swarbrick et al (94)). B. Mean 24 hour TG and C. TG AUCs (23 h) before and after 2, 8 and 10 week consumption of glucose or fructose-sweetened beverages at 25% of daily energy intake in overweight/obese humans (G=glucose group: n= 14; F= fructose group: n= 17); values are means ± SEM, * :p < 0.05 vs 0wk in the fructose group (figures adapted from Stanhope et al [23]).
Figure 3
Figure 3
LDL particle size in 6 to 14 years old Swiss children, values are means ± SD, (Figure adapted from Aeberli et al [4].

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