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No, even the reanalysis doesn't say that a bit more protein, alone, will make you look like this ;-)

I've written about both observational and experimental studies that show how increased protein intakes can improve your body composition. So why mention another one?

Well, the study at hand which has been conducted by scientists from the Purdue University is interesting, because (a) it's not as extreme as Jose Antonios 2014 study in which the subjects consumed "Fivefold More Than the FDA Allows" (learn more), (b) it is not a simple short-term diet intervention where the high protein diet comes - as usual - out victorious and it is (c) actually a re-analysis of one of those studies that is often cited to "prove" that increased protein intakes, let alone the use of whey protein, wouldn't be advantageous for overweight and obese individuals trying to shed body fat.

But let's tackle one thing after the other. The original goal of the study at hand was to re-assess the data from Weinheimer's 2012 study which concluded that "whey protein supplementation [10, 20, 30, or 30 g of whey protein twice daily] does not affect exercise [2x resistance training 1x cardio per week] training-induced changes in body composition and indices of metabolic syndrome in middle-aged overweight and obese adults" (Weinheimer. 2012 | just to make sure you're not confused: While the lead authors changed Weinheimer <> Campbell, it's still the same team).
Instead of dealing with absolutes and overall averages, only, Campbell et al. reanalyzed their data to elucidate the influence of total protein intake (TPro) and changes in protein inatke (CTPro) on exercise-induced changes in body composition and metabolic syndrome indexes. As the scientists point out in the introduction to their soon-to-be-published paper, they conducted this assessment from 3 perspectives for protein intake as follows (Campbell. 2015):

1. TPro as a continuous variable with the use of a multiple linear regression model;
2. CTPro during the intervention vs. each subject s usual protein intake (post-intervention value minus pre-intervention value) with the use of multiple linear regression; and
3. TPro as a categorical variable, <1.0, ≥1.0 to <1.2, and ≥1.2 g per kg bodyweight, using a stratified analysis approach.

In that, Campbell et al. (2015) already expected that they would be able to correct their original findings. More specifically, they hypothesized that they'd find that a higher total protein intake, expressed as a continuous or categorical variable, would enhance the training-induced reduction of fat mass (FM) and gain of lean mass (LM), but not influence responses of MetS indexes (these were waist circumference, glucose, TGs, HDL cholesterol, and blood pressure).

Table 1: Overview of the results of the multiple linear regression analysis the beta² are quantitative indicators of the link between total protein intake (TPro) and change in protein intake (CTPro) (Campbell. 2015).

In addition, the scientists were quite convinced that they'd be able to show that the changes in body composition had been the most pronounced in those subjects with the highest increase in total protein intake over the course of the 36 week study period. And guess what!? Campbell et al. were able to confirm both hypotheses in their ahead-of-print paper:

• In conjunction with exercise training, higher total protein intakes promoted positive changes in body composition. What the higher protein intakes did not do, however, was to promote further improvements in critical markers of metabolic syndrome in the 117 overweight and obese middle-aged adults who participated in the 2012 original 36-week intervention.
• In addition, the changes in body composition, Weinheimer et al. observed when they conducted the study three years ago were the most pronounced in those subjects who recorded the largest changes in total protein intake via diet or supplements.

Figure 1. Temporal changes in the most important markers of body composition according to total protein intake of the subjects during Weinheimer's 2012 36-week intervention study (Campbell. 2015).

That's all great and certainly supports the physique improving benefits of high protein diets. What's a bit disappointing, though, is that similar correlations between higher or increased total protein intakes were not observed for any of the markers of metabolic syndrome (waist circumference, glucose, TGs, HDL cholesterol, and blood pressure).
References:

• Antonio, Jose, et al. "The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals." Journal of the International Society of Sports Nutrition 11.1 (2014): 19.
• Campbell, et al. "Higher Total Protein Intake and Change in Total Protein Intake Affect Body Composition but Not Metabolic Syndrome Indexes in Middle-Aged Overweight and Obese Adults Who Performed Resistance and Aerobic Exercise for 36 Weeks." J. Nutr. jn213595 (2015): Ahead of print.
• Weinheimer, Eileen M., et al. "Whey protein supplementation does not affect exercise training-induced changes in body composition and indices of metabolic syndrome in middle-aged overweight and obese adults." The Journal of nutrition 142.8 (2012): 1532-1539.

"If some is good, more is better!" Unfortunately, this simple maxime does rarely apply when it comes to the physiological response to certain foods and/or supplements. For protein, however, it appears as if the relation holds - at least as long as protein does not become the only energy source in your diet.

I guess by now I can simply skip the lengthy introduction telling you about how I didn't want to cherry pick only three out of more than twenty newsworthy studies that were presented at the Twelfth International Society of Sports Nutrition (ISSN) Conference and Expo in 2015, when I started writing this series right (click here if you have missed the previous articles)?

Well, that's good because it leaves more room for a brief preview of the studies I am about to discuss in today's third serving of the waredownloadsoft ISSN Research Review 2015 - studies that are all related (in one way or another) to increased protein intake. Either in overweight or obese people, for whom higher protein meals increase the post-prandial increase of the "satiety hormone" GLP-1, or in vegans, vegetarians and everyone else who wants to make the most of his vegetable protein sources (pea and rice protein, to be precise) by adding digestive enzymes to the mix, or - last but not least - gymrats who ramp up their protein intake from 2.3 to 3.8 g/kg body weight to see even more pronounced improvements in body composition.

• High protein, high GLP-1, ... highly beneficial? As a waredownloadsoft reader you are aware of the far-reaching metabolic effects of GLP-1 on appetite (suppression | Näslund. 1999), glucose and fat metabolism, as well as thermogenesis (Lejeune. 2006). Against that background, you will know that the small, but statistically significant increase in GLP-1 Franklin et al. (2015) observed in their latest study which compared the effects of a high protein and high mono-unsaturated fat meal on the well-known incretin hormone may have significant long-term effects even though the blood glucose levels of the study's twenty-four overweight or obese participants (male/female: 12/12; age: 38.7 ± 15.3 (mean ± standard deviation) years; BMI: 31.6 ± 4.0kg/m²), who consumed isocaloric meals containing either 35.2% energy from fat and 20.7% from monounsaturated fat (HMF meal) or 31.9% energy from protein (HP meal), did not trigger differences in post-prandial glucose levels at 30, 60, 120, and 180 min.
  
  

  Figure 1: Levels of active GLP-1 in response to high protein (HP) or high MUFA (HMF) meals (Franklin. 2015).

  To believe that "simply eating more protein" is going to solve all your weight problems, though, would be short-sighted - especially for the overweight obese for whom the study at hand as well as previous studies investigating the effects of GLP-1 on glucose metabolism suggest that they may benefit to a lesser extent from protein induced increases in GLP-1 than lean individuals, in whom the "satiety hormone" will trigger much more pronounced β-cell responses that in in patients with sign. insulin resistance and pre- or full-blown type 2 diabetes (Kjems. 2003).
  
  If that sounds like you, using the high(er) protein meals in conjunction with an energy restricted diet to lose weight and thus to improve your insulin sensitivity can obviously still be beneficial. Without a planned, reasonable caloric deficit, however, high(er) protein intakes alone are probably not going to "cut it" (all puns intended).

References:

• Detzel, Christopher J., et al. "Functional animal proteins activate mTOR and bind pro-inflammatory compounds." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P35.
• Ellerbroek, Anya, et al. "The effects of heavy resistance training and a high protein diet (3.4 g/kg/d) on body composition, exercise performance and indices of health in resistance-trained individuals-a follow-up investigation." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P37.
• Franklin, Brian, et al. "The effect of meal composition on postprandial glucagon-like peptide-1 response in overweight/obese participants." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P12.
• Galvan, E., et al. "Effects of 28 days of two creatine nitrate based dietary supplements on bench press power in recreationally active males." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P17.
• Jäger, Ralf, et al. "Analysis of the efficacy, safety, and regulatory status of novel forms of creatine." Amino Acids 40.5 (2011): 1369-1383.
• Lejeune, Manuela PGM, et al. "Ghrelin and glucagon-like peptide 1 concentrations, 24-h satiety, and energy and substrate metabolism during a high-protein diet and measured in a respiration chamber." The American journal of clinical nutrition 83.1 (2006): 89-94.
• Näslund, E., et al. "Energy intake and appetite are suppressed by glucagon-like peptide-1 (GLP-1) in obese men." International journal of obesity 23.3 (1999): 304-311.
• Nystrom, M. G., et al. "Nutrient timing habits of Division I NCAA athletes." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P33.
• Minevich, Julie, et al. "Digestive enzymes reduce quality differences between plant and animal proteins: a double-blind crossover study." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P26.

Want to maximize net protein retention? Order another one... another steak ;-)

In view of the WHO's recent epidemiological bogus publication, ... ah I mean their review of the epidemiological research that said that "red meat kills", it is quite surprising that the study Il-Young Kim and colleagues conducted in healthy young adults was even approved by the ethics committee of their respective research institutions. After all, the study involved measuring the whole body protein kinetics of young men and women after the consumption of ~40g (moderate protein, or MP) or, even "worse", ~70g (higher protein, HP) of protein in form of red meat (85% lean ground beef) in a regular food matrix (=as part of a normal meal | see Table 1 for an exact overview of the macronutrient content).
Whole protein kinetics? Yes, that's different from what you see in the average "whey protein builds muscle study", in which the researchers measure only the fractional protein synthesis. Kim et al. went one step further and measured the protein synthesis (PS), breakdown (PB), and net balance (NB) in their subjects, twenty-three healthy subjects [18 – 40 yrs] who were recruited from the Little Rock area using local newspaper advertisements and flyers posted around the University of Arkansas for Medical Sciences (UAMS) campus and the Little Rock area. Now, it's not like humans had a display you can use to read these variables, so eventually, they were still calculated based on the determinations of the rate of appearance (Ra) into the plasma of phenylalanine and tyrosine, and the fractional Ra of endogenous tyrosine converted from phenylalanine as in a previous study by the same team of researchers (Kim. 2015a). Since this technique is unable to distinguish between the different sites of protein breakdown.and storage, the results of the study at hand could describe increases or decreases in splachnic (=organ) protein synthesis or breakdown, too. It is thus not possible to exclude a null effect on skeletal muscle protein synthesis and breakdown based on the available data.

Whole protein kinetics, two different amounts of protein, with and without exercise

There were yet other things Kim's study had in common with many of the aforementioned "whey protein studies": The study had a run-in that was included to minimize any potential effects of the protein content of the subjects' baseline diets. The subjects ate their high or medium protein meals in the fasted state and the participants - or at least some of them - also trained. To be more specific, the subjects were randomly assigned into an exercise group (X, n=12) protocol consisting of 3 sets of 10 repetitions of bench press, lateralis pull-down, leg press, and leg extension each at 80% of 1 repetition maximum (1 RM, the maximum weight that can be lifted for one repetition) at a pace of 30 sec per set (rest interval between sets was less than 2 min, and the entire exercise bout was completed in ~45 – 50 min), or a resting group (R, n=11).

Table 1: Overview of the macronutrient intake during the 4-day run-in and the actual experiment (Kim. 2015b)

So much for the study design. Let's take a look at the results now: When the scientists analyzed the data from the 7-h stable isotope tracer infusion protocol that was used to determine the rate of protein synthesis (PS), breakdown (PB) and net protein balance (NP), they realized that...

• exercise did not significantly affect protein kinetics and blood chemistry, while 
• feeding, in general, resulted in a positive net protein balance at both levels of protein intake,

Boring? You're right. This would hardly be a 'waredownloadsoft newsworthy' study if the researchers had not also confirmed what most of you probably already suspected: The high protein meal lead to a significantly greater increase in net protein balance than the medium protein meal.

Figure 1: It's the decrease in protein breakdown, not the marginal increase in protein synthesis that makes the difference between the net protein balance after the high and medium protein meals (Kim. 2015b).

Interestingly enough, this increase in net protein balance was achieved primarily through a greater reduction in PB and to a lesser extent stimulation of protein synthesis (for all, p<0.0001). This is an important results, because it suggests that all previously reported ceiling effects for protein synthesis could be irrelevant when we are talking about a potential limit of protein intake beyond which you won't be able to see further beneficial effects on body composition in general and the accrual of lean mas in particular.
References:

• Fukagawa, N. K., et al. "Insulin-mediated reduction of whole body protein breakdown. Dose-response effects on leucine metabolism in postabsorptive men." Journal of Clinical Investigation 76.6 (1985): 2306.
• Kim, Il-Young, et al. "Quantity of dietary protein intake, but not pattern of intake, affects net protein balance primarily through differences in protein synthesis in older adults." American Journal of Physiology-Endocrinology and Metabolism 308.1 (2015): E21-E28.
• Kim, et al. "The anabolic response to a meal containing different amounts of protein is not limited by the maximal stimulation of protein synthesis in healthy young adults." Am J Physiol Endocrinol Metab (November 3, 2015b). doi:10.1152/ajpendo.00365.2015.

Is it really bad to drink that whey shake before you eat the bananas, strawberries and blueberries, because whey makes you insulin resistant? Sounds "bogussy" and a closer look at the questionable methodological choices of the scientists who conducted the study don't make the results sign. more credible.

In the fitness community, whey protein is the #1 on the "must have supplement" list. Multi-vitamins? Creatine? Who cares, as long as you get your 30g of whey per day, you're good... really? One of you recently send me a study that would suggest that "good" is not exactly the right word to describe the effects of whey protein on at least one out of the set of well-established parameters of optimal metabolic health: Your muscles' insulin sensitivity.

In the paper that has been published in the reputable scientific journal "Diabetes", Gordon I. Smith and colleagues describe an experiment the results of which clearly suggest that whey doesed at 0.6g/kg fat free mass has a sign. insulin-desensitizing effect in twenty-two sedentary (<1.5 hour of exercise/w) and weight-stable (<2 kg change for at least 6 months), 50-65y old postmenopausal women who participated in this acute response study.
Acute response? Yes, there it is, the first in a line of problems that reduces the significance of the results. After all, testing the acute response to a certain health cannot tell you anything about the long-term effects on said parameter... especially if your subject group due to being sedentary and in an age where the parameter in question is deteriorating, anyway.

But let's not be the "it's not bros, so it's not valid for bros"-guys. Let's rather take a look at (a) the procedures and (b) the results and make up our minds later. And let's first take a look at a handful of important parameters of the study design: To determine the insulin sensitivity, the scientists used two hyperinsulinemic-euglycemic clamp sessions with the subjects being randomly assigned to do the procedure with vs. without whey protein first.

If you've got brawn and brain you cannot ignore that whey is much more than a potent muscle builder | learn more

"Before each clamp procedure, subjects were instructed to adhere to their usual diet and to refrain from vigorous physical activities for three days. Subjects were admitted to the Clinical Research Unit in the late afternoon, where they consumed a standard dinner between 1800 and 1900 h, and then fasted, except for water, until the next morning. At 0600 h, a catheter was inserted into an arm vein for the infusion of a stable isotope labeled glucose tracer; catheters for blood sampling were inserted into the radial artery of the opposite arm and in retrograde fashion into the femoral vein of one leg. At ~0645 h, a primed, constant infusion of [6,6- 2 H2]glucose (priming dose: 22 µmol·kg body wt-1, infusion rate: 0.22 µmol·kg body wt-1·min-1), purchased from Cambridge Isotope Laboratories Inc. (Andover, MA), was started and 4 h later the hyperinsulinemic-euglycemic clamp procedure was initiated with two 5-minute priming doses (first 200 mU·m-2 body surface area (BSA)·min-1 then 100 mU·m-2 BSA·min-1) of human insulin (Novolin R, Novo Nordisk, Princeton, NJ); for the remaining 230 min, insulin was infused at a rate of 50 mU·m-2 BSA·min-1. Euglycemia (at blood glucose concentration ~5.6 mM) was maintained by variable rate infusion of 20% dextrose (Baxter, Deerfield, IL) enriched to 2.5% with [6,6-2H2]glucose" ().

During the "whey trials", the subjects consumed 0.6 g of whey protein (unflavored Unjury®, ProSynthesis Laboratories, Inc, Reston, VA) per kg FFM dissolved in 360 ml water or the same volume of water alone. In addition, the researchers conducted a trial in which the subjects consumed the same amount of leucine.
To figure out if any effect they would observe was induced by whey, i.e. a complex protein, or just the most-applauded whey ingredient, i.e. leucine, the scientists ran a follow-up test (1-4 weeks later) in which the subjects consumed either 0.0684 g/kg FFM of pure leucine (that's equivalent to the amount of leucine in the whey protein)  dissolved in 360 ml Kool-Aid® (Kraft 94 Foods, Inc, Northfield, IL) or the same volume of the Kool-Aid® solution alone during the clamp procedure. I don't have to tell you that this was a mistake that makes the results of this follow-up useless for comparisons to the previous trial, in which the whey protein was mixed with water - Kool-Aid is after all all-carbohydrate - with 0.9g carbohydrates per ml of junk... ah, I mean per ml of the soft-drink.

Figure 1: Clearance of glucose during the hyperinsulemic clamp for the whole body and the legs (Smith. 2015). It is noteworthy that there control vs. active treatment signalling protein response (mTOR, p-AKT, ACC, etc. - not shown in figure) did not show differences that could explain the alleged negative effects of whey on glucose uptake (see Figure 2).

This does not mean that we couldn't use the data from the leucine trial, at all, though. But let's be honest, who cares about the non-significance of the effects of a non-gluconeogenic amino acid (meaning that leucine cannot be converted to glucose by the liver) if you cannot compare them to the significant decrease in insulin-mediated glucose disposal (38.8 vs 51.9 µmol glucose per µU insulin/ml / min; P<0.01) the scientists observed in the whey condition, because the test was messed due to the use of a different and by no means "neutral" control?

Figure 2: Don't worry, while the scientists cleverly call the glucose disappearance into the legs "leg glucose uptake" it's just the product of blood flow to the legs times whole body glucose disposal and suffers from the same methodological short-come as the whole body glucose disposal that assumes that whey was non-gluconeogenic (data from Smith. 2015)

Rather than as a basis to argue that whey is bad and leucine is good, you can use the Kool-Aid glitch and the fact that leucine cannot be converted to glucose in the liver to substantiate the following hypothesis: If the scientists had accounted for the gluconeogenic glucose load from whey when they tested their allegedly sugar-free (manufacturer claim) whey protein vs. water in the previous trial, they would probably have found no significant effect of whey protein on muscular glucose uptake, because the test wouldn't have been unfairly thwarted in favor of the water control which came without the additional glucose load from the whey-induced gluconeogenesis in the liver.

Figure 3: Both, acute and chronic realistic and thus relevant studies show beneficial effects of whey on glycemia (Petersen. 2009) and insulin sensitivity (Pal. 2010) - you decide which studies to trust ;-)

Plus, even if we assume that this hypothesis wasn't true (I am pretty convinced it is), the results of the study at hand would still be an inexplicable artifice that stands in stark contrast to the well-proven multi-facetted acute and chronic beneficial effects of whey protein on glucose- and weight-management in healthy, diabetic and pre-diabetic individuals (Layman. 2004; Frid. 2005; Peterson. 2009; Akhavan. 2010; Pal. 2010) - effects of which no one ever claimed that they were mediated by acute increases in muscular insulin sensitivity, by the way; and that despite the fact that the data from Pal (Figure 3, left) clearly indicates that these benefits occur in the real world.

References:

• Akhavan, Tina, et al. "Effect of premeal consumption of whey protein and its hydrolysate on food intake and postmeal glycemia and insulin responses in young adults." The American journal of clinical nutrition 91.4 (2010): 966-975.
• Frid, Anders H., et al. "Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects." The American journal of clinical nutrition 82.1 (2005): 69-75.
• Layman, Donald K., and Jamie I. Baum. "Dietary protein impact on glycemic control during weight loss." The Journal of nutrition 134.4 (2004): 968S-973S.
• Morifuji, Masashi, et al. "Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats." British journal of nutrition 93.04 (2005): 439-445.
• Pal, Sebely, Vanessa Ellis, and Satvinder Dhaliwal. "Effects of whey protein isolate on body composition, lipids, insulin and glucose in overweight and obese individuals." British journal of nutrition 104.05 (2010): 716-723.
• Petersen, Brent L., et al. "A whey protein supplement decreases post-prandial glycemia." Nutr J 8.47 (2009): 1475-2891.
• Smith, Gordon I., et al. "Protein ingestion induces muscle insulin resistance independent of leucine-mediated mTOR activation." Diabetes 64.5 (2015): 1555-1563.

This could have been the HP breakfast. Egg-based pancakes + ham.

It is almost like the question "to carb" or "not to carb" and the almost religiously maddish discussions between carb-eaters and ketophiles: The debate revolving around the useful- or uselessness of breakfast, when it comes to health and physique issues.

In my more recent articles about the topic I have repeatedly exposed the claim that "not having breakfast is bad for everyone" is total bogus; and while I am not going to go back on that I am about to discuss a study that demonstrates that the right breakfast, i.e. one that's high in protein, may be extremely better than having no breakfast at all.
Said study has been conducted by scientists from the University of Missouri and the Purdue University (Leidy. 2015). It's an investigation into the effects of normal-protein (NP) vs. high-protein (HP) breakfast meals on appetite control, food intake, and body composition in “breakfast skipping” young people with overweight/obesity.

As a waredownloadsoft reader you'll know that previous studies suggest that as habitual breakfast skippers, the youths are actually not the ideal study object for a study to show beneficial effects of breakfast. After all, a recent study by Thomas et al. showed quite convincingly that "Whether Skipping Breakfast Increases Insulin, Hunger and Blood Lipids Depends on One's Breakfast Habits" (read the article). Is this a problem? Well, it could be if the new study yielded negative results. After all, we'd have to argue that this was to be expected if the subjects were habitual breakfast skippers.

Table 1: Subject characteristics at baseline (Leidy. 2015). As you can see the subjects were randomly assigned to the three groups at a ratio of 1:2:2 to breakfast skipping, normal protein (NP) and high protein (HP) breakfast.

Luckily, the results were positive and the study with its 12-week study period probably long enough to overcome the effects of habituation which mess with the results of all studies which test the effect of having vs. skipping breakfast on only one or two occasions.

Figure 1: Macronutrient composition (g) of the test meals used in the study (Leidy. 2015)

The study at hand, however, had its fifty-seven adolescent subjects (age: 19 +/- years; BMI: 29.7 +/- 4.6 kg/m²) complete a 12-week randomized controlled trial in which the adolescents consumed either a 1,464 kJ NP breakfast (13 g protein), an isocaloric breakfast with a high protein content (HP | 35 g protein), or continued to skip breakfast (CON). The main outcome variables were the subjects' pre- and post-study appetite, their food intake, body weight, and body composition, which was assessed assessed via DXA scans (which are as you know still the "gold standard" for measuring the body composition of subjects in scientific studies)
The NP and HP groups were provided with specific breakfast meals to consume between 6:00 and 9:45am each day, while the CON group continued to skip breakfast (with nothing to eat/drink, besides water) before 10:00am - with significant consequences as the in parts significant inter-group differences in Figure 2 can tell you.

Figure 2: Comparison of the changes in fat mass, the daily food intake, hunger and fullness ratings in the subjects from the CON (=kept skipping breakfast), NP (normal protein) and HP (high protein) breakfast groups (Leidy. 2015).

The superiority of (a) having breakfast and (b) consuming a high protein breakfast are not debatable. With its 12-week study duration, the study at hand obviously allowed for a full habituation and did thus - much in contrast to many short-term studies - yield all the benefits that are usually ascribed to having breakfast. In particular, having breakfast...

• "Breakfast!? An (Un-)Biased (?) Review of the Breakfast Myth" | read it!

  made the subjects magically lose (HP) or at least not gain (NP) superfluous body fat.
• significantly reduced the daily energy intake in the high protein condition and buffered the significant increase in energy intake in the no breakfast condition if the breakfast had a normal protein content,
• reduced the total time during which the subjects were hungry not just in the morning, but 24/7, and
• increased the subjects' fullness, especially in the morning.

• Dhurandhar, Emily J., et al. "The effectiveness of breakfast recommendations on weight loss: a randomized controlled trial." The American journal of clinical nutrition 100.2 (2014): 507-513.
• Leidy, Heather J., et al. "A high‐protein breakfast prevents body fat gain, through reductions in daily intake and hunger, in “Breakfast skipping” adolescents." Obesity (2015).
• Schlundt, David G., et al. "The role of breakfast in the treatment of obesity: a randomized clinical trial." The American journal of clinical nutrition 55.3 (1992): 645-651.
• Thomas, Elizabeth A., et al. "Usual breakfast eating habits affect response to breakfast skipping in overweight women." Obesity 23.4 (2015): 750-759.