Scientific Opinion on the substantiation of health claims related to fructose
and reduction of post-prandial glycaemic responses (ID 558) pursuant to
Article 13(1) of Regulation (EC) No 1924/2006[sup]1[/sup]
EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA)2, 3
European Food Safety Authority (EFSA), Parma, Italy
Słowa kluczowe:
Fructose
glucose
health claims
post-prandial glycaemic response
sucrose
1. Charakterystyka żywności / składnika
The food constituent that is the subject of the health claim is fructose.
Fructose (a ketohexose) is a 6-carbon monosaccharide with the same molecular formula (C6H12O6) as glucose (an aldohexose), but with a different structure. Fructose is found in many foods, especially fruits. Purified fructose is a white solid which dissolves easily in water. Together with glucose, fructose is a component of sucrose. Fructose is derived from the digestion of sucrose, and absorbed directly in the small intestine (Vasankari and Vasankari, 2006).
From the information provided, the Panel assumes that fructose should replace sucrose or glucose in foods or beverages in order to obtain the claimed effect. Fructose is used commercially in foods and beverages because of its sweet taste, which is about 1.3-1.7 times as sweet as sucrose. Fructose, sucrose, and glucose can be determined quantitatively in foods and beverages by established methods.
The Panel considers that the food constituent which is the subject of the health claim, fructose, and the food constituents which fructose should replace in foods or beverages in order to obtain the claimed effect, sucrose and glucose, are sufficiently characterised.
2. Znaczenie oświadczenia dla zdrowia człowieka
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Spożycie fruktozy powoduje mniejszy wzrost glikemii (stężenia glukozy we krwi) niż spożycie sacharozy bądź glukozy
The claimed effect is “carbohydrate metabolism and insulin sensitivity”. The Panel assumes that the target population is individuals who wish to reduce their post-prandial glycaemic responses.
In the context of the proposed wordings and the references provided, the Panel assumes that the claimed effect refers to the reduction of post-prandial glycaemic responses.
Postprandial glycaemia is interpreted as the elevation of blood glucose concentrations after consumption of a food and/or meal. This function is a normal physiological response which varies in magnitude and duration, and which may be influenced by the chemical and physical nature of the food or meal consumed, as well as by individual factors (Venn and Green, 2007). Decreasing post-prandial glycaemic responses may be beneficial to individuals with, for example, impaired glucose tolerance as
long as post-prandial insulinaemic responses are not disproportionally increased. Impaired glucose tolerance is common in the general population of adults.
The Panel considers that reduction of post-prandial glycaemic responses (as long as post-prandial insulinaemic responses are not disproportionally increased) may be a beneficial physiological effect.
3. Naukowe uzasadnienia wpływu na zdrowie człowieka - Zmniejszenie stężenia glukozy we krwi (glikemii) po posiłku
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Spożycie fruktozy powoduje mniejszy wzrost glikemii (stężenia glukozy we krwi) niż spożycie sacharozy bądź glukozy
The references provided in relation to the claim included two narrative reviews and an internet page which did not provide original data that could be used for the scientific substantiation of the claim. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claim.
Two human intervention studies investigated the effects of fructose on post-prandial glycaemic and insulinaemic responses compared to other carbohydrates (Bantle et al., 1983; Crapo et al., 1980).
In a test meal study by Bantle et al. (1983), 10 healthy subjects, 12 patients with type 1 diabetes, and 10 patients with type 2 diabetes (none taking oral hypoglycaemic medications) received in a random order five test breakfasts containing 42-43 g of different test carbohydrates (glucose, fructose, sucrose, potato starch and wheat starch) and nearly identical amounts of energy (685-742 kcal), of total carbohydrates (84-89 g), of protein (31-38 g) and of fat (25-26 g). Blood samples were obtained at 0, 15, 30, 60, 90, 120, 180 and 240 minutes after each breakfast. In healthy and type 2 diabetic subjects, the breakfast containing fructose induced significantly smaller peak increments in post-prandial blood glucose concentrations when compared to glucose, but not to sucrose. Similar results were obtained in healthy and type 2 diabetic subjects for the mean incremental area under the curve. No significant differences between carbohydrate sources were observed with respect to post-prandial insulin responses. The Panel notes that in this study fructose replaced sucrose and glucose in solid foods.
In another test meal study by Crapo et al. (1980), 9 healthy subjects, 10 subjects with impaired glucose tolerance, and 17 type 2 diabetic subjects received in a random order 50 g loads of glucose, sucrose and fructose, given alone in a drink or in combination with protein and fat, in a liquid formula meal. Diabetic subjects on oral hypoglycemic agents had discontinued medications two weeks before testing. Blood samples were obtained at 0, 15, 30, 45, 60, 120 and 180 minutes after each meal. Fructose consumption induced significantly lower blood glucose and insulin responses than sucrose or glucose consumption in all study groups, either when given alone or in the test meal, with the exception of post-prandial insulin responses, which in the diabetic group were flat and not significantly different for all three sugars. The post-prandial blood glucose response to fructose was directly proportional to the degree of glucose intolerance (i.e. post-prandial glycaemic responses to fructose were significantly higher in glucose-intolerant and type 2 diabetic subjects). The Panel notes that this study shows a significant decrease in post-prandial blood glucose responses when fructose replaces either sucrose or glucose in liquid meals or beverages.
Another reference provided was “the international table of glycemic index and glycemic load values: 2002” (Foster-Powell et al., 2002), which provides glycaemic index values from individual studies or groups of studies on a variety of foods, including fructose and fructose-containing beverages. Post-prandial glycaemic response expressed as the glycaemic index for fructose using glucose dissolved in water as a reference has a mean value of 19±2, and using white bread as a reference 27±4, whereas such values for sucrose were 68±5 and 97±7, respectively. The Panel notes that these values support a significant decrease in post-prandial blood glucose responses when fructose replaces either sucrose or glucose.
The Panel notes that fructose induces lower glycaemic and insulinaemic responses compared to other hexoses, including glucose, and compared to sucrose, both when consumed alone or with other macronutrients.
Regarding the mechanism by which fructose could exert the claimed effect, fructose is more slowly absorbed in the gastro-intestinal tract than glucose, and the rapid entry of fructose into the liver, as well as its initial steps of metabolism, are insulin independent. Fructose is converted into glucose or triglycerides in the liver, and most of the glucose is stored as glycogen, resulting in only a modest increase in blood glucose concentrations.
Some recent short- and longer-term intervention studies, which compared the consumption of
beverages sweetened with fructose, glucose or sucrose, have shown that high fructose intakes ( 25 % of total energy) induce dyslipidaemia, insulin resistance and increased visceral adiposity in healthy and in hyperinsulinaemic insulin-resistant subjects (reviewed in Le and Tappy, 2006; Stanhope and Havel, 2008; Stanhope et al., 2009; Stanhope and Havel, 2010; Tappy and Le, 2010). However, these effects are generally not observed at lower doses of fructose intake (about 40-50 g/day in place of starch or sucrose (reviewed in Wolever, 2006)). Whether free fructose and fructose in sucrose have different metabolic effects is a matter of debate.
In weighing the evidence, the Panel took into account that the few intervention studies in healthy and type 2 diabetic subjects provided showed a consistent significant reduction in post-prandial glycaemic responses following fructose consumption compared with sucrose and glucose, without disproportionally increasing post-prandial insulinaemic responses, and that the mechanism by which fructose (in place of sucrose or glucose) could exert the claimed effect is well established.
The Panel concludes that a cause and effect relationship has been established between the consumption of fructose in place of sucrose or glucose in foods or beverages and reduction of post-prandial glycaemic responses.