Het afvallen lukt niet echt :(

ik vind dat iedereen zijn eigen plan moet trekken en niet zijn oren moet laten hangen naar anderen. Succes hoor usena, het zal je wel lukken.

quote:camomille schreef op 30 januari 2013 @ 23:37:

wat doe je dan dat je 2200 calorieen per dag nodig hebt? beroepsmilitair? Sportleraar? Ik weet dat als ik meer dan 1630 ckal eet ik aan kom. Want dat is wat ik verbruik, als ik drie keer per week sport (high impact). Maar ik ben misschien kleiner (1.70) dan jij bent. Maar 2200 ckal verbrandt bijna geen een vrouw op een dag zonder dat ze 5 keer per week intensief traint. Ik schrok daar ook van hoor want ook ik ben opgevoed met het idee dat een vrouw 2000 ckal per dag verbruikt. Dat is dus niet zo......



Het idee is eigenlijk heel simpel, als je minder eet dan je verbrandt, val je af.... Val je niet af, dan neem je dus te veel ckal tot je.



het is eigenlijk niet mogelijk om zonder laboratorium te bepalen hoeveel je verbruikt. Dat is afhankelijk van heel veel factoren waaronder je bouw maar ook je karakter. De nerveuzere types verbranden honderden calorieën per dag meer dan de wat relaxter karakters bijvoorbeeld. Maar 2200 is voor een matig actieve vrouw

van gemiddelde lengte een logischer gemiddelde dan 1600. 1600 calorieen per dag is een dieetgemiddelde. Ik als intensieve sporter zit in de winter ver boven die 2200, heel ver zelfs.

vergeet de colalight Usena, ook light frisdranken zetten aan tot insulineproductie en vetopslag, ook al bevatten ze geen calorieen. Bovendien is aangetoond dat je van light frisdranken een grotere eetlust krijgt.



wat is in vredesnaam tintelfruit?

quote:Kapitein_Onderdeurtje schreef op 31 januari 2013 @ 00:03:

[...]





Ik ben er voor het eerst achtergekomen via een video presentatie van Vegetarian Society of Hawaii maar kan de videolink niet 1,2,3 vinden. Daarin werd een wetenschappelijk onderzoeksresultaat gepresenteerd waaruit blijkt dat de meeste mensen eigenlijk te weinig b12 binnenkrijgen.het binnenkrijgen van vit. B12 door voeding of pillen speelt geen enkele rol bij het B12 tekort. Een B12 tekort is het gevolg van een resorptieprobleem in je darmen. Pillen slikken helpt niet, ook niet ter preventie. Je zal injecties moeten halen. Deze (ernstige) aandoening komt wel veel vaker voor bij veganisten. Een goede reden om geen veganist te worden.

@meds:



En ik mezelf maar altijd als een actief persoon bestempelen, ben ik misschien gewoon erg nerveus

quote:Kapitein_Onderdeurtje schreef op 31 januari 2013 @ 00:12:

[...]

Ik ben niet zo voor alles-of-niets-denkerij (sorry dat ik het even zo bestempel) maar anderen zijn daar wat mij betreft ook vrij in.



En ook al is het maar een onvolmaakt streven, het is toch een significante stap.No offence hoor Kapitein, ik was nogal onder de indruk van het gemak waarmee je zei dat je dan gewoon veganist wordt. En ja, ik ben nogal een mierenneukert wat dat betreft

@perzosa niks mis met een natural zenuwpees.

sabbaticalmeds, 16 minuten geleden vergeet de colalight Usena, ook light frisdranken zetten aan tot

insulineproductie en vetopslag, ook al bevatten ze geen calorieen.





In een ander topic zijn we eens heel hard op zoek geweest naar bewijs voor deze veelgehoorde stelling en dat hebben we niet gevonden.

Mocht jij wel een link naar onderzoek hebben, ik ben erg geinteresseerd.





Dit is een post uit dat topic (Eten met je verstand deel V) , via google kan je de rest terugvinden:



Ik kan nog steeds niks vinden dat erop wijst dat je van zoetstof honger

krijgt of dik wordt.

Ik loop nu weer tegen een hoogleraar voedingsleer aan die zegt dat

het onzin is: Vragen van lezers

Vraag: Er werd mij verteld dat er onderzoek is gedaan naar zoetstoffen

en dat zoetstoffen de lever voor de gek houden, omdat het de zoete

smaak toch registreert en vervolgens maakt dat je daardoor juist meer

gaat eten en dus zoetstoffen een averechts effect zouden hebben. Je

valt er niet van af, maar komt er juist van aan. Antwoord: 25 jaar geleden vatte een Engelse onderzoeker het idee op

dat het eten van zoetstoffen honger veroorzaakt. Dat idee is intussen

uitgebreid getest en het blijkt niet zo te zijn. Het blijft echter circuleren. http://www.mkatan.nl/



dit gaat dan meer over het vermeende honger krijgen door zoetstof, maar ook dat insulineverhaal hebben we nergens terug kunnen vinden.

Ik heb gelezen dat je lichaam zoetstoffen zoals aspartaam niet "herkent" en daarom je insulinewaarden verhoogt, niet dat je er meer van gaat eten. Ik weet niet of iedereen daar zo van aankomt. Ik ken mensen die veel diet Coke drinken en gewoon slank zijn maar dat is uiteraard geen wetenschappelijk bewijs.



Als ik kijk naar mijn eetgewoontes en die van mijn moeder vroeger toen ze mijn leeftijd had: gewoon vier boterhammen met mager beleg, paar koppen koffie zonder suiker of cream en avondeten (aardappelen, groente, vlees en jus). Nou, vooruit, nog een appeltje voor wat vitamines. Tegenwoordig is het toch anders. In die tijd was de supermarkt maar tot een uurtje of zes open, dus toen mijn ouders allebei werkten moesten ze op koopavond of zaterdag boodschappen doen. Wat je niet in huis hebt, kun je ook niet eten natuurlijk.



Ik hoor vaker dat je gewoon moet zoeken naar wat bij jou past. Mijn schoonmoeder eet bij een dieet overdag twee boterhammen en eet 's avonds liever een groot vol bord leeg. Daar valt zij wel mee af, terwijl dieetgeleerden zeggen dat je beter je ontbijt of lunch je grootste maaltijd kunt laten zijn. Een vriendin van mij kwam door sporten juist vijf kilo aan; ze was skinny fat, en haar spieren maakten haar veel zwaarder.



Ik volg overigens geen dieten waar ontbijt lunch diner en tussendoortjes al zijn uitgestippeld; is voor mij veel te beperkend. Ik hou het nu bij minimaal vijf keer per week dagelijks een half uur bewegen en een caloriebeperkend dieet van 1400 calorieen. Ik ben al wel wat kwijt, maar ik wacht even met juichen tot ik een paar weken lang wat af kan vallen.

Afvallen met een dieet van 1800-2000kcal gaat niet lukken. Ook niet als het allemaal gezonde caloriën zijn. De enige manier om met dat aantal kcal af te vallen is door er lekker flink bij te sporten.



Het basisprincipe blijft nog altijd: Minder binnen krijgen dan je verbrandt.

Eydis_, 35 seconden geleden Ik heb gelezen dat je lichaam zoetstoffen zoals aspartaam niet

"herkent" en daarom je insulinewaarden verhoogt, niet dat je er meer

van gaat eten.



Ja dat wordt de laatste tijd steeds gezegd, maar is het wel zo? Yvonne Lemmers zegt het bv in haar boek Grip op koolhydraten, maar zij geeft ook geen bron. Er is wel oz gedaan naar kinderen en light vs suiker drinken en de lightdrinkers vielen af.

quote:usena schreef op 30 januari 2013 @ 23:11:





Als ik mijn calorieën tel dan kom ik elke dag min op 1800 uit en max op 2000.





Ik vraag me eerlijk gezegt wel af wat jij allemaal wat niet drinkt daarbij als je maaltijden zo gezond zijn en jij zoveel kcal binnen krijgt.



Mijn otnbijt met 200 grm magere yoghurt, muesli zonder suiker en fruit

3 vk boterhammen zonder boter met mager beleg én groente op elke boterham

150 gr aardappelen 200 gr groente en 125 gr vlees.



En als ik tussendoro honger krijg 250 ml magere zuivel of 1 stuks fruit extra tussendoor.

Mag ik BLIJ zijn als ik de 1600 kcal haal volgens voedingscentrum



drinken: water en thee zonder suiker

quote:impala schreef op 31 januari 2013 @ 01:08:

Eydis_, 35 seconden geleden Ik heb gelezen dat je lichaam zoetstoffen zoals aspartaam niet

"herkent" en daarom je insulinewaarden verhoogt, niet dat je er meer

van gaat eten.



Ja dat wordt de laatste tijd steeds gezegd, maar is het wel zo? Yvonne Lemmers zegt het bv in haar boek over grip op koolhydraten, maar zij geeft ook geen bron. Er is wel oz gedaan naar kinderen en light vs suiker drinken en de lightdrinkers vielen af.





Wat ze zegt klopt. Als je bijv. slapjes wordt omdat je niet eet, en je eet een suikerklontje, voel je je beter nog voordat de suiker in je bloed is opgenomen.



Er is ooit een onderzoek gedaan naar mensen die suikerriet oogsten. Ik weet niet exact de opzet meer, maar het kwam hier op neer: 3 groepen.. Alle 3 de groepen mochten niet eten. Huppa aant werk.. Tijdens de lunch kreeg groep 1 iets met suiker. Groep 2 kreeg iets met zoetstof zonder kcal. Groep 3 kreeg niets zoets of kcalrijks. De groepen communiceerden niet met elkaar en wisten niet wat ze kregen.



Na een uurtje of 2 werd gekeken hoe elke groep na de lunch functioneerde.



Groep 1 die suiker kreeg werkten flink door. Laten we ff zeggen 100kg oogst.

Groep 2 had ook 100kg oogst.

Groep 3 had veel minder geoogst.



Aan het einde van de dag was groep 2 echter meer afgepeigerd dan de andere 2 groepen.



De conclusie was dat de smaak van suiker al maakt dat het lichaam denkt dat er voedingstoffen binnen komen waardoor de werkers in groep 2 nog steeds goed konden doorwerken. Echter, maakte hun lichaam meer insuline aan wat alle aanwezige suikers omzette in (voor het lichaam niet direct bruikbare) glycogeen. Toen er vervolgens niks binnenkwam was hun bloedsuikerspiegel zo laag dat ze daarna enorm inkakten en eigenlijk dubbel zo veel trek hadden/suiker nodig hadden.



Was leuk om te zien!





Mijn eigen ervaring bevestigd bovenstaande. Ik heb lang last gehad van een eetstoornis. Ik kon makkelijk de hele dag niet eten. Ik dronk dan de hele dag water. 1 dag heb ik echter van 8 uur 's ochtends tot 15:30 op school crystal clear gedronken ( had een 1.5L fles mee). Toen ik thuis kwam had ik zo'n ontzettende honger dat ik misselijk was van de trek. Ik trilde, zweette en viel uiteindelijk flauw. Mijn theorie op basis van bovenstaande is dus dat ik idd door de zoete crystalclear "dacht" dat ik suiker binnen kreeg en meer insuline aanmaakte. Daardoor onderdrukte ik de glucagon dat glycogeen omzet in glucose (wat gebeurt als je spiegel te laag is, als jebijv niet eet). En daardoor kreeg ik een veel te lage suikerspiegel.

quote:impala schreef op 31 januari 2013 @ 01:08:

Eydis_, 35 seconden geleden Ik heb gelezen dat je lichaam zoetstoffen zoals aspartaam niet

"herkent" en daarom je insulinewaarden verhoogt, niet dat je er meer

van gaat eten.



Ja dat wordt de laatste tijd steeds gezegd, maar is het wel zo? Yvonne Lemmers zegt het bv in haar boek Grip op koolhydraten, maar zij geeft ook geen bron. Er is wel oz gedaan naar kinderen en light vs suiker drinken en de lightdrinkers vielen af.



Misschien is het een aanrader om het boek van Ronald van wankum eens te lezen: voeding zoals voeding voor u moet zijn



Daarin staat ook besschreven dat mensen met suikerziekte vaak idd overgaan op light producten en ze toch niet afvallen.

Onderzoek toont uit hoe dit komt:

De zoetstoggen verhogen snel je suikerspiegel, waarna die na een tijdje ook weer heel snel daalt en onder de onderst lijn komt van waar die tussen moet blijven waardoor mensen gaan naar suiker hunkeren en méé'r gaan eten omdat hun suikerspiegel niet goed is

quote:kleinmeisje_89 schreef op 31 januari 2013 @ 01:19:

[...]





Misschien is het een aanrader om het boek van Ronald van wankum eens te lezen: voeding zoals voeding voor u moet zijn



Daarin staat ook besschreven dat mensen met suikerziekte vaak idd overgaan op light producten en ze toch niet afvallen.

Onderzoek toont uit hoe dit komt:

De zoetstoggen verhogen snel je suikerspiegel, waarna die na een tijdje ook weer heel snel daalt en onder de onderst lijn komt van waar die tussen moet blijven waardoor mensen gaan naar suiker hunkeren en méé'r gaan eten omdat hun suikerspiegel niet goed isBedoel je niet de insuline spiegel? Want die stijgt idd onder invloed van de smaakt en daardoor verlaagt de bleodsuiker veel te veel (Er kwam onverhoopt niks binnen aan suikers!) en dan heb je de suikers ineens nóoooodig! En dan ga je ernaar hunkeren.

quote:Ephina schreef op 31 januari 2013 @ 01:25:

[...]



Bedoel je niet de insuline spiegel? Want die stijgt idd onder invloed van de smaakt en daardoor verlaagt de bleodsuiker veel te veel (Er kwam onverhoopt niks binnen aan suikers!) en dan heb je de suikers ineens nóoooodig! En dan ga je ernaar hunkeren.



ja precies



Maar ik blijf er in iedr geval bij dat TO veel meer nuttigt dan zij aangeeft.



Als je echt wat over voeding wil leren en WAT het met je lichaam doet: lees het boek. Het is geen dieet, het is een levenswijze. Simpel uitgelegt. Als je gezond eten en af en toe eens zondigen kunt volhouden is het voor iedereen te doen.

Je ogen zullen door de uitleg geopent worden

Ik zou er niet teveel\dieettheorieën op loslaten. Al dat gezeur over de hoeveelheid calorieën en zoveel maaltijden per dag. Je moet t tenslotte toch je leven lang volhouden. Je eet prima, niet erg veel trouwens. Gun jezelf elke dag iets lekkers en als je been beter is, lekker gaan sporten net als Meds zegt. Ben er zelf 30 kilo mee afgevallen en al 2 jaar op gewicht. Niks geen bijzonder dieet: gewoon volkoren brood, muesli, yoghurt, fruit, weinig aardappels en pasta, veel groente en matig vlees. Maar dat doe je al. Dus lekker doorgaan zo en als t zo blijft, even langs de dokter. Je weet niet of t nog een andere oorzaak kan hebben. Succes!

Daarin staat ook besschreven

dat mensen met suikerziekte

vaak idd overgaan op light

producten en ze toch niet

afvallen.

Onderzoek toont uit hoe dit komt:

De zoetstoggen verhogen snel

je suikerspiegel,



mensen met suikerziekte maken toch helemaal geen insuline aan. Dus dit kan toch niet kloppen? Of gaat dit alleen om diabetes type 2 ? Maar een collega met type 2 meet geen verschillen in zijn bloed na drinken van light.

Ik ben nog steeds op zoek naar een wetenschappelijk onderzoek.

Zoetstoffen verhogen de suikerspiegel ook niet. Ze verhogen (door met smaak je brein te foppen) je insuline waarde en daardoor daalt de bloedsuikerspiegel.



Bij een diabeet is dit afhankelijk van het type en de persoon zelf. Probeer anders het onderzoek eens op te zoeken dat ik hierboven vermeldt. Was op Discovery of NG. Wetenschappelijk opgezet.

Hoeveel weeg je TO en sport je? Hoeveel kcal je met een dieet mag hangt af van je gewicht. Voorbeeld als je net als ik 129 weegt is 2000 kcal ok op sportdagen. Als ik niet sport eet ik 1500 kcal op een dag aan gezonde voeding. En ik loop tegen hetzelfde probleem als jou aan ik val niet af. Ik drink zelf een blikje cola light per dag.

ja die quote was niet handig omdat die niet klopte maar we bedoelen wel hetzelfde. Ik ga kijken of ik jouw oz kan vinden. Ik wil weten of het echt waar is. Want drink ook graag een cola light.

Ik ben ff op pubmed gaan zoeken en kwam dit tegen. Heb alleen het abstract gelezen maar volgens mij komt het aardig overeen.

Ze meten iig ook de glucose en insulinelevels na de maaltijd. Het enige foutje t.o.v. onze situatie is dat die mensen minder kcal binnen krijgen. I.p.v. 200kcal (normale cola) v.s. 0.1kcal (light).

Ik zoek nog ff verder want dat is wel belangrijk.



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900484/

Wauw dit is ook best heftig..

Gaat over de dissociatie tussen zoete smaak en de reactie van ons lichaam. Door frisdrank zonder kcal te drinken trainen we ons lichaam om suikersmaak niet te associeren met kcal inname waardoor we meer gaan eten en ons metabolisme veranderd.





http://www.sciencedirect. ... cle/pii/S0031938409004089



He, voor die link moeten jullie inloggen. Da kan dus niet.

Sorry voor deze enorme post, maar anders kan ik het jullie niet laten lezen..



High-intensity sweeteners and energy balance

Susan E. Swithers, , Ashley A. Martin, Terry L. Davidson

Department of Psychological Sciences, Purdue University, West Lafayette, IN, USA

http://dx.doi.org.ezproxy ... 16/j.physbeh.2009.12.021, How to Cite or Link Using DOI

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Abstract

Recent epidemiological evidence points to a link between a variety of negative health outcomes (e.g. metabolic syndrome, diabetes and cardiovascular disease) and the consumption of both calorically sweetened beverages and beverages sweetened with high-intensity, non-caloric sweeteners. Research on the possibility that non-nutritive sweeteners promote food intake, body weight gain, and metabolic disorders has been hindered by the lack of a physiologically-relevant model that describes the mechanistic basis for these outcomes. We have suggested that based on Pavlovian conditioning principles, consumption of non-nutritive sweeteners could result in sweet tastes no longer serving as consistent predictors of nutritive postingestive consequences. This dissociation between the sweet taste cues and the caloric consequences could lead to a decrease in the ability of sweet tastes to evoke physiological responses that serve to regulate energy balance. Using a rodent model, we have found that intake of foods or fluids containing non-nutritive sweeteners was accompanied by increased food intake, body weight gain, accumulation of body fat, and weaker caloric compensation, compared to consumption of foods and fluids containing glucose. Our research also provided evidence consistent with the hypothesis that these effects of consuming saccharin may be associated with a decrement in the ability of sweet taste to evoke thermic responses, and perhaps other physiological, cephalic phase, reflexes that are thought to help maintain energy balance.



Keywords

Sweet taste; Body weight; Pavlovian conditioning

1. Introduction

A variety of recent epidemiological evidence points to a link between the consumption of sweetened beverages and incidence of obesity and other disorders associated with positive energy balance. For example, although not all studies have agreed, in recent years a number of reports have revealed that intake of sugar-sweetened beverages (SSBs; primarily soda and juices) is strongly and positively correlated with elevated body weight and also with increased incidence of the metabolic syndrome which includes Type II diabetes, hypertension, and cardiovascular disease ([1], [2], [3], [4] and [5]; see also Hu, this volume).



Because SSBs are calorically-dense, it may not be surprising that increased consumption is associated with positive energy balance. Based on this fact, one approach to combating the current obesity crisis is to reduce access to SSBs. In the U.S., a much publicized application of this strategy has been a program to remove SSBs from primary and secondary school vending machines, replacing them with diet sodas and other non-nutritively sweetened or unsweetened beverages (see, for example, Storey, this volume). However, some question whether or not this program can reduce SSB intake enough to have a significant impact on childhood, and subsequently, adult obesity (e.g. Popkin, this volume).



As a means of weight control, the substitution of non-nutritively sweetened beverages for SSBs may also be questioned on other grounds. Several studies that have linked intake of SSBs to increased incidence of obesity and the metabolic syndrome also report a similar, and sometimes stronger, relationship when intake of diet soda is correlated with the same weight and health outcomes. For example, using both cross-sectional and longitudinal data from the Framingham Heart Study, Dhingra et al. [2] reported positive relationships between consumption of diet soda and the prevalence of the metabolic syndrome that were larger than that obtained with consumption of regular soda. Similar results have also been reported as part of independent studies by Lutsey et al. [6] and Nettleton et al. [7]. Furthermore, Fowler et al. [8] reported that for humans who were normal weight or nonobese (BMI < 30) at baseline, intake of > 21 non-nutritively sweetened beverages per week (diet sodas and artificially sweetened coffee and tea) was associated with about double the risk of obesity compared to nonusers at follow-up 7 to 8 years later.



Of course, these epidemiological data are limited with respect to what they can say about how intake of non-nutritive sweeteners may be related causally to obesity and the metabolic syndrome. The mere finding that consumption of non-nutritively sweetened foods and beverages is positively correlated with weight gain is necessary, but clearly not sufficient, to confirm the hypothesis that the use of non-nutritive sweeteners causes increased weight gain. Nor can such information differentiate this interpretation from the alternative view that weight gain is the impetus for increased use of non-nutritive sweeteners. Indeed, there may be no causal relationship in either direction (i.e., other factors could cause both increased use of non-nutritive sweeteners and increased body weight gain). Furthermore, even if body weight gain does cause increased use of non-nutritive sweeteners, the question remains whether consuming these substances helps or hinders weight management in humans [9]. The available data relevant to this question are controversial [10], and the debate is sometimes heated. For example, holding everything else constant, substituting non-nutritive for high-calorie sweeteners obviously reduces the energy content of food and beverages. But some data from humans suggest that these kinds of substitutions may not reduce, and may even increase, total energy intake by stimulating appetite [11].



Research on the possibility that non-nutritive sweeteners promote food intake, body weight gain, and metabolic disorders has been hindered by the lack of a physiologically-relevant model that describes the mechanistic basis for these outcomes. The purpose of the present paper is to consider a theoretical account that may fill this gap in understanding and to review recent experimental findings from our laboratories that have been generated by this model.



2. A Pavlovian perspective on energy regulation

Perhaps the most fundamental and well-established concept in psychology is that organisms learn about events that signal important biological outcomes. Pavlov's [12] finding that dogs would come to salivate to the sound of a metronome that preceded the delivery of meat powder provided the first experimental demonstration of this signaling relationship. Sensitivity to such simple Pavlovian contingencies is ubiquitous across species from the simple sea slug (e.g., Aplysia californicus[13]) to humans, and can be demonstrated with a diverse array of stimuli and with a wide variety of response systems (see [14]).



Among the most robust forms of Pavlovian conditioning are those that involve the establishment of taste stimuli (e.g., sweet and bitter) as signals for postingestive (e.g., nutritive and gastric malaise) consequences and that measure intake as the behavioral index of this learning [15] and [16]. Similar to ideas originally proposed by Pavlov, current models of the physiological controls of energy regulation suggest that Pavlovian conditioning also enables tastes and other orosensory cues to evoke not only food intake, but a variety of hormonal, neural, and metabolic conditioned responses that prepare for and promote the efficient utilization of energy [17]. One implication of these models is that circumstances that degrade the ability of tastes to predict the occurrence of caloric outcomes will also weaken the evocation of these physiological or “cephalic phase” responses with the effect that energy regulation would become less effective [18], [19], [20] and [21].



In nature, and throughout most of our evolutionary history, sweetness has been a reliable predictor of the energy content of food. Accordingly, within the Pavlovian framework outlined above, sweet taste should be a potent elicitor of the cephalic phase responses that promote energy regulation. The available data provide strong confirmation of this suggestion [22]. However, we have suggested that beginning in the 1960's with the mass introduction of non-nutritive sweeteners into the food environment, the relationship between sweet taste and the caloric density of food may have changed (e.g., [18], [19], [20] and [21]). That is, for consumers of non-nutritive sweeteners, sweet tastes are no longer always accompanied by energetic outcomes. Based on Pavlovian conditioning principles, because sweet tastes are no longer consistent predictors of strong nutritive postingestive consequences, the ability of sweet taste to evoke cephalic phase responses would be degraded, with the result being less effective energy regulation and increased caloric intake when normal sweet (and high-calorie) foods are consumed.



3. An animal model of energy dysregulation

Pavlov was awarded the Nobel Prize in Medicine in 1904 for his research with dogs on digestive physiology. He then spent almost all of the remainder of his career investigating the implications of that work for the understanding of simple learning process, also using primarily non-human animal models. Pavlov's findings in both digestive physiology and in learning have been robustly confirmed in other species, including rats and humans, and have been the basis of important theoretical accounts of both types of processes [17] and [23]. The research described next is based on the integration of principles from physiology and learning, and uses the control afforded by an animal model (the rat) to study how intake of non-nutritive sweeteners affects energy and body weight regulation.



Our research has investigated the effects of degrading the ability of sweet tastes to predict increments in the postingestive nutritive consequences of eating on several behavioral and physiological indices of energy regulation. We reasoned that if sweet tastes are normally valid predictors of increased caloric outcomes, then exposing rats to sweet taste that is not associated with these increased calories should degrade this predictive relationship and impair energy intake and body weight regulation. Some of our work has studied the effects of giving different groups of rats semi-solid dietary supplements (plain yogurt) that have either non-nutritive or nutritive sweeteners (glucose) added. We will begin by describing these findings before turning to studies that compared the effects on intake and body weight of consuming fluids that were mixed with nutritive or non-nutritive sweeteners.



4. Sweet taste–caloric relations: semi-solid foods

4.1. Body weight gain, adiposity, and food intake

In our basic design, in addition to ad libitum lab chow and water, we gave adult male rats access to both plain and sweetened low-fat, yogurt in addition to their regular lab chow and water. One group (Predictive) received 30 g of plain unsweetened yogurt (0.6 kcal/g) on some days and 30 g of yogurt sweetened with 20% glucose (1.2 kcal/g) on other days. Thus, for this group, sweetened diet predicted more calories than unsweetened diet. The second group (Non-Predictive) received plain unsweetened yogurt on some days and yogurt sweetened with 0.3% saccharin on the other days. Thus, for this group, sweetened yogurt did not predict more calories than unsweetened diet. With this arrangement, although the rats could differentiate between the sweetened and unsweetened forms of the yogurt, they were not given the opportunity to directly compare the taste or palatability of the caloric sweetener to the non-caloric sweetener. All rats (ns = 8–9 per group) were given 30 g of sweetened or unsweetened yogurt daily 6 days per week (3 days sweetened and 3 days unsweetened) in random order for 5 weeks in addition to ad libitum chow and water. At the end of 5 weeks under these training conditions, rats in the Non-Predictive group, for which sweet taste did not signal an increase in the energy density of the yogurt, gained significantly more weight (Fig. 1A) and had significantly higher body adiposity (Fig. 1B) compared to the rats in the Predictive group for which sweet taste provided a valid signal for calories.





Fig. 1. Body weight gain (A) and adiposity (B) were significantly greater in rats (ns = 8–9 per group) given access to saccharin-sweetened yogurt diet supplements in which sweet taste did not predict increased calories (Non-Predictive group) compared to animals given glucose-sweetened yogurt diet supplements (Predictive group) in which sweet taste did reliably predict increased calories. *p < 0.05 compared to Predictive.

Adapted from [21]. Used with permission.



Figure options

Weekly total caloric intake (yogurt plus lab chow) intake over the same 5-week period is shown for the Non-Predictive and Predictive groups. Fig. 2 shows that total caloric intake (yogurt plus chow) tended to be higher in the Non-Predictive group. However, this difference did not achieve statistical significance.





Fig. 2. Total caloric intake tended to be greater in rats given access to saccharin-sweetened yogurt diet supplements in which sweet taste did not predict increased calories (Non-Predictive group) compared to animals given glucose-sweetened yogurt diet supplements (Predictive group) in which sweet taste did reliably predict increased calories (ns = 8–9 per group).

Adapted from [21]. Used with permission.





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4.2. Caloric compensation

Additional findings show that consumption of saccharin-sweetened yogurt can promote excessive intake relative to yogurt sweetened with glucose by reducing caloric compensation. Caloric compensation is exhibited when animals adjust for calories consumed on one occasion by reducing their caloric intake at subsequent opportunities to eat [24], [25], [26] and [27]. Therefore, weakened caloric compensation could result in excess energy intake and ultimately increased weight gain. We gave adult male Sprague–Dawley rats (ns = 8–9 per group) 30 g of low-fat, plain yogurt (Dannon) daily for 14 days in addition to ad libitum lab chow and water. Similar to the design described above, rats in the Glucose group received plain, unsweetened yogurt for 7 of the 14 days and yogurt sweetened with 20% glucose for 7 of the 14 days. In contrast, rats in the Saccharin group received plain, unsweetened yogurt for 7 days and yogurt sweetened with 0.3% saccharin for 7 days. Thus, as above rats in the Glucose group were trained under conditions in which sweet taste was a highly valid predictor of increased calories, whereas for rats in the Saccharin group, sweet taste did not predict more calories. After this training, both groups were food-deprived overnight before being tested for caloric compensation using a novel, sweet-tasting food. One test day, the rats were given a premeal of 5 g of Chocolate Ensure Plus thickened with guar gum (1.4 kcal/g) for 30 min and they were given no premeal on another test day, in counterbalanced order. On each test day, all rats were then given free access to lab chow and the amount eaten was recorded after 1, 2, and 4 h.



The results of the caloric compensation test showed that for the Glucose group (Fig. 3A) caloric compensation was virtually complete in that the total amount of calories consumed (premeal and lab chow combined) was almost the same when the rats were tested following the premeal compared to the no-premeal condition. To achieve this outcome, the rats in the Glucose group had to reduce their intake of lab chow by an amount equivalent to the caloric content of the Ensure premeal. In contrast, much weaker caloric compensation was shown by the rats in the Saccharin group. As can be seen in Fig. 3B, for this group, total energy intake was significantly greater following the Ensure premeal compared to the no-premeal condition. This outcome indicates that rats in the Saccharin group were less able to reduce their intake of lab chow to compensate for calories contained in the premeal compared to rats in the Glucose group. If continued over the long-term, reduced caloric compensation could contribute to excess body weight gain. Within our theoretical framework, weaker caloric compensation by the Saccharin group was expected to the extent that the control of energy intake relies, at least in part, on the ability of sweet taste to signal the caloric content of the Ensure premeal. This signaling relationship would be degraded by prior exposure to sweet but non-nutritive saccharin, but not by prior exposure to sweet and high-calorie glucose.





Fig. 3. Rats given experience with Predictive experience with sweet tastes and calories (A) showed strong caloric compensation for calories provided in a novel, sweet-tasting premeal. Total caloric intake was not significantly different on days when a premeal was provided compared to days on which a premeal was not provided. In contrast, rats given experience with Non-Predictive relations between sweet taste and calories (B) failed to compensate for calories provided in a novel sweet premeal (ns = 8–9 per group). *p < 0.05 compared to No Premeal.

Adapted from [21]. Used with permission.



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4.3. Generality and persistence of the phenomenon

Additional research showed that the effects of degrading sweet taste–calorie relations on body weight gain are not specific to saccharin but are also obtained when 0.3% Acesulfame Potassium (AceK), a non-nutritive sweetener with a chemical structure that is distinct from saccharin. AceK has been employed in a variety of sweetened beverages including Diet Coke with Splenda, Diet Pepsi Lime and Diet Pepsi Vanilla, Minute Maid Light, and Dasani and Aquafina sweetened waters. In one study [19], three groups of adult male rats were given 23-h access to 30 g of low-fat, unflavored yogurt each day in addition to ad libitum chow for 14 days; on 7 days, plain yogurt was provided while sweetened yogurt was provided on the other 7 days with order of presentation quasi-randomized. As in our previous studies, the yogurt was sweetened with 20% glucose for one group and was sweetened with 0.3% saccharin for a second group. Extending our earlier research, body weight gain for these groups was compared to a third group that received yogurt sweetened with 0.3% AceK. Fig. 4 shows that while body weight gain over the 14 days of training differed little for rats given saccharin-sweetened relative to those given AceK-sweetened yogurt, both of these groups gained significantly more weight than the group given yogurt sweetened with glucose. A similar pattern of results with the same statistical outcome was obtained in another study (see Experiment 2, [19]) that compared body weight gain for rats given only 1-h access to yogurt sweetened with saccharin, AceK, or glucose (data not shown).





Fig. 4. Body weight gain was significantly greater in rats given yogurts sweetened with saccharin or AceK compared to rats given yogurts sweetened with glucose (ns = 8 per group). *p < 0.05 compared to AceK and Saccharin.

Adapted from [19]. Used with permission.



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We also compared the persistence of body weight differences following the discontinuation of the yogurt supplements sweetened with saccharin or glucose. Following 14 days of training with daily 1-h access to 20 g of plain or sweetened yogurt, presentation of the yogurt supplements was discontinued and body weight gain was measured for an additional 2 weeks. Replicating our previous findings, body weight gain during the period when the yogurt supplements were presented was significantly greater for rats that ate saccharin-sweetened compared to glucose-sweetened yogurt (Fig. 5A). In addition, body weight gain after yogurt presentation was terminated did not differ among these groups (Fig. 5B) indicating that body weight differences that emerged during prior training with yogurt persisted over the course of the subsequent two-week period without yogurt.







Fig. 5. Body weight gain was significantly greater during 2 weeks exposure (A) to saccharin-sweetened yogurt compared to glucose-sweetened yogurt. Following discontinuation of yogurt access (B), animals in the saccharin-sweetened group failed to compensate for the prior excess weight gain (n = 13 per group). *p < 0.05 compared to Glucose.

Adapted from [19]. Used with permission.



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4.4. Reversibility of the effects of non-nutritive sweeteners on weight gain

We also assessed the effects of reversing the predictive and non-predictive relationships on weight gain and energy intake. Specifically, using a factorial design, we compared the effects on body weight gain of shifting adult, male, rats trained with saccharin-sweetened diets to diets sweetened with glucose (saccharin–glucose) and vice-versa (glucose–saccharin) and compared these groups to unshifted (saccharin–saccharin and glucose–glucose) controls. In addition, the sweeteners were presented mixed not only with plain yogurt, but in separate groups, mixed with refried beans (pilot work established that rats would readily consumed both sweetened and unsweetened refried beans). For all rats, training occurred with one base diet (yogurt or beans) and testing occurred with the other. Because the base diets were shifted from training to test for all groups, differences in body weight for the shifted versus unshifted sweetener conditions could not be attributable changes in the base diet. The training and test phases were each 2 weeks in duration, and daily 23-h access to 30 g of the base diet, plain on half the days and sweetened on the other half, were presented in quasi-randomized order.



The results of the training and test phases are presented, collapsed across the yogurt and refried bean base diets, in Fig. 6 and Fig. 7, respectively. Confirming our previous findings, the results of training (Fig. 6) showed that weight gain was significantly greater for rats that consumed saccharin-sweetened compared to glucose-sweetened base diets. Furthermore, shifting from a base diet sweetened with glucose to one sweetened with saccharin was followed by a significant increase in weight gain relative to the unshifted glucose–glucose control. In fact, weight gain for the glucose–saccharin shifted group achieved the level of the unshifted saccharin–saccharin control group by the end of the testing. In contrast, shifting from a saccharin- to a glucose-sweetened base diet (Fig. 7) produced little change in body weight gain relative to the unshifted saccharin–saccharin control. Thus, the results of this experiment showed not only that the effects on body weight of exposure to a non-predictive sweet–calorie relationship (as a result of training with saccharin) are persistent, but also that they are difficult to reverse when a predictive sweet–calorie relation is established by training with glucose.





Fig. 6. During exposure to yogurt or refried bean diets sweetened with saccharin, body weight gain was significantly greater compared to the same base diets sweetened with glucose (ns = 12–14 per group).

Adapted from [19]. Used with permission.



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Fig. 7. Body weight gain in all rats given saccharin-sweetened yogurt or refried beans was significantly greater compared to animals given access to glucose-sweetened diets (ns = 12–14 per group).

Adapted from [19]. Used with permission.



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5. Thermogenesis: a potential physiological mechanism

It is well-established that food intake elicits a reflexive cephalic phase thermogenic response in both human and non-human animals. This form of heat production appears to be mediated, in part, by orosensory stimuli that precede and signal the absorption of nutrients in the gut. In humans when food is tasted but not swallowed, as well as in dogs allowed to taste food but not digest it, the thermogenic response to the oral stimulation produced by food has been reported to exceed that produced by a meal that is ingested normally [28]. Alternatively, when nutrients bypass the oropharyngeal cavity (e.g., via feeding tube) cephalic phase thermogenic responses for both humans and dogs are either not observed or much weaker than those produced by normal feeding [29] and [30]. These responses, along with other cephalic phase reflexes (e.g., hormonal, gastric and exocrine), are generally thought to perform anticipatory functions that prepare the GI tract for the arrival of nutrients, increase the efficiency of nutrient utilization, and minimize the degree to which those nutrients perturb homeostasis by producing positive energy balance [17], [31] and [32].



One component of this thermogenic response is an increment in core body temperature, the magnitude of which is determined primarily by the energy content of the food [33] and [34]. If sweet tastes evoke thermic responses based, in part, on the degree to which they predict the arrival of calories in the gut, one might expect that tasting a sweet, high-calorie food would evoke a greater increase in core body temperature for rats that have been exposed to a highly reliable predictive relationship between sweet tastes and calories compared to rats that for which sweet taste is a less reliable signal for calories. One implication of this hypothesis is that if consuming non-nutritive sweeteners reduces the validity of sweet taste as a signal for calories, then one effect of consuming these sweeteners would be a reduced ability for sweet-tasting foods to evoke increments in core body temperature.



We tested this prediction by implanting miniature radio-frequency transmitters in the abdominal cavity of 16 adult male rats to allow us to measure remotely changes in core body temperature immediately before, during, and after the rats consumed premeals and test meals that contained nutritive or non-nutritive sweeteners [21]. During training, rats received 30 g of a low-fat, plain yogurt daily for 14 days in addition to ad libitum lab chow and water. As in our earlier studies, the yogurt was sweetened on a quasi-random half of the training days, and was unsweetened on the remaining days. For half of the rats, the sweetener used was always saccharin, whereas glucose was the sweetener for the other rats. When training was complete, all the rats were tested following overnight food deprivation with a premeal of 5-g thickened Chocolate Ensure Plus. During training and testing temperature was recorded at 1-min intervals.



Fig. 8A shows core temperature data during the first 60 min after presentation of sweetened and unsweetened yogurt, averaged across all training sessions, for rats that received yogurt sweetened with glucose. Comparable data for rats that received yogurt sweetened with saccharin are shown in Fig. 8B. The results indicate that while intake of yogurt sweetened with glucose produced a larger and more sustained increment in core temperature relative to unsweetened yogurt, consuming yogurt sweetened with saccharin did not have this effect. This is not surprising given that the energy content of glucose-sweetened yogurt was substantially greater than for unsweetened yogurt, whereas the energy content of saccharin-sweetened and unsweetened yogurt were the same. However, this pattern of results indicated that our measures of core temperature were consistent with previous reports showing that energy density is an important determinant of the thermic effect of food [35].





Fig. 8. Increases in core body temperature across 2 weeks of exposure to plain, unsweetened yogurt and yogurt sweetened with glucose (A) or saccharin (B) (ns = 6–8 per group). *p < 0.05 compared to unsweetened yogurt.

Adapted from [21]. Used with permission.



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Of greater interest are the results from when the rats in the glucose-trained and saccharin-trained groups were tested with a common novel, sweet, and high-calorie supplement, Chocolate Ensure Plus. We reasoned that compared to the rats trained with glucose, rats trained with saccharin should exhibit a weaker thermic response to the sweet taste of the Ensure. That is because, for those rats, prior consumption of sweet, non-nutritive saccharin should have reduced the ability of sweet taste to predict calories and thus, should have reduced the ability of sweet taste to evoke increments in core temperature. This prediction was confirmed (see Fig. 9). That is, the increment in core temperature that occurred for the saccharin group was significantly smaller than that for the glucose group when both groups were tested with same novel sweet-tasting diet. These results suggest that experience with non-nutritive sweeteners may perturb at least one physiological mechanism involved with energy regulation, in a manner that was anticipated with a theoretical framework based on Pavlovian conditioning [21].





Fig. 9. Increases in core body temperature following a premeal of a novel, sweet diet were significantly higher in animals with previous experience consuming glucose-sweetened yogurt diets compared to animals with previous experience consuming saccharin-sweetened yogurt diets (ns = 6–8 per group). *p < 0.05 compared to saccharin group.

Adapted from [21]. Used with permission.



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6. Sweet taste–caloric relations: fluids

6.1. Caloric compensation

As noted in Section 1, much of the concern about the effectiveness using non-nutritive sweeteners as a method of weight control stems from epidemiological studies that indicate a link between body weight gain and the consumption of diet beverages. We have also used our animal model to investigate this link.



As an initial test of this idea, Swithers [18] assigned juvenile male and female rats (∼ 35 days old) to one of two groups. The first group (Consistent) experienced two sweet diets that contained calories — 10% sucrose and 10% glucose (w/v). The second group of rats (Inconsistent) experienced one caloric sweet diet, 10% glucose, and one non-caloric sweet diet, 0.3% saccharin. All diets were flavored with 0.1% grape or cherry Kool-Aid. The order of presentation of the diets and the Kool-Aid flavor associated with each diet were counterbalanced across litters. The rats were given 5 days of training where a fluid supplement was offered for 24 h, then removed and replaced with the alternative supplement. Following this training, the rats were food-deprived overnight, then given a small (10 g) preload of a novel, sweet-tasting, and high-caloric premeal of Rich Chocolate Ensure Plus® to consume for 1 h. One hour after the end of this premeal period, intake of their regular rat chow diet was assessed.



Analogous to our account for the data obtained with semi-solid foods, our hypothesis was that rats in the Inconsistent group would compensate less well for the sweet-tasting preload compared to rats for which sweet taste was a consistent predictor of calories (i.e., the Consistent group). The results showed (see Fig. 10) that although intake of the premeal did not differ between the groups, subsequent chow intake for the Inconsistent group was significantly greater compared to the Consistent group, for which sweet taste was a highly reliable signal for calories. These data indicate that inconsistent experiences with sweet tastes and calories may have impaired compensation for the calories in the sweet premeal.





Fig. 10. In juvenile rats given experience with Inconsistent relations between sweet taste and calories (glucose and saccharin solutions), chow intake following a novel, sweet premeal was significantly greater compared to juvenile rats given previous experience with Consistent relations between sweet taste and calories (glucose and sucrose solutions; n = 10 per group). *p < 0.05 compared to Consistent group.

Adapted from [18]. Used with permission.



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6.2. Food intake and body weight gain

In addition to data showing that exposure to sweet, but non-nutritive fluids may increase short-term intake by impairing caloric compensation, very recent studies in our laboratories have assessed the effects of such exposure on food intake and body weight gain. In one study, adult male rats were assigned to one of two groups, matched on ad libitum body weight. One group was given water sweetened with 10% glucose (n = 16) and the other was given water sweetened with 0.3% saccharin (n = 13). The solutions were presented overnight for ten consecutive days. Each rat received 10 ml of its sweetened solution for the first 2 days, after which they were given 20 ml of the solution on each of the next 8 days. The rats were also given free access to lab chow and water throughout the experiment. Body weight and amount of lab chow consumed were recorded for all rats on days 1, 5, and 10 of this period.



Fig. 11 shows mean body weight for the groups given saccharin or glucose solutions on the day immediately before, and 1, 5, and 10 days after the solutions were presented. Mean daily intake of lab chow is shown for each group over the same period in Fig. 12. The results indicate that the rats given the saccharin solutions both gained weight significantly more rapidly and ate significantly more chow overall than the rats given the glucose solution.







Fig. 11. Body weight gain was significantly greater in rats (n = 13–16 per group) following 10 days exposure to saccharin solutions compared to glucose solutions. *p < 0.05 compared to saccharin.

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Fig. 12. Chow intake was significantly greater during 10 days exposure to saccharin solutions compared to 10 days exposure to glucose solutions (n = 13–16 per group). *p < 0.05 compared to saccharin.

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6.3. Stevia solutions have effects on body weight gain similar to saccharin solutions

Recently, sweeteners extracted from the leaves of the Stevia rebaudiana plant have been introduced as “natural” non-nutritive sweeteners in the U.S. market. Like the “artificial” sweeteners AceK and saccharin, stevioside is reported to be significantly sweeter than sugar (250 to 300 times). To assess the generality of the effects of consuming saccharin solutions on body weight gain that we found in the preceding study, we gave one group of adult male rats access to a 30–50 ml of a solution of Stevia extract (Steviva) mixed in water (0.1% w/w) overnight for 15 days and compared body weight gain for this group with that of rats given the same type of exposure to 0.3% saccharin or 10% glucose solutions (n = 18 for each group). Lab chow and tap water were available throughout the experiment. Weight gain for rats given Stevia and those given saccharin did not differ significantly any point during this training (Fig. 13). In contrast, by the end of 15 days of exposure weight gain for each of these groups was significantly greater than that for the group given the glucose solution. Thus, just as the effects on body weight gain of consuming semi-solid yogurt mixed with non-nutritive sweeteners are not specific to saccharin, the results of this study support the same conclusion when sweet, non-nutritive solutions are consumed.





Fig. 13. Body weight gain was significantly greater in animals consuming either saccharin solutions or Stevia solutions compared to animals consuming glucose solutions (n = 18 per group). *p < 0.05 compared to saccharin or Stevia.

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7. Summary and conclusions

The research reported here provides an answer to the question “Can consuming non-nutritively-sweetened foods or fluids promote increased energy intake and body weight gain compared to sugar-sweetened foods and fluids?” In principle, the answer clearly seems to be yes. Using a rodent model, we found that intake of foods or fluids containing non-nutritive sweeteners was accompanied by increased food intake, body weight gain, accumulation of body fat, and weaker caloric compensation, compared to consumption of foods and fluids containing glucose. Our research also provided evidence consistent with the hypothesis that these effects of consuming saccharin may be associated with a decrement in the ability of sweet taste to evoke thermic responses, and perhaps other physiological, cephalic phase, reflexes that are thought to help maintain energy balance. Furthermore, our studies were generated within a theoretical framework provided by Pavlovian conditioning, and the results we obtained seem readily interpretable within a mechanistic approach that integrates fundamental concepts from learning and physiology. Thus, the claim that there is no viable mechanistic explanation of how intake of non-nutritive sweeteners could promote weight gain can be repudiated.



However, it is always possible to question whether any “in principle” demonstration, obtained with an animal model, under well-controlled laboratory conditions, can shed light on factors that are currently promoting excess energy intake and body weight gain in the much more complex and uncontrolled human food environment. Yet, despite this complexity, it is plausible, if not probable, that (a) both human and non-human animals rely on learning about the relationship between the sensory properties of foods and their nutritive postingestive consequences to help maintain energy balance; and (b) consuming diets in which the orosensory properties of foods and beverage are not strongly predictive of their caloric consequences can disrupt energy regulation. Thus, it is conceivable that just as exposure to non-predictive sweet taste–calorie relationships in the laboratory promotes increased intake, body weight and body adiposity in rats, the widespread use of non-caloric sweeteners by humans outside of the laboratory may have similar effects on the predictive validity of sweet tastes and ultimately on the ability of humans to control their intake and body weight.

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