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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.”






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.






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.





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.







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 


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

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

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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.

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In this article I'll be using "cheat day" and "feasts" interchangeably but they are both synonyms for short-term overfeeding of various durations and magnitudes. The same general principles will apply, more or less. A "refeed" is often used in the context of a structured diet approach. It tends to be more strict and planned in terms of macronutrient composition (high-carb, low-fat.)

While I will discuss refeeds in brief, this article will mainly discuss overfeeding of a mixed diet - that is, what you should take into consideration on Thanksgiving, at the Christmas dinner table, or any other occasion where you will be presented with lots of tasty foods.

My plan is not to tell you exactly what to eat or how much of it - that would be absurd. I don't encourage someone to count calories on Thanksgiving Day or similar such occasions. Instead, I'll talk about some factors that will determine how much fat you end up putting on and how you can potentially reduce the time spent making up for your splurging.

First, let's look at the general effects of overfeeding and do some myth debunking in the process.



Effects of Overfeeding

I tend to look at cheat days and feasts mostly as psychological relief and fun, but you'll often see some overly optimistic claims about cheat days being made in the fitness community; how it boosts your metabolic rate and tricks your body into "fat burning mode" for the rest of the week. There's some truth to this, but the real impact of cheat days are exaggerated if you look at the numbers you're dealing with.

Studies on overfeeding shows that metabolic rate typically increases about 6-8% for up to 24 hours after feeding. There's also large differences in between individuals, illustrated by the fact that the magnitude of the increase ranges from 3-10%. Those prone to obesity ("thrifty" phenotypes) tend to be in the lower range (3%), while the naturally lean ("spendthrifty" phenotype) tend to be in the upper range (10%). Either way, from a fat loss perspective it's not really justified to eat thousands of surplus calories to burn a few hundred calories extra.

The other argument, about tricking your body into fat-loss mode, usually alludes to the effect of overfeeding carbs on leptin. For a lean person, or for someone one a prolonged dieting stint, low leptin is an issue. This hormone, the king of hunger regulation, controls metabolic rate, appetite, motivation and libido, among other things. Leptin drops whenever your body senses a calorie deficit and when fat mass is lost.

The reverse happens when your body senses a calorie surplus. A surplus temporarily boosts leptin, which leads to downstream effects on fat oxidation, thyroid, dopamine and testosterone. In the context of dieting, refeeds are therefore beneficial.

However, similar to the effects of overfeeding on metabolic rate, a leptin-boost is also rather transient and drops again once you resume your diet and your body senses the deficit. It's for this reason I prefer to use frequent but moderate overfeeding, or refeeds, as part of the Leangains approach. Usually in conjunction with weight training to take advantage of the anabolic effects.

What macronutrient causes the greatest boost in leptin calorie per calorie? The hierarchy looks like this:

1. Carbohydrate. (Glucose - not sucrose or fructose.)

2. Protein. Glucose is superior to protein, but I suspect it might be a better choice to sucrose or fructose. (I'm quite sure that protein hasn't been compared to sucrose and fructose, but I'll look into it just in case.)

3. Dietary fat.

4. Alcohol. Ethanol has not been directly compared to the other macronutrients. However, the effect is a negative one. While one study actually found a positive effect on leptin, most studies point towards an inhibitory effect. Strangely, a reverse effect has been seen in women from red wine. I wonder if this has something to do with the fact that alcohol consumption is associated with lower body weights in women but not men. I'll have to look into that.

Due to the superior effects of carbs on leptin, and leptin's downstream effects on metabolism and anabolic hormones, a high-carb, moderate-protein and low-fat refeed is traditionally recommended for dieting purposes.

Lyle Mcdonald has written a great deal on this topic, most extensively in "The Ultimate Diet 2.0." Though I am no fan of the diet itself, the book is a tremendous resource for anyone interested in the physiology of dieting and its impact on various hormonal parameters.

Lyle has also written a lengthy and detailed article series on leptin. I highly recommend it if this topic piques your interest: "Body Weight Regulation: Leptin Part 1."

However, a low-fat, high-carb refeed is obviously not so doable during Thanksgiving Day, Christmas, or any other such occasions. A few different factors should be taken into account on cheat days and feasts.

This is a quick primer on nutrient metabolism, as it will help you understand some of the concepts discussed later on.

The easiest way to think about nutrient metabolism is in terms of the Respiratory Quotient (RQ) and insulin. They are associated - when insulin is high, RQ is high, and vice versa. Here's a quote from "Intermittent Fasting and Stubborn Body Fat":

"After you eat, insulin and fatty acids are elevated. You are in the fed state and there's zero fat burning going on. Your body is relying completely on glucose oxidation during the hours following the meal."

This doesn't mean that you'll be burning more body fat if you follow a low-carb high fat diet, or that you'll never burn fat on high-carb diets. In energy balance, 24-hour RQ is reflective of the macrocomposition of the diet rather than fat gain or fat loss per se. Dietary fat has insulin-independent storage mechanisms (ASP) and "fat balance" (net storage of dietary fat) is primarily dictated by total calorie intake at the end of the day. The time course and trend in substrate metabolism will be different dependent of the carb:fat-ratio, but not the net effect.

Overfeeding elevates RQ for several hours - up to a day even - and indicates that glucose metabolism is dominant. Since glucose metabolism is high, fat burning is low or insignificant. This metabolic state allows net storage of dietary fat. Carbs, protein and alcohol all elevate RQ and affects fat burning negatively. Dietary fat does not affect RQ but has insulin-independent ways of getting into fat cells.

Knowing this is, are there some ways to limit fat gain in mixed-diet overfeeding or is it all about calories? To answer this, let's look at the energy costs for fat storage of various macronutrients.

During overfeeding, surplus calories are stored as fat with a great deal of varying efficacy.

The energy cost for storage of dietary fat is minimal (0-2% depending on saturation.)

The conversion of carbs to fat, de novo lipogenesis (DNL), is hardly significant in humans and usually only occurs when glycogen stores are saturated (i.e. prolonged high-carb overfeeding). This does not matter much in practical terms, as there will be plenty of dietary fat in mixed-diet overfeeding. Carbs promote fat gain by reducing fat oxidation, as explained before. There's some variance between individuals here, based on genetics, metabolic state and habitual diet-patterns. Enzymes that modulate DNL are up-regulated in habitual high-carb diets and in the obese. Another factor that play a role is insulin sensitivity. There are similar individual aspects to the storage of dietary fat as well (mediated by LPL and ASP.)

In metabolically healthy humans, the energy cost for DNL is approximately 25%. In practical terms, this means that 3 out of 4 calories can be used for fat synthesis once a "carbohydrate surplus" is achieved (after saturated glycogen stores). Given that glycogen stores are never full in conditions of energy balance, people have a large "carb-sink" to use up before carbs contribute to fat gain directly. (Until then, the effect of carbs is indirect via suppression of fat metabolism. Am I being redundant yet?)

The above is in particular reference to glucose; sucrose and fructose are more lipogenic due to some differences in metabolic pathways. Fructose do not go to muscle glycogen stores, but to liver glycogen - and this glycogen depot is significantly smaller than muscle glycogen. One study comparing DNL from glucose and sucrose overfeeding in lean and obese people, showed DNL to be 10% and 20% higher respectively after the sucrose-experiment.*

* From results: "The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group." Which means that the difference (10-20%) was not enough to be deemed significant from a scientific standpoint. Fructose-overfeeding has not be compared to glucose in a controlled study, but judging from this study, DNL would likely be substantial (sucrose is half fructose, half glucose)