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Official websites use. Share sensitive information only on official, secure websites. Supported by PHS grant no. Reprints not available. E-mail: popkin unc. Nonnutritive sweeteners NNS are ecologically novel chemosensory signaling compounds that influence ingestive processes and behavior. These sweeteners have the potential to moderate sugar and energy intakes while maintaining diet palatability, but their use has increased in concert with BMI in the population. This association may be coincidental or causal, and either mode of directionality is plausible. A critical review of the literature suggests that the addition of NNS to non-energy-yielding products may heighten appetite, but this is not observed under the more common condition in which NNS is ingested in conjunction with other energy sources. Substitution of NNS for a nutritive sweetener generally elicits incomplete energy compensation, but evidence of long-term efficacy for weight management is not available. The addition of NNS to diets poses no benefit for weight loss or reduced weight gain without energy restriction. There are long-standing and recent concerns that inclusion of NNS in the diet promotes energy intake and contributes to obesity. Most of the purported mechanisms by which this occurs are not supported by the available evidence, although some warrant further consideration. Resolution of this important issue will require long-term randomized controlled trials. The intake of nutritive sweeteners NS has increased markedly in the United States and globally over the past 3 decades, coincident with the increased incidence and prevalence of overweight and obesity 1. This has prompted considerable research on the role of NS in energy balance. Numerous reviews 2 — 9 have attempted to summarize the literature, but no consensus has emerged. Nevertheless, recommendations have been made to moderate the intake of NS 10 , Given the contribution of sweeteners to food palatability and recognition that adherence to diets of moderate or low palatability is likely to be limited, one approach to limit intake is to substitute nonnutritive sweeteners NNS for NS in products and discretionary applications. The success of this approach is open to debate and requires resolution to determine the best clinical practices and public health recommendations. This review describes recent trends in the use of NNS and current knowledge of their effects on short-term appetite and food intake as well as longer-term energy balance and body weight. More importantly, given the current controversy about NNS and energy balance, we critically reviewed the reported mechanisms by which they may exert their effects on these outcomes. In addition, stevia, an herb extract of intense sweetness, is used in limited applications. Although research on NNS began more than a century ago, it was not until concerns about diabetes and weight control intensified that the food industry began to move NNS to market and to obtain regulatory approval for their inclusion in the diet Table 1. Thus, there has been relatively little time to assess the long-term effects of these substances, which mimic certain sensory properties ie, sweetness but lack the energy value of the class of compounds that have provided the mainstay of dietary energy during human evolution. Cyclamate was designated as generally recognized as safe GRAS in , but was banned in the United States in because of evidence that high concentrations in the diet were associated with bladder cancer in rats. Subsequent review of the evidence has raised questions about the physiologic relevance of the trials, but the sweetener remains unapproved in the United States. Cyclamate is approved for use in the European Union and in more than countries. There are published safety standards for the consumption of NNS. Data on the amounts of NNS in foods and beverages are not readily accessible. Total estimates of tons of aspartame produced based on sales data are available, but there is no direct measure of use. Because all of the approved NNS are regarded as GRAS, producers and manufacturers are not required to provide content data on food labels or to release this information to federal agencies. A few studies directly measured the amounts of NNS in foods, specifically in beverages. For instance, one was a safety study undertaken in Hong Kong It documented wide ranges of concentrations and multiple combinations of NNS in products, as would be expected because each product has different properties. Others in small selected samples have published overall NNS consumption but not the content of NNS in specific foods 13 — Given the absence of reliable data on the concentrations of NNS in the food supply, estimates can only be derived from information about foods that contain them. In the present article, 2 methods were used to identify foods that contain NNS: 1 a method based on an earlier toxicity study 17 that identified aspartame-containing foods was used to locate these same foods in the US nutrient monitoring system food-composition tables and 2 keyword searches were conducted using food descriptions that included the terms low-cal , low calorie , reduced calorie , dietetic , sugar-free , sugarless , sugar substitute , lite or light , sweetener , aspartame , splenda , sucralose , and stevia. The nutrient content of each of these items was then reviewed by using the USDA food-composition table to eliminate items with names that did not match their content. It places foods and beverages into nutrient-based subgroups according to their fat and fiber content. However, these food groups varied widely with respect to added sugar values. An estimate of foods with NNS are shown in Table 2. Thus, it is estimated that in —, the average American consumed g For foods, Based on the Nationwide Food Consumption Surveys for , —, and — and the National Health and Nutrition Examination Survey —, —, and — The results were weighted to be nationally representative. NS included a wide variety of monosaccharides glucose and fructose and disaccharides sucrose and saccharose that exist either in a crystallized state as sugar or in thick liquid form as syrups. Included in sweeteners are maple sugar and syrups, caramel, golden syrup, artificial and natural honey, maltose, glucose, dextrose, isoglucose also known as high-fructose corn syrup , other types of fructose, sugar confectionery, and lactose. Foods and beverages with added NNS were consumed by a relatively small proportion of the population. Beverages with NNS were consumed by Overall, only The amount per consumer for the beverages containing NNS was g Of the foods with NNS, the amount consumed per capita was g. The consumption trends for foods and beverages containing NNS are clearly increasing, but are different between categories. The proportion of consumers ingesting NNS in beverages remained relatively stable between and 6. However, in , this still represented only 5. If anything, we expect that these figures for the proportion of the sample consuming foods with NNS might be overestimated. The literature shows an underestimation of less healthy, more energy-dense foods and an overestimation of healthier ones 19 — Following this logic, it is possible that amounts per consumer are also overestimated. The influence of NNS on appetite, energy intake, and body weight has been the topic of a number of scholarly reviews 8 , 9 , 23 — Although these authors represent different disciplines and are supported by various funding agencies, the consistencies in their findings are striking. Although there have been reports to the contrary 31 — 33 , earlier reviews faithfully summarized the preponderance of then existing evidence indicating acute exposure to NNS in vehicles providing little or no energy, such as water or chewing gum, augments hunger relative to effects of exposure to the vehicle alone 31 , 34 — The interpretation of such trials was that the sweetness of NNS enhances postingestive hunger. However, a study of comparable design, using sodium chloride in soup replicated the findings, which suggests that the phenomenon may be attributable, more generally, to oral exposure to a palatable stimulus in the absence of an energy load Subsequent studies explored the addition of NNS to energy-yielding foods, beverages, or meals and commonly observed no alteration of hunger relative to vehicle alone or vehicle sweetened with sucrose 38 — This holds when the foods are equally energetic, sweet, and palatable, which indicates a lack of effect of sweetener type. Additional support for this latter finding is provided through studies reporting no effects on hunger when sweeteners are delivered via a nasogastric tube 41 or capsules 31 , 42 — 44 to eliminate orosensory stimulation. Some work suggests that the ingestion of aspartame in a capsule actually decreases hunger 42 , 43 , although the validity of this observation and a likely mechanism remain to be established. The doses of aspartame were similar in trials, regardless of whether effects were observed. With the addition of this evidence, later reviews consistently concluded that NNS have little effect on appetite 26 , 29 , Evidence that NNS promote hunger when delivered without energy, but not when incorporated into an energy-yielding food, requires this effect to be weighed in light of the fact that beverages are the primary source of NNS This is a medium that commonly does not supply energy, but is most often ingested periprandially 39 , 47 , negating the conditions apparently required for the increase in hunger. Furthermore, if an increase in hunger is elicited, the question arises as to whether this translates into increased energy intake. Preload design trials are the most common approach for assessing appetitive effects on intake, but, because they are short-term by design, they fail to reflect known 48 — 50 longer-term dietary compensation responses. Thus, their value for predicting energy intake over intervals likely to impact body weight is questionable. On the basis of modeling with data from the Beltsville One Year Dietary Study, it was predicted that carbohydrate replacement in core foods would result in increased fat and protein consumption 51 , thereby offsetting a reduction in energy intake. The authors noted that their findings were predicated on substitution rather than addition of reduced carbohydrate products. Whereas controlled feeding trials, in which sugars were replaced with NNS, have yielded mixed support for the model's predictions 52 , 53 , a test in free-living populations has not been conducted because consumers largely use products with NNS as additions to the diet. Absolute quantities of carbohydrates, sugars specifically, and NNS products have increased over the past 2 decades 2. Indeed, the contribution of carbohydrate as a percentage of energy intake has also increased 1 , There are reports from controlled trials in humans of enhanced energy intake after ingestion of a sweetened, non-energy-yielding beverage 54 — However, the preponderance of evidence indicates that NNS exert no short-term effect on energy intake 28 , 35 , Longer-term feeding trials generally indicate that the use of NNS results in no change or a reduction in energy intake. When the sucrose-sweetened products were reintroduced, energy intake exceeded baseline by 7. Thus, these data suggest that the covert introduction of NNS can lead to a reduction in energy intake over days, but with uncertain sustainability. The covert manipulation and controlled test setting were appropriate for the hypotheses under study, but left unanswered questions about the extrapolation of the data to free-living individuals, who largely know when they are consuming products with NNS. Relative to the no-soda condition, daily energy intake rose significantly with NS and declined with NNS. However, poor dietary compensation for beverages with different energy sources has been reported 61 ; therefore, it is not possible to attribute the effects to sweetness or to the sweetener. A more recent trial 62 examined the effects of a wk intervention in which overweight males and females were required to consume specific minimum amounts of sucrose or NNS products daily, but otherwise intake was ad libitum. The diets provided 3. There was a significant group difference, but the change in energy intake in the NNS group over the trial was not statistically significant. Thus, short-term trials of NNS consumption provide mixed evidence supporting reduced energy intake, whereas longer-term trials consistently indicate that the use of NNS results in incomplete compensation and slightly lower energy intakes. The latter studies are arguably the more nutritionally relevant. These conclusions are consistent with those of previous reviewers 9 , 23 , 24 , 26 — 29 , 45 , The primary interest in the effects of NNS on feeding is based on the assumption that a stimulatory effect will result in weight gain or reduced weight loss in those attempting to lose weight. The pendulum of concern about the contribution of NNS use on body weight has made a full cycle in the past 2 decades. The potential for NNS consumption to promote weight gain drew attention in based on findings from an American Cancer Society ACS survey conducted over 1 y in 78, women 50—69 y of age After adjustment for initial body weight, those who used NNS were significantly more likely to gain weight than were nonusers. Despite the conservative interpretation of the data, the hypothesis generated considerable debate. Although some additional supporting data were published 65 , the noted shortcomings in the ACS data 66 and proposed alternative explanations of the findings eg, the association was equally well explained by reverse causality combined with the publication of data from shorter-term \[ie, 10 d 53 , 3 wk 60 , 10 wk 62 , 12 wk 58 , and 16 wk 67 \] intervention trials that failed to support the original hypothesis, allayed concerns. Inverse associations were also reported in some observational studies The largest intervention trial with NNS aimed to promote weight loss through substitution of NNS for sucrose in the diet A sample of adults participated in a 3-wk run-in, wk intervention, 1-y maintenance, and 2-y follow-up. At the end of the intervention, there was no difference in weight loss between groups using and avoiding aspartame, but the former group better maintained the loss during the subsequent 2 y. Whereas the reports of Stellman and Garfinkel 64 and Blackburn 67 are often cited as support for antithetical views about the role of NNS in body weight regulation; they, in fact, draw essentially the same conclusions. However, with the popularity of higher-fat diets and renewed implication of carbohydrate in obesity incidence and prevalence during the late s and early s, attention again focused on a role for NNS. Since this reversal, no new large-scale intervention trial has been published, and, as before, the recent observational evidence has failed to clarify the issue. In contrast, findings from the San Antonio Heart Study indicate a direct relation. The mean BMI gain was 1. Reverse causality remains a likely explanation for a portion of the findings, but changes noted for nondieting, normal-weight individuals fit less well with this interpretation. Whether these findings hold true when total use of NNS is considered is an important question. Limiting analyses to use of beverages containing NNS may bias the data toward significant effects because this is a medium more consistently associated with NNS augmentation of appetite and intake Thus, intervention trials consistently fail to document that NNS promote weight gain, and observational studies provide only equivocal evidence that they might. Reflecting these findings, conclusions from prior reviews are ambivalent about a contribution of NNS to weight gain 9 , 23 , 24 , 26 — 29 , 45 , Nevertheless, concern about their use persists. This is fueled by existing and evolving evidence for plausible mechanisms. They appear to be afforded greater weight given the noted methodologic difficulties in documenting associations between use of NNS, feeding, and BMI. Thus, a critical examination of commonly evoked mechanisms linking NNS to appetite and feeding should help clarify the issue. NNS have been introduced into the food supply to achieve several aims. From an economics perspective, NNS may be less expensive than NS, and supplies of NNS are more reliable, which results in reduced costs and greater profitability to the food industry NNS may also yield products with desirable sensory properties 74 not easily achieved with NS and thereby increase product sales. Health considerations are also a driving force. NNS provide greater food choices to diabetic individuals attempting to moderate their ingestion of NS. They also provide options to healthy consumers interested in limiting consumption of NS for reasons unrelated to energy balance eg, dental health, behavioral disorders , although, clearly, concerns have been voiced about the health effects of NNS as well. Perhaps the most widely recognized function of NNS in the food supply is to help maintain the palatability of foods that are low in energy and, as a consequence, aid in weight management. On a metabolic level, no data indicate that the intrinsic properties of NNS modify energy balance independently of their influence on macronutrient and energy intakes. With respect to the former, if it is assumed that substitution of NNS for NS only results in decreased carbohydrate intake, the fat and protein to carbohydrate ratios of the diet would increase. Although weight loss is achievable with energy-restricted diets of varying macronutrient composition 75 , recent evidence supports the efficacy of an unrestricted diet with elevated fat and protein to carbohydrate ratios 76 , However, the degree to which NNS may contribute to this macronutrient shift is not established and could be low in free-living individuals, in whom trends indicate that NNS are commonly used as dietary additions rather than as substitutes for NS 2. The preponderance of research on NNS and weight management has focused on their ability to promote negative energy balance through maintenance of the appeal and consumption of an energy-diluted food. It is an uncontested maxim that, with free choice, consumers will not purchase or consume products on a chronic basis that do not meet their sensory expectations. Neurally mediated physiologic responses to sensory stimulation reportedly prime the body to optimize the digestion of foods and the absorption and use of the energy and nutrients they yield 78 — Some researchers hypothesize that lack of activation of cephalic phase responses may increase the risk of obesity Conversely, others hypothesize that activation of cephalic phase responses, through eating in general 82 , 83 or exposure to sweet items in particular 84 , will be problematic by stimulating appetite and intake. One proposed mechanism for the latter view entails an effect of NNS on insulin secretion and glucose metabolism. However, supportive evidence is lacking. An independent effect of sweetness stimulation on insulin release in humans has been reported in some studies 85 , 86 , but not in others 87 — This may be due, in part, to differences in the effectiveness of sweeteners because a cephalic phase insulin response CPIR has been reported in humans with glucose and saccharin 86 , 87 but not with aspartame 88 , 90 — Still, if sweet exposure provided through NNS does prompt an increase in insulin, it cannot be assumed that it will enhance hunger. Elevated concentrations of insulin in the brain decrease feeding in animals, and hunger responses in humans do not track insulin concentrations during euglycemic clamp studies Clamp studies also show that hunger does not track glucose concentrations. However, if glucose was an appetitive signal, a decline in hunger due to the stimulating effect of NNS on insulin is unlikely because CPIR moderates glucose excursions 94 , 95 rather than augments swings. Moreover, other cephalic phase responses might counter mechanisms promoting hunger. For example, the thermogenic response, particularly to palatable stimuli 96 , is associated with reduced hunger 97 , although not consistently As with CPIR, this response may not be elicited by all sweeteners \[eg, aspartame 99 \]. The results combined do not show adequate support that NNS stimulate hunger via cephalic phase responses. The stomach provides primarily volumetric-based appetitive signals, whereas the intestines are more responsive to nutrient cues , However, these properties are not absolute as there are intestinal osmoreceptors and gastric chemoreceptors Gastric distention promoted by mechanical inflation of a balloon , or nutritive fill 41 , is associated with enhanced satiety. Within a beverage type, those containing NS have a higher energy content and osmotic load Beverages of higher energy density empty from the stomach more slowly , , independent of osmotic effects , Similarly, the gastric emptying rate is reduced with higher osmotic challenges — , independently of energy content Activation of both gastric stretch and intestinal nutrient signals results in synergistic effects on satiety , Consequently, it is hypothesized that beverages with NNS may weaken satiety properties associated with NS. However, the absolute importance of these properties is uncertain. The osmotic effects on gastric emptying are transient. Within 30 min of ingestion of beverages with marked differences in osmotic load, emptying rates equilibrate as the greater gastric volume generated by the high osmotic load itself promotes increased emptying Furthermore, nutritive effects are inconsistent. Sucrose empties from the stomach more quickly than an isoenergetic load of maltose, yet the former results in greater fullness Also, an isoenergetic and iso-osmotic load of fructose empties more quickly than does a load of glucose Thus, the nature of the sweetener is also a factor. Ultimately, the gut is only one source of a highly redundant matrix of appetitive signals, and its contribution may be overridden by cognitive, sensory, metabolic, and other sources of input Long-term gastrectomized individuals differ little from healthy control subjects in appetitive sensations and food intake regulation Thus, changes in the osmotic and nutrient properties of foods and beverages through substitution of NNS for NS would not be predicted to enhance hunger or diminish satiety. Dietary macronutrients are differentially effective at stimulating the release of gut peptides. Carbohydrate is an adequate stimulus for secretion of glucagon-like peptide-1 GLP-1 — —a potent incretin and satiety factor , Failure of NNS to elicit the release of such peptides could theoretically result in lower satiety and augmented energy intake. Recent evidence suggests that receptors with properties similar to sweet taste receptors on the tongue are present in the gastrointestinal tract and are involved in GLP-1 release Sucralose is a ligand for the gut receptor and elicits GLP-1 secretion However, just as aspartame was not an effective elicitor of cephalic phase responses, it is also not effective for GLP-1 secretion Thus, with these data, the hypothesis that NNS will be less effective stimuli for carbohydrate responsive satiety hormones is uncertain. There may be compound specificity in responsiveness. A primary motivation to add NNS to foods or beverages is to enhance their palatability. Often they are added to improve the acceptability of low-energy or energy-reduced foods or diets with the aim of increasing their intake over more energy-dense versions. NNS may also be added to items with real or perceived health benefits independent of their energy content eg, high-fiber or nutrient-fortified foods or with desired physiologic effects eg, caffeinated products to promote intake. However, support for this view is very limited. One report noted that hunger increased in anticipation of eating a preferred food , but most trials have monitored appetite within an eating occasion. As reviewed previously , greater palatability has been associated with augmented , , unchanged , or diminished , hunger after adjustment for intake. Studies monitoring appetitive effects beyond the meal eg, rebound hunger have also yielded mixed findings , — Thus, there is inconclusive evidence that palatability influences appetitive sensations. Part of the explanation may be that the relation is not static and, with repeated exposures to a food, its hedonic tone changes Generally, the acceptability of less-palatable foods improves with familiarity. Strictly replacing NS with NNS will, by definition, result in a higher proportion of energy from fat in the diet. Less straightforward are claims that use of NNS may preferentially stimulate an absolute increase in fat intake. On the basis of mathematical modeling, a g reduction of NS in core foods through the substitution of NNS would shift food choice and result in an increase of 10 g fat and 6 g protein to the diet. Given that the increased use of NNS has not been accompanied by a reduction of NS, as documented elsewhere 1 , 46 , the assumption that NNS are used as a substitute for NS likely does not hold. Second, the replacement of foods providing energy only in the form of sugars, such as sodas, would not directly influence the intake of other macronutrients. Intervention trials provide limited support for the modeling prediction of increased fat intake and they do not confirm an impact on body weight. Several acute feeding trials, testing the effects of beverages containing NNS or NS on intake, noted no significant changes in dietary fat or energy intake 55 , A 4-wk intervention in which adults were provided supplementary beverages containing either NS or NNS showed no change in fat intake with either beverage. Additionally, use of NNS for 10 wk by free-living adults was not accompanied by significant shifts in macronutrient or energy intakes or body weight Taken together, published evidence does not indicate that use of NNS leads to increased fat consumption and thus in greater energy intake. An enhanced efficiency of energy use with a higher proportional fat composition of the diet would likely be offset by incomplete energy compensation. Nutrient labeling allows consumers to make informed decisions about the nutritive quality of their diet, but this may be counterproductive if the information is not correctly interpreted. Labeling foods as lower in energy could lead consumers to alter their feeding behavior and paradoxically increase their energy intake. This may occur if the expected savings in energy attributed to the substitution of an energy-diluted product is greater than any subsequent indulgence rationalized by the prior savings. This may also hold true if information about an energy reduction leads to the mistaken belief that such products may be added to the diet without consequence. Acutely, beliefs about the energy content of foods may exert stronger effects on hunger than their true energy value , and coupling knowledge of energy loading with activation of digestive processes augments satiety responses relative to physiologic challenges alone Short-term studies have yielded mixed data on expectations and intake. In one crossover trial , participants ingested breakfast cereals that contained no sweetener, sucrose, or aspartame. The sweet versions were matched on energy, sweetness, and palatability. Half of the participants were informed about the sweetener used and half were not. Informed aspartame use was associated with a nonsignificant, but noteworthy, increase in total daily energy intake. However, other studies failed to observe this effect 55 , , In a long-term trial in which participants were motivated to maintain weight loss, use of NNS was associated with lower weight regain. The importance of this mechanism remains poorly characterized. It is not specific to sweeteners or sweetness. Indeed, more pronounced effects may occur with manipulated expectations of fat content , where small errors lead to larger energy differences because of the higher energy density of fat. In this instance, the purported problem stems from an inappropriate use of NNS rather than an inherent problem with such products. Sweetness is inherently pleasant , but the sensation acquires salience through associative learning. That is, based on acquired knowledge of the metabolic consequence of ingesting a food through previous exposures, its sensory properties signal information about the impending metabolic challenge posed by ingestion of the item. This allows decisions about what type and quantity of food to eat as well as initiation of an appropriate postingestive physiologic response Combined, such a homeostatic system contributes to maintenance of energy balance. NNS and other means of diluting the energy density of foods pose a challenge to this system. Repeated exposure to low-energy foods containing NNS could lead to a noncognitive expectation that their consumption would contribute little energy to the diet. Thus, if presented with a higher energy version with similar sensory properties, intake may reflect the expected, rather than the true energy value, which leads to greater energy consumption. This was shown in a recent trial in rats in which chow energy intake was higher after ingestion of a premeal with a flavor previously paired to a low-energy food than after ingestion of the same preload with a flavor previously paired to a comparable high-energy food Preliminary data in humans have also documented this effect, albeit not solely through the manipulation of sweeteners , However, the long-term nutritional consequences of such misguided feeding are uncertain. The frequency of exposures to these conditions is likely to be low and energy compensation may occur at a later time point. Furthermore, associative learning is continuous, so each exposure to a food results in a recalibration of the sensory signal's meaning and, as a consequence, its influence on intake. Another variation on this concept entails repeated pairings between a single sensory property, such as sweetness, and inconsistent metabolic consequences. Again, the predictability of the signal may be compromised 84 , , Recent provocative findings from rat models suggest diminished predictability results in positive energy balance. In one set of studies , 2 groups of rats were provided sweet solutions overnight for 10 nights. This was followed by an acute feeding test in which a sweet, chocolate-flavored caloric beverage was consumed before the meal and was followed by ad libitum access to chow. Whereas intake of the sweet premeal was comparable for both groups, those that received inconsistent pairings consumed more energy from the chow than did the group receiving consistent pairings. Thus, when a sensory cue, such as sweetness, lacks predictive power, energy regulation is disrupted and is biased toward positive balance. The longer-term implications of this acute trial were shown in a subsequent 5-wk study The rats receiving inconsistent training consumed more energy, gained more body weight, and gained more body fat because of a weaker dietary compensation response. It is unclear whether these findings can be extrapolated to humans who eat a more varied diet and when nonnutritively sweetened foods are ingested concurrently with high-energy foods eg, diet soda with a hamburger, nonnutritively sweetened coffee with pie. Under such conditions, associative learning would be considerably more complicated and subtle. Will signal veracity be compromised if a meal contains kJ compared with kJ by the substitution of a beverage containing NNS for a beverage containing NS? Beverages sweetened with NNS are most commonly consumed with food Other recent evidence indicates that learning does occur in humans, but is counter to predictions from the animal studies Participants reported consuming beverages containing NNS alone on at least some occasions, so their energy-taste associations would be inconsistent. In short-term tests, participants failed to report increased appetite or energy intake in response to consumption of NNS, whereas nonusers of NNS reported heightened appetite and energy intake after such stimulation. These findings indicate inconsistent exposure to NNS paired or not paired with energy from beverages results in blunted responses to their consumption and no elevation in risk of weight gain. However, this work explored only one source of exposure, beverages, and short-term 1 d responses. The implications of chronic, widespread use of NNS on taste-energy associations and their influence on appetite and feeding are questions open to study. Given that a high proportion of NNS are consumed in beverage form Table 2 , the effects of hydration state on feeding are relevant. A reciprocal association between food and water intake is widely recognized. Animals reduce their food intake when water is restricted, and reduce their water intake when food deprived Similar responses are observed in humans However, hydrational effects on feeding are also apparent in animals provided ad libitum access to food and water This relation prompted an early hypothesis that obesity stemmed from excess fluid consumption, independent of energy provided by the fluids That is, drinking begets eating. The hypothesis is that drinking may initiate eating events to address the osmotic challenge posed by hypotonic beverage ingestion. There has been considerable research on feeding induction of drinking, but much less on the reverse — Whether consumption of NNS stimulates drinking and, as a consequence, compensatory eating, has not been adequately evaluated. The concept of reward in feeding is difficult to define and is proposed to be multifaceted with elements of liking, wanting, and learning Sweetness is a prototypical stimulus to document each of these elements There is increasing recognition that reward systems activated by the anticipation and actual act of feeding interact with, and may dominate, appetitive systems in modulating food and beverage consumption — One way to operationalize reward is to document the effects of sensory exposures on its neural substrates. Sweetness is an effective stimulus for the release of mediators of reward, such as dopamine — and opioids , , that can stimulate food intake. However, the view that sweet foods are preferred and consumed because of the activation of these systems is only one proposed mechanism. Higher intake may also be due to a lack of responsiveness of these systems , Thus, overeating can stem from a lower reward value of foods or motivation to seek them , Recently, it was proposed that these phenomena coexist , but it may also be argued that the data are presently more descriptive than mechanistic. Behaviorally, common experience indicates that food palatability can initiate eating in the absence of energy need and increase energy intake within a meal , , — Reduced palatability during a meal is not a primary determinant of its termination Although there is no evidence that NNS are uniquely able to stimulate feeding acutely, their addition to an energy-yielding food or meal has been associated with greater intake 45 , , The effect is magnified if intake occurs when individuals are hungry and persists, albeit to a lesser degree, in a state of higher satiety Whether longer-term intake is increased by this mechanism is not established. With repeated exposure, less palatable foods gain acceptability and intake can match initially preferred items Similarly, palatability may decline for foods with a high hedonic quality with frequent exposure , Individuals with heightened reward sensitivity may be at particular risk of palatability driven feeding as preliminary evidence indicates that this characteristic is directly related to food intake and BMI , However, it cannot be assumed that obese individuals derive greater pleasure from foods , Indeed, some work indicates that there are no differences between lean and obese individuals , or that the former actually provide higher hedonic ratings to a standard list of foods The importance of postingestive learning in the establishment of food preferences has been well documented and often attributed to flavor cues. However, recent findings raise questions about a unique role of sweet taste in reward-mediated feeding. In this model, NNS are not as effective at stimulating dopamine release, flavor conditioning, or promoting intake. Existing evidence does not support nor refute a role for NNS in enhanced palatability on reward motivated feeding. This is best exemplified by the wide variety of cuisines in a global population with largely common inherent hedonic predilections. A primary mechanism by which flavor preferences are entrained is through repeated exposure. This phenomenon has been most clearly described for salt and fat. Observational data indicate a direct association between customary salt intake and the preferred concentration of salt in food Some evidence suggests a more specific association between use of discretionary salt and intake , which underscores the contribution of sensory exposure. Experimentally, the required addition of salt to food, which increases sensory exposure to the taste, leads to a preference for higher levels of salt in the food In contrast, no hedonic shift occurs when same quantity of salt is added to the diet via capsule, which matches the metabolic challenge posed by salting food but without the same sensory exposure. With the exception of extreme sodium depletion , systematic reduction of salt exposure for more than several weeks has the opposite effect — Similarly, placing individuals on the same reduced-fat diet, in which one group is deprived of sensory exposure to fats while another is allowed to use fat replacers to simulate continued sensory exposure, leads to a preference for lower fat levels in foods in the former group, but not in the latter , With respect to sweetness, several — , although not all , observational studies note a significant association between hedonic ratings for sweet items and customary sweetener exposure. Infants repeatedly provided sweetened water early in life exhibit a heightened acceptance of sweetened water at 2 y of age This preference is not apparent for a novel fruit-flavored beverage, which indicates that the effect is food-specific. However, ethnographic studies suggest that sweet preferences learned by children generalize, at least to other sweet beverages Broader associations have also been noted between the percentage of energy ingested from predominantly sweet foods and beverages and optimal concentrations of sweetness in foods in adults In other work, the dietary sweetness level, calculated as the gram sum of fructose, sucrose, and alternative sucrose equivalents, correlated with peak hedonic ratings of a fruit-flavored beverage containing graded sucrose concentrations These observations are supported by limited data from a controlled intervention trial in which 59 children mean age: 9. A significant increase in preferred sweetness level for the beverage and a trend in this direction for the yogurt were observed in the children, but not in the adults. Interestingly, a similar effect was not noted with a comparable manipulation of sourness. However, this may have been attributable to the short duration of exposure, because the acceptance of novel sweet items is more rapid than the acceptance of novel sour items Collectively, these observations suggest that repeated exposure to a taste or flavor leads to increased acceptance of foods or beverages characterized by the taste or flavor and that the desired intensity of the sensation is directly related to the concentration of the compound responsible for the sensation in dietary items. Furthermore, the sensory property may exert a stronger influence on the preferred concentration of a taste or flavor compound in a food than would the metabolic effect of consuming the relevant compound. Thus, repeated exposure to NNS would be expected to establish and maintain a preference for sweet items in the diet. To the extent that NNS are included in energy-yielding items and that the liking for sweetness contributes to intake, their use may be predicted to contribute to energy intake. Generally, there is a direct relation between hedonic ratings for foods and intake Amelioration of a learned liking for a highly sweetened diet will likely require restricting exposure to sweet foods and beverages, including those that are not significant sources of energy. Such an approach clearly conflicts with one that encourages the use of NNS to dilute the energy content of the diet while maintaining its palatability. It may be that each approach holds merit, but for different subsets of the population who are consuming energy from sweet items in excess of need for different reasons eg, reward sensitivity, health concerns. There is widespread agreement that sweetness is an inherently pleasant sensation , However, there is marked individual variability in its behavioral manifestation , This has prompted exploration of the genetic basis of sweet taste. To date, there is little evidence of a heritable component for the ability to detect or rate the intensity of sweetness and only slightly more support for individual differences in hedonics There are several recent reports of a genetic basis for sugar intake , that may be mediated by sweetener-sensing mechanisms , There are receptors in the intestine, analogous to sweet taste receptors TR1s in the oral cavity, that increase glucose transport via rapid glucose transporter type 2 GLUT2 insertion into enterocyte cell membranes when activated by NS and NNS Identification of a polymorphism of GLUT2 showed that individuals who were Ile carriers had higher intakes of sugars from items such as baked goods and chocolate, but not inherently sweet items such as fruit. This suggests that, even if there is an inherent predisposition to ingest sweet items, it will be modulated by nonphysiologic factors such as food availability, health concerns, and custom and, possibly, other inherited traits influencing food choice \[eg, neophobia \]. From an evolutionary perspective, NNS are a novel dietary stimulus that have been introduced into our diets in only the past few decades. Although the safety of approved NNS has been established with respect to acute toxicity and longer-term pathologies eg, carcinogenesis , their influence on appetite feeding, energy balance, and body weight has not been fully characterized. Questions remain regarding the effects of both properties of the compounds themselves eg, sweet, palatable and the way consumers choose to use them dietary additions rather than substitutes. However, this number is growing, so the implications of their use in addressing overweight and obesity requires more complete understanding. Early acute feeding studies indicate that NNS inclusion in products that provide little or no energy is associated with heightened hunger, but subsequent work showed that when incorporated into energy-yielding products, this does not occur. Because beverages containing NNS are commonly consumed with foods, augmented hunger may not be a concern. Furthermore, it is unclear whether heightened hunger necessarily translates into increased energy intake. However, evidence that use of NNS in free-living individuals results in improved weight loss or maintenance is lacking. This void has permitted speculation that NNS ameliorate or, more commonly, exacerbate the problem of positive energy balance. A critical review of the literature, addressing the mechanisms by which NNS may promote energy intake, reveals that none are substantiated by the available evidence. There is no clear evidence that NNS augment appetite by activating cephalic phase responses, altering osmotic balance, or enhancing food palatability. Indeed, there is emerging evidence that selected NNS may stimulate the release of satiety hormones, although the link between these hormones and energy intake in free-living individuals is also open to debate. With respect to energy intake, there is no substantive evidence that inherent liking for sweetness or NNS activation of reward systems is problematic. Use of NNS may result in greater proportional energy contributions from fat, but work on this issue also indicates that total energy intake is moderated by NNS, and the latter is the dominant factor with respect to body weight. Knowledge of use of NNS has been shown to result in energy compensation or even overcompensation in short-term trials, but less so with chronic use. This may be because those who compensate, and therefore fail, to achieve weight goals cease using NNS; therefore, only those less susceptible to cognitive influences remain to be evaluated. The concept that use of NNS disrupts responsiveness to signals aiding energy balance has been substantiated theoretically, but there is no evidence available to assess the validity of the mechanism in humans. The question of whether drinking is promoted by the appeal and availability of beverages containing NNS and thus stimulates eating, which leads to positive energy balance, remains unsettled. Use of NNS likely promotes a preference for higher sweetener levels of foods and beverages, but whether this compromises efforts to reduce energy intake has not been explored. Taken together, the evidence sum-marized by us and others suggests that if NNS are used as substitutes for higher energy yielding sweeteners, they have the potential to aid in weight management, but whether they will be used in this way is uncertain. This will require additional information about use patterns of NNS, clarification of remaining potential counterproductive mechanisms, and long-term randomized, controlled trials in free-living populations. The authors' responsibilities were as follows: RDM and BMP were involved with the conceptualization of the manuscript, review of the literature, and the drafting and editing of the document. Neither author had a conflict of interest with respect to this manuscript. As a library, NLM provides access to scientific literature. Am J Clin Nutr. Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms 1 2 , 3 Richard D Mattes Richard D Mattes Find articles by Richard D Mattes. Open in a new tab. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Foods containing added NS 2.

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