Download Fitness Tools

Whether having breakfast will help or hinder glucose control will also depend on its macronutrient composition and carbohydrate content. In their 2011 study Pereira et al. were able to show that a high carbohydrate, high GI breakfast will have a similarly negative impact on glucose control of adults and children as having no breakfast at all (Pereira. 2011).

Intermittent fasting (IF), i.e. skipping breakfast and/or other meals in order to stay fasted for ~16h+ per day is no longer "all the rage", but still highly popular among people who believe in its health and weight loss benefits. And in fact, there is some research (also from a couple of Ramadan studies) that appears to confirm the notion that it is healthy and may - even without deliberate caloric restriction - facilitate weight and more importantly fat loss.

On the other hand, intermittent fasting conflicts with everything we've been (falsely?) told about the benefits of frequent meals. Benefits of which waredownloadsoft readers know that they are quasi-non-existent, in most healthy individuals and sometimes even counter-productive in obese and diabetic individuals, where most studies refute that eating more frequently provides significant weight loss benefits in the context of a calorically restricted diet.
Now, a recent study from the Diabetes Unit, Wolfson Medical Center of the Sackler Faculty of Medicine at the Tel Aviv University, the Lund University in Sweden and the Hebrew University of Jerusalem (Jakubowicz. 2015) suggests that extending your overnight fast by skipping breakfast may have real (not just corollary) detrimental effects on habitual breakfast eaters (learn why this is important) who are suffering from type II diabetes (with glycated hemoglobin (HbA1c) levels of 7–9% (the subjects in the study at hand were more than just pre-diabetic).

In this group of subjects, skipping breakfast increases post-prandial hyperglycemia (PPHG) after lunch and dinner. It lowers the important GLP-1 response to the meals (learn more about how GLP-1 is important in "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?") and impairs the subjects' already messed up insulin response. More specifically,

• Three meals may be ok, but six meals are actually counterprodutive in T2DM.

  the lunch AUC0-180 for glucose, FFA, and glucagon were 36.8, 41.1 and 14.8% higher, respectively, and the AUC0-180 for insulin and  iGLP-1 17.0% and 19.0% lower, respectively, on the NoB[reakfast] day compared with the YesB[reakfast] day (P < 0.0001), 
• the dinner AUC0-180 for glucose, FFA, and glucagon were 26.6, 29.6, and 11.5% higher, respectively, and the the AUC0-180 for insulin and iGLP-1 were 7.9% and 16.5% lower on the NoB day compared with the YesB day (P < 0.0001), on the other hand

Whether the conclusion that "[b]reakfast consumption could be a successful strategy for reduction of PPHG [prostprandial hyperglycemia] in type 2 diabetes" applies to every type II diabetic is yet as questionable as the assumption that you could extrapolate the data from this acute phase study and use it to predict the long-term response in diabetics, let alone health individuals.

Figure 2: Hunger, satiety, plasma glucose and insulin in the Eaters and Skippers in the two conditions in Thomas (2015).

If we go back to Thomas' recently published study (I have discussed it in detail here), it is after all obvious that the scientists choice of subjects who consume breakfast regularly may have thwarted their results. I mean, the researchers from the University of Colorado School of Medicine and the Denver Health Medical Center have shown quite conclusively that one's breakfast habits will determine whether skipping breakfast increases insulin, hunger and blood lipids or not.
References:

Yogurt does not have to be served this way to be healthy, but I bet many of your friends and relatives would be amazed and much more likely to pass on the cream cake or tiramisu if the option was an appetizing dessert like that.

In a world where being vegan is "the new sexy" and eating animal products "the new smoking", dairy has lost much of its former appeal. I mean, we all remember how the literal "glass of milk" has been marketed as a daily health booster, right? Well, times have changed and that despite the fact that an impartial review of the evidence suggests more benefits than downsides to dairy consumption. Specifically fermented dairy, first and foremost yogurt, but also cheese can, and in the case of yogurt maybe even should be part of your of your diet. And that's not just because both are an often forgotten, but essential part hailed "Mediterranean diet" (Vasilopoulou. 2013). The same diet of which recent studies say that it's associated w/ a -30% reduced CVD risk (Estruch. 2013).
How's that? Well, cheese may be full of saturated fat and cholesterol. In controlled trials, however, even high fat cheese has - in contrast to butter, for example (Hjerpsted. 2011) - no or even beneficial effects on the total and LDL cholesterol levels of otherwise healthy individuals. In addition, real dairy cheese has been found to have neutral effects on body weight when it is consumed as part of an otherwise healthy diet. Some traditional types of cheese even share the anti-hypertensive effects of yogurt, which is still the real star among the fermented dairy products. A star that has been shown to prevent weight gain, reduce cholesterol and more meaningful makers of heart disease risk, to improve glycemia, and to prevent the development and/or progression of type II diabetes in both experimental and observational studies (Tholstrup. 2006; Nestel. 2008; Mozaffarian. 2011, Tapsell. 2015).

Figure 1: A study comparing the effects of getting 13% of one's total daily fat intake from cheese vs. butter on the blood lipids in healthy men and women shows increases in TC and LDL only with butter (Hjerpsted. 2013). In contrast to the total and LDL cholesterol levels, the total / HDL cholesterol ratio wasn't affected sign. by butter though. You can thus expect both forms of high fat dairy having negligible cholesterol mediated effects on the heart health of healthy indiv.

In short, the existing scientific evidence leaves little doubt that yogurt is, maybe next to whey (learn why), the star among the dairy based health foods. Part of its beneficial effects are probably mediated by its ability to improve integrity of our digestive tracts and thus to prevent the influx of pro-inflammatory, obesogenic, and pro-atherogenic endotoxins into the bloodstream. With it being available for almost 10,000 years, yogurt is thus the first and oldest "functional food" to act on the recently discovered link between "leaky gut", obesity and cardiovascular disease (Lam. 2011).

Figure 2: Proposed mechanisms by which yogurt consumption exerts beneficial health effects (Marette. 2015)

Some scientists like Marette & Picard-Deland even go so far as to argue that an early introduction of yoghurt into the diets of children is vital to establish a microbial community that supports long-term health. And while Taspell et al. are right to highlight that "[m]ore research is needed" (Tapsell. 2015). There's little doubt that "yogurt can deliver essential nutrients with high bioavailability and relatively low energy density" (ibid).
The fact pertinent trials still show ambiguous results, when it comes to the effects of yogurt on body weight and composition (Chen. 2012) is mostly a results of the study designs which usually require subjects to simply increase their intake of dairy products, in general, or yogurt, in particular. As Taspell (2015) points out in a recent review this is a problem "if the energy content of the diet is not managed, particularly with high-fat varieties and with added ingredients such as sugar" (ibid). If it is managed, as in habitual consumers, though, high(er) yogurt intakes have been shown to be associated...

• Prevalent Nutrient Deficiencies in the US: More Than 40% are Vitamin A, C, D & E, Calcium or Magnesium Deficient and >90% Don't Get Enough Choline, Fiber & Potassium | read more

  with higher scores for the Dietary Guidelines Adherence Index (DGAI) and higher intakes of key micronutrients, as well as significantly higher potassium and fiber intakes - two nutrients the average Westerner usually doesn't get enough of (Wang. 2013)
• with reduced weight gain in a large US cohort study that tracked the food intake and weight development of 22 557 men and 98 320 women for four years; with R = -0.89 the correlation is similar to the one for the recommended amount of physical activity vs. being sedentary and thus nothing you should ignore as being practically irrelevant
• with reduced inflammation as measured by C-reactive protein, IL-6 and TNF-a in the ATTICA study that involved 3042 healthy Greek adults for whom only 8 servings of dairy products, in general (full fat and low fat!), were linked with already significant reductions in inflammation; since a greater proportion of the cohort reported consumption of fermented dairy foods such as feta cheese (93%), hard yellow cheese (92%) and low-fat yogurt (50%) compared to low-fat milk (46%), we can yet safely assume that many of these anti-inflammatory benefits were actually due to fermented dairy products
• with reduced type II diabetes risk (-12% or both yogurt and cheese) in the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct Study (Sluijs. 2012);
  

  Table 1: HRs for risk of type 2 diabetes associated with the substitution of yoghurt (137 ga) for snacks and desserts: EPIC-Norfolk study (n=4,127 | O'Connor. 2014)

  with 28% reduced diabetes risk the results of the EPIC-Norfolk cohort study in the UK were even more impressive (O’Connor. 2014); as you can see in Table 1 the results of this study do yet also underline that the benefits will occur only if yogurt replaces other, less healthier ingredients of ones diet.

References:

• Asemi, Zatollah, et al. "Effects of daily consumption of probiotic yoghurt on inflammatory factors in pregnant women: a randomized controlled trial." Pakistan journal of biological sciences: PJBS 14.8 (2011): 476-482.
• Chen, Mu, et al. "Effects of dairy intake on body weight and fat: a meta-analysis of randomized controlled trials." The American journal of clinical nutrition 96.4 (2012): 735-747.
• de LeBlanc, Alejandra de Moreno, and Gabriela Perdigón. "Yogurt feeding inhibits promotion and progression of experimental colorectal cancer." American Journal of Case Reports 10.4 (2004): BR96-BR104.
• Douglas, Steve M., et al. "Low, moderate, or high protein yogurt snacks on appetite control and subsequent eating in healthy women." Appetite 60 (2013): 117-122.
• Elwood, Peter C., et al. "The consumption of milk and dairy foods and the incidence of vascular disease and diabetes: an overview of the evidence." Lipids 45.10 (2010): 925-939.
• Estruch, Ramón, et al. "Primary prevention of cardiovascular disease with a Mediterranean diet." New England Journal of Medicine 368.14 (2013): 1279-1290.
• Fisberg, Mauro, and Rachel Machado. "History of yogurt and current patterns of consumption." Nutrition reviews 73.suppl 1 (2015): 4-7.
• Hjerpsted, Julie, Eva Leedo, and Tine Tholstrup. "Cheese intake in large amounts lowers LDL-cholesterol concentrations compared with butter intake of equal fat content." The American journal of clinical nutrition 94.6 (2011): 1479-1484.
• Lam, Yan Y., et al. "Role of the gut in visceral fat inflammation and metabolic disorders." Obesity 19.11 (2011): 2113-2120.
• Lithell, H., and B. Zethelius. "Glucose Tolerance and Cardiovascular Mortality." Arch. Intern. Med. 161 (2001): 397.
• Marette, André, and Eliane Picard-Deland. "Yogurt consumption and impact on health: focus on children and cardiometabolic risk." The American journal of clinical nutrition 99.5 (2014): 1243S-1247S.
• Moreno, Aznar LA, et al. "[Scientific evidence about the role of yogurt and other fermented milks in the healthy diet for the Spanish population]." Nutricion hospitalaria 28.6 (2012): 2039-2089.
• 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.
• Nestel, Paul J. "Effects of dairy fats within different foods on plasma lipids." Journal of the American College of Nutrition 27.6 (2008): 735S-740S.
• Nestel, Paul J., et al. "Effects of low-fat or full-fat fermented and non-fermented dairy foods on selected cardiovascular biomarkers in overweight adults." British Journal of Nutrition 110.12 (2013): 2242-2249.
• Neyestani, Tirang R., et al. "Improvement of vitamin D status via daily intake of fortified yogurt drink either with or without extra calcium ameliorates systemic inflammatory biomarkers, including adipokines, in the subjects with type 2 diabetes." The Journal of Clinical Endocrinology & Metabolism 97.6 (2012): 2005-2011.
• Nikooyeh, Bahareh, et al. "Daily consumption of vitamin D–or vitamin D+ calcium–fortified yogurt drink improved glycemic control in patients with type 2 diabetes: a randomized clinical trial." The American journal of clinical nutrition 93.4 (2011): 764-771.
• O’Connor, Laura M., et al. "Dietary dairy product intake and incident type 2 diabetes: a prospective study using dietary data from a 7-day food diary." Diabetologia 57.5 (2014): 909-917.
• Ortinau, Laura C., et al. "The effects of increased dietary protein yogurt snack in the afternoon on appetite control and eating initiation in healthy women." Nutr J 12.71 (2013): 10-1186.
• Panagiotakos, Demosthenes B., et al. "Dairy products consumption is associated with decreased levels of inflammatory markers related to cardiovascular disease in apparently healthy adults: the ATTICA study." Journal of the American College of Nutrition 29.4 (2010): 357-364.
• Sluijs, Ivonne, et al. "The amount and type of dairy product intake and incident type 2 diabetes: results from the EPIC-InterAct Study." The American journal of clinical nutrition 96.2 (2012): 382-390.
• Struijk, E. A., et al. "Dairy product intake in relation to glucose regulation indices and risk of type 2 diabetes." Nutrition, Metabolism and Cardiovascular Diseases 23.9 (2013): 822-828.
• Tapsell, Linda C. "Fermented dairy food and CVD risk." British Journal of Nutrition 113.S2 (2015): S131-S135. 
• Tholstrup, Tine. "Dairy products and cardiovascular disease." Current opinion in lipidology 17.1 (2006): 1-10.
• Vasilopoulou, Effie, Vardis Dilis, and Antonia Trichopoulou. "Nutrition claims: a potentially important tool for the endorsement of Greek Mediterranean traditional foods." Mediterranean Journal of Nutrition and Metabolism 6.2 (2013): 105-111.
• Wang, Huifen, et al. "Yogurt consumption is associated with better diet quality and metabolic profile in American men and women." Nutrition Research 33.1 (2013): 18-26.
• Zemel, Michael B., et al. "Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults." Obesity research 12.4 (2004): 582-590.

With the right diet and lifestyle, stem cell treatments, probiotic supplements or xylose-laden "functional foods" wouldn't be necessary in the first place.

You're probably used to it, but I am in the mood for bragging: The waredownloadsoft is where you'll read about the latest nutrition, exercise and supplement related studies first. In research updates like the one today, I am trying to provide a little more information than in the SV Facebook News, though, where I usually stick only to the main results of studies that have just been published or at least accepted for publication.

In today's installment of what I often call the "Short News", I will discuss three papers that are going to be published in one of the next issues of the peer-reviewed scientific journal Nutrition News.

Studies dealing with a pre-clinical, but promising stem cell therapy for diabetics, the verdict on probiotic supplements (including my evaluation of the scientists' verdict ;-) for weight loss and an update on the effects of the xylitol precursor d-xylose and its effect on mammalian fat cells in vivo.

• Stem Cells as Diabetes Treatment (Xing. 2015) - In software development you'd probably call the latest study from the Cangzhou City Central Hospital an "early alpha version" of an intriguing new way of treating type II diabetes.
  
  In their latest rodent study, Baoheng Xing et al. build on previous experiments in which pancreatic progenitors derived from human embryonic stem cells were shown to be able to effectively treat diabetes in mice (Kroon. 2008). In their study, however, Xing et al. went one step further and developed a system for treating diabetes using human embryonic stem cell–derived pancreatic endoderm in a mouse model of gestational diabetes mellitus.
  

  Figure 1: Glucose (a), insulin (b) and body weight (c) levels of wild type (wt) and treated (db/+PE) vs. untreated (db/+) pregnant mice before and during gestation, as well as Kaplan-Meier survival curves of litters show significant improvement right into the normal range in response to treatment (Xing. 2015)

  To this ends, the researchers had human embryonic stem cells differentiate in vitro into pancreatic endoderm, which were then transplanted into db/+ mice suffering from gestational diabetes mellitus.
  
  As the data in Figure 1 goes to show you, the transplant, of which the researchers expect that it could be used in humans, too, greatly improved the glucose metabolism and reproductive outcome of the treated female rats compared with the control groups. With their results Xing et al. do thus contribute to the growing evidence that diabetes may (sooner or later) be a "curable" disease when we are eventually mastering the use of differentiated human embryonic stem cells for treating general and gestational diabetes mellitus patients.
• Probiotics and weight loss - reviewed (Park. 2015): What's the verdict? You will remember that I am still skeptical with respect to the real world benefits of the new en-vogue supplements that contain billions of life or dead bacteria and promise benefits from increased gut health to... you guessed it, the most marketable of all benefits: weight loss!
  
  A recent systematic review by scientists from the Hoseo University and the Keimyung University in Korea presents the first attempt to summarize and critically evaluate the evidence from clinical trials that have tested the effectiveness of probiotics or foods containing probiotics as a treatment for weight loss. Literature searches of electronic databases such as PubMed, Cochrane Library, and EMBASE were conducted. Methodological quality was assessed using body weight and body mass index (BMI). Initial searches yielded 368 articles. Of these, only 9 met the selection criteria. Because of insufficient data, only 4 of the studies were randomized controlled trials (RCTs) that compared the therapeutic efficacy of probiotics with placebo.
  
  As my skepticism would have made me believe, the meta-analysis of these data showed no significant effect of probiotics on body weight and BMI (body weight, n = 196; mean difference, −1.77; 95% confidence interval, −4.84 to 1.29; P = .26; BMI, n = 154; mean difference, 0.77; 95% confidence interval, −0.24 to 1.78; P = .14).
  

  Figure 3: It's not like there were no benefits. You just have to look at the right parameters to see them. Studies like Kadooka et al. show that the effects on BMI are small compared to those on metabolically more relevant markers like total fat mass, waist circumference and visceral fat (Kadooka. 2015).

  That does not mean that there are no benefits at all, though. I reviewed the few studies that measured not just body weight and BMI, but also the subjects' body fat levels. This is an important difference, because a focus on BMI ignores potentially health relevant changes in body composition. Changes as they were observed by Kadooka et al. (2013; see Figure 3), for example, who found a significant time x group differences for visceral fat, fat percentage, fat mass, and waist circumference with much less pronounced effects on BMI (too low to influence the result of a systematic review significantly) in their 12-week study. In this context, it is also worth mentioning that Sanchez et al. (2014) observed a significant beneficial effect in obese women (but not man) for whom the consumption of 1.6 × 10^8 colony-forming units of LPR/capsule with oligofructose and inulin made it significantly easier to maintain their body weight after a weight loss intervention. Another benefit that must not be ignored.

• Overall, I still feel obliged to repeat what I wrote in my recent article on the effects of sweeteners on the microbiome: We still have to learn very much about the effects of probiotics in general and individual types of gut bacteria, in particular, before we can actually give good strain-specific supplement recommendations. It's after all possible that the same strains that work in the obese subjects of studies like Kadooka (2015) won't work or even do the opposite in lean individuals.
• D-Xylose Exerts Epigenetic Anti-Obesity Effects and Stops Fat Cell Growth (Lim. 2015) - Yes, this is not the first study to show that the provision of D-Xylitol or, as in the case of a 2011 study by Amo,et al., its cousin and "artificial sweetener" xylitol can reduce the weight gain due to obesogenic diets. What makes it interesting, though, is that it involved two different, relatively low dosages of D-xylitol as they could easily be added to our own food chain.
  

  Figure 4: While the effects on body weight and fat gain were significant, the differences (expressed relative to the rodents on regular chow) are still significant, so even if you replace 5-10% of the sugar in your junkfood diet with the low calorie sweetener (2.4kcal/g), you will get fat. If anything it may completely prevent the increase in liver fat - albeit only if the dosage is high enough and the effects are identical in humans (data from Lim. 2015)

  With only 5% and 10% of the sucrose content of the high fat chow of the rodents in Lim et al.'s latest study being replaced by D-Xylose, the scientists observed
  • significant reductions in weight and more importantly fat gain
  • significant reductions in hepatic steatosis (NAFLD),
  • a reduction of the genes that are responsible for the storage of fat to normal (5%) and sub-normal (10% D-Xylose) levels, and
  • significant reductions in total cholesterol and low-density lipoprotein cholesterol, low-/high-density lipoprotein, and the important total cholesterol/high-density lipoprotein ratio.
  In view of the fact that replacing just a relatively small amount of sucrose in our diet with D-Xylose (and probably xylitol) can ameliorate the weight and adipose tissue gain, normalize blood glucose levels and blood lipid profiles and lower the lipid accumulation in the liver by "regulating expression of lipogenesis- and β-oxidation–related genes" (Lim. 2015), it is probably actually warranted to speculate, just like Lim et al., about a "possible application of d-xylose as a dietary supplement for the prevention of obesity-related metabolic disorders" (Lim. 2015) - even though clinical human trials are still warranted.

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 ;-)

Creatine, whey and - at least optionally - casein are on the list of "must have" supplements for anyone who has been following a solid workout routine a decent high(er) protein diet for a year or longer. And even though this makes any news study on one of the three potentially interesting for a huge part of the waredownloadsoft readers, the results are often so unsurprising that they are hardly worth an individual waredownloadsoft article...

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.
Study #1 sheds some light onto the intricate differences between the way(s) whey and casein may differently affect our energy balance, gut hormones, glucose metabolism, and taste preference (Pezeshki. 2015), while study #2 is actually a meta-analysis that makes a first attempt to actually quantify the average effect of creatine on leg strength (Lanhers. 2015).

• 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.
  If you take a look at my compilation of the most relevant data in Figure 1, you will see significant improvements in glucose management in all groups (Figure 1 | G). You should yet also be able to see that the most significant increase in GLUT-4 expression and thus the muscles ability to take up glucose occurred in the casein and mixed protein groups. In the whey group, on the other hand, where the insulin levels were the highest the increase in GLUT4 receptor expression was negligible and the 60 minutes post value for glucose after the glucose tolerance est was higher, but not significantly higher than in either the mixed protein or casein group.
  

  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).

  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. 

• 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...
  

  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).

  ... 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. 
• 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!).
  

  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).

  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.
  
  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 ;-)

• 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.