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The Paradoxical Effects of Non-Calorically Sweetened Beverages on Weight Gain
Kristin L. Bater
October 1, 2010
Obesity (defined as having a Body Mass Index>30) is becoming commonplace in United States culture, with a reported age-adjusted prevalence 33.8% in 2007-2008 (Flegal et al 2010). In an effort to avoid the consumption of excess calories, once sugar-sweetened beverages are being supplemented with counterparts containing non-caloric sweeteners. However, it has been suggested that the replacement of sugar with non-caloric sweeteners (NCS) may yield paradoxical effects ultimately causing weight gain (http://articles.mercola.com/sites/articles/archive/2005/06/30/diet-sodas.aspx).
These paradoxical effects are thought to be, in part, a result of augmented appetite and increased caloric consumption due to increased insulin secretion from the pancreas (http://articles.mercola.com/sites/articles/archive/2005/06/30/diet-sodas.aspx). Therefore, it is imperative to understand the relationship between insulin release and glucose levels in the blood. Insulin is produced by the beta cells located in the pancreas. When there are elevated levels of glucose in the blood, the beta cells are stimulated to secrete insulin. As a result, insulin is released via capillary islets into the blood stream, and glucose is stored in an attempt to maintain stable glucose levels (Karp 2010). However, if the consumption of NCS is triggering the secretion of insulin from the pancreas and the storage of glucose when there is not really an increase in blood glucose concentration, the homeostatic blood glucose will fall below its ideal concentration. Low blood glucose levels will signal a decrease in available energy, cause hunger, and promote the consumption of calories as compensation.
It is important to consider the variety of non-caloric sweeteners utilized in diet beverages in order to assess their individual effects on weight gain, as it is very possible that each variety could have a distinct effect on the biological mechanisms responsible for an ultimate increase in weight. While there are five non-caloric sweeteners approved by the Food and Drug Administration (Mattes et al 2009), this review will focus on three sweeteners - acesuflame-K, saccharin, and aspartame.
Additionally, it is important to consider any variation in effects of NCS amongst the different groups being studied animals, children/adolescents, and adults. Weight fluctuation in a singular group could be the result of factors other than the consumption of NCS. This being the case, the most comprehensive way to consider the effects of NCS is to consider the effects of each NCS on each of the groups separately and then conclude by looking at effects shared between groups.
The primary goal of this review article is to assess the effects of non-caloric sweeteners in order to determine if the consumption of diet beverages ultimately causes weight gain.
The Effects of Non-caloric Sweeteners
Due to the wide variety of non-caloric sweeteners, it is entirely feasible that each agent could have a different effect on insulin secretion. However, some NCS share similar characteristics and are therefore grouped together and studied based on these commonalities. For example, Malaisse et al (1998) divided NCS into those possessing bitter and non-bitter tastes. Those with a bitter taste, which include saccharin and acesuflame-K, in addition to sodium cyclamate and stevioside, in varying quantities between 1.0-10.0 mM, were shown to increase insulin production and secretion from rat pancreatic islets. The non-bitter NCS, aspartame, did not effect secretion of insulin in rat pancreatic islets.
The conclusions about each of the above sweeteners reached by Malaisse et al (1998) were further supported by more specific studies, each focusing on the effects of one of the aforementioned NCS. Liang et al (1987) tested the effects of acesuflame-K, in vitro, on pancreatic islets of Male Wistar rats. The findings of this particular experiment show that acesuflame-K affects both stages of insulin secretion. Another study, Berthoud et al, investigated the possibility that insulin release could be triggered, in part, due to oral sensory signals. This study concluded that upon the consumption of 1 mL of a 0.15% saccharin composition generated a rapid increase of insulin levels consistent with the previously stated findings of Malaisse et al (1998) that the consumption of saccharin does increase insulin secretion.
While the above animal trials measured the effects of the NCS quantitatively, using measures of glucose and insulin concentrations in the blood, the following studies employed a more qualitative approach. Human subjects were observed, their appetite ratings reported on a subjective basis, and the number of calories consumed by each subject was measured.
Child and Adolescent Trials. Anderson et al (1989) studied the effect of aspartame consumption on appetite and food intake on children aged 9-10 years old. This study attempted to avoid experimental error by testing the effects of aspartame in the presence and absence of a carbohydrate group. The children were given a standard breakfast, followed by a beverage some containing aspartame and others without. Following this allocation, the amount of food consumed at lunch was measured. In both the absence and presence of a carbohydrate group, aspartame showed no significant effects in feelings of appetite or calorie consumption.
The above findings are consistent with the results of an experiment that utilized a different age group children 2-5 years old. In this study, by Birch et al (1989), children showed appetite suppression following the consumption of both sucrose and aspartame, relative to the consumption of a water control. While the suppression that existed following the aspartame was less than the appetite suppression that followed the consumption of sucrose, they were not significantly different.
Adult Trials. Canty and Chan (1991) studied the affects of saccharin, aspartame, and sucrose on the caloric consumption and indices of hunger of 20 healthy adult subjects. This study showed, consistently, that hunger ratings were greatest for the water control group, then for the non-caloric sweeteners, and the least hunger was reported for those who had consumed sugar-sweetened beverages. The food intake following beverage consumption correlated with the hunger ratings, those who had consumed water consumed the greatest number of calories and those who had consumed a sugar-sweetened beverage the least. However, the only significant differences that existed in this experiment were those between the water control group and the sugar-sweetened beverages. The NCS, aspartame and saccharin, did not produce any significant increase in hunger ratings or caloric intake.
Rolls (1990) compared the effects of soft drinks sweetened with aspartame versus sucrose in 42 male subjects. The findings show that between three distinct groups of males, each given their respective drinks at different times with a meal, 30 minutes prior to a meal, and 60 minutes prior to a meal, no significant differences in hunger ratings or caloric consumption at the meal could be detected between the groups that consumed the NCS and the groups that consumed sugar-sweetened beverages.
Based on the above studies, the effects of the three NCS being considered: acesuflame-K, saccharin, and aspartame, on insulin release, appetite stimulation, and caloric consumption can be summarized as follows:
Acesuflame-K The consumption of acesuflame-K was shown to effect not only one, but both stages of insulin secretion in the rat pancreatic islets (Liang Y et al 1987). Its bitter taste was also reported, in another study, to augment the release of insulin, from rat pancreatic islets, into the blood (Malaisse et al 1998). This increase in insulin production directly correlates with an increased level of glucose uptake. Upon the storage of glucose, caloric cravings ensue in order to compensate for low energy due to low blood glucose concentrations (Karp 2010). Because of its direct effects on the process of insulin secretion, acesuflame-K can be correlated with appetite stimulation and thus increased caloric intake, which could result in weight gain.
Saccharin The conclusions about this particular NCS varied between the animal and human trials. Malaisse et al (1998) classified saccharin as a bitter-tasting non-caloric sweetener, a classification that is linked to augmented insulin release. However, when 20 adult subjects were asked to report their hunger ratings following the consumption of beverages containing saccharin, no significant increase in these ratings could be noted. Additionally, the caloric intakes of these individuals following this consumption were not significantly increased when compared to those who had consumed water (Rolls 1990). Due to the inconsistency between the animal trials and human trials, no definitive conclusion about the effects of saccharin on weight gain can be drawn.
Aspartame The effects of aspartame were reviewed in all of the above studies and showed consistent results throughout. Aspartame, classified as a non-bitter NCS, was shown not to augment insulin secretion from rat pancreatic islets (Malaisse 1998). In two distinct studies, Anderson et al (1990) and Birch et al (1989), performed on children, neither one showed increased hunger ratings or caloric consumption based on the presence of aspartame in a beverage consumed before lunch. Furthermore, the effects of aspartame in the presence of a carbohydrate group were studied, and still proved not to have a significant effect on the hunger ratings or caloric consumptions of children aged 9-10 years old (Anderson et al 1990). Twenty healthy adults also showed no significant increases in appetite ratings or caloric consumption after drinking beverages sweetened with aspartame (Canty and Chan 1991). This was consistent with the study of 42 male subjects, in the study performed by Rolls (1991). The correlation between the findings of these five studies, in spite of their great variation in subjects, shows that aspartame does not yield significant increases in any of the following: insulin secretion, appetite stimulation, or increased caloric intake.
The purpose of this review paper was to analyze whether or not diet beverages are an appropriate dietary supplement for individuals trying to lose weight. Making this determination requires comparing the caloric consumption of individuals drinking sugar-sweetened beverages to those drinking NCS-sweetened beverages. In the trial, by Birch et al (1989), that tested the effects of sucrose versus aspartame in children aged 2-5, results showed that appetite suppression was greatest with sucrose-sweetened drinks. However, the number of calories consumed was not reduced by this appetite suppression due to the fact that the sugar-sweetened drinks were calorically dense. The same results were shown in the Canty and Chan (1991) study of 20 healthy adults, who reported lower hunger ratings when consuming sucrose sweetened beverages but whose caloric intakes were increased simply due to the calories present in the sucrose-sweetened beverages. Based on the caloric density of sucrose-sweetened drinks, logic follows that if aspartame does not show effects on weight gain that diet beverages would be an acceptable alternative.
However, while the studies discussed in this literature review paper consistently show aspartame to have no significant effects on the secretion of insulin, appetite stimulation, or increased caloric intake; this does not mean that the consumption of diet soda is completely without consequence. Aspartame is often found in tandem with acesuflame-K in diet beverages. Acesuflame-K showed, in two separate studies, to augment the release of insulin from rat pancreatic islets. Because of this frequent pairing, it might prove beneficial to further explore the effects of acesuflame-K on human insulin release, and then additionally to study to effects of these two NCS when paired together. Until more information is obtained about their individual effects, and the effects of both aspartame and acesuflame-K together, it cannot be ascertained whether their consumption can be correlated with weight gain.
(The two images above picture the ingredient lists of two distinct diet beverages, Coke Zero Cherry and Diet Fanta, both of which include the combination of aspartame and acesuflame-K.)
Taking the myriad of effects associated with the consumption of both sucrose- and non-calorically sweetened beverages into account and trying to weigh the pros and cons, based on a handful of studies, is probably not a worthwhile endeavor. The only definite conclusion that can be drawn is that sugar-sweetened beverages contribute to weight gain purely because they are a source of calories. The lack of information about the range of effects of all the NCS makes it difficult to conclude anything definitive about the correlation between their consumption and weight gain. Until further research is performed, it would be most beneficial to simply replace beverages, sugar-sweetened or diet, with water if striving to maximize weight loss.
Anderson G.H., Saravis S., Schacher R., Zlotkin S., Leiter LA. (1989). Aspartame: Effect
on lunch-time food intake, appetite and hedonic response in children. Appetite, 13(2), p.93-103.
Berthoud H.R., Trimble E.R., Siegel E.G., Bereiter D.A., Jeanrenaud B. (1980) Cephalic-
phase insulin secretion in normal and pancreatic islet-transplanted rats. The American Journal of Psychology, 238(4), p. 336-340.
Birch L.L., McPhee L., Sullivan S. (1989). Children's food intake following drinks
sweetened with sucrose or aspartame: Time course effects. Psychology and Behavior, 45(2), p. 387-395.
Canty D.J., Chan M.M. (1991). Effects of consumption of caloric vs noncaloric sweet
drinks on indices of hunger and food consumption in normal adults. American Journal of Clinical Nutrition, 53(3), p. 1159-1164.
Flegal K.M., Carroll M.D., Odgen C.L., et al. (2010). Prevalence and Trends in Obesity
Among US Adults, 1999-2008. The Journal of the American Medical Association, 303, p. 235-241.
Karp G. (2010). Cell and Molecular Biology, 6th Edition (p.618-620). Hoboken, NJ:
John Wiley & Sons, Inc.
Liang Y., Maier V., Steinbach G., Lalić L., Pfeiffer E.F. (1987). The Effect of Artificial
Sweetener on Insulin Secretion II. Stimulation of Insulin Release from Isolated Rat Islets by Acesulfame K (In Vitro Experiments). Hormone Metabolic Research, 19(7), p. 285-290.
Malaisse W.J., Vanonderbergen A., Lochami K., Jijaki H, Malaisse-Lagae F. (1998)
Effects of Artificial Sweeteners on Insulin Release and Cationic Fluxes in Rat Pancreatic Islets. Cellular Signaling, 10(10), p.727-733.
Mattes R.D., Popkin B.M. (2009). Non-nutritive sweetener consumption in humans:
Effects on appetite and food intake and their putative mechanisms. American Journal of Clinical Nutrition, 89(1), p. 1-14.
Mercola, J. (2005) Diet Sodas May Double Your Risk of Obesity. Retrieved from
Rolls R.J., Kim S., Fedeoroff I.C. (1990) Effects of drinks sweetened with sucrose or
aspartame on hunger, thirst and food intake in men. Psychology and Behavior, 48(1), p. 19-26.
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