Carbohydrate Mouth-Rinses Activate Brain Areas Involved in Visual Perception & Reward - Are There Implication For Athletes & Obese Individuals You Need to Know?

CHO Mouth rinsing? Cyclist do it, but they do a lot of things ;-)

You know what a "mouth-rinse" is, right? That's when you wash some sort of liquid "through" your mouth and spit it out without swallowing. Over the past years, I have probably read a dozen of papers on this topic and although I did not keep exact record, I am pretty sure that six of them presented positive results (meaning the carbohydrate mouth-rinse increased performance), while the other six reported a null-result (no performance increase).

The former is also the main reason I did not address this topic in any previous articles in detail. A couple of days ago, I hit on a study that made me reconsider my previous decision that the contemporary evidence would suggest it's not really worth talking or rather writing about carbohydrate mouth rinses.

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The study is about to be published in the renowned pee-reviews scientific journal "Appetite" and it is the first study to replace the performance measures (physical or cognitive ones) with neuroimaging... with intriguing results, as I may say.

The good old mantra is that you ingest carbs, they are absorbed, your blood glucose levels increases and all sorts of good an bad things happen. In the course of the whole diabesity debate, here at the SuppVersity, you have already learned that this is not just an oversimplification - if it's not seen in perspective, it's simply false. Still, before the publication of the study at hand, we had only little experimental evidence of the impressive downstream effects of sweet taste receptors in the mouth.

The data Turner et al. present in their latest paper, appear to confirm that there is in fact a hitherto mostly overlooked energy signalling pathway capable of improving human performance that's triggered by the presence of carbohydrates in the mouth.

Figure 1: Performance increases (power output) observed in response to serial carbohydrate mouth rinsing during a cycle sprint - data from one of the most recent studies (Phillip. 2014)

The scientists from the University of Auckland believe that this pathway may form part of homeostatic energy systems that govern and promote feeding behaviour via the transduction of information specific to energetically-useful nutrients (Sclafani. 2004); and - as mentioned before - this pathway has already been shown to enhance corticomotor output (Gant. 2010) - the data in Figure 1 is only from one of the latest studies.

Table 1: Overview of the study results Jeukendrup et al. reviewed in their most recent overview of the literature (Jeukendrup. 2010)

Ok, the results may be inconclusive, and the dependence on exercise duration or other confounding parameters may be under-researcher, but the observed benefits are there. Being in the range of 2-4% they may seem "insignificant" (from a practical perspective, not a statistical one; see Table 1), but 4% more mileage during 1h cycling, that's worlds apart - at least in the in the world of the pro cycling. In short, The ameliorating effects CHO mouth rinses have had on the observed declines in motor function in previous studies was associated with reduced fatigue significant enough to provide a neural basis for enhancements in motor performance observed in many behavioural studies (Jeukendrup. 2010).

The protocol of the study at hand is complex, but in essence, it should suffice to know that the subjects, 10 healthy volunteers, had "mouth-rinse" with either carbohydrate (CHO) or - this is important! - a taste-matched placebo (PLA) solution in a double- blind, counterbalanced study. As the scientists point out, "[t]his protocol eliminates post-oral factors and controls for the perceptual qualities of solutions", and guarantees that the functional magnetic resonance imaging of the brain  identifies only those cortical areas which are actually responsive to oral carbohydrate during rest and activity phases of a hand -grip motor task.

Figure 2: Effect of carbohydrate on brain activity. Group level contrast images displaying areas of activation from the contrast CHO > PLA (Turner. 2014)

In particular, the scientists measure that the mean blood-oxygen-level dependent signal change experienced in the contralateral primary sensorimotor cortex was larger for CHO compared to PLA during the motor task when contrasted with a control condition. Now what's interesting is that the differences were observed not just in those areas of which we know already that they belong to the primary taste cortex.

In fact, another region that was heavily involved in the CHO mouth-rinse response was the area of the brain that's usually responsible to process visual perception, as well as regions deep down in the the limbic system that have been previously associated with reward.

How is a performance enhancing mouth rinse done? Let's take a look at the study with the largest performance leap, i.e Pottier et al. (2008):

The total rinsed/ingested amount of the solution was set at 14 mL/kg body weight and the subjects were instructed to "rinse" equally distributed over the course of the time trial. The actual rinsing lasted for 5s, afterwards the liquid hat to be spit out. The drink that was used was standard Gatoratde with 5.4 g sucrose, 0.46 g glucose, 41.7 mg Na 1 , 12.5 mg K 1 , citric acid, salt, sodium citrate, natural flavor and the other "Gatorade-ish" additives that are in there though no-one wants or needs 'em.

Bottom line: The observation of difference in both, the areas that are responsible for visual perception and the reward center are relevant for both, athletes and gymrats who are increased in maximal performance (think of a tennis player who need maximal visual acuity and enough dopamine (reward) to perform!) and overweight individuals.

The latter usually don't need a heightened visual acuity, of course. The lack of reward ... or rather their constant struggle for food-rewards on the other hand is a massive problem. In this context the superiority of the CHO vs. the artificially sweetened mouth-rinse shines a whole new light on the "diet products for weight loss debate?" and could rekindle a discussion about the timing of the measurement the dopaminergic / brain / reward response to these foods - the latter could be "instant" and any study measuring the effects in the postprandial phase may miss the most important, immediate, taste-receptor-mediated effects completely.

Plus: You want to learn more about artificial sweeteners of food reward, click on the links (RSS compatible browser required)!

References:

• Gant, Nicholas, Cathy M. Stinear, and Winston D. Byblow. "Carbohydrate in the mouth immediately facilitates motor output." Brain research 1350 (2010): 151-158.
• Jeukendrup, Asker E., and Edward S. Chambers. "Oral carbohydrate sensing and exercise performance." Current Opinion in Clinical Nutrition & Metabolic Care 13.4 (2010): 447-451.
• Phillips, Shaun M., et al. "The Influence of Serial Carbohydrate Mouth Rinsing on Power Output during a Cycle Sprint." Journal of sports science & medicine 13.2 (2014): 252.
• Pottier, Andries, et al. "Mouth rinse but not ingestion of a carbohydrate solution improves 1‐h cycle time trial performance." Scandinavian journal of medicine & science in sports 20.1 (2010): 105-111.
• Sclafani, Anthony. "The sixth taste?." Appetite 43.1 (2004): 1-3.
• Turner, Clare E., et al. "Carbohydrate in the mouth enhances activation of brain circuitry involved in motor performance and sensory perception." Appetite (2014).

Sucralose, Hazardous or Innocent? Part II: Appetite, Gut Health & Food Reward | Sucralose, Gluttony & Adiposity?

Plain mineral water is still the best thing to quench your thirst.

Today we are going to continue our thorough, educated reading of the recently published overview over the biological issues with sucrolase, a "popular" artificial sweetener most of you will probably know by its brand name Splenda. The focus of part I of this series was on the potential pro-diabetic effects of this agent that belongs to a class of molecules that has originally been hailed as a solution to the diabetes problem (it goes without saying that I am talking about artificial sweeteners here, right?). In a way we are thus only continuing the discussion, when we are trying to verify Schiffman's & Rother's argument that the consumption of sucralose is associated with an increase in obesity risk... or, put more simply that using sucralose is going to make you fat, not lean.

The good old "energy in" vs. "energy out" argument

As SuppVersity readers you are well aware that the oversimplified concept of an "energy balance" is fundamentally flawed. My recent post "Anorexia study suggests: Your body can easily reduce its resting metabolic rate by 10%" in the SuppVersity Facebook News is only one out of thousands of scientific papers you could quote to point out that replacing 420kcal of energy from pure sugar, i.e. three cans of regular coke, with its diet variety is not going to produce a net weight, let alone fat loss of 420g per week (suggested read: "Busting the 3,500kcal = 1lbs Weight Loss Myth!" | learn more).

This is part II of a multi-part series:

Sucralose, insulin, glucose, GLP-1

Appetite, Obesity & Gut Health

Cancer, Drug & Hormone Interact.

I know that Mark Sisson likes to says this, but this website is not written by a machine, but by a man who has the same "short" 24h days you have... basically, what I am trying to say is that I had to split this review of the review into a "trilogy" - and be honest, you wouldn't want an article thrice as long as this one, would you?

Thus being "in the know", you can only shake your head, when you read how Schiffman and Rother (ab-)use a recent study by Ruyter et al. (2012) to support the non-significant, not sufficiently differentiated data from epidemiological studies which inform us that obese people are more likely to consume artificial sweetened products than lean ones, to subliminally imply that artificial sweeteners would not help, in some cases even hinder weight loss.

"In an 18-mo trial with children, participants were randomly assigned to receive an 8-oz can per day of either a noncalorically sweetened or a sugarsweetened beverage that provided 104 kcal (de Ruyter et al., 2012). [...] The calorie consumption from these beverages was 46,627 kcal greater for children in the sugar-sweetened group than in the sucralose-sweetened group (5.8 × 77.3 × 104). In spite of this highly significant difference in calories consumed from the beverages, the total weight gain over this 18-mo study was only 1 kg greater for children in the sugar-sweetened group compared to sucralose group. No explanation was provided to account for the small difference in weight gain given the large difference in caloric consumption from the beverages." (Schiffman. 2013)

Despite the fact that Schiffman & Rother acknowledge that the scientists would not have been able to detect, if the children who consumed the sugar-sweetened beverages compensated by reducing their food intake, the reviewers fail to point out that neither this, nor the second "evidence" they cite, a 2-year study by Ebbeling et al. (2012), where Schiffman & Rother simply ignore the fact that the mere provision of diet sodas to the families of the adolescent subjects did reduce the weight gain in the active intervention period (1st year, see Figure 1, below), would confirm a negative real-world effect on body weight.

Figure 1: Change in body fat percentage (vs. basleline) of adolescents during the intervention & follow up period in the Ebbeling study (2012), of which the reviewers only cite the results of the follow up.

Let's be honest: If you actually take a look at the results from the Ebbeling study (Figure 1), you will have to concede that this study refutes the claim that artificial sweeteners make you fat. During the active treatment period, in the course of which the adolescent participants were...

• 

  "What Really Happens, When Nutrition Science Meets Real Life" | more

  ... supplied with noncaloric beverages (e.g., bottled water and “diet” beverages for the whole family) every 2 weeks, getting monthly motivational telephone calls with parents (30 minutes per call), 
• ... having three check-in visits with participants (20 minutes per visit), and 
• ... receiving written intervention messages with instructions to drink the delivered beverages and not to buy or drink sugar-sweetened beverages, were mailed to participants

...they do exactly what we originally expected them to do: They ameliorate the body fat gain in the adolescent subjects. In other words: As long as respective products are available, and dietary adherence is encourages, replacing regular sugar sweetened with artificial sweetened or unsweetened beverages can have a significant ameliorative effect on the body fat gains of adolescents - irrespective of the fact that they were obviously free to compensate with chocolate, cookies, etc..

Contemporary evidence from RCTs suggest either no, or beneficial effects

If you follow Schiffman's and Rother's lead and discard potential differences between sucrose and other sweeteners, acknowledge the fact that the results from previous rodent experiments have repeatedly failed to translate to human beings and take into account that this data is "inconsistent and conflicting" (Schiffman. 2013), anyways, you will be hard pressed to find arguments to support the claim that artificial sweeteners could hinder weight loss.

"No-Carb Foods, Artificial Sweeteners & The Cravings" | more

Potential mechanisms for the obesogenic effects: In a very detailed review Mattes & Popkin list a whole host of hypothesis ranging from the disproven stimulation of insulin and differences in the GLP-1 response, over osmotic effects and increase food palatability, up to the "Zero sugar, great, I'll have 10 instead of one of those cookies!" effect and the development of an extremely sweet tooth. What's important, though, is that none of this mechanisms is "supported by the available evidence, although some warrant further consideration" (Mattes. 2009).

In fact, the vast majority of RCTs clearly supports the assumption that non-nutritive sweeteners (NNS), artificial or not, promote weight loss and blunt weight (re-)gain (De la Hunty. 2006; Bellisle. 2007). The argument that these effects do satisfy the calories in vs. calories out hypothesis is pathetic, to say the least. Even a 100% controlled diet won't comply to an equation that is about as accurate as "1+2=343". We can thus register that:

1. There is ample evidence to support the beneficial effects of artificial sweeteners (including sucralose) as a tool during controlled dietary interventions.
2. There is insufficient evidence to support the claim that their regular consumption has a negative effect on body weight.

With respect to (2) we would even have to say that the limited amount of useful* evidence we have would rather suggest beneficial than detrimental effects (*a 'useful' study is not a study that tells me that obese individuals are more likely to consume artificially sweetened products than lean ones like the often cited epidemiological data). This is particularly true, for controlled interventions where sugar-sweetened beverages were replaced by their artificially sweetened counterparts.

The great unknown: Hunger, appetite and food reward

If data on the real-world effects of sucralose consumption on body weight gain is "scarce", consistent, experimentally verified hypotheses that would explain the potential underlying mechanism are quasi non-existent... or, I should clarify: They are still in their infancy. Against that background it's quite astonishing that more and more people appear to take it for granted that the consumption of artificially sweetened foods will mess with both, (a) your ability to control your energy intake and (b) the hedonistic response you derive from foods.

Table 1: Sweetness, dose to stimulate the sweet taste receptor (EC50; based on Matsuda. 2011) and correlation of sweetness and EC-50 value.

It goes without saying that there is no sucralose-specifc data out there, but the decrease in hypothalamic sweet taste receptor density I mentioned in the first installment of this series is something I'd expect to see in response to all artificial sweeteners that make it across the blood brain barrier (Note: Even Schiffman & Rother acknowledge that we do not know if they even do that!) - probably "sweetness" dependent,  by the way.  This would imply that sucralose would be the worst, cyclamate the least offender among the common artificial sweeteners in Table 1. With a sweetness that's 300x higher than that of sucrose, stevia would end up being the "(un?)happy medium".

Despite the fact that Schiffman & Rother don't really address this issue in their paper, I still want want to address the practical and thus relevant aspect of the various proposed theories for potential sweetener-induced increases in energy consumption.

Figure 2: Mean effective change in energy intake (%) in RCTs investigating the degree of energy compensation in response to the provision of artificial sweetened products (De la Hunty. 2006)

As the data from De La Hunty's 2006 meta-analysis of 32 study outcomes in Figure 2 clearly demonstrates, there is a statistically highly significant (p < 0.001) trend towards reduced energy consumption in the RCT [randomized controlled trial]. In that, the degree of compensation for the sudden energy reduction due to ingestion of calorically less dense, since artificially sweetened product ranged from statistically non-significant 18% to statistically highly significant 86% in trials such as Porikos et al. (1982), where 6 men lost and gained 0.8kg of body weight within 2x12 days in a metabolic ward on artificially sweetened and sucrose sweetened ad-libitum diets, respectively.

Non-nutritive sweetener (NNS) intake 1965-2004 (Mattes. 2009)

So, sweeteners can't ever make you hungry? I would not necessary subscribe to this idea. While the consumption of artificial sweetened foods as part of your regular diet, e.g. diet coke with your dinner, does not seem to be a problem, Mattes & Popkin (2009) rightly point out that "non-energy-yielding products may heighten appetite", when they are not "ingested in conjunction with other energy sources". So, if you are guzzling diet coke all day, this may very well trigger binge eating. With an ever increasing consumption of sweeteners from partially / totally artificially sweetened beverages (see table to the left), this could thus well be part of our obesity problem.

Just like the previously discussed (relatively short term) effects on insulin, GLP-1 and co, the #2 on the list of most frequently heard objections against the use of artificial sweeteners, i.e. dietary overcompensation, does thus appear to have little basis in fact. What we do not know, though, is whether the results will be identical for all types of sweeteners, or whether sucralose may be the toxic (this aspect will be covered in the next installment) or gut microbiome disrupting exception to the rule.

Sucralose induces changes in the gut microbiome

The last issue I want to address in this second installment of the "Sucralose, Hazardous or Innocent Trilogy" will thus revolve around the question, whether a modulatory effect of sucralose on the microbial composition of your gut could induce potential negative long-term effects that would not show up in the hitherto discussed RCTs.

Under the headline "Effect of Sucralose on the Number and Relative Proportions of Different Intestinal Bacterial Types", Schiffman & Rother argue that it has long been known that bacteria from the oral cavity and soil cannot use sucralose as a growth substrate. If the same was true for the bacteria in our guts the replacement of regular sugar with sucralose would thus starve our (beneficial) subtenants.

Table 2: Differences (%) in bacterial counts in feces of rodents on diets containing what in human terms would be ~14mg, 43mg, 71mg and 156mg of sucralose per day after 12 weeks treatment and 12 weeks into "recovery" (Abou-Donia. 2008)

Based on the fecal bacterial count of rodents on diets that would be equivalent to 14mg, 43mg, 71mg and 156mg of sucralose per day in human beings (see Table 2), Schiffman & Rother argue that chronic (12-week) ingestion of relatively low amounts of sucralose (a single can of Diet Crush Cream Soda, for example, has 42mg of sucralose) lead to highly significant reductions in the numbers of total anaerobes, bifidobacteria, lactobacilli, Bacteroides, clostridia, and total aerobic bacteria.

In view of the fact that Abou-Donia et al. (2008) observed the most significant losses in bifido- and lactobacillus strains, i.e. those strains that have repeatedly been implicated as the driving forces of the beneficial health effects of probiotic supplementation, this and not the previously discussed pro-diabesity effects should be the point where people start to freak out.

Table 4: Other sweeteners are preferred food for certain bacteria and may also alter the gut microbiome (Payne. 2012).

This is particularly true if you take into account that at least part of the beneficial effects of lactobacilli may be related to their ability to keep the number of enterobacteria, a large family of Gram-negative bacteria that includes both harmless symbionts, as well as a whole host of familiar pathogens, such as Salmonella, Escherichia coli, Yersinia pestis, Klebsiella and Shigella, Proteus, Enterobacter, Serratia, and Citrobacter in check (Liévin-Le Moal. 2006) - exactly those bacteria, which produce the nasty lipo polysaccharides (LPS) that have been associated with inflammation and its downstream metabolic effects, such as obesity, diabetes, heart disease, gastrointestinal cancer etc. and, as the data in Table 2 tells you. Now, unfortunately, the these villains are all part only type of bacteria that was not significantly decimated by the sucralose challenge.

As Schiffman et al. point out these reductions are not, as Brusick et al. (2009) suggest simply a result of "normal variation". In fact, the probability to see a similar random reduction in bifidobacterial count occur "naturally"within 12 weeks would be 1/5000. It is thus more than just unlikely that the71.9%, 76%, and 77.7% reductions in bifidobacteria counts Abou-Donia et al. observed at dosages of 3.3, 5.5, and 11 mg/kg/d were coincidental.

Prebiotics, anyone? In view of the alleged neg. effects on your gut microbiome, you may feel inclined to increase your prebiotic intake. If that's the case, this top 10 list of food items with prebiotic fiber contents of up to 65% of total weight may help:

1. Chicory root - 65%
2. Jerusalem artichoke - 32%
3. Dandelion greens - 24%
4. Garlic - 18%
5. Leek - 12%
6. Onion - 9% 
7. Cooked Onion - 5% 
8. Asparagus - 5% 
9. Wheat bran - 5% 
10. Banana - 1% 

Remember: These are the "richest" not necessary the "best" sources ;-)

If there is reason to be concerned it's about your gut health and its downstream metabolic effects: In view of the important role of bacteroides for the health of the intestinal eco-system (Lee. 2013) and their persistent reduction even after the 12-week recovery period, the selective antibiotic activity of sucralose is as of now the by far most disconcerting negative health effect discussed in this series.

If the changes Abou-Donia et al. observed in their rodent studies were to be confirmed in human studies, where the subjects consumed a balanced whole foods diet with a high prebiotic content. The profound changes the researchers from the Duke University Medical Center report in their paper from September 2008 would be reason enough to revise my previous conclusions about a potential contribution of sucrose to the diabesity (=obesity + diabetes) epidemic.

In fact, a revision of the potential long(er) term downstream effects of sucralose on your metabolic health could be all the more indicated, if it turns out that the alleged toxic and endocrine-disrupting effects I will discuss in the next installment of this series turn out to be substantiated, as well.

Reference:

• Abou-Donia, M. B., El-Masry, E. M., Abdel-Rahman, A. A., McLendon, R. E., & Schiffman, S. S. (2008). Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. Journal of Toxicology and Environmental Health, Part A, 71(21), 1415-1429.
• Bellisle, F., & Drewnowski, A. (2007). Intense sweeteners, energy intake and the control of body weight. European Journal of Clinical Nutrition, 61(6), 691-700.
• De la Hunty, A., Gibson, S., & Ashwell, M. (2006). A review of the effectiveness of aspartame in helping with weight control. Nutrition Bulletin, 31(2), 115-128.
• de Ruyter, J. C., Olthof, M. R., Seidell, J. C., & Katan, M. B. (2012). A trial of sugar-free or sugar-sweetened beverages and body weight in children. New England Journal of Medicine, 367(15), 1397-1406.
• Ebbeling, C. B., Feldman, H. A., Chomitz, V. R., Antonelli, T. A., Gortmaker, S. L., Osganian, S. K., & Ludwig, D. S. (2012). A randomized trial of sugar-sweetened beverages and adolescent body weight. New England Journal of Medicine, 367(15), 1407-1416.
• Liévin-Le Moal, V., & Servin, A. L. (2006). The front line of enteric host defense against unwelcome intrusion of harmful microorganisms: mucins, antimicrobial peptides, and microbiota. Clinical Microbiology Reviews, 19(2), 315-337.
• Mattes, R. D. (1996). Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiology & Behavior, 59(1), 179-187.
• Mattes, R. D., & Popkin, B. M. (2009). Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms. The American journal of clinical nutrition, 89(1), 1-14.
• Payne, A. N., Chassard, C., & Lacroix, C. (2012). Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity. Obesity Reviews, 13(9), 799-809.
• Porikos, K. P., Hesser, M. F., & Van Itallie, T. B. (1982). Caloric regulation in normal-weight men maintained on a palatable diet of concentional foods. Physiology & behavior, 29(2), 293-300.
• Schiffman, S. S., & Rother, K. I. (2013). Sucralose, A Synthetic Organochlorine Sweetener: Overview Of Biological Issues. Journal of Toxicology and Environmental Health, Part B, 16(7), 399-451. 

No-Carb Foods, Artificial Sweeteners & The Cravings: In The End, It's The Glucose, Not The Taste Our Brains Crave

Despite the fact that candy is per definition (literally) made of sugar, you can buy "no carb candy" at every corner. The results of this study tell you why these aren't worth the money.

I have written extensively about artificial sweeteners in the past and would thus hope that it's not necessary to recount all the information about how they interact with insulin, potential toxicity risks, their (non-existent) effects on satiety... ah, well actually I do want to talk about the last point, because it is highly relevant to understand the implications of the results of recent Yale study (Tellez. 2013).

I know, it's just a rodent study, but I guess you will feel reminded of yourselves during your diet, when I tell you about the observations Luis A Tellez, Xueying Ren, Wenfei Han, Sara Medina, Jozelia Ferreira, Catherine Yeckel and Ivan E de Araujo made an experiment that is the first to demonstrate that the lack of glucose utilization in the brain makes artificial sweetener totally unattractive to mice.

Did you ever realize that sweeteners just won't cut it, when you're hungry?

Many of you may know that: You are dieting and you are craving - food in general, but pasta, candy and all the other carbohydrate-laden foods even more so. You've been training hard and feel that your blood glucose levels are right in the no-man's land between "just high enough to keep standing" and "already so low that you have to sit down". This is the time when you will begin to feel cold. You are sweating or getting shaky (these symptoms vary from person to person), get moody or feel like you had to run even more just to abstain from doing the one thing of which you know that it would solve all your problems (temporarily): Heading over to the kiosk next door and buying the next best Snickers or Mars bar.

Yes, Adelfo Cerame is a professed, but reformed carbophobic. Learn more about how reintroducing carbs into his diet finally got him his pro-card in this and his other guest posts

The poor critters in the study Tellez et al. conducted did not have a kiosk available. What they did have, though, was glucose and artificially sweetened water. Now, the scientists conducted the same experiment in two conditions.

• During condition one, the rodents were fed, satiated and happy (fed). 
• During condition two, however, they had been glucose deprived and were in a similar state as you may have been after the previously described workout. 

What's quite telling (and by the way new) is that the glucose availability had a major impact on their sweetener preferences. When fed and happy, the mice went for the super-sweet sugar- and calorie-free artificially sweetened water.

The disgustingly sweet but glucose-free water did however lose all its appeal once the mouse brains realized that the glucose supply was becoming tight:

"Consistently, hungry mice shifted their preferences away from artificial sweeteners and in favour of glucose after experiencing glucose in a hungry state." (Tellez. 2013)

And what's more, this deliberate(?), or probably instinctive, decision to turn their back on the fake sugars and avail themselves of the "real sweet deal" of which they new it would deliver what the mice needed was immediately rewarded. Rewarded in the most physiological sense of the word: with a whopping dose of dopamine, the very hormone that entrains stimulus < > response relationships like these.

Sugar will increase dopamine, sweeteners won't

You can tell how real this "conditioning" effect was from another observation the researchers made, when they analyzed the brain activity of their lab animals and found that a big gulp from the sugar water did not just bring the blood glucose of the sugar-deprived animals back up, it

"was [also] found to produce significantly greater levels of dopamine efflux compared to artificial sweetener in dorsal striatum" (Tellez. 2013)

When the scientists artificially disrupted the oxidation of glucose directly at the level of the dorsal striatum, which is also known as the neostriatum or striate nucleus that is activated by stimuli associated with reward and aversive, novel, unexpected, or intense stimuli, the sweetness preferences of the mice remained the same. This observation directly supports the conclusion that we are in fact dealing with a fundamental food-reward effect here; and effect, of which you can be certain that is is also involves in "past addiction" ;-)

So what does this tell you about fake foods?

Suppversity highly suggested read: "Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | read more

As the researchers themselves point out, their results demonstrate that glucose oxidation controls the intake levels of "sweet tastants"  (=umbrella term for everything that stimulates the sweet taste receptors) by modulating the extracellular dopamine levels in dorsal striatum.

For you, this means that you know better than believe that you could get away with that low carb, sugar free candy bar, chewing gum or whatever else it may be that you are using to soothe your sweet tooth you are effectively cheating yourself. It works only in conjunction with your free will to avoid the carbs and usually only for so long as you allow yourself planned and controlled refeeds.

Note: When you are in full ketosis, things may be different; although the effects of ketones on dopamine levels are - afaik - not well researched, yet.

Let's finally try to draw some more general conclusions about carbohydrate intake in general - I mean beside the real sweet stuff, like candy, etc. Let's take the no-carb noodles you or hopefully not you, but your obese neighbor just bought, for example. They may taste just like the real deal. In the absences of the (expected) subsequent influx of glucose and its oxidation in the brain, they will yet never provide the hedonic response you are looking for. They are fake, a good one that may fool the first line of nutrient sensors, but a fake that's not good enough to reproduce the expected downstream effects on neurotransmitters.

Now, the good news is: No-carb noodles are probably non-addictive. The bad news, however, is: No-carb noodles are also highly, or I should say utterly unsatisfying replacement for real pasta, because the lack of carbohydrates, or rather the glucose that would get oxidized right in your brain, when you consume a bowl of real pasta is the critical physiological signal that makes pasta what it is: A highly addictive comfort food. For the average pasta junky, a "no-carb noodle" is thus never going to cut it, unless he or she is willing to cure him- or herself of her sugar addiction first.

---

SuppVersity suggested read: "Coke vs. Diet Coke vs. Milk - The "Unhealthy Beverage Shoot-Out": Milk Reduces, Coke Increases Visceral Fat. Dreaded Diet Coke on Par With Plain Water" | read the complete article

Bottom line: Unlike "zero carb candy" or "no-carb noodles" an effective "diet aid", or let's rather say, one of the foods you should select, whenever you are trying to rid yourself of body fat (low GI starches, fruits and even vegetables (*I write "even" because the amount of carbs in some veggies borders zero)) can offer this "second line" effects in your brain; effects, none of the fake foods you buy at the supplement store, the super market and as of late even some kiosks will ever be able to produce. These real foods are the ones that will have you feel satisfied and they are the ones that should make up more than just the figurative lion's share of your diet - not the calorie, carbohydrate and nutrient free no-carb noodles and their low-carb brethren that will just have you crave the "real deal" even more.