Guyenet and Hall demonstrate that what does happen cannot really happen

(versión en español: pinchar aquí)

NOTE: a calorexic is a person that believes in the energy balance pseudoscience.

I reproduce below a text from Woo’s blog. Its authors are Stephan Guyenet, Kevin Hall and a third author. The bold type hightlighting is mine.

If decreased circulating fuels caused the development of common human obesity as described by the CIM, then experimentally decreasing circulating fuels should result in increased energy intake, decreased energy expenditure, and body fat accumulation. The drug acipimox reduces FFA levels by mimicking the effect of insulin to inhibit adipocyte lipolysis. In a 6-month trial, acipimox induced a persistent 38% reduction of plasma FFA levels in adults with obesity but did not impact energy or macronutrient intake, resting energy expenditure, or body composition. Thus, a key prediction of the CIM was not experimentally supported.

Woo argues that not to use results from insulin experiments, when it is clearly possible to do so, when they want to demonstrate something about insulin is a clear attempt to deceive (see). She obviously has a point, because it is difficult to understand how they do something like this.

Basically what the argument of Hall and Guyenet says is that no physiological factor can be fattening per se, because it would increase energy intake, reduce energy expenditure and fat accumulation would happen. According to these authors, since in a specific experiment with the drug acipimox none of the three things was observed, they deduce that it cannot happen in any case, including insulin.

In my opinion, to use a drug (acipimox) instead of insulin to demonstrate something about insulin, is quite relevant, since the extension of those results to a different physiological factor, such as insulin, necessarily implies that what they want to establish is a general principle valid for any supposedly fattening physiological factor. Otherwise, Hall and Guyenet would have only used experimental results related to insulin. What their text conveys is that they are questioning the causality of the carbohydrate-insulin model. That is the reason why they talk about the reduction of circulating fuels, something not necessarily caused by insulin, and they use a physiological factor different from insulin. They are trying to establish a general principle, which, according to them, the carbohydrate-insulin hypothesis fails to fulfill.

In short, their argument is that:

no physiological factor can produce energy accumulation in a tissue

because according to them neither the caloric intake nor the energy expenditure nor the accumulation of fat can be altered by a physiological factor. If they thought they could be altered, they would not use acipimox instead of insulin. I insist that it is the causality of the carbohydrate-insulin theory what they try to make believe that has no experimental support:

A key prediction of the CIM was not experimentally supported.

The argument is not limited to adipose tissue, since the accumulation of energy in any format and in any tissue within the body must have the same consequences from the point of view of the energy balance equation. And they clearly speak of “decreased circulating fuels” which is common to any tissue that stores metabolites. If it is argued that it cannot happen for adipose tissue, then it cannot happen for any tissue, since the effects on the terms of the energy balance equation of the accumulation/release of metabolites in a tissue are, a priori, similar for all tissues. Otherwise, their argument would be that when, for example, the liver accumulates fat there is no problem for the body due to having a little less fat to use, but that same body does not know what to do with a gram less of dietary fat when it is stored in the adipose tissue. Nonsense.

I suppose that at this point you are already asking yourself how is it possible that they are arguing this. They are Hall and Guyenet: that is the only explanation. It is time now to analyse their argument. My analysis is structured in the following sections:

  1. The main argument is a straw man
  2. It is false that they are talking about a key concept of the carbohydrate-insulin hypothesis
  3. If you want to know if there is fattening, look if there is fattening
  4. It is false that there must be effects in the terms of the energy balance
  5. Do we apply this criterion to other accumulations of energy in tissues?
  6. It is false that it has to happen. Other reasons
  7. Apart from being false, it is not measurable and may be never will be
  8. The CICO theory cannot explain the scientific results
  9. Conclusion

1. The main argument is a straw man

If decreased circulating fuels caused the development of common human obesity as described by the CIM, then experimentally decreasing circulating fuels should result in increased energy intake, decreased energy expenditure, and body fat accumulation.

Does the decreased circulating fuels cause accumulation of body fat? Let’s think about it for a moment. Is that what the carbohydrate-insulin hypothesis says?!!! Really? Let’s look at the figure, taken from an article that defends the carbohydrate-insulin model: do we see what causes the accumulation of body fat in that model?

The irrelevant, unnecessary and possibly non-existent decreased circulating fuels, is a possible consequence —a symptom that may not even exist!— of the accumulation of body fat, not its cause! Have you ever read an advocate of the carbohydrate-insulin hypothesis say that we gain weight because circulating fuels are reduced? Does this argument really have three authors? Have they no shame? Have they no shame?!!! Are they really twisting what the carbohydrate-insulin model really says in this way?

Moreover, the carbohydrate-insulin hypothesis says that insulin causes accumulation of triglycerides in the adipose tissue, triglycerides that would no longer be available to other tissues, for example to be dissipated as heat in muscle tissue (see,see). If there is no fattening, it is absurd to suggest that the circulating fuel will be reduced due to fattening. Can it be used to question that that causality is possible, an experiment with acipimox that, according to Hall and Guyenet, did not cause changes in body composition!!? What changes in energy intake and energy expenditure can we expect to find in these conditions? What changes?!!!! And they argue that the reduction of circulating fuels, which supposedly is the consequence of gaining weight, also did not cause weight gain. And that there were no effects on the energy balance terms caused by a fattening that did not happen for them is proof that … Fuck Hall and Guyenet!!!

Note that if they had not attributed to the carbohydrate-insulin model a false causality, different from the one actually proposed by this model, they could not have talked about the experiment with acipimox, because in the absence of fattening they could not justify their search for effects in the terms of the energy balance equation. That search only exists from the moment they make up that fattening is produced by a reduction of the circulating fuels. And that is a lie.

Moreover, it is the CICO theory the one that proposes that a decreased circulating fuels forces the adipocytes to release body fat, that is, makes us lose weight.

That is, Hall and Guyenet falsely attribute a fake causality to the carbohydrate-insulin model but that causality is the causality of their own model.

The drug acipimox reduces FFA levels by mimicking the effect of insulin to inhibit adipocyte lipolysis. In a 6-month trial, acipimox induced a persistent 38% reduction of plasma FFA levels

If in a drug experiment circulating free fatty acids are systematically reduced, if that does not result in a reduction in body weight, the causality that would be called into question, in any case, is that of the CICO theory!

In my opinion, the acipimox experiment doesn’t demonstrate that the CICO causality is false. What I find relevant is that Hall and Guyenet have conveniently attributed to the carbohydrate-insulin model a false causality, pretending to conclude that this model is not supported by the experimental evidence.

2.It is false that they are talking about a key concept of the carbohydrate-insulin hypothesis

On the other hand we have the idea that the terms of the energy balance equation cannot respond to the action of a tissue that decides to capture fatty acids.

A key prediction of the CIM was not experimentally supported.

Note that the idea that changes in energy intake and energy expenditure are a consequence of fattening is not a key idea of ​​the carbohydrate-insulin hypothesis. This is another straw man created by Hall and Guyenet to make believe that they are falsifying that theory by dismantling one of its pillars. In the carbohydrate-insulin hypothesis, fattening is a physiological process in which insulin plays a fundamental role, while the terms of the energy balance do not matter a cent! We only talk about changes in the terms of the energy balance for didactic reasons, trying to make calorexics understand at once that the carbohydrate-insulin hypothesis does not violate any law of physics, but not because those terms play a relevant role in this model. Of course calorexics do not understand that the energetic terms on which they have based their career are irrelevant. And they insert these terms even in the speech of those who deny the relevance of these terms.


Have a look at the figure above. In this model the energy balance terms cut no ice in the process of getting fat! According to the carbohydrate-insulin hypothesis, the changes in the terms of the energy balance are irrelevant for fattening, unnecessary for fattening and possibly non-existent in the presence of fattening symptoms. Key idea? !! Only if you try to deceive and you just do not understand that your believes are pure and simple charlatanism.

What is relevant in the carbohydrate-insulin model? The hormonal changes and if there is fat gain or there is not. Energy balance equation, they say? What is that?

3.If you want to know if there is fat gain, you check if there is fat gain

Another important problem with Hall and Guyenet’s argument is that if you want to know if a physiological factor is making you fat, what you have to do is a controlled experiment in which that physiological factor is applied and you check if there is growth in the adipose tissue. The terms of the energy balance are not relevant for that check, except when, as is the case here, someone wants to make us believe that what does happen cannot really happen.

It’s simple: if you want to test if insulin makes you gain fat,

  1. you use insulin and
  2. you check if there is fat gain.

That’s it!

If you use a drug that is not insulin and you look for changes in secondary, unnecessary, irrelevant and probably absent markers for fat gain, in that case do not dare to say you are not trying to deceive.

For example, in this experiment, with the same energy intake and the same levels of physical activity, injecting insulin produced body fat accumulation.



Have Guyenet and Hall demonstrated that this experiment, the one I am referring to, is wrong, because what happens in it is impossible? Not at all.

This one must be also wrong: the mice injected with insulin consumed less food, but finished the experiment with a percentage of body fat that was 65% higher than in those mice that were injected saline.



Or this one, in which with the same energy intake, the more insulin injected the more body fat accumulated:



And we have an epidemic of poorly done studies, because in this one at 12 months the group injected with insulin had a body fat 4.2 times greater than the other, with no differences in energy intake.


There are also experiments in humans in which while the caloric intake was reduced, body fat increased, in people who were injected insulin (see).

And insulin is not the only physiological factor that can cause increased body fat without increased intake: example, example, example, example, example.

I do not want to explain further here the experiments. The links lead to blog entries where you can check their details. I go on.

4. It is false that there must be effects in the terms of the energy balance

It is not true that if a physiological factor directly produces body fat accumulation, we must detect effects on the energy intake and energy expenditure terms of the energy balance equation. The energy balance of the adipose tissue is NOT the energy balance of the whole body (see,see).

For example, in these experiments a hormonal change caused body fat gain, without the concurrence of an increase in the energy intake. I mentioned above experiments with insulin injection where we find the same. The fact that there is no increase in the caloric intake does not mean that there has been no fat gain, or in other words, to gain fat does not imply that the caloric intake has to be changed.

For example, it is possible to lose body fat while muscle mass is increased, or just the opposite (see,see), a situation in which there is not necessarily a cahnge in the difference between energy intake and energy expenditure. And yet there is fat gain!! In this experiment the mice that gained more body fat were those that gained less weight, which shows that is nonsense to think that an increase in the size of the fat tissue must be accompanied by an increase in the caloric intake and a reduction in the energy expenditure.

Another example: in ventromedial hypothalamus lesions, body fat can accumulate without changes in the body weight or in the caloric intake (see).

It’s not true, because as I said,

the energy balance of the adipose tissue is NOT the energy balance of the whole body

Everyone understands this, except, apparently, Hall and Guyenet.

5. Do we apply this criterion to other energy accumulations in tissues?

Do you think it is possible for your liver to accumulate body fat due to physiological causes that are not related to the energy balance terms, for example due to the presence of sugar and fructose in the diet? (see) Do you think that the accumulation of energy in the liver is caused by an energy intake that exceeds your energy expenditure, because Hall and Guyenet have demonstrated it must be so? So, do you think it is possible to accumulate fat in the liver due to physiological causes not related to the whole body’s energy balance equation?

Do you think that not measuring changes in the energy intake or in the energy expenditure while accumulating fat in the liver (I’m not saying that the body weight changes) would show that the cause of the fatty liver cannot be physiological? Note that not measuring it does not mean that they the changes do not exist, just that they are not seen.

How are connected the accumulation of fat in the liver and the terms of the energy balance equation for the whole body? What are the physiological mechanisms that link them?

Are they really arguing that there cannot be physiologic causes for the accumulation of body fat in a tissue? A bad argument that is used only because someone doesn’t want to back down is called an ad-hoc argument. They cannot defend their argument, but that fact has not prevented them from using to advance their agenda.

Let’s talk about anabolic steroids. They make muscle mass grow (see). Do they work through a direct physiological/hormonal action in the muscle tissue, or is that impossible, as Hall and Guyenet have demonstrated, because our body would not know how to manage having a few grams less of metabolites, the ones used in that growth? Is the increase in the energy accumulated in the tissuemediated by changes in the terms of the whole body’s energy balance, or are the terms of the whole body’s energy balance irrelevant in the growth of the tissue? If the only thing anabolic steroids do is to increase the appetite and make us sedentary, can we achieve the same results just by eating more and moving less?

6. It is false that it has to happen. Other reasons

Kevin Hall says that an excess of just one gram of fat in our food intake explains the current obesity epidemic (30 kJ /d = 7.2 kcal/d):

A small persistent average daily energy imbalance gap between intake and expenditure of about 30 kJ per day underlies the observed average weight gain (source)

I think it is important to highlight this fact to be aware of the dimension of the obesity problem: we deal with a few grams per day net accumulation in the adipose tissue.

Suppose that of the 400g of food you consume today, 1 gram goes directly to your adipose tissue. What will be the effect in the following days? Voracious hunger? An increase in your caloric intake? You will feel tired due to the lack of nutrients? Are we kidding? Is that what you actually notice when one day you consume 399 g instead of the 400 g you eat on an average day?

Have you thought about the variation in your food intake from day to day? Do you think that when you eat 1 g less than an average day this causes some response in the caloric intake that is bigger than the natural and inevitable variations in your daily caloric intake? Do you think there is such an effect if you consume 5 g less than an average day?

Apart from the above, our body “wastes” much of what we eat as body heat. And the amount is not fixed: it is adaptive. If you eat a little more or a little less, your body can adapt without any problem to the intake of that day and dissipate as heat what is left over, maybe more, maybe less than the day before. There is no reason to eat more in the next days: your body has not felt deprived of food neither of the two days. It is not true that the fact that your adipose tissue accumulates triglycerides must have an effect on your caloric intake. The variation in the amount of available nutrients can be perfectly absorbed by a very slight change in the energy expenditure. The efficiency of the human body is variable and adaptive (see,see,see,see,see,).

If instead of eating 1g less than normal, your adipose tissue stores 1g of what you eat, is your body an impossible situation? How is this situation different from eating 1g less than the average you consume? Is the second case a problem, but not the first one? That’s what Hall and Guyenet are telling us:

  • Today you eat 1 g less than yesterday —> The body has no problem at all.
  • Today your adipose tissue decides to accumulate 1 g of what you eat as body fat —> That is an impossible situation, as demonstrated by not detecting changes in the energy intake nor in the energy expenditure in an experiment with acipimox.

The body would not know what to do with 1 gram less of food, but only in the second case … Ummmm, are they serious?

7. Apart from being false, it is not measurable and may be never will be

Another fallacy is to try to draw conclusions from what not only does not have to occur, but cannot be measured either.

If today you eat 1g less than normal (it is not an erratum, it is the hypothesis of Hall and Guyenet), what changes do you expect to find in your energy intake or energy expenditure the next day? Do you think that if this effect existed, it could be measured, as a change that is distinguishable from the natural daily variations in your energy expenditure and energy intake? And how would you distinguish it from those natural variations?

What do you think is the resolution and precision of the state-of-the-art measure systems that can be used to measure the food that actually enters the body and the energy expenditure you have on a specific day? Even if you do not understand the concepts of precision and resolution, do you think that with current technology you can reliably measure that your body has spent 10 kcal less than the previous day, while controlling the actual caloric intake (food actually absorbed) with better accuracy than those 10 kcal? Are Hall and Guyenet pretending that these measures can be made in order to draw valid conclusions from them?

In any case, as I explained before, there does not even have to be an effect to measure.

8. The CICO theory cannot explain the scientific results

Hall and Guyenet are two of the greatest advocates of the energy balance charlatanism. Their ridiculous attack to the carbohydrate-insulin hypothesis can only be explained by the interest of these two gentlemen to defend the dogmas on which they have based their career and their book, respectively.

Do they question their dogmas with the same intensity with which they question the carbohydrate-insulin hypothesis? I would say they do not.

If there is no local effect of insulin, unrelated to the energy balance, how is it explained that insulin injections change the distribution of body fat in the body? An effect mediated by changes in the energy intake and the energy expenditure cannot explain that observation (see).

How does the CICO theory explain the spatial correlation between insulin concentration and adiposity detected especially before insulin resistance develops? (see)

If a physiological factor cannot cause fat gain by mechanisms different of changing the caloric intake and the energy expenditure, how can this experiment be explained in which the rats that consumed half the calories than others gained more body fat? How does the CICO theory explain this experiment? It is important to highlight that the CICO theory is not what the First Law of Thermodynamics says (see).

In this experiment, there were no differences in the caloric intake, but there was greater body fat accumulation in the group injected with insulin. If we store as body fat what is left over when our body has spent to meet its needs, did the mice in one of the groups suddenly have less “energy needs”?


Is it possible that the body spends what is left after we have gained body fat? (see) Have they considered this possibility? Why do they discard it? What would we expect to find in the uncoupling proteins activation in each case?

9. Conclusion

Theories have to be coherent with scientific experiments, not the other way round (see). If someone wants to say that the composition of the diet has no effect on the adipose tissue, or that there are no effects in that tissue that the calories and the distribution of macronutrients cannot explain, they must first give an explanation for what has been published in the scientific literature (see). Hundreds of perfectly controlled experiments are wrong? Really? Do we have to believe that Hall and Guyenet have not seen all that evidence?

these findings nonetheless corroborate a substantial body of evidence showing the uniquely potent fattening effect of insulin, regardless of calories consumed (source)

Hall and Guyenet have not found all that evidence published in scientific journals, but they have found an experiment with acipimox. They are amazing!

In short, Hall and Guyenet say that they have shown that what the scientific evidence shows, does not really happen. Oh my!

Note: This is not the first time that Stephan Guyenet, PhD has used BS arguments to make people believe that insulin does not make you fat (example,example,example,example,example,example). And his arguments in defense of sugar are inappropriate for someone with an academic degree (see,see).

Note: Guyenet and Hall’s paragraph has 125 words, my comment has 4000. Brandolini’s Asymmetry Principle.

Further reading:


80 years of energy balance pseudoscience

The prejudice and stupidity cycle:

Further reading:

The CICO Theory, a pseudoscience based on rhetorical tricks

(Spanish language version: click here)

The main goal of this article is to explain that the Energy Balance theory (also known as the CICO Theory) is wrong. It is important to understand that this is so, because otherwise we will continue trying to prevent or reverse our weight problems with principles that have no real basis. These wrong ideas are:

  • The cause of gaining weight is a caloric surplus.
  • The obvious solution for excess weight is to eat less and move more. Without a caloric deficit you can’t lose weight.

Yes, both ideas are wrong, fraudulent and fallacious.

I will focus the explanations on two key concepts:

  • The CICO Theory is not the First Law of Thermodynamics
  • The CICO Theory is based on unjustified premises

The First Law of Thermodynamics

Principle of energy conservation applied on the physical limits of our body (our skin):


Nobody here denies that this law is fufilled in the human body. I repeat this point: nobody here denies the fulfillment of this law.

The CICO Theory

The CICO theory is based on two unjustified assumptions:

  1. Only the energy stored in the adipose tissue is allowed to change.
  2. The adipose tissue is passive: the amount of triglycerides stored in this tissue can not change by itself (i.e. in response to physiological stimuli, such as the hormonal environment).

In the figure below, those terms with a green circle are allowed to change by themselves. The CICO Theory does not allow the third term, the one with the red circle, to change by itself.


Why cannot a food product, such as sugar, directly affect term #3? Why cannot a food product be “fattening”, by itself, regardless of the calories consumed/spent? The answer is that the CICO Theory does not allow this to happen, because one of its unjustified premises is that it cannot happen. For no reason: it is just not allowed.

“Caloric excess” and “caloric deficit”

This terms imply that that there is a difference between the first two terms (the two terms with the green circle), and that difference, by means of the energy balance equation, forces a change in the third term (the one with the red circle). Note that the third term changes because the other two terms change: it is an unwarranted behavior of our body created by the unjustified premise that the adipose tissue is passive.

Note that under the unjustified premises of the CICO Theory, any solution to obesity will always be based on managing the energy intake and the energy expenditure, that is, acting on the two terms with the green circle in the figure above.

For example, when weight loss stalls, some of the defenders of this pseudoscience attribute the stall to the fact that there is a “slowing down of the metabolism”. What is a slowdown of the metabolism? A change in the second term of the equation. Or they say that you are lying and you eat more food than you say. In this case, they are talking about the first term of the equation. These diagnosis and solutions respect the unjustified premise that only the first two terms of the equation have the capacity to change by themselves. Why can’t be the cause of the plateau that the adipose tissue has the drive to store fat? It can’t be because the CICO Theory doesn’t allow this possibility.

Note that if we follow the CICO logic, if the weight loss stalls because the metabolism slows down, the only possible solution is that you have to eat even less. No solution will ever be based on understanding the adipose tissue’s physiology, because the CICO Theory says its physiology is non-existent.

And that “eating less” has to work, because that metabolism slowdown “is not that big”. As I said at the beginning: understanding that the CICO Theory is a hoax is key to understand that almost everything we think we know about what to do to lose weight or not gain it, is unfounded.

As a key idea: the CICO Theory does not violate the First Law of Thermodynamics, but it is not the First Law of Thermodynamics. This theory assumes a behavior of the human body that does not legitimately derive from the laws of physics, although it does not violate them.

How relevant is that the CICO Theory is based on unwarranted premises?

I will answer that question by proposing an alternative theory to the CICO Theory. This alternative theory is also compatible with the First Law of Thermodynamics. It is utterly irrelevant if this alternative is correct. What really matters is that it is possible, which

  1. makes it clear that the CICO Theory is a fraud, and
  2. helps to understand that ideas totally opposed to the CICO Theory could be the key to managing our body weight.


In this model we allow the adipose tissue to change by itself, but now the energy expenditure can’t. An unjustified premise? Exactly! A premise as unjustified as in the CICO Theory. This is precisely what I want to convey with this article.

If the adipose tissue can vary by itself, to control its size or changes we need to understand what causes fatty acids to enter or leave it: what hormones are involved, what are the physiological factors that alter those processes, etc.

Under this premise, in order to control our body weight we have to pay attention to everything that the CICO Theory considers, with no good reason, irrelevant in the processes of gaining and losing weight.

In this model a food can be fattening per se.

In this model, if the weight loss stalls, the cause lies in the adipose tissue itself, which has decided not to continue reducing its size, perhaps in response to a lack of food that our body sees as a threat to survival.

In this model the plateau has nothing to do with a “slowdown of the metabolism”, which in any case would be a symptom, not the cause of the weight loss stall.

On the other hand, remember that there is a second unjustified premise in the CICO Theory: “only the energy stored in the adipose tissue can change“. Is that premise relevant? It obviously is.

We see this point clearly if, instead of imposing that only the energy stored in the adipose tissue can change, we impose that only the energy stored in a tumor can change:


Is a “caloric excess” the obvious cause of a tumor growth? Is establishing a “caloric deficit” the obvious solution to reduce its size? We know that these questions are nonsense, and they are for two reasons:

  1. The energy balance of the whole body has nothing to do with the change in the energy stored in a specific tissue: there is no justification for assuming that only the energy stored in the tumor can change.
  2. We know that the tumor does not grow nor it is reduced by the establishment of a “caloric surplus/deficit”. We know that the tumor takes the initiative to grow/decrease, and we know that there is no justification for assuming that its role in its own growth is passive.

Are relevant the tricks on which the CICO Theory is based? We have seen that for sure they are.

Please note that the CICO Theory can be complex, but the complexity is only allowed in 2 of the 3 terms of the energy balance equation. A complex CICO Theory is still pseudoscience.


The CICO Theory is not the First Law of Thermodynamics.

The CICO Theory is based on unjustified premises.

A “caloric surplus” is NOT the obvious cause of obesity.

A “caloric deficit” is NOT the obvious solution to obesity.

Thinking about the effects of what we eat in our adipose tissue is not charlatanism nor it is a denial of the fulfillment of any law of physics, although it does indeed mean denying the correctness of the CICO Theory.

We have to be aware of the trap: we want to continue talking about calories, because the CICO Theory allows us to eat whatever we want, be it real food or be it an edible product. We want that theory to be correct. And the food and diet industries take advantage of that desire. But the CICO Theory is not a correct theory. And it does not work in practice either.

CICO denial

— Last summer I gained 5 kg of muscle mass
— How did you do that?
— I consistently ate more than I expended
— That’s not a way to gain muscle, bro
— What are you, a CICO denier? Increasing your muscle mass is an energy balance problem: when people gain muscle mass, it’s always because more calories were consumed than were expended. This is a hard fact, man
— You are right. No one can break the Laws of Thermodynamics


The simple, unavoidable fact of human physiology is that you can’t increase your muscle mass without creating a calorie surplus. Whether you do this by eating more, moving less or a combination of the two, is a matter of preference.

Making up a physiologic behaviour from a physics constraint

(versión en español: pinchar aquí)

When you eat more calories than you burn, the excess calories are primarily shunted into your adipose tissue. Your adiposity, or body fatness, increases. It really is as simple as that (Stephan Guyenet, PhD)

No, it is not as simple as that. As a matter of fact, that idea is a perfect example of the energy balance pseudoscience. The laws of physics do not tell you how things work, but rather the constraints under which they work. Whatever happens in a system, its behaviour cannot violate nature laws: matter cannot be created from nothing, an object will not accelerate unless a net force is applied or energy can not be created nor destroyed. Nevertheless, those limitations are often irrelevant in practice. For example, according to the Law of Conservation of Matter, you cannot accumulate matter in your body unless more matter enters the body than exits. But that fact is irrelevant for understanding growths in a living being.

What I want to explain in this blog entry is that the fraud in the energy balance theory does not lie in the maths —since this theory is indeed compatible with the physics constraint imposed by The First Law of Thermodynamics—, but in the physiologic behaviour that this theory makes up by using language tricks.

I am going to use a water tank as an analogy. Water is poured regularly into the tank and part of its contents is lost through a drain. We know that water cannot accumulate in the tank unless more water comes in than is lost through the drain. That is a true as useless, because it is just saying accumulation with different words. But, do you think that when more water comes in than goes out, the excess water is accumulated in the tank?

I am going to present two simple models based on a water tank. Both of them are compatible with the physics laws, since water is not created nor destroyed in any of them, but they behave differently. I insist: my point is that the energy balance theory is a fraud not because of its maths but because it makes up a physiologic behaviour.


Model #1


Let us assume, for example, the following behaviour of the drain: the rate at which water flows from the tank is constant. In this case, if the rate of water flowing into the tank is bigger than the drain rate, water will accumulate in the tank. We could say “excess water” accumulates in the tank.

But let us assume that the drain rate is adaptative and equal to the rate of water poured into the tank. Would you say that, in this case, “when more water comes in than goes out, excess water accumulates in the tank“? No it does not and, in this case, there is no such thing as excess water. Not always it is correct to say that “when more water comes in than goes out, the excess water is accumulated in the tank“.

It is our physiology knowledge what would lead, where appropriate, to talk about “caloric excess”. From the First Law of Thermodynamics we cannot deduce a physiologic behavior, which is what the fraudulent energy balance theory does.

For example, the storage of carbohydrates as glycogen cannot be caused by an intake that exceeds their oxidation, because that would mean that by increasing our carbohydrate intake we could gain as much weight as we wanted. But physiology says it is not like that.

a chronic imbalance between carbohydrate intake and oxidation cannot be the basis of weight gain because storage capacity is limited and controlled, conversion to fat is an option which only occurs under extreme conditions in humans, and oxidation is increased to match intake (Broskey et al.)

Physiology determines if it is correct to speak of a specific “excess” as a cause of a specific accumulation.

Model #2

In this model part of the contents of the tank is lost through the drain, but part is lost because it overflows the walls of the tank.


Please note that our body has physiologic mechanism that can dissipate unnecessary nutrients as heat. One of these mechanisms are the uncoupling proteins, which can be found in several organs and tissues in our body.

Moreover, in this model the walls of the tank are not fixed, but they can dynamically expand or contract, changing the total volume of the tank. In this model the position of the walls is regulated by the concentration of specific substances in the water.


Let us assume that a specific substance is present in the water and it makes the tank expand. As a consequence of that expansion, the total volume of water stored in the tank increases. Would you say that, in this case, “when more water comes in than goes out, excess water accumulates in the tank“? No, this not correct. The use of the term “excess water” is unwarranted.

Water is not accumulated because more water comes in than goes out, although more water will come in than go out when water accumulates.

This model does not violate universal laws of physics —water is not magically created nor destroyed— and the existence of another model that is also compatible with the physics laws, but with a behaviour different from that of the energy balance theory, clearly shows that this theory goes beyond the physics constraint that the First Law of Thermodynamics establishes: it introduces an unwarranted physiologic behaviour. As I said before, the fraud of the energy balance pseudoscience does not lie in the maths but in the unwarranted physiologic behaviour that it makes up.

Fundamentally, obesity is a problem of energy imbalance, which only develops when energy (food) intake exceeds total energy expenditure (Schrimpton et al.).

Obesity is not a problem of energy imbalance: it is a problem of excessive triglyceride accumulation in the adipose tissue. There is no physiologic basis for talking about “energy” or “energy excess” in regard to weight changes in the human body.

Energy Balance Pseudoscience and Causality Hoax (2/2)

The messages I want to convey with this second part of the blog post are as follows:

  • To complete the explanations from the first part, which can be summarized as that the energy balance theory does not rightfully derive from the laws of thermodynamics. Energy intake and energy expenditure are not necessarily neither the cause nor the solution to the obesity problem
  • To clarify the causality fraud and its consequences in practice by means of a simple mathematical model of body weight dynamics, but also to explain the limitations of mathematical models.

I will use a very simple model of body weight dynamics, taken from an article (see) from Kevin Hall, a well-known promoter of the energy balance pseudoscience. In the past I have criticized the pretensions of this gentleman to interpret the forecasts of his mathematical model as scientific evidence, something always reprehensible but it is especially so in his case because he uses his results to blame the victims, the obese, for not being able to lose weight (see, see).

Please, do not bother criticizing the modifications I’m going to introduce in the mathematical model: I do not intend to propose an alternative model nor to improve the model. The ideas I want to convey are others and the model I use seems quackery to me, because instead of modelling the phenomenon of interest, which is the accumulation of triglycerides in the adipose tissue, what the model does is model the terms of the energy balance. Any model that is based on the energy balance theory is, in my opinion, insurmountable quackery (see first part of this entry).

Model #1: A model that lacks a physiological adaptation

I assume hereafter that the daily energy intake is as the picture below shows (it is the relatice change with respect to the baseline, which is supposed to be a point of intake&weight equilibrium):

The model is very easy to understand. The energy intake is the input (on the left side) and the body weight is the output (on the right side). Each day we calculate (yellow block) the difference between caloric intake and energy expenditure and, in this model, that value determines the daily weight gain. The body weight is calculated as the cumulative sum (orange block) of all these daily changes.

This model does not include a physiological adaptation mechanism.

In the graph below, on the left I show the body weight evolution with time and on the right the energy expenditure evolution. By design of this model, when the energy expenditure is reduced around 200 kcal/d the body weight will stabilize. It can be shown that when the energy intake is a constant the model stabilizes its output at weight=intake/epsilon, which in this case is -200/25.8 =-7.75 kg. There is no need to run the model to know that result because, as I said above, it is part of the design of the model.

We are not seeing a rebound effect (i.e. a physiological adaptation) because in the Model #1 we do not include a physiological adaptation mechanism.

Do we deduce from this simulation that the physiological adaptation does not exist in real life and that what happens is that obese people simply eat more than they tell us? (see).

Model #2: A model that does include a physiological adaptation

Let us suppose that, triggered by the food restriction, our physiology has changed. In Model #@ we maintain that there is a certain tendency to lose body fat, driven by the fact that we are eating too little, but now our adipose tissue has become especially prone to accumulate body fat (see the lightgray block and a new yellow block that adds these two effects in the figure below):

In this new version of the model, the body weight evolves as shown in the pictures below (blue curve on the left side). The energy expenditure is reduced as shown by the blue curve on the right side. The graph on the right shows that the simulated energy expenditure has been gradually reduced by around 50 kcal/d additional to what we expected (which would be the red curve):



In this model, the body weight is not regained by “eating more than it is expended”, but rather by the opposite, because the physiological adaptation that has been modeled is caused by the food restriction, i.e., for “eating an insufficient amount of food” in a sustained way. Does this model violate any laws of physics? Please consider that for our body functioning with the substrates that have not been stored is like we’ve just consumed a few grams less of food each day. It is not that hard to understand that Model #2 does not violate any law of physics or suppose an impossible situation for our body.

I believe there is no point in explaining how I implemented the physiological adaptation mechanism in Model #2. What I want to explain is that when I believe that there is a physiological adaptation and, therefore, I include an adaptation mechanism in the model, the model shows a physiological adaptation. And Model #2 is not doing anything clearly impossible: we are talking about an additional reduction of the energy expenditure of 50 kcal/d after two years. Note that the Hall calculations were that the CALERIE2 participants were consuming around 37 kcal/d more than they actually consumed (difference between black and white bars in the graph), which is a difference of the same order of magnitude of those 50 kcal/d that I have simulated. What the Hall model attributes to an increased energy intake when compared with actual data is probably caused by the physiological adaptation whose effects Hall despises.

In short, the message here is that when Hall argues that there is no physiological adaptation in reality because his model does not show a physiological adaptation, his argument is fallacious: if he included the appropriate mechanism in his model, his model would show a reduction of the energy expenditure that goes beyond his present prediction. Just as I have done. In short, his argument can be summarized as follows: “the physiological adaptation does not exist in real life because I did not want to include it in my mathematical model”.

This simulation illustrates the very long equilibration time for weight loss in obese subjects and demonstrates that the weight loss plateau observed after 6 mo cannot be a result of physiological adaptation (source)

Model #3: An “energy” model that does include a physiological adaptation

Model #3 is, mathematically speaking, identical to Model #2. It also includes a physiological adaptation mechanism, but the magnitude of that reaction now changes directly the total energy expenditure and the energy balance equation is applied to compute the magnitude of the daily body fat accumulation.

Note that the evolution in time of intake, energy expenditure and body weight are identical to those of Model #2, because mathematically models #2 and #3 are identical (it has only changed at which point of the feedback loop the physiological adaptation is applied). What is different between these two models is the assumed causality.

  • Model #2. Your adipose tissue stores more fat–> Your body has less fuel to spend–> your body reduces its energy expenditure
  • Model #3. Your body reduces its energy expenditure–> your body has more fuel to store–> your adipose tissue stores more fat

In Model #2 the adipocytes have changed their behavior and they seek to recover the lost body fat, and the rest of the body can not spend what has already been stored in the adipose tissue. Therefore, as a consequence of gaining weight, the energy expenditure is reduced exactly like in Model #3. A reduction in the total energy expenditure would only be a consequence of the underlying physiological process that is actually causing the changes in the accumulated body fat.

For the sake of clarity, these are the  weight (blue curve on the left) and energy expenditure (blue curve on the right) for Model #3:

The energy balance pseudoscience assumes that if you are regaining weight this is caused by an energy imbalance. What I am showing here is that other causalities are compatible too with the first law of thermodynamics: it is possible that the cause of gaining weight is a physiological adaptation regardless of the calorie intake or the energy expenditure. The adaptation can be driven by starvation, by losing weight, by a change in the mean size of the adipocytes or by another physiological cause. In this case, the energy expenditure would be an irrelevant possible symptom of the underlying physiological process that is indeed being caused by food scarcity. Model #2 does not violate any law of physics but it does highlight the causality fraud of the pseudoscientific energy balance paradigm.

it can be calculated that a weight loss of 20-kg body weight in an obese patient will result in an obligatory average reduction of 400 kcal in daily EE. Besides this obligatory or passive energy economy, further reductions in daily EE can also be expected as it has repeatedly been demonstrated that the fall in EE is greater than predicted by the loss of body mass, thereby underscoring the operation of mechanisms that actively promote energy conservation through adaptive suppression of thermogenesis. (source)

May be it doesn’t happen “through” suppression of thermogenesis: they are assuming that an effect is the cause.

How to avoid the physiological adaptation

From the point of view of the energy balance theory, if there is a physiological reaction equivalent to 50 kcal/d, if you eat 50 kcal less you will compensate for the physiological effect. But understanding the process requieres understanding causality: if the cause of the physiological adaptation were an excessive intake, reducing the energy intake would make the reaction disappear and the weight would remain stable. But the cause of that reaction is not necessarily that you eat “too much”, but rather the opposite. The adaptation may be caused by losing weight “eating of less”, i.e. by scarcity of food. If we confuse energy expenditure, a symptom, with the cause of weight regain, we will not prevent that weight regain.

What does the model predict if we even consume 50 kcal/d less? That the physiological reaction will continue to exist, because its cause is not an excessive energy intake. Reducing the energy intake is treating a symptom, the “energy balance”, not fixing the actual cause of that reaction.

I do not intend to draw any conclusions as if in real life there is or not a physiological adaptation similar to the one that I have included in the model. My message is exactly the opposite! What I try to explain is that no useful conclusion can be drawn from a simulation, about the existence or inexistence of such adaptation, because a mathematical model simply does what we command it to do.

And the other conclusion has to do with causality: if a factor makes us fatter, it has to make us fatter, not necessarily have a direct effect on our energy intake or on our energy expenditure. We save money for reasons that can not be deduced by examining the factors that affect our incomes or expenses.

Further reading: