“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.
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).
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.
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.
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.
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- 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