Nutrition Research Update: Meal Timing & Energy Intake, Full Fat Dairy for Zero Fat Waist-Lines, D-Sorbose for Glucose Control, Broccoli for Your Brain & More

From Meal Timing Over Broccoli & Full-Fat Dairy to Anti-Diabetic Sweeteners

Based on the number of visitors you like a number of short news that will bring you up to speed on a certain topic better than a longer in-depth analysis of just one study. This and the fact that the number of recent papers that would be worth being discussed at length is not exactly huge are the reason today's SuppVersity article falls into the "short news" category again.

Basically the title says it all. All of the individual items in today's news article are from the latest issue of Nutrition Research and thus related to the effects the stuff that enters your body through your mouth is going to have on your health and overall well-being.

You can learn more about meal frequency at the SuppVersity

Grazin' Bad For the Obese!

Breakfast Keeps You Lean?!

Frequent Protein Consumption

Myth: Few Meals More Bodyfat

8 Meals = Stable, But High Insulin

Int. Fasting & Exercise

• Meal timing matters, but only because it has a significant effect on the amount of food we eat. According to the latest study by Kathryn J. Reid, Kelly G. Baron, and Phyllis C. Zee, factors that correlate with an increased energy intake in 59 individuals, whose rest/activity patterns were assessed using 7 days of wrist actigraphy, and whose caloric intake was evaluated using 7 days of diet logs, are:
  • eating more frequently , 
  • later timing of the last meal, and 
  • a shorter duration between last meal and sleep onset
  Again, none of these factors will mechanistically make you store more body fat. What they will do, however, is to make you eat more. Basically this is also what the scientists imply, when they say that "In a mediational model, eating frequency explained the relationship between eating closer to sleep onset and total caloric intake" (Reid. 2014).

  

  Table 1: Associations between total calories, BMI, meal timing, meal frequency, and measures of sleep (Reid. 2014)

  It is thus not, as you may assume based on the latest studies on the intricate relationship between meal timing and the workings of your biological clock, the timing that makes late eaters more prone to obesity, but simply the fact that they're eating more than the early birds. 
• Whole fat dairy intake is associated with lower obesity risk, findings from the Observation of Cardiovascular Risk Factors in Luxembourg study show. Bear in mind that we are dealing with observational data with all its usual flaws and shortcomings, before you start shoveling down extra amounts of whole fat dairy or throw all your low fat dairy products out of the window.

  

  Figure 1: Multivariate adjusted (Model 1: M1 | Model 2: M2, details see text) difference in risk of being abdominally obese (WC ≥102 cm for men and 88 cm for women) in men and women consuming 3 vs. 1 serving of the given type of dairy per day (Crichton. 2014).

  Although the data in Figure 1 has been adjusted for age, education, sex, smoking, physical activity (in min/wk), total carbohydrate (in g/d), total protein (in g/d), total fat (in g/d), total fiber (g/d), alcohol (in g/d), calcium (in mg/d), and total energy intake (in kcal/d), and in model 2 even for HDL (in mg/dL), LDL (in mg/dL), triglycerides (in mg/dL), and systolic and diastolic BP (in mm Hg), this is still statistical shenanigan and could well be messed up by a correlation between being fat and choosing fat foods in the (false?) believe that they would help you lose weight. 
• D-sorbose as an anti-diabetes sweetener. In an attempt to develop d-sorbose as a new sweetener that could help in preventing lifestyle-related diseases, scientists from the University of Nagasaki Siebold investigated the inhibitory effect of d-sorbose on disaccharidase activity, using the brush border membrane vesicles of rat small intestines - put simply they checked if d-sorbose would inihibt the breakdown of disaccharides into monosaccharides and thus have the ability to slow down the absorption of glucose from "complex" carbs.

  

  Figure 2: Effects of adminstration of sucrose, the same amount of sucrose and + 10% d-sorbose or l-sorbose on the glucose and insulin response in rodents (Oku. 2014)

  I've marked the "benefits", i.e. the decrease in blood glucose (left) and the reduced insulin spike (right) in Figure 2. As you can see the effect is - at least in rodents - physiologically relevant, so that it is reasonable that Oku et al. assume that
  

  "[...] d-sorbose might also suppress postprandial elevation of levels of glucose and insulin due to ingestion of sucrose or maltose in humans and could be used as a sweetener that may reduce risk for lifestyle-related diseases but requires more research" (Oku. 2014).

  In view of the fact that the technology that is necessary to produce large amounts of d-sorbose has become available only relatively recently it is yet unlikely that you will be able to buy this stuff at the health food store next door, already.

• 

  Green veggies like broccoli have also been shown to reduce postprandial glycemia + insulin and noost the production of the anti-obesogenic satiety hormone GLP-1 | learn more

  Broccoli may ameliorate "brainflammation" in the eldery. That's at least what the latest rodent study from the University of Illinois would suggest.
  
  The study that was conducted by Brigitte E. Townsend, Yung-Ju Chen, Elizabeth H. Jefferya, and Rodney W. Johnson showed marked reductions in age-elevated cytochrome b-245 β, an oxidative stress marker, and reduced glial activation markers in aged mice who were fed a diet containing 10% broccoli diet for 28 days. Overall the effects are obviously modest; and yet, the study still provides good evidence to keep broccoli on your "foods I consume regularly" list.

Does eating veggies reduce inflammation? Yes, it does, 8 servings per day will significantly reduce CRP (Watzl. 2000), 68g of avocados will reduce IL-6 & NF-kappaBeta (Li. 2013), high intakes of alpha- and beta-caro- tene containing foods is associ- ated with decreased coronary heart disease risk and CHD mortality (Osganian. 2003 ; Bujisse. 2008), tomatos may protect against prostate cancer (Etminan. 2004), tomato juice makes LDL molecules resistant to oxidation (Upritchard. 2000), toma- to paste protects your skin from UV radiation (Rizwan. 2011), etc.

You want more? Well I have another study for you. One that attempts to explain why fruits an veggies in general and plant carotenoids in particular are good for you. It's a study from the Environment and Agro-biotechnologies Department in Luxemburg (Kaulmann. 2014) that analyzed the effect of carotenoids on intracellular signaling cascade and the corresponding effects on gene expression and protein translation and found that (1) carotenoids are able to interact with the nuclear factor κB pathway and thus inhibit the downstream production of inflammatory cytokines, (2) carotenoids can block oxidative stress by interacting with the nuclear factor erythroid 2–related factor 2 pathway and activating phase II enzymes and antioxidants, such as glutathione-S-transferases, and concludes that we (3) still have an incomplete understanding of what exactly carotenoids and other phytochemicals can do for our health | Any comments? If so, leave them on Facebook!

References:

• Buijsse, Brian, et al. "Both α-and β-carotene, but not tocopherols and vitamin C, are inversely related to 15-year cardiovascular mortality in Dutch elderly men." The Journal of nutrition 138.2 (2008): 344-350.
• Crichton, Georgina E., and Ala'A. Alkerwi. "Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study." Nutrition Research (2014). 
• Etminan, Mahyar, Bahi Takkouche, and Francisco Caamaño-Isorna. "The role of tomato products and lycopene in the prevention of prostate cancer: a meta-analysis of observational studies." Cancer Epidemiology Biomarkers & Prevention 13.3 (2004): 340-345.
• Kaulmann, Anouk, and Torsten Bohn. "Carotenoids, inflammation, and oxidative stress—implications of cellular signaling pathways and relation to chronic disease prevention." Nutrition Research (2014).
• Li, Zhaoping, et al. "Hass avocado modulates postprandial vascular reactivity and postprandial inflammatory responses to a hamburger meal in healthy volunteers." Food Funct. 4.3 (2013): 384-391.
• Oku, Tsuneyuki, et al. "D-sorbose inhibits disaccharidase activity and demonstrates suppressive action on postprandial blood levels of glucose and insulin in the rat." Nutrition Research (2014). 
• Osganian, Stavroula K., et al. "Dietary carotenoids and risk of coronary artery disease in women." The American journal of clinical nutrition 77.6 (2003): 1390-1399.
• Reid, Kathryn J., Kelly G. Baron, and Phyllis C. Zee. "Meal timing influences daily caloric intake in healthy adults." Nutrition Research (2014). 
• Rizwan, M., et al. "Tomato paste rich in lycopene protects against cutaneous photodamage in humans in vivo: a randomized controlled trial." British Journal of Dermatology 164.1 (2011): 154-162. 
• Upritchard, JANE E., W. H. Sutherland, and J. I. Mann. "Effect of supplementation with tomato juice, vitamin E, and vitamin C on LDL oxidation and products of inflammatory activity in type 2 diabetes." Diabetes care 23.6 (2000): 733-738.
• Watzl, Bernhard, et al. "Prolonged tomato juice consumption has no effect on cell-mediated immunity of well-nourished elderly men and women." The Journal of nutrition 130.7 (2000): 1719-1723.

2x40g, 4x20g or 8x10g of Whey? Which Feeding Strategy Yields the Greatest Net Protein Retention? Plus: What the Results Can Tell Us About Intermittent Fasting on a "Bulk"

In know, after reading the headline you are probably already urgently waiting for the results of the latest study on protein timing, but before we get to the facts, let me briefly announce that this "bolus vs. intermittent vs. pulse" protein study, which is incidentally the result of an international cooperation between researchers from the Nestlé Research Centre in Lausanne, Switzerland, Canadian researchers from the University of Guelph, the Canadian Sport Centre and (you guessed it) Stuart M Phillips' group at the McMaster University, and their colleagues from the Australian Institute of Sport and the RMIT University in Melbourne, will be one of the topics of today's SuppVersity Science Round Up on Super Human Radio.

Other things I hope Carl Lanore and I will be able to squeeze into today's show, which airs, just as every Thursday live at 1PM EST and will also be available as a podcast later today, either right from the nav-bar on the right ("Physical Culture for Your Ears") or at www.superhumanradio.com, are ...

• the latest news on natural nitrate supplementation with beet root juice, 
• how stress and laziness increase breast cancer risk more than hormonal imbalances, and
• how you can prepare your own powerful stevia-based wound ointment  

There is obviously more to the list, but I have learned from past mistakes and won't announce all I have piled up, when I know that's simply not possible to squeeze all of them into a single 1h show ;-)

A note for those of you who are looking for Adelfo Cerame's weekly contest prep blog: Don't worry it's still alive! You must have over-read that he has switched to a bi-monthly format!

Ok, ok... but NOW tell me hod do I have to spread my protein across the day"

While we know already that more is not necessarily better, when it comes to protein intake and that timing plays a significant role with respect to the returns in protein synthesis, and more importantly net protein retention you get for each gram of additional protein you consume, the question how you best spread your roughly 1.5-2.0g of protein per kg body weight across the day is still a matter of contemporary research and bro-scientific debate.

Suggested read: Protein Synthesis "Beyond the 20g Limit: Study Shows Exercise Facilitates 32% Greater Increases in Fractional Protein Synthesis With 40g vs. of 20g of Whey PWO" (click here to read)

What appears to be widely accepted, though, is the notion that both, the ingestion of a slow digesting protein before, and the intake of a fast digesting protein after a workout can effectively increase protein synthesis and net protein retention. If we assume that the combination of both strategies will yield further benefits (this has to my knowledge not been shown yet and is certainly not necessarly the case!), and regard the peri-workout supplementation as a "stand alone" that's not part of the 1.5g-2.0g /kg body weight baseline protein intake, we still end up with at least 80g of high quality protein (for the real light-weights or ladies ;-) we would have to spread in one way or another across the rest of the day.

8 x 10g, 4 x 20g or 2 x 40g? What's "optimal"?

Now, Moore et al. obviously won't have had my allegedly botchy "real-world" scenario on their minds, when they came up with the exact experimental design of their latest study. Still, if we forget about the 20g+ of protein post-workout, I believe none of you will be willing to abandon, their experimental setup fits the framework pretty nicely. After all, the scientists deliberately picked the 12h period after a workout "to standardise and take advantage of the accentuated protein synthesis in the exercised muscle over this period" and investigate three archetypal means of spreading a total amount of 80g of protein across the day: In 2 x 40g servings, 4x 20g servings or 8x 10g serving (Moore. 2012).

Suggested read: "3.2kg of Lean Mass Over Night W/ 40g of Slow Digesting Protein 30min Before Bed!?" (click here to read more)

The 24 male subjects who were advanced trainees working out 4–6 times per week in what the researchers call a "high intensity resistance training regimen" (note: I don't think this denotes a classic low volume HIT regimen) had to

"[...] follow standardized diet for the 72h prior to the trial that provided an energy availability of 45 kcal/kg fat-free mass with a macronutrient contribution 1.5 g protein/kg/d and 4 g carbohydrate/kg/d, respectively. [Moreover, s]ubjects were instructed to refrain from training and other vigorous physical activity during the 72h period."

When the men reported to the laboratory on the testing day, they had refrained from training or performing any other vigorous activity during the 72h period leading to the intervention and had been fasting 10h (over night). In absence of any other information I assume they remained in the fasted state for the subsequent standardized acute bilateral leg extension exercise session (4x10 sets at 80% 1-RM with 3 min recovery between sets), after which they were randomly allocated to receive their 80g of protein from whey as

• pulsed feeding (PULSE), 8x10g every 1.5h; 
• intermediate feeding (INT), 4x20g every 3h ; or 
• bolus feeding (BOLUS), 2x40g every 6h. 

The supplementation regimen was started right after the workout and the protein synthesis, breakdown and net balance were determined based on previously tested and verified procedures (Hartmann. 2006).

Figure 1: Comparison of effect sizes, p-values (remember only p < 0.05 would be a statistical significant difference) and the scientists qualitative inference's based on the effect of feeding pattern on whole body net protein balance (left) and a detailed breakdown of the feeding specific effects on 12h protein synthesis expressed relative to the bolus group (based on data from Moore. 2012)

As the data in figure 1 goes to show you, the results clearly confirm that the pattern according to which you consume your daily allotment of protein does matter, what it does yet not really tell us is how this will translate into a real-world scenario, in which, as I have pointed out before, not having at least 20g of whey / other protein sources after a workout appears almost negligent. The provision of a 20g whey + 10g casein mix right after a workout could, for example, have undone the minimal (and statistically non-significant) advantage in net protein retention of the intermediate feeding group. And that may still have been the case if the latter had been "upgraded"  to a 4x25g whey pattern.

On the other hand, if we wanted to pick on the study design, the "workout" (leg extension) and the absence of other nutrients (or the lack of information about those in the paper?), which could easily have reduced the amino acid breakdown that nullified the advantage the pulse feeding had with respect to its ability to trigger and sustain (over 12h) protein synthesis, would be more relevant points of critique, anyway. That said the "study" at hand is actually only a "short communication", and I am pretty sure there is more to come in the future (it stands to reason that the SuppVersity is the place to go to read about that, right?)

Note: I still maintain that overnight fasting is healthy, and IF probably one of the best, r at least a very effective way to shed body fat, but that does not mean that it should be the only diet strategy in your "nutritional toolbox", in which other tools are probably better suited to pack on slabs of muscle!

(Preliminary) bottom line: The results Moore et al. present certainly don't provide a definitive answer on "the very best" way to time your protein intake (and even if there was an "optimal" way, no single study will ever be able to elucidate it). They do however make one thing pretty clear: My gut feeling that intermittent fasting and here especially those varieties with very long fasting and very short feeding windows, is probably not the best way of dieting to gain muscle. After all, there is no debating that the bolus regimen (2x40g 6h apart!) is trailing behind.

You can certainly tweak and thus optimize it by (a) adding a third meal in between and (b) cleverly using / combining fast and slow acting proteins (cf. "Whey and Casein Work Hand in Hand for Protein Anabolism"), but if you want level playing fields you would have to apply similar tweaks to the more frequent 4 x 20g and 8x 10g regimen as well... and I that would probably restore, if not magnify the difference.

Update on the real world significance of the advantage: I know that SuppVersity readers are smart and therefore was not suprised that only minutes after I posted this article, Steven Arcera objected that long-term studies don't show this advantage. Now, while Steven is right the implicit assumption that this implies that there is no advantage of spreading your protein across meals is false. If we simply take the exact figures from the study, which would be an added ~0.02g/kg body weight in protein retention over 12h, assume (which is obviously not valid) that the protein retention would be identical over the other 12h of the day in all groups and do the math for the study participants who weighed 80kg, this would be an additional 1.6g of protein retention for the whole body (remember this is whole body protein retention) and therfore even in a long-term study of 12 weeks only 134.4g! This would still be 134.4g more than with bolus feeding but would NEVER make a statistical significant difference in any study. And even the 584g "advantage" you would accumulate over a whole year would make it past the p < 0.05 line! So much about "optimal feeding strategies" and the real world outcomes of the latter :-)

References:

• Hartman JW, Moore DR, Phillips SM. Resistance training reduces whole-body protein turnover and improves net protein retention in untrained young males. Appl Physiol Nutr Metab. 2006 Oct;31(5):557-64.
• Moore DR, Areta J, Coffey VG, Stellingwerff T, Phillips SM, Burke LM, Cléroux M, Godin JP, Hawley JA. Daytime pattern of post-exercise protein intake affects whole-body protein turnover in resistance-trained males. Nutr Metab (Lond). 2012 Oct 16;9(1):91.

Meal Timing, Glycemic Index & Load: Human Study Probes Whether "Hitting Your Macros" Really is All That Counts

High or low GI, carbs in the morning or in the evning, cookies and dingdongs or all bran. So many questions and way too many answers from rodent studies or studies in obese diabetics... but what are Mr. and Mrs. Healthy Average Joe supposed to do?

In a recently published paper, Linda M. Morgan, JiangWen Shi, Shelagh M. Hampton and Gary Frost take yet another look on a concept that has lost much of the momentum it had only a decade ago: The GI and / or GL paradigm (GI: glycemic index (abstract unit); GL: glycemic load, i.e. GI / actual amount of food) and combines another paradigm, which is still gathering momentum within the medical science community - the issue of nutrient timing, in order to answer the following questions:

• Will a large evening energy and carbohydrate load cause an increase in postprandial glucose that is comparable to the same amount of energy and carbohydrates in the morning?
• Will a high glycaemic excursions in the evening be ameliorated by decreasing the glycaemic index (GI) of the meal?

Or put simply: Does carbohydrate and energy timing make a difference and can this difference be mitigated by chosing the "right", i.e. low glycemic carbs (e.g. sweet potato vs. white bread)?

White bread king or all-bran pauper - is that  the question?

To answer this world-shattering question and actually prove their hypothesis that both, i.e. having carbs in the evening and having those in the form of high glycemic index foods, will have negative consequences on postprandial glycemia, the scientists picked six healthy volunteers (four females, two males; mean age 30 +/- 4.3 years, BMI 21·6 +/- 1.3 kg/m²) and randomly assigned them to a follow one of the four following dietary protocols:

• Low GI (average GI = 34), with the majority of energy load consumed in the morning (LGI-am)
• Low GI, with the majority of energy load consumed in the evening (LGI-pm)
• High GI (average GI = 84), with the majority of energy load consumed in the morning (HGI-am)
• High GI, with the majority of energy load consumed in the evening (HGI-pm)

with identical energy content of approx. 8368 kJ (2000 kcal) for the whole day on four individual intervention days with a minimum of 7 days between each of the tests. Breakfast was given at 09.30 hours, lunch at 13.30 hours and the evening meal at 20.30 hours - subjects were at the laboratory for the whole day. Blood samples were taken 2h postprandial and blood glucose levels were monitored continuously via a "MiniMed continuous glucose monitoring system" that senses interstitial glucose by electrochemical detection in subcutaneous interstitial fluid in 5 min intervals.

Figure 1: Composition of the two test diets (low GI, blue; high GI read) and individual macronutrient breakdown of the test meals the subjects consumed on two seperate occasions (based on Morgan. 2012)

It does not take a nutrition expert to see that despite the obvious differences with respect to the glycemic index and load, even the allegedly healthy low GI diet with all-bran for dinner* and a macronutrient composition 72% carbohydrates 14% protein and 14% fat is not exactly what the latest research would suggest to be a healthy, let alone a "physique enhancing" diet.

*note: The scientists probably chose similar foods for breakfast and dinner, because the study design required those to be exchangeable.

Against that background it is still astonishing how much of a difference...

• 99% higher fiber content,
• -60% lower glycemic index (GI), and
• -63% lower glycemic load (GL)

... actually make when it comes to the effect of isocaloric meals with identical macronutrient compositions (see figure 1, right):

Figure 2: Total area under the curve for interstitial glucose (0–20 h), postprandial plasma insulin, TAG (**mind the text for info a potential typo, here) and NEFA (0–2 h after each meal) in six healthy volunteers following either a high-glycaemic index (HGI) or a low-glycaemic index (LGI) diet, with most of the energy consumed either early (LGI-am, HGI-am) or late (LGI-pm, HGI-pm); all values expressed relative to respective statistical mean (data calculated based on Morgan. 2012)

I guess I don't have to tell you that the image that emerges here stands in line with the as of late largely ignored glycemic index paradigm the underlying message of which is: It is not simply the amount of sugar you eat,  but rather how fast / hard it hits your blood stream that determines it's impact of on your glucose metabolism. And with respect to the latter, the researchers remark:

"Glucose and insulin responses showed broadly similar patterns. Both meal timing and quality of carbohydrate affected postprandial glucose and insulin responses (P < 0.01). The area under the glucose and insulin response curves was greatest for the HGI-pm meal regimen. The HGI-pm meal regimen produced a significantly greater postprandial area under the glucose curve than for any of the other three meal regimens (P < 0.05). The postprandial area under the insulin curve was significantly greater than both the LGI regimens (P < 0•05). Postprandial insulin resistance measured by homeostatic model assessment was also significantly greater for the HGI-pm meal than for the two LGI meals (P < 0•05)."

However, since Morgan, Shi, Hampton and Frost also state that "[p]ostprandial TAG and NEFA levels were not affected by meal timing or carbohydrate quality", I do suspect that there is a typo in table 3 of the original study, where it says that the TAG would be 5.04 mmol/l x h (probably is 6.04) and thus more than 15% lower than the average (TAG levels and insulin resistance usually go hand in hand, so it is really very unlikely that the 5.04 mmol/l x h is correct).

So what's the take home message here?

The only question that still has to be answered would be "King or pauper? At least with regard to the former, the best thing I can to is to suggest you read both the posts on "Breaking the Fast" and the "Carbs Past 6PM Posts"  (Part 1 & Part 2). When you have done that your perspective on the importance of breakfast and the purported fallacy of having a large dinner should already have changed. The things that are still left to do is not fool yourself into the false belief that you can pound whatever junk you want (as long as it fits your macros). As the glucose curve of the high GI arms (light color) in the figure above goes to show you, your body won't be happy when you get your "carb macros" from sugary junk.

Stick to starchy (or "save carbs", if you will) and fruit. Use veggies to fill you up. Use coconut & olive oil and the fats that are already in your meats, fish and dairy products to achieve baseline fat intake of at least 40-50g (all together). Aim for a 100-120g carbohydrate basis, diverge towards the lower side, when your body fat is high, you can't train or you're dieting and towards the higher side, when you are already very lean, have a high training volume, or are trying to build muscle. Complement that with min. 20g of quality protein with each meal. Don't deprive yourself on any nutrient completely and ramp up the total amount of food (at the given ratio) to fulfill your energy requirements.

In that, avoid processed food sand rely on whole foods, whenever possible (>90%),. Use food supplements* only where it makes sense, e.g. a protein shake post workout (*creatine for example would not be a "food supplement", since you can NEVER get the amounts that are necessary to supersaturate your stores from meat alone) and don't forget to live about all that "dieting" and thinking about the best ways to eat, please!

So if we assume that my assumption with respect to the triglyceride values in the originally published study are correct and we are simply dealing with a typo here, the next questions which arise here, are...

1. What is / are the reason/s that the lipid metabolism did not suffer?
2. How reliable is the HOMA-PP, i.e. the postprandial assessment of insulin sensitivity via the homeostasis model assessment? 
3. What does all this mean for you? Does meal timing not make a difference and are macros all that counts? 

As far as (1) goes, the answer is pretty simple: With a diet that was that low in fat and not overabundant in energy (2,000kcal for both diets) any potential the negative downsides on lipid metabolism will take their time to show. The acute ingestion of three high GI meals on a single day or modifications in their distribution across the day won't have much of an effect in healthy individuals, such as the four women and two men in the study at hand (in diabetics and especially patients with NAFLD things will probably look different, though).

The absence of changes in lipid metabolism after one day on high vs. low GI diets w/ different meal timing patterns yields answer #1 to question (3): If you are healthy the occasional day with junk food won't hurt you as long as you keep the total amount of energy at bay and jump back on the "healthy diet" wagon the very next day.

On the other hand, if only a single day of high GI food consumption can have such a pronounced impact on the postprandial HOMA levels, this raises the question how reliable this "long term measure" of glucose sensitivity actually is. Obviously, you should not go to the doctor's office and have your HOMA measured, at a morning after a day with three SuperSize Meals from McDonalds (even if you have been fasting after supper at night before, as the participants in the study at hand did) - unless you want a prescription for meformin, of course ;-)

It would however be likewise unwise to "do everything right" for three (maybe even just one day) before you head to the doctor to get blood drawn, just to be able to rejoice over a HOMA reading that does by no means represent your "normal" insulin sensitivity. This may make your doctor happy and spare you getting ticked off, but could have you run around pre-diabetic unnoticed for months if not years - maybe so long until the first irreversible damage has already been done.

The high susceptibility of HOMA measures to acute dietary modifications yields answer #2 to question (3): If you want know where you stand, don't make last minute changes to your diet before you get blood drawn. After all, the 90:10 rule (better 95:5 rule ;-) applies both ways - the 90/95 days of consistent eating patterns will decide whether you are lean, muscular and above all healthy or fat, undermuscled and sick.


References:

• Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr. 2012 Oct;108(7):1286-91.

Fasting or Caloric Restriction, What Holds Greater Promise as a Means of Life Extension? Plus: Does Exercise "On Empty" Increase Muscle Damage?

"70 Years Between Meals? Indian Mystic Promotes Atmosphere Diet" that's the title of a Times newsfeed, but is it also the secret to longevity? Or is 70 years too much of an intermittent fast ;-)?

It is undeniable that many of the centenarians are known for their rather modest energy intake and is has been long established that there is a direct mechanistic connection between "living on the high energy fast track" and increased aging. The border between calorie restriction on the one hand and malnutrition on the other is however fluid and where one may effectively add a couple of years to your life-span the other is not only going to make it shorter, it will also make it miserable. Within the past years fasting and intermittent fasting have emerged as potential alternatives.

The purpose of today's article is now to take a closer look on whether they are equally or better suited to lead a long, healthy life that is not going to wast you away.

Longevity effect of caloric restriction: More than a long-lived myth?

Scientists were pretty excited, when the first realized that a reduction in caloric intake without malnutrition, will initiate metabolic adaptations that can extend the lifespan of a variety of species.

"Key early studies in rodents revealed that mice fed 55–65% caloric restricted diets through their life exhibited a 35–65% greater mean and maximal lifespan than mice eating a non-purified ad libitum diet (Weindruch. 1996). Although attenuated, these effects remain present even when moderate caloric restriction (20–40%) is implemented in middle-aged mice (Weindruch. 2001)."

At least in rodents (Weinbruch. 2001) and nonhuman primates (Colaman. 2009) these beneficial effects on life expectancy were partly mediated by reductions of exactly those diseases that are currently carrying off increasing parts of the population of the Western Obesity Belt, namely cancer and diabetes.

Insulin surprise: Higher not lower fasting insulin levels are associated with better cognitive performance in Chinese nonagenarians and centenarians. At the same time, the worst cognitive function was found in subjects with hypoglycemic (=low) blood glucose levels (Yan-Ling. 2013).

Evidence that similar beneficial effects can occur in human beings comes mostly from studies on overweight subjects on calorically restricted diets. Unsurprisingly, the latter have been associated with

• reductions of several cardiac risk factors (Fontana. 2004 + 2007; Lefevre. 2009), 
• improved insulin-sensitivity (Larson-Meyer. 2006), and
• enhanced mitochondrial function (Civitarese. 2007). 

These health improvements went hand in hand with a reduction in oxidative DNA damage (Heilbronn. 2003 + 2006; Hofer. 2008), but support the benefits of general caloric reduction only in those who have been eating well than they needed for years.

But what about the healthy, lean physical culturist?

Those of you who have already tried to live off a calorically reduced diet for months, may however have noticed that this does come with significant downsides for the someone who does not carry a health-deteriorating, but "nourishing" (in times of caloric reduction) amount of body fat around. For those increasingly rare specimen without a pouch, an intermittent, instead of a chronic caloric reduction and / or a fasting regimen appears to be a much more favorable way to slow down the clock that's ticking for all of us.

"Evidence that [fasting for hours and up to days] may have beneficial effects on longevity first appeared several decade ago (Carlson. 1946). Since this time, a growing body of literature suggests that fasting periods and intermittent fasting regimens can trigger similar biological pathways as caloric restriction (i.e., increased autophagy and mitochondrial respiratory efficiency), which can result in a host of beneficial biological effects including increased circulation and cardiovascular disease protection, and modulation of reactive oxygen species and inflammatory cytokines (Lee. 2011)" (Anton. 2013)

Fasting periods have also been shown to have direct antimutagenic, antibacterial and anticarcinogenig effects (Lee. 2011). In a recent special on the effects of fasting on all things longevity & health in the Journal of Experimental Gerontology, there are three different papers with direct relevant to the topic:

1. 

   Suggested read: "More Muscles For Old Chaps, Less Fat for Baby Boomers W/ HMB" | read more

   Waters et al. did a review of the controversies related to current lifestyle recommendations promoting diet-induced weight loss in obese adults 65 years and older (Waters. 2013).
   
   Obesity in those > 65 years of age is prevalent and linked to negative health outcomes. The review found that diet & exercise facilitate weight loss in frail obese older adults.
   
   Muscle quality and physical function improved with weight loss. The weight loss observed in all studies included bone & lean body mass, issues to be addressed in future studies, this as well as the unsatisfying long-term effects argue against the current use of chronically energy-reduced diets in the elderly.
    
2. Avena et al. compared the effects of both food restriction and overeating on brain reward systems (Avena. 2013).
   
   The aging population has been shown to exhibit altered reward sensitivity and decreased caloric consumption. Moreover, members of this population appear to be increasingly affected by the current obesity epidemic. Food, like alcohol or drugs, can stimulate its own consumption and produce similar neurochemical changes in the brain. Age-related loss of appetite, decreased eating, and caloric restriction are hypothesized to be associated with changes in the prevalence of substance misuse, abuse, and dependence seen in this cohort.
   
   Overall, the results appear to suggest that the hedonistic effects of eating play an important role with respect to the impact our diets can have on longevity, as well. And in that, malnutrition in response to anorexia is as detrimental to our health as gluttony.
    

3. 

   Suggested read: "Sugar Addicted or Just Stressed Out? Study Investigates Modulatory Effects of Different Macronutrient Compositions on Serotonin in the Presence and Absence of Stress" | read more

   Shriner et al. revisited the concepts of "detox and abstinence" as they relate to food addition, as well as the effects of abstinence on clinical outcomes in metabolic pro-inflammatory conditions (Shriner. 2013).
   
   The researchers point out that geriatric diabesity is confounded by the obesity paradox (healthy people with high BMI) and sarcopenia (sick people with low BMI and no muscle). Interestingly, neuroimaging results show same pattern in obese and cocaine/opioid addicts - an observation the researchers relate to the combined fat and sugar (especially HFCS) overload which is not just pro-inflammatory, but also highly addictive. For the live-long fast food junkie, fasting (chronic or intermittent) is thus the "new abstinence". To"detox" the body it does therefore require metabolic, addictive and relationship treatment in most of the patients, which is why diabese geriatric patients need careful supervision by physician and dietician.

These reviews are topped of with an intriguing study by Dannecker et al. who investigated the effects of fasting on indicators of skeletal muscle damage in humans.

Figure 1: NO (µmol/L) in 12 young female subjects (22 years) before & after biceps curls in the fasted (8h water fast during the day) and 4-5h after meal with ca. 30g / 100g / 35g fat/carbs/protein (Dannecker. 2013)

• Dannecker et al. tested the effects of fasting on exercise-induced muscle damage in humans (Danecker. 2013). Daily 8-hour fasts were compared to a controlled meal within 4–5 h of visit. The indicators of muscle damage were collected before and across five days after exercise. The fasts did not robustly protect against exercise-induced muscle damage, but it did not ameliorate the damage either.
  
  However, both the baseline and post-workout nitric oxide levels [NO] were higher (figure 1) and the TNFa levels, a marker of oxidation damage was lower in the fasting group across time. Therfore, the researchers conclude that fasting may in fact have an ameliorative effect on muscle damage.

All of these studies are relevant to the initially raised question and they appear to confirm that despite the fact that it is "currently unknown if all humans benefit from engaging in caloric restriction", the contemporarily available research supports the notion that "we" are probably all living on the metabolic fast lane.

In other words, lean or not - that's more of a matter of how much more food you consume than you actually need, or put more simply: With the current energy intake we are already at the upper end of the adaptation scale.

Suggested read: "A Low Fat Advantage For Alternate Day Fasting? While the Improvements in Body Composition Are Virtually Identical, Only the 25% Fat Diet Will Improve Arterial Blood Flow" | read more

Intermittent fasts are thus actually only bringing us back to the mid-range and closer to what would be "necessary" for weight maintenance and metabolic flexibility without having the nasty side effect of favoring permanent reductions in caloric expenditure. The latter are actually the result of our body shifting into a new "steady state" that will leave us in a position, where it is becoming increasingly hard to maintain our weight and health in a society that is characterized by 24/7 nutrient abundance and portion sizes that are way beyond good and evil. The consequence is a constant overexpression of the "anabolic", but autophagy and thus recycling / repair impairing IGF-1/p-AKT/m-TOR pathway I talked about during Thursday's installment of the Science Round-Up on SuperHumanRadio.com (download the podcast, here).

Fasting induced ravenous feasts, a potential problem!?

Contrary the controlled "intermittent fast" as it is propagated among others in the infamous "lean gains" regimen, the increasingly popular ever-other-day or two-days-a-week fasting regimen, in the course of which people tend to go totally overboard on the "feasting days", have been implicated as one of the reasons for the undeniable trend that breakfast-skippers tend to consume a low quality diet and display significantly increased obesity rates (cf. Niemeier. 2006; Deshmukh-Taskar. 2012).

The diet quality is in fact so important, that even the often hailed "Eat Breakfast Like a King and Supper Like a Pauper" appears to entail significant negative metabolic downsides for exactly those people who are now jumping on the said "intermittent fasting for dummies" train without making the most important qualitative dietary and lifestyle changes first.

• In 2008, for example, Devaraj et al. observed that the ingestion of a high-fat, energy-dense, fast-food-style breakfast results in an increase in oxidative stress in metabolic syndrome people with metabolic syndrome compared to a control breakfast that was formulated according to the suggestions of the American Heart Association (Devaraj. 2008)

  

  Figure 2: The increases in oxidation markers in response to a single large fast-food-style (FFS) breakfast counter all potential benefits of intermittent fasting (Devaraj. 2008)

  As the corresponding markers of postprandial inflammation and lipid oxidation go to show you, a single-meal strategy aka "If It Fits Your Macros" that does not take food quality into considerations well, is the best way to ruin the already wrecked health of an obese individual completely.

Of the latter, namely the lifestyle changes, there is little question that the inclusion of intense (=challenging) exercise regimen will probably going to yield the most significant benefits for obese and lean individuals alike. Lee et al., for example, found statistically highly significant risk reductions in all-cause mortality, when they reviewed the data from 17 321 healthy men with a mean age of 46 years. And to achieve the -13% reduction in all-cause mortality it takes nothing, but  a weekly exercise induced energy expenditure of 800-900kcal - as long as you are burning them 
during exercises that consume at least >6x the amount of your resting energy expenditure.

---

Suggested read: "Intermittent Thoughts On Intermittent Fasting - AMPK I/III: Zoning in on Its Effects on Body Composition" | read more

Reckless IIFYM Intermittent Fasting for the sluggish obese will probably worsen, not improve the situation: Intermittent, continuous fasting and exercise are, at least from a very fundamental, mechanistic perspective equivalent. They all promote autophagy + cell-recycling over anabolism + cell differentiation.Optimal health does yet reside somewhere on a sine that oszillates between AMPK and mTOR and that is probably better served with an intermittent fasting than with a chronic fasting regimen.

Without exercise and finally getting rid of the illusory dream that you could eat "whatever you want" and "as much as you want", as long as you don't eat it "whenever you want" intermittent fasting can easily backfire - specifically for those whose already compromised health could turn an already not exactly healthy super-size meal into a highly inflammatory, pro-artherogenic binge.

On the other hand, I personally don't see significant evidence why a devoted fitness maniac and "3-meals a day person", like myself, would have to "fast" (I would rather call it not eat) for more than his regular 8-12h a day to help the AMPK pathway come into its own. When you are actually trying to cut weight, on the other hand, there are few better ways to easily "drop" 20% of your daily energy intake without even noticing it than intermittent fasting (=skipping one of these meals / preferably breakfast; learn why).

References:

• Anton S, Leeuwenburgh C. Fasting or caloric restriction for Healthy Aging. Exp Gerontol. 2013 Apr 29. 
• Avena NM, Murray S, Gold MS. Comparing the effects of food restriction and overeating on brain reward systems. Exp Gerontol. 2013 Mar 25.
• Carlson AJ, Hoelzel F. Apparent prolongation of the life span of rats by intermittent fasting. J Nutr. 1946 Mar;31:363-75. 
• Ceriello A. Acute hyperglycaemia: a 'new' risk factor during myocardial infarction. Eur Heart J. 2005 Feb;26(4):328-31. Epub 2004 Nov 30. Review. 
• Dannecker EA, Liu Y, Rector RS, Thomas TR, Sayers SP, Leeuwenburgh C, Ray BK. The effect of fasting on indicators of muscle damage. Exp Gerontol. 2012 Dec 22.
• Devaraj S, Wang-Polagruto J, Polagruto J, Keen CL, Jialal I. High-fat, energy-dense, fast-food-style breakfast results in an increase in oxidative stress in metabolic syndrome. Metabolism. 2008 Jun;57(6):867-70.
• Deshmukh-Taskar P, Nicklas TA, Radcliffe JD, O'Neil CE, Liu Y. The relationship of breakfast skipping and type of breakfast consumed with overweight/obesity, abdominal obesity, other cardiometabolic risk factors and the metabolic syndrome in young adults. The National Health and Nutrition Examination Survey (NHANES): 1999-2006. Public Health Nutr. 2012 Oct 3:1-10. 
• Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6659-63. Epub 2004 Apr 19.
• Larson-Meyer DE, Heilbronn LK, Redman LM, Newcomer BR, Frisard MI, Anton S, Smith SR, Alfonso A, Ravussin E. Effect of calorie restriction with or without exercise on insulin sensitivity, beta-cell function, fat cell size, and ectopic lipid in overweight subjects. Diabetes Care. 2006 Jun;29(6):1337-44. 
• Lee C, Longo VD. Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients. Oncogene. 2011 Jul 28;30(30):3305-16.
• Niemeier HM, Raynor HA, Lloyd-Richardson EE, Rogers ML, Wing RR. Fast food consumption and breakfast skipping: predictors of weight gain from adolescence to adulthood in a nationally representative sample. J Adolesc Health. 2006 Dec;39(6):842-9. Epub 2006 Sep 27
• Waters DL, Ward AL, Villareal DT. Weight loss in obese adults 65years and older: A review of the controversy. Exp Gerontol. 2013 Feb 10.

Protein Timing Does Matter! Yet Only in Trained Men. More Than 2x Higher Relative Protein Retention W/ Immediate vs. 6h Post Whey Consumption in Bodybuilders vs. Rookies

Drop the weights, grab the shake! Timing matters for advanced trainees.

I guess you'll all have followed my suggestion to read Brad Schoenfeld's, Alan Aragon's and James Krieger's excellent review of the effects or protein timing on skeletal muscle hypertrophy, last year. In said paper, the two conclude that their review would "refute the commonly held belief that the timing of protein intake in and around a training session is critical to muscular adaptations" (Schoenfeld. 2013)

Certainly a reasonable conclusion based on the evidence they present. With the recent publication of a study by Hiroyasu Mori from the Department of Nutrition Management at the Hyogo University, future reviews will yet probably have to distinguish according to the training status of the athletes.

You can learn more about protein intake at the SuppVersity

Are You Protein Wheysting?

5x More Than the FDA Allows!

Protein requ. of athletes

High EAA protein for fat loss

Fast vs. slow protein

Less Fat, More Muscle!

In his latest study, Mori investigated the effect of the timing of protein and carbohydrate intake after resistance exercise on nitrogen balance in trained and untrained young men. By dividing his 20 healthy male subjects between the age of 20 and 29 into two groups, i.e.

• those Mori calls "bodybuilders" and who regularly performed resistance exercise were assigned to the trained group (n = 10; mean age, 23 ± 4 years; height, 173.8 ± 3.1 cm; weight, 72.3 ± 4.3 kg) and
• those of which Mori writes that they were "recreationally trained" but without resistance training experience were assigned to the untrained group (n = 10; mean age, 23 ± 1 years; height, 171.8 ± 5.0 cm; w eight, 64.5 ± 5.0  kg),  respectively,

Mori added an element to the equation that has been overlooked in previous studies. An element that would allow him to answer the question:

Do the same rules apply for untrained subjects and bodybuilders with 6.2 ± 2.8  years of training experience?

In view of the fact that the majority of studies that investigate the long(er) term hypertophy effects of resistance training are conducted with training noobs to make sure you can measure meaningful and statistically significant changes after only a few weeks, the previously cited conclusion by Schoenfeld et al. is also based mostly on data from rookies or the infamous "recreationally active" study participants.

Figure 1: Overview of the experimental design (Mori. 2014)

As you can see in Figure 1, both groups, i.e. the bodybuilders and recreationally active rookies, were subjected to the same exercise + supplementation protocol in this 4-week randomized crossover trial.

"In the P0 experimental period, subjects consumed protein and carbohydrate supplements 5 min after resistance exercise, and in the P6 experimental period, subjects consumed the same supplements 6 h after exercise. A washout period >7 days was applied before each experimental period. During each 11-day experimental period, the first 8 days were defined as an adaptation period for muscle to adapt to the energy and nutrients from the experimental food and supplements prepared by the examiner. During the next 3-day period (day 9 to day 11), 24-h urine samples were collected. The two experimental schedules are shown in Figure 1. " (Mori. 2014)

Because at least 7 days of adaptation and 3 days of urine collection are needed to calculate nitrogen balance (Jordan. 2010), the resistance exercise schedule in the P0 and P6 experiments lasted for 11 days: 8 days of adaptation (two cycles of resistance exercise for 3 days and rest for 1 day) and 3 days of urine collection.

Are urine collections valid measures of protein retention? I would prefer a 12-week study that measures the net muscle gain in response to immediate vs. 6h post supplementation as well. In the end, the 3+ day urine collection is probably still a better measure of the amount of protein that's actually used to "build lean mass" (remember this way we cannot distinguish where the protein was stored - we only know that is was not metabolized and excreted!) than the acute measures of protein anabolic signalling you see in many other studies - a measure of which Mitchell et al. have shown that it does not correlate with resistance training-induced muscle hypertrophy in young men (Mitchell. 2014), only recently.

Prior to each experimental period, body composition and one-repetition maximum (1RM) were measured, and questionnaires on daily activity were completed.

 "In daily experimental sessions, subjects performed the following resistance exercises: 4 sets of 8 to 10 repetitions of resistance exercise consisting of leg press, leg extension, and leg curl on experimental days 1, 5, and 9; bench press, shoulder press, and triceps pushdown on experimental days 2, 6, and 10; and lat pulldown, biceps curl, and rowing on experimental days 3, 7, and 11. All exercises were performed at 80% RM, and each set was followed by a 2-min break." (Mori. 2014)

Before the experimental session each day, subjects used a cycle ergometer (Aerobike 800; Combi Wellness Corporation, Tokyo, Japan) at 100 W for 10 min to warmup. Each exercise session was scheduled to take place between 10:00 and 11:00. The subjects were instructed not to participate in any other sports activities during the experimental period.

The diets were standardized to 1.5g/kg body weight

In spite of the fact that the bodybuilder group consumed ~13% more energy per day, both the total (1.5g/kg per day), as well as the supplemental protein intake (0.5g/kg of whey protein + 0.8 g/kg dextrin body weight) were standardized. In that, the amount of protein per meal was defined as follows:

• P0 experimental period: Subjects had to ingest protein (0.3 g/kg body weight) and carbohydrate (0.8 g/kg body weight) immediately after resistance training.
• P6 experimental period: Subjects had to ingest protein (0.3 g/kg body weight) and carbohydrate (0.8 g/kg body weight) 6 h after resistance exercise session.

The total energy intake, total protein intake, and protein intake per  body  weight  (kg) were  calculated  by  a  registered dietitian and the protein balance was assessed by analyzing the nitrogen excretion in the urine.

Figure 2: Net protein balance per body weight and per lean body mass (LBM) when the post-workout protein + carbohydrate shake was consumed immediately after or 6h after the workout (Mori. 2014)

And, as you can see in Figure 2, a comparison of the net protein balance in the two groups during the immediate post vs. 6h post consumption periods clearly indicates that protein timing does matter, even if it's just for the experienced resistance trainee, for whom the study at hand shows that his nitrogen balance is less positive than that of the rookie anyway.

Apropos total protein intake and nitrogen balance, the average total protein intake in the studies reviewed by Schoenfeld et al. was after all slightly higher (1.66 g/kg/day). This, as well as the general believe that bodybuilders should consume tons of protein make me question whether the results would have been different, if total protein intake had been 2.0 or even 2.5g/kg per day instead of just 1.5g/kg. Personally, I don't thinks so, but it would be worth a try, anyway.

(1) Thou shalt not wait 6h to consume protein after a workout (2) Thou shalt not wait 6h to consume carbs (not necessarily ultra fast digesting, though) after a workout either | learn why

Bottom line: If you're striving for maximal muscle and performance gains, specificity is key; and the study at hand specifies that you have to specifically make sure to get your post-workout nutrition "immediately" post workout and not 6h later if you (a) want to maximize net protein retention and (b) are already beyond those first happy months in the course of which you just have to look at a dumb- or barbell to grow ;-)

Ah, and when you're at it, I suggest you also include 5g of creatine monohydrate in your postworkout shake. The latter has after all also been shown to work a tad better, when it's consumed after the workout | learn more.

Reference:

• Jordan, Leora Y., et al. "Nitrogen balance in older individuals in energy balance depends on timing of protein intake." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 65.10 (2010): 1068-1076.
• Mitchell, Cameron J., et al. "Acute Post-Exercise Myofibrillar Protein Synthesis Is Not Correlated with Resistance Training-Induced Muscle Hypertrophy in Young Men." PloS one 9.2 (2014): e89431.
• Mori, Hiroyasu. "Effect of timing of protein and carbohydrate intake after resistance exercise on nitrogen balance in trained and untrained young men." Journal of Physiological Anthropology 33 (2014): 24.
• Schoenfeld, Brad Jon, Alan Albert Aragon, and James W. Krieger. "The effect of protein timing on muscle strength and hypertrophy: a meta-analysis." Journal of the International Society of Sports Nutrition 10.1 (2013): 53.

Calorie Shifting (-45%) Beats Calorie Reduction (-55%): Four Meals, Spaced 4h Apart Induce Greater Hunger(!) & Body Weight Reduction Than More Restrictive Regular Dieting

4x4 are those the optimal numbers?

Alright, if you have 500,000kcal worth of fat to lose, you'd sure as hell lose it faster if you're running a kcal deficit of 55% vs. 45%, right? Yeah, I know. As a SuppVersity reader you're smart enough to question the validity of this simple mathematical question and I have to admit that this is in fact one of the major weaknesses of the study at hand. However, let's postpone the criticism to the conclusion and simply assume it would be obvious that someone cutting back by 55% would lose more fat or at least more body weight than someone who consumes only 45% less calories.

Let's further assume this "someone" was an obese and overweight (BMI ≥ 25), nonsmoking adult (age 26-50 years) woman who has been selected from two clinics related to Weight Loss and Weight Gain Unit, Shohaday Tajrish Hospital and Private Clinic in Esfahan between April 2010 and September 2012.

You can learn more about meal frequency at the SuppVersity

Grazin' Bad For the Obese!

Breakfast Keeps You Lean?!

Frequent Protein Consumption

Myth: Few Meals More Bodyfat

8 Meals = Stable, But High Insulin

Int. Fasting & Exercise

Now, if you took 74 of these women and randomly allocated them to either the 45% or the 55% arm of the study, you would expect to see a weight loss advantage for the latter, right? Right.

But what if there was another twist to the study? A twist that says: "Eat 4 times per day for eleven days and make sure you leave at least 4h of time to digest between those four meals. Then, eat regular for three days and repeat!" Ha? What would happen?

Figure 1: Relative weight and fat loss after 12 weeks of dieting and after 4 week follow up (Davoodi. 2014)

Surprised? Well honestly, I would not have expected to see a difference like the one in Figure 1, either. Eventually, the study at hand which was conducted to test whether you can tackle some or all of the following downsides of classic weight loss interventions, i.e. non-adherence due to being  hungry, metabolic shutdown reduced physical activity, by nutrient timing provides more compelling evidence to a truth some people in the health and fitness industry have been propagating for decades: Timing matters!

Figure 2: Reduced hunger and no drop in resting metabolic rate - still asking for the reasons?

It matters not only because the subjects in the "eat 4 times a day at fixed 4h intervals"-group lost significantly more body weight. It matters above all, because...

• their "resting metabolic rate tended to remain unchanged" during the CSD phases,
• their plasmaglucose, total cholesterol, and triacylglycerol reductions were greater, and
• their geeling of hunger actually decreased over the course of the 4-week study

Now, all that is certainly fantastic. What's not so fantastic, though, is the minor "flaw" in the study design of which I've already pointed out in the introduction that it is based on the (imho) false believe that increases in caloric deficits in the 40%+ region would yield improved weight loss results.

No, no and no! Don't be stupid! Eat to satiety and fast or stay fat forever! Frequent meals will hamper not improve dietary T2DM treatment. Eating four times a day with 4h+ between the meals, on the other hand, is a promising approach to dieting.

Bottom line: Due to the extra -15% deficit in the "regular" diet group, the study at hand fails to "prove" the sole influence of meal timing on weight loss and improvements in glucose and fatty acid metabolism. That's a pity, but it does not mean that we could not conclude that "meal timing", or as I would rather like to call it "meal spacing" is an important and effective strategy to improve your weight loss results - I mean, on which -45% energy restricted diet does your hunger decrease over time?

So how can we conciliate the results of the study and hand with those of the "Many Small Meals Suck" (read it) study from  a couple of weeks ago? Well, easy! We're dealing with four, not 6 meals and they were spaced 4h, not just 2h apart. This + the fact that the women were  obese or overweight, but not diabetic could easily explain the difference.

Reference:

• Davoodi, Sayed Hossein, et al. "Calorie Shifting Diet Versus Calorie Restriction Diet: A Comparative Clinical Trial Study." International journal of preventive medicine 5.4 (2014): 447.

Breakfast!? An (Un-)Biased (?) Look at the Contemporary Scientific Evidence For and Against the Benefits of Having Breakfast and The Negative Effects of Skipping Meals

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).

Learn more about fasting and eating / skipping breakfast at the SuppVersity

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Breakfast & Glucose Metab.

Breaking the Fast, Cardio & the Brain

Does the Break- Fast-Myth Break?

Fasting = Muscle- Loss - Always?

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 you and 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).