Can MCTs Help You Lose Weight Yes They Can! Latest Meta Analysis Says MCTs Safe But Not Super Effective

Yes, coconut oil does contain MCTs, but it is not as some people believe pure MCT. Only ~50% of the fat in coconut oil is actually in MCT form. If you want pure MCTs you have to resort to specific MCT supplements / oils.

The mechanisms by which medium-chain triglycerides (MCTs) may help you to lose fat are manifold. They are not only hard to store for your body. They also counteract fat deposition in adipocytes by increasing thermogenesis and satiety.

MCTs contain 8 to 12 carbon atoms and include caprylic acid (C8:0, octanoic acid), capric acid (C10:0, decanoic acid), and lauric acid (C12:0, dodecanoic acid). Foods high in MCTs include coconut oil (58%), palm kernel oil (54%), desiccated coconut (37%), and raw coconut meat (19% of total energy) (USDA). Average intakes of 1.35 g/day (0.7% of total energy intake | USDA. 2008) MCTs have been reported in the United States and 0.2 g/day in Japan | Kasai. 2003).

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MCT is cleaved into glycerol and medium-chain fatty acids in the gut lumen.5 The medium chain length makes a smaller, more soluble molecule compared with a longchain fatty acid, giving it a preferential absorption and metabolic route in the body. As the authors of the latest meta-analysis of the effects of MCTs on body weight say:

"[t]his physicochemical nature of medium-chain fatty acids allows them to pass into the portal vein on route to the liver to be rapidly metabolized via b oxidation with no requirement of reesterification in intestinal cells, incorporation into chylomicrons, or the rate limiting enzyme carnitine acyltransferase for intramitochondrial transport. In comparison, long-chain fatty acids have a slower route, being re-esterified in the small intestine and transported by chylomicrons via the lymphatic and vascular system before being oxidized for energy or stored. Thus, rapid metabolism of MCTs reduces their opportunity of adipose tissue uptake." (Mumme. 2015)

Several human intervention studies have been conducted investigating the weight-reducing potential of MCT, with mixed results. In their latest meta-analysis, Mumme et al. set out to separate the wheat from the chaff in order to answer the question whether MCTs, specifically C8:0 and C10:0, provide significant weight loss benefits and/or trigger changes in body composition compared to "regular" long-chain fatty acids (LCT).

Figure 1: Meta-analysis for changes in body weight (in kilograms) in randomized control trials that compared dietary medium-chain triglycerides (MCTs) with a longer-chain triglyceride (control) shows a favorable effect of MCT intervention on body weight. *Oleic acid as control. **Myristic acid as control. #Body mass index < 23. ##Body mass index > 23. IV inverse variance. SD standard deviation (Mumme. 2015).

The researchers primary outcome measures were body mass, waist and hip circumference, total body fat, and subcutaneous and visceral fat. Secondary outcomes were blood lipids, including triglycerides (TG), total cholesterol, high-density lipoprotein (HDL) cholesterol, and LDL cholesterol. Of the latter the foremost values are those that are of greatest interest and among them the body mass shows a measurable, albeit not earth-shattering reduction in almost all trials. Only the in the 2001 study by Matsuo et al. there was an increase in body weight in response to an MCT supplement that contained almost no medium chain triglycerides.

No, you wont lose slabs of body fat by adding MCTs to your diet! Unless, the satiety effect of MCTs makes you eat less on other meals, you are going to gain body fat by adding MCTs to your diet, because you are effectively increasing the total amount of energy in your diet - Dont be stupid.

Figure 2: Meta-analysis for changes in total body fat, total subcutaneous fat, and visceral fat (Mumme. 2015).

In view of the fact that the most relevant obesity parameters, i.e. the waist and hip circumferences and body fat percentages (Figure 2) dropped in all studies that investigated this parameter and considering the fact that there were no significant deterioration - rather improvements - in blood lipids, it appears warranted to assume that the replacement (!), but not the addition, of 2g/day MCTs (1% of the energy) to 54 g/day MCTs (20% of the total energy intake)  over a duration of 4 to 16 weeks leads to measurable and potentially health relevant weight loss, compared to bacon, butter & co, i.e. regular long chain fatty acids.

Bottom line: With an average weight loss of 0.51 kg (range 0.80 to 0.23 kg) over an average 10-week period, the weight loss may be marginal. In conjunction with similarly marginal, but measurable reductions in waist and hip circumferences, total body fat, subcutaneous fat, and visceral fat and in the absence of significant changes in blood lipids, even this amount of weight may be health relevant. Hamman,et al. were after all able to show that even marginal reductions in body weight (1kg) are associated with a 16% reduced type II diabetes risk in - albeit only in obese subjects (Hamman. 2006).

Trying to gain weight? Learn more in the Overfeeding Overview | go for it!

What MCTs are not, though, is the weight loss wonder as some people appear to believe they were. If you dont stop stuffing yourself with long-chain fatty acids and replace the latter with MCTs in your diet its unlikely that you are going to see any results.

Since the benefits also appear to decline with baseline body weight, buying tons of expensive and by no means delicious MCTs is probably a useless undertaking for 95% of the SuppVersity readers | Comment on Facebook.

References:

• DeLany, James P., et al. "Differential oxidation of individual dietary fatty acids in humans." The American journal of clinical nutrition 72.4 (2000): 905-911.
• Hamman, Richard F., et al. "Effect of weight loss with lifestyle intervention on risk of diabetes." Diabetes care 29.9 (2006): 2102-2107.
• Kasai, Michio, et al. "Effect of dietary medium-and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans." Asia Pacific journal of clinical nutrition 12.2 (2003): 151-160.
• Mumme et al. "Effects of Medium-Chain Triglycerides on Weight Loss and Body Composition: A Meta-Analysis of Randomized Controlled Trials." EAT RIGHT - Research Review (2015).
• US Department of Agriculture. Nutrient Intakes From Food: Mean Amounts Counsumed per Individual, One Day, 2005-2006. Washington, DC: US Department of Agriculture, Agricultural Research Service; 2008.

Amino Acid Supplement With High Amount of Isoleucine Increases Clearance of Dextrose Supplement But Impairs Post Workout Glycogen Resynthesis in Man Implications

Post-Workout High Isoleucine AA+CHO Decreases Glucose Spikes, But Impairs Musclular Glyocogen Resynthesis - Reason Enough to Skip Amino Acids?

If you put any faith into the promises of the supplement industry, amino acid supplements are the solution to all your problems - including those you havent even known about, yet. Against that background its always interesting if scientists study the real world effects of amino acid supplements in a realistic scenario like after strenuous exercise.

In their latest study Wang and colleagues from the University of Texas at Austin and the Shanghai Research Institute of Sports Science did just that: They studied the effects isoleucine and four additional amino acids, on blood glucose homeostasis and glycogen synthesis after strenuous exercise.

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As the scientists point out, the results of their study "could provide a practical and safe means of increasing the rate of muscle glycogen synthesis after exercise and enhancing the rate of recovery" (Wang. 2015).

Table 1:  Subjects’ characteristics (Wang. 2015).

Ten healthy active adults volunteered for the study. All subjects were accustomed to cycling for prolonged periods of 3–5 h during an exercise session. The ,aximum oxygen uptake (VO2max) was measured in all subjects on a cycle ergometer by using a TrueOne 2400 metabolic measurement system (ParvoMedics, Sandy, Utah) to verify adequate aerobic fitness levels (results see Table 1).

Figure 1: Basically the AA supplement contained almost exclusively isoleucine. It was administered in the dosage shown above and at twice that amount in the LAA and HAA trials (Wang. 2015)

"Two to three days after the VO2max test, the subjects reported to the laboratory to perform a practice ride to familiarize them with the laboratory environment and the experimental protocol. The practice ride was also used to adjust and verify appropriate workloads for the experimental trials. The practice rides simulated the protocol ride but without blood samples or muscle biopsies being taken. The ride consisted of cycling at 70 % VO2max for 2 h, which was followed by five 1-min sprints at 85 % VO2max. The sprints were separated by 1 min cycling at 45 % VO2max. During the first 15 min of each hour, oxygen uptake was measured for 5 min to verify workload.

Water (250 mL) was provided every 20 min of exercise. Heart rate (HR) was monitored and ratings of perceived exertion (RPE) on a Borg-scale (ranging from 6 to 20) were collected every 30 min of exercise. The practice ride and each of the following three experimental trials were separated by a minimum of 7 days and maximum of 12 days" (Wang. 2015).

The actual tests consisted of cycling on an ergometer to deplete muscle glycogen. Blood sampling and a muscle biopsy were performed immediately on cessation of exercise. After the muscle biopsy, subjects were given the first of two supplement doses. More specifically they received either...

• 1.2 g carbohydrate/kg body weight (CHO), 1.2 g carbohydrate/kg body weight plus 6.5 g AA (CHO/LAA) or 
• the same carbohydrate supplement plus 6.5g (CHO/LAA) or 13 g AA (CHO/HAA) 

immediately after the first muscle biopsy and at 120 min of recovery. The carbohydrate base consisted of simple dextrose dissolved at a ratio of 100g/296 mL in an orange flavored drink (SUN-DEX, Fisher Healthcare, Houston, Texas). The additional amino acids contained 0.046 g cystine 2HCl, 0.023 g methionine, 0.045 g valine, 6.342 g Isoleucine, and 0.044 g leucine per person, or twice that amount in the CHO/HAA trial. The amino acids were simply added to the dextrose drink.

Why would you even believe that there may be benefits from AA supplementation?

As Wang et al. point out, "this amino acid mixture was selected as it was previously reported to be more effective in lowering the blood glucose response to a glucose challenge than isoleucine alone" (Wang. 2015) by Bernard et al. (2011).

Figure 2: Blood glucose AUC during the oral glucose tolerance test (OGTT). Sprague-Dawley rats were gavaged with either glucose (CHO), glucose plus a 5-amino acid mixture (CHO-AA-1), glucose plus a 5-amino acid mixture with increased leucine concentration (CHO-AA-2), or placebo (PLA). Blood was taken from the tail immediately before the gavage and 15, 30, 60, and 120 min afterward (Bernard. 2011).

The three test beverages were similar in color, taste, and texture to allow a double-blinded and counter-balanced study design. All test drinks were randomly assigned and dispensed by a laboratory technician who was not involved in the data collection.

Figure 3: Blood glucose postexercise and during the 4-h recovery. Treatments were with CHO (circle), CHO/LAA (triangle), and CHO/HAA (filled circle) supplements provided immediately after and 2 h after exercise. Values are mean ± SE. CHO/HAA vs. CHO (*p < 0.05). CHO/LAA vs. CHO (# p < 0.05) - left; Blood glucose area under the curve (AUC) during the 4-h recovery. Treatments were CHO, CHO/LAA, and CHO/HAA supplements provided immediately after and 2 h after exercise. AUC was calculated with baseline (pre). Values are mean ± SE. CHO/HAA vs. CHO (*p < 0.05). CHO/LAA vs. CHO (# p < 0.05) - right (Wang. 2015).

As the data in Figure 3 indicates,There was a similar effect in humans as it has previously been observed in rodents. An effect of which you as a SuppVersity reader know that it is probably mostly ascribable to isoleucine (see "The Glucose-Repartitioning Effects of Isoleucine" | more).

Glucose modulation without glycogen optimization?! How does that work? Well, obviously glucose can also be oxidized or used to replete ATP in the muscle. It is at least no real news that isoleucine will decrease glucose levels in the blood and increase glucose uptake in the muscle without, however, producing increased glycogen levels. For example, Doi et al. (2005) reported that an oral administration of 1.35 g/kg isoleucine in food-deprived rats significantly decreased the plasma glucose concentration and increased glucose uptake in the muscle of rats without an increase in muscle glycogen storage.

Figure 4: Total muscle glycogen storage in the vastus lateralis during the 4-h recovery from intense cycling. Treatments were CHO, CHO/LAA, and CHO/HAA supplements provided immediately after and 2 h after exercise. Values are mean ± SE. CHO/HAA vs. CHO (*p < 0.05 | Wang. 2015)

What is a bit disappointing is the fact that the decrease in blood glucose did not come with an increase in glycogen storage.

As the data in Figure 4 shows, the exact opposite was the case. After 4h of recovery the muscle glycogen levels were not higher, but lower in the amino acid supplemented trials.

For diabetics this wouldnt be a problem. For athletes its yet clearly a disadvantage that the 4-g recovery glycogen levels were lower and significantly lower in the low and high dose amino acid supplement trials.

Eventually this result is surprising because specifically in the high amino acid group (a) the insulin levels, (b) the AS160, a protein that controls insulin mediated glucose uptake, (c) the mTOR & p-AKT levels, (d) the "exercise hormon" levels of serum irisin  and (e) the levels of glycogen synthase which stores carbs in forms of glycogen in the high dose AA trials were significantly elevated.

Bottom line: While the study at hand did confirm that isoleucine (in conjunctio with other, but probably irrelevant amino acids) will improve the glucose response to high GI carbohydrates, it did not confirm the assumption that this makes isoleucine the ideal intra- and/or post-workout amino acid to optimize glycogen synthesis and thus post-workout recovery. For diabetics the increase in insulin and the corresponding decrease in glucose response still is a major plus. This assumes that the insulin increase occurs in the obese (in previous studies by Wang et al. (2012) an increased insulin release to a high isoleucine AA mixture was not observed) and / or that there is an independent effect of the amino acid mixture on glucose uptake in the muscle or the periphery.

In contrast to the high isoleucine amino acid supplement that was used in the study at hand, plain whey protein does increase glycogen storage after workouts - significantly, as the data Ivy et al. generated in a 2004 randomized controlled human study involving well-conditioned subjects observed (Ivy. 2004).

For athletes, however, it appears to be detrimental as it reduces the rate of muscle glycogen synthesis after workouts and puts a questionmark behind the "repartitioning effects" of amino acids - if there is a repartitioning effect involved, here, it would be away from the glyocogen stores of your muscle. An effect that may be related to the increase in mTOR which triggers protein synthesis via p70S6k which inactivates the glycogen synthase kinase-3 (Armstrong. 2001). This would indicate that you cannot have both maximal protein & glycogen synthesis and thus relativize the obvious conclusion that isoleucine supplements are not suitable for athletes. What it wont do, though, is to provide the missing evidence that amino acid supplements have an advantage over whey, which has been shown to increase glycogen synthesis and storage (Morifuji. 2005, 2010; Zawadzki. 1992; Ivy. 2002, 2008) - why would you use AAs, then? | Comment on Facebook!

References:

• Armstrong, Jane L., et al. "Regulation of glycogen synthesis by amino acids in cultured human muscle cells." Journal of biological Chemistry 276.2 (2001): 952-956.
• Bernard, Jeffrey R., et al. "An amino acid mixture improves glucose tolerance and insulin signaling in Sprague-Dawley rats." American Journal of Physiology-Endocrinology and Metabolism 300.4 (2011): E752-E760.
• Doi, Masako, et al. "Isoleucine, a potent plasma glucose-lowering amino acid, stimulates glucose uptake in C2C12 myotubes." Biochemical and biophysical research communications 312.4 (2003): 1111-1117. 
• Ivy, John L., et al. "Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement." Journal of Applied Physiology 93.4 (2002): 1337-1344.
• Ivy, J. L., et al. "Post exercise carbohydrate–protein supplementation: phosphorylation of muscle proteins involved in glycogen synthesis and protein translation." Amino acids 35.1 (2008): 89-97.
• Morifuji, Masashi, et al. "Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats." British journal of nutrition 93.04 (2005): 439-445.
• Morifuji, Masashi, et al. "Post-exercise carbohydrate plus whey protein hydrolysates supplementation increases skeletal muscle glycogen level in rats." Amino acids 38.4 (2010): 1109-1115.
• Wang, Bei, et al. "Amino acid mixture acutely improves the glucose tolerance of healthy overweight adults." Nutrition Research 32.1 (2012): 30-38.
• Zawadzki, K. M., B. B. Yaspelkis, and J. L. Ivy. "Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise." J Appl Physiol 72.5 (1992): 1854-9.

Sweet But Not Innocent! The Fattening Effects of the Non Nutritive Sweeteners Erythritol Aspartame Are On Par With Equally Sweet Sugar Water

I just hope that todays SuppVersity article is not going to cause scenes like this, because when it all said and done it may be less likely, but not impossible that it is (for whatever vexed reason) still aspartame that caused the negative effects observed in the study at hand.

It is one of the recurring motifs here at the SuppVersisty and at the same time one of the most popular issues of dispute in the health and fitness community: The Obesogenic Effects of Artificial Sweeteners. Or, in plain English, the question  

"Can I use Sucralose, Aspartame and Acesulfam-K without taking the risk of getting fatter - not leaner, as I actually intended?"

For all three of the explicitly mentioned agents human studies clearly suggest that the answer is "Yes, you can!" And I will now dare saying that the of the most recent study from the Oita University in Japan are not going to change that - as long as you use them instead of carbs in your diet the said zero-calorie sweetener are going to help not block weight loss.

So why did the mice in the Mitsutomi study get obese then?

By anticipating the most important conclusion, I have made things easy for us, after all the only questions we still have to answer are:

• Why did the mice in the Mitsutomi study get obese?

• Is it possible that this is an erythritol-specific effect?

It would appear as it it could not be all too difficult to answer the first question. It was after all part of the research interests of the Japanese scientists, so that you would expect it to be answered in the discussion of their result. Well, lets see then, ...

Exactly what the energy drinks promise, the sugar water got the rats "on sucrose" going: They were >40% more active than their peers - without caffeine as you may notice (Mitsotomi. 2013)

"Compared with sucrose supplementation, NNS supplementation decreased the serum glucose level. Interestingly, compared with the control treatment, NNS supplementation increased the serum insulin level in mice with DIO. In addition, NNS administration influenced glucose tolerance compared to controls.

These observations suggest that NNS supplementation induced insulin resistance by increase of tissue triglyceride, although some NNSs are used to control hyperglycemia.

NNS supplementation increased the WAT leptin level in DIO mice in the present study.

It is possible that the high leptin level was related to body adiposity. Indeed, NNS administration increased the weight of epididymal fat. Thus, it is possible that the high leptin level was related to the influence on body adiposity." (Mitsotomi. 2013)

No, I dont see an explanation, rather a concise summary of the results, that tells us that the addition of plain sugar (33%)  to the drinking water did - as the scientists already expected - lead to a decrease in food intake and an increase in obesity and its nasty unhealthy side effects.

Figure 1: Differences in food intake & body composition of mice with 33% sucrose and 4% erythritol + aspartame in the drinking water (left) expressed relative to control w/ plain water, histology of lover (top) and white adipose tissue (WAT, bottom) of mice with regular (control) and sucrose respectively NNS drinking water (Mitsotomi. 2013)

Much to their own surprise, Mitsotomi et al. did also observe that the group that received the "non-nutritive sweeteners" as a 4% solution (99% of which were erythritol and 1% was aspartame) in their drinking water got exactly as fat (see Figure 1), had a slightly less pronounced increase in adipocyte size, and experienced a similar fatty acid deposition in the liver (NAFLD). And as if that had not been bad enough, there were also pathological changes in the "fat burning brown adipose tissue" (BAT) of the rodents in the NNS group - a physiological deterioration, Mitsotomi et al. observed exclusively in the erythritol + aspartame goup.

Figure 2: Leptin resistance (in WAT) and the major downregulation in UCP-1 (in BAT; both left) are candidates of which the researchers believe that they were responsible for the visible defect (right) in the BAT architecture (Mitsotomi. 2013)

Lets be honest, if you take another look at the BAT histology in Figure 2 (right) even you as a non-expert will see that there is a major difference between the meshed BAT in the rodents on the control diet and the messy BAT of the NNS group, compared to which the brown fat cells of the sugar guzzlers still look very healthy.

Remember: All this mess happened in the absence of an increase in calorie intake

Just to make this clear: This is not the first study to show that artificial sweeteners can have obesogenic effects in rodent models. In contrast to Naismith et al. (1995) and Blundell & Hill (1986) who observed a "pradoxical effects" of  artificial sweeteners on the appetite of their lab rodents, the rats in the study at hand did not overeat, though! They also moved about as much as their peers in the control group and still got fat and sick.

Want to change your "Fat-o-type"? Work out! | read more

In other words, the weight gain the Japanese researchers recorded was neither a result of a mismatch between energy intake and expenditure nor the consequence of a promotional effect of artificial sweeteners on the "sweet tooth" of the rodents. Rather than that it was either brought about or accompanied and promoted by the impairment of the thermogenic capacity of the brown adipose tissue, of which you can argue, based on histologies in Figure 2 that the brown adipose tissue of the furry "subjects" of this study was not just functionally, but also structurally compromised by the ingestion of the non-nutritive sweeteners.

The defective brown adipose tissue (BAT) and the correspondingly reduced UCP 1 expression (UCP increases mitochondrial uncoupling in BAT and burns off energy to increase the body temperature), led to a significant reduction in oxygen consumption. With the latter being a direct marker of fatty acid oxidation the it is difficult to say which came first, the defect in BAT or the onset of obesity. What we can say for sure, though, is that the defective BAT had its share in the rapid weight gain and the corresponding metabolic deterioration.

This could be an erythritol specific effect

Despite the fact that Mitsotomi et al. did not address the potential influence the type of artificial sweetener they used, it is not unlikely that the use of erythritol, of which I have seen dozens of toxicity studies, but no long(er) term feeding studies in a potentially obesogenic diet scenario, could explain the unexpected study outcome. So: "Is this an erythritol specific effect?"

An advantage of erythritol is that it has almost the same sweetness profile as sugar (sucrose), but is 30-40% less sweet (de Cock. 2012)

Without further studies, it is obviously not possible to answer this question, it does however not appear to be unlikely that it were the 99% of erythritol in the commercial erythritol + aspartam mixture the researchers used in their study thats to blame for the obesogenic effects. If this was a general NNS effect, a similar impairment of the brown adipose tissue and corresponding increases in body, muscle and liver fat should after all have been observed in previous studies, already. To my knowledge these studies do not exist - specifically not for aspartame. Without speculating about unpredictable interactions within the two we are thus left with erythritol as out only culprit.

While erythritol has only 60% to 70% of the sweetness of sucrose (comparing 10% solutions in water; this means you need much more of it to achieve a similar sweetness) it has an almost identical sweetness profile (no "off" tastes; cf. de Cock. 2012). This is not the only reason both scientists and the food industry are fond of the low-calorie sweetener. Its rather the combination of its gut- and tooth-friendliness that makes it such a valuable addition to everything sweet. So, despite the fact that it does share the the anti-caries effects with sugar alcohols like xylitol, it is so easy on the gut that its use is not restricted to chewing gums and other "food" items that need only marginal amounts of sweeteners to achieve the desired degree of sweetness. If you want to sweeten larger amounts of foods / beverages, erythritol is thus the sugar alcohol of choice

There is evidence that suggests aspartame reduces insulin - at least during workouts | learn more

Why dont you suspect aspartame? The reason that I am scrutinizing erythritol and not aspartame is simple. Despite or rather because of all the hoopla around potential toxic effects of aspartame it is one of the best researched artificial sweeteners and evidence for obesogenic effects in the absence of increases in food intake are simply non-existent. It may thus make this article more popular among the high number of aspartame haters out there, but it would not help us understand the experimental results,if I started lamenting about how Coke and Pepsi are trying to kill us.

If you take a peak at the Wikipedia article and many scientific papers, you will learn that erythritol has been shown to be mostly (90%) absorbed before the chyme enters the colon (Bernt. 1996). The non-negligible rest of the erythritol  (10%), on the other hand, is said to pass through the short and long intestine, where it is generally believed not to fermented by the gut bacteria (Arrigoni. 2005).

The cholesterol increase scientists observed in response to a high sucralose diet is another of the many yet not fully understood side effects of artifical sweeteners | learn more

In view of a more recent study by Beards et al. (2010) it is however more than questionable that this assumption for which researchers usually cite the in vitro results Arrigoni et al. presented in a 2005 paper is accurate.

Beards and her colleagues from the University of Reading in the UK were after all able to show that erythritol is not simply excreted undigested. Rather than that it is fermented and leads to changes in the bacterial composition and a 6.25x increase in acetate production.

In view of the beneficial effects of SFCA (acetate, propionate and butyrate) on the production of satiety hormones this certainly appears to be a good thing. From studies by Patil et al. we do however know that chronically high SCFA levels and decreased relative bacteroides levels are characteristic of features of human obesity (Patil. 2012; see Angelakis. 2012, as well).

If we include the comparatively short timespan (24h) in the course of which the said changes in the bacterial composition and acetate production in the Beards study occured and assume that this may, after days of constant erythritol exposure have destabilized the previous "ecosystem" in the gut, it does not appear too far fetched to assume that the rodents may have suffered from weight gain and all sorts of metabolic deterioration as a consequence of the potential lactobacilli + Atopobium overgrowth in response to the erythritol in their drinking water.

By now it should no longer appear totally odd to assume that neither artificial sweeteners per se, nor the "bad bad" aspartame are to blame for the "fat effects" the researchers observed in the study at hand, right? I mean, of all the three short chain fatty acids, butyrate, acetate and propionate, acetate is the one with the weakest antiobesogenic effects (Lin. 2012) and in view of the fact that it is preferentially used as a substrate for de novo lipogenesis (=deposition of fat) in colonocytes, hepatocytes and adipocytes (Samuel. 2008), both the fatty liver and the 172% increase in body fat could be explained by the constant influx of acetate from a dysbiotic gut - right?

Suggested Read + Podcast: "he Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | read more

Reason to be afraid - yes or no?"It could be possible...", these are the four little words that would have to go before each and every of the sentences in this conclusion. It could be possible that the interaction of erythritol with the gut microbiome of the rodents drove the accumulation of lipids in the liver, which would in turn have lead to the development of insulin and leptin resistance and could have compromised the function of the "fat burning brown adipose tissue" of our furry friends. The latter could have sped up the weight gain and may eventually explain why the mice in the "non-nutritive sweetener" group were by no means better off than their similarly obese peers in the sucrose group.

Despite the fact that it could also be possible that similar negative effects on the accumulation of liver and whole body fat would be observed in humans, the failure of the brown adipose tissue wouldnt be much of a problem for us, a species that has long lost most of its brown fat stores (learn more). Against that background and in view of the fact that Id hope that no one of you follows a 60% fat, 20% carbohydrate diet and tries to sooth his / her sweet tooth with 2-3l of erythritol + aspartame sweetened water per day, Id suggest you refrain from freaking out until we do have more compelling evidence that the stress hormones you will be producing are not more harmful than the few mg of sugar alcohols in your protein bars.

References:

• Angelakis E, Armougom F, Million M, Raoult D. The relationship between gut microbiota and weight gain in humans. Future Microbiol. 2012 Jan;7(1):91-109.
• Arrigoni E, Brouns F, Amadò R. Human gut microbiota does not ferment erythritol. Br J Nutr. 2005 Nov;94(5):643-6. 
• Beards E, Tuohy K, Gibson G. Bacterial, SCFA and gas profiles of a range of food ingredients following in vitro fermentation by human colonic microbiota. Anaerobe. 2010 Aug;16(4):420-5.
• Bernt WO, Borzelleca JF, Flamm G, Munro IC. Erythritol: a review of biological and toxicological studies. Regul Toxicol Pharmacol. 1996 Oct;24(2 Pt 2):S191-7. Review.
• Blundell JE, Hill AJ. Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet 1986;1(8489):1092–3.
• de Cock P. Erythritol. In "Sweeteners and Sugar Alternatives in Food Technology". 2nd edition. Ed. ODonnell & Kearsley. Wiley. 2012.
• Lin HV, Frassetto A, Kowalik EJ Jr, Nawrocki AR, Lu MM, Kosinski JR, Hubert JA, Szeto D, Yao X, Forrest G, Marsh DJ. Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. PLoS One. 2012;7(4):e35240. 
• Mitsutomi K et al. Effects of a nonnutritive sweetener on body adiposity and energy metabolism in mice with diet-induced obesity. Metabolism. Oct. 2013 [ahead of print]
• Naismith DJ, Rhodes C. Adjustment in energy intake following the covert removal of sugar from the diet. J Hum Nutr Diet 1995;8:167–75.  
• Patil DP, Dhotre DP, Chavan SG, Sultan A, Jain DS, Lanjekar VB, Gangawani J, Shah PS, Todkar JS, Shah S, Ranade DR, Patole MS, Shouche YS. Molecular analysis of gut microbiota in obesity among Indian individuals. J Biosci. 2012 Sep;37(4):647-57.
• Samuel BS, Shaito A, Motoike T, Rey FE, Backhed F, Manchester JK, Hammer RE, Williams SC, Crowley J, Yanagisawa M, Gordon JI. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41. Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16767-72.
• Sell H, Deshaies Y, Richard D. The brown adipocyte: update on its metabolic role. Int J Biochem Cell Biol 2004;36: 2098–104.