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So for these reasons, I am thankful to Alan Aragon for the aptly titled 'Intermittent fasting: After over a decade of research, where are we today?' in which he writes about the current state of affairs of intermittent fasting. The article appeared in the December edition of the Alan Aragon's Research Review (AARR) which I have been a subscriber of since the first issue.

I asked Alan for permission to publish the article on my site, as I had a few comments on the content therein, and housed no doubts that our readership would be interested in taking part of it all. You'll find that most of my thoughts doesn't have to do with the article itself, but rather with some of the statements and issues raised.

Alan has previously published A Critique of the ISSN Position Stand on Meal Frequency on this site. If you enjoy reading about nutrition and exercise with a scientific twist, check out Alan Aragon's Research Review.

Now enjoy this article, folks. You will find my comments prefixed with MB after the relevant paragraphs below.

Intermittent fasting and body composition: After over a decade of research, where are we today?

Speaking of decades...

The last time I wrote an article about intermittent fasting (IF) was almost a decade ago. A rich body of research on the topic has been published since then. The ongoing interest in IF is not surprising, given its mystique that’s wrapped in ancient spiritual origins, all the way to its modern applications to clinical and aesthetic goals. The aim of this article is to bring the reader up- to-date on the scientific findings, with a particular focus on comparing IF regimes with conventional/linear dieting. After all, the question is not whether IF works – it obviously does, as does any mode of caloric restriction. The question is whether it works better than conventional dieting for improving body composition, and if so, to which contexts can we apply it.

Variations on a theme

Let’s get some labeling/classification aspects out of the way. In the literature, the broad categories that I call linear and non- linear dieting have been called daily caloric restriction and intermittent caloric restriction, respectively. They have also been called continuous energy restriction and intermittent energy restriction. The intermittent category (what we call IF) can be further divided into three subclasses (1):  alternate-day fasting (ADF), whole-day fasting (WDF), and time-restricted feeding (TRF).

Alternate-day fasting

The most extensively studied IF variant is ADF, which typically involves a 24-hour fasting period alternated with a 24-hour feeding period. Complete compensatory intake on the feeding days (to offset the fasting days’ deficit) does not occur, and thus total weight loss and fat loss occurs on ADF. Lean mass- retention has been an intriguing effect of ADF reported by Varady et al (2-4). Lean mass loss in ADF conditions has also been observed by other investigators (5-7). However, the latter effect might be attributable to more severe energy deficits. The more lean mass-friendly The ‘fasting’ period in the Varady model is actually an energy-restricted period (~25% of maintenance requirements, typically in the form of a single meal at lunchtime) alternated with a 24-hour ad libitum (as desired) feeding period.

On the note of alternating fasting and feeding periods of the same length, alternate-week energy restriction (one week on ~1300 kcal/day, one week on the usual diet) has only a single study to-date, but is worth mentioning since it was as effective as continuous energy restriction for reducing body weight and waist girth at 8 weeks and 1 year. (8)

Time-restricted feeding

TRF typically involves a fasting period of 16-20 hours and a feeding period of 4-8 hours daily. The most studied form of TRF is Ramadan fasting, which involves approximately 1 month of complete fasting (both food and fluid) from sunrise to sunset. Unsurprisingly, significant weight loss occurs, and this includes a reduction in lean mass as well as fat mass (11-12). 

Aside from Ramadan fasting studies, there’s a scarcity of human TRF research in the peer-reviewed literature. Stote et al (13) compared 1 versus 3 meals per day in eucaloric (weight–maintenance) conditions for 8 weeks and surprisingly found 1 meal resulted in fat loss and lean mass gain, while no significant improvements were detected in the 3-meal group. Unfortunately, the use of bioelectrical impedance (BIA) keeps these results questionable. Perhaps the only other longitudinal TRF study was done back in 1971 by Young et al, (14) who found no significant differences in weight loss and body composition change between 1, 3, or 6 meals per day

As for TRF programs in the lay press, Hofmekler’s Warrior Diet (15) published in 2002, was perhaps the first popular diet book to expose the general audience to TRF for weight loss. It involves a 4-6 hour feeding period at night, and an 18-hour “under-feeding” period during the day. The diet draws inspiration and justification from the purported habits of our Stone Age ancestors, as well as other leaps of faith involving the sympathetic and autonomic nervous systems. 

Berkhan’s Leangains system of TRF has a 16-hour ‘fasting’ period and an 8 hour feeding period (16). What separates this protocol from others is its attention to macronutrition, and its administration of branched chain amino acids (BCAAs) during the fasting period. As a matter of trivia that you might enjoy, Hofmekler and Berkhan’s were recently referenced in the peer-reviewed literature (17).
MB: Let me translate that. What Alan means to say is that Hofmekler's Warrior Diet is full of pseudoscientific nonsense and I agree wholeheartedly. 

Article continues...

The most comprehensive systematic review on IF to-date

Seimon et al (18) recently published the largest systematic review of IF research to-date. Importantly, they compared the effects of intermittent energy restriction (IER) to continuous energy restriction (CER) on bodyweight, body composition, and other clinical parameters. Their review included 40 studies in total, 12 of which directly compared an IER with a CER condition.

They found that overall, the two diet types resulted in “apparently equivalent outcomes” in terms of bodyweight reduction and body composition change. In addition, neither IER or CER was superior to the other at improving glucose control/insulin sensitivity. No different effects on thyroid, cortisol, and sex hormones were seen between IER and CER, though the authors concede that there’s insufficient research comparing neuroendocrine effects of the two diet types to draw definitive conclusions in this area.

Interestingly, IER was superior at suppressing hunger. The authors speculated that this might be attributable to ketone production in the fasting phases. However, this effect was somewhat immaterial since it failed to translate into superior improvements in body composition or greater weight loss.

MB: Well, that's not quite true. These studies didn't have a suitable control group, as the participants served as their own controls. Thus, you can't say that it didn't translate into "superior improvements in body composition or greater weight loss" - it might have done so for that that group, even if that conclusion can't be drawn from the collected brunt of data. That's the problem with these systematic reviews Like it says in the paper:

Only 12 of the 40 publications included in this review directly compared IER with CER: the lack of direct comparison makes it difficult to determine whether IER is superior to CER, or for whom.

- Seimon, et al. (2015)



Article continues...

Limitations of the review included the standard ones – relatively small sample sizes, relatively short trial durations, and heterogeneous study designs making comparisons outside of the same study difficult. An acknowledged limitation worth highlighting was that 14 of the 40 studies were by the same research group (Varady et al, University of Illinois at Chicago). Ideally, a more diversified and less concentrated set of labs is less likely to repeat the same errors or preserve the same biases.

Speaking of the potential for bias, Varady has published a lay- directed book titled, The Every-Other-Day Diet (19). I’m not claiming that Varady is destined to make sure her ADF study results will always square up with her book, but it’s one of the potential caveats nevertheless. I would add to these limitations that there’s a severe lack of IER (and IER vs CER) studies that include a structured training component.

Of the 152 industry-funded studies she has examined, 140 boast results that favor the funder. That's more than 90 percent.

- Food companies distort nutrition science. Here's how to stop them.


If you want to read more about this topic as it pertains to nutritional science, check out Marion Nestle and her writings. She's quite brilliant.





Why Calories Count by Marion Nestle. I found this book in a large box of bullshit that I ordered from Amazon two years ago. It was the only thing worth scavenging and I intend to read it after I'm done with a few horror novels. I figure that I'd be properly warmed up by then. A book about food politics and marketing shenanigans can get quite dark and depressing no doubt.


But food companies are as unlikely to fund research on intermittent fasting, as Coca Cola is unlikely to fund research on ketogenic diets. What Alan brings up is the potential for bias on the researcher's part, Krista Varady to be specific. Aside from researching intermittent fasting, she is also involved in selling books, namely books based off of the research she is doing. What gives?

Well. While I haven't read The Every-Other-Day Diet, but I have mixed feelings about Krista Varady. She does try a bit too hard for my liking. I covered her work* before in "Intermittent Fasting For Weight Loss Preserves Muscle Mass?" back in the days and found several problems. Note that I'm wrongfully referring to Varady as "he" in that article. In short, she published a pretty shitty review of the subject, but then again, there weren't that many data points around in 2011. Five years later, it's gotten a little better, but there's still not enough good data around to draw any definitive conclusions - and like Alan says, a lot of that data comes from the same lab (Varady's).

It's worth mentioning that Varady appeared in a laughable infomercial documentary called "Eat, Fast and Live Longer" on BBC Horizon. In it, Michael Mosley - the show host and soon-to-be-author, interviews researchers working in the field of intermittent fasting and Varady is one of them. After rewatching the segment she appeared in, I found her to be matter of fact and professional even though she dutifully suffered through all the TV show gimmicks thrown at her - they gorged on hamburgers and fries to show that you could stuff your face and still lose weight on ADF, for example.

By the way, this "documentary" served as a launching pad for Michael Mosley's worthless book The FastDiet. Seems like there was some kind of falling out between Varady and Mosley after that. Anyway. Don't waste your money. If you want a book on intermittent fasting, pick up Eat Stop Eat.

Now, speaking of Varady, there's nothing wrong with pushing your agenda, but don't shove it down peoples throats by publishing bad research and doing shady shit like failing to disclose your conflicts of interest, because that makes you suspect in my eyes.

That said, there's nothing fishy about her recent work, as far as I can tell. It's entirely possible that Varady and her colleagues got together one night and decided amongst themselves to doctor the results, but I find that very unlikely.





It's kind of spooky, but a client just sent me this two minutes ago. I'm mentioned on the same page as Mosley and Varady, and I'm reading it just as I finish up this paragraph. I believe he was reading a book by his doctor, Robin Willcourt. I'll have to ask about the title, so I'll add it here later for those interested. Update: Name of the book is  Chasing Antelopes: Why All This Caused All That


When fuckery strikes in science, it's usually a lot more subtle and sinister. I would know, because years ago, I approached Alan with this subject. See, I had uncovered some sophisticated tampering with the results of a study that received a lot of spin on social media and the mainstream news. I was slightly distressed over the fact that he had missed it - the studies appeared in the AARR, not only once, but twice - and presented my findings. I needed a second opinion, because maybe I was making a hen out of a feather.

Nope. Alan agreed, it was some shady shit. In fact, it was a case study in deceit. Career-ending, if you ask me. But to this day, no one has debunked the findings, and the researcher is still active; polluting the journals with more bullshit for every new study that gets published. Who knows, maybe one day I'll put an end to it.

The key point of all this, is that science can't be trusted for shit, unless you do your due diligence and read the fine print. But in this particular case, concerning Krista Varady, I'm not worried.


Article continues below...


This limitation also plagues the body of research comparing various within-day meal frequencies. Readers familiar with my work know that Brad Schoenfeld, James Krieger, and I did a meta-analysis on the effect of meal frequency on body composition, and found that higher meal frequencies were associated with greater losses of fat mass and greater retention of lean mass (20). However, sensitivity analysis revealed that the removal of a single study (21) completely eliminated the significant effect of meal frequency on changes in body composition.

It’s worth noting that the studies in our analysis (and in this entire body of literature) lacked sufficient protein. An exception was Arciero et al (22) who found that 6 meals per day at 35% of total kcal as protein was superior to 3 meals per day for reducing total body fat and abdominal fat. Furthermore, 6 meals per day increased lean mass despite hypocaloric conditions.


MB: Sure thing. Something like that only happens in a study sponsored by EAS, Alan.
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What about muscle gain? 

The retention of lean mass in IF studies has been seen repeatedly. However, the question of muscle gain via IF remains unanswered since the investigative focus of IF research has been on weight/fat loss and accompanying clinical effects. No IF studies in the current literature have focused on the goal of gains in muscle size and/or strength. As such, No IF studies to-date (at least none that have passed peer review) have included a structured, progressive resistance training program.

This is untreaded ground fresh for the taking by researchers with the desire to do so. With that said, a poster presentation by Tinsley et al (23) at the The 12th ISSN Conference and Expo provided a summary of their study that compared the effects of TRF (on non-training days, all calories consumed in a 4-hour period) and progressive esistance training (RT) 3 days a week for 8 weeks – versus an RT group presumably on their usual diet. No between-group differences were seen in body composition, but interestingly, TRT+RT outperformed the RT in leg press maximal strength and in bench press endurance. The full text of this will be interesting to dig into if/when this study makes it into publication.

The Editor’s Cut of the May 2012 issue of AARR pondered the question of what might be the lower threshold of meal frequency for optimizing muscle gain. I concluded that this threshold, based on what we knew at the time, was probably 3 protein-rich meals. I contended that a lower daily meal frequency than that would compromise maximal rates of muscle gain. Since that time, a replication of well-controlled studies has shown the superiority of 4 doses of 20 g whey eliciting a stronger anabolic response during a 12-hour period than 2 doses of 40 g or 8 doses of 10 g (24, 25). These findings made me re-think my position of a 3- meal minimum. It’s plausible that folks with the goal of maximizing rates of muscle gain should look to a minimum of 4 daily doses of protein at of at least 20-40 g (older subjects require 35-40 g to maximize the anabolic response). (26-28)



MB: This is all nice and dandy in theory, if it weren't for the fact that...

1. The studies that made Alan "re-think" his position of a 3-meal minimum are all funded by Néstle - a controversial company who likes to be addressed as the “world’s leading nutrition, health and wellness company.” The former Néstle-owned supplement company Musashi supplied the whey protein used in at least one of the two studies Alan cites.

Remember the quote from Marion Nestle - no relation to the company Nestlé - earlier in the article? Here it is again:

Of the 152 industry-funded studies she has examined, 140 boast results that favor the funder. That's more than 90 percent.

If you think the supplement industry is any different, you're batshit crazy. I'm willing to go out on a limb and say that it's closer to a 100% when it comes to the supplement industry.


2. The results obtained in these studies are unlikely to be relevant for real-world eating habits and real-world results.

However, it is important to note that this response was characterised when protein was ingested alone, and as the authors acknowledge, this finding cannot be evaluated in the context of a mixed meal. Indeed, it is commonplace to consume protein in the form of a mixed-macronutrient meal. Therefore, it is reasonable to postulate that macronutrient co-ingestion could alter intestinal transit, thus influencing amino acid absorption kinetics (Deutz et al. 1995) and perhaps MPS. Moreover, this study used high-quality whey protein

Of course, the big limitation is that acute studies can measure protein synthesis but they can’t measure changes in body composition. Recent work by MacKenzie-Shalders found no significant difference in lean mass increase between a high protein intake (2.6-2.7 g/kg) spread across 4 vs 6 meals in elite rugby players. This findings are interesting, but once again, 3 meals per day remains a gray area in the question of a minimum for maximizing muscle growth. Perhaps future studies will compare 3 meals versus 5 or 6 for this purpose – while imposing an energy surplus and a progressive resistance training program. Seems like just a matter of time before someone in the current or newer generation of researchers attacks this gap in the literature.

Concluding perspectives & applications 

IF has proven itself to be an effective approach to dieting, and has outperformed conventional dieting in some cases. In the interest of cohesion to the topic, this article didn’t delve into IF’s effect on athletic performance. However, it’s important to keep in mind that IF protocols can compromise performance goals if careful modifications are not made. In general, IF is best applied to goals oriented toward altering body composition and clinical markers that occur alongside body fat reduction. This is not to say that muscle gain cannot occur with IF – it’s just that the rates of gain will not likely be maximised.

As for which IF variant to chose (ADF, WDF, TRF, etc) if one decides to try IF, the good news is that they all have demonstrated effectiveness in the literature, and therefore can be chosen on the basis of personal preference. Just remember that there is no special metabolic magic in IF, just like there’s no stoking the metabolic furnace with 6 meals a day.


Article ends.

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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.