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Why does my breakfast make me hungry?

Warum macht mich mein Frühstück hungrig?

"Why does my breakfast make me hungry?" After someone asked me this question for who-knows-how-many times, I decided to delve deeper into the possible reasons and mechanisms. I thought it would be a good idea to share my thoughts on the subject with you.

The average person eats their breakfast

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

Welcome to the average guy, who is about as average as it gets - with all the implications that means he's fat, has poor insulin sensitivity and is out of shape - so he fits the standard of modern man used in the scientific literature.

The average guy sits down and eats his breakfast and, due to the influence of cortisol, his pancreas responds with a rapid and - relative to other times of the day when all else is equal - strong insulin release. This lowers blood glucose levels back to baseline more quickly than later in the day, which is a desirable effect in this context.

Although the food-induced insulin peak occurs much faster and is much higher due to the coincidence with the peak cortisol daily rhythm, the net effect should be that average insulin secretion and average blood glucose levels are lower during the breakfast phases than later in the day when food intake occurs at low cortisol levels. In some ways, our average guy's sluggish pancreas might even benefit from the increased insulin response in the morning.

That was our average guy. But what about an above average fit person? This is where things start to get interesting.

Insulin sensitivity and insulin resistance: a brief introduction

I've noticed something very strange and I've observed it far too often to dismiss it as coincidental.

When I first started dieting, I was doing well with a typical high meal frequency with the typical fitness-oriented, oatmeal-based breakfast. I started out quite fat at around 100 kilos and lost almost 20 kilos using a fairly generic approach.

Of course, I made rookie mistakes galore - especially in the cardio area where I overdid it - and suffered as a result. I had my setbacks - like everyone else - but I got through them all.

However, it took a while in terms of my leanness before breakfast started to become a problem. First of all, I always felt that it was an unnecessary caloric burden that interfered with my dieting. I wasn't hungry in the morning, but I was even hungrier in the evening.

Of course, if I had known better back then, I would have started skipping breakfast sooner, but back then everyone was preaching the important benefits of breakfast and I didn't really dare to break all those golden rules of fitness.

Secondly, it seemed like the post-breakfast hunger pangs would increase in both frequency and strength with every damn gram of body fat I lost after a certain point. At a certain point, this hunger became excessive and that's when I started to tread water in terms of progress. This continued until I decided to do my own research and stop swallowing the nonsense that so-called fitness gurus and other dubious sources were feeding me. The rest is history.

Anyway, let me put on my lab coat and explain to you how this fits in with everything I've told you so far. We have now reached the second key point in this hypothesis behind the phenomenon of hunger after breakfast. The first key point, as you may remember, was the Cortisol Awakening Response (CAR) and its maximum value, which coincides with breakfast.

The second key point is insulin sensitivity. What happens when a person with high insulin sensitivity eats something? In a nutshell, rising blood glucose levels send a signal to the pancreas and the pancreas responds with insulin. The insulin then transports the glucose from the blood to places where it is needed (e.g. liver and muscles), lowering blood glucose levels and preventing glucose from accumulating in the blood.

When blood glucose levels are elevated for an extended period of time (as seen in untreated type 2 diabetes, insulin resistance, poor insulin sensitivity, etc.) this causes all kinds of bad things to happen, which is the reason we should try to bring them back down to baseline as quickly as possible. This is the reason that high insulin sensitivity is a good thing.

When your body has a high insulin sensitivity, your pancreas responds quickly to glucose with a strong insulin surge, which slowly subsides when it is no longer needed. A rapid rise in insulin levels followed by a rapid drop. The net result is lower blood glucose and insulin levels after eating.

In contrast, insulin resistance results in a sluggish insulin response with a small insulin surge followed by a slow drop in insulin levels. The net result is higher blood sugar and insulin levels after eating.

Imagine a graph showing insulin release in the post-meal phase with time on the x-axis and insulin levels on the y-axis. Now imagine a pulse-like pattern for a person with high insulin sensitivity and a mountainous pattern for an insulin-resistant person - this is what it would look like.

An important point in the above scenario is that insulin levels reach a higher maximum in the person with high insulin sensitivity.

Insulin and blood glucose regulation

Remember that cortisol increases insulin secretion. If you have high cortisol levels (e.g. at peak CAR) and eat something, insulin secretion will be boosted. Your pancreas reacts faster and more strongly.

But our fit example person already has a really robust insulin response because they have a high insulin sensitivity. And now add to that the enhancing effect of CAR on insulin secretion. What do you get? In theory, a very strong and sharp insulin pulse. And what is the consequence of this?

In other words - just as an example - what is the consequence of injecting too much insulin relative to your needs? If you overdo it with this, you risk all the serious consequences of life-threatening hypoglycemia, resulting in extreme hunger, confusion, coma, brain damage and death - in that order.

While the above is a real danger for diabetics, there is no such danger for healthy individuals. Over the course of evolution, we have developed an extremely efficient regulatory system to prevent our blood sugar levels from dropping too low, to the point where our bodily functions and cognition are impaired and our chances of survival are reduced.

In fact, blood glucose regulation is a very safe system with redundant mechanisms that are able to increase glucose release to meet our needs even if one system fails. Glucagon, epinephrine (adrenaline), cortisol and growth hormone are different hormones that work together to fulfill each other's role in the event that one cannot do its job properly.

But this system has not evolved to take care of blood sugar levels that are just low enough to trigger hunger without having serious side effects beyond that. In fact, low blood sugar levels as a hunger signal were the focus of one of the earliest theories of appetite regulation.

Why does breakfast make the average fit person hungry?

As part of the "glucostatic theory", Jean Mayer postulated in the 1950s that blood sugar served as the primary hunger-inducing signal that made us want to eat (Mayer, 1953). Later studies have taught us that appetite regulation is far more complicated, but that blood sugar plays a clear role in the equation.

Building on Mayer's theory, Campfield proposed a more complex and refined theory in which, in brief, he suggested that falling blood glucose levels could serve as a hunger signal (Campfield & Smith, 2003). This has been echoed elsewhere in the sense that the rate at which blood glucose levels fall may in some sense serve as an alarm signal - while a prompt drop in blood glucose levels after eating is desirable, too sharp and rapid a drop may be interpreted as a danger and trigger a hunger signal.

So if our insulin-sensitive, fit person eats their breakfast directly to the maximum value of the Cortisol Awakening Response (CAR), then a lot of insulin is released in response to this meal, resulting in a rapid drop in blood glucose levels.

Now let's look at the meal itself. What does the typical breakfast of a fit person look like? Chances are that this meal is high in protein and carbohydrates, low in fat and quite often includes a source of dairy or milk protein. Each of these components independently contributes further to insulin secretion.

As a consequence of the above, hunger rears its ugly head shortly after a meal. Either as a result of blood sugar levels dropping a little too low or as a result of it dropping too quickly within a narrow window of time.

Let's put it all together

And that, my friends, was my abbreviated version of the explanation for post-breakfast hunger. When I think about it a bit, it fits perfectly with my personal experience, my observations and many anecdotes I've heard over the years.

Hunger after breakfast is something that occurs more frequently and to a greater extent in fairly lean people. I would estimate that this phenomenon is quite common in the 12 to 14% body fat range. And as you approach a single-digit body fat percentage, this phenomenon is indeed quite common - and becomes a serious obstacle for many.

As we get leaner, our insulin sensitivity gradually improves. And as insulin sensitivity increases step by step, we get hungry faster after breakfast and this hunger becomes more and more annoying until we finally wonder why we feel like we are starving 1 to 2 hours after a reasonable sized meal.

In a sense, it's funny that blood sugar regulation works best in the fasting state and not in the aforementioned breakfast scenario. This becomes understandable when you consider that in the fasting state there is a balance between supply and removal - in this case glucose and insulin. Blood glucose levels are low and are well maintained by low insulin levels in a person with good insulin sensitivity.

After breakfast, clearance is disproportionate to intake (breakfast) due to cortisol - an imbalance that would not occur in other circumstances (i.e. the same meal later in the day with low cortisol or in a person with lower insulin sensitivity).

All this raises interesting questions about the role of the cortisol-insulin link - or breakfast consumption and adaptation (or lack of adaptation) in the course of human evolution and its consequences for modern humans with their modern meal pattern.

This is very interesting indeed when you consider the events that take place at a metabolic and transcriptional level when you combine cortisol and insulin. Not to mention the role of cortisol in conditioning and getting leaner and the fact that even if breakfast first thing in the morning is an artificial habit coined by one of the first and possibly biggest giants of the food industry (Kellogs), this habit is certainly one that we get into very quickly.

But that's a topic for another time. Or for another person intelligent enough to recognize the references to something I've just made - always assuming anyone cares at all.

Final reflection

In conclusion, I would like to emphasize that there are a few things I had to leave out, as this article has already become quite long. I should perhaps at least mention these briefly and succinctly by saying that there is a high degree of individual variance in the Cortisol Awakening Response and that this could also influence insulin secretion (i.e. a stronger Cortisol Awakening Response could have a greater influence on food-induced insulin secretion).

In addition, food and macronutrient choices obviously play a large role in all of this, but this role may be different than most would expect. For example, some protein sources - or should I say amino acids - are not only highly insulinogenic, but also elicit a cortisol response. Coincidentally, these tend to be the protein sources that are often consumed at breakfast.

Perhaps I should mention that protein can elicit a cortisol response depending on the context (Benedict et al., 2005; Gibson et al., 1999; Slag et al., 1981). Oh, you thought it was the other way around - that protein lowers cortisol levels? Well, then you've learned something new today.

References

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  2. 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
  3. 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
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  6. 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.
  7. MAYER, J. (1953). Glucostatic mechanism of regulation of food intake. The New England journal of medicine, 249(1), 13-16. doi:10.1056/NEJM195307022490104
  8. Newport, D.J. and Nemeroff, C.B. (2002) Stress. In: (Ed. in chief), Encyclopedia of the Human Brain, Vol. 4. Elsevier, pp. 449-462.
  9. 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
  10. 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.
  11. 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
  12. 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

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