Meta-Analysis: Dieting Reduces Food, Fat, Sugar, Starch & Junk-Food Cravings | In Whom? Why? Is it Diet Dependent?

Believe it or not - At least after some time, a severely energy restricted diet will reduce your cravings for donuts, pizza, pasta, and even chocolate statistically significantly - the questions from the headline do yet remain: Who benefits? What's the mechanism? And do the effects depend on your diet / its macros?

If you browse blogs and read e-books, you will read highly popular claims like "Dieting is useless, it just makes you hungry. If you want to lose weight, you got to stop eating carbs and reduce insulin." Those claims are popular because they entail the (unwarranted) claim that you could lose weight without cutting back on your energy intake. WRONG!

Fortunately, more and more people seem to understand that. One thing that will still be hard for them to swallow is the conclusion of the latest meta-analysis that addresses the ubiquitous claim that "calorie restriction may increase food cravings" (Kahathuduwa 2017), would thus ruin all your weight loss efforts and should be shunned in favor of macronutrien modulations that would promote satiety and thus allow for effortless weight loss.

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The study that addresses this important, if not crucial question was conducted by researchers from the Texas Tech University and the Pennington Biomedical Research Center. For their meta-analysis, C. N. Kahathuduwa, M. Binks, C. K. Martin, and J. A. Dawson dug up studies that were

• conducted on subjects with obesity, 
• implemented calorie restriction for at least 12 weeks, and 
• measured food cravings pre-intervention and post-intervention. 

The eight studies the scientists found mostly used the Food Craving Inventory. "Other comparable methods were," as the authors point out "converted to a similar scale" (Kahathuduwa 2017). For studies w/ multiple follow-ups, the authors used the duration ≥12 weeks, but closest to 16 weeks for studies and performed DerSimonian–Laird random-effects meta-analyses (this is the most widely used method to estimate between studies variance) using the ‘metafor’ package in r software.

Cravings for food, in general, sweets, high-fat foods, starchy foods, and fast food declined significantly over the course of the dieting period in obese subjects.

The above, i.e. the significant reductions in almost all relevant domains of food cravings were observed with a certain heterogeneity (meaning the reductions varied between studies) across all studies; a heterogeneity of which the scientists' analysis of potentially confounding variables revealed that it was explained by baseline body weight, type of intervention, duration, sample size and percentage of female subjects.

For whom are the results of the study at hand relevant? To answer this question we have to take a closer look at both: the subjects and the design of the eight studies that were analyzed for the meta-analysis at hand. Since all subjects were obese and thus equipped with more than ample energy stores to compensate for the 500-1200kcal deficit, it is more than questionable that the results are relevant for a hard-training athlete in his contest prep.

Before we delve further into the intricate differences due to (a) subject characteristics or (b) study design, though, let's briefly appreciate the mean reductions in craving scores I plotted for you in Figure 1. As previously highlighted, the scientists observed observed reductions in pooled effects for overall food cravings (−0.246 [−0.490, −0.001]) as well as cravings for sweet (−0.410 [−0.626, −0.194]), high‐fat (−0.190 [−0.343, −0.037]), starchy (−0.288 [−0.517, −0.058]) and fast food (−0.340 [−0.633, −0.048]) in the meta‐ analysis.

What does it mean if the scientists say that cravings for sweet reduced by "0.410" pts?

As previously pointed out, Kahathuduwa et al. used the "Food Craving Inventory" (FCI | learn more in White 2002) for their comparisons. For studies which used different methods to quantify the food cravings of their subjects, the authors converted the corresponding scale(s) accordingly. As White et al. point out in their 2002 paper that introduced this tool to the scientific community, "[t]he FCI was designed to measure specific food cravings using two subscales: subjective cravings and consumption of particular foods." White et al. further explain:

"Low Carb(-ing) Reduces Fat & Fast Food (10-20%) Cravings Plus 60% Less Hunger After Meals in Obese Men/Women" - This 2017 study by Heimowitz et al. is not yet part of the meta-analysis at hand.

"We chose to develop these subscales to distinguish between a craving for a food and consumption of that food. Because previous research had often defined craving as consumption, our intention was to determine whether craving and consumption were psychometrically different constructs. The first subscale (subjective) assessed the frequency of subjective cravings for 47 different foods. The foods were chosen according to the classifications provided by Harvey et al. and additional foods were included on the basis of theory and literature review. The second subscale (behavioral) was intended to measure the extent to which participants gave in to craved foods. Participants completed the subjective and behavioral subscales for the same 47 foods" (Kahathuduwa 2017). 

Exemplary foods from the analysis are fried chicken, sausage, milk, tuna, beef, gravy, fried fish, bacon, corn bread, hot dogs, steak, brownies, cookies, cheese, candy, chocolate, donuts etc. As you may already have guessed based on this incomplete list, the FCI includes both, foods people typically crave (cookies, donuts, gravy, etc.), as well as foods you'd not necessarily put on a "food addiction" list, such as steak, veal, milk, tuna, etc.

The FCI assesses both subjective (craving) and objective (eating) factors asking subjects: "Over the past month, how often have you experienced a craving for the food?" and "Of those times in the past month during which you craved a particular food, how often did you 'give in'?". Subjects answer questions with values from 1-5 implying: 1 = never, 2 = rarely (once or twice), 3 = sometimes, 4 = often, and 5 = always/almost every time.

Despite the fact that the meta-analysis at hand refutes the assumption that energy restriction per se will trigger cravings, there's another feature common dieting attempts have in common: dietary monotony (Pelchat 2000). Just like the meta-analysis at hand, the increase in food cravings in response to a monotonous diet in young people on nutrient sufficient diets support the notion that food cravings have an important psychological component.

How can that be true? If you're dieting, you got to crave more... Well, that's what common sense and the "deficit theory" (Weingarten 1990 | cravings occur owing to a deficiency of energy or nutrients) may say. As the authors of the meta-analysis at hand point out, though, their results do not support the "deficit theory". Rather than that, the findings of the scientists from the Texas Tech University support the notion that - at least in the obese - "craving develops as a result of a conditioned association between repeated consumption of a specific type of food with a particular stimulus, environment or occasion (i.e. classical conditioning)" (Kahathuduwa  2017). The scientists speculate that after 12 weeks on an energy restricted diet that doesn't allow for the regular consumption of these usually energy‐dense foods, a dissociation of consumption of food and associated stimuli would have taken place and the hard-wired food cravings would have been erased.

In fact, scientists have observed that extended calorie restriction may suppress food‐cue reactivity of brain regions that regulate food reward and increase activity in regions that have been implicated in inhibitory control over drives towards food ingestion (Rosenbaum 2008) - a phenomenon that would be the "neurophysiological surrogate for ‘craving’" (Kahathuduwa  2017)

Kahathuduwa et al do also point out that "it should be noted that a food craving is likely a complex bio‐psycho‐social phenomenon that cannot be fully explained using a simple psychological model alone" (ibid.). Two of the missing physiological phenomena I would suspect to have an impact - especially on sweet, starch and fast food cravings - are (a) the ongoing reductions in inflammation and insulin resistance that will help restore a functional energy sensing system over the course of the diet and the restoration of normal sweet and fat taste perception. Obviously, further research is warranted to confirm or falsify this assumption. If we do yet assume that they're true, they point to a previously highlighted problem with the study at hand: as all studies were conducted with obese individuals, the chances to see similar effects in lean athletes are slim.

The -0.41 point reduction Kahathuduwa et al. report calculated for the sweet cravings of their subjects, is yet not a -0.41 reduction from say 4.0 to 3.59 pts on the Likert scale of the FCI, but an effect size the scientists calculated based on their analysis of all 8 studies. Effect sizes tell you something about the efficacy of an intervention. In this particular case, a negative effect size means that the intervention, i.e. the reduction in energy intake due to the diet, lead to reduced cravings. A positive effect size, on the other hand, would indicate that the cravings increased.

Figure 1: If one pools the data from all studies in the meta-analysis, both, the overall food cravings, as well as all individual food cravings, the scientists assessed (figure shows only fast food) were reduced significantly (Kahathuduwa 2017).

With effect sizes of -0.246 for general food cravings, -0.410 for sweet foods, -0.190 for high-fat foods, -0.288 for starchy foods and -0.340 for fast-food, the effect of dieting was generally positive, all cravings that were assessed in the study were reduced. Furthermore, the scientists observed a...

• small effect (d<0.30) on general, high-fat, and starchy food cravings, and 
• medium effect (0.30 < d < 0.50) on cravings for sweet and fast-food.

Accordingly, you cannot expect that category 5 cravings (FCI: almost craving) will be reduced to category 1 (FCI: never craving) if you start dieting. What's also worth knowing is that the scientists' meta-regression analysis shows that for all food cravings...

• a  higher baseline weight was associated with a decreased effect size - this means the heavier participants saw greater reductions in cravings 
• a higher percentage of women in the study population was likewise associated with increased effect sizes - in other words, women are more prone to develop cravings, accordingly, studies with more women found slightly lower (d-0.016) reductions in cravings
• a more extensive list of items the subjects were not allowed to eat at all was associated with an increased effect size (d+0.707) - this means that the more restrictive (in terms of food choices) the diet was, the smaller the beneficial effect on food cravings

In other words: (1) The more body fat you have to draw on while you're dieting, the less prone you're going to be to suffer from cravings. (2) Being a woman makes it a bit more difficult to diet. And (3) restricting certain food items, groups and/or macronutrients can, in line with both, the deficiency theory and hedonistic explanations of food cravings, trigger increased cravings for the prohibited (macro)nutrients [deficiency theory] or food groups [hedonistic explanation].

Figure 2: The link between low-carb and increased cravings for sweet/starch is mainly due to a single study (red), which isn't even a true low-carb vs. high-carb comparison - another study (green) even shows low-carb advantages.

The last-mentioned conclusion, however, seems to be driven by the inter-group differences in the low-carb vs. high-carb group of a 2012 study by Jakubowicz et al., a study that used a diet the defining feature of which was that it was low calories and comparatively high in protein: With a significantly reduced energy intake (-1400-1600kcal total) and whopping ~180g protein, the diet left room for only a marginal inter-group difference of carbohydrate intake of 10% (20% vs. 10% of total energy came from carbs in the high vs. low carb group). This is obviously hardly what you would expect from a "low-carb vs. high-carb" comparison and would warrant only one conclusion:

A low-calorie high protein (52%) medium-fat (38%), low-carb diet (10%) will increase your cravings for sweet, starch and all the other sources of readily available energy.

The only 'real" low vs. high carb comparison in the meta-analysis, confirms the notion that low-carb or, I should say, high-fat, low-carb diets will not make you crave carbs. After all, Martin et al. who compared a diet with only 20 g carbs per day (in the form of low-glycemic index vegetables) to an isocaloric diet that contained 55% of the energy intake in form of carbs in 2011, found no detrimental effects of a significantly reduced carbohydrate intake in terms of either starch and sweet cravings (see Figure 2, green) - and that despite the fact that their diet had a similar energy deficit as it was used by Jakubowicz et al (see Figure 3, red).

Other "craving news": Even though it seems unlikely that the results of studies in obese, sedentary individuals translate to avid gymrats, it is worth noting that Rocha et al. have recently demonstrated that moderate intensity activity will decrease total food cravings, specific cravings of high-fat foods, fast-food fats, and carbs (moreover, there was a trend with a large effect size for cravings of sweets (p = 0.052, d = −0.86) to be lower after the exercise intervention) within the same 12-week time frame that was investigated in the meta-analysis at hand - albeit not in the obese, but in healthy, normal weight, untrained young men (Rocha 2016).

Another study that's worth mentioning comes from School of Medicine, The University of Leeds. It found that resisting food cravings is rewarded with significantly increased weight loss - in view of the fact that even the meta-analysis at hand shows that dieting will only reduce the cravings, this finding should remind us that it's not necessarily the severity of the craving, but the ability to resist that's relevant; and the effects of dieting on the latter has not been studied, yet.

Bottom line: The overall message of Kahathuduwa is that a mere reduction in food intake will not increase your general and/or special food cravings for sweet, high-fat, high starch and/or fast foods after 12 weeks of dieting. While this sounds awesome, there are some caveats we must not forget: the effects are (a) only small to medium, you cannot expect to no longer have to think about chocolate or a burger if you're dieting; the meta-analysis (b) didn't investigate cravings in the first weeks of dieting - the latter may be significantly elevated or at least not reduced - this is also supported by the negative correlation of study duration and food cravings observed in the study at hand (i.e. longer diet = reduced cravings);  the benefits (c) have been observed exclusively in obese individuals, and can be expected to differ significantly in dieting athletes, who (i) don't have the (fat) resources of an obese individual to draw on and (ii) don't see the same improvements in glucose management with every pound they lose; lastly, there's (d) the potential effect of limiting both, the energy intake and the intake of certain foods/macronutrients that could nullify if not reverse the beneficial effects of dieting.

With respect to (d), i.e. the effects of restricting certain food groups and macronutrients, it's, however, worth pointing out that the conclusion that this study would prove that low-carbing will increase your hunger for sweets and starchy foods is unwarranted. This assumption is supported only by one study in the meta-analysis and this study did not compare classic low- vs. high-carb diets (cf. previous elaborations) - both, the study by Martin et al that was part of the meta-analysis and a more recent study by Heimowitz et al., I discussed in March 2017, clearly refute the assumption that carbohydrate reductions would trigger cravings for sweets/starches... what we shouldn't forget, however, is that this study was also conducted in obese, inactive individuals and is thus of questionable relevance for athletes | Comment! 

References:

• Jakubowicz, Daniela, et al. "Meal timing and composition influence ghrelin levels, appetite scores and weight loss maintenance in overweight and obese adults." Steroids 77.4 (2012): 323-331.
• Joyner, Michelle A., Ashley N. Gearhardt, and Marney A. White. "Food craving as a mediator between addictive-like eating and problematic eating outcomes." Eating behaviors 19 (2015): 98-101.
• Kahathuduwa, C. N., et al. "Extended calorie restriction suppresses overall and specific food cravings: a systematic review and a meta‐analysis." Obesity Reviews (2017).
• Martin, Corby K., et al. "Change in Food Cravings, Food Preferences, and Appetite During a Low‐Carbohydrate and Low‐Fat Diet." Obesity 19.10 (2011): 1963-1970.
• Pelchat, Marcia Levin, and Susan Schaefer. "Dietary monotony and food cravings in young and elderly adults." Physiology & behavior 68.3 (2000): 353-359.
• Rocha, Joel, et al. "Effects of a 12-week aerobic exercise intervention on eating behaviour, food cravings, and 7-day energy intake and energy expenditure in inactive men." Applied Physiology, Nutrition, and Metabolism 41.11 (2016): 1129-1136.
• Rosenbaum, Michael, et al. "Leptin reverses weight loss–induced changes in regional neural activity responses to visual food stimuli." The Journal of clinical investigation 118.7 (2008): 2583.
• Weingarten, Harvey P., and Dawn Elston. "The phenomenology of food cravings." Appetite 15.3 (1990): 231-246.
• White, Marney A., et al. "Development and validation of the food‐craving inventory." Obesity 10.2 (2002): 107-114.

Western vs. Ketogenic Diet - Greater 'Gains' Materialize Only After Glycogen-Loading in 12-Wk Study in Trained Subjects

Unfortunately, I cannot tell you if the "Western" diet was also full of junk food. I just know that its 20/55/20 ratio of PRO/CHO/FAT is everything but ideal for one's body composition.

While it has not officially been published, yet, I am pretty sure that Jacob M. Wilson's latest paper is going to be one of the most-downloaded articles in the upcoming issue of the Journal of Strength and Conditioning Research it's about to be published in. You're asking yourself why I am so sure about that? Well, it's already the most-discussed ahead-of-print article in months (see any Facebook Fitness / Exercise Research group or bulletin board), because it claims to confirm that ketogenic diets "can be used in combination with resistance training to cause favorable changes in body composition, performance and hormonal profiles in resistance-trained males" (Wilson 2017) - a claim that gets both ketophiles and keto-haters absolutely fired up.

Would be interesting to compare keto to high-protein, not western diets, right?

Practical Protein Oxidation 101

5x More Than the FDA Allows!

Low Carb Unfit for Crossfit(ters)

Protein Oxidation = Health Threat

Keto Diet ⇒ Perform. ↓

Keto for Superior Weight Loss?

Before I will delve into a brief discussion of what the study is actually about, I would like to point outu that I have revised the original draft several times - both, to incorporate/answer questions that I've found online and in response to a brief conversation with the authors, who were by no means the first to "examine resistance training adaptations using a human model" (Wilson 2017). What Wilson et al. can boast of, though, is that their paper is the first to address the issue using a decently realistic resistance training program in healthy, previously trained young men. A scenario in which the authors hypothesized a priori that ...

"the KD [ketogenic diet group] would decrease body fat to a greater extent than a WD [western diet] group, while maintaining skeletal muscle hypertrophy, strength, and power" (Wilson 2017).  

In that, the effects of the heavily criticized glycogen load you may have read about elsewhere, was not a means to make this hypothesis come true, but an effort to generate a level playing field of which the authors write that it also constitutes a "tertiary purpose" of the study, which was thus also intended as a means to investigate "the effects of carbohydrate refeeding following KD adaptation on body composition and performance" (ibid.)

The glycogen loading was not meant to skew, but to create a level playing field.

Unfortunately, this strategy backfired in a way that's currently getting people all over the interwebs so "excited" (to say the least) that they focus exclusively on this failed attempt to compensate for the glycogen advantage and do not acknowledge the strengths of the study.

Update from April 21, 2017: You can read more about the study from the authors themselves if you want to. Ryan Lowery also addresses the "glycogen loading" making practically the same point I did: anybody who would have invested time and effort to read the whole paper, would have read that they never claimed the aprupt increase in lean mass in the final week was anything but water.

Strengths such as (1) the selection of trained subjects and exclusion of those with a squat performance that was significantly below 1.5 times the subjects' own body weight (here we have one of the criticized issues with the reporting, though, because the value Wilson et al. provide is 1.56 ± 0.14 and thus below 1.5 if you subtract the standard deviation from the arithmetic mean), as well as the prescription of (2) a realistic resistance training routine with a hypertrophy focus (see Table 1).

Table 1: Training protocol; *rest was 60-90 seconds on hypertrophy days and 3-5 minutes on strength days (Wilson 2017).

Extra cardio or other endurance training and/or other athletic activity outside of the three weekly workouts was strictly prohibited. All exercises were either performed for the given number of reps or to failure. The load utilized for weeks 3-6 ranged from 65 to 95 % of subjects’ initial 1RM. However, these loads were increased by 2-5 % for the final 7-9 weeks of training depending on subject’s ability to perform the prescribed repetitions during weeks 3-6.

Figure 1: Visualization of the macronutrient composition of the diets (Wilson 2017).

As the authors explain, the "subjects tapered by decreasing volume by 40-50 % through decreasing sets on auxiliary lifts on Monday and Wednesdays and only performing 1RM testing on Fridays" (Wilson 2017) in the final two weeks of the study period, of which it may be worth mentioning that it lasted 12 weeks: a two-week lead-in, 9 weeks until the highly debated glycogen repletion protocol began and another week until the final measurements of exercise performance and body composition.

How different were the diets in reality? Unfortunately, the researchers don't elaborate (and probably didn't even review) which foods their subjects actually eat. Accordingly, we're left with the macros and some extra information on the saturated, poly-, and monounsaturated fat and fiber content of the diet. What I can tell you is this: the average protein intake in both groups was identical, amounting to ~130g/day; the fiber intake was 2-fold higher in the WD group; and the percentage of saturated, monounsaturated and polyunsaturated fat in the diet were similar (47%, 30% and 23% in the KD and 48%, 34% and 18% in the WD group, respectively) - if that's relevant for the results is questionable, though. Unless, obviously, you believe in the myth of the tooth fairy... ah, I mean, the "anabolic prowess of saturated fats" that was born out of a single study showing increased testosterone levels on higher SFA-diets.

Dietwise, the subjects, N=25 resistance-trained males who had an average max squat performance of 1.56 ± 0.14 times their body weight and an average of 5.5 ± 3.8 years of training experience, were randomly assigned to...

• 

  Only recently scientists have been able to show that coffee can kickstart ketosis, even if you eat a sign. number of carbs for breakfast | learn more.

  the WD = western diet - 20% calories from protein, 55% from total carbohydrate, and 25% from fat
• the KD = ketogenic diet - 20% calories from protein, 5% from carbohydrate including fiber, and 75% from fat 
• in both groups, subjects were instructed to consume food immediately following training that contained a minimum of 20-30g of protein, with the remainder of the meal reflecting the accurate ratios prescribed throughout the day

The individual energy content was calculated based on maintenance calories determined by the Mifflin St. Jeor equation. Now, while this is standard procedure in metabolic research it is still problematic, as the equation can be 15% off the actual requirements. Accordingly, it is not clear, whether the subjects were in a caloric deficit. Since this holds true for both groups and the overall energy intake was identical in both groups, though, this is not relevant to the study's original research goal, which is to determine differences between a ketogenic and a western diet.

Excellent dietary adherence and full ketosis in the main part of the study

What we can tell, though, is that the subjects' adherence to the diets was excellent (2608.6 ± 157.5kcal/day vs.  2549.5 ± 212.5 kcal/day,  217.02 ± 15.5 g fat per day vs.  83.4 ± 13.3 g fat/day, 133.6 ± 10.8 g protein per day vs. 132.2 ± 13.3 g protein per day, 30.9 ± 5.9 g carbohydrates per day vs. 317.6 ± 31.1 g carbohydrates per day in the KD vs. WD group, respectively) and confirmed by both both food logs and weekly urinary ketone measurements.

Does the study "fly in the face of all other research" and present "totally unrealistic results"? That's at least what I read on Facebook several times - alongside accusations of scientific fraud that have no basis in facts, by the way.

Let's take a look at the little research there is: There's the recent revelation that low carbohydrate dieting impairs the adaptive response to aerobic training in Louise Burke's excellent paper in the Journal of Physiology (Burke 2017); a paper, of which not even its authors would claim, though, that it settles the debate once and for all - neither for endurance athletes, of whom Cox et al. write that "five separate studies of 39 high-performance athletes" show that "this unique metabolic state [ketosis] improves physical endurance by altering fuel competition for oxidative respiration" (Cox 2016; further evidence e.g. Ball 1995; Gore 2001), nor for athletes competing in anaerobic sports, where studies studies in gymnasts (Paoli 2012), or dieting martial artists (Rhyu 2014) report favorable results with ketogenic diets.

Comparison of the body composition changes in Jabekk 2010, a study in untrained overweight women w/out dietary restriction and the results Wilson et al.. report before the glycogen reload in week 11 that's obviously absent in the Jabekk study.

Let's get more specific, though: If we exclude the effects of the glycogen reload (i.e. stick to the body composition changes from week 1-10) and compare these to the observations of a 2010 study by Jabekk et al., it also becomes obvious that the changes in body composition are not as "unrealistic", as some critics have claimed: With almost identical macronutrient compositions, i.e. 6%, 66%, and 22% in the "low carbohydrate" (de facto ketogenic) diet and 41%, 34%, 17% of the energy from carbs, fats and protein in the "normal" (de facto western) diet, Jabekk's study has a very similar dietary composition as the study at hand.

Due to fundamental differences in the subject selection (untrained, overweight women vs. trained, lean men) and other aspects of the study design, including a non-restricted energy intake and non-hypertrophy-specific workouts, it should be obvious that the results of the studies cannot be 'identical'. Within the statistical margins of error (which are unfortunately not provided in Wilson 2017; that's also why the error bars are missing in the figure on the left) and in view of the previously mentioned design differences, Jabekk's results are yet similar enough to refute the claim that Wilson's study results were "totally unrealistic" or had to be discarded, altogether, because they would "fly in the face of all previous research" (my emphasis).

The last-mentioned ketone tests confirmed that all subjects in the ketogenic dieting group (KD) had reached full ketosis at the beginning of the 2nd week of the two-week lead-in - an important observation that was not made (either because it was not tested or because the high protein content of the diet allow the subjects to reach full ketosis) in some previous "low carbohydrate diet"-studies.

Figure 2: Changes in body composition (in the given timeframe in kg) according to DXA scans (Wilson 2017).

So far, so good... I guess, it's about time to address the catch, then: Before the final DXA scans (results see Figure 2), muscle circumference and strength tests were done, the subjects in the KD group were subjected to a classic glycogen loading protocol consisting of two days on 1g/kg carbohydrates, followed by two days on 2g/kg carbohydrates and 3g/kg carbohydrates in the last 2 days before the DXA scan - obviously, with an isocaloric decrease in dietary fat that maintained the caloric intake at the previously described calculated maximum.

Hindsight is easier than foresight: If you glycogen-load, it'd be logical to do so in both groups

In general, there's nothing wrong about this. To create a truly equal playing field, however, it would yet have been smarter to either glycogen-load (or, alternatively, -deplete) both groups. With only one group getting the extra boost in muscle fullness, however, the DXA data from week 11 is as skewed (albeit into the other direction) as the measures that were taken in week 10, when the emptied glycogen stores in the KD group gave the similarly elusive impression that the consumption of a ketogenic diet had impaired the subjects' lean mass gains while extremely augmenting their fat loss.

Percent changes in leg lean and fat mass vs. baseline following glycogen depletion and creatine and glycogen loading with and without creatine (Bone. 2016) | learn more in my previous article about the study.

Glycogen or real muscle gains? If you scrutinize the data in Figure 2, you will realize that the keto group was trailing 50% behind in weeks 1-10, i.e. while the subjects were actually consuming a ketogenic diet. Only after the increase in carbohydrate intake in week 11 that was not all-too-different from the glycogen loading protocol in a recent study by Bone et al. (2016), they caught up and overtook the western diet group. The ~2kg (~3% of baseline lean mass) extra lean mass in the ketogenic vs. western diet group, however, is pretty much identical to the 2.0 ± 0.9 % increase in DXA-measured lean mass Bone et al. observed in response to a similar glycogen loading protocol in their study.

If we assume that the effects of the loading protocol were similar to those Bone et al. (2016) observed with an almost identical protocol in their recent study (see discussion in the red box, above), the extra glycogen would appear as a ~3% increase in lean mass on the DXA scans - and that's pretty much what we see in the study at hand. Accordingly, the "real" muscle gains in the KD group are probably somewhere in-between what we see in Figure 2 (left) for the 1-10 wk and 1-11 wk period. This, however, would imply that the "real" lean mass gains (and the increase in muscle thickness, see Figure 3) over the course of the study would - within the usual statistical margins of error - be identical for both diets.

It's not true that Wilson et al. do not address the issue of glycogen-driven 'extra gains'

In view of the harsh criticism Wilson et al. have received over the Easter weekend, it should be mentioned that the authors come to a very similar conclusion (without, however, citing the study Bone et al.), when they write in the discussion of their results that "the abrupt, yet not unexpected, changes in LBM were primarily driven by drastic changes in water flux during the last week of the study" (Wilson 2017) - and conclude, just as I did, that both "groups gained similar amounts of muscle mass throughout the entire study" (ibid.).

Figure 3: Rel. changes (%) in muscle thickness and performance data from week 1-10 and 1-11 (left) and absolute DXA data with lean mass at the top and fat mass at the bottom (full bars = KD, open bars = WD | Wilson 2017).

The fact that the authors do not make this more explicit in the abstract and, even more importantly, speak of a body composition "advantage" for the KD diet in the "practical implications" section of the paper, is in fact reason for warranted criticism. After all, the alleged improvements in fat loss vanish just as the increases in lean body mass did, if we subtract the ~6% "virtual" loss of body fat Bone et al. observed as a result of glycogen depletion, alone, and/or estimate the "real" body fat loss by averaging over the fat mass Wilson et al. measured in week 10 and 11, respectively.

If there's no inter-group difference, the study at hand still shows just what the first part of the conclusion of the abstract says: "The KD can be used in combination with resistance training to cause favorable changes in body composition, [and] performance" (Wilson 2017).

So, even if we assume that the extra gains were an experimental artifice and assume that a potential fat loss advantage did not exist, we should at least be able to agree that the study at hand confirms, irrespective of its methodological problems and 'suboptimal' reporting of the results, that ketogenic diets can build the same amount of lean mass and strip the same amount of fat off the bodies of trained young men, when all other parameters are kept equal. Whether the "western diet", a high carb, lowish protein, medium fat diet, is an adequate yardstick when it comes to the question "What's the best diet for gymrats, physique athletes and/or bodybuilders?", however, is yet another story.

Figure 4: Despite all the criticism: There's one major problem with the study that has gone largely unnoticed: In the absence of data from the last week the subjects were actually consuming a ketogenic diet it is IMHO unwarranted to conclude that a KD "cause[s] favorable changes [...] in hormonal profiles" (Wilson 2017).

So, keto-dieting rules, right? If we try to average the effects of the glycogen load out, the study at hand still yields an important result: it confirms that there is no body composition and muscle size disadvantage to consuming a ketogenic diet compared to an isocaloric "western" high carbohydrate, lowish protein diet.

How's that? Well, due to the fact that the scientists' well-meant effort to level the playing field by restoring their subjects glycogen stores in week 11 backfired, it is impossible to say, whether the "favorable changes", Wilson et al. point out in the conclusion of the abstract were more or less pronounced in the ketogenic compared to the western diet group.

What is possible, however, is to speculate based on data from before and after the glycogen-load. If we thus try to 'fix' the data by (a) averaging over the data from weeks 10 and 11, respectively, or by the means of (b) logical inference based on the results of Bone's previously discussed study that used an almost identical protocol to determine the effects of glycogen loading on DXA scans (Bone 2016), we will arrive at a conclusion that mirrors the one Wilson et al. phrase in the discussion of their results - that both "groups gained similar amounts of muscle mass throughout the entire study" (Wilson 2017); and that's, if we are honest, exactly what the first part of the heavily criticized and, as I believe, largely misunderstood conclusion of the study's abstract says: "The KD can be used in combination with resistance training to cause favorable changes in body composition" (Wilson 2017; my emphasis).

Unfortunately, the person who wrote the "practical applications" section of the paper seems to have 'forgotten' about that when he wrote that the KD was overall "advantageous for body composition [...] as compared to a WD" (ibid; my emphasis). That's clearly not in line with the message that emerges in the authors' previously cited discussion of the results.

What is likewise questionable is whether the study outcome would have been similar for the practically more relevant comparison of a ketogenic diet to a classic bodybuilding-style high protein, medium carbohydrate control diet - a diet with lower amounts of carbs and fats and significantly more protein than the unquestionably suboptimal "western" diet in the study at hand. Ah... and one last thing: It is not just questionable, but, in my humble opinion, simply unwarranted to claim that the ketogenic diet had beneficial effects on the subjects' testosterone levels when the latter were assessed after one week of glycogen loading (cf. Figure 4) | Comment!

References:

• Ball, Thomas C., et al. "Periodic carbohydrate replacement during 50 min of high-intensity cycling improves subsequent sprint performance." International Journal of Sport Nutrition 5.2 (1995): 151-158.
• Bartlett, Jonathan D., John A. Hawley, and James P. Morton. "Carbohydrate availability and exercise training adaptation: too much of a good thing?." European journal of sport science 15.1 (2015): 3-12.
• Bone, Julia L., et al. "Manipulation of Muscle Creatine and Glycogen Changes DXA Estimates of Body Composition." Medicine and science in sports and exercise (2016).
• Burke, Louise M., et al. "Low Carbohydrate, High Fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers." The Journal of Physiology (2017).
• Cox, Pete J., et al. "Nutritional ketosis alters fuel preference and thereby endurance performance in athletes." Cell Metabolism 24.2 (2016): 256-268.
• Gore, Christopher J., et al. "Live high: train low increases muscle buffer capacity and submaximal cycling efficiency." Acta physiologica scandinavica 173.3 (2001): 275-286.
• Jabekk, Pal T., et al. "Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat." Nutrition & metabolism 7.1 (2010): 17.
• Paoli, Antonio, et al. "Ketogenic diet does not affect strength performance in elite artistic gymnasts." Journal of the International Society of Sports Nutrition 9.1 (2012): 34.
• Roberts, Michael D., et al. "A putative low-carbohydrate ketogenic diet elicits mild nutritional ketosis but does not impair the acute or chronic hypertrophic responses to resistance exercise in rodents." Journal of Applied Physiology 120.10 (2016): 1173-1185.
• Wilson et al. "The Effects of Ketogenic Dieting on Body Composition, Strength, Power, and Hormonal Profiles in Resistance Training Males." J Strength Cond Res. 2017 Apr 7. doi: 10.1519/JSC.0000000000001935. [Epub ahead of print]

True or False: A High Protein Intake Nullifies the Benefits of Diet-Induced Weight Loss (10%) on Glucose Metabolism

With high protein diets often being falsely equated with misguided varieties of keto diets where you eat nothing but sausages and bacon, the public jumps at 'news' like "A new study suggests there's a downside to all that protein" (time.com) and ignores that high protein dieters like you and me limit the amounts of these foods and eat way more veggies and fruits than Mr. Average is often forgotten in the debate.

You will probably remember the headlines: "It’s Time to Rethink High-Protein Diets for Weight Loss" (time.com). Now, that the notion that an increased protein intake can help you shed body fat by increasing your satiety, reducing your cravings and improving the ratio of lean-to-fat-mass you will lose while dieting is finally becoming common knowledge (Leidy. 2007; Mettler, 2010), the impact of biased reporting on studies such as Smith, et al. (2016) could become a public health problem of its own.

That's a daring hypothesis, I know, but my own bias towards higher protein diets is not the only reason I do not subscribe to the what Bettina Mittendorfer, co-author of the study and a professor of medicine, argues in the previously cited article on time.com: "There’s no reason to [follow a high(er) protein diet], and potentially there is harm or lack of a benefit" (quote from the time.com article).

High-protein diets are much safer than some 'experts' say, but there are things to consider...

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Satiety: Casein > Whey? Wrong!

Protein Timing DOES Matter!

High Protein not a Health Threat

So what are the reasons, there's no reason to panic... yet? Let's first take a look at the study design. In the study, the author compared the effects of 10% weight loss (took ~28 weeks in both groups) w/...

• a hypocaloric diet (-30% energy intake) containing 0.8 g protein/kg/day (NP) to a
• a hypocaloric diet (-30% energy intake) containing 1.2 g protein/kg/day (HP)

on muscle insulin action in postmenopausal women with obesity and found that "HP intake reduced the WL-induced decline in lean tissue mass by 45%" (Smith. 2016).

Figure 1: Flow of study participants (from supplemental material for Smith. 2016)

In view of the only recently fully appreciated importance of lean mass (muscle, organ and bone mass) in metabolic health and healthy aging (Han. 2010) and considering the special needs of the study population, postmenopausal women of whom studies indicate that the will regain only the fat, but not the lean mass (Beavers. 2011) and thus set themselves up for the dreaded yo-yo effect, the lack of loss of lean mass clearly is - as the scientists (allegedly) acknowledge - very good news.

Good news #1: Eating 150% of the RDA for protein while dieting reduces postmenopausal women's diet-induced lean mass losses significantly.

Unfortunately, the often-cited abstract to the study (and the press release that's at the heart of the mass media coverage I hinted at in the introduction) creates the impression that this was the only positive result, the scientists observed in a study the most important finding of which was that the "HP [high protein] intake also prevented the WL[weight loss]-induced improvements in muscle insulin signaling and insulin-stimulated glucose uptake".

Figure 2: Changes in body weight and composition. Percent changes in body mass (A), intra-hepatic triglyceride (IHTG) content (B), intra-abdominal adipose tissue (IAAT) volume (C), percent contribution of fat-free-mass(FFM) to total weightloss(D) as measured after 28 weeks and 10% weight loss (Smith. 2016).

If we take a closer look at the evidence as a whole, however, this conclusion is obscured by the following observations: There was/were ...

• no difference in basal and insulin and glucose levels, or the insulin and glucose levels in response to a hyperinsulinemic-euglycemic clamp test you would expect to see both if the subjects' glucose management worsened significantly due to the increased protein intake,
• no difference in free fatty acid levels at rest and during the hyperinsulinemic-euglycemic clamp as you would expect them if the high protein intake had had a negative effect on the subjects' glucose and subsequently fatty acid metabolism, 
• no difference in the reduction of the amount intra-hepatic triglyceride (liver fat), which has been associated with significant decreases in full-body insulin resistance,
• no difference in the effect of the global inflammation markers hs-CRP and IL-6, which could explain the allegedly worsened glucose metabolism in the HP group,
• no differences in the loss of intra-abdominal fat, which is among the most important determinants of whole body inflammation and thus - again - one's insulin sensitivity
• no difference in the small and mostly non-significant effect of the treatment on the expression of genes involved in lipogenesis, and fatty acid oxidation and mitochondrial function in muscle that could potentially explain the emphasized "downside to all that protein" (time.com)
• no difference in the change of AMPK, the master regulator of cellular energy homeostasis 
• no difference in serum BCAA levels, of which previous studies have shown that their accumulation in the blood is at least correlated with the development of obesity and a worsening of glucose management (She. 2007)

I guess you will agree that each and every of these eight observations stands in contrast to the "bottom line" the authors of the press release propagate. They do, after all, contradict the notion that the increase in protein intake would ruin any benefit of high(er) protein intakes while dieting and refute the assertion that's resonating in the placative title "It’s Time to Rethink High-Protein Diets for Weight Loss" (time.com) of the previously referenced article on time.com (similar articles can be found on other media outlets, as well).

Good news #2: Eating 50% more protein does not significantly affect the value and/or change of eight other biological markers you'd expect to differ if eating 1.2g/kg protein while you are dieting would ameliorate, if not reverse the benefits of body weight and fat loss.

Now, none of these "good news" invalidates the scientists' analysis of glucose dynamics during the hyperinsulinemic-euglycemic clamp procedure (HECP), of which the scientists say (not without reason, by the way) that they were indicative of the fact that a "HP intake also prevented the WL-induced improvements in muscle insulin signaling and insulin-stimulated glucose uptake" (Smith. 2016). What these "good news" do, however, is to warrant the question how practically significant this observation actually is - after all, you would expect, and I know that I am repeating myself here, insulin, glucose, inflammation, visceral fat and the other parameters listed above and/or the way they changed over the course of the study to differ between groups, as well.

Food for thought: What does the HECP actually measure and how representative is that of what you would see under 'real-world conditions'?

A lack of changes outside of the HECP makes the quest for potential mechanisms even more important. The scientists, however, cannot even explain the "adverse effect of HP intake on insulin
action", in general. They call it "unclear" (Smith. 2016) and argue, just like me, that this is particularly true in view of the "absence of any major differences in body weight, body composition, plasma FFA availability, and inflammatory markers" (Smith. 2016). Based on the increase of the glutathione recycling gene GSTA4 and expression of PRDX3 a muscle-specific gene that's increased when animal muscle is exposed to oxidative stress, Smith et al. argue that eventually their results

"[...] suggest that the adverse effect of HP intake on insulin action during weight loss therapy may have been mediated through its effects on oxidative stress because it prevented the WL-induced decrease, and even increased, metabolic pathways involved in oxidative stress response in muscle" (Smith. 2016).

This is yet only one possible explanation. Another hypothesis that would explain the differences in the extreme situation of the HECP, i.e. the continuous infusion of glucose under hyperinsulinemic conditions as you would like and in 99% of the cases can avoid them in reality, can be derived based on data from a Y2K study by Linn, et al. In this study, the authors investigated the long-term effects of high protein diets (1.8g/kg vs. 0.7g/kg) on glucose metabolism without weight loss and found one effect of high protein diets, Smith et al. ignore completely:

Figure 3: The chronic consumption of a high protein diet (1.7 g/kg vs. 0.7g/kg) has been shown to increase fasting glucagon and the endogenous production of glucose (gluconeogenesis) in the fasted state. This finding from a human study that was conducted by Linn et al. in 2000, alone, could explain the unexcepted difference in the HECP results.

Alongside the increases in glucagon concentrations, the endogenous glucose production aka the gluconeogenesis increases significantly. And that's something that is most pronounced in the fasted state - the same state in which the HECP was conducted in the Smith study. It is thus simply math: If more glucose is produced by the liver (esp. at the beginning of the HECP), the total amount of glucose that has to be stashed away (or oxidized) increases. This increase, however, is not quantified by the rate of glucose infusion that's measured in the HECP, where the glucose infusion rate and the disappearance of marked exogenous glucose that's injected into the subjects are measured and any endogenous production, is ignored.

Remember: Irrespective of the argument that the result may be a methodological artifice and potentially of limited practical significance, a more important and non-hypothetical argument against panicking is that we are dealing with a single study in a very specific part of the population. It's thus not the time for over-generalizations and hectic responses, yet.

Figure 4: Studies like Farnsworth et al. (2003) show that increasing the protein content of  the diet of overweight subjects from ca. 60g  to ca. 120g has beneficial effects on both the glucose (HP -8.6%; HC -2.6%)  and insulin (HP -25.4%;  HC -4.2%levels during the classic oral glucose tolerance test in the Farnsworth study.

In the nutritional practice, however, where the increased insulin response that begins as early glucose (and to a certain extent protein) from a real meal are ingested orally, will - at least in healthy individuals - counter this effect.

In the HECP, on the other hand, the insulin levels of both groups will be the same, namely maxed out. The previously described compensation that occurs in the real world and in response to real food and the other gold-standard of measuring an individual's glucose metabolism, the oral glucose tolerance test, is thus physiologically impossible in the artificial hyperinsulinemic-euglycemic clamp procedure - and the 2003 study by Farnsworth would confirm that: In the "real world", i.e. under dynamic insulin conditions as you would see them with both, the oral glucose tolerance test, Farnsworth et al. conducted and the ingestion of a real meal, practically relevant disadvantages of the chronic consumption of a high protein diet don't exist.

I openly admit that I am, based on the plethora of scientific evidence in its favor, biased towards high(er) protein diets. What I am not, though, is blind to potential downsides of high protein intakes. You can read about one I've discussed only recently in "Protein Oxidation 101: 8 Simple Rules to Minimize PROTOX and Maximize the Proven Benefits of High(er) Protein Diets" I don't ignore potential downsides of  this way of eating and for me, the Smith study alone does not provide convincing evidence of another downside of high(er) protein intakes.

So, do I have to stop eating more protein / suggesting higher protein intakes to clients? In my humble opinion the answer to this question is "no"; and this answer is not based on my personal bias... well, at least not primarily ;-) It's rather based on my knowledge of previous evidence from studies that compared high protein (HP) to high carbohydrate (HC) weight loss diets, studies like Piatti et al. who found, likewise with HECP, that "glucose disposal and glucose oxidation significantly increased after the HP diet and significantly decreased after the HC diet" - the exact opposite of what Smith et al. report in their more recent study. Ok, the diet Piatti et al. prescribed was consumed for 'only' 21 days, the caloric deficit was sign. more pronounced (800kcal/day) and the 25 obese, female subjects were pre-, not postmenopausal women and still... the "one study suffices to 'Rethink High-Protein Diets for Weight Loss'"-approach the time.com article takes appears even more questionable in view of these and similar study results (e.g. Farnsworth. 2003 - sign. improvements in the classic glucose tolerance test; see Figure 4).

What all studies, including the one at hand, report, though, is that the increase in protein intake will have beneficial effects on the subjects' body composition by preserving lean, and in many cases promoting fat mass loss without messing with the classic measures of glucose metabolism: insulin, fasting glucose, HOMA-IR, HbA1c, or the previously mentioned oral glucose tolerance test (Brinkworth. 2004 a,b; Sargrad. 2006; Claessens. 2009; Hession. 2009) | Comment!

References:

• Brinkworth, G. D., et al. "Long-term effects of a high-protein, low-carbohydrate diet on weight control and cardiovascular risk markers in obese hyperinsulinemic subjects." International journal of obesity 28.5 (2004a): 661-670.
• Brinkworth, G. D., et al. "Long-term effects of advice to consume a high-protein, low-fat diet, rather than a conventional weight-loss diet, in obese adults with type 2 diabetes: one-year follow-up of a randomised trial." Diabetologia 47.10 (2004b): 1677-1686.
• Claessens, M., et al. "The effect of a low-fat, high-protein or high-carbohydrate ad libitum diet on weight loss maintenance and metabolic risk factors." International journal of obesity 33.3 (2009): 296-304.
• Farnsworth, Emma, et al. "Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women." The American journal of clinical nutrition 78.1 (2003): 31-39.
• Han, Seung Seok, et al. "Lean mass index: a better predictor of mortality than body mass index in elderly Asians." Journal of the American Geriatrics Society 58.2 (2010): 312-317.
• Hession, M., et al. "Systematic review of randomized controlled trials of low‐carbohydrate vs. low‐fat/low‐calorie diets in the management of obesity and its comorbidities." Obesity reviews 10.1 (2009): 36-50.
• Leidy, Heather J., et al. "Higher protein intake preserves lean mass and satiety with weight loss in pre‐obese and obese women." Obesity 15.2 (2007): 421-429.
• Linn, T., et al. "Effect of long-term dietary protein intake on glucose metabolism in humans." Diabetologia 43.10 (2000): 1257-1265.
• Mettler, Samuel, Nigel Mitchell, and Kevin D. Tipton. "Increased protein intake reduces lean body mass loss during weight loss in athletes." Med Sci Sports Exerc 42.2 (2010): 326-37.
• Piatti, P. M., et al. "Hypocaloric high-protein diet improves glucose oxidation and spares lean body mass: comparison to hypocaloric high-carbohydrate diet." Metabolism 43.12 (1994): 1481-1487.
• Sargrad, Karin R., et al. "Effect of high protein vs high carbohydrate intake on insulin sensitivity, body weight, hemoglobin A1c, and blood pressure in patients with type 2 diabetes mellitus." Journal of the American Dietetic Association 105.4 (2005): 573-580.
• She, Pengxiang, et al. "Obesity-related elevations in plasma leucine are associated with alterations in enzymes involved in branched-chain amino acid metabolism." American Journal of Physiology-Endocrinology and Metabolism 293.6 (2007): E1552-E1563.
• Smith, Gordon I., et al. "High-protein intake during weight loss therapy eliminates the weight-loss-induced improvement in insulin action in obese postmenopausal women." Cell Reports 17.3 (2016): 849-861.

Carb Up to Burn More Fat!? True or False: High CHO Diet Allows for 64% Greater Intra-, Post- & Total Fat Oxidation

You could use this exercise to deplete your glycogen levels before "cardio".

The title alone will be considered an atrocity by Taubes' evangelists: "High-CHO diet increases post-exercise oxygen consumption after a supramaximal exercise bout" (Ferreira. 2016 | title of the paper in the Brazilian Journal of Medical and Biological Research). I mean, more carbs = lower fat oxidation, that's what they've been told for years. And in fact, the title says "after a supramaximal exercise bout" and thus appears to leave enough room for the low-carb run to still burn significantly more total fat. Unfortunately (for Taubes and co.), though, that's not the case.

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If you take a look at the data in Figure 1, you will notice that the rate of fatty acid oxidation was significantly higher both during (EXERCISE) and after the workout (EPOC).

Figure 1: VO2 as a marker of fatty acid oxidation during (EXERCISE) and after (EPOC = excess post-exercise oxygen consumption) in 5 physically active males in response to submaximal exercise on high- vs. low-CHO diets (Ferreira. 2016).

Accordingly, the total amount of fat the subjects burned was larger, not smaller; and the effect size of ES = 1.8 further somehow reminds me of a sentence that I haven't heard ever since the rise of low-carb dieting: 'Fat burns in the fire of carbohydrates'.

Don't be fooled - Increased fatty acid oxidation does not necessarily translate to increased fat loss! If this is not your first SuppVersity article, you probably know that already. For the occasional newcomer, however, it is vital to understand that the lipids you burn during and after your workouts (a) won't necessarily come from your belly and (b) can be easily restored after the workout even if they came from your more or less abundant adipose energy stores.

Before we get deeper into the discussion of the implications of the results, however, it is imperative to take a look at the methodology of the experiment the scientists from Vitória de Santo Antão, the Universidade de São Paulo, and the Universidade Federal de Lavras have conducted last year.

Low(er) Carb Crossfitters May be Missing Out Significantly | more

"[A]fter receiving verbal and written explanations, and signing an informed consent, 5 physically active males (age 31.0±7.7 years, height 180.2±4.3 cm, body mass 77.0±7.7 kg, body fat 13.3±2.9%, V̇O2 peak 48.6±11.5 mL·kg-1·min-1) volunteered to participate in this study [...]

In order to produce a large difference in CHO availability, pre-SE endogenous CHO stores were altered by a combination of exercise and diet" (Ferreira. 2016)

Now these "alterations" comprised (a) a glycogen-depletion exercise protocol 48 h before each experimental session. As Ferreira et al. point out, "[t]his protocol consisted of a 90-min cycling at 50% of the difference between LT1 and LT2, followed by 6×1 min exercise bouts at 125% of V̇O2 peak; 1 min recovery was allowed between effort sets" (Ferreira. 2016), and (b) different baseline diets (see light-blue box for more information about the diet - will be updated, if possible).

Figure 2: Experimental design. After the preliminary and familiarization test, and a 7-day period, participants were submitted to a glycogen-depletion exercise protocol (GDEP), followed by 48 h having either a high- or low- carbohydrate (CHO) diet. At the end of the 48-h period, participants returned to the laboratory and performed the test experiment for data collection. After a washout period of 7 days, the process was repeated with participants who had the high CHO diet previously, receiving the low CHO diet, and vice-versa (Ferrera. 2016).

After the standardized glycogen-depletion exercimse protocol, participants followed the sequentially prescribed high- or low- carbohydrate (CHO) diet for 48h. At the end of the 48-h period, participants returned to the laboratory and performed the test experiment for data collection. After a washout period of 7 days, the process was repeated with participants who had the high CHO diet previously, receiving the low CHO diet, and vice-versa (crossover design, Figure 2).

UPDATE: Exact macronutrient and energy content of the diets: Yes, it is a bummer that the exact macronutrient composition is not mentioned in the article, but I've gotten a pretty fast response from the authors who tell me that the low-CHO diet with 10% carbohydrate, 35% lipids, and 55% protein is not a high fat, but a high protein diet, while the high-CHO diet is, more or less, a low fat, low protein diet. Any conclusions about a truly ketogenic (as being in full ketosis 24/7 due to high fat, low carbohydrate and relatively low protein intakes) diet are thus unwarranted - too much protein (and likely gluconeogenesis) going on with only 35% of lipids and 55% of the energy from protein; wha is not surpring, though, is that a diet with the lion's share of energy being delivered in form of protein is rather ergolytic than ergogenic.

In the test day, participants arrived at 8:00 am in the laboratory after a 12-h overnight fast and rested on a chair during 20 min for the assessment of resting V̇O2 value (Quark b2, Cosmed, Italy). Then, they underwent a 5-min warm-up at 50 W, followed by an SE at 115% of V̇O2 peak until exhaustion, which was assumed when participants were unable to maintain the pedal cadence above 60 rpm. Immediately after the test, they sat comfortably on a chair for 60 min. The V̇O2 peak was measured continuously from the baseline to the end of the 60-min post-exercise period (Quark b2, Cosmed).

You have already seen the results of the O2 analysis (baseline values were similar for both groups) in Figure 1. So, I will stick to the results I haven't reported, yet:

• 

  Two-A-Day Training - That's Bogus, Right? No - You Will Reward Yourself w/ Increased Fat Oxidation and more

  time to exhaustion increases in the high-CHO group (4.4±0.6 vs 3.0±0.6 min, P=0.01, ES=2.4 large, power effect=0.98),
• total mechanical work was greater in the high-CHO group (76.9±16.5 vs 50.9±9.4 kJ, P=0.001, ES=2.0 large, power effect=0.91) and
• the V̇O2 measured at exhaustion was slightly higher in high- compared to low-CHO diet (48.6±11.0 and 45.2±11.0 mL·kg-1·min-1, respectively, P=0.004, ES=0.3 small, power effect=0.08)

To summarize it in the authors' words: "The high-CHO diet increased exercise duration (∼32%) and total mechanical work (∼34%) during a single SE bout. The increased tolerance further led to an increased exercise energy expenditure (i.e., ∼30% VO2 increase)" (Ferreira. 2016).

Going to raid the fridge? You better don't do this after a workout. Myth says: Going to bed glycogen depleted will boost mitochondrial biogenesis - true of false?

Things to keep in mind, when interpreting the results: Now, before you start crying "foul play", let's address a few issues that must not be overlooked when you're talking about the practical implications of the study at hand. (A) With the preceding glycogen depletion protocol, we will probably have relatively low glycogen stores in both groups. This, in turn, will have lead to an increase of AMPK in the muscle during both conditions and could thus have produced similar rates of muscular fatty acid oxidation. (B) The "fat advantage" would thus, as the authors hint at in the previously quoted part from their discussion, simply a function of the increased exercise time.

That's not bad, but it is unlike the result that's implied in the title of the paper, not in opposition to previous studies which suggest that a high carbohydrate diet will increase the respiratory ratio (RER) and thus reduce the relative amount of fat to carbohydrates subjects (energy from fat:energy from carbs) will burn during the standardized workouts.

Now, from (A) and (B) follows that, unless you're doing glycogen-depleted cardio workouts (e.g. after leg training or as described in the "Sleep Low"-study from early 2016), there's only a relatively slim chance that you'd see an effect size of the magnitude Ferreira et al. report in their paper. In view of the fact that the previously explained RER is not a determinant of exercise-induced body fat loss, however, it's still (with and without glycogen depletion) possible that the ergogenic effects of the high(er) CHO diet and its ability to increase both, the total mechanical work and the workout duration (and thus the total energy expenditure), may still allow you to burn more body fat. Whether that's indeed the case, and high-carbing alongside glycogen depletion is, as Ferreira et al. speculate "[f]rom a practical standpoint, [...] an appealing strategy for a less time-consuming training and weight loss" (Ferreira. 2016), however, requires, as usual, further research | Comment!

References:

• Ferreira, G. A., et al. "High-CHO diet increases post-exercise oxygen consumption after a supramaximal exercise bout." Brazilian Journal of Medical and Biological Research 49.11 (2016).