The Latest Gut Microbiome Modulators: Beneficial Effects of Cacao, Negative Effects of Acidic Water and Preliminary Evidence of the Negative Impact of Gluten & Whole Grains

Pancakes al cacao & your gut: Bad grains and good cacao?

There is an increasing amount of interesting scientific publications on the role of the gut microbiome in health and disease. Unfortunately, the evidence on what exactly influences the number and types of bacteria in our gut in a beneficial way and even what exactly a "beneficial way" actually is, is yet largely unknown.

In today's installment of the SuppVersity Short News, I am going to take a closer look at a selection of recent studies that may shed at least some light at the previously mentioned questions.

You can learn more about the gut & your health at the SuppVersity

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

• Cacao as a gut microbiome modulator - The first study we're going to look at deals with cacao. Cacao and its effect on the gut microbiome. In said study, 3-week-old Wistar and Brown Norway rats were fed, for 4 weeks, either a standard diet or the following three isoenergetic diets containing increasing proportions of cocoa flavonoids from different sources: one with 0·2 % polyphenols (from conventional defatted cocoa), and two others with 0·4 and 0·8 % polyphenols (from non-fermented cocoa, very rich in polyphenols).
  
  

  

  Only the regular theobromine containing cacao did also reduce the weight gain in the three-week study (Massot-Cladera. 2014).

  What the scientist found, when they analyzed the serum Ig concentrations, faecal IgA levels, microbiota composition and IgA-coating bacterial proportion at the end of the study and compared them to those at the beginning was a significant beneficial effect on the mucosal IgA levels and microbiota composition from all supplements. The 0.2 % cacao diet which contained a higher proportion of theobromine and fibre, however, had a more profound impact on the aforementioned parameters - in spite of the fact that there was less cacao in the diet. Obviously, the caffeine-like bitter alkaloid from cacao is contributes to the beneficial effects of cacao in a similar way as the polyphenols.
  
  As the body weight data in Figure 1 shows, the theobromine containing conventional cacao was also the only one that was able to reduce the diet induced weight gain in the rats. This could, but does not necessarily have to be related to the higher levels of Bacteroides, Bifidobacterium and Lactobacillus bacteria in the gut of the rodents that received the "cheap" conventional cacao.
• Acidic water triggers type I diabetes - probably by modulating the gut microbiome - No, I am not trying to advertise bicarbonate, here. I am just reporting the results of a recent study from the Medical University of South Carolina which found that a stain of mice that's particularly susceptible to type I diabetes developed insulitis and hyperglycemia rapidly, only when the mice were maintained on acidic pH water (AW).
  
  

  

  Suggested Article: "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals! Causative or Corollary? Plus: Are Grains, not Meats the Main Offenders in Our Diet?" | read more.

  The scientists also observed that this effect could be countered by fecal transplants and was obviously triggered by changes in the diversity of the gut flora that occurred, when the pH of drinking water was in the acidic range and were probably related to the proinflammatory cytokine response in the intestinal mucosa.
  
  As you as a SuppVersity reader know previous studies in humans have already shown that a "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals!" (read more) - Who knows, this could also be related to the effect on the gut microbiome!?
• Gluten and whole grains as modulators of the gut microbome - In two recent randomized cross-over trials, researchers from the University of Copenhagen determined the impact of dietary gluten or whole grains on the gut microbiome and host metabolic health.
  
  What the researchers found was what the recent backlash against gluten and "healthy" whole grains on the internet would suggest the already overweight "[p]articipants had slightly elevated fasting glucose levels and increased waist circumference" (Ibrügger. 2014).
  

  

  Table 1: Overview of the products used in the randomized controlled cross-over trials (Ibrügger. 2014)

  Whether that's related to the effects on the gut microbome is unfortunately something I can't tell you, yet. Why? Well, the currently available paper refers to a future publication that would outline the detailed results. All I can tell you now is that the study used the products listed in Table 1 and, more importantly, that it is its high statistical power, which, due to the large sample size and the crossover design, "allows detecting even small diffrences in the outcome variables" (Ibrügger. 2014).

Suppversity Suggested: "Stevia Kills Good Gut Bacteria - One Study Enough to Stop Using the Natural Sweetener? Probably Not in View of its Anti-Diabetes, Anti-LDL, Anti-Viral & Anti-Cancer Effects" | more

Bottom line: It's a pity that we still can't tell for sure what the "optimal" gut microbiome looks like. Moreover, the currently available scientific evidence suggests that what is considered "optimal" may well depend on your type of diet and / or your metabolic health.

Against that background the previously presented results offer nothing but a brief glimpse at what may become one of the hottest topics in obesity and diabetes prevention in the future. At the moment, though, all the results and any recommendations that are based on these results have to be considered preliminary. And this is also true for the gluten + whole grain study of which you will certainly read again, here at the SuppVersity | Comment on Facebook!

References:

• Ibrügger, S., et al. "Two Randomized Cross-Over Trials Assessing the Impact of Dietary Gluten or Wholegrain on the Gut Microbiome and Host Metabolic Health." J Clin Trials 4.178 (2014): 2167-0870.
• Massot-Cladera, Malen, et al. "Impact of cocoa polyphenol extracts on the immune system and microbiota in two strains of young rats." British Journal of Nutrition 112.12 (2014): 1944-1954.
• Sofi, M. Hanief, et al. "pH of drinking water influences the composition of gut microbiome and type 1 diabetes incidence." Diabetes 63.2 (2014): 632-644.

Weight Loss Supplements Exposed: Green Tea & Probiotics. Fat Loss, Energy Expenditure, Fat Oxidation, Sex & More

Yesterday at Starbucks: "I just ordered a bottle of probiotics!"

In view of the fact that all the feedback I got in response to the re-installment of the Short News was positive, I guess you won't mind if I use the chance and bundle the two soon-to-be-published weight loss studies from the British Journal of Nutrition into a Weight Loss Supplement Mini-Special of the SuppVersity Short News.

If you were actually sitting next to you, I would probably ask you, whether you'd prefer the good, or the bad news, first!? Well, I guess I'll start with the bad one, then: Green tea sucked - again!

ZERO effect of EGCG supplementation in overweight women

To examine the effects of green tea epigallocatechin-3-gallate (EGCG) on the changes in body composition (! not just weight), energy and substrate metabolism, cardiometabolic risk factors and liver function enzymes after an energy-restricted diet intervention in obese women, a group of researchers from the University of the Basque Country in Spain recruited a group of 83(!) obese (BMI 30-40 kg/m2) pre-menopausal women (Mielgo-Ayuso. 2013).

The women were randomly assigned to consume either 3x100 mg/d of EGCG or placebo (lactose) with each of their three main meals for 12 whole weeks. During those twelve weeks, all women followed a specifically designed low-energy mixed (55 % carbohydrates, 30 % lipids and 15 % proteins) diet that provided ca. 600 kcal/day energy less than the women would need to maintain their body weight. The energy content and macronutrient composition of diets were designed to achieve a weight loss of 0.5 to 1 kg per week, as it was observed by Davis et al. (2006) and Bantle et al. (2008) on very similar regimen. As the scientists point out, the "dietary instructions were reinforced weekly by a dietitian" (Mielgo-Ayuso), to optimise compliance.

Figure 1: Changes in body composition, energy expenditure and fat oxidation, left; changes in glucose, cholesterol metabolism and inflammation, right (Mielgo-Ayuso. 2013)

I am not sure how compliant the participants actually were, but in view of the fact that the women were advised not to change their physical activity habits during the energy restriction program, the relatively meager and statistically non-significant changes in body weight (-0·3 kg, p > 0.05) and fat mass (-0·7 kg, p > 0.05) are probably not really surprising. It is nice to see, though, that the women lost more fat than total mass - muscle loss was thus not an issue for the ladies.

What was not to be expected, though, - at least if you believe a single word of the hype about green tea supplements - were the non-existent effects of the purported weight loss supplement on  energy expenditure, fat metabolism, HOMA-IR (insulin sensitivity), total cholesterol, LDL-cholesterol, or triglycerides. In fact, the only good thing about the whole EGCG intervention was that the recently observed negative effects on the liver did not occur, either.

SIGNIFICANT Effect W/ 16 Million CFU of Nestlé's Lactobacillus rhamnosus strain

Want to check out the patent?

Despite the fact that the overall results are much more exciting than those in the previously discussed green tea study, I'd advise you to keep calm. We are after all dealing with another Nestlé study on a patented strain of Lactobacillus rhamnosus (LPR), i.e. "CGMCC1.3724" (date patented: 2012-05-10; #20120114622), and cannot tell how many never published negative study results the Nestlé guys had to dispose of, before Marina Sanchez et al. finally produced study results that pleased the marketing division of this multinational corporation.

What? Ok, ok... let's get back to the facts: The scientists from the Laval University and the Nestlé Research Center randomized a group of one-hundred fifty-three 18 to 55 year-old obese men and women to receive either a placebo or the said LPR formulation with 1·6 × 10⁸ colony-forming units of LPR and additional oligofructose and inulin per cap for a total of 24 weeks.

In the course of the first 12 weeks (phase 1), each participant received a personalised diet plan that would have him or her consume 500 kcal/d less than he or she'd need for weight maintenance (just as an aside, that's 100kcal more than for the subjects in the green teas study). During phase 2, each participant received a personalised diet plan without energy restriction. The good thing, the resting energy expenditure (REE) was actually measured: after a 12 h overnight fast in subjects having had rested for at least 15 min in a standardised supine position. This procedure was repeated thrice: (1) At baseline, (2) after the weight-loss and (3) after the second phase weight-maintenance periods using indirect calorimetry.

Figure 2: Changes in body composition (all data in kg) in men (left, blue) and women (right, orange) after weight loss (ΔW12) and weight maintenance (ΔW24) phase (Sanchez. 2013)

The data in figure 2 confirms what the abstract says: "The intention-to-treat analysis showed that after the first 12 weeks and after 24 weeks, mean weight loss was not significantly different between the LPR and placebo groups when all the subjects were considered."

Figure 3: Changes in metabolic parameters, i.e. energy intake (kcal/day), resting energy expenditure (REE, kcal/day) and respiratory quotient (RQ, remember: low RQ = high fat, low carb oxidation) after 12 and 24 weeks (Sanchez. 2013)

It does yet also confirm - and that there was a significant treatment × sex interaction, observed with the women in the treatment group losing significantly more weight than those in the placebo group (P= 0·02). More importantly, though...

"[...w]omen in the LPR group continued to lose body weight and fat mass during the weight-maintenance period, whereas opposite changes were observed in the placebo group."

For the unlucky men, on the other hand, the (unquestionably expensive) supplement didn't do sh*t: Their "changes in body weight and fat mass during the weight-maintenance period were similar" irrespective of whether they received the placebo or the active treatment.

Whether this was the reason or a consequence of the fact that the the men didn't show similar significant reductions in circulating leptin, as the women is questionable. Based on the fact that the relative abundance of bacteria of the Lachnospiraceae family in faeces increase only in women, we do yet have to assume that the missing reduction in leptin, as well as the absence of the significant body fat reductions, the researchers observed in their female subjects was simply a results of ...

• under-dosing - the same the 1·6 × 10⁸ colony-forming units of LPR that was sufficient for the average woman (body weight ~89kg) could have been too low for the guys (body weight ~104.3kg) 
• dietary interference - there could have been something in the diets of the guys that ruined the effects of the supplementation (lactobacilli are not exactly friends of meats and we all know that men love their meat ;-)
• different baseline gut microbiome - it goes without saying that you cannot place a group of rabbits in forest full of predators and expect them to survive; similarly the LPR spores may have come off second in the guts of the men, because they have a less "LPR-friendly" baseline colinization
• fundamental sex differences - at the moment I am not sure what the underlying reasons could be, but it's not impossible that hormonal difference could have played a role as well

I am pretty sure that I could come up with a whole host of additional, increasingly bizarre ad-hoc explanations for the null-effect Marina Sanchez and her colleagues from the Laval University and the  Nestlé Research Center in Lausanne observed in their male study but would rather conclude this news-item with the scientists own funky, but not unlikely explanation: Men are simply too good at dieting!

True: Women have a harder time losing weight even with high protein | more

As the authors point out, we know from previous trials (and corresponding SuppVersity posts, read more) that men are generally more prone to respond to a negative-energy balance intervention than women - and that's true irrespective of whether it is an exercise-training programme (Tremblay. 1984), a diet– exercise programme (Doucet. 1999), or a session of exercise and of mental work (Pérusse-Lachance. 2013). Plus, if you look at the data in figure 2, you'll see that this is actualy "concordant with the results of the present study that shows higher weight loss in men in the placebo group than in the women". Sanchez et al. do now believe that the high baseline success "abolished this difference" (Sanchez. 2013).

In view of the fact that there was a difference in a single low-abundance taxonomic group  (Prevotellaceae) between the baseline gut microbiome of the male and female study participants, I would still not exclude that the different baseline gut microbiomes could at least have added to the 'effect abolishing effect' of the sex-specific ease of weight loss in men. I mean, why wouldn't the feces of the men show an increase in lactobacillus spores, if the supplement worked?

Bottom line: Today's installment of the short news is very characteristic of the dilemma with weight loss supplements. We are just realizing that the classic thermogenic 'rodent fat burner' don't really work in humans. Against that background the rise of supplements that target the gut microbiome and exert much more complex body recompositioning effects comes in the nick of time.  Unfortunately, our understanding of the complex interactions between the gut microbiome and our immune system in the context of the emerging science of immunonometabolism is so incomplete (Mathis. 2011) that we are more or less groping in the dark, whenever we supplement subjects, patients or even ourselves with allegedly healthful bacteria.

All alleged benefits aside,  "specificity", the 2nd Principle of Sensible Supplementation, should keep you away from the next best GNC or online supplement store. The two studies at hand do after all not warrant the use of either green tea or lactobacillus supplements as weight loss aids in lean, healthy and active  men or women.

Accordingly, the observation that green tea supplements won't help sedentary over-weight women to lose weight appears to be much more reliable than the allegedly impressive weight loss effects of the probiotic during the "maintenance phase" of the Sanchez study.

We must however not forget the respective constraints of the research design and irresponsibly over-interpret the results of the EGCG study to (a) the potential benefits of regular 'whole' tea consumption in the average, non-obese individual (Wu. 2003) or (b) visceral fat loss in diet + exercise interventions in obese individuals (cf. Maki. 2009). Similarly, the fact that obese women will lose weight on a LPR supplemented maintenance diet is very unlikely going to translate to lean, athletic folks like you and me. According to the 2nd Principle of Sensible Supplementation, which is "specificity" (learn them all), I don't see you or me heading over to the next best online shop to buy LPR or EGCG supplements - irrespective of the promising results of the Sanchez trial.

References: 

• Bantle JP, Wylie-Rosett J, Albright AL,et al.(2008) Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care31, Suppl. 1, S61– S78.
• Davis NJ, Emerenini A & Wylie-Rosett J (2006) Obesity management: physician practice patterns and patient preference. Diabetes Educ32, 557 – 561. 
• Maki, K. C., Reeves, M. S., Farmer, M., Yasunaga, K., Matsuo, N., Katsuragi, Y., ... & Cartwright, Y. (2009). Green tea catechin consumption enhances exercise-induced abdominal fat loss in overweight and obese adults. The Journal of nutrition, 139(2), 264-270.
• Mathis, D., & Shoelson, S. E. (2011). Immunometabolism: an emerging frontier. Nature Reviews Immunology, 11(2), 81-83.
• Mielgo-Ayuso J, Barrenechea L, Alcorta P, Larrarte E, Margareto J & Labayen I (2013). Effects of dietary supplementation with epigallocatechin-3-gallate on weight loss, energy homeostasis, cardiometabolic risk factors and liver function in obese women: randomised, double-blind, placebo-controlled clinical trial. British Journal of Nutrition, available on CJO2013. 
• Tremblay, A., Despres, J. P., Leblanc, C., & Bouchard, C. (1984). Sex dimorphism in fat loss in response to exercise-training. Journal of obesity and weight regulation.
• Wu, C.-H., Lu, F.-H., Chang, C.-S., Chang, T.-C., Wang, R.-H. and Chang, C.-J. (2003), Relationship among Habitual Tea Consumption, Percent Body Fat, and Body Fat Distribution. Obesity Research, 11: 1088–1095.

Stevia Kills Good Gut Bacteria - One Study Enough to Stop Using the Natural Sweetener? Probably Not in View of its Anti-Diabetes, Anti-LDL, Anti-Viral & Anti-Cancer Effects

Study indicates stevia kills healthy gut bacteria. So, how bad is it? Are the effects significant, will they have an impact on your overall health and does this mean you must not use stevia any longer?

A recent study from the Institute of Microbiology and Biotechnology at the University of Latvia in Riga shows the impossible: Stevia, the "natural" sweetener that's everybody's darling, could mess up your gut microbiome by killing large numbers of the beneficial Lactobacillus Reuteri bacteria in your tummy - exactly those bacteria of which several studies have shown that supplementing will help cure acute diarrhea in young children (Shornikova. 1997), is capable of reducing frequency and intensity of antibiotic-associated side-effects during eradication therapy for H. pylori. (Lionetti. 2006), confers broad-spectrum protection against disease in humans and animals (Casas. 2000), has cholesterol lowering effects (Jones. 2012) and much much more.

You can learn more about the gut & your health at the SuppVersity

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

In view of the fact that it would appear as id Lactobacillus reuteri was clearly one of the "good guys" it seems that the results I. Denin a, P. Semjonovs, A. Fomina, R. Treimane and R. Linde report on their latest study in Letters in Applied Microbiology (Denin. 2014) were really bad news:

Figure 1: Influence of stevioside (a) and rebaudioside A (b) on biomass formation in Lactobacillus reuteri strains (24 h | Denin. 2014).

"In samples supplemented with stevia glycosides, the growth of all Lact. reuteri strains was slightly inhibited – however, a statistically significant concentration-dependent inhibitory effect was not observed for all strains (Fig. 1).

Comparing both the glycosides, the inhibitory effect of stevioside was more pronounced for strains 44 and 16, while the effect of rebaudioside A was more pronounced for strains 16 and 19. Statistically significant concentration-dependent inhib itory effect was observed for lactic acid and acetic acid synthesis. The decrease in lactic acid and acetic acid production was observed for both stevioside and rebaudioside A. [...] Although the inhibitory effect of stevioside on pH was observed at different stevioside concentrations, the effect was evident for all strains. Rebaudioside A had a more pronounced inhibitory effect on pH values of certain strains including Lact. reuteri 12, 16, 43 and 44" (Denin. 2014 | my emphasis).

The good news, however, is in the details: The inhibitory effect was "slight" (see quotation above) and the design of the study leaves it open, whether similar effects would occur in vivo and thus outside of a glycoside, stevioside and rebaudioside laden Petri dish.

Previous studies seem to refute significant effects of stevia on the human microbiome! In 2003, Gardana et al. found no effect of stevia on the make-up of human fecal cultures when they were incubated with either stevioside or rebaudioside A. Only the fact that bacteroides, i.e. the "enemies" of lactobacilli, were the most efficient in hydrolyzing Stevia sweeteners to steviol would suggest that there may be an overall effect on the human microbiome form stevia (ab-)use.

And while we have little in vivo evidence that stevia is bad for you, a brief review of the contemporary scientific literature on Stevia yields the following "proven" (mostly only in a handful, if not just a single study) benefits:

• Stevia has been implicated in diabetes and hyperlipidemia treatment and its effects on blood glucose levels are not a mere result of the corresponding reduction in sugar intake.

  

  Figure 2: Effects of stevia vs. diabetes drug Glibenclamide on blood glucose and lipid levels in diabetic rodents; data expressed relative to healthy control (Singh. 2014)

  In a recent rodent study that compared the effects of stevia against those of the often-prescribed diabetes-drug Glibenclamide, the natural sweetener outperformed the drug in many in its ability to reduce LDL and blood sugar and was not far off of what the Glibencamide did for the diabetic lab animals in terms of its effects on HDL and VLDL (see Figure 2).
  
  Previous human studies indicate that stevia extracts will also increase the increased 16 healthy human volunteers whose plasma glucose levels during an oral glucose tolerance tests were significantly lower after having consumed 5 grams of aqueous leave extract at regular 6-h intervals for 3 days (Curi. 1985).

  

  Figure 3: Effects of stevia and aspartame replacement of sucrose in test meals that were fed to obese and normal-weight volunteers on postprandial blood glucose levels (Anton. 2010)

  Moreover, in a more recent study by Anton et al. where stevia was compared to aspartame, it had the same beneficial effects on total energy intake and let to statistically significant reductions in postprandial glucose levels of both obese and lean study subjects (see Figure 3) that did not reach significance when the sucrose content of the test meal was replaced by aspartame.
• In-vitro stevia appears to have anti-cancer effects, as well. That's at least what studies by  Jayaraman et al. (2008) observed with stevia extracts. An effect that may be related to both it's anti-microbial, as well as its potent anti-oxidant activity (Tadhani. 2007) of the whole leaves and leave extracts of which Tahani et al. found that they contain significant effects of folic acid (52.18 mg/100 g) and vitamin C, as well as 130.76 μg catechin and 15.64 μg quercetin for leaves and 43.99 μg catechin and 1.57 μg quercetin for cellus at mg of water extracts, respectively.
  
  Furthermore, Tadhani et al.'s results showed that the leaf extracts contained higher amounts of free radicals, hydroxyl radicals and superoxide anion radical scavenging activities than those of the callus extracts or the anti-mutagenic effects Cariño-Cortés et al. report in their 2007 study. Whether anything similar can be observed with the white "stevia" powder that is used by most people to sweeten their foods is yet questionable - it's after all pure steviosid and thus devoid of all of the previously mentioned compounds.

  

  Figure 1: Several natural constituents of the stevia plant, including steviosides, which are the naturally sweet agents in stevia have potent anti-viral activity against Epstein-Barr virus; values in brackets
  represent % of untreated control dish (Konoshima. 2002)

  Another possible anti-cancer mechanism may be related to stevia's ability to kill viruses like the Epstein-Barr virus that has been implicated in the pathogenesis of Burkitt’s lymphoma, Hodgkin’s disease, non-Hodgkin’s lymphoma, nasopharyngeal carcinoma, and lymphomas, as well as leiomyosarcomas arising in immunocompromised individuals.in humans (Thompson. 2014).

Against that background it seems questionable that the new evidence of negative effects on allegedly healthy gut bacteria (just want to remind everyone that we have no clue what the optimal gut microbiome would look like) is significant enough to have us all reconsider our use of tiny amounts of stevia as a sweetener in our foods.

Read more about the effects artificial sweeteners have on the microbiome in a prevoius article | go ahead!

Interim conclusion: While I am not all too scared that stevia will mess with my gut microbiome in a way that makes me sick, fat and what not, I truly believe that the effects of artificial sweeteners on the make-up and density of the human gut microbiome is still massively under-researched - and that in spite of the fact that it could have a significant effect on the health of us all.

As s SuppVersity reader you will also be aware that this is not a stevia-specific effects. Only recently I have written about similar effects for a bunch of artificial sweeteners - an article I can only recommend to anyone who hasn't read it yet | Comment on Facebook.

References:

• Anton, Stephen D., et al. "Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels." Appetite 55.1 (2010): 37-43.
• Casas, Ivan A., and Walter J. Dobrogosz. "Validation of the probiotic concept: Lactobacillus reuteri confers broad-spectrum protection against disease in humans and animals." Microbial ecology in health and disease 12.4 (2000): 247-285. 
• Curi, R., et al. "Effect of Stevia rebaudiana on glucose tolerance in normal adult humans." Brazilian journal of medical and biological research= Revista brasileira de pesquisas médicas e biológicas/Sociedade Brasileira de Biofísica 19.6 (1985): 771-774.
• Deniņa, Ilze, et al. "The influence of stevia glycosides on the growth of Lactobacillus reuteri strains." Letters in applied microbiology 58.3 (2014): 278-284. 
• Gardana, Claudio, et al. "Metabolism of stevioside and rebaudioside A from Stevia rebaudiana extracts by human microflora." Journal of agricultural and food chemistry 51.22 (2003): 6618-6622. 
• Jayaraman, Sathishkumar, Muthu Saravanan Manoharan, and Seethalakshmi Illanchezian. "In-vitro antimicrobial and antitumor activities of Stevia rebaudiana (Asteraceae) leaf extracts." Tropical Journal of Pharmaceutical Research 7.4 (2008): 1143-1149.
• Jones, M. L., C. J. Martoni, and S. Prakash. "Cholesterol lowering and inhibition of sterol absorption by Lactobacillus reuteri NCIMB 30242: a randomized controlled trial." European journal of clinical nutrition 66.11 (2012): 1234-1241.
• Konoshima, Takao, and Midori Takasaki. "Cancer-chemopreventive effects of natural sweeteners and related compounds." Pure and applied chemistry 74.7 (2002): 1309-1316.
• Lionetti, E., et al. "Lactobacillus reuteri therapy to reduce side‐effects during anti‐Helicobacter pylori treatment in children: a randomized placebo controlled trial." Alimentary pharmacology & therapeutics 24.10 (2006): 1461-1468.
• Shornikova, Aino-Vieno, et al. "Lactobacillus reuteri as a therapeutic agent in acute diarrhea in young children." Journal of pediatric gastroenterology and nutrition 24.4 (1997): 399-404.
• Singh, Sunanda. "Antidiabetic, Antidyslipidymic and Antioxidative potential of methanolic root extract of Stevia rebaudiana (Bertoni) on Alloxan induced Diabetic Mice Sunanda Singh and Veena Garg Department of Bioscience and Biotechnology, Banasthali Vidyapeeth, Banasthali, Rajasthan, India." (2014). 
• Tadhani, M. B., V. H. Patel, and Rema Subhash. "In vitro antioxidant activities of Stevia rebaudiana leaves and callus." Journal of Food Composition and Analysis 20.3 (2007): 323-329. 
• Thompson, Matthew P., and Razelle Kurzrock. "Epstein-Barr virus and cancer." Clinical Cancer Research 10.3 (2004): 803-821.

Vitamin A Educates T-Cells, Joins Forces With Vitamin D Against Liver Cancer. Milk Better Than Sugary Electrolyte Solutions for Rehydration? Helicobactor Pylori: Probiotics from Breast Milk & Feces Better Than Amoxicillin!

Lactobacilli are hip, vitamin A is not - at the SuppVersity you still get news on both

1kg! That's the amount of weight you could probably lose if you rid yourself of all the microbes in your gut - from the weight of the bacteria alone, of course. Whether this would be a good idea or not, is however very questionable. On the one hand, we do have the still not fully understood studies on obesity-resistant germ free mice and an accumulating amount of evidence that having the "wrong" bacteria in the gut is at least associated with an increased obesity risk (Blaut. 2012). On the other hand, however, we are seeing new studies on the various benefits of having the "right" gut microbiome being published on an almost daily basis. So what?

Before we take a closer look at a definite benefit of having the "right" gut bacteria, though, let's start out with another likewise gut-related news item on the role of retinoic acid in T-cell education. In a way it's funny, it starts right where the bacteria reside, could have immune-modulatory effects that are way more pronounced and far reaching than probiotics and is still hardly discussed.

Vitamin A is of critical importance to (intestinal) T-cell education

If you have ever asked yourself how the immune cells in your body know what they are supposed to do, Catharine Ross' latest paper that was published in the American Journal of Clinical Nutrition and is based on a short talk the researcher from the Department of Nutritional Sciences at the Pennsylvania State University held at a conference earlier this year may provide at least some additional insides into the role a still way underrated molecule plays in this "T cell education" (Ross. 2012): Vitamin A!

Figure 1: Model of T cell differentiation, from uncommitted naive T cells into different T cell subsets that produce different cytokines and thus promote different functional activities (adapted from Ross. 2012)

As you can see in figure 1, retinoic acid does not simply promote the differentiation of regulatory T cells, which help to suppress inflammatory reactions, it also plays a significant role in normal mucosal immunity (in the gut, the airways and elsewhere) by modulating T cell activation and regulating cell trafficking. Moreover, vitamin A promotes antibody responses to T cell–dependent antigens. Needless to say that

"[...] in a state of vitamin A deficiency, inflammatory T cell reactions may be inadequately opposed and therefore become dominant [...] Although data from human studies are still needed, the framework now developed from studies in mice and rat models suggests that adequate vitamin A status, [...] is  important for maintaining a proper balance of well-regulated T cell functions and for preventing excessive or prolonged inflammatory reactions." (Ross. 2012).

Discovery a beta carotene derived vitamin A receptor blocker is only one of a couple of intriguing findings wrt to vitamin A.

One thing that sticks out from the complex interactions (see figure 1), really is the way by which the interaction of vitamin A with the T-cells in the gut crucially determine the efficiency of the 'fist line defenses' and their downstream effects on the whole organism. It is by no means co-incidental that diarrhea is rampant in areas of the "third world", where a large amount of the population is vitamin A deficient (Beaton. 1994). And in fact studies have shown consitently that

"RA is essential for 'imprinting' gut-homing specificity on T cells activated by intestinal DCs [dendritic cells] and suggested that MLN DCs are a source of RA that drives T cell differentiation toward the gut-homing phenotype" (Ross. 2012)

Moreover, oral tolerance to foreign antigens and thus an allergy free live requires a form of immune suppression, which can be proffered or hampered by sufficient and insufficient vitamin A intakes. In that, the exact effects of vitamin A will depend on the cytokine milieu the T-cells are exposed to. Examples are...

• an exaggerated IL-17 response with vitamin A deficiency, on the one hand, and
  
• an increase of the inflammatory response due to high vitamin A in an IL-15 environment 

Based on these observations, Ross rightly points out that "when RA is used for therapeutic purposes, it should be used cautiously in subjects with various inflammatory bowel conditions and sensitivities to dietary antigens." (Ross. 2012) People with gluten intolerance, celiac and other allergic reactions, for example would probably be better off avoiding the consumption of any form of supplemental vitamin A (on top of what's in their regular diet). Someone with high IL-17 and IL-6 levels as they have been observed in non-celiac inflammatory bowel disease, type 1 diabetes, multiple sclerosis and rheumatoid arthritis, on the other hand, could actually benefit from vitamin A's (especially ATRA) presence during activation of CD4⁺ T cells, because it will - even in the presence of IL-6 - "favor the development of the a Treg lineage at the expense of T cells secreting IL-17" and could thus help reduce chronic inflammation and keep autoimmune reactions at bay (Schambach. 2007; also Ramgolam. 2010).

More news

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  Figure 2: Who cares about cell viability, the survival time (in days) matters

  Combination therapy with vitamin A and a vitamin D (not D3, but calcitriol) analog EB1089 kills liver cancer cells. And it does so more effectively than any of the two molecules alone. That's the actually unsurprising result of a study that has been conducted at the Beijing Army General Hospital in China. The researchers injected nude mice with molecules that made them develop hepatocellular cancer. Afterwards, the rodents received either 10 μmol/L retinoic acid (vitamin A), 10 nmol/L EB1089 or both as a combination treatment.
  
  Compared to vitamin A or the calcitriol analog alone, the combination treatmend resulted in a significanlty higher reduction of the viability of hepatocellular cancer cells. Based on TUNEL analysis, Zhang et al. did also establish that individual cancer cells had a higher apoptotic ratio in the combined drug group than in the groups for which the drugs were used separately. Most importantly, however, the tumor weight was decreased and the mice on the combination treatment lived significantly longer (see figure 2; Zhang. 2012)

• 

  In the same publication, Pritchett and Pritchett recommend 1.0-1.5ml / kg body weight per hour of chocolate milk as the optimal post-workout drink to be consumed in the 2 h after a workout.

  Skimmed milk, the ideal post-workout rehydration formula? According to L James' paper in Lamprecht's compendium Acute Topics in Sport Nutrition, milk is a way better choice then the standard sugar + electrolyte rehydration formulas. Interestingly this is not due to the minerals in the milk, or the sugar, but, as James argues, a direct consequence of the milk proteins, which help restore "fluid balance after exercise-induced dehydration to a greater extent than a carbohydrate-electrolyte sports drink." As James points out it will yet have to be elucidated, whether the simple addition of whey protein to a standard sugar + electrolyte formula would exert similar effects (James. 2013).
• Probiotics to kill Helicobacter Pylori? While not every bacteria stands a chance against the nasty gut bug H. Pylori, certain Lactobacillus spp. strains obviously do. At least, if the results of a recent in-vitro + in vivo rodent study by Pei-Shan Hsieh can be replicated in human studies.

  

  Figure 3: Urease activity in H. pylpori after co-incubation with the specific probiotic and resulting bacteriostatic ratio (100% = bacteria free; data adapted from Hsieh. 2012)

  Lactobacillus acidophilus TYCA08, L. acidophilus TYCA15, L. johnsonii MH-68, and L. salivarius subsp. salicinius AP-32 were the most effective strains the researchers from National Chung Hsing University in Taichung, Taiwan, analyzed. And believe it or not, the latter of these, i.e. L. johnsonii MH-68, and L. salivarius subsp. salicinius AP-32, both of which are  by the way found in feces, were even minimally more potent effective than Amoxicillin, a moderate-spectrum, bacteriolytic, β-lactam antibiotic used to treat bacterial infections. L. acidophilus TYCA15, however, steals the show. This probiotic that occurs naturally in breast milk reduced the urease activity of H. Pylori by -97.1% (see figure 3).
  
  In the consecutive rodent study, Hseieh et al. did yet still use 10⁹ CFU/mL of either AP-32 alone, MH-68 alone, or an equal mix of cultures of the two strains and both, "either alone or as a mixture in powder form were effective in reducing H. pylori load in gastric mucosa and help in reducing gastric inflammation and in regulation of gastric acid production." (Hsieh. 2012)

Thats it for today and for this weekend. As mentioned yesterday, there was simply not enough time to do the necessary research for the follow up to the Athlete Triad Series, so that this will have to wait. So don't dig an even deeper whole in the mean time. Maybe you want to do some of the psychomotor tests mentioned in yesterday's news, and check whether you are already overtrained!? How steady are your hands, for example? And whatever the result may be, don't forget to enjoy the rest of the weekend!

References:

• Beaton GH, Martorell R, Aronson KA, Edmonston B. McCabe, G, Ross, AC, Harvey, B. Vitamin A supplementation and child morbidity and mortality in developing countries. Food Nutr Bull 1994;15(4): 282–9.
• Blaut M, Klaus S. Intestinal microbiota and obesity. Handb Exp Pharmacol. 2012;(209):251-73.
• Hsieh PS, Tsai YC, Chen YC, Teh SF, Ou CM, King VA. Eradication of Helicobacter pylori Infection by the Probiotic Strains Lactobacillus johnsonii MH-68 and L. salivarius ssp. salicinius AP-32. Helicobacter. 2012 Dec;17(6):466-77.
• James L. Milk Protein and the Restoration of Fluid Balance after Exercise. In Lamprecht M (ed): Acute Topics in Sport Nutrition. Med Sport Sci. Basel, Karger, 2013, vol 59, pp 120–126. 
• Pritchett K, Pritchett R. Chocolate Milk: A Post-Exercise Recovery Beverage for Endurance Sports. In Lamprecht M (ed): Acute Topics in Sport Nutrition. Med Sport Sci. Basel, Karger, 2013, vol 59, pp 127–134.
• Ramgolam VS, Markovic-Plese S. Interferon-beta inhibits Th17 cell differentiation in patients with multiple sclerosis. Endocr Metab Immune Disord Drug Targets. 2010 Jun;10(2):161-7.
• Ross AC. Vitamin A and retinoic acid in T cell-related immunity. Am J Clin Nutr. 2012 Oct 10.  
• Schambach F, Schupp M, Lazar MA, Reiner SL. Activation of retinoic acid receptor-alpha favours regulatory T cell induction at the expense of IL-17-secreting T helper cell differentiation. Eur J Immunol. 2007 Sep;37(9):2396-9. 
• Zhang J, Zhang H, Zhang X, Yu Z. Synergistic effect of retinoic acid and vitamin D analog EB1089-induced apoptosis of hepatocellular cancer cells. Cytotechnology. 2012 Oct 16.

Performance Enhancing Gut Microbes - First Study to Show: Having (The Right?) Gut Bugs Doubles Exercise Endurance

Yogurt & Co are good for athletes. But is this due to the bacteria?

As a regular here at the SuppVersity, you are well aware of the far-reaching effects of having the "right" or "wrong" bacteria in your tummy. The claim that having the "right" bacterial make-up in the gut could have beneficial effects on your performance in the gym or on the track is something you should not believe too credulously. If we had a study to prove these benefits, things would be different, though - a study like the one a group of researchers from the National Taiwan Sport University are about to publish in the scientific bible of resistance training, the Journal of Strength and Conditioning Research (Hsu. 2014).

In said study which is still available only as an accepted manuscript, Hsu et al. investigated the association of intestinal bacteria and exercise performance in specific pathogen-free (SPF), germ-free (GF), and Bacteroides fragilis (BF) gnotobiotic mice (animals in which only certain known strains of bacteria and other microorganisms are present).

You can learn more about the gut & your health at the SuppVersity

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

To this ends, the scientist had the rodents swim to exhaustion to determine whether enteric bacteria alter antioxidant enzyme levels, exercise performance and physical fatigue. In addition, they tested the antioxidant enzyme activities, physical performance and anti-fatigue function after monocolonizing GF mice with B. fragilis (BF).

Figure 1: Time to exhaustion during exercise test and body composition of the miceaccording to the make-up of their gut microbiome; data expressed relative to group means (Hsu. 2014)

What they found was an increased time to exhaustion for the previously germ-free (GF) mice after they'd been colonized with B. fragilis (BF). Similar results were observed for the specific pathogen-free and Bacteroides fragilis gnotobiotic mice, who were also more enduring than the obesity resistant (Bäckhed. 2007) germ-free mice.

Do we have human data, as well? No, we don't have human data that's comparable to the one presented in the study at hand, but we do have evidence of beneficial (ergogenic) effects of probiotics and prebiotics in human "athletes". Examples? Well, the oral administration of the probiotic Lactobacillus fermentum VRI-003 and mucosal immunity in endurance athletes (Cox. 2010). Improved oxidative status in athletes during intense exercise training (Martarelli. 2011). Reduced risk of infection (Gleeson. 2011; West. 2011). And if that's not enough, what about keeping on top of your game by preventing and managing travellers’ diarrhoea (Tillett. 2006)!

As any SuppVersity veteran would expect, the germ-free mice were leaner than the rest of the pack. At the same time, the "sterile" mice did yet also have a lower liver, muscle, brown adipose, and epididymal fat pad weight than the SPF and BF mice.

Figure 2: Selected markers of antioxidant status in serum and liver; expr. rel. to group means (Hsu. 2014)

The markers of antioxidant defenses, the scientists measured were highest in the lean + light germ-free mice and their specific pathogen-free cousins. Against that background it's at least somewhat surprising that the performance differences are pretty significant.

Pre- instead of probiotics: Personally, I believe that prebiotics, i.e. substances that promote the growth of the "right" bacteria are more promising agents than probiotics ("live" bacteria). Studies have shown that prebiotic at dosages above 2.5 g, which is far higher than that occurring in natural foods, increases the abundance of lactic acid and butyrate-producing bacteria. In that, galacto-oligo- saccharides (GOS) and  fructo-oligo- saccharides (FOS), are the prebiotics with the most positive outcomes.

As West points out in a 2012 mini-review as part of the BJSM "A–Z of nutritional supplements" series, the "potential benefits of supplementation with prebiotics on athletic performance are most likely indirect: they may be associated with the maintenance of gut health and perhaps a reduced risk of some illnesses which might enhance the athlete’s ability to train and compete." (West in DiMarco. 2012). Altering GI microbiota through the use of prebiotics may yet also favourably influence host metabolism. Athletes who are dieting, for example, will benefit from the reduction in appetite increase in gut peptide concentration in response to thec consumption of 16 g per day of FOS (Cani. 2009).

So what are the practical implications, then? As the authors emphasize, "[t]his is the first study to show that the intestinal microflora plays an important role in exercise performance." The way the microbial make-up regulates the antioxidant enzyme defense system is yet not in line with the observed reduction in physical fatigue Hsu et al. observed in the study at hand.

In view of the fact that the general assumption is that " intensive and sustained exercise training and high-level competition generate large amounts of free radicals that likely exceed the buffering capacity of the biological system, leaving athletes susceptible to oxidative stress", you would expect the Bacteriodes fragilis mice to perform the worst.

On the other hand, the mice harboring Bacteroides fragilis are significantly more muscular than the lightweight germfree mice... well, we could continue this discussion forever, but eventually the one result that may have a practical implication is the increased performance after mono-colonization in the germ-free mice. If nothing else, this result which happens to be the first evidence of performance enhancing effects of having a gut microbiome, would imply that you better recolonize your gut as soon as possible after a course of antibiotics. How the various different microbial status might regulate performance, on the other hand, will have to be elucidated in future studies - human (!) studies, that is | Comment on Facebook!

References:

• Bäckhed, Fredrik, et al. "Mechanisms underlying the resistance to diet-induced obesity in germ-free mice." Proceedings of the National Academy of Sciences 104.3 (2007): 979-984.
• Cani, Patrice D., et al. "Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal." The American journal of clinical nutrition 90.5 (2009): 1236-1243.
• Cox, Amanda J., et al. "Oral administration of the probiotic Lactobacillus fermentum VRI-003 and mucosal immunity in endurance athletes." British Journal of Sports Medicine 44.4 (2010): 222-226. 
• DiMarco, N. M., et al. "A–Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance—Part 30." British journal of sports medicine 46.4 (2012): 299-300.
• Gleeson, Michael, et al. "Daily probiotic's (Lactobacillus casei Shirota) reduction of infection incidence in athletes." (2011). 
• Hsu et al. "Effect of Intestinal Microbiota on Exercise Performance in Mice." Journal of Strength and Conditioning Research.  DOI: 10.1519/JSC.0000000000000644 | Publish Ahead of Print.
• Martarelli, Daniele, et al. "Effect of a probiotic intake on oxidant and antioxidant parameters in plasma of athletes during intense exercise training." Current microbiology 62.6 (2011): 1689-1696.
• West, Nicholas P., et al. "Lactobacillus fermentum (PCC®) supplementation and gastrointestinal and respiratory-tract illness symptoms: a randomised control trial in athletes." Nutrition journal 10.1 (2011): 30.

They Dictate What You Like, They Dictate What You Crave and They May Even Determine Whether You're Lean or Fat: The Bacteria in the Gut - The Latest Evidence Reviewed

The alien inside - billions of bacteria in your gut interact with your central nervous system and take command over your metabolism and - probably - even about what you want to put into your mouth.

Wouldn't it be great if it was not your lack of willpower and your unhealthy food choices that were to blame for the potbelly you're carrying around? Wouldn't it be awesome if you could blame your misery on someone else? And wouldn't it be best if that someone was a dirty little microbe in your gut? Someone who cannot fight back, when you chose him as a scapegoat? That would be great, right?

Well, in today's SuppVersity Article we're going to take a look at a bunch of studies and hypothesis that may actually allow you to find a new excuse for your inability to lose weight. But beware! While I wouldn't say that researchers who favor the "evolutionary conflict between host and microbes" theory as an alternative explanation for the ever-increasing obesity rates are totally off. What I will say, however, is that this is at best a contributing, maybe even just a corollary factor in the etiology of the obesity epidemic.

You can learn more about the gut & your health at the SuppVersity

Fiber for Female Fat Loss

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

We know for quite some time that individual members of the microbiota, and consortia of those microbes are highly dependent on the nutrient composition of the diet.

• Prevotella grows best on carbohydrates; dietary fiber provides a competitive advantage to Bifidobacteria (González‐Rodríguez. 2013)
• Bacteroidetes has a substrate preference for certain fats (Wu. 2011)

Scientists have also found some specialist microbes, e.g. mucin degrading bacteria such  as Akkermansia mucinophila. They thrive on secreted carbohydrates provided by host cells. Other butyrate producing microbes, e.g. Roseburiaspp., fare better when they are delivered polysaccharide growth substrates in the diet. Specialist microbes that digest seaweed have been isolated from humans in Japan (Hehemann. 2010). African children raised on sorghum have unique microbes that digest cellulose (De Filippo. 2010). Many other examples exist (Fava. 2012).

We have tons of associations, but little experimental evidence: All this does yet not mean that the specialized gut microbiome will also affect the dietary intake of the host. You could after all argue that you could get rid of Prevotella by simply cutting out all carbs from your diet, but scientists believe that the specialization works both ways.

There is circumstantial evidence for a connection between cravings and the composition of gut microbiota. Individuals who are “chocolate desiring” have different microbial metabolites in their urine than “chocolate indifferent” individuals, despite eating identical diets (Rezzi. 2007).

Figure 1: A study by Rezzi et al. showed that chocolate cravers have a different microbiome than their peers (Rezzi. 2007)

In spite of these intriguing results and a plethora of evidence for mood and central nervous system effects of certain bacteria in rodents, the definite evidence of a causal relationship between gut microbes A, B & C and certain food preferences, let alone "addictions" is still missing.

It's not as if there was no evidence, it's just not really compelling (yet?)

An area where the mechanisms appear to be more evident is the effect of certain bacteria on the expression of certain molecular receptors in the gut. Germ-free mice for example have altered taste receptors for fat on their tongues and in their intestine compared to mice with a normal microbiome (Duca. 2012). Since an increase in fat receptors is associated with an increased preference and intake for fatty foods and energy, an over-expression of these receptors could certainly be involved in the etiology of obesity.

Both, low dose penicillin at weaning (blue) and at birth (red) lead to significant obesity in male pups later in life (Cox. 2014).

Latest research says: Disruption of gut bacteria early in life can lead to obesity in adulthood! Certain microbes found in the gut may protect against obesity and diabetes. A study published by Cell Press August 14th in the journal Cell reveals that these microbes shape their hosts' metabolism very early in life and that disrupting them with short-term exposure to antibiotics during infancy can cause metabolic changes that appear to increase the risk of obesity in adulthood.

These findings in mice are helping researchers identify which gut bacteria are crucial to metabolic health. Such information could be used to help restore levels of those helpful microbes after an infant has received life-saving antibiotics, thereby promoting healthy metabolism in adulthood.

In conjunction with other scientific evidences, such as the increased intestinal expression of cannabinoid and opioid receptors in mouse and rat intestines in response to the oral supplementation of L. acidophilus NCFM in rats and similar effects in human epithelial cell culture (Rousseaux. 2006), the Duca study suggests that the composition of microbes in our guts could in fact actively alter our food preferences by modulating the receptor expression or transduction (Collins. 2012).

Is a "gut dysbiosis" the reason we are fat?

The idea that not having the "right" bacterial make-up could be at the heart of the obesity epidemic has recently received significant scientific attention. Backhed and colleagues showed that mice genetically predisposed to obesity remained lean when they were raised without microbiota (Bäckhed. 2004).

Figure 2: Germ-free mice stayed lean, in spite of the fact that they were genetically predisposed to become obese and irrespective of their increased food intake (Bäckhed. 2004). When they were inoculated with the microbiota from regular obese mice (CONV-D), however, they became just as obese as their conventional peers (CONV-R)

When the mice were "infected" with fecal pellets from a conventionally raised obese mice, they became obese again. That this could happen in humans as well is supported by data from Ridaura et al. (2013) who observed that the inoculation of germfree mice with microbiota from an obese human produced similar results.

Let's put everything together, now!

As you can see in the graphical illustration in Figure 3, the taste receptor interactions are not the only scientifically proven changes. There are also well-known endotoxin induced effects on mood and anxiety (Amaral. 2008; Chiu. 2013) of which Hill et al. have shown (albeit in a different context) that it will affect food cravings (Hill. 1991).

Beware! If the scientists are right, the same probiotics that are good for people on a mixed diet may be bad for those who consume a low carb or ketogenic diet. I would thus be very reluctant to make any form of one-size-fits it all supplement recommendation! If there is one take home message from what we already know, it's that, in the long run, unbalanced diets (low-to-no whatever) will obviously put you at greater risk of developing a highly specialized obesity-promoting gut microbiome.

Figure 3: Like microscopic puppetmasters, microbes may control the eating behavior of hosts through a number of potential mechanisms including microbial manipulation of reward pathways, production of toxins that alter mood (shown in pink, diffusing from a microbe), changes to receptors including taste receptors, and hijacking of neurotransmission via the vagus nerve (gray), which is the main neural axis between the gut and the brain (Alcock. 2014)

Now Alcock et al. who created this illustration speculate that the weight loss and inhibition of weight gain we've seen in trials using probiotic yogurts (Kadooka. 2010; Mozaffarian. 2011) could be mediated, at least in parts, by microbial interactions with the vagus nerve:

If microbial control is mediated through the vagus nerve, then microbial signals should interfere to some extent with the physiological regulation coordinated by the vagus nerve. [...] We predict that people experiencing cravings should have lower vagal tone. Furthermore, it is possible to block or sever the vagus, which we predict would subdue microbial signaling via the vagus nerve, and thereby alter food preferences. This would be consistent with studies showing that blocking the vagus nerve can lead to weight loss." (Alcock. 2014)

In conjunction with the aforementioned effects and the influence of population size and composition on cravings and high fat, high carbohydrate preferences foods Alcock et al. believe to have enough evidence for the existence of what they call an "evolutionary conflict between the host and microbiota" which may lead to cravings and cognitive conflict with regard to food choice.

Will Engineered Super-Bacteria Help Even Gluttons to Stay Lean? Scientists "Produce" Anti-Obesity Bacteria to be Administered in the Water | more

Personally I don't consider the evidence convincing enough to assume that the suppression oo modification of microbial signals from the gut alone will fix what is currently deemed a problem of self-control and bad food choices | What's your take? Comment on Facebook!

I do not doubt though that "acquired tastes" may at least be reinforced by corresponding microbial selection in the gut. Resetting the microbial make-up and/or modifying it via pre- and probiotic foods and supplements is thus unquestionable an interesting, yet still not fully understood strategy to complement lifestyle intervention that focus on diet and exercise.

And let's not forget: Both diet and exercise have been shown to have a major impact on the gut microbiome, as well (Gotthardt. 2014; Hold. 2014)!

References:

• Alcock, Joe, Carlo C. Maley, and C. Aktipis. "Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms." BioEssays (2014).
• Amaral, F. A., et al. "Commensal microbiota is fundamental for the development of inflammatory pain." Proceedings of the National Academy of Sciences 105.6 (2008): 2193-2197.
• Bäckhed, Fredrik, et al. "The gut microbiota as an environmental factor that regulates fat storage." Proceedings of the National Academy of Sciences of the United States of America 101.44 (2004): 15718-15723. 
• Chiu, Isaac M., et al. "Bacteria activate sensory neurons that modulate pain and inflammation." Nature (2013).
• Collins, Stephen M., Michael Surette, and Premysl Bercik. "The interplay between the intestinal microbiota and the brain." Nature Reviews Microbiology 10.11 (2012): 735-742.
• Cox et al. "Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences." Cell 158 (2014):705–721.
• De Filippo, Carlotta, et al. "Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa." Proceedings of the National Academy of Sciences 107.33 (2010): 14691-14696.
• Duca, Frank A., et al. "Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota." PloS one 7.6 (2012): e39748. 
• Fava,Francesca, et al. "The type and quantity of dietary fat and carbohydrate alter faecal microbiome and short-chain fatty acid excretion in a metabolic syndrome ‘at-risk’population." International Journal of Obesity 37.2 (2012): 216-223.
• González‐Rodríguez, Irene, et al. "Factors involved in the colonization and survival of bifidobacteria in the gastrointestinal tract." FEMS microbiology letters 340.1 (2013): 1-10.
• Gotthardt, J. D., et al. "Exercise Promotes Enhanced Gut Microbial Diversity Compared to Sedentary Counterparts." International Journal of Exercise Science: Conference Proceedings. Vol. 9. No. 2. 2014. 
• Hehemann, Jan-Hendrik, et al. "Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota." Nature 464.7290 (2010): 908-912.
• Hill, Andrew J., Claire FL Weaver, and John E. Blundell. "Food craving, dietary restraint and mood." Appetite 17.3 (1991): 187-197. 
• Hold, Georgina L. "The gut microbiota, dietary extremes and exercise." Gut (2014): gutjnl-2014.
• Kadooka, Y., et al. "Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial." European Journal of Clinical Nutrition 64.6 (2010): 636-643.
• Miras, Alexander D., and Carel W. le Roux. "Mechanisms underlying weight loss after bariatric surgery." Nature Reviews Gastroenterology and Hepatology 10.10 (2013): 575-584.
• Mozaffarian, Dariush, et al. "Changes in diet and lifestyle and long-term weight gain in women and men." New England Journal of Medicine 364.25 (2011): 2392-2404.
• Rezzi, Serge, et al. "Human metabolic phenotypes link directly to specific dietary preferences in healthy individuals." Journal of proteome research 6.11 (2007): 4469-4477.
• Ridaura, Vanessa K., et al. "Gut microbiota from twins discordant for obesity modulate metabolism in mice." Science 341.6150 (2013): 1241214.
• Rousseaux, Christel, et al. "Lactobacillus acidophilus modulates intestinal pain and induces opioid and cannabinoid receptors." Nature medicine 13.1 (2006): 35-37. 
• Wu, Gary D., et al. "Linking long-term dietary patterns with gut microbial enterotypes." Science 334.6052 (2011): 105-108.