Showing posts with label on short notice. Show all posts
Showing posts with label on short notice. Show all posts
Wednesday, November 4, 2015
Kids' Low GL Breakfast Boosts Cognitive Performance 24h Later | Maternal Low Protein Diet Programs High Myostatin, Low Muscularity | Beef Beats Pickled, Not Baked Herring
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| 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. |
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 waredownloadsoft
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.
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.
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).
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.
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.
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).
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 waredownloadsoft 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.
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.
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).
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.
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| 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 |
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.
From BodyPump to HIIT, From Weight Lifting to Cardio - How Much Energy & Fat Do You Burn During & After Your Workouts and How do PWO Carbs or Protein Affect This
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| BodyPump is a fast paced workout with barbells. Light(er) weights, high reps, loud music and a drill instructor... if you know one, you'll know all of these group based "resistance training" workouts. |
While exercise and the exercise-induced increase in energy-expenditure is an important pillar of diet (+ exercise) induced weight loss. The dietary component is what makes you lose weight, while the exercise component is meant to (a) maximize the retention of lean muscle tissue and (b) improve your overall fitness and health. If you're just "working out to burn energy" you're destined to fail; not least because you will never be able to tell exactly how many kcals you've "left in the gym". And beware: Especially while dieting, it's usually much less than you think ;-)
Read more about exercise-related studies at the waredownloadsoft
Tri- or Multi-Set Training for Body Recomp.?
Alternating Squat & Blood Pressure - Productive?
Pre-Exhaustion Exhausts Your Growth Potential
Full ROM ➯ Full Gains - Form Counts!
Battle the Rope to Get Ripped & Strong
Study Indicates Cut the Volume Make the Gains!
Tri- or Multi-Set Training for Body Recomp.?
Alternating Squat & Blood Pressure - Productive?
Pre-Exhaustion Exhausts Your Growth Potential
Full ROM ➯ Full Gains - Form Counts!
Battle the Rope to Get Ripped & Strong
Study Indicates Cut the Volume Make the Gains!
- People overestimate the energetic demands of "intense" exercise (Berthiaume. 2015) - In view of the fact that everyone knows the (inaccurate) rule of thumb that says that the amount of energy (in kcal) you expend when you're jogging is roughly your body weight times 10 (it's actually rather body weight times 7, unless you're running really fast, by the way), it's not surprising that Berthiaume et al.'s latest study shows that their subjects, 40 healthy men and women (age: 31.7±5.8 years, body mass index [BMI]: 24±2.6 kg/m²), significantly overestimated the amount of energy they expended during a (perceived) "intense" BodyPump(TM) workout.
Instead of the 394.1±116 kcal, the subjects thought they'd burned, the scientists measurements yielded an average energy expenditure of only 250.3±67.8 kcal during the 60 minute workout. Now, that's not really a problem if do BodyPump, because you like group workouts like these. In view of the fact that the typical clientele of programs like these tends to charge the energy they expend during workouts against the energy from extra food they'd like to eat (BIG mistake, learn why), this may be problematic.
Figure 1: Young, healthy BodyPump practitioners overestimate the energetic demands of this kind of equipment based group workouts by over 36% (Berthiaume. 2015).
Now, you may remember the results of Vezina's 2014 study (see Figure 2 and previous article). In said paper they used a much more precise method to arrive at the actual energy expenditure. In Berthiaume's study, a simple SenseWear armband was used. That's not the "traditional calc." in Figure 2 that proved to be so unreliable in Vezina's study, but it may still suffer from the same shortcomings when it comes to measuring anaerobic vs. aerobic energy expenditure. It would thus be prudent to be at least somewhat skeptical of the exactness of Berthiaume's results.
Figure 2: Just a reminder: The energy expenditure (kcal per kg of body weight per hour) due to body weight exercises calculated based on oxygen uptake during the exercises (traditional) or during the rest periods has been shown to be rather under- than overestimated (Vezina. 2014 | read more) - Exercise type and post-workout supplementation influence post-exercise resting energy expenditure and respiratory exchange ratio (Wingfield. 2015) - I know, I have written about EPOC, which is actually nothing else than the total post-exercise energy expenditure in relation to the respiratory exchange ratio, repeatedly. There is a reason, though, that the latest study from the University of North Carolina still made it into the waredownloadsoft news: It compared six exercise sessions, consisting of three exercise modalities and two acute nutritional interventions - that's extraordinary, for sure.
- AEE - aerobic endurance exercise - 30-min on the treadmill at 45% to 55% of the heart rate reserve), high-intensity interval running
- HIIT - ten rounds of a 60-s treadmill run at 85% to 95% HRR with a 60-s passive rest period), and
- HIRT - high-intensity resistance training consisting of leg presses and bench presses, lunges, shoulder presses, biceps curls, and triceps extensions using free weights for three sets of 6RM to 8RM followed by a 20- to 30-s rest for each set of a given exercise and 2.5 min between each exercise
- CHO and PRO (25 g of CHO (maltodextrin) or PRO (whey isolate) mixed with 6 oz of water in an opaque bottle.
Next to the post-exercise resting energy expenditure (REE) and respiratory rate (RER), which were analyzed via indirect calorimetry at baseline, immediately post (IP), 30 minutes (30 min) post, and 60 minutes (60 min) post exercise, the scientists obtained salivary samples, as well (both didn't change sign.). The latter were used to determine estradiol-β-17 and cortisol levels before the workouts. To exclude any influence of dietary changes, the subjects were asked to eat diets similar to those they had consumed when they wrote their 3-day food logs at the beginning of the study. Practically speaking, this meant that, on average, subjects ingested 2,078.7 ± 679.9 kcal, 253.7 ± 97.6 g CHO (approximately 48.8% CHO), 84.3 ± 29.9 g PRO (approximately 16.2% PRO), and 80.9 ± 36.7 g of fat (approximately 35.0% fat) per day.
Figure 3: Overview of the study design (Wingfield. 2015).
Interestingly, a statistical significant effect for the resting energy expenditure (REE) was observed only in the HIIT, yet not in the HIRT trial (Figure 4, A). This is a result you may not have expected based on the assumption that any form of intense activity (like resistance training in this case) should have some sort of "afterburn" effect.
Figure 4: Only the HIIT modality yielded sign. inter-group differences as far as the resting energy expenditure is concerned. Even those were very transient, though, and disappeared 30 min after the workout (Wingfield. 2015).
Cortisol is not your enemy - at least in the short run: As expected the hardest workout, the HIIT workout, produced the most significant increase in cortisol. The change was still not statistically significant, but I decided to mention it anyway, in order to take the chance and remind you of the fact that cortisol is a glucocorticoid that will not just gnaw away your muscles (it does so if it's chronically elevated), but is also involved in a host of beneficial processes including acute increases in performance and the facilitation of body fat loss (learn more).
- What is less surprising is the relatively small, but "significant" (statistically, only!) increase in REE in response to protein vs. carbohydrate (Figure 4, B). So, protein is thermogenic even after a workout. Unfortunately, the increase in energy expenditure and the increase in fatty oxidation as signified by the reduced respiratory exchange ratio in Figure 5 B are way too small to be of any practical relevance.
Eventually, the same can be said of the decrease in RER (=increase in fatty oxidation) in response to the HIIT and the increase in RER (=decrease in fatty acid oxidation) in response to the HIRT regimen. Both are statistically significant and look large enough to be relevant. When all is said and done, it does yet not really matter if you burn fat directly or glucose first. Whether you lose or gain body fat is after all a matter of the total energy balance over days and weeks, and not the fatty acid oxidation during and 60 minutes after your workouts.
Figure 5: Effect of exercise modality and CHO vs. PRO supplement on the respiratory exchange ratio (RER); lower values indicate greater fat and lower carbohydrate oxidation (Wingfield. 2015).
So, what did we learn today? I guess the most important message is that even if it would make sense to charge the energy you expend at the gym against the amount of energy you consume in form of foods, you would fail miserably, because your estimation of how many kcals you've actually "left at the gym" are going to be hilariously inaccurate.
Against that background the results of the Wingfield study are still interesting, but of highly questionable practical value. Your decision whether you do steady state medium intensity cardio, resistance training or high intensity interval training should always be based on your training goals, not the energetic demands of the workouts. In that, fitter individuals (like yourself?) will see better results with high intensity interval training than classic cardio - assuming their training goal are increases in cardiovascular fitness. To maintain the fitness you have, steady state cardio can obviously still be an option; and weight training + optional protein supplements are the perfect choice for anyone who's interested in being and looking fit | Comment!
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| Five Good Reasons Why At Least 50% of Your 2015 'Cardio' Training Should Be High Intensity Interval Training (HIIT) | more |
References:
- Berthiaume, M. P., et al. "Energy expenditure during the group exercise course BodypumpTM in young healthy individuals." The Journal of sports medicine and physical fitness 55.6 (2015): 563.
- Vezina, Jesse W., et al. "An Examination of the Differences Between Two Methods of Estimating Energy Expenditure in Resistance Training Activities." Journal of strength and conditioning research/National Strength & Conditioning Association (2014).
- Wingfield, et al. "The acute effect of exercise modality and nutrition manipulations on post-exercise resting energy expenditure and respiratory exchange ratio in women: a randomized trial." Sports Med Open. (2015)
Whey vs. Casein - Casein-Exclusive Increase in GLUT-4 Expression Beats Whey's Insulinogenic Effect // Creatine Builds Legs of Young & Old, Rookie & Pro, BB & Cyclist
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| If you drink "old school" protein shakes with milk and eggs, you don't have to worry if casein or whey is better on hypercaloric diets ;-) |
I mean, let's be honest: You wouldn't be excited if I wrote about study #1023 showing a practically irrelevant acute increase in protein synthesis, let alone totally meaningless increases in mTOR in response to the ingestion of whey protein, would you?
For today's installment of the short news, I will picked two studies that are at least not as simplistic (and useless) as the previously mentioned 1023rd whey protein study.
Want to become stronger, bigger, faster and leaner? Periodize appropriately!
30% More on the Big Three: Squat, DL, BP!
Block Periodization Done Right
Linear vs. Undulating Periodizationt
12% Body Fat in 12 Weeks W/ Periodizatoin
Detraining + Periodization - How to?
Tapering 101 - Learn How It's Done!
- Whey or casein? The answer to this question probably depends on your goals - That's at least what the complex results of a similarly complex series of experiments from the Snyder Institute for Chronic Diseases at the University of Calgary appears to suggest (Pezeshki. 2015). In the corresponding study, the researchers determined the effects of dietary whey, casein, and a combination of the 2 on energy balance, hormones, glucose metabolism, and taste preference in rats.
Yes, this does mean that we must not uncritically transfer the results to humans. It does not mean, however, that we cannot use the results of Pezeshki's study, at all. Much of what we know and have later proven in human studies about our metabolism has initially been observed in rodents. Doing the same experiments with humans would not just have been significantly more expensive, it would also have been thwarted by misreported energy intakes and a lack of dietary control. So, if you belong to the "it's a rodent study, so I ignore it, if the results don't fit my world-view" faction, you are free to fast forward to the Lanhers study. If not, here's the elevator pitch on the two experiments the scientists conducted:- The hormone / energy expenditure experiment: Obesity Prone CD (OP-CD) rats were fed a high-fat control diet (33% fat energy) for 8 wk, and then randomly assigned to 4 isocaloric dietary treatments (n = 12/group): the control treatment (CO; 14% protein energy from egg white), the whey treatment (WH; 26% whey + 14% egg white), the casein treatment (CA; 26% casein + 14% egg white), or the whey plus casein treatment (WHCA; 13% whey + 13% casein + 14% egg white) for 28 d. Measurements included food intake, energy expenditure, body composition, metabolic hormones, glucose tolerance and key tissue markers of glucose and energy metabolism.
- The food intake / preference experiment: Naive Obesity Prone CD (OP-CD) rats (not the same rats as in experiment 1) were randomly assigned to 3 groups (n = 8/group). During an 8 d conditioning period, each group received on alternate days either the CO or WH, CO or CA, or CO or WHCA. Subsequently, preferences for the test diets were assessed on 2 consecutive days with food intake measurements at regular intervals.
Since you will usually hear that whey is the #1 glucose repartitioner this may seem odd. In view of the fact that insulin can only drive glucose into the cells if they actually "stretch out their glucose "suckers", i.e. the GLUT-4 receptors, it is yet only logical - and that despite the fact that we cannot (yet) explain the differential GLUT-4 response.
Figure 1: 0-60 minute hormone, glucose, cytokine and gene response to glucose tolerance test in diet-induced obese rodents fed diets containing either low amounts of protein or high amounts from whey, casein or a combination of whey + casein (Pezeshki. 2015).
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| Whey or casein hydrolysate - or rather no protein - what to use in your intra-workout beverage for endurance? Find out in this SV Classic |
- What remains to be seen, though, is whether this measurable, but not in all details statistically significant difference actually matters. If you look at the food intake and preference data in Figure 3. It would seem as if it didn't. I mean, if we apply "Taubes'ian" logic, here, the high(er insulin levels in the whey group should have made the rats overeat...
... a brief glimpse at the data in Figure 2, however, tells you that this was clearly not the case. It is thus not surprising that the final lean and fat mass percentages in Figure 3 did not differ significantly between the groups, even though some of you will notice a non-significant lean vs. fat mass advantage for the casein group.
Figure 2: Daily food intake during conditioning trials. Rats were fed, on alternate days, a control diet or whey (A), casein (B), or a combination of whey and casein (C). Mean hourly food intakes on 2 consecutive days of preference testing, with access to both control and one of the high protein diets (D, E, F | Pzeshki. 2015). - Eventually, it would still appear unwarranted to use the study at hand to argue in favor of casein instead of whey protein as your protein supplement of choice. If you are yet already following my suggestion to mix the two (read even more), the results of the study at hand would be another reason to stick to that practice.
Overall, we do yet have to remember that significant treatment effects in response to the increase in protein were observed in all groups. In that, it may be true that the casein group had the highest reduction in food intake (30-43% reduction) and appears to have ended up with a slightly better body composition, but hey, we are talking about non-significant differences in a study that was not just done on rodents, but on obese rodents ... and you know that the weight status obese vs. lean / athletic can make more of a difference in the way people / lab animals react to supplements than the difference between man and mouse. - Creatine and lower limb strength - what to expect? You are probably asking yourself now: "Why on earth is Adel so interested in this meta-analysis?" Well, the answer is as simple as it is personal: The only body part of mine that appears to to have ever really benefited from creatine supplementation, strength-wise, are my legs. Accordingly, I was attracted to the Lanhers' meta-analysis, because I hoped to find some clues on why this may be the case.
Now, I guess I don't give away too much, when I say that the paper didn't provide me with new insights in this respect. What the scientists' compilation and meta-analysis of the data did do, however, was to confirmation that I am not the only one whose "wheels" respond extremely favorably to creatine supplementation: One of the main results of Lanhers' meta-analysis of 60 (!) studies is after all that the effect of creatine supplementation on leg strength is not just statistically significant in almost every study they reviewed, it is also and maybe even more importantly and astonishingly independent of population characteristics, training protocols, and supplementary doses and duration (reread this - you don't have to superdose it!).
In that, I find it particularly striking that even training for mostly aerobic team sports, like handball, for example, can trigger significant increases in squat performance if the players are consuming 3-5g of creatine before or after their training sessions (Note: In the corresponding study by Izquierdo, the handball players also saw significant increases in bench press performance - It's thus by no means as if creatine was a "leg strength booster", only!).
For the total workout volume (not shown in Figure 4), Lanhers et al. report almost identical effect sizes as the researchers determined them based on the absolute increase in squat performance in kg (see Figure 4); and just like the relative strength gains, the relative volume increases did not depend on the training status or age (subjects were 21-69 years old) of the subjects.
Figure 4: Meta-analysis on maximal weight lifted (kg) in squat. CI confidence interval, M male, SD standard deviation, T0 baseline, T1 following supplementation (Lanhers. 2015).
In view of these results, there's really no good reason to doubt the scientists' conclusions that (a) "[c]reatine supplementation is effective in lower limb strength performance" and (b) works "for exercise with a duration of less than 3 min". If you also take into account that the average effect size for weight and volume are in the range of ~30% irrespective of the population characteristic, training protocols, and supplementary doses and duration, I hope that you can agree that there's also no reason to doubt my repeatedly voiced recommendation to "take your creatine bros" ... ah, and take it with sodium bicarbonate, obviously ;-)
Bottom line: In view of the fact that both items of today's short news already have their own bottom lines, I am not sure if you even need an extra summary, but here you go: With the Pezeshki study we have initial evidence to question the longstanding, but hardly researched assumption that whey is the protein of choice for weight loss and glucose management. In spite of the fact that the results show only trends towards better body composition and improved glycemia with casein vs. whey and need confirmation in non-obese, even better athletic human beings, I will keep an eye on potential follow-up or related studies.
In that, I don't believe we will see an earth-shattering difference between the two protein sources in any potential follow-up, but what I really would like to know is the reason and mechanism behind the unexpected and unexplaind casein-induced increase in GLUT-4 receptor expression on the cell surface Pezeshki et al. observed in the study at hand (other studies often measure only total GLUT4!).
In contrast to the Whey vs. Casein study, Lanhers' meta-analysis of the effects of creatine on leg muscle strength and maximal training volume is so simple to interpret that you can summarize its implications in one sentence: "If you know that creatine will make you stronger, irrespective of how old you are, how you train and whether you take only 3g of much more, you either want to be weak or must be an idiot if you don't take it" | Comment on Facebook!
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| Suggested waredownloadsoft Classic: "10+ Things You Probably Didn't Know Whey & Peptides That Form During its Digestion Can Do" - When you've read this article, I promise you will (re-)appreciate the benefits of whey and forget the Pezeshki study until a follow-up / related study is published | more |
In contrast to the Whey vs. Casein study, Lanhers' meta-analysis of the effects of creatine on leg muscle strength and maximal training volume is so simple to interpret that you can summarize its implications in one sentence: "If you know that creatine will make you stronger, irrespective of how old you are, how you train and whether you take only 3g of much more, you either want to be weak or must be an idiot if you don't take it" | Comment on Facebook!
References
- Izquierdo, M. I. K. E. L., et al. "Effects of creatine supplementation on muscle power, endurance, and sprint performance." Medicine and Science in Sports and Exercise 34.2 (2002): 332-343.
- Lanhers, Charlotte, et al. "Creatine Supplementation and Lower Limb Strength Performance: A Systematic Review and Meta-Analyses." Sports Medicine (2015): 1-10.
- Pezeshki, et al. "Dietary Whey and Casein Differentially Affect Energy Balance, Gut Hormones, Glucose Metabolism, and Taste Preference in Diet-Induced Obese Rats." The Journal of Nutrition. First published ahead of print August 26, 2015.
Gluten Research Update: Cesarean Section, Breast Feeding, Noocebo Effects and the ‘Right’ & ‘Wrong’ Bacterial ‘Poop’
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| 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. |
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 waredownloadsoft
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
Is Gluten Intolerance Real?
- 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.
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.
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).
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.
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).
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).
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.
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.
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) - 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.
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).
Table 1: Cultivable bacteria involved in gluten metabolism isolated from faeces of healthy subjects, active coeliac disease patients and firstdegree relatives (Caminaro. 2015).
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).
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).
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 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.
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 ;-).
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).
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?
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| 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 |
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!
- 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.
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