Water Before Meals Doubles Weight Loss Success - Study Said to Confirm Diet Myth Gets Falsely Overgeneralized

Could this large glass of water really be the "diet game changer" some mainstream media make it look like? Or, are we - once again - dealing with the abuse of science to attract readers by propagating dubious dieting myths?

The advice to "drink a glass of water before every meal" is about as old as human efforts to lose weight. Yet despite the fact that an increase in daily water consumption is widely advocated as a useful tool to aid weight loss and even included in popular weight loss programs like Weight Watchers, there is, according to the latest systematic review of the association between water consumption and body weight,  little evidence to support this practice outside of energetically restricted interventions (Muckelbauer. 2013).

In other words: While we do have evidence that replacing caloric beverages with water/diet beverages works (Tate. 2012), we have little evidence that simply drinking more will accelerate weight loss and almost no evidence of the potential benefits water preloading before meals, in particular.

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Quite surprising, isn't it. I mean, it should be obvious that drinking a glass or two of water before a meal would be a highly promising strategy to reduce meal energy intake by modifying an individuals’ perception of fullness prior to eating by, as Parretti et al. (2015) put it, "consuming a 'preload' of water". Nevertheless, Daniels' 2010 systematic review identified only two small laboratory studies that specifically investigated whether water preloading reduced energy intake. As Parretti et al. point out in the introduction to their own study,

"[b]oth studies compared participants given a water preload of 500 ml for 30 min before an ad libitum meal with those not given a preload and found that energy intake at the meal was lower for the preload group compared with the no-preload group" (Parretti. 2015). 

Thus, evidence to suggest that water preloading may improve the effectiveness of weight loss programs is there. Experimental evidence to confirm that is yet ultra-scarce. In fact, the only RCT (Dennis. 2015) to directly examine the effects of water preloading before meals on weight loss was published five years ago. In said study, 48 adults with overweight or obesity were allocated to a hypocaloric diet plus 500 ml of water before meals every day (water preload group) or a hypocaloric diet alone intervention (nonwater group) over 12 weeks.

Figure 1: Dennis et al. were the first to show that drinking 500 ml of water before meals everyday can boost the weight loss success of overweight and obese individuals participating a 12-week diet intervention (Dennis. 2010).

As you can see in Figure 1, the subjects in the water group lost ~2kg more weight than their peers and showed a 44% greater decline in weight over the 12 weeks than the nonwater group. That's interesting because the energy intake during test meals was suppressed by the additional water load only at baseline, yet not after 12 weeks on the preloading protocol (see Figure 2).

Figure 1: In a previous study the beneficial effect of the water preload on food energy intake wore off. The subjects in Dennis' study still lost more weight with the preload, but with respect to the long-term efficacy of drinking 500ml of water before every main meal this is an important result we should not forget (Dennis. 2010).

One of the things we will have to look for when analyzing Paretti's more recent study is thus whether she made sure to check if the appetite reducing effects persist. After all, their study was very similar to the one by Dennis, with an important difference in the study population which was not predominantly middle aged or older white men and women in Paretti's study. Otherwise there are only very few surprises with regard to the study design. Here's what we're talking about:

• a two-group randomized controlled trial with eighty-four adults with obesity 
• all participants were given a face-to-face weight management consultation at baseline (30 min) and a follow-up telephone consultation at 2 weeks (10 min)
• participants were randomized to either drinking 500 ml of water 30 min before their main meals or an attention control group where participants were asked to imagine their stomach was full before meals (*)
• primary outcome was weight change at 12-week follow-up

In that, the "(*)" denotes something you might consider weird... and what should I say? It is weird to imagine that your stomach is full before a meal, but that's Parretti's way of turning a regular RCT into an attention controlled RCT, where the dummy procedure disguised the true intent of the study and provided a nonspecific intervention that in some ways matched preloading.

Table 1: Self-reported adherence for both groups - (I) intervention group, (C) control group (Parretti. 2015).

It is thus not really surprising that the subjects in the control group (C) hardly managed to follow the scientists advise once a week, while the majority of the subjects in the intervention group (I) consumed their water preload on at least two of three meals per day. The data in Table 1 does yet still leave no doubt that the adherence declined significantly over the 12-week period. Whether the Parretti study is able to answer the previously raised question, if the chronic use of water preloads may reduce their efficacy, is thus highly questionable. I mean, after 12 weeks, almost half of the subjects didn't use the preload anymore.

Table 2: Self-reported fullness and satiety scores for both groups - (I) intervention group, (C) control group; fullness and satiety scores can range from 1 to 10 (Paretti. 2015)

Against that background, I would not interpret the stable satiety and fullness levels from week 2-9 as evidence that there is no such habituation effect. And in view of the lack of data on the actual food intake, the satiety and fullness data is pretty much irrelevant, anyways (just as there's a disconnect between mTOR and actual muscle gains, there are also disconnects between appetite, fullness and food / energy intake - if you don't measure the relevant outcome you're groping in the dark).

Figure 2: Weight loss (in kg) over the 12-week study period (unadjusted values | Parretti. 2015)

What is relevant and hard to reject, though ,is the fact that the water preloading group lost 1.3 kg more than the subjects in the control group (see Figure 2) - with a statistically significant difference of 1.2 kg still remaining when the data was adjusted for ethnicity, deprivation, age, and gender, the lack of which had been an issue in the previously referenced study by Dennis et al. (2010).

The reason I am still not thrilled is simple: Parretti's study was celebrated in the laypress as the breakthrough research that demonstrates that you can easily lose weight by simply drinking 500ml of water before each and every of your meals. Unfortunately, this is not just a broad overgeneralization of the results it is simply a completely false interpretation of the study. What Parretti's study does suggest (not prove) is that drinking 500ml will accelerate the weight loss on energy reduced diet.

"Chewing gums will help you lose weight" - That's another commonly heard dieting myth. One that may actually be true, though... albeit only if the gum is a nicotine gum, which could in fact promote fat loss | more

Trigger vs. support - That's an important difference! The most significant result of the initially referenced meta-analysis by Muckelbauer et al. was after all the disparity between studies of individuals dieting for weight loss and those who were on ad libitum diets. A disparity which suggest a weight-reducing effect of increased water consumption occurs only if you are on an energetically reduced diet (just like the subjects in the study at hand). In studies in general mixed-weight populations like you and me, however, such an effect has - as of yet - not been observed. It is thus more than questionable, whether pre-diluting each and every of your meals with 500ml water is going to help you stay lean. What it may do - and that's in fact something the Peretti study suggests - is to help you stick to a calorically restricted diet and thus lose weight faster and more effectively | Comment on Facebook!

References:

• Daniels, Melissa C., and Barry M. Popkin. "Impact of water intake on energy intake and weight status: a systematic review." Nutrition reviews 68.9 (2010): 505-521.
• Dennis, Elizabeth A., et al. "Water Consumption Increases Weight Loss During a Hypocaloric Diet Intervention in Middle‐aged and Older Adults." Obesity 18.2 (2010): 300-307.
• Muckelbauer, Rebecca, et al. "Association between water consumption and body weight outcomes in children and adolescents: A systematic review." Obesity 22.12 (2014): 2462-2475.
• Parretti, Helen M., et al. "Efficacy of water preloading before main meals as a strategy for weight loss in primary care patients with obesity: RCT." Obesity (2015).
• Tate, Deborah F., et al. "Replacing caloric beverages with water or diet beverages for weight loss in adults: main results of the Choose Healthy Options Consciously Everyday (CHOICE) randomized clinical trial." The American journal of clinical nutrition 95.3 (2012): 555-563.

Strength & Conditioning Update - Sep '15: Reduced Rest, 200kcal Extra-EE (+30%) | Dehydration Turns Sprint to Jog | Knee Wraps More Power, Lower ROM & Vastus Activity

No, this is not the first time you read about "battling the rope" and how it could be an excellent form of fat burning and conditioning HIIT training. In my previous article "Want to Get Ripped & Strong? 'Battling the Rope' Could be THE Exercise to Do!" I've already discussed the proven long-term benefits of this intense conditioning exercise | learn more.

Usually, I handpick the three best studies for overviews like this, but with the Journal of Strength and Conditioning research, this is not always easy. With the September issue, only some studies are interesting, and there are no real "blockbuster" that would deserve an article on their own. Don't get me wrong. There's still interesting information, there but I guess what's most interesting is significantly more open to debate than usually.

Accordingly, today's research update contains my very personal favorites from September 2015 issue of this journal. Well, my favorites minus one study by Soares et al. (2015) about which I've written in my April 2015 article "Single- vs. Multi-Joint, Rookie vs. Gymrat - How Much Rest is Required in Trained Athletes if Noobs Need 72h or More?" (read it!), when the study was published initially as an online exclusive "ahead of print" print article five months ago.

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• Rest intervals and their effects on metabolism and velocity loss during battling the rope and ballistic bench press exercises - With the studies by Ratames, et al. (2015) and Garcia-Ramos et al. the latest issue of the JSC contains not one but two studies that deal with the effects of reducing the inter-set (rope) and inter-rep (ballistic bench press = "bench throws") times.
  

  

  Figure 1: Aerobic and anaerobic energy expenditure with 2 and 1 minute rest between 30s bouts of battling the rope in the welve men and 10 women (age = 20.8 6 1.3 years) who participanted in Ratamess study (ibid. 2015).

  While Ratames' study shows the expected increase in energy expenditure and fatty oxidation, as well as the lactate levels and heart rates of the female subjects, when the rest-time between the 8 sets of 30-second intervals (15 seconds of single-arm waves and 15 seconds of double-arm waves) of battling the rope were reduced from two to one minute, the results of the study by Garcia-Ramos (2015) require a correlation analysis to confirm that increasing the inter-set rest during "bench throws" (=ballistic bench presses) with 30%RM, 40%RM, or 50%RM from 6 to 12 seconds ameliorated the otherwise linear decrease in the maximal number of reps significantly.
  
  

  

  Want to Design a Killer Workout? Reduce the Rest Times and Burn 37% More Energy During Your Workout!

  In view of the effect that both outcomes where expected, it may be most intriguing that the 33% and 32% increases in total energy expenditure in the men and women (respectively) in Ratamess study were significantly more pronounced than what one may have expected from a mere reduction in rest times. Based on Ratamess previously discussed study that involved a full body resistance training workout and increases in energy expenditure of up to 37%, SuppVersity veterans should not be too surprised by the efficacy increase due to the reduction of the rest times. One thing you should keep in mind, however, is that any decrease in rest times will also lead to an increase in fatigue. In the Ratamess study, the increased in the rate of perceived exertion was 14% in the female and 21% in the male subjects.
• No, hydration doesn't matter for marathoners, only - While we usually think of endurance athletes when we talk about the effects of (de-)hydration on exercise performance, the reality is that everyone can experience the ergolytic (=performance decreasing) effects of dehydration. Against that background, it's sad that the number of studies that quantify these effects is very limited. With Davies et al.'s (2015) latest contribution we do now have the first detailed study on the effects of dehydration on repeated sprint performance which is highly relevant for almost every teamsport and may also give us insights into the effects of dehydration on high(er) rep strength training.
  
  In their study, the researchers from several universities had eight male collegiate baseball players complete intermittent sprints either dehydrated (DEHY) by 3% body mass or euhydrated (EU). To induce the state of dehydration the men were subjected to heat with controlled fluid restriction occurring 1 day before the trial. During the actual trial, which was repeated with appropriate time for recovery, the participants completed twenty-four 30-m sprints divided into 3 bouts of 8 sprints with 45 seconds of rest between each sprint and 3 minutes between each bout.
  

  

  SuppVersity Suggested: Learn why sodium restriction in athletes is a stupid idea (learn more)

  The study outcomes, perceived recovery status (PRS), heart rate (HR), ratings of perceived exertion (RPE) (0–10 OMNI scale), and perceived readiness (PR) scale, as well as the session RPE (SRPE), were recorded after every sprint, and 20 minutes after completing the entire session, respectively.
  

  

  Figure 2: Sprint times and rates of perceived exertion after each bout of exercise (Davies. 2015).

  The authors'  2 (condition) × 3 (bout of sprints) repeated-measures ANOVA revealed a significant main effect of condition on mean sprint time (p = 0.03), HR (p < 0.01), RPE (p = 0.01), and PR (p = 0.02).
  
  In addition, the scientists' post hoc tests showed significantly faster mean sprint times for EU vs. DEHY during the second (4.87 ± 0.29 vs. 5.03 ± 0.33 seconds; p = 0.01) and third bouts of sprints (4.91 ± 0.29 vs. 5.12 ± 0.44 seconds; p = 0.02). Heart rate was also significantly lower (p ≤ 0.05) for EU during the second and third bouts. Post hoc measures also showed significantly impaired (p ≤ 0.05) feelings of recovery (PRS) before exercise and increased (p ≤ 0.05) perceptual strain before each bout (PR) during the second and third bouts of repeated sprint work (i.e., RPE and PR) and after the total session (SRPE) in the DEHY condition.
  
  

  

  Every Sip of Plain Water Can Reduce Your Type II Diabetes Risk | more

  It is thus hard to argue with Davis' conclusion that all three observed effects, i.e. the impaired sprint performance, the negatively altered perception of recovery status before exercise, and the increased RPE and HR response are reasonable arguments to make sure you're always staying well hydrated. Plus: If you think of the recently discussed study on the way hydration can help you avoid type II diabetes (read it again), this advise is just as relevant for non-athletes.
• Expected but often disclaimed reduction in vastus lateralis activity when squatting with knee wraps - Ok, ok... there's one thing that's missing here: The reduction occurs if the weight that's used with and without the knee wraps is identical. If, however, you are able to squat 10% more, which is very likely, since studies indicate increases of >20% in maximal isometric force during the squat exercise, independent of the level of stiffness of the knee wrap (Gomes. 2014), the results of Gomes' latest study (2015) are no real reason to worry about your gains.
  

  

  Figure 3: Changes in vastus lateralis (A), gluteus maximimus (B) EMG activity and knee and hip angles (C) when doing back squats with (KW) or without (NW) knee wraps (Gomes. 2015).

  Eventually it would just have been a reduction in vastus lateralis activity, anyway. For the gluteus the activity doesn't change, anyways; and that in spite of the fact that the range of motion (the knee angle | Figure 3, right, black bars) is reduced when you're squatting with knee wraps (KW) vs. without wraps (NW).

Bottom line? You don't really need one, do you? So, instead of giving you another summary of the already dicussed implications of the (in part unsurprising) results of the previously discussed studies, I am inclined to give you a second serving in form of an extra-study.

Figure 4: Hooper and his colleagues from the Ohio State University believe that the increased fast ball, and driving / approach shot accuracy in high-level baseball pitchers and golfers they observed when the athletes wore upper body compression garments is mediated by improved proprioceptive cues during upper-body movements (Hooper. 2015).

The study was conducted at the Ohio State and dealt with the effects of upper-body (!) compression garment on athletic performances. Now, while we do have ample evidence of often subtle, but significant benefits of lower body compression garments, the study at hand is the first one I have read that reports significant performance improvements in eleven Division I collegiate pitchers (age: 21.0 ± 2.9 years; height: 181.0 ± 4.6 cm; weight: 89.0 ± 13.0 kg; body fat: 12.0 ± 4.1%) and 10 Division I collegiate golfers (age: 20.0 ± 1.3 years; height: 178.1 ± 3.9 cm; weight: 76.4 ± 8.3 kg; body fat: 11.8 ± 2.6%) in terms of fastball accuracy (30% improvement) and driving (21%) as well as accuracy (17%), respectively. That's quite a significant benefit for high-level athletes - an effect of which the authors, Hooper et al. (2015), believe that it was "most likely mediated by improved proprioceptive cues during upper-body movements" (Hooper. 2015) | Comment on FB!

References:

• Davis, J.-K, Laurent, CM, Allen, KE, Green, JM, Stolworthy, NI, Welch, TR, and Nevett, ME. Influence of dehydration on intermittent sprint performance. J Strength Cond Res 29(9): 2586–2593, 2015
• García-Ramos, A, Padial, P, Haff, GG, Argüelles-Cienfuegos, J, García-Ramos, M, Conde-Pipó, J, and Feriche, B. Effect of different interrepetition rest periods on barbell velocity loss during the ballistic bench press exercise. J Strength Cond Res XX(X): 000–000, 2015 
• Gomes, Willy Andrade, et al. "Acute effects on maximal isometric force with and without knee wrap during squat exercise." Int J Sports Sci 4.2 (2014): 47-49.
• Hooper, DR, Dulkis, LL, Secola, PJ, Holtzum, G, Harper, SP, Kalkowski, RJ, Comstock, BA, Szivak, TK, Flanagan, SD, Looney, DP, DuPont, WH, Maresh, CM, Volek, JS, Culley, KP, and Kraemer, WJ. Roles of an upper-body compression garment on athletic performances. J Strength Cond Res 29(9): 2655-2660, 2015
• Ratamess, NA, Smith, CR, Beller, NA, Kang, J, Faigenbaum, AD, and Bush, JA. Effects of rest interval length on acute battling rope exercise metabolism. J Strength Cond Res 29(9): 2375–2387, 201
• Soares, S, Ferreira-Junior, JB, Pereira, MC, Cleto, VA, Castanheira, RP, Cadore, EL, Brown, LE, Gentil, P, Bemben, MG, and Bottaro, M. Dissociated time course of muscle damage recovery between single- and multi-joint exercises in highly resistance-trained men. J Strength Cond Res 29(9): 2594–2599, 2015.

Gluten Research Update: Cesarean Section, Breast Feeding, Noocebo Effects and the ‘Right’ & ‘Wrong’ Bacterial ‘Poop’

As read on the SV Facebook: Baking makes gluten resilient to digestion, the presence of protein does the opposite. The food matrix makes the difference.

In view of the fact that "gluten" is or isn't (literally) in everyone's mouth or tummy, I thought that it may make sense to keep you up-to-date on the latest interesting research in the area of non-celiac gluten sensitivity and celiac disease.

Don't worry I am not going to bother you with the typical Internet bogus about how cancer, obesity and everything else we are or are not suffering from (yet) is triggered by gluten. What I will do, though, is to summarize and discuss the results of two recent studies and one review on the connection between our microbiome and our very individual susceptibility to gluten-related health problems

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

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• Celiac disease and non-celiac gluten sensitivity may be all about the microbiome and begin at the very moment you're born via cesarean section and worsen when you're not breastfed - In a soon-to-be-published review in Nutrients Cenit et al. try to elucidate whether gluten intolerance and celiac disease are consequences or triggers of significant imbalances in the bacterial composition of the human microbiome and how one or the other may eventually come about..
  
  As the authors point out, there are in fact studies which suggest that the early colonization of the infant’s gut in conjunction with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of our kids' oral tolerance to gluten.
  

  

  Figure 1: Proposed model for celiac disease (CD) pathogenesis. Specific host genetic makeup and environmental factors could promote the colonization of pathobionts and reduce symbionts, thus leading to dysbiosis. Dysbiosis may contribute to disrupting the immune homeostasis and gut integrity, thereby favoring CD onset and aggravating the pathogenesis (Cenit. 2015).

  In that, the early colonization of the intestinal tract is of particular importance, because it programs a normal or abnormal immune reaction to gluten (and other potential allergens). It is thus no wonder that celiac disease and a whole host of other autoimmune diseases have been linked to a lack of, or an improper early colonization of the intestinal tract and the consequential misprogramming of the immune cells. In that, it has been suggested that the resulting dysbiosis may affect autoimmunity by altering the balance between tolerogenic and inflammatory members of the microbiota and, therefore, the host immune response.
  
  Needless to say that the increased risk of autoimmune diseases is a standalone problem. It is after all not a mere reaction to the bacteria, but a bacterially induced phenomenon that involves the epigentic reprogramming of a whole host of genes. This process is however (unfortunately) so complex that we haven't yet fully understood the individual bacteria-gene and gene-gene interactions. Everyone, who tells you otherwise is lying - probably to sell his snake oil or snake oilish lifestyle advise.
  

  

  Figure 2: While there's one outlier, 3/4 studies on the effects of breastfeeding when the first gluten containing foods are introduced show significantly reduced risks of developing celiac disease (Akobeng. 2006).

  Among the few things we do know, though, is that breastfeeding and the way it promotes the early colonization of the gut with Bifidobacterium spp. is associated with a reduced risk of gluten intolerance. This is particularly true, if gluten containing foods are introduced while the kids are still breastfed (-52% according to a meta-analysis by Akobeng et al. 2006).

Breast milk contains a gliadin specific anti-body - What does that mean? Özkan et al. were the first to describe the presence of gliadin-specific IgA antibodies in breast milk (Özkan. 2000). The presence of significant amounts of this anti-body in the breast-milk (and even more in the colostrum) of 105 healthy mothers (aged 17 – 36 years) is generally understood to be one of the potential pathways by which breast milk and colostrum can protect children from celiac disease by educating the immature immune system of newborn children.

• The fact that these benefits do not apply for every breastfed child may be explained by (epi-)genetic polymorphisms of the mother, such as the altered concentration of several immune markers that have been observed by several researchers in the breast milk of mothers with celiac disease (Olivares. 2014). If that's in fact the case, it's hardly astonishing that the number of celiac patients began to rise when the use of formula peaked and is exploding now that more and more women with celiac disease (or non-celiac gluten sensitivity) are feeding their children with "non-protective" breast milk. We must be careful, though, not to jump to conclusions. There are, after all, as Cenit et al. point out "no robust prospective studies revealing how differences in breast milk composition and intestinal microbiota acquisition and evolution early in life might ultimately protect or contribute to CD onset" (Cenit. 2015).
  
  A similar healthy skepticism is necessary with respect to the link of cesarean sections and an increased susceptibility to gluten sensitivity (Dominguez-Bello. 2010). While it would appear logical to assume that the lack of exposure to the vaginal microbiome may contribute to the previously mentioned misprogramming of the immune system, it would be overtly simplistic to assume that gluten wouldn't be a problem if we were all breastfed and born the natural way.
  

  

  Figure 3: Increases in risk of full-blown celiac, intestinal inflamation and the presence of markers of celiac disease in the blood in subjects with previous exposure to antibiotics; in all fairness it must be said that the risk increase decreased when individuals who were exposed within the last 24m were excluded - even then the reduced 30% increase was statistically significant and practically relevant, though (Mårild. 2013)

  In conjunction with the indisputable link between the (early) use of antibiotics (Mårild. 2013 | see Figure 3) and the first successful efforts to ameliorate the chronic inflammation in celiac guts with prebiotics, there is yet little doubt that the "right" microbial make-up may be what distinguishes celiacs from patients with non-celiac gluten insensitivity and the still large number of people who don't appear to react to gluten at all.
• Study in healthy subjects, celiacs and their relatives suggests that the way your bacteria metabolize gluten may make you sick - From the first study, or rather review, I've analyzed in this feature article we've already learned that the inability to digest or handle gluten may be transmitted via certain immune factors in the breast milk from mother to child. It is thus particularly interesting that scientists from the Universidad de Léon in Spain who compared the stool of sixteen healthy volunteers on normal diet, eleven healthy volunteers on gluten-free diet (GFD), seventy-one relatives of CD patients on normal diet and sixty-nine relatives on GFD for several proteolytic activities, cultivable bacteria involved in gluten metabolism, SCFA and the amount of gluten found that significant differences in how celiac disease patients metabolized gluten.

Good news for celiacs: With the increasing awareness of celiac disease and gluten intolerance and the ever-increasing market shares of gluten-free products, it has become relatively easy to eat gluten-free, these days. Against that background it is all the more important that a recent study shows remission rates of 37% and general improvements in more than 50% of the patients in a recent study investigating the efficacy of gluten-free diets in celiacs over a four-year period (Newnham. 2015). The only potentially "bad" news is that all subjects gained significant amounts of body fat - specifically in the first year. The lean body mass indices, which did also improve, on the other hand, improved only very slowly and irrespective of status at diagnosis.

• 

  Table 1: Cultivable bacteria involved in gluten metabolism isolated from faeces of healthy subjects, active coeliac disease patients and firstdegree relatives (Caminaro. 2015).

  In contrast to healthy volunteers, their feces showed a significantly higher glutenasic activity (FGA), tryptic activity (FTA), SCFA, but lower levels of faecal gluten. That's interesting, yet counter-intuitive. After all, we've previously thought that one of the main problems of celiac disease and non-celiac gluten sensitivity is that the proteins are not broken down. Rather than that the results of the study at hand suggest that celiacs harbour bacteria that generate immunogenic peptides or pro-inflammatory metabolites which are the actual triggers of the problem (otherwise they'd have to poo out at least as much gluten as the other subjects on the gluten-free diets).
  
  Needless to say that this result does, once more, point toward fecal transplants or prebiotics as potential future treatment options celiac disease and non-celiac gluten sensitivity... with the only problem being: We don't know yet which bacteria we want to support and which to annihilate to solve the problem. If you look at the data in Table 1, though, killing the Clostridium and promoting the Lactobacillus population could be a first step to reinstalling a less celiac-prone gut microbiome.
• More 60% of non-celiac gluten patients don't react to gluten in randomized clinical study - That's certainly an impressive number Zanini et al. report in their latest paper in Alimentary Pharmacology and Therapeutics (Zanani. 2015).
  
  

  

  Let's hope aspergillus niger does not produce the wrong proteins when breaking down gluten otherwise it would make NCGS worse not better. Thus, further studies are needed. 

  In the corresponding study the researchers studied 35 non-CD subjects (31 females) that were on a gluten-free diet (GFD), in a double-blind challenge study. Participants were randomised to receive either gluten-containing flour or gluten-free flour for 10 days, followed by a 2-week washout period and were then crossed over. The main outcome measure was their ability to identify which flour contained gluten. Secondary outcome measures of the study from the University and Spedali Civili of Brescia in Italy were based upon Gastrointestinal Symptoms Rating Scale (GSRS) scores (criteria & results see Figure 4).
  
  In contrast to what the Internet experts are trying to make you believe, only 12 and thus hardly more than 34% of the allegedly highly gluten-intolerant patients were able to tell when they were fed gluten-containing flour based on increases in pain, reflux, indigestion, diarrhoea, and constipation.
  

  

  Figure 4: Increased severity of symptoms according to whether subjects were able to distinguish whether they were fed a gluten-containing or gluten-free diet (Zanani. 2015).

  Seventeen participants (49%), on the other hand, swore black and blue that they had been fed the gluten-containing flour when they were on the gluten-free diet (and if you look at the data in Figure 4, they even felt worse than those who were actually sensitive ;-).
  
  Now, what's most intriguing about this is that the study proves that there's a non-negligible noocebo effect involved, when it comes to non-celiac gluten sensitivity. One that's powerful enough to have people experience real increases in pain, reflux, indigestion, diarrhoea, and constipation... that tells you something about how infections reading too much bogus on the internet is, right?

Is Noneliac Gluten Sensitivity Legit? A Recently Published Review of the Latest Scientific Evidence on NCGS by Alex Leaf (Guestpost) May Help You Decide Whether you Even Want to Do the Painstaking Test | more

Bottom line: By including yet another study that puts a huge question mark behind the allegedly ever-increasing prevalence of non-celiac gluten intolerance into this write-up I am not trying to suggest that this pathogenesis does not exist. I am just trying to remind you that there is good evidence that it can also be triggered by the mere assumption that you have NCGS.

With that being said, the actual topic of this feature article is not the noocebo effect of the aggressive gluten-free propaganda, but rather the evidence of the existence of a physiological link between "dysbiosis" (in the broadest sense), the subsequent mal-metabolism of gluten by the "wrong" bacteria in your gut and the occurence of gluten sensitivity and full-blown celiac disease.

As bad as this may sound, the potential existence of this link between the gut microbiome and gluten sensitivity is actually good news: If the influence of your current gut bugs is in fact as huge as some of the scientists speculate, it should be possible to ameliorate, if not annihilate, the symptoms by reinstalling a "corrected" gut microbiome that helps celiacs and individuals with non-celiac gluten sensitivity metabolize gluten "correctly". This in turn could eventually even reverse the epigenetic changes that are causally involved in the inflammatory immune response to gluten and thus alleviate at least the nasty problems that occur if celiacs consume really small amounts of gluten incidentally. Whether it will fully reverse celiac disease, though, appears more than just questionable to me | Comment on Facebook!

References:

• Akobeng, Anthony K., et al. "Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies." Archives of disease in childhood 91.1 (2006): 39-43.
• Caminero, et al. "Differences in gluten metabolism among healthy volunteers, coeliac disease patients and first-degree relatives." British Journal of Nutrition (2015): Ahead of print.
• Dominguez-Bello, Maria G., et al. "Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns." Proceedings of the National Academy of Sciences 107.26 (2010): 11971-11975.
• Mårild, Karl, et al. "Antibiotic exposure and the development of coeliac disease: a nationwide case–control study." BMC gastroenterology 13.1 (2013): 109.
• Newnham, Evan D., et al. "Adherence to the gluten‐free diet can achieve the therapeutic goals in almost all patients with coeliac disease: A five‐year longitudinal study from diagnosis." Journal of gastroenterology and hepatology (2015).
• Olivares, Marta, et al. "Human milk composition differs in healthy mothers and mothers with celiac disease." European journal of nutrition 54.1 (2014): 119-128.
• Özkan, T., T. Özeke, and A. Meral. "Gliadin-specific IgA antibodies in breast milk." Journal of international medical research 28.5 (2000): 234-240.
• Zanetti, et al. "Randomised clinical study: gluten challenge induces symptom recurrence in only a minority of patients who meet clinical criteria for non-coeliac gluten sensitivity." Alimentary Pharmacology and Therapeutics (2015): Ahead of print.

Kids' Low GL Breakfast Boosts Cognitive Performance 24h Later | Maternal Low Protein Diet Programs High Myostatin, Low Muscularity | Beef Beats Pickled, Not Baked Herring

We all know this is not a healthy breakfast. What we don't or rather didn't know, though, is that you have to test on two consecutive days to find out how unhealthy it actually is for your kids' brains. With Young's study we learned that.

In what? That's probably what you are asking yourself now that you've read that beef beats pickled, but not baked herring, right? Well the answer to this question can be found in my brief summary of the results of Svelander's recent meal-response study. It's, as you may have guessed, the insulin response that sucks for pickled herring. What sucks even more, though, are mothers who are afraid of protein. After all, Liu's latest study shows that they may be setting their kids up to a life as skinny fatness.

When I come to think about it, this may yet be better than giving your kids a high glycemic load breakfast to take to school. After all, Young's latest study shows quite impressively what previous studies may have missed. The ill effects of high GL breakfasts on cognition are neither immediate, nor restricted to the late AM. No, they rather last for 24h+ and maybe even longer.

Learn more about fasting and eating / skipping breakfast at the SuppVersity

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Breaking the Breakfast Habit

Fasting, Cardio & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

• Maternal low-protein diet affects myostatin signaling and protein synthesis in offspring's skeletal muscle - Ok, we are talking about swine, but (a) many human beings behave much worse than swine and (b) swine are actually a much better model of human metabolism than rodents and many primates (the real reason they are not the standard model is that they are too large and too long-lived, which means they need too much space, the studies last too long and get much too expensive).
  
  It is thus more than likely that a very similar effect on myostatin and protein synthesis as it was observed by Liu et al. in their latest study in the European Journal of Nutrition where the swine who were fed a protein-deficient diet with only 6% of the energy from protein gave birth to piglets with (a) significantly reduced body weight, (b) significantly reduced muscle weight, (c) extremely reduced relative muscle weight (to body weight) and (d) small muscle with miniscule intramuscular domains.
  

  

  Figure 1: Body weight, muscle weight (LD), myofiber cross sectional are and rel. muscle weight (LD/BW) of piglets born to sows on protein sufficient (12% | SP) and deficient (6% | LP) diets (Liu. 2015).

  While you can see all of that in Figure 1, the reasons for the lack of muscularity can be seen in Figure 2 which tells you that the piglets that were born to mothers on the low protein (LP) diet had significantly increased myostatin (remember myostatin blocks protein synthesis) and accordingly reduced S6K levels.
  
  With the former being the controller and the latter being the executor of protein synthesis, the results of Liu's study leave little room for speculation: A diet that contains only 6% protein - for humans ~20-30g (depending on your baseline intake) - may increase your offspring's risk of becoming under-muscled and skinny fat... what? No, I didn't say "beware vegans" - that was you!
• Herring (pickled & baked) vs. beef, round one - fight! When it comes to the postprandial lipid and insulin responses among healthy, overweight men, the baked herring is said to be the #1 "health choice" - and here's why.
  
  In the corresponding study, scientists from the Chalmers University of Technology, and the Gothenburg University had seventeen healthy, overweight men (mean age 58 years, BMI 26.4–29.5 kg/m2) consume standardized lunches together with 150g of baked herring, pickled herring or baked, minced beef on three occasions in a crossover design. Blood samples were taken just before and up to 7 h after the meal. The postprandial response was measured as serum concentrations of triglycerides (TG), total cholesterol and lipoproteins (LDL, HDL and VLDL), insulin, 25-OH vitamin D (which did not change, by the way) and plasma fatty acid composition.
  

  

  Figure 2: Insulin response of eventeen healthy, overweight men (mean age 58 years, BMI 26.4–29.5 kg/m2) to std. lunches w/ baked or pickled herring, or baked, minced beef (Svelander. 2015). 

  In contrast to the pickled version, where the added sugar messed with the insulin and insulin response (the latter is not shown in Figure 2), both, the baked herring and the baked, minced meat did quite well. Differences in the cholesterol response as you'd expect them did not exist. There was however a small, albeit allegedly statistically significant advantage for the fish(es) in terms of the triglyceride response, which was lower than in the minced beef trial.
  
  Whether that's actually due to the extra omega-3s and whether it is even half as health-relevant as the scientists conclusions that their result "supports previous studies on the beneficial effects of herring on cardiovascular health" (Svelander. 2015) is yet highly questionable, if you asked me.
• Isomaltulose effectively reduced the GL of kids breakfasts and has beneficial effect on their cognitive performance in the late AM and on a 2nd day! If you are following the SuppVersity news on Facebook, you will know that although previous research has associated the glycaemic load (GL) of a meal with cognitive functioning, typically the macro-nutrient composition of the meals has differed, raising a question as to whether the response was to GL or to the energy, nutrients or particular foods consumed.
  
  With the latest study from the University of Wales Swansea, this different. The study that was conducted by Hayley Young, and David Benton contrasted two breakfasts that offered identical levels of energy and macro-nutrients, although they differed in GL, i.e. the insulinogenic effect of the (otherwise identical) carbohydrate content

  "Using a repeated-measures, double-blind design, 75 children aged 5–11 years, from socially deprived backgrounds, attended a school breakfast club and on two occasions, at least a week apart, they consumed a meal sweetened with either isomaltulose (Palatinose™) (GL 31.6) or glucose (GL 59.8). Immediate and delayed verbal memory, spatial memory, sustained attention, reaction times, speed of information processing and mood were assessed 1 and 3 h after eating" (Young. 2015).

  Now, what is interesting and quite revealing with respect to the mixed results of previous investigations is that the nature of the meals did not influence any measure of cognition or mood after an hour; however, after 3 h, children’s memory and mood improved after the lower-GL breakfast.
  

  

  Figure 3: Kids who consumed the low GL meal with isomaltulose vs. glucose on day one had sign. improved information processing (left) and spatial memory (right) on day two (Young. 2015).

  What is even more striking, though, is the second-day effect on the speed at which the kids processed information faster and their spatial memory, which improved significantly when on the day after the kids had consumed the low GL meal. This observation is total news and it clearly suggest that the benefits of low GL meals on cognition are not necessarily acute, but may rather be accumulating.
  
  Overall, the kids were thus able to process information faster and had better spatial memory later in the morning, when they had the low glycemic load (GL) breakfast that was prepared with isomaltulose vs. glucose. The reason why you need any form of "sugar" (isomaltulose is still a sugar) in your kids' breakfast is still beyond me, though.

Is myostatin relevant for mass monsters only, or for normal trainees, as well? You can find the answer to this smart and justifiable question in this SV Classic Article: "More Evidence That Myostatin is an Important Inhibitor of Diet and Exercise Induced Muscle Gains in You & Me" | read more

Bottom line: If I had to pick only one study, I'd pick the Young study as my highlight of this brief nutrition science review and I'd say that it should be obvious why. I mean, come on: Who would have expected that eating a low glycemic load breakfast would yield significant cognitive benefits on the day after you consumed it even if your "day two"-breakfast does not have a low glycemic load?

For me, this is even more exciting than the sad revelation that low protein diets trigger epigenetic changes that are associated with significant increases in myostatin, subsequent decreases in protein synthesis and a significantly reduced muscle weight ... I can thus only hope that no pregnant woman actually believes that eating less than 10% protein would be good for her own health or the health of her unborn child | Comment on Facebook!

References:

• Liu, Xiujuan, et al. "Maternal low-protein diet affects myostatin signaling and protein synthesis in skeletal muscle of offspring piglets at weaning stage." European journal of nutrition (2014): 1-9.
• Svelander, Cecilia, et al. "Postprandial lipid and insulin responses among healthy, overweight men to mixed meals served with baked herring, pickled herring or baked, minced beef." European journal of nutrition (2014): 1-14.
• Young, Hayley, and David Benton. "The effect of using isomaltulose (Palatinose™) to modulate the glycaemic properties of breakfast on the cognitive performance of children." European journal of nutrition (2014): 1-8.