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1 From the Department of Nutritional Sciences, Faculty of Medicine, University of Toronto.
2 Presented at the Sugars and Health Workshop, held in Washington, DC, September 18–20, 2002. Published proceedings edited by David R Lineback (University of Maryland, College Park) and Julie Miller Jones (College of St Catherine, St Paul). 3 Manuscript preparation supported by ILSI NA; research supported by ILSI Japan. 4 Address reprint requests to G Harvey Anderson, Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Fitzgerald Building, 150 College Street, Toronto, Ontario, Canada M5S 3E2. E-mail: harvey.anderson{at}utoronto.ca.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUGARS, APPETITE, AND FOOD...SUGARS, GLYCEMIC RESPONSE, AND...SUGARS AND FOOD INTAKE...FUTURE RESEARCHREFERENCES |
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Key Words: Sucrose • sugars • food intake • satiety • preloads • young men • blood glucose
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUGARS, APPETITE, AND FOOD...SUGARS, GLYCEMIC RESPONSE, AND...SUGARS AND FOOD INTAKE...FUTURE RESEARCHREFERENCES |
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50% of carbohydrates, or 22%, of the total energy intake in 1987–1988 (2). Sugars are either monosaccharides or disaccharides and include sucrose, lactose, maltose, glucose, and fructose. Carbohydrate ingestion promotes satiety (3, 4). However, in recent years, the prevalence of obesity has increased despite reported declines in fat intake (5) and a subsequent rise in carbohydrate consumption. Thus, it has been suggested by some that because sugars and high–glycemic index (GI) carbohydrates have contributed to this increase, they are the cause of overeating and obesity (6–8).
The relation between the consumption of sugars and their immediate (up to 2 h) effects on satiety and food intake are explored here. Also examined is the hypothesis that the glycemic response to sugars predicts their effects on satiety and food intake. An evaluation of the effect of the consumption of sugars over the longer term, that is over a day or several days, on energy metabolism and body weight control is provided in a separate review (9).
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SUGARS, APPETITE, AND FOOD INTAKE |
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Sweet taste alone has been proposed to contribute to the reduction of hunger and increased feelings of fullness (12). Some studies support this hypothesis. For example, in the studies by Woodend and Anderson (13) (Table 1
), the effect on food intake of drinks containing 25 g (418 kJ) and 50 g (836 kJ) sucrose was not different from that of the noncaloric sweetened control but was different from the water control. In another study of adult subjects, noncaloric sweetened beverages reduced hunger ratings to an amount intermediate between sucrose (20 g) and the water control (8). Similarly, an aspartame-sweetened beverage led to suppression of food intake in children compared with the effects of a water control (14).
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Evidence for an association between sugars and overweight has been derived from epidemiologic, observational, and experimental studies. Although epidemiologic studies consistently report an inverse association between body mass index and sugar intake in adult populations (16–18), a relation between the form of sugars consumed and overweight in children has been identified. Consumption of sweet beverages, especially soft drinks, was found to be associated with overweight in youths in one study (19) and with reported higher energy intakes in children in another study (20). Similarly, a prospective observational study reported an association between increased soft drink consumption and the development of obesity in children over a 19-mo period (6). Because one report suggested that the sugars consumed in liquid rather than in solid form are less likely to be compensated for during the day (21), it has been hypothesized that sugars, especially those used as caloric sweeteners, when consumed in drinks, contribute to excess energy intake through bypassing regulatory systems and by exacerbating hunger (6–8, 21).
The literature, however, provides no evidence that sugars bypass regulatory systems and, for this reason, create excess energy intakes. Experimental studies that have been designed to test the effect of quantity and the time interval between the dose and the test meal, and to compare sugars with other carbohydrates, show remarkably precise compensation in a subsequent meal (the short-term response) for the energy contained in sugars consumed 30–60 min before the meal. Furthermore, the compensation is better in the short term for high-glycemic than for low-glycemic carbohydrates.
Sucrose
Both adults and children are satiated by sucrose and reduce food intake if the time intervals between the preload and the test meal are appropriate for the dose consumed. Most of the literature shows that food intake is reduced after ingestion of 
50 g sucrose in drinks presented 20–60 min before a meal (22). Larger amounts would be expected to prolong satiety, and this was shown recently. A beverage containing 135 g sucrose caused a stronger feeling of fullness and reduced ratings of prospective consumption and hunger compared with the water control for 2–3 h (15).
Even small amounts of sucrose decrease food intake. For example, when young men were given drinks (300 mL) containing 25, 50, or 75 g sucrose, the lowest dose of 25 g (418 kJ) increased subjective satiety, as assessed by visual analogue scales (Figure 1) and suppressed food intake from a pizza meal 1 h later (Table 1
) (13). There was 123% compensation, compared with the water control, at 1 h for the 418 kJ (100 kcal) provided in the 25-g sucrose beverage. Compensation for the 50- and 75-g doses was 62% and 90%, respectively. Clearly the compensatory responses under similar conditions within an experiment are not precisely related to the energy contained in the drinks. However, there is no evidence that the variability in compensation is less and the response is more precise for other carbohydrates. Indeed, when comparisons were made among drinks equally sweetened with a noncaloric sweetener and containing 75 g sucrose, polycose (a linear oligosaccharide of glucose), or glucose, the energy compensation—in relation to the noncaloric sweet control, sucralose (Splenda; Tate & Lyle, Reading, United Kingdom)—was not different at a test meal consumed 1 h later (42 ± 14%, 36 ± 16%, and 48 ± 25%, respectively) (23). In another experiment, equally sweetened preload drinks containing 75 g sucrose and polycose led to significant compensation in a meal 1 h later (44 ± 13% and 65 ± 19%, respectively), whereas amylopectin and amylose did not (0 ± 22% and 23 ± 16%, respectively) (23). Again the comparison is with a noncaloric sweet control. Thus, the response to sucrose in pure form and not mixed with foods is at least as precise as for other sugars and better in the short term than for carbohydrates with a lower GI.
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The 25-g dose of sucrose may be at the low end of the detection limit for an energy preload to have an effect at a meal 1 h later in adults. Drinks containing 20 g sucrose (76 kcal) did not show a statistically significant suppression of food intake 1 h later in 20 subjects (18 females, 2 males) (8). However the difference in the mean intakes between the sucrose and the water treatment was 85 kcal. Possibly, if only the 2 treatments had been given in a paired design rather than a comparison of 4 treatments in a repeated-measures design, statistical significance could have been achieved.
Young children also compensate for sugar consumed as a beverage. In children aged 2–5 y (n = 24), 90 kcal from a sucrose drink was sufficient to suppress intake at test meals 0, 30, or 60 min after the preload (14). The compensation observed at 30 min was 100%, which the authors attributed to the ability of young children to rely solely on internal hunger cues. Although not found to be as precise, older children also compensate for energy derived from sucrose. When children aged 9–10 y consumed a cherry-flavored drink containing either 45 or 90 g sucrose, lunchtime food intake was reduced 30 min later (24). Compensation for the 45- and 90-g sucrose beverages was 68% and 63%, respectively.
The importance of timing of the test meals in relation to the size of the treatment dose is illustrated by the failure of 50–60 g sucrose to suppress food intake of children aged 9–10 y when the test meal was given 90 min later. However, hunger and desire-to-eat ratings were lower after the drinks containing sucrose than after the drinks containing aspartame at 85 min (25).
It is clear therefore, that under laboratory conditions, sucrose contributes to satiety and suppresses subsequent food intake. Thus, the data refute the hypothesis that sucrose leads to obesity by bypassing regulatory systems (6–8).
The literature does not report comparisons of the effects of corn syrups or of high-fructose corn syrups given in similar quantities with the effects of sucrose on short-term food intake. Some of the corn syrups are a source of sugars in the diet, although many used by the food industry are composed of long chains of glucose and are used for functional, not sweetening, purposes. The high-fructose corn syrups commonly used as sweeteners in foods and beverages have a monosaccharide composition similar to that of sucrose, ie, they contain a mixture of 
55% fructose and 45% glucose. It seems unlikely that there would be a difference in satiety between a beverage containing sucrose and one containing high-fructose corn syrup.
Glucose and fructose
Because sucrose and high-fructose corn syrups are composed of glucose and fructose, one or both of these monosaccharides may explain their effect on food intake regulatory mechanisms. In general, when given as a beverage, the consumption of glucose alone decreases food intake but the reduction is less than that produced by fructose.
In young men, the consumption of 75 g (23) or 50 g (26) glucose in drinks or 50 g in yogurt (27) reduces food intake 1 h later. Fructose consumed alone also suppresses food intake. In many studies, 50 g fructose in a drink suppressed energy intake and did so to a greater extent than did glucose at test meals from 38 min (28) to 2.25 h later (29–31).
When fructose is consumed with another carbohydrate, its advantage over glucose disappears. For example, equicaloric cereal preloads containing additions of fructose (30 g) or glucose (33.5 g) reduced energy intake in meals consumed either 30 or 120 min later, but there were no differences between the treatments (32; Table 2). Similarly, no differences in food intake were observed between 50 g fructose and 50 g glucose at 2.25 h, when they were given in a mixed nutrient meal containing starch (31). As little as 15 g starch or glucose added to 50 g fructose prevents the decrease in food intake 2.25 h after a 50-g fructose preload (31).
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At this time there is no evidence that the effect of sucrose or high-fructose corn syrups of similar composition on food intake can be attributed solely to one of their monosaccharide components. It is clear, however, that sucrose and its component sugars suppress food intake, even when consumed in small quantities if the time between consumption and eating is short. The duration of the effect has not been fully defined but is dose dependent.
Maltose and lactose
Only one study examined the effects of maltose using the preload paradigm, and it suggests that maltose can suppress appetite (15). An oral preload of 135 g maltose in a lemon-flavored solution decreased hunger compared with water 150–180 min later but did not increase fullness or decrease prospective consumption ratings as did sucrose (15). No reports of the effect of lactose preloads on food intake in humans were found in the published literature.
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SUGARS, GLYCEMIC RESPONSE, AND FOOD INTAKE |
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The effect of sugars on blood glucose can be described by measuring the total glycemic response over time. The GI was developed to provide a basis for comparing glycemic responses to carbohydrates in foods (38, 39). This index compares the incremental area under the blood glucose response curve of 50 g glycemic carbohydrate in a test food relative to 50 g carbohydrate of a standard food such as white bread, when ingested by the same subject (38). Because the GI standardizes the glycemic response to a test food, it corrects for between-subject variation, thereby allowing glycemic responses from different studies to be compared.
A range of glycemic responses is observed after ingestion of sugars (40). Glucose produces a more rapid and higher increase in postprandial blood glucose and insulin than does fructose (30, 31). Sucrose tends to elicit a postprandial blood glucose concentration that is intermediate between glucose and fructose (39, 40). The GIs of glucose, fructose, and sucrose—expressed relative to 100 for white bread—are 149, 32, and 87, respectively (40, 41). Contrary to the belief that sugars produce higher blood glucose concentrations than does an equivalent amount of starch, fructose and sucrose have lower GI values by up to 50% compared with most common starchy foods (41, 42). For this reason, replacing a portion of the starch with sucrose in a high-GI breakfast cereal lowers the glycemic and insulin responses (43).
In the short term, high but not low glycemic responses are associated with satiety and reduced food intake (13, 44). For example, when pure isovolumetric (400 mL) preloads of 75 g polycose, sucrose, glucose, or a fructose-glucose mixture were consumed by young men, the glycemic response, calculated as blood glucose area under the curve from time 0 to 60 min, was inversely related to food intake 1 h after treatment (23) (Figure 2). Glucose and sucrose decreased food intake compared with a control, but food intake after the fructose-glucose and polycose treatments was not different from that after all other treatments. Polycose, glucose, and sucrose produced a rapid increase in blood glucose between baseline and 20 min, which remained elevated above baseline at 65 min. The combined fructose-glucose treatment elicited a smaller increase in blood glucose than did all other carbohydrate treatments, and blood glucose returned to baseline by 65 min. Overall, there was a weak inverse relation between food intake from a pizza meal 1 h after treatments and both the incremental area under the curve for blood glucose and blood glucose concentrations at 37 min (r = -0.24, P < 0.05) and 60 min (r = 0.23, P = 0.06). Consistent with this observation is a study of the effect of 38 common foods on food intake 2 h later (44). Insulin area under the curve was inversely related to food intake. Thus, these studies suggest that the greater the response in blood glucose and in insulin, the greater the satiety after carbohydrate consumption, at least to 2 h.
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SUGARS AND FOOD INTAKE REGULATION |
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Consistent with the glucostatic hypothesis are the observations that carbohydrate consumption and the resulting increase in blood glucose are associated with satiation (23, 49, 50). Also consistent with the hypothesis are the correlations observed between the duration of a rise in blood glucose and the intermeal interval (48). A rapid increase and then decline in blood glucose after sucrose (1000 kJ) ingestion was found to correspond to a shortened intermeal interval, whereas a small but sustained rise in blood glucose was found to be associated with a longer intermeal interval after a low glycemic preload. The results of this study were interpreted to support the view that a sustained elevation in postprandial blood glucose concentrations is the mechanism by which satiety is maintained. However, the low glycemic food in this study was one high in fat, leading to a possible alternative explanation. Because fat produces weaker but sustained satiety compared with carbohydrates (51), the delayed intermeal interval may reflect a satiety mechanism unrelated to blood glucose. For instance, fat stimulates the release of cholecystokinin, which can act peripherally to signal satiety (52).
Although the data provide indirect support for the hypothesis that satiety is associated with the effects of carbohydrates on blood glucose, a primary role for blood glucose in determining satiety remains uncertain (53). A lack of association between the blood glucose response and food intake is also easily shown. For example, the glycemic response as measured by the blood glucose incremental area under the curve to 2 h was 85 ± 10 and 175 ± 20 mmol • L-1 • min-1 after breakfast cereals containing either 30 g fructose or 33.5 g glucose, respectively, but food intake was not significantly different 30 or 120 min after consumption (32) (Table 2).
Further evidence that blood glucose is neither the only nor the best predictor of satiety is provided by studies in which blood glucose concentrations have been altered through intravenous administration of glucose. Early studies showed either no effect (54) or an increase in hunger and food intake under hyperinsulinemic and hyperglycemic (10 mmol/L) conditions (55). In contrast, more recent studies have found that acute hyperglycemia (15 mmol/L) induces satiety over 240 min (50) and decreases food intake at 140 min (49).
From the foregoing studies it cannot be concluded that the effects of low- and high-GI carbohydrates on satiety are mediated by mechanisms sensitive to their effect on blood glucose concentrations. It is more likely that the glycemic response to carbohydrates serves to depict their absorption characteristics and not necessarily the specific mechanism by which they provide satiety signals (53). Many other mechanisms, including those based on the rate of gastric emptying and gut hormones, may account for the effects of carbohydrates on food intake. For example, contact of nutrients with the small intestine is postulated to be a major source of postgastric satiety (34, 35). Many peptides with the potential to influence satiety are released in response to the presence of food in the small intestine. These include, but are not limited to, cholecystokinin, glucagon, bombesin, gastrin, somatostatin, neurotensin, and glucagon-like peptide 1 (56)
Sugars also mediate satiety through mechanisms not directly involving their effect on blood glucose. For example, a rapid increase in the occupancy of glucoreceptors would be expected after ingestion of glucose, sucrose, or high-fructose corn syrups. Thus, a surge of preabsorptive satiety signals would be produced, but they would be expected to dissipate relatively quickly as the glucose is transported from the gut lumen into the bloodstream. A more extended effect of sugars on satiety might arise from the slowing of gastric emptying and the release of glucagon-like peptide 1. Glucagon-like peptide 1 has received considerable attention as a putative satiety peptide involved in regulating carbohydrate-induced satiety (57–59) and is released when glucose comes into contact with the L cells of the lower small intestine (60). A rise in blood glucose concentrations has been associated with a slowing of gastric emptying (61), which would also contribute to fullness and short-term satiety (62).
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FUTURE RESEARCH |
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TOPABSTRACTINTRODUCTIONSUGARS, APPETITE, AND FOOD...SUGARS, GLYCEMIC RESPONSE, AND...SUGARS AND FOOD INTAKE...FUTURE RESEARCHREFERENCES |
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Further research is required to answer several questions that are unresolved on the topic of sugars and appetite control: 1) Is there a difference between solid and liquid forms of the different sugars? Is it due to a caloric or sweetness response? 2) What is the duration of the satiety response to sugars, and how does this compare with the duration of effect of other carbohydrates? 3) How do sugars added to food affect satiety and food intake compared with the addition of polysaccharides? 4) What is the effect of daily consumption of drinks containing sugars compared with the chronic consumption of drinks containing low-GI carbohydrates on body weight and energy intake? 5) Does a glycemic rebound occur after usual servings of sugars in beverages, and does this cause increased hunger? 6) What is the role of satiety signals from the gut in controlling food intake and satiety after sugars compared with other carbohydrates?
In conclusion, sugars produce satiety and decrease food intake in the short term similar to other high-GI carbohydrates but to a greater extent than low-GI carbohydrates. Their effect is also greater than that of fat. Although the effect on food intake of high-GI sugars and carbohydrates often is associated with their effects on blood glucose, the mechanism by which sugars modulate food intake is unlikely to be solely based on this effect, as proposed by the glucostatic hypothesis of food intake regulation. The release of putative satiety peptides, mediated by the intensity and length of interaction of carbohydrates in the gastrointestinal tract, is no doubt a crucial component of the mechanisms by which they initiate and sustain satiety.
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ACKNOWLEDGMENTS |
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REFERENCES |
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
), sweet control (sucralose + water; 
), 25 g sucrose (
), 50 g sucrose (
), and 75 g sucrose (•). The treatments, except for the water control, were equalized for sweetness with the addition of the noncaloric sweetener sucralose, and all treatments were provided as isovolumetric (300 mL) beverages. Within-subject design; n = 14 young males. *An overall treatment effect (P < 0.05) was observed at 15, 30, and 60 min. The calculated incremental areas under the curves were different between treatments as follows: 