Nutrition

The hidden fat loss hormones
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Control them and get hard and defined more easily

When you think of hormones, especially in the fitness and bodybuilding world, you probably think of things like testosterone, insulin, cortisol and growth hormone. You probably won't think of GLP and GIP.

GLP and GIP are hormones of the digestive tract and your ability to get hard and defined can stand or fall with them. The funny thing is, most people have never heard of these hormones and even experts didn't fully understand their full impact until recently.

The unexpected revelations of a gastric bypass

Gastric bypass surgery has become the treatment of choice for severely obese patients. This surgery can also be seen as proof that the calorie model of metabolism is correct.

When this surgery was originally developed, the idea was to reduce the volume of food that could be eaten. It was believed that the observed fat loss was based solely on the fact that patients were eating less or absorbing less food. It was believed that this reduced calorie intake was the only reason for the weight loss.

If you physically reduce the size of the stomach, then the patient can't eat as much as before and loses weight. That was the theory and reducing calorie intake definitely plays a role. But is that the whole story?

Slowly, a new understanding of what is happening developed. There is an unintended and only recently discovered consequence of these gastric bypass operations: reduced hunger and (to a lesser extent) reduced cravings. How can this be? This surgery does not take place in the brain, which is the area that controls these feelings.

Even more interesting is the fact that in a high percentage of patients who suffered from diabetes or insulin resistance before the surgery, these problems disappeared completely. Imagine that before the surgery you were plagued by constant hunger, insatiable cravings and diabetes and as you recover from the surgery you realize that your hunger and cravings have disappeared and your diabetes has been cured.

What is happening here?

The positive effects that this surgery has on metabolism and weight loss are not simply a matter of calories, but are related to an unintended manipulation of the endocrine properties of the mucous membranes of the digestive tract. Endocrine in this context refers to the hormonal activity of the digestive tract.

The digestive system is not simply a place where food is digested and absorbed. The digestive system also secretes hormones.

In order to absorb food and regulate metabolism, the body needs a way to enable communication between the brain, pancreas and other organs and tissue types regarding the type of food being fed. Is the food a large bowl of sweet cereal that requires a large amount of insulin? Or is it a huge steak that will linger in the stomach for a while to be digested?

Our digestive tract is lined with sensory cells that "examine" the food that has been eaten. These cells provide the body with information about the quantity and composition of the food consumed and send signals via hormones/peptides to the brain, pancreas, fat cells, etc.

It is now believed that these hormones of the digestive tract are the primary mechanism by which these operations exert their effects.

GLP and GIP

The glucose-dependent insulinotropic peptide (GIP) and the glucagon-like peptide (GLP) are probably the two most important hormones. These hormones are also known as incretins.

These two hormones switch off hunger in the brain and stimulate the release of insulin as soon as they perceive large amounts of glucose. These two hormones are the reason why glucose injected directly into a vein causes much less insulin to be released than the same amount of glucose consumed.

GIP is secreted by so-called K sensory cells that line the digestive tract in the upper small intestine where food leaves the stomach (the duodenum). GLP is secreted by the L sensory cells, which are also located in the duodenum, but have a higher concentration in the lower part of the intestine.

With gastric bypass, GIP concentrations are reduced while GLP levels are increased. This is because the area of the intestine that contains most of the GIP-secreting cells is bypassed and no longer has contact with the food, while most of the areas that secrete GLP remain intact.

GIP and GLP have very different effects on metabolism, they both suppress appetite and both cause insulin secretion (but only in the presence of glucose). Obese people and diabetics have reduced GLP activity and the influence of GIP on the pancreas is suppressed.

GPL has several effects that make it very beneficial for diabetics and obese people compared to GIP. GLP reduces the levels of the hormone glucagon - a hormone that is out of control in diabetes and causes glucose to be continuously released from the liver. GLP also helps the body to produce new, more functional pancreatic cells, restoring the correct function of the insulin mechanism.

GLP also reduces the breakdown of muscle tissue. It also slows down the release of food from the stomach, which means that other hunger hormones (such as ghrelin) remain suppressed for longer.

All of this leads to more GLP, less GIP, lower glucagon levels (which normalizes blood sugar), restoration of insulin sensitivity and reactivity, suppressed appetite, reduced cravings and increased fat burning. These changes positively influence the amount of calories consumed.

Note: We do not yet know how long this effect lasts, as some patients regain the weight they have lost over the years, but rarely to the weight they once had.

What does this mean for us?

All of this shows us that weight loss is not simply a matter of calorie math, but involves complex interactions of hormonal biochemistry.

Most people do not need to undergo expensive and risky surgery to reap the same effects and benefits. GLP and GIP levels can also be manipulated with food. Fiber (especially viscous fiber), protein, bitter foods, probiotics and other factors are also able to manipulate the sensory cells of the digestive tract, thereby reducing hunger, helping with cravings and restoring insulin sensitivity.

How can you use this science for fat loss?

  1. Use GIP and GLP to your advantage by eating foods that stimulate their appetite suppressing effects but not their insulin stimulating effects. This means protein, fat and fiber without starch and sugar. Protein, fat and fiber will all have an impact on GIP and GLP, and as long as you don't eat large amounts of starch or sugar during the same meal, you will get full faster and stay full longer.
  2. Never combine fat and starch/sugar. This combination will greatly increase GIP levels and lead to higher insulin secretion over time.
  3. Choose viscous fiber. This type of fiber lines the digestive tract and makes it "think" there is more food in the digestive tract than there really is. Using a fiber-based drink as a snack is an excellent way to take advantage of this effect. The best fibers for this purpose are oat bran, acacia and glucomannan. But be careful, because if these fibers are consumed in combination with sugar or starch, you can achieve exactly the opposite effect. Remember that you are using fiber to control your appetite, not to eliminate it. Avoid products that are designed to eliminate appetite and are overloaded with sweeteners.
  4. Eat the right carbohydrates. High-fiber carbohydrates such as non-starchy vegetables and less sweet fruits have the best fiber to sugar/starch ratio. These are the carbohydrates you should prioritize.
  5. Branched-chain amino acids - and leucine in particular - can have a special effect on GLP. A BCAA supplement that is used as a snack and not simply to promote post-workout recovery may be a wise choice.

References

  1. Shalev A1, Holst JJ, Keller U. Effects of glucagon-like peptide 1 (7-36 amide) on whole-body protein metabolism in healthy man. Eur J Clin Invest. 1997 Jan;27(1):10-6.
  2. Vendrell J1, et al. Study of the potential association of adipose tissue GLP-1 receptor with obesity and insulin resistance. Endocrinology. 2011 Nov;152(11):4072-9. doi: 10.1210/en.2011-1070. Epub 2011 Aug 23.
  3. Chen Q1, Reimer RA. Dairy protein and leucine alter GLP-1 release and mRNA of genes involved in intestinal lipid metabolism in vitro. Nutrition. 2009 Mar;25(3):340-9. doi: 10.1016/j.nut.2008.08.012. Epub 2008 Nov 26.
  4. Bueter M1, le Roux CW. Gastrointestinal hormones, energy balance and bariatric surgery. Int J Obes (Lond). 2011 Sep;35 Suppl 3:S35-9. doi: 10.1038/ijo.2011.146.
  5. Tadross JA1, le Roux CW. The mechanisms of weight loss after bariatric surgery. Int J Obes (Lond). 2009 Apr;33 Suppl 1:S28-32. doi: 10.1038/ijo.2009.14.
  6. Shin AC1, Berthoud HR. Food reward functions as affected by obesity and bariatric surgery. Int J Obes (Lond). 2011 Sep;35 Suppl 3:S40-4. doi: 10.1038/ijo.2011.147.

By Dr. Jade Teta

Source: https://www.t-nation.com/diet-fat-loss/the-hidden-fat-loss-hormones

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The supplement dream team: BCAAs and glutamine!
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Although branched-chain amino acids (BCAAs) have many interesting properties on their own and can help to promote and optimize anabolic and anti-catabolic processes, BCAAs and glutamine represent a powerful synergistic combination that is in many ways clearly superior to the use of BCAAs or glutamine alone.

While BCAAs are the most abundant amino acids in muscle protein, glutamine is the most abundant free amino acid in the bloodstream and cells. Glutamine is essential for the function of the immune system and the cells involved in the regeneration and repair of muscle tissue. In addition, glutamine is said to have many other beneficial effects, ranging from healing the stomach lining to being used as a supplement to reduce cravings for alcohol and nicotine.

Similar to BCAA levels, it has been shown that there is a correlation between the concentration of glutamine in the body and the rate of protein synthesis. In other words, glutamine levels are a good indicator of an anabolic state. When blood glutamine levels are high, the chances of positive adaptations in muscle mass and strength in response to weight training are higher and low blood glutamine levels are a clear sign of overtraining and/or malnutrition. The synergy between BCAAs and glutamine exists because not only do both induce many of the same anabolic and anti-catabolic effects, but BCAAs can directly contribute to increasing glutamine stores under stressful conditions by serving as precursors for the formation of glutamine.

A combination of glutamine and BCAAs has been shown to dramatically improve nitrogen balance and reduce muscle breakdown in patients with burns and after major surgery. In addition, a relatively low-dose combination of 3 grams of BCAAs and 5 grams of glutamine has been shown to produce significantly greater gains in muscle mass and strength in athletes than whey protein alone. Anecdotal reports suggest that some athletes can make significantly greater gains when using higher doses of BCAAs and glutamine in conjunction with optimal nutrition and training. Although BCAAs and glutamine have many benefits on their own, the combination of these two supplements appears to significantly increase the potential benefits.

What is the correct dosage?

In order to maximize the numerous anabolic effects of BCAAs and glutamine, it is important that sufficiently high dosages are used. Although it has been shown that as little as 3 grams of BCAAs per day can provide benefits, studies using higher doses of BCAAs in the range of 20 grams per 50 kilograms of lean body weight show much more dramatic results. Even better results can be achieved during intense training phases or a strict diet with BCAA dosages of up to 0.45 grams per kilogram of lean body mass. The optimum dosage for this purpose can be easily calculated by subtracting the weight of the body fat from the body weight and multiplying the result by 0.45. So if you weigh 100 kilos and have a body fat percentage of 10%, then your fat-free body mass is 90 kilos, which, multiplied by 0.45, results in a quantity of approx. 40 grams of BCAAs per day.

The minimum dosage for glutamine is 0.1 grams per kilogram of lean body mass. However, significantly better results are achieved with dosages of between 0.2 and 0.45 grams of glutamine per kilogram of lean body mass. The same trainee with a body weight of 100 kg and a body fat percentage of 10% should therefore consume between 10 and 40 grams of glutamine per day, whereby the higher dosages make the most sense, particularly during intensive training phases in conjunction with a high calorie deficit and a reduced carbohydrate intake.

The right timing

Perhaps the biggest differences of opinion among experts in the field of BCAA or glutamine supplementation are regarding the correct timing of these nutrients. Depending on who you ask, you will get different answers. I think everyone agrees that the greatest physical stress on an athlete occurs during training sessions or sporting events. Since BCAA and/or glutamine supplementation provides its greatest benefits during these periods of peak stress, it makes sense that supplementation with these compounds should take place prior to training to ensure that high levels of BCAAs and glutamine are present in the body during exercise.

It is important to remember that dietary protein is broken down in the digestive tract into individual amino acids including BCAAs and glutamine. It is also important to remember that carbohydrates will help to conserve BCAA and glutamine stores in the body. If you eat well, provide your body with adequate protein at regular intervals and maintain a normal lifestyle, then there should be sufficient amounts of BCAAs and glutamine in your body for most of the day. However, when a sudden catabolic load is placed on the body during exercise, BCAA and glutamine stores are drawn upon as glycogen stores begin to be depleted.

This is the time when strategically increased BCAA and glutamine levels will have their greatest anabolic and anti-catabolic effect. For this reason, the first thing to do is to ensure high BCAA and glutamine levels during training by splitting the daily dosage of these two nutrients in half, taking the first half 30 minutes before training or at the start of the training session and the second half immediately after training. This way you will get the most bang for your buck. You should try this approach for two weeks and see if you notice a substantial difference in terms of recovery, delayed onset muscle soreness, fat loss, muscle growth and energy levels during training.

There will of course be additional benefits if you increase your daily BCAA and glutamine dosage and use these supplements at other times of the day. During a strict diet, where both calorie intake and carbohydrate intake are significantly reduced, supplementing with 2 to 5 grams of BCAAs and glutamine between meals will help maintain a positive nitrogen balance and protect existing muscle mass from breakdown. In addition, glutamine between meals can help reduce cravings for sweets and carbohydrates. Another point that should not go unmentioned is the effect on the release of growth hormone.

Both BCAAs and glutamine have been shown to independently increase growth hormone levels when using a dosage of just 3 grams. By using 3 to 5 grams of BCAAs and 3 to 5 grams of glutamine between meals and an additional 5 to 10 grams of glutamine before bed, athletes - and especially athletes over the age of 30 - can benefit from increased growth hormone levels. This can lead to a lower body fat percentage, increased energy and accelerated regeneration after training.

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Why does my breakfast make me hungry?
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"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

  1. Benedict, C., Hallschmid, M., Scheibner, J., Niemeyer, D., Schultes, B., Merl, V., Fehm, H. L., et al. (2005). Gut protein uptake and mechanisms of meal-induced cortisol release. The Journal of clinical endocrinology and metabolism, 90(3), 1692-1696. doi:10.1210/jc.2004-1792
  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
  4. 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.
  5. Fries, E., Dettenborn, L., Kirschbaum, C., 2009. The cortisol awakening response (CAR): facts and future directions. Int. J. Psychophysiol. 72, 67-73.
  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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Why does my breakfast make me hungry?
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"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.

This is quite a long article, but I hope it is interesting enough to keep your attention and interesting enough to teach you a few things.

My heart was in my mouth a few months ago when it seemed like there was overwhelming evidence for the benefits of breakfast, but I was able to disprove it.

Why does breakfast make some people hungry?

As mentioned earlier, it was not without reason that this question piqued my interest beyond what could be attributed to food choices. In questionnaires, clients often stated that eating in the morning made them hungry before lunch and that this was sometimes the case less than an hour after breakfast.

On Facebook, in emails and in conversations, similar anecdotal experiences were mentioned too frequently to be explained by mere coincidence - or to be dismissed with a half-hearted response based on the assumption that everyone ate an unhealthy breakfast.

These people hadn't eaten fruit loops and a peanut butter sandwich with a glass of orange juice for breakfast - you know, the average person's breakfast that would make anyone hungry an hour later.

No, these people had eaten a typical fitness athlete's breakfast that included all kinds of foods that most of us have eaten for breakfast at one time or another - oatmeal, dairy, eggs, etc. It was often a meal characterized by moderate to high amounts of carbohydrates and protein, relatively low amounts of fat, and usually a useful amount of fiber.

You can spend all day debating how healthy or unhealthy whole grains and dairy are, but the fact remains that these foods can't provide a blanket explanation for the fact that breakfast triggers hunger in some people.

Heck, all you have to do is google "why does my breakfast make me hungry", "hungry after breakfast" or "breakfast makes me hungry" and you'll see that the forums are full of people reporting similar experiences.

I would count myself as one of those people. Skipping breakfast was by far the best change I made to my diet when I started Intermittent Fasting in 2006.

Like many other Intermittent Fasting practitioners, breakfast was something really annoying for me and skipping it made a huge difference. Compared to before, dieting almost went by itself.

Not to mention the long-term maintenance of weight. No more counting down the hours until lunchtime and no more feeling like I was on a diet - regardless of whether I was actually dieting, maintaining my weight or gaining weight.

For me and many others, skipping breakfast keeps hunger at bay much better than eating something in the morning - as paradoxical as this may sound. This is of course very interesting to me as it's a damn strange thing. Why are some people better off not eating anything at all in the morning? How can it be that under these specific circumstances you are better off with zero calories than with hundreds of calories. It just doesn't make sense...

So I set about trying to find an answer to this question and eventually came up with a satisfying hypothesis regarding the mechanism underlying this mysterious post-breakfast hunger surge that so many of us feel.

The original article ended up being 12000+ words long and had an over-the-top ridiculously academic feel to it, branching off into all sorts of only remotely related topics. The article was far too long for most people's attention span and far too technical for most people's level of understanding.

So yesterday I sat down and rewrote the whole thing, trying to get it across in the same way I would explain the topic to my girlfriend or an invisible friend I've told the whole thing to a few times now.

Note: As for the term breakfast, in the context of this article, I mean breakfast in the traditional sense, i.e. breakfast right after getting up - and not in the original sense of the word as the first meal after an overnight fast.

Let's define hunger after breakfast

Trying to define hunger after breakfast is something completely pointless. It's something you'll understand immediately because you've had the same experience, or something that will make you wonder what the hell I'm talking about because you simply don't have that problem. I suspect most of my readers will fall into the first category, which is why I won't spend much time on an academic discourse explaining the phenomenon beyond what I've already done. Simply put, some people get hungry - very hungry - and experience cravings of varying intensity shortly after eating breakfast in the morning.

In the realm of scientific literature, scientists who specialize in research on appetite, hunger, and addiction make a distinction between the previously mentioned terms (i.e. hunger, cravings, etc.), but since hunger after breakfast is described by clients and on forums as a subjective experience, without more detailed research on my part, I would guess that most people are referring to the same phenomenon when they talk about hunger after breakfast and use terms such as cravings, feeling hungry, ravenous hunger, etc. Personally, I would describe this feeling as hunger in the sense that most people would use the term hunger.

Hunger after breakfast sets in sometime between morning and noon - usually 30 minutes to 2 hours after breakfast and doesn't usually manifest itself in any symptoms beyond noticeable hunger. However, some people have mentioned that irritability and an impaired ability to concentrate on tasks that require greater amounts of focus occur at the same time as hunger after breakfast.

An important point is that the same meal does not produce this early and/or pronounced hunger when consumed later in the day. Hunger after breakfast cannot be explained by differences in food choices, but by certain individual factors and their interactions with a time-dependent effect of food intake on hormonal profile and metabolism.

An introduction to cortisol

Cortisol is the main culprit when it comes to post-breakfast hunger. Most of you will probably associate cortisol with stress and muscle catabolism and consequently with 'bad' and 'avoidance'. While this is partially correct, it is largely incorrect.

Since "partially correct" is responsible for many of the bullshit nutrition myths out there, it's useless. People who claim that eating six meals a day will boost your metabolism and that fasting results in starvation mode are "partially correct" - but most of what they say is just nonsense.

Context is often key and this is especially true when it comes to cortisol - which is why I'm going to give a brief introduction to this complex and multi-faceted hormone here. There are almost as many different definitions of stress as there are myths out there about cortisol but in terms of the former, the definition that appeals to me most from a minimalist perspective is the following:

"Stress can be defined as any challenge to an individual's homeostasis that necessitates an adaptive response by that individual."

Newport & Nemeroff, 2002.

Cortisol is released in response to a stressor to help you deal with that stressor efficiently - whether that stressor is a 20 repetition set of squats to complete exhaustion or an approaching deadline for an article that needs to be published. The role of cortisol during these challenges is to give you a boost, not to hinder you - whether the stressor is physical (e.g. training, injury, cold) or psychological (e.g. a complex cognitively demanding challenge).

Elevated cortisol levels during exercise allow us to go far beyond our non-stressed comfort zone and maintain an adequate rate of exertion without being unduly distracted by pain, hunger and fatigue for a longer period of time than would otherwise be the case. Cortisol improves muscle and glycogen metabolism, increases pain tolerance, reduces fatigue and boosts motivation.

Oh yes, does this answer the questions of those who have asked me about my thoughts on the use of cortisol blockers before training? No? Okay, then all I can say is good luck with those squats buddy....

Because of the cortisol response to a cognitive challenge, we can remember important facts faster and in more detail, maintain our concentration, stay alert and work on the computer all night if necessary. Cortisol improves our sensory perception, memory and alertness.

Most of this 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. In short, prolonged stress results in chronically elevated cortisol levels, which then do all kinds of bad things. There is a time and a place for cortisol. But in our hectic times, the thin line between work (stress) and leisure (rest) is often blurred.

With constant demands placed on oneself, never-ending obligations and endless opportunities to work (at the office, at home, etc.), the stressors of modern society are of great psychological variety and they are omnipresent if you allow them to be.

In stark contrast, the stressors of the past were more often short-term and physical in nature. Even though these were probably more serious and often life-threatening, there was a clear line between start and finish. And this explains the title of Sapolsky's book, which I cannot recommend enough and which should be read by anyone seeking a more detailed explanation of stress and the work of cortisol.

What Sapolsky does not explain in detail, however, is the cortisol response upon waking and the acute effects of cortisol on insulin secretion.

The cortisol response after waking up

Most people understand the concept of exercise and work as stressors - challenges to homeostasis - that require an adaptive response (cortisol). However, few people think of waking up after sleep and getting up in the morning as a particularly stressful event. However, waking up after sleep is indeed a major challenge to homeostasis.

The transition from a passive state of sleep to an active state of wakefulness is - in some ways - like going from a leisurely walk to a sprint where you have to give it your all. In the field of endocrinology, there is a special name for the events that follow waking up in the morning: The Cortisol Awakening Response (CAR - in German Kortisol Aufwachreaktion), on which there is a substantial amount of scientific research.

"Awakening stimulates ACTH release in the pituitary gland, which then stimulates cortisol release by the adrenal cortex. The rapid increase and peak in cortisol levels after waking is known as the Cortisol Awakening Response (CAR). Although CAR is believed to be part of the cortisol diurnal rhythm, CAR and cortisol diurnal rhythm represent two separate adrenocortical activities."

Shin et al, 2011.

As the body prepares to start the day, cortisol levels begin to rise steadily during the second half of the night, reaching a peak around the time you open your eyes. But as you struggle to get out of bed, cortisol levels continue to rise on the way to the shower. They will peak around 30 to 45 minutes later, which is around breakfast time.

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

The cortisol awakening response and insulin secretion

So you've showered, gotten dressed for the day and done all the things you do in the morning that are none of my business and now you sit down to eat your breakfast before work, school or whatever. I'm guessing it's now 30 to 45 minutes after you get out of bed, if you're like most people.

By the time you sit down to eat - or sometime around that period - your cortisol levels will be at their highest of the day, which should be around 20-30 nmol/l. In comparison, cortisol levels in the evening are around 2-5 nmol/l, which corresponds to the lowest value of the cortisol daily rhythm, if you're interested in the numbers. Of course, cortisol levels could rise further later in the day depending on the amount of stress you are exposed to, but this has nothing to do with our analysis.

"The early insulin response to a meal is higher in the morning than in the afternoon and this fact can only be partially explained by a moderate increase in incretin secretion. Rapid non-genomic effects of high cortisol levels in the morning may be at least partially responsible for this observation."

Vila et al, 2011.

The point is that the peak of the cortisol diurnal rhythm coincides with breakfast and that this is the only time during the day when cortisol levels reach sufficiently high levels to have an acute and marked effect on the food-induced insulin response.

If this sounds vague to the endocrinology enthusiast and those familiar with cortisol, let me briefly explain in plain language. What I mean here is that during the CAR maximum, cortisol levels rise high enough to "tantalize" the glucocorticoid receptors. This changes the non-genomic interaction between cortisol and insulin action from a suppression by the former, as can be observed at other times during the day due to mineral corticoid binding dominance, to a non-genomic stimulation or synergistic effect (Vila et al., 2010; Dallman et al., 1995)

If the last paragraph doesn't make much sense to you, then you now know why I had to rewrite and simplify the entire article.

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

* As opposed to long-term exposure, which has the opposite effect.

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Creatine myths
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Anyone who is even remotely involved in sport or fitness will almost certainly have heard something about creatine. Equally, you will almost certainly have heard one or two horror stories or completely exaggerated claims about the performance-enhancing effects of creatine.

This often leads to athletes who could actually benefit from using a creatine supplement not being sure whether they should use creatine or not, as they doubt its safety and harmlessness to health. As a rule, most of these statements are nothing more than myths that have little to do with reality. The fact is that creatine is one of the safest and most effective supplements in the fitness world and is completely safe for long-term use.

This article will address some of the most common creatine myths and explain why they are nothing more than myths.

Is creatine comparable to anabolic steroids?

Anabolic steroids are synthetic analogs of the male sex hormone testosterone. The possession and use of these compounds is illegal in many countries. Anabolic steroids are more or less widespread on the black market, but you certainly can't buy them legally in a supplement store.

In contrast, creatine is a completely legal sports supplement that is widely available in many stores, which now even include ordinary supermarkets. Creatine has been freely available without a prescription for several decades and is considered very safe and harmless to health based on a huge amount of scientific research.

Although creatine certainly has performance-enhancing capabilities based on increasing strength and muscle endurance while promoting cell volumization, unlike steroids, all of these effects are based on non-hormonal pathways.

Can creatine damage the kidneys?

As with any supplement, it is of course advisable to consult your doctor before using creatine. There are also numerous scientific studies on creatine that clearly show that creatine can be considered safe and harmless to health for healthy adults without pre-existing kidney damage, even with long-term use.

Even if there are isolated anecdotal reports of kidney damage in creatine users, these health problems are very likely based on undetected kidney damage that already existed prior to creatine use.

Can creatine cause muscle cramps or injuries?

This is probably the most widespread creatine myth among athletes, repeated so often by so many people that potential creatine users who have never used creatine themselves unfortunately often take this statement as fact.

If an athlete using creatine gets a muscle cramp, they are quick to blame it on the creatine used, even though the actual reason for the cramp is more likely to be a lack of hydration, poor electrolyte balance or a number of other factors that can result in cramps.

In a large-scale study of over 1500 participants, creatine supplementation in athletes did not result in an increased incidence of muscle cramps. In fact, the members of the group that used creatine reported fewer muscle cramps than the members of the control group that did not use creatine.

Similarly, many athletes mistakenly believe that creatine can increase their risk of injury. However, scientific research has shown that creatine does not increase the likelihood of injury.

A study conducted with 72 professional football players as subjects concluded that athletes who supplemented creatine experienced fewer muscle cramps, less muscle stiffness, fewer strains, less dehydration and fewer overall injuries.

Perhaps even more interesting is a study conducted in 2001, which showed that creatine supplementation could accelerate rehabilitation in subjects after immobilization of one of the extremities during exercise training.

Conclusion

The creatine myths debunked in this article are merely the most common misconceptions. If you dig a little deeper, you will find many more. I hope that this article has encouraged readers to take a healthy dose of skepticism about anything they hear in the future that is overly negative about creatine.

I can only encourage everyone to search relevant search engines such as PubMed or Google Scholar for legitimate scientific literature and studies when it comes to creatine or other supplements. You shouldn't necessarily rely on personal anecdotes or statements from training colleagues or coaches, but instead consult meaningful, independently peer-reviewed studies when in doubt.

Of course, all this advice also applies to overly positive claims about a particular supplement. If you look at the exaggerated advertising claims made by some companies about the effects of creatine or other supplements, you should always bear in mind that creatine is not a steroid but a natural supplement and therefore you cannot expect steroid-like results - even if some manufacturers like to claim this.

To conclude this article, it should be mentioned that there are well over a thousand if not thousands of studies conducted with creatine, the vast majority of which show that creatine is a safe and effective supplement. Whether you are a recreational or professional athlete, or simply want to maintain good health, creatine can be a useful addition to your personal supplement plan.

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