A recent study that was conducted by a group of researchers from the Roehampton University, and the Universities of Northampton and Hull in London took an interesting and totally overdue approach to dispel the myths that revolve around the anti-obesity effects of breakfast. In the said study, a team of researchers recruited 37 participants who were assigned to one out of four groups on the basis of their body mass index (BMI) - normal weight BMI <25 kg/m² | or overweight/obese BMI > 25 kg/m² | habitual breakfast eaters | habitual breakfast omitters.
Subsequently, even the latter, i.e. the breakfast eaters were requested to eat breakfast for an entire week. The BREAKFAST week was followed by a one week wash-out and an entire week during which the subjects had to omit breakfast.
Over the course of the whole study period, all subjects hat do keep detailed 7-day food diaries, reporting what was consumed and the timing of consumption were completed for each breakfast condition.
Figure 1: Lean (left) and overweight (right) subjects react very different to breakfast skipping (Reeves. 2014)
As the data in Figure 1 already reveals, the total energy intake was significantly higher during the breakfast than the no breakfast week. But just as the scientists say, the present study did also reveal a "significant effects of timing on energy intakes": More energy was consumed during the afternoon in the no breakfast week compared to the breakfast week.
Timing and body weight, both make a difference!
In general, overweight participants consumed greater amounts of energy than normal weight participants (surprise ;-) in the early evening - the effect was even more pronounced for those of them who were regular breakfast omitters and thus used to feasting in the afternoon / evening.
Overall, this sounds as if having breakfast regularly was a very good idea, but unlike some people want to make you believe, the total energy intake does count. The same is yet also true for the amount of sugar, which skyrocketed in the overweight subjects in the no breakfast week. Running around on empty and being unable to tap into their affluent energy depots on the hips and around the waist, the insulin resistant (don't tell me about "healthy obesity!") overweight part of the study participants gravitated towards readily available energy intake.
Table 1: Mean sugar and micronutrient intakes in breakfast and no-breakfast conditions (Reeves. 2014)
Bottom line: Paired with the reduced folate and iron intake in the non-breakfast week, the previously outlined results of the study at hand highlight once more the practical value of having breakfast for the average American who is neither willing nor able to track his energy and macronutrient intake on a daily basis. In a controlled diet scenario, on the other hand, lean individuals have no reason to eat breakfast, if they feel that intermittent fasting (=breakfast skeeping) helps them to stick to their planned energy intake.
If you take another look at the data in Table 1 to the right, you will after all realize that the lean study participants were able to live of their fat stores and did not have to resort to Snickers, Twinkies and *bs* "protein bars" with a sugar content of 85% - the sugar intake of the habitual breakfast eaters decreased significantly by 31% while their fibre intake remained stable in conjunction with the 26% reduction in energy intake this alone should have been enough to she a couple of pounds of body fat... So what? Good bye "healthy" breakfast cereals ;-)
References:
Reeves, Sue, et al. "Experimental manipulation of breakfast in normal and overweight/obese participants is associated with changes to nutrient and energy intake consumption patterns." Physiology & Behavior | Available online 24 May 2014.
Do you know that grumbling? This strange feeling you get, when you are "running on empty" - not the appetite or desire you feel when you pass by the ice cream parlor. I am talking about hunger, real physiological hunger, the one where you start towards your fridge and, regardless of what is in there, stuff it down your pie-hole. This ravenous desire for food is the direct psycho-physiological response to surges of the "hunger-hormone" ghrelin.
So, if high ghrelin levels make you eat everything that cannot escape fast enough, it seems quite obvious that this would be the underlying reason for obesity in rats injected with exogenous ghrelin.
This, however, was not the case in a recently conducted study by Perez-Tilve et al. from the Department of Internal Medicine at the University of Cincinnati (Perez-Tilve. 2011).
Figure 1: Food intake of ghrelin injected or control rats on low fat or high fat diets. (data adapted from Perez-Tilve. 2011)
The scientists had administered intracerebroventricular ghrelin injections to two groups of rats. One group received a low-fat chow, while the other was on the famous high-fat diet scientists use to emulate our modern westernized gluttony (cf. yesterday's news, fig. 1). As expected, the rats that were fed the low-fat chow significantly increased their food intake (cf. Figure 1). Unexpectedly, though, ghrelin failed to statistically significantly increase food intake in the high fat diet group, yet ...
in rats fed the HFD, ghrelin nonetheless increased adiposity [fat mass increase of 14±2 g (ghrelin+HFD) vs. 1±1 g (saline+HFD), P<0.001] up-regulating the gene expression of lipogenic enzymes in white adipose tissue.
These results are of great interest, because they clearly show that your typical "fast", where you diet really hard for a few days (and thus increase your ghrelin levels), until you get so ravenously hungry that you end up (deliberately or not) "refeeding" yourself with pizza and ice-cream set the scene for further undesirable fat gain by setting your body's metabolic switches to fat storage mode.
Believe it or not, but the question "low or high carb for breakfast" is non-sense, because there is no general answer. It depends on who is asking and what he is going to spend the rest of his day.
Before we can start reviewing the contemporary literature, we will have to define the term "breakfast" as the first meal in the day which is eaten in the AM. This definition differs from the "literal" one, I've used in a previous article with the title "Circadian Rhythmicity - "Breakfast" or "Breaking the Fast"? Fasting as Zeitgeber & All About King, Prince & Pauper" (read it) and is thus in line with the mainstream idea of standing up, showering and... yes, you got it: having breakfast.
If you google "breakfast" and "obesity" you're served a colorful potpourri of "pro breakfast" articles which will inform you about "facts" like "Eating a big breakfast fights obesity and disease" (ScienceDaily), or "Breakfast Combats Obesity and Diabetes in Young People" (medscape).
Could all these "experts" be wrong? For the obedient average Joe this sounds crazy. Like one of those theories from your average Internet conspiracy theorist, but if you look at the actual evidence you have to admit:"A definitive conclusion can be made concerning the role of breakfast skipping in weight change." (McCrory. 2014)
The reasons for our cluelessness are manifold
There is for example a very good reason I anteceded this article with a definition of "breakfast". The latter is after all something you won't find in the average study, which could therefore consider eating a donut at 11am in as much as "breakfast", as it would discard having a protein shake immediately after you wake up as "not breakfast".
If we look at the actual "average Joe" (according to US National survey data), we're getting into even more trouble. This guy was eating 2.76 meals in 1971–75, while he is now up to 2.96 in 1999–2002 (Kant. 2007).
In other words: Americans eat more frequently these days, but are still fatter
Obviously frequency alone doesn't tell us whether one of those "almost three" meals was actually the holy breakfast. I mean, if it wasn't it's obvious the Americans became fatter and fatter - right (sarcasm)? The data we are interested in, is thus not the total number of meal (if you want to know more about that, take a look at "Many Small Meals Suck!" | go for it!). The data we are interested in is the data in Figure 1, the number of non-obedient US citizens who don't listen to the well-meant advice from the USDA and simply skip one of their holy meals.
Figure 1: Prevalence of skipping meals (breakfast, lunch, dinner) and snacking in the US, 2009–10 (McCory. 2014).
As McCorey highlights in a recent review (2014), their number rose. This seems to be a contradiction. I mean, if the number of meal skippers increases, shouldn't the number of meal (on average) decrease, when it in fact rose from 11% to 18%? Well, it should, if it was not for the snackers and grazers who either skip breakfast and snack all-day or are over-obediently grazin' on 20+ small meals per day.
Figure 2: Prevalence of breakfast skipping among US men and women (USDA)
What's interesting, is that we will find that the was a decrease in breakfast skippin' from 2002 to 2009, of which I am pretty sure that it was (at least partly) mediated by headlines like the ones I quoted in the introduction to this article (USDA)
USDA shows a slight decrease in the prevalence of breakfast skippingin both men and women by about 4%. If not having breakfast was the root cause of the obesity epidemic, the average American should thus have lost a few pounds over the past decade - right?
Right! This should be the case if breakfast was the mythical "lean-maker" the "experts" want us to believe. The figures, i.e. the constantly increasing rate of obesity, don't disprove that (those who don't eat breakfast could simply gain even more weight), but they certainly put another "?" behind the statement that having breakfast has anti-obesogenic effects.
23% of males and 20% of females skip lunch!
Apropos "?", I am missing one, here! One behind the consequences of skipping lunch. With all the upheaval about skipping breakfast, people seem to have forgotten that lunch, not breakfast, was the most commonly skipped meal among most age groups in 2009–10. In most age groups, 23% of males and 20% of females are skipping this important (?) meal... and are - you bet - having an unhealthy snack later in the afternoon.
How careless is it not to have breakfast :-) According to the latest meta-analysis of cross-sectional studies (epidemiology) with the telling title "Belief beyond the evidence: using the proposed effect of breakfast on obesity to show 2 practices that distort scientific evidence." skipping breakfast is associated with a +55% increased obesity risk. A risk increase without any evidence of a causal relationship between the two epidemiologically assessed parameters.
Anyway! This is the breakfast skipping research summary and no afford to dig up the two or three studies that dealt with skipping lunch explicitly. Let's thus, just for the time being, assume breakfast does in fact keep you lean. How on earth would eating some extra-food do that, when we all agree that the root cause of the obesity epidemic is after all the ravenousness of the average Westerner and the ways in which his / her diet multiplies these effects...oh, I guess the latter will lead us right to one of the answer to our question.
Proposed reasons for the anti-obesity effects of breakfast
I am not sure if I will be able to list all of them, but the following list of explanations that have been brought forward to explain the cross-sectionally observed negative association between body weight and breakfast eating is probably pretty comprehensive:
skipping breakfast leads to lower satiety than if breakfast had been eaten, thus
overeating will ensue later in the day, which
over time would result in weight gain
What? Yeah, in the end, this is all the "breakfastpromoters" have to tell you: It's an overcompensation for the energy missed at breakfast they blame the alleged fattening effects of not having breakfast on. As McCroy points out, in what's probably the most recent peer-reviewed analysis of the contemporary evidence, one could easily imagine another scenario
"in which breakfast skipping could result in no weight change over time, if breakfast skipping does not lead to overeating (i.e., if there is perfect compensation for the missed meal), or to weight loss if there is lack of compensation." (McCrory. 2014)
In his review McCory provides an enlightening overview of each of these possible scenarios, I don't want to keep from you. The“control” in this imaginary case study is a habitual breakfast eater with energy needs of 2000kcal/day, whose energy intake distribution across breakfast, lunch, snacks and dinner is 2000 kcal/day and therefore who is maintaining body weight.
Figure 3: Theoretical models illustrating different types of breakfast skippers vs. a habitual breakfast eater (McCrory. 2014).
There are potentially three types of habitual breakfast skippers: those with perfect compensation and maintain body weight, those who overcompensate and gain weight, and those who undercompensate and lose weight over time. In his consecutive review, in which McCrory considered only studies in adults (≥18 years on average) and focusing primarily on experimental studies (short-term acute feeding trials or longer-term feeding trials) and longitudinal studies (prospective or retrospective, with the outcome of body weight change), the scientists from the Purdue University draws the following conclusions:
Acute feeding studies on breakfast skipping effects on energy intake and appetite later in the day show equivocal results.
Longer-term (2–3 weeks) randomized controlled trials do not show effects of breakfast skipping on weight change.
In prospective studies with 3.7–10 years follow-up, individuals who consume breakfast more frequently gain less weight.
McCrory also points out that the lack of standardization is a major obstacle that makes it difficult, if not impossible to compare the results from different labs / different experimental setups.
Let's assume you decide you want to have breakfast, because this works for youand you don't belong to the unfortunate people with an APO-E4-genetyp - in that case I'd suggest you consider having one or multiple eggs, incl. the yolk, to boost your cholesterol reverse transport and improve your cholesterol profile | learn more.
Bottom Line: Considering all the previously presented facts, we have to admit that we are currently, not at a point where anyone could prove a causal relationship between breakfast skipping and an increased obesity risk. Personally, I don't believe that there is a general connection - specifically not in those of us who eat clean and keep an eye on their overall food intake.
Furthermore, the average American breakfast consists of sugar-coated breakfast cereals with bacon... well, sort of. So skipping a meal like this is probably not going to hurt anyone. What's really intriguing, though, is the number of lunch skippers. A number I haven't been aware of, when I started writing this article, and a number I am planning to address in a future article - assuming I find more evidence than the two potentially relevant studies that popped up in my first cursory database search.
References:
Brown, Andrew W., Michelle M. Bohan Brown, and David B. Allison. "Belief beyond the evidence: using the proposed effect of breakfast on obesity to show 2 practices that distort scientific evidence." The American journal of clinical nutrition 98.5 (2013): 1298-1308.
Kant, Ashima K., and Barry I. Graubard. "Secular trends in the association of socio-economic position with self-reported dietary attributes and biomarkers in the US population: National Health and Nutrition Examination Survey (NHANES) 1971–1975 to NHANES 1999–2002." Public health nutrition 10.02 (2007): 158-167.
McCrory, Megan A. "Meal skipping and variables related to energy balance in adults: A brief review, with emphasis on the breakfast meal." Physiology & Behavior (2014).
How much of the protein you can eat and how much of it you need two keep the status quo are very different questions.
Don't worry, this article is not about the notorious "Anabolic Barndoor" or the purported magic of "nutrient timing" and post.workout supplements. The thing I want to discuss in today's SuppVersity article is of a more general nature and revolves around the upregulation of the ubiquinase enzymes and consequent proteolysis (=catabolims) of skeletal muscle tissue ... or if you want to use my buddy Carl Lanore's term: "The loss of metabolic currency" we all know you better avoid at all costs, if you care about aging healthily.
You can learn more about protein intake at the SuppVersity
Are You Protein Wheysting?
Cod protein for recovery
Protein requ. of athletes
High EAA protein for fat loss
Fast vs. slow protein
Too much ado about protein?
What we are going to deal with today is protein breakdown, or the purported general anticatabolic effect of high protein diets. To this ends, we will be taking a closer look at the ubiquitin proteasome system (UPS) response to constant energy deficits (ED) at varied dietary protein intakes before and after the consumption of a high protein meal replacement. An issue, by the way, that was also addressed in a paper that has been published a couple of days ago in the peer-reviewed scientific journal FASEB (Carbone. 2013).
No, this is not a deja vue! You've actually read about the same experiment, yet a different portion of the results back in June, in one of my previous articles on optimal protein intake / supplementation | read more
In said paper by scientists from the School of Health Sciences at the Eastern Michigan University, the Nutrition Division at the U.S. Army Research Institute of Environmental Medicine, the Human Nutrition Research Center that's located at the U.S. Department of Agriculture, and the School of Medicine and Health Sciences at the University of North Dakota thirty-nine young, fit and healthy adult volunteers, who were caged in a metabolic ward, were randomized to one out of three groups with different baseline protein intakes:
0.8g/kg body weight of protein (RDA)
1.6g/kg body weight (2 -RDA), or
2.4g/kg body weight (3 -RDA)
The participants, 32 men and 7 women, had to be between the ages of 18 and 42 yr and of stable weight ( 2 kg for a period of 2 mo), to have a body mass index (BMI) between 22 and 29 kg/m², and to be physically fit [peak oxygen intake (Vo2peak) 40–60 ml/(kg ·min)].
The subjects followed the prescribed dietary protocol for a whole month (31 days), went into a tightly controlled 10-day weight maintenance phase and started fasting for 21 days, immediately thereafter (Note: To keep the protein intake stable, the dietitians who planned and prepared the meals for all study participants had to prepare meals with a significantly higher relative protein content),
In this study: 30% energy restriction +10% physical activity = "fasting"
Just to avoid any confusions: The above, i.e. a 30% reduction in energy intake and a 10% increase in physical activity, is what John W. Carbone and his colleagues talk about, when they use the word "fasting". It does not mean that the subjects have been sitting in one of those tents, where you can actually measure the energy expenditure for 21-days eating nothing, but their finger and toe nails.
An important note on the accuracy of calculated: While Carbone et al. state that their -30% intake, +10% expenditure protocol will produce an energy deficit of 40%, I'd hope that you as seasoned SuppVersity students see through the futility of calculations like these and let go off figures that signify a degree of exactness that's simply not there.
In view of the fact that the term "fast" is contemporarily used to designate "diets" that are really low in energy (up to ZERO calories, intermittently), I suspect I should also mention that I personally would call the last 21 days of the study the "diet" not "fasting" phase.I mean, 30% reduced energy intake and +10% physical activity? We all know that the health and physique 90% of our fellow men and women would benefit from this regimen.
Muscle biopsies and enzyme expressions
The scientists took muscle biopsies before (fasted) and 2h after (fed) the ingestion of "a commercial nutrition supplement (Boost; Nestlé HealthCare Nutrition, Florham Park, NJ, USA)" with a total energy content of 480 kcal and 20 g of protein to assess the degree of intracellular proteolysis on day 10, i.e. right before the "fast", and day 31, i.e. right after the "fast", of which Carbone et al. write that it was based on individualized menus that were administered under supervision, to ensure compliance.
"To maintain fitness, the volunteers performed resistance type physical activity 3 d/wk, and daily endurance-type exercise, at levels comparable to those they had reported in their prestudy activity logs. To minimize the potential that an unaccustomed training stimulus would influence skeletal muscle outcomes and to ensure accuracy, research personnel closely controlled and monitored the intensity and volume of physical activity. For resistance-type exercise, the volunteers performed 1 single-joint movement per major muscle group (3 sets of 15 repetitions), using workloads determined during the prestudy period. The intensity of the endurance-type activity (40 – 60% VO2peak) was based on prestudy measurements, and verified by indirect calorimetry (ParvoMedics) and the corresponding heart rate during familiarization trials conducted before the study, and by the heart rate reserve-method throughout the interventio." (Carbone. 2013)
The 10% increase in physical activity was achieved by an increase in the length of the daily endurance training sessions that would accommodate for the corresponding increase in energy expenditure
Figure 1: Changes in lean body mass and fat mass (kg) that occured during the 21-days on 40% energy restricted diets with varying amounts of dietary protein in it (based on Pasiakos. 2013)
As you can see in Figure 1, which is based on results the researchers presented in a previous publication that was likewise discussed, here at the SuppVersity, this intervention was not without consequences on the body and fat mass of the study participants who lost on average 3.2 ± 0.2 kg body mass, but at very different lean:fat-mass ratio (learn more).
What's the more important "-bolism": Cata- or ana-bolism?
In contrast to their previous paper that focused exclusively on the increase in muscle protein synthesis, this "follow up"* discards the influx of dietary protein into the muscle of the subjects and focuses on the proteolytic enzymatic response to the diet (*I assume both were filed at the same time, but the one in FASEB was published ahead of print, while the one at hand did not).
Figure 2: Enzymatic activities for 26S 1(A), 26S 2(B), 26S 5(C), and caspase-3 (D). Open bars, weight maintenance; solid bars, energy restriction.
Put differently, instead of asking the likewise important question: "What's more anabolic?" that was already answered in the paper by Pasiakos et al. (read more). Carbone et al. focus on the similarly or even more important question: "What's more catabolic?" - with a quite intriguing outcome, if I may say.
I mean, you would expect that the activity of the catabolic enzymes would vary depending on the protein content of the diets, wouldn't you? No? Well, maybe you did expect that the response to the 20g protein shake the subjects consumed would have an effect on their expression (black bars in Figure 2)?
You didn't? Tthat's awesome, you must be a genius, 'cause nothing of that actually happened. In other words, the expression of proteolytic enzymes did not in any way or form depend on the total amount of protein, the healthy young subjects in the study at hand consumed on a daily basis - once, twice or thrice the RDA of 0.8g/kg body weight.
Take home message #1 -- Your daily total protein intake has no effect on the expression of catabolic enzymes in your musculature. Even your total energy intake has little effect on the expression of catabolic enzymes in your musculature.
And if we are honest, most of us would probably also have expected a much more pronounced difference in these markers of muscle catabolism, when comparing the weight maintenance to the fasting phase (white vs. black bars) - a difference that existed for some yet not all of the ubiquinase enzymes, but was statistically significant for none of them.
Figure 3: mRNA expression of the Ub ligases MuRF1, atrogin-1 and TNF-alpha (Carbone. 2013)
And just in case you find all that not yet surprising enough, I'd suggest you take a parting look at the Murf-1 and atrogin-1 expression in Figure 3 -- what do you see? Correct, Murf-1 and atrogin-1 are the most prominent members of muscle-specific proteases that are highly expressed during muscle atrophy (Gomes. 2001; Witt. 2005); and you are also correct, if you are now scratching your head thinking:
"But how come that both are increased with higher protein intakes?"
Actually you know the answer already. It's after all not just take home message #2 of today's SuppVersity article, but has been addressed in many previous articles on total protein intake and the effects of protein supplementation here at the SuppVersity, as well.
Take home message #2 -- The more protein you eat the more wasteful your body will be (note: this does not mean that the net protein retention does not increase, but it means that you will see diminishing at intakes of thrice the RDA even non-existent returns; cf. "Are you Protein Wheysting?")
So what's left do discuss then? Ah, right, aside from the proteolytic enzymes, the scientists also tested for changes in the expression of TNF-alpha & co and observed that the expression of TNF- mRNA and activation of NF- B1 increased as protein intake exceeded the RDA.
This increase in TNF-alpha and NF-B1 may at first surprise you - TNF [tumor necrosis factor] and consequent NF- B activation are, after all, generally associated with increased muscle proteolysis. If you look back at "take home message #2", however, you'll realize that this, i.e. an increase in muscle proteolysis is exactly what's going on, in the 2x and 3x RDA groups. It is thus also logical that this increase in tumor necrosis factor occurs only in the fed state - a state, when dietary protein is abundantly available.
So what's to be learned on the practical side of things, then? In view of the results of the study at hand, it appears as if we may in fact have overrated the influence of the loss of skeletal muscle protein, i.e. proteolysis, in the past. Compared to the amplitude, or differences between ups and downs of protein synthesis the activity of the proteolytic enzymes is (a) very constant and does (b) depend inversely, but non-linearly on the total amount of protein you eat.
Remember the recent article about the myostatin reducing and thus potentially muscle building effects of low protein diets? | read more
Practically speaking this means that there is a relatively low threshold beyond which the "loss" of protein (=protein not being incorporated into the muscle tissue) keeps increasing, while the storage of protein stagnates. A hypothesis that stands in line with the results of experiments that investigated the differential effects of bolus (=all at once) vs. staggered (=in 4x20g or 8x10g) ingestion of protein supplements (see "Slow or Fast, Bolus or Pulse? Protein Synthetic Response is Identical!" | read more) and the revelation that protein fasting can decrease the expression of myostatin and thus ramp up the capacity for and efficacy of muscular protein storage (see "36% Decrease In Myostatin, With Low Protein (0.1g/kg BW) Diet" | read more).
References:
Carbone, J. W., Margolis, L. M., McClung, J. P., Cao, J. J., Murphy, N. E., Sauter, E. R., ... & Pasiakos, S. M. (2013). Effects of energy deficit, dietary protein, and feeding on intracellular regulators of skeletal muscle proteolysis. The FASEB Journal, 27(12), 5104-5111.
Gomes, M. D., Lecker, S. H., Jagoe, R. T., Navon, A., & Goldberg, A. L. (2001). Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy. Proceedings of the National Academy of Sciences, 98(25), 14440-14445.
Pasiakos SM, Cao JJ, Margolis LM, Sauter ER, Whigham LD, McClung JP, Rood JC, Carbone JW, Combs GF Jr, Young AJ. Effects of high-protein diets on fat-free mass and muscle protein synthesis following weight loss: a randomized controlled trial. FASEB J. 2013 Jun 5. [Epub ahead of print].
Schakman, O., Dehoux, M., Bouchuari, S., Delaere, S., Lause, P., Decroly, N., ... & Thissen, J. P. (2012). Role of IGF-I and the TNFα/NF-κB pathway in the induction of muscle atrogenes by acute inflammation. American Journal of Physiology-Endocrinology And Metabolism, 303(6), E729-E739.
Witt, S. H., Granzier, H., Witt, C. C., & Labeit, S. (2005). MURF-1 and MURF-2 target a specific subset of myofibrillar proteins redundantly: towards understanding MURF-dependent muscle ubiquitination. Journal of molecular biology, 350(4), 713-722.
