Showing posts with label Meal Frequency. Show all posts
Showing posts with label Meal Frequency. Show all posts
Thursday, June 28, 2012

Why Does Breakfast Make Me Hungry? (Major Update July 16th)

Share

“Why does breakfast make me hungry?” When someone asked me that question for the umpteenth time since my methods became popular, I finally decided to indulge in a deeper exploration of what the plausible mechanism might be. I thought I’d share my thoughts on that with you today.

Note: Major Update July 16th and July 17th. See "Closing Point: Addendum" and "Short addendum" at the end of the article, a few P.S's, and a complete list of references.

It’s a fairly lengthy article, but hopefully interesting enough to keep your attention, informative enough to teach you a few things, and decent enough to mark my return back into the love-hate-relationship I maintain with the Internet (…and its potpourri of good and bad, smart and dumb, facts and bullshit).




My heart sank when it seemed they had provided overwhelming evidence for the benefits of breakfast a few months ago. But I proved them wrong.



Why Does Breakfast Make Some People Hungry?


As mentioned, it wasn’t without grounds that the question piqued my curiosity beyond that which could be attributed to food selection. In questionnaires, clients would often note that eating in the morning made them ravenous before noon, and sometimes no more than an hour after a steady breakfast.

On Facebook, in emails, and in casual conversation, anecdotes to a similar effect kept popping up too frequently to be explained by mere coincidence. Or to be shrugged off with a half-assed answer, with the underlying assumption that everyone’s eating crap for breakfast.

These folks weren’t eating Cheerios rounded off with a peanut butter sandwhich and a large glass of orange juice – you know, the usual Average Joe breakfast that would make anyone hungry an hour later.

No, these guys had your typical fitcentric breakfast with the kinds of foods that most of us ate at one point or another – oatmeal, dairy, eggs, etc. Often, but certainly not that often since the increasing popularity of Paleo, a meal characterized by moderate to high amounts of carb and protein, relatively low on fat, and more often than not a decent chunk of fiber.

You can spend all day arguing about the healthiness of whole grains and dairy (just not here, thanks), but fact remains that these foods could not singlehandedly explain the fact that breakfast triggered hunger in some people.

Hell, just google “why does breakfast make me hungry”, “hungry after breakfast”, or “breakfast makes me hungry”, and you’ll see that forums are swamped by people with the same experiences.

I’ll add myself to the aforementioned crowd. Omitting breakfast may have been the single greatest improvement to my diet when I embarked on my intermittent fasting regimen back in ’06, adherence wise.

For me, like countless other Leangains practitioners, breakfast was a huge pain in the ass and skipping it made all the difference in the world. Compared to before, dieting became almost effortless.

Not to mention long-term maintenance. No more counting the hours ‘till noon, and feeling like I was on a diet, regardless of whether I was actually dieting, maintaining, or “bulking.”





My favorite "breakfast" these days is the all-you can-eat-beef-buffet at 6 PM or later.


For me and many others out there, skipping breakfast keeps hunger away far better than eating in the morning – paradoxically enough. This is of course very interesting to me, because it’s a damn strange thing. Why is it that some people are better off not eating anything at all in the morning? How can you be better off with zero calories than hundreds of calories under these specific conditions? It just doesn’t make sense.

So I set out trying to answer that question, and finally arrived at a satisfying hypothesis a mechanism behind that mysterious post-breakfast hunger surge that so many of us experience.

The original article ended up being 12000+ words long with a ridiculously pretentious academic tone, branching out in all kinds of directions on semi-related issues. Far too long for most people’s attention spans, and way too technical for most peoples level of understanding.

Yesterday I sat down and rewrote the whole thing, trying to convey it all in the same manner I’d use when explaining it to my girlfriend, bro, or invisible friend, to which I’ve retold this whole thing to numerous times now. That’s Berkhanese for “some things are simplified from my perspective, but it’s still complex enough for the lay man, and hopefully decent enough to satisfy the expert.” Enjoy.

* In regards to breakfast, I will be referring to breakfast in the traditional sense of the term throughout this article, i.e. eating upon arising. Not breakfast in the original sense of the meaning, i.e. as the first meal after an overnight fast.


Defining Post-Breakfast Hunger 


Trying to define post-breakfast hunger is an exercise in futility. It’s something you’ll instantly be able to relate to, because you have the same experience, or something that makes you wonder what the hell I’m talking about, because you simply don’t have that problem. I’m guessing most of my readers fall into the former category, so I won’t be spending much time on academic discourse in attempting to define the phenomenon beyond what I’ve already done. Simply put, some people get hungry, very hungry, and/or experience cravings of various magnitude shortly after eating breakfast in the morning.

In the scientific literature, researchers who specialize in research on appetite, hunger and addiction, make a distinction between the aforementioned terms (i.e. hunger, craving, etc), but since post-breakfast hunger has been described in subjective experiences from clients, forum posts, etc, and without any truly detailed inquiry from my side, I’m guessing most people refer to the same phenomena when they talk about post-breakfast hunger in terms of getting cravings, feeling hungry, feeling ravenous, and so forth. For me personally, the sensation can be described as hunger, in the sense most of you probably think of hunger.

Post-breakfast hunger sets in somewhere between morning and noon, usually 30 mins to 2 hours after breakfast, and doesn’t usually manifest in any symptoms beyond noticeable hunger. However, some people have mentioned that irritability and impaired ability to focus on tasks that require sustained amounts of concentration, co-occurs with post-breakfast hunger.

An important point is that the same meal will not trigger this early and/or pronounced sensation of hunger if consumed later in the day. Post-breakfast hunger cannot be explained by differences in food choice, but by certain individual factors, and their interaction with a time-of-day effect of feeding on hormonal profile and metabolism.




Cereal will make anyone hungry soon again, but an important point of this article is that post-breakfast hunger is independent of food choice (i.e. it cannot be attributed to the simple fact that people tend to eat different type of foods in the morning versus later in the day). By the way, the above is part of my post-workout meal, when I occasionally include a box of cereal. I might be having some beef, potatoes, and ice cream afterwards to celebrate the new deadlift PB I just scored. 600 lbs x 4 in case anyone's curious. Stay tuned for the video


A Primer on Cortisol


Cortisol is the main culprit behind for post-breakfast hunger, the up-until-now mysterious affliction that is the topic behind this article. Most of you probably associate cortisol with stress and muscle catabolism, and consequently with “bad” and “avoid.” This is partly correct, but mostly erroneous.

Since “partly correct” is to blame for many of the nonsensical diet myths out there, it’s useless. People claiming that eating six times a day will stoke your metabolism, and that fasting causes starvation mode, are “partly correct” – but mostly full of shit, as I explained in “Top Ten Fasting Myths Debunked.”

The context is often critical, and this is especially true in regards to cortisol - which is why I’m going to give you a very brief primer on this complex and multi-facetted hormone. There are almost as many definitions of stress as there are myths about cortisol, but in regards to the former, the one that appeals to me from a minimalist perspective is:

Stress can be defined as any challenge to homeostasis of an individuum that requires an adaptive response of that individuum.

- Newport & Nemeroff, 2002.

Cortisol is secreted in response to a stressor, in order to help you cope with the stressor efficiently, whether that stressor is a balls-to-walls-set of 20-rep squats, or a looming deadline for an article that needs to be finished. The role of cortisol during these challenges is to boost you, not cripple you, whether the stressor is physical (e.g. exercise, injury, cold) or psychological (e.g. a complex or cognitively demanding challenge) in nature (or both).

Thanks to increasing cortisol levels during training, we can push way past our non-stressed comfort level, and maintain an adequate rate of exertion for a longer period of time than what would have been possible otherwise, without being overtly distracted by pain, hunger and fatigue. Cortisol improves muscle and glucose metabolism, increases pain tolerance, diminishes fatigue and strengthens motivation.

By the way, does this answer those of you who have asked me about my thoughts on pre-workout cortisol blockers? No? OK, then all I can say is good luck with those squats, buddy..

Due to cortisol in response to a cognitive challenge, we can recall important facts faster and in greater detail than otherwise, maintain focus, stay alert and pull all-nighters in front of the computer if needed. Cortisol increases sensory perception, memory recall, and wakefulness.






Most of the above is covered in Robert Sapolsky’s excellent book Why Zebras Don't Get Ulcers, in which he also explains when and why cortisol becomes bad for us. Briefly, prolonged exposure to a stressor results in chronically elevated cortisol, which then does all sorts of bad things to us. There’s a time and place for cortisol. In this day and age, the line between work (stress) and leisure time (rest) is often blurred.

With constant self-imposed demands, never ending obligations, and endless opportunities to work (in the office, at home, etc), the stressors of modern society are of the psychological variety and they are always present if you allow them in.

In stark contrast, the stressors of the past were more often of the intermittent and physical variety. While they were probably more severe and often life threatening, there was a clear-cut line between the start and the end. And this explains the title of Sapolsky’s book, which I cannot recommend highly enough, and which I urge you to read if you want a more detailed explanation of stress and the workings of cortisol.

What Sapolsky doesn’t cover in great detail however, is the cortisol awakening response and the acute effects of cortisol on insulin secretion.



The Cortisol Awakening Response


Most people get the concept of exercise and work as stressors, “challenges to homeostasis”, which require an adaptive response (cortisol). But few people think of waking up from sleep and rising out of bed as a particularly stressful event. However, waking up from sleep is indeed a profound challenge to homeostasis, if you think of stress in those terms.

The transitioning between the passive sleeping state to the active wake state is – in a way – like a leisurely walk interrupted by an all-out-sprint. In endocrinology, there’s a special name for the events that transpire to wake you up in the morning: the cortisol awakening response (CAR), on which there exists a substantial amount of research.

Awakening stimulates ACTH secretion in the pituitary, which then stimulates cortisol secretion in the adrenal glands. The rapid increase and peak in cortisol level after awakening is termed the cortisol awakening response (CAR). Although it is thought that CAR is a distinct part of diurnal cortisol rhythm, CAR and diurnal cortisol rhythm actually represent two separate adrenocortical activities.

- Shin et al., 2011.


As the body prepares to start up for the day, cortisol gradually starts to rise in the second half of the night, almost resulting in a climax as you open your eyes. But as you waddle out of bed on the way to the shower, cortisol will continue to climb. It will reach a peak 30-45 minutes later – which is right around breakfast time.

We’ve now reached a key point in this hypothesis behind post-breakfast hunger, because the precise timing of the circadian cortisol peak (CAR) and breakfast consumption has some very interesting effects on insulin secretion.


The Cortisol Awakening Response and Insulin Secretion


So you’ve taken your shower, dressed for the day, and done whatever else you like to do in the morning that’s none of my business, and now you sit down to eat breakfast before work, school, or whatever else. I’m guessing it’s now some 30-45 minutes after you stepped out of bed if you’re like most people.

As you sit down to eat, or at some point right around that time, cortisol reaches the highest point of the day, which would be 20-30 nmol/l. That’s compared to 2-5 nmol/l between evening and midnight, which is the lowest point during the circadian cycle if you want some numbers. It might go higher later during the day depending on the magnitude of stress you’re exposed to, but that’s besides the point.

The early insulin response to a meal is higher in the morning than in the afternoon, and this fact can only partially be explained by a moderately increased secretion of incretins. Rapid non-genomic effects of higher cortisol levels in the morning might be, at least in part, responsible for this finding.
- Vila et al., 2011.


The point is that the circadian cortisol peak coincides with breakfast, and that this is the only point during the day that cortisol reaches high enough levels to exert an acute and pronounced effect on feeding-induced insulin secretion.

If that sounds vague for the endocrinology enthusiasts out there and those of you who are familiar with cortisol, allow me to provide you with a brief explanation in language you can appreciate it. What I mean here is that, at the CAR peak, cortisol climbs high enough to agonize glucocorticoid receptors. This changes the non-genomic interaction between cortisol and insulin action from being permissively restraining by the former, as seen at other times during the day due to mineralocorticoid binding dominance, to a non-genomic stimulating, or synergistic if you will, effect (Vila et al., 2010; Dallman et al., 1995)

If the last paragraph doesn’t make much sense to you, then you know why I had to rewrite the whole article and simplify it.

Short-term* exposure to cortisol powerfully augments insulin secretion and this is the key point here.

* In stark contrast, long-term exposure has the opposite effect.


Average Joe Eats Breakfast


So, what happens then, as you start eating? Bad things? No, not necessarily, depending on the other variables in this equation – more on that very soon.

Enter Average Joe, who is average as it gets, with all its implications. Meaning fat, poor insulin sensitivity, and out of shape, according to our standard, but average according to the standard for modern man used in the scientific literature.

Average Joe sits down to eat his breakfast, and due to the influence of cortisol, his pancreas responds with a rapid and – relative to other points during the day, all else equal – high burst of insulin. This forces blood glucose down faster to baseline than later in the day, which in this context is a desirable effect.

Although the feeding-induced insulin peak comes much faster and is much higher, due to the meal coinciding with the circadian cortisol peak, the net effect should be that average insulin secretion and blood glucose in the post-prandial period post-breakfast is lower than later in the day, under a low-cortisol fed condition. In a way, Average Joe’s sluggish pancreas might actually benefit from the augmented insulin response in the morning,

That’s Average Joe. But what about Fit Joe? This is when it gets interesting.


Insulin Sensitivity and Insulin Resistance: Brief Primer


Something has always struck me as very peculiar and far too common of an observation to be coincidental.

When I first started dieting way back in the day, I did just fine with on your run-of-the-mill high meal frequency diet, with your run-of-the-mill fitcentric oatmeal based breakfast. I started out pretty fat at around 225 lbs, and lost about 40 lbs give or take, on a fairly generic approach mostly.

Sure enough, I did tons of beginner mistakes, especially in the cardio department (overdoing it), and subsequently suffered for it. I had my setbacks, like everyone else, but I powered through them all. I wrote about this journey a few years ago, in case you care to read more about it. There’s a few photos from back in the day too, which does a decent job of showing my overall development throughout the years.

Anyway, it wasn’t until at a later stage, leanness wise, that breakfast really started becoming a problem. First of all, I always felt that it was an unnecessary caloric burden that interfered with dieting. I wasn’t that hungry in the morning, but more so in the evening.




I would never have been able to maintain this conditioning with breakfast.

Had I known better back then, I would have started skipping breakfast earlier, of course, but back then everyone was preaching the virtues of breakfast and you didn’t really dare to break all these golden rules of the fitness game.

(And you’d still be eating breakfast if I didn’t put my ass on the line to set you straight 5-6 years ago, or whenever you first read my stuff. Am I right or am I right?)

Second of all, it seemed like the post-breakfast hunger surge increased in amplitude and frequency for every damn ounce of body fat I lost beyond a certain point. At some point, it became overwhelming, and that’s when the wheel-spinning started, progress wise. Until I finally decided to do my own research, no longer swallowing down the bullshit fed to me by so-called fitness gurus and the Journal of Broscience. The rest is history.

Anyway, let me put my labcoat back on again, and explain to you how this fits in with everything else I’ve talked about so far. We’ve now reached the second key point in this hypothesis behind post-breakfast hunger. The first key point, as you might recall, was the CAR and its peak coinciding with breakfast.

The second key point is insulin sensitivity. What happens when an insulin sensitive person eats something? Briefly, rising blood glucose levels feeds back to the pancreas (i.e. tells it that insulin is needed), and the pancreas responds with insulin. In turn, insulin then shuttles glucose from the blood to places where its needed (e.g. liver and muscle), which lowers blood glucose and prevents it from accumulating in the blood.

High blood glucose levels for longer periods of time (as seen in untreated type 2 diabetes, insulin resistance or poor insulin sensitivity, etc) does all sorts of bad things to us, which is why we want to bring it back to a healthy baseline as soon as possible. This is why high insulin sensitivity is a good thing.

If you’re insulin sensitive, the pancreas responds fast, with a big burst of insulin, in response to glucose, and then tapers off when it’s no longer needed. A sharp peak of insulin, with a prompt decline. The net result is lower readings of post-prandial blood glucose and insulin levels.

In contrast, insulin resistance results in a sluggish response, with a small burst of insulin, and a slow decline. The net result is higher readings of post-prandial blood glucose and insulin.

Imagine a graph tracking insulin secretion in the post-prandial period, with time on the X-axis and insulin on the Y-axis. Now picture a peak-like pattern for an insulin sensitive person, and a hill-like pattern for an insulin resistant person – that’s how it would look.

An important point in the above scenario is that insulin reaches a higher max in the insulin sensitive example.


Insulin and Blood Glucose Regulation

Recall that cortisol augments insulin secretion. When you have high levels of cortisol (i.e. at the peak of the CAR) and eat something, insulin secretion is boosted. The pancreas responds faster and stronger.

But Fit Joe already boasts a really robust insulin response, because he is insulin sensitive. Now add the insulin boosting effect of CAR on top of that, and what do you get? In theory, a very strong and sharp insulin surge. And what is the consequence of that?

Put differently – just as an example – what is the consequence of injecting too much insulin relative to needs (i.e. glucose)? If you overdo it by a wide margin, you risk all the horrors of life threatening hypoglycemia, with the result being extreme hunger, confusion, coma, brain damage and death, in that order.

While the above presents a real danger for diabetics, it doesn’t for healthy individuals. We have evolved an extremely efficient regulatory system for preventing blood glucose from dropping too low, to levels where it can compromise bodily functions and cognition, and impair our chances for survival.

Indeed, blood glucose regulation is a very secure system, with redundant mechanisms able to increase glucose output to meet needs in case one part of the system fails. Glucagon, epinephrine (adrenaline), cortisol and growth hormone are different hormones that cooperate to fulfill the role of another in case it fails to do its job properly.

But this system has not evolved to deal with blood glucose that is just low enough to trigger hunger, without any serious side effects beyond that. In fact, low blood glucose as a hunger signal was the focus of one of the earliest theories on appetite regulation.


Why Does Breakfast Make Fit Joe Hungry?


In the “glucostatic theory”, Jean Mayer in the 1950’s proposed that low blood sugar served as the primary hunger-triggering signal that prompted us to feed (Mayer, 1953). Later studies has taught us that appetite regulation is way more complicated than that, but there is clearly a role for blood glucose in this equation.

Building on Mayer’s theory, Campfield has proposed a more complex and refined theory, in which he – briefly summarized – suggests that falling blood glucose levels might serve as a hunger signal (Campfield & Smith, 2003). This has been echoed elsewhere, in the sense that the speed of which blood glucose falls can serve as an alarm signal in a sense – while a prompt lowering of post-prandial blood glucose levels is desirable, too steep of a decline can be interpreted as danger, and trigger a hunger signal.

So when insulin sensitive Fit Joe eats breakfast right at the peak of his CAR, he gets a lot of insulin to go with that meal, with the result being a very speedy drop in blood glucose.

Now consider the meal itself. What does a typical fitcentric breakfast look like? Odds are that it’s higher on the protein and carb side of things, low on fat, and quite often includes a source of dairy or milk protein. Any one of these components further contributes to insulin secretion, independent of each other.

As a consequence of the above, hunger rears its ugly face shortly after the meal. Either as a result of blood glucose dipping slightly to low, or as a result of it dropping too fast within a narrow time-frame.


Putting It All Together


And that, my friends, was my abbreviated explanation for post-breakfast hunger. If you give it some thoughts, it fits right in with my personal experience, my observations, and the many anecdotes I’ve come across throughout the years.

Post-breakfast hunger is something that occurs more frequently, and more noticeably so, in fairly lean individuals. I’d estimate that it’s fairly common in the 12-14% range. As you close in on single digit body fat percentage, it becomes very common indeed - and a serious obstacle for many.

Gradually, as we get leaner, we become more insulin sensitive. Little by little, as insulin sensitivity goes up, we get hungrier faster and more annoyingly so after breakfast, until we start wondering why we’re starving a mere 1-2 hours after a decently sized meal.

In a sense, it’s funny that blood glucose regulation works better in the fasted state, relative to the aforementioned breakfast scenario. It’s understandable when you consider that in the fasted state, you have balance between input and output, which in this analogy would be glucose and insulin. Glucose input to the blood is low and is well maintained with a low level of insulin in an insulin sensitive person.

With breakfast, insulin output is disproportionate to the input (breakfast), due to cortisol. A mismatch that would otherwise not be present under different circumstances (i.e. the same meal eaten later in the day, with low cortisol, or by someone with lower insulin sensitivity).

All of this raises interesting questions regarding the role of the cortisol-insulin connection, or dare I say breakfast consumption, and adaptation (or absence thereof) in the role of human evolution and its consequences for modern man, with his modern meal patterns.

Very interesting indeed, when you consider the events that transpire on a metabolic and transcriptional level once you combine cortisol and insulin. Not to mention the role of cortisol in place preference conditioning, learning, and the fact that even though breakfast-first-thing-in-the-morning is an artificial habit, manufactured by one of the first and possibly largest giant of the food industry (The Kellogg’s Company), it certainly is a habit we learned very fast.

But that’s for another time. Or for another one smart enough to recognize the clues to something big that I just handed them. Assuming they give a shit.


Closing Point

As a closing point, I want to point out that there were a few things that I had to cut out, since this article is long enough as it is. I figure that I should mention them very briefly by stating that there is a high degree of individual variance in the CAR, and that this might affect insulin secretion as well (i.e. a high CAR may have a larger influence on the feeding-induced insulin surge).

Furthermore, there is obviously a big role of food and macronutrient choice in all of this, but the role played may not be one that people typically expect. For example, some protein sources – or should I say, amino acids - are not only highly insulinogenic, but also trigger cortisol secretion. Incidentally, it tends to be the ones often consumed with breakfast.

Perhaps I need not mention that protein triggers a cortisol response, depending on the context (Benedict et al., 2005; Gibson et al., 1999; Slag et al., 1981). Oh, you thought that it was the other way around – that protein lowers cortisol? Well, then you learned another little something new today.

Maybe I’ll talk more about this another day, because there were many related and interesting semi-related parts to the topic of this article that I had skimp on, or cut out. Hopefully, time and motivation permits. I don’t trust myself to give any guarantees for the latter, unfortunately. But for the time and being, I’m back.


Closing Point: Addendum (July 16th)


An important point, which I should have accentuated and expanded upon, is the high degree of individual variability present among the hormonal factors within the equation that might predispose people to post-breakfast hunger. I wrote:

Post-breakfast hunger cannot be explained by differences in food choice, but by certain individual factors, and their interaction with a time-of-day effect of feeding on hormonal profile and metabolism.

More appropriately, my hypothesis states that it's the magnitude of these certain individual factors. Obviously, there are plenty of people who eat breakfast and do just fine. Some of whom probably need to eat breakfast in order to function optimally, and a portion of those that tolerate fasting poorly.

It should also go without saying that leanness and high insulin sensitivity does not inevitably bring about post-breakfast hunger, since there are tons of lean people who do not experience it. High insulin sensitivity are merely one of the factors that I believe plays a key role - and although leanness correlates strongly with insulin sensitivity*, there is a good degree of individual variance at any fixed level of body fat percentage.

*Specifically, visceral adipose tissue - not subcutaneous - predicts insulin sensitivity. However, low body fat means relatively low amounts of visceral fat, if you got to that point with a healthy and wholesome diet (i.e. with a decent fatty acid composition).

What are the other key factors - or variables - that determines the response? On top of insulin sensitivity, there is a very high degree of intra-individual variability when it comes to the CAR. I wrote:

 ...There is a high degree of individual variance in the CAR, and that this might affect insulin secretion as well (i.e. a high CAR may have a larger influence on the feeding-induced insulin surge).

My original article included a much longer section on CAR, in which I mentioned a few factors that should predict a high CAR, which in turn would predispose one to post-breakfast hunger. However, there are so many discrepancies and inconsistent findings on the subject within the scientific literature, that I choose to not delve into in such great detail. It would have been too speculative for my taste. This is also the current consensus on the topic in the scientific literature:

...The CAR literature is so inconsistent with regard to associations with trait psychosocial and health measures. 
...It is likely that different trait factors may be associated with different aspects of the regulatory puzzle, making it very difficult to tease apart.

- Clow et al., 2010.


Insulin sensitivity is easy to predict (body fat percentage), CAR is not - but I know there's some companies that provide kits for measuring salivary cortisol at home, and those are fairly reliable, I think. Anyone who's really interested in knowing their CAR might consider going that route.

There is one fairly consistent finding when it comes to the CAR; it's higher among women (Fries et al., 2009; Clow et al., 2010. Coincidentally, quite a few women have reported to me that they experience post-breakfast hunger - but  the role of CAR in all of this is anyone's guess, as is the relative contribution of each of these factors. After all, all of this is a hypothesis of mine, based on empirical research, endocrinology, and scientific theory.

The third important factor, which unquestionably plays a very important role in this, is food and meal composition, where you would have rapidly absorbing high-glycemic and highly insulinogenic meals (think toast, or cereal and milk) on one extreme end and low-glycemic low-insulinogenic meals on the other. The standard fitcentric breakfast that made me so ravenous for all those years falls somewhere in between. I usually had oatmeal, cottage cheese, whole grain bread, protein shakes, etc, in various combinations.

Someone in comments asked what you should eat if you happen to break the fast shortly after awakening. First of all, you need to ask yourself if you're hungry after whatever it is you're eating right now. No? Then there's obviously no need to start fixing and changing because you read a bunch of yang-yang on Leangains.com. All this theory and speculation, however fancy and educated that speculation happens to be, is always secondary to real life results.

That said, assuming you do seem to be experiencing post-breakfast hunger after breaking the fast in the morning, I would definitely recommend cutting down on carbs in favor for fat and a solid protein source. Solid meaning chewable, meaning meat.

Aside from a change in macrocomposition, I would also consider some common sense fixes depending on needs. Cutting down on caloric density and increasing volume (e.g. by replacing some food items with veggies, ideally crucificerious veggies) is almost always a good idea.


Short addendum, July 17th


I added a quote by Vila (2011) to the article. Nothing new, just a little something in support of what I wrote about the CAR and insulin secretion:



The early insulin response to a meal is higher in the morning than in the afternoon, and this fact can only partially be explained by a moderately increased secretion of incretins. Rapid non-genomic effects of higher cortisol levels in the morning might be, at least in part, responsible for this finding.


Lastly, I should mention that the original article included a few more mechanisms by which breakfast may trigger hunger in some. However, I felt that the article was already too long, and would get way too technical and confusing for most people if I veered off into several directions. Furthermore, the blood glucose mechanism for post-breakfast hunger seemed like the most likely candidate. That said, it's interesting to note that Vila (2011) also demonstrated a direct effect of concurrent glucose and cortisol administration on PYY, a key hormone involved in appetite regulation:

The modulation of PYY plasma levels suggests the possible non-genomic effects of glucocorticoids on appetite-regulatory hormones.

However, in that study they used intravenous glucose, which makes the relevance of these results to real life settings questionable.


P.S.


In case anyone’s wondering where I’ve been, especially those of you used to reading my frequently updated nonsense on Twitter and Facebook, only to see me disappear from the face of the Earth for the last two months.

An “I’ve been busy” type of response won’t do this time around. That would be a disservice to my true and loyal fans, many of who do a terrific job of directing others to the enlightenment they come to discover here. Not to mention an insult to those I’ve had to break important obligations to – you know who you are, and you will hear from me soon.

To make a long story short, an unfortunate chain of events forced me to take time off from everything. Literally everything on the online side of things, which is more or less like saying time off from work.

In either case, I’m back now. I understand that my work here is not yet done, and I shall finish what I started. Or die trying.

A special thanks to those of you who emailed me and wrote about the role I played in your life, development, career choice, inquired about my health, and reminded me of the important role I have come to play for some people. The few times I checked my inbox, it seems that there was yet another email from one of you, and I appreciated every single one of them. Here’s to hoping that I’ll get back to you one day.




Thanks for the support.



P.S. That deadlift video I talked about earlier in the article: deadlifting 600 lbs x 4 on Leangains intermittent fasting. Stay tuned for more videos. You can subscribe to my YouTube channel to be sure you don't miss 'em.

P.S.S. By the way, while you're over on YouTube, you might also want to check out the Hodge Twins talking about Leangains and intermittent fasting. Nothing new if you've read my stuff, but these guys are pretty hilarious. I can certainly appreciate them spreading the good word about intermittent fasting and killing off all these diet myths the way I've done here for years.

Lastly, I thought I'd mention that I'm once again quite active on Twitter and The Leangains Facebook Page. Feel free to follow me and join in the conversation.



Reference List 


Benedict, C., Hallschmid, M., Scheibner, J., Niemeyer, D., Schultes, B., Merl, V., Fehm, H. L., et al. (2005). Gut protein uptake and mechanisms of meal-induced cortisol release. The Journal of clinical endocrinology and metabolism, 90(3), 1692–1696. doi:10.1210/jc.2004-1792

Campfield, L. A., & Smith, F. J. (2003). Blood glucose dynamics and control of meal initiation: a pattern detection and recognition theory. Physiological Reviews, 83(1), 25–58. doi:10.1152/physrev.00019.2002

Clow, A., et al., The cortisol awakening response: More than a measure of HPA axis function. Neurosci. Biobehav. Rev. (2010), doi:10.1016/j.neubiorev.2009.12.011

Dallman MF, Akana SF, Strack AM, Hanson ES, Sebastian RJ. The neural network that regulates energy balance is responsive to gluco- corticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. Stress: Basic Mechanisms Clin Implicat 1995; 771: 730±742.

Fries, E., Dettenborn, L., Kirschbaum, C., 2009. The cortisol awakening response (CAR): facts and future directions. Int. J. Psychophysiol. 72, 67–73.

Gibson, E. L., Checkley, S., Papadopoulos, A., Poon, L., Daley, S., & Wardle, J. (1999). Increased salivary cortisol reliably induced by a protein-rich midday meal. Psychosomatic Medicine, 61(2), 214–224.

MAYER, J. (1953). Glucostatic mechanism of regulation of food intake. The New England journal of medicine, 249(1), 13–16. doi:10.1056/NEJM195307022490104

Newport, D.J. and Nemeroff, C.B. (2002) Stress. In: (Ed. in chief), Encyclopedia of the Human Brain, Vol. 4. Elsevier, pp. 449-462.

Shin, I.-Y., Ahn, R.-S., Chun, S.-I., Lee, Y.-J., Kim, M.-S., Lee, C.-K., & Sung, S. (2011). Cortisol Awakening Response and Nighttime Salivary Cortisol Levels in Healthy Working Korean Subjects. Yonsei Medical Journal, 52(3), 435. doi:10.3349/ymj.2011.52.3.435

Slag, M. F., Ahmad, M., Gannon, M. C., & Nuttall, F. Q. (1981). Meal stimulation of cortisol secretion: a protein induced effect. Metabolism, 30(11), 1104–1108.

Therrien, F., Drapeau, V., Lupien, S. J., Beaulieu, S., Doré, J., Tremblay, A., & Richard, D. (2008). Awakening cortisol response in relation to psychosocial profiles and eating behaviors. Physiology & Behavior, 93(1-2), 282–288. doi:10.1016/j.physbeh.2007.08.019

Vila, G., Krebs, M., Riedl, M., Baumgartner-Parzer, S. M., Clodi, M., Maier, C., Pacini, G., et al. (2010). Acute effects of hydrocortisone on the metabolic response to a glucose load: increase in the first-phase insulin secretion. European journal of endocrinology / European Federation of Endocrine Societies, 163(2), 225–231. doi:10.1530/EJE-10-0282

Thursday, June 16, 2011

Is Late Night Eating Better for Fat Loss and Health?

Share

If late night eating interferes with fat loss, why do people who eat more in the evening lose more fat than people who don't?

If carbs become fattening after 6 PM, how come people who eat more carbs after 6 PM lose more fat than those who eat them earlier in the day?

If we should "eat breakfast like a king, lunch a queen, dinner like a pauper", then why does breakfast skipping and nightly feasts lead to fat loss and improved blood lipids?

If eating late is bad for you, why does almost every controlled study show that eating later in the day is better than eating earlier in the day?

And if the above statements are true, why do people still believe that late night eating is bad for you...?


The Late Night Eating Myth


It's commonly believed that it's better to eat more earlier in the day and less later in the day; eating late can supposedly interfere with fat loss and/or cause unwanted weight gain. In a nutshell, this myth is summed up by the saying that you should "eat breakfast like a king, lunch a queen, dinner like a pauper."

You will often find proponents of broscience clinging to the notion that carbs somehow become more fattening after 6 P.M. This is nonsense of course.




You might already know that this is BS, as I debunked the late night eating myth in "Top Ten Fasting Myths Debunked" (Myth 10). In "Top Ten Fasting Myths Debunked" I concluded that there was no scientific evidence in support of the late night eating myth or the notion that we should eat more earlier in the day.

But the facts are actually more interesting than what I've previously stated; in controlled studies, late eating patterns are superior for fat loss and body composition.

In this article, I'll review studies on temporal distribution of calorie intake and summarize the results. I will devote a bit of extra attention to the latest study, "Greater Weight Loss and Hormonal Changes After 6 Months Diet With Carbohydrates Eaten Mostly at Dinner", which is what caused me to revisit this topic in the first place.

One pressing question first: Why is the late night eating myth still around if there are studies showing the exact opposite..?


Late Night Eating in Dietary Epidemiology


Someone asked this in comments:

"Is it ok to eat dinner 1-2h before bedtime? Note that every damn meat eating mammal goes to sleep after consuming massive amounts of food e.g lions, dogs, bears but apparently somewhere down the line, nutritionist´s came up with the conclusion that we somehow evolved. So it would be nice if someone came with some evidence that you shouldn´t eat before bed. I really don't understand why not, could you please explain?"

Yes, how did nutritionists arrive at the conclusion that eating before bedtime is bad for you?

The late night eating myth is mainly another consequence of mistaking correlation for causation in dietary epidemiology. There are plenty of observational studies that have found a positive association between calories consumed in the evening and a higher BMI in the general population.

This association is solely attributed to the fact that Average Joe's who like to eat more in the evening also consume more calories overall. In this study, it was deducted from food logs that late eaters consumed on average 248 calories more than the other group.

Similar relationships are commonly found in other observational studies on meal patterns. People who skip breakfast, skip meals and eat late at night are on average fatter and worse off than people who eat breakfast, regular meals and eat less in the evening. This has nothing to do with meal timing per se, but the lifestyle that goes in hand with "dysregulated" eating habits (as discussed in "Top Ten Fasting Myths Debunked").

Meal pattern with omission of breakfast or breakfast and lunch was related to a clustering of less healthy lifestyle factors and food choice leading to a poorer nutrient intake. (Ref.)

Late night eating is not only correlated to a higher calorie intake, but also less sleep time and more sedentary activities, i.e. watching TV and more time spent in front of the computer, which are additional confounders that can predispose people to weight gain.


Shift-Work and Circadian Rhythms


The imagined hazards of late night eating might also be the result of the scientific literature on shift-workers and metabolic health. Shift-workers are predisposed to a myriad of health disorders; obesity, poor mental health, cardiovascular disease, peptic ulcers and gastrointestinal problems (likely a result of chronic stress).

The negative effects of shift-work on health is mainly the result of a compromised diet, sleep deprivation, and stress - these tend to go hand. However, it's possible that feeding under conditions of a disrupted circadian rhythm and an irregular meal pattern is an independent factor in the predisposition towards poor health amongst shift-workers.

Humans can adapt to a wide variety of feeding regimens depending on the habitual meal pattern. This entrainment takes place on a cellular level and is regulated by ghrelin, a hormone that increases during meal times and prepare your metabolism to best handle a nutrient load. Similarly, the circadian rhythm - when you awake and go to sleep - is regulated by daylight and habitual sleep/wake-cycle, and adapts your metabolism accordingly.

Simply put, your body expects a certain routine every day, depending on habitual diet patterns and sleep/wake cycles, and adjusts its hormonal profile and metabolism accordingly. If this pattern is haphazardly and constantly shifted back and forth, and never allowed to adapt, as is the case with many shift-workers - it's very possible that it would be an independent factor in predisposing people to disease and health disorders. The hormonal profile of shift-workers tend to be less favorable than non-shift workers, for example.

It should be noted that permanent shift-workers, i.e. those who always work nights, or work nights on consecutive days, are better off than other shift workers, which is partly be explained by re-entraining the circadian rhythm; it seems that an "unpredictable" pattern, i.e. rotating day and night-shifts is the main culprit, as the circadian rhythm is constantly desynchronized. However, given the many confounders present amongst shift-workers, i.e. stress, sleep loss, calorie intake, it's hard to isolate which factor does what, i.e. is feeding during biological night worse than sleep deprivation, etc.


Dietary Epidemiology vs Controlled Studies


The aforementioned studies are of no interest to us. We are interested in controlled studies, not dietary epidemiology and observations in the general population. If you use dietary epidemiology to tell people how they should be eating you get this: The USDA Dinner Plate. When you use controlled studies to draw a conclusion, you get something that looks a little bit more like this. Throw some veggies in there and you're all set.

Controlled studies answers questions like "I'm on a 2000 calorie diet. How will fat loss be impacted if I eat most of those calories in the later part of the day versus the earlier part of the day?" That's what interesting to us, so let's look into this now.


Early Meal Patterns vs Late Meal Patterns: Controlled Studies


In all of these studies, calories were controlled and fixed for all groups. The only variable that differed was the temporal daily distribution of calorie intake. In late meal patterns, 67-100% of total daily caloric intake was eaten between 6 PM and bed time, and this was compared against an early meal pattern with an opposite pattern.

Starting with the earliest study and working myself down to the latest study, I'll briefly summarize the results, comment on the validity of the study, and interject whatever else of interest I find in each study.

Note that I will not include studies on Ramadan fasting. In loosely controlled studies on Ramadan fasting, fat loss and improvements in health markers is commonly found. This is a paradoxical and interesting finding, simply for the fact that people eat in the middle of the night, shortly before bedtime, along with a concomitant increase in intake of sugary treats and baked goods (and sometimes total calorie intake). However, these are rarely calorie-controlled studies, i.e. participants do not have strict guidelines about what they should eat, which is why I will not include them in this review.


Study #1


Results: In the very first calorie-controlled study on meal timing from 1987, it was found that weight loss did not differ when participants ate their daily calorie intake in the morning (10 AM) or evening (6 PM).

While it's interesting to note that lipid oxidation (fat burning) was consistently higher in the PM-group, the duration of the study (15 days) was very short, which makes it hard to draw any meaningful conclusion from it. Aside from lipid oxidation, there were no differences in cortisol levels, blood pressure or resting energy expenditure between the groups.


Study #2



Results: In this well-designed 12-week study, participants were habitual breakfast eaters and non-breakfast eaters, who were assigned a breakfast or non-breakfast diet. Interestingly, fat loss was greatest among ex-breakfast eaters who followed the breakfast skipping diet. This group ate lunch and supper and consumed 2/3 of their daily calorie intake at supper (6 PM or later). 

In contrast, baseline breakfast skippers who were put on a breakfast diet got more favorable results than those who continued the breakfast skipping pattern. The implication of these seemingly paradoxical findings might be related to impulse-control; dysregulated eating habits, such as breakfast skipping, tend to go hand in hand with uninhibited and impulsive eating. Eating breakfast might therefore be of benefit for those with poor self-control, such as the ex-breakfast skippers in this study. 

On the other hand, more favorable results were had with breakfast skipping amongst the "controlled" eaters (habitual breakfast eaters). This group would be more representative of us, meaning people who are used to count calories, follow an organized diet and not just mindlessly eat whatever is in front of us.

There were no differences between groups in regards to the weight loss composition (75% fat / 25% lean mass) or resting metabolic rate.

Interesting tidbit: The breakfast eating groups showed a slight increase in depression-induced eating whereas the subjects in the no-breakfast group showed a slight decrease. Furthermore, subjects in the breakfast group saw the diet as more restrictive than the no-breakfast group. Quote:

...the larger meal size of the no-breakfast group caused less disruption of the meal patterns and social life than did the smaller meal sizes in the breakfast condition. 

Perhaps it was these favorable effects on their social life that also resulted in the no-breakfast groups showing superior compliance rates at the follow-up 6 months later (81% vs 60%).


Study #3



Results: In this study participants alternated between two 6-week phases of the same diet of which 70% of the daily caloric intake was eaten in the morning or evening respectively. Larger morning meals caused greater weight loss compared to evening meals, but the extra weight lost was in the form of muscle mass. Overall, the larger evening meals preserved muscle mass better and resulted in a greater loss in body fat percentage.

The greater weight loss associated with the AM [morning] pattern that we found in our study was due primarily to loss of fat-free mass, which averaged about 1 kg more for the AM pattern than for the PM pattern.

An interesting study with a few glaring limitations, mainly the small sample size (10 participants) and the way body composition was measured (total body electrical conductivity, which is somewhat similar to BIA discussed in "Intermittent Fasting for Weight Loss Preserves Muscle Mass?").

This study also included weight training 3x/week, which was a serious confounder in this specific study design. Given that the PM-group consumed a greater percentage of their calorie intake post-workout, this study might simply show the benefits of nutrient timing, and not bigger PM meals per se.

AM-Setup:

Breakfast, 8-8.30 AM: 35% of total daily calorie intake
Weight training (circuit style), 9-9.30 AM
Lunch, 11-12 PM: 35%
Dinner, 4.30-5 PM: 15%
Evening snack, 8-8.30 PM: 15%

PM-Setup:

Breakfast, 8-8.30 AM: 15% of total daily calorie intake
Weight training (circuit style), 9-9.30 AM 
Lunch, 11-12 PM: 15% 
Dinner, 4.30-5 PM: 35%
Evening snack, 8-8.30 PM: 35%

As you can see, the PM-setup is quite similar to the "One Pre-Workout Meal" protocol of Leangains.





My client Gary here demonstrates the fattening effects of post-6 PM carbs. Gary followed the Leangains one pre-workout meal protocol and ate more than 75% of his daily calorie intake and >200 g carbs after 6 PM.

Finally, the researchers speculate on the muscle sparing effects of the PM-pattern:

Certain endocrine influences might have contributed to the difference in fat-free mass change between the meal patterns. Growth hormone secretion displays an endogenous rhythm that is partially linked with the sleep cycle. At night pulsatile secretion increases after 1-2 hours of sleep, with maximal secretion occurring during stages 3 and 4 of sleep.
Although the effect of prolonged changes in dietary intake or meal patterns on growth hormone release are not known, it is conceivable that a greater flux of dietary amino acids with the large evening meals, coupled with the known protein anabolic effect of growth hormone, might combine to favor deposition of lean tissue.

Study #4





Results: Using almost the exact same setup as the aforementioned study by Sensi & Capani (1987), it was found that splitting the daily calorie intake evenly into five meals consumed every other hour between 9 AM-8 PM, eating all calories in the morning (9-11 AM), or in the evening (6-8 PM) did not affect weight loss, metabolic rate or cortisol differently. The limitations here are once again a very short study duration for each phase (18 days). Quote for those worrying about cortisol and fasting:

At the end of the stages studied, we found no significant changes in the circadian rhythm of cortisol secretion regardless of the timing of diet ingestion, even after 22 h of fasting.

It might be worth noting that nitrogen loss, which is a rough marker for muscle loss, was not affected by eating time or meal frequency; there was no difference between the 5-meal phase or the 22-hour fasting phases with one AM/PM-meal. 


Study #5



In this latest and well-designed 6-month study on calorie distribution throughout the day, participants who ate most of their daily carb-intake at dinner (8 PM or later) lost more fat, experienced greater fullness throughout the diet, and saw more favorable hormonal changes than those who ate their carbs earlier in the day.


Background: This study was founded on the premise that the diurnal peak in leptin can be altered, as noted during the month of Ramadan. (I've covered leptin and intermittent fasting here: "Intermittent Fasting, Set-Point and Leptin.")


Previous studies have described a typical diurnal pattern of leptin secretion that falls during the day from 0800 to 1600 hours, reaching a nadir at 1300 hours and increases from 1600 with a zenith at 0100 hours. Ironically, this crucial hormone responsible for satiety is at its highest levels when individuals are sleeping.
It was hypothesized that consumption of carbohydrates mostly in the evening would modify the typical diurnal pattern of leptin secretion as observed in Muslim populations during Ramadan. 

Simply put, the goal of this study was to see whether it was possible to shift leptin secretion to strategically induce greater satiety and diet adherence during the morning and noon of the next day, instead of having leptin peak during night time (as it does on a standard diet).

...it was predicted that the diet would lead to higher relative concentrations of leptin starting 6–8 h later i.e., in the morning and throughout the day. This may lead to enhanced satiety during daylight hours and improve dietary adherence.

Note that leptin displays significant latency in response to carbs; if you eat carbs before you go to sleep, you won't be experiencing the peak until you wake up in the morning (an added bonus is that you sleep good with some carbs pre-bedtime).

This study also sought to examine the effect of the experimental diet on adiponectin.

Adiponectin is considered to be “the link between obesity, insulin resistance, and the metabolic syndrome”. Adiponectin plays a role in energy regulation as well as in lipid and carbohydrate metabolism, reducing serum glucose and lipids, improving insulin sensitivity and having an anti-inflammatory effect. Adiponectin’s diurnal secretion pattern has been described in obese individuals (particularly with abdominal obesity), as low throughout the day.

* Low adiponectin = bad. High adiponectin = good.

* When insulin is low, adiponectin is high, but adiponectin also follows a diurnal pattern; low during night time, high during daytime (in normal weight individuals).

...it was also hypothesized that adiponectin concentrations would increase throughout the day improving insulin resistance, diminishing symptoms of the metabolic syndrome and lowering inflammatory markers.

* In the obese, chronically high insulin causing chronically low adiponectin is a problem as it increases insulin resistance and inflammation. By omitting carbs during the earlier part of the day, the researcher's hypothized that this would increase adiponectin and improve health markers more than the conventional diet.


Setup: Both groups received the same diet divided into breakfast, lunch, dinner and as three "snacks" (morning, afternoon, night):

1300-1500 kcal
45-50% carbs
30-35% fat
20% protein

Group A received the carbs evenly split throughout the meals and snacks. Group B received the great majority of the total carb allotment (~170 g) at dinner. There are no details concerning the exact macronutrient amounts provided at each meal but the full-text paper contains the menus of each respective group. I would estimate that approximately 100-120 g carbs were consumed at dinner in group B.

Results: Both groups lost weight and saw improvements on several health markers, but group B lost more weight (-11 kg vs -9 kg), body fat (-7% vs -5%), stayed fuller and more satiety, and improved their hormonal profile more than group A:

Hunger scores were lower and greater improvements in fasting glucose, average daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were observed in comparison to controls.

As predicted, the big carb-rich dinner was able to alter leptin and adiponectin in a way that might have favored greater fullness and a better hormonal profile:

The experimental diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity.

But what I found most interesting, at least for those of us who want to maintain low body fat, was that the carb-rich dinner increased average leptin levels compared to the standard diet:

Our experimental diet might manipulate daily leptin secretion, leading to higher relative concentrations throughout the day. We propose that this modification of hormone secretion helped participants experience greater satiety during waking hours, enhance diet maintenance over time and have better anthropometric outcomes.

Perhaps this is why me, and many others with me, have found Leangains/intermittent fasting to be such an easy way of staying lean once you've reached your goals.

This study was solid, but for some reason there was no mention of how body fat percentage was measured. Similarly, calorie intake was not set individually and according to energy needs. However, given that everyone had the same job (police officer), it's fair to assume that physical activity did not vary much on an individual basis. Furthermore, sample size was very large (78 participants), which makes it unlikely that the results were confounded by these factors.


Summary


Dietary epidemiology commonly find associations between certain meal patterns and higher BMI / body fatness. However, this association can solely be attributed to lifestyle-related factors and eating behaviors; snacking in front of the TV in the evening, making poor food choices in general, and so forth. People who eat more in the evening simply eat more calories, which explains why they weigh more.

Calorie-controlled studies looking at the effects of distributing a fixed caloric load differently throughout the day are scarce; I have listed all of them above. These tell a much different story than the one found in dietary epidemiology. While short-term studies (15-18 days) do not find a statistically significant difference between early and late meal patterns, long-term studies (>12 weeks) show that late eating patterns produce superior results on fat loss, body composition and/or diet adherence. This might be explained by more favorable nutrient partitioning after meals due to hormonal modulation.

I understand that these facts might be hard to swallow for some people, given everything we've heard about late night eating being bad, fattening, and so forth. But then again, we hear a lot of strange things in the fitness and health community. Rarely do these old wives' tales mix with reality; think of all the myths about fasting, alcohol and meal frequency, for example.

That's all for tonight. I hope you've enjoyed the article and will rest easy knowing there's nothing bad about late night eating and big meals before bedtime.


Monday, April 4, 2011

A Critique of the ISSN Position Stand on Meal Frequency

Share

When International Society of Sports Nutrition (ISSN) released their position stand on the topic of meal frequency, two things stood out to me.

First of all, a number of questionable conclusions are made in the abstract. With my last article in mind, the claim that "...increasing meal frequency during periods of hypoenergetic dieting may preserve lean body mass in athletic populations" seems a bit presumptuous, wouldn't you say? An inquiring mind would like to know what conclusive data these gentlemen are sitting on.

Furthermore, given yesteryear's study on meal frequency and appetite control, the claim that "Increasing meal frequency appears to help decrease hunger and improve appetite control" is also rather interesting.

I could go on and on and give you numerous examples to counter some of the statements made in the abstract. But that is not the role I'm going to play today.

What was the second thing that stood out to me? You may recognize some names amongst the authors; the more notable ones are John Berardi - author of several diet books and articles - and Jose Antonio, CEO and co-founder of ISSN.

Is John Berardi - who, aside from making numerous scientifically unsound claims, has been one of the strongest proponents of high-meal frequency eating - unbiased enough to be allowed to participate in this publication? Berardi considers HMB a worthwhile supplement for athletes and wholeheartedly recommends it on his site. For those of you who don't know, HMB is damn near worthless. Buying it is as close to throwing your money away as you can possibly get (just like Glutamine - which Berardi also recommends). What does this say about his credibility as a scientist?

Jose Antonio? He's been the nutritional consultant to several supplement companies, among them Met-Rx, the king of meal replacements. What position do you think is most beneficial to maintain in order to keep the supplement industry spinning - that high-frequency eating is superior or that there's no difference between 3 and 6 meals a day? When people feel that the need to eat every other hour or so, what is it that they add to their diet? Protein shakes, protein bars, recovery drinks and meal replacements.

There's more here if you do some digging. Suffice to say, I was not convinced that this was the best team for an unbiased "position stand" on meal frequency. And the greatest joke of all? At the end of the paper, you'll find this: "Competing interests: The authors declare that they have no competing interests." When pigs fly, perhaps.

But never mind that for now. Let's judge this paper on its own merits and forget everything else. But I've talked myself blue in the face about the topic of meal frequency and it would be refreshing to have someone else dissect this paper for us. For that purpose, there is no one more fitting than Alan Aragon.




I've been a subscriber to Alan Aragon's Research Review since the first issue. AARR provides unbiased and critical analyses of the latest research on nutrition, exercise and supplementation. Adding to that, it also contains commentaries and analyses on the latest "hot topics" in the fitness industry and blogosphere. I'm giving it two thumbs up and recommend anyone interested in nutrition and exercise science to check it out. Download a free issue here. 



A Critique of the ISSN Position Stand on Meal Frequency
By Alan Aragon 
Originally Presented at Leangains.com, April 4th, 2011


Introduction

The International Society of Sports Nutrition (ISSN) is a forerunner in the movement toward providing reliable nutrition information for sports and fitness professionals. By virtue of its academically decorated staff and peer-reviewed research journal (JISSN), the ISSN is in a justifiable position to consider itself one of the world’s top authorities on sports nutrition. Thus, when they issue a position statement on any given topic, it’s frequently cited as solid evidence, and not taken lightly. For example, along with other literature reviews, I regularly cite their position paper on protein requirements for athletes [1]. However, I typically follow that up with what I do in personal practice, which isn’t always research-backed. It’s important to keep an eye on both the research and the trenches, since field knowledge can take years and sometimes decades to make it into academic publication.

It’s clear that the focus of their latest position stand is meal frequency’s effect on body composition. Right from the start, the authors illustrate the importance of this topic by citing the obesity epidemic in the United States. Setting the tone as such implies that weight/fat loss is the most pressing concern of the position stand, more so than other aspects such as muscle gain and exercise performance. This focus is justified, given the prevalence of obesity in industrialized nations, not just the United States. This justification is bolstered by the myriad health complications that accompany a chronic state of excess body fat. The next question becomes, how well does the ISSN support their meal frequency assertions to this end? I encourage you to have the ISSN’s position stand open while you read through this critique of the evidence used to support their key claims. The full text of the paper is freely available, see the reference list [2].  


Body Weight & Body Composition

The authors begin the above-titled section by discussing uncontrolled/observational studies, including animal data. We can safely skip those, since the threats to their validity are numerous & obvious. They then move on to discuss experimental studies in humans. They correctly note that on the whole, the evidence in this area fails to indicate the superiority of increased meal frequency for improving weight loss. An interesting and important detail is the authors’ point that the minority of studies that did show improvements as a result of increased meal frequency happened to be in athletic subjects, whereas the ones that did not examined overweight/obese subjects. Three studies were provided to support this, which I’ll discuss next.

First up is Benardot et al, who compared the effects of three 250 kcal between-meal snacks with a noncaloric placebo [3]. A significant increase in anaerobic power and lean mass was seen in the snacking group, with no such improvements seen in the placebo group. Obviously, it’s impossible to credit the superior results to a higher meal frequency since this was also accompanied by a higher overall energy intake. The next study cited was by Deutz et al, which was not a controlled comparison of the isolated effects of different meal frequencies [4]. Instead, it merely drew correlations between body composition and the results of a 24-hour recall of diet and physical activity variables. The final study was by Iwao et al, who found that boxers consuming 6 meals a day lost less lean body mass (LBM) and showed lower molecular measures of muscle catabolism than the same diet consumed in 2 meals per day [5].

Of the three aforementioned studies, one was correlational. Of these two studies that demonstrated causation, only one of them (the boxer study) equally matched the intakes of each group. However, its design flaws compromise its relevance. Aside from flaws common to studies on both sides of the fence (short trial duration, subpar assessment methods, small sample size), the total energy intake at 1200 kcal was artificially low compared to what this population would typically carry out in the long-term. It’s also important to note that the protein intake, at 20% of total kcals, amounted to a paltry 60g/day. This translated to slightly under 1.0g/kg. To illustrate the inadequacy of this dose, recent research by Mettler et al showing that protein as high as 2.3g/kg and energy intake averaging 2022 kcal was still not enough to completely prevent LBM loss in athletes under hypocaloric conditions [6]. Therefore, the ISSN’s claim that increased meal frequency in athletic populations may improve body composition is based on a single study with questionable applicability.

Missing Research on Body Composition 

In addition to the aforementioned limitation, the authors failed to mention research that runs contrary to their assertion that, “Interestingly, when improvements in body composition are reported as a result of increasing meal frequency, the population studied was an athletic cohort.” Introducing the topic of comparative drops in LBM opens up a can of worms that does not support the ISSN’s claims. A recent review by Farady concluded that although daily caloric restriction (DCR) and intermittent calorie restriction (ICR) have similar effects on total bodyweight reduction, ICR has thus far been more effective for retaining lean mass [7]. The results of 11 DCR studies 7 ICR studies were clearly laid out. Here are a couple of key stats that contributed to Farady’s conclusion:

  • 3 of the ICR studies showed no significant decrease in LBM, while all of the DCR studies showed decreases in LBM.
  • In studies lasting 8-12 weeks, average LBM loss was 1.25% in ICR and 4% in DCR.

Adding to the body of contrary data to the ISSN’s position, there are two more studies showing the superior effects on LBM status via lower meal frequency. An 8-week trial by Stote et al found the group consuming one meal per day gained lean mass and lost body fat, while the group consuming 3 meals per day showed no improvements in body composition [8]. It should be noted that just like the study by Iwao et al, Stote et al’s results are limited by the use of BIA to assess body composition. Oyvind et al compared the 12-week effects of eating 3 versus 6 meals per day in subjects on a resistance training program, and the lower-frequency group gained significantly more LBM [9].

Collectively, this body of research refutes the ISSN’s claim that superior effects on body composition have only been seen in athletic subjects with higher meal frequencies.


Blood Markers of Health

As an obligatory introduction, the authors begin their above-titled section by discussing observational/uncontrolled studies. Again, there’s no need to wade through this, given the availability of controlled studies. The first controlled intervention discussed is by Stote et al, where blood pressure and total cholesterol (both HDL & LDL) were higher in the group consuming 1 meal per day compared to the 3-a-day group [8]. However, Stote et al noted that the difference in blood pressure may have been due to differences in circadian rhythm since it was measured in the late afternoon in the 1-meal group, and in the early morning in the 3-meal group. No speculations were made over what might have caused the cholesterol increase in the 1-meal group.

Another concern of the ISSN was the potentially adverse effect of lower meal frequency on glucose homeostasis. In support, they cited work published in the 1960’s. They also cited subsequent work done in the same proximity with contrary outcomes. Notably, they discussed a study by Jenkins et al, which compared 3 versus 17 feedings per day and found no difference in mean blood glucose levels [10]. Although the latter failed to show improvements in blood glucose levels, benefits from the (unrealistically) high meal frequency improved insulin levels and blood lipid profile. Although the data in this area is equivocal, the ISSN recommends increasing meal frequency for the purpose of improving health markers.

Missing Research on Glucose Control

An 8-week trial by Carlson et al found that subjects consuming 3 meals instead of 1 meal per day had more favorable results on an oral glucose tolerance test (OGTT) [11]. However, the authors of this study acknowledge that this may have been due to a much larger consumption of food in closer proximity to the OGTT in the single-meal group. Testing was first thing in the morning, and the single-meal group consumed their day’s intake in a 4-hour window before bed.

A very recent study adds to the evidence contrary to this idea, and was likely unavailable at the time of the ISSN position stand was written. Holmstrup et al found that glucose levels remained elevated throughout the day with frequent 6 meals compared to 3 meals, and no differences in insulin levels were seen [12]. The key design strengths this study has over predecessors were the frequent sampling used to track blood glucose and insulin levels, and the use of healthy non-obese subjects with normal glucose tolerance. These aspects make it more relevant to active & athletic populations, to whom the ISSN’s position stand is directed in the first place. Another trial too recently published to make it into the position stand was by Harvie et al, who found that intermittent energy restriction was as effective as continuous energy restriction for decreasing bodyweight and increasing insulin sensitivity [13].

In sum, due to the inconsistency of the data, it appears that increasing meal frequency for the purpose of improving health-related biomarkers is a premature recommendation.     


Metabolism

The aspects of metabolism discussed in this section are diet-induced thermogenesis (DIT – also called the thermic effect of food), resting metabolic rate, and protein metabolism. As for DIT, differences between varying meal distributions across several studies are negligible. The same lack of difference was also seen in several studies, including tightly controlled designs involving metabolic chambers to measure resting metabolic rate and total energy expenditure. These data further serve to invalidate the dying cliché of stoking the metabolic fire with frequent small feedings.

The discussion of protein metabolism mainly involved the effects of meal frequency on nitrogen retention. The ISSN duly notes that most studies discussed in this section used nitrogen status as a proxy for muscle protein status, which is not always reliable. The nitrogen balance technique measures whole-body (systemic) nitrogen flux, rather than directly measuring protein turnover within skeletal muscle. Although the nitrogen balance method has limited applicability, it provides clues & hypotheses to test through more rigorous & direct means. The literature on meal frequency and nitrogen retention is reviewed, and the bulk of the data shows no differences despite meal frequencies ranging from one to six meals per day.

The discussion of effects on protein metabolism begins by citing work by Garrow et al, who saw less nitrogen loss in obese subjects in hypocaloric conditions consuming 5 meals per day, compared to consuming 1 meal per day, and lean mass preservation was more pronounced in the higher protein treatments [14]. However, the extrapolability of this research to real-world scenarios in non-sedentary & athletic populations is highly questionable. Total energy of the diets was 800 kcal, and the protein levels tested ranged from 10-15% of total kcals, amounting to 20-30g of protein per day. This amount represents about a tenth of the protein typically consumed by adult male athletes. The limitations of this study’s design are obvious.

The authors then proceed down a slippery slope by discussing the potential benefit of maximizing muscle protein synthesis (MPS) on a per-meal basis. In acute (short-term or immediate-effect) studies on individuals of average body weight, the protein dose that tops out MPS is roughly 20-30g of high-quality protein, or about 10-15g of essential amino acids (EAA). Given this, the authors make a logical leap by presuming that more frequent occasions of maxing-out MPS would ultimately lead to faster rates of muscle gain. To support this idea, they cite rodent research by Wilson et al [15] and short-term human research by Paddon-Jones et al [16]. I’ll comment on the latter since rat data pales in relevance when there’s human data available to examine.  

Paddon Jones et al found that MPS was greater when an EAA + carbohydrate liquid supplement was consumed between the 3 regular-sized solid meals [16]. As a result, this study is often cited to support both the idea of increasing protein feedings as well as the benefits of dosing EAA between meals. The problem is, the group receiving the inter-meal supplementation ended up with 45g EAA + 90g carbs more than the control group by the end of the 16-hour test period. This treatment imbalance in both total calories and macronutrition is compounded by low protein intakes, averaging 23g per meal, totaling 64g per day. The experimental group’s supplemental intake boosted protein intake to 109g. So, not only was there the confounding element of unmatched macronutrition between groups, it essentially was a comparison of insufficient protein intake versus barely adequate intake.

After examining the literature on protein metabolism/nitrogen retention, the ISSN concluded that, “…it appears as if the protein content provided in each meal may be more important than the frequency of the meals ingested, particularly during hypoenergetic intakes.”  Still, this statement is collectively based on the Garrow study involving 20-30g protein per day, the Wilson rodent study, and the Paddon-Jones study, all of whose limitations are critical. Nevertheless, the ISSN made the redeeming point that increasing meal frequency isn’t likely to increase metabolic rate. To their credit, they repeatedly acknowledged that there’s a lack of research on the effect of meal frequency on various aspects of metabolism in athletic & physically active subjects.  

Missing Research on Markers of Protein Metabolism

Missing from this section of the paper was any mention of recent work by Soeters et al, who saw no difference in glucose, lipid, or protein metabolism between an intermittent fasting treatment (involving 20-hour fasting cycles) and a standard diet [17]. Similarly, Arnal et al saw no significant difference in body composition & nitrogen retention in subjects consuming most of their daily calories in 1 meal versus 4 evenly-spread meals throughout the day [18].  In older subjects, the same research team actually found better nitrogen retention with most of the day’s calories from 1 meal instead of 4 meals [19].

Although the ISSN isn’t firm with it, there’s an underlying implication that increasing the frequency of protein dosing at the threshold known to max-out MPS (20-30g protein or 10-15g EAA) would optimize the rate of net muscle protein gains. If this were true, then more muscle would be lost in lower-frequency treatments. Conversely, greater gains would be seen in higher-frequency treatments over time. The majority of the research thus far has simply not supported either one of these phenomena [7-9, 17-19, 21, 22].

   
Hunger and Satiety

This section begins by discussing short-term (within-day) effects of meal frequency on hunger and satiety. These designs involved the pre-loads of varying meal distributions, and measuring subsequent ad libitum food intake. Unanimously, the higher-frequency meal preloads resulted in better appetite control, evidenced by lesser subsequent intakes. Additionally, a study by Smeets et al found higher satiety ratings over a 24-hour period in subjects consuming 3 meals instead of 2 [20].

The important question is whether the hunger-controlling effects of higher meal frequency persist beyond a single day. The ISSN only mentions 2 such studies, and they happen to have conflicting outcomes. Stote et al’s 8-week trial reported greater hunger levels in subjects consuming 1 versus 3 meals per day [8]. A more recent trial by Cameron et al compared 6 meals per day (technically 3 meals + 3 snacks) with 3 meals per day, and found no significant differences in appetite ratings [21]. Additionally, there were no trends suggesting a significant effect of increased meal frequency on the levels of the appetite-regulating peptides ghrelin and peptide YY (PYY). As seen consistently in other research, there were no differences bodyweight decrease or body composition change. Curiously, despite the equivocal results of these two trials, the ISSN concluded that increasing meal frequency is likely to decrease hunger and control intake in subsequent meals. But as we’ll see, more recent data continues to challenge this idea.  

Missing Longer-Term Research on Hunger & Satiety

An important study is missing from the ISSN’s review. In fairness, it’s likely because it wasn’t yet available at the time it was written. Leidy et al compared varying protein levels consumed across either 3 or 6 meals per day [22]. Predictably, the higher-protein level (25% vs. 14%) promoted greater satiety. Interestingly, the higher meal frequency led to lower daily fullness ratings regardless of protein level. Meal frequency had no significant impact on ghrelin levels, regardless of protein intake. PYY, which is associated with satiety, was 9% lower in the higher meal frequency.

When focusing mainly on the short-term (within-day) studies, increasing meal frequency appears to have beneficial effects on appetite control. However, these results for the most part have not been supported by longer-term research. Thus, the blanket recommendation to increase meal frequency in order to decrease hunger is not based on the weight of the evidence.


Athletic Populations

This section of the position paper was basically a reiteration of the outcomes of 3 studies discussed earlier, in attempt to emphasize the point that more is potentially better when it comes to meal frequency. In response, I’ll briefly review my contentions with the applicability of this data. Deutz et al was a retrospective correlational study, not a controlled intervention capable of demonstrating causation [4]. Iwao et al’s study on boxers used a protocol that was artificially low in total kcals and unrealistically low in protein compared to what athletes typically consume [5]. Benardot et al’s design did not match total energy and macronutrition between groups, so it’s not surprising that the greater performance and lean mass gains occurred in the group with the higher fuel consumption [6]. In addition to the crucial limitations of these studies, research with contrary results (and equal or better design quality) is missing from this position stand [7-9].

The authors go on to assert that data on the eating habits of competitive athletes (in primarily endurance-based sports) shows a range of roughly 5-10 eating occasions per day. They suggest that this is optimal because it enables athletes to consume a culturally normal meal pattern in addition to meals proximal to the training bout. In response to this, I’d say that this range of frequencies is fine for this population. But, I’d also contend that the energy needs of competitive athletes in endurance-based sports can be 2-4 times greater than that of recreationally active individuals (who make up the bulk of the nonsedentary adult population). Therefore, applying the meal frequency of competitive athletes to less active populations is unnecessary & impractical, at best. In my private practice, I’ve seen recreational athletes succeed long-term with as little as 2 meals per day. The most common meal frequency range I’ve observed in physically active clients with long-term success is rather broad (3-6 meals per day). Whether individuals choose the higher or lower end of that range is based solely on personal preference and tolerance.   


Boiling Things Down: The Position Statements

Credit is due to the ISSN for preemptively stressing that the research on physiological & morphological effects of meal frequency in physically active and athletic populations is scarce. They responsibly state that this prevents definitive conclusions from being made. The following are the exact statements that comprise the ISSN position stand on meal frequency, which I’ll follow with my comments & conclusion.

  1. Increasing meal frequency does not appear to favorably change body composition in sedentary populations.
  2. If protein levels are adequate, increasing meal frequency during periods of hypoenergetic dieting may preserve lean body mass in athletic populations.
  3. Increased meal frequency appears to have a positive effect on various blood markers of health, particularly LDL cholesterol, total cholesterol, and insulin.
  4. Increased meal frequency does not appear to significantly enhance diet induced thermogenesis, total energy expenditure or resting metabolic rate.
  5. Increasing meal frequency appears to help decrease hunger and improve appetite control.

When examining the above points, 1 & 4 have a substantive, cohesive, and adequately-designed body of research backing them. Thus, they possess the strongest evidence basis of the bunch. Number 3 sits right on the fence, since it’s a particularly complex and delicate area with much conflicting data. It’s my hunch that the differential effects of varying meal frequencies on blood markers of health would greatly diminish in the presence of a formal exercise program. Again, the potentially profound impact of training that’s missing from the current meal frequency research leaves big questions unanswered. Points 2 & 5 have the least scientific support, and the largest leaps of faith and bias from the ISSN.

In Closing

I’d advise everyone with enough motivation to dig into the references and question the conclusions of all parties involved. It’s clear that position stands of authoritative organizations are far from being completely accurate, complete, and bias-free. With that said, the ISSN provides plenty of food for thought. Again, read the full text of their paper in order to get the most out of my critique of it [2]. Meal frequency research is becoming increasingly more active, so it’s safe to predict that in the coming years, more relevant designs will narrow the gap between the questions and answers. Something I can wholeheartedly agree with is the paper’s closing quote: “Nonetheless, more well-designed research studies involving various meal frequencies, particularly in physically active/athletic populations are warranted.”


References

1.      Campbell B, et al. International Society of Sports Nutrition position stand: protein and exercise. J Int Soc Sports Nutr. 2007 Sep 26;4:8. [Medline]
2.      La Bounty PM, et al. International Society of Sports Nutrition position stand: meal frequency. J Int Soc Sports Nutr. 2011 Mar 16;8(1):4. [Epub ahead of print] [Medline] [JISSN]
3.      Benardot D, et al. Between-meal energy intake effects on body composition, performance, and total caloric consumption in athletes. Med Sci Sports Exerc. 2005;37(5):S339. [MSSE]
4.      Deutz RC. et al. Relationship between energy deficits and body composition in elite female gymnasts and runners. Med Sci Sports Exerc. 2000 Mar;32(3):659-68. [Medline]
5.      Iwao S, et al. Effects of meal frequency on body composition during weight control in boxers. Scand J Med Sci Sports. 1996 Oct;6(5):265-72. [Medline]
6.      Mettler S, et al. Increased protein intake reduces lean body mass loss during weight loss in athletes. Med Sci Sports Exerc. 2010 Feb;42(2):326-37. [Medline]
7.      Varady KA. Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? Obes Rev. 2011 Mar 17. [Epub ahead of print] [Medline]
8.      Stote KS, et al. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J Clin Nutr. 2007 Apr;85(4):981-8. [Medline]
9.      Oyvind H, et al. The effect of meal frequency on body composition during 12 weeks of strength training. 12th Annual congress of the European College of Sport Science, 2007. [ECSS]
10.  Jenkins DJ, et al. Nibbling versus gorging: metabolic advantages of increased meal frequency. N Engl J Med. 1989 Oct 5;321(14):929-34. [Medline]
11.  Carlson O, et al. Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women. Metabolism. 2007 Dec;56(12):1729-34. [Medline]
12.  Holmstrup ME, et al. Effect of meal frequency on glucose and insulin excursions over the course of a day. Eur e-J Clin Nutr Metab. 2010 Dec;5(6):277-80. [e-SPEN]
13.  Harvie MN, et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond). 2010 Oct 5. [Epub ahead of print] [Medline]
14.  Garrow JS, et al. The effect of meal frequency and protein concentration on the composition of the weight lost by obese subjects. Br J Nutr. 1981 Jan;45(1):5-15. [Medline]
15.  Wilson GJ, et al. Equal distributions of dietary protein throughout the day maximizes rat skeletal muscle mass. The FASEB Journal, 2010. 24(740.17). [FASEB J]
16.  Paddon-Jones D, et al. Exogenous amino acids stimulate human muscle anabolism without interfering with the response to mixed meal ingestion. Am J Physiol Endocrinol Metab. 2005 Apr;288(4):E761-7 [Medline]
17.  Soeters MR, et al. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. Am J Clin Nutr. 2009 Nov;90(5):1244-51. [Medline]
18.  Arnal MA, et al. Protein feeding pattern does not affect protein retention in young women. J Nutr. 2000 Jul;130(7):1700-4. [Medline]
19.  Arnal MA, et al. Protein pulse feeding improves protein retention in elderly women. Am J Clin Nutr. 1999 Jun;69(6):1202-8. [Medline]
20.  Smeets AJ,  Westerterp-Plantenga MS. Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency. Br J Nutr, 2008. 99(6): p. 1316-21. [Medline]
21.  Cameron JD, et al. Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet. Br J Nutr. 2010 Apr;103(8):1098-101. [Medline]
22.  Leidy HJ, et al. The influence of higher protein intake and greater eating frequency on appetite control in overweight and obese men. Obesity (Silver Spring). 2010 Mar 25. [Epub ahead of print] [Medline]




My name is Martin Berkhan and I work as a nutritional consultant, magazine writer and personal trainer.

Welcome to the Internet's leading resource on intermittent fasting and all things related.


FeedBurner FeedCount

Google Friend Connect

Join Me on Twitter

Facebook

Follow Me on Facebook

Recommended Reading

Lame Title, Good Book

Recommended Reading

Intermittent Fasting for Fat Loss

Recommended Reading

Covers All Bases

Recommended Reading

Awesome Recipes for The Paleo Diet
Recipes for the Paleo Diet - Two Cookbooks - 120 Recipes Each!>

Recommended Reading

Fat Loss Made Easy

Great Interval Timer

+1 If You Think Leangains is Awesome