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.

The short-term effect of a diet may have nothing to do with its long-term effect (2 of 2)

(Versión en español: pinchar aquí)

In the first part of this article we have seen an experiment that clearly shows that the CICO theory is wrong.

Let us assume that the following premises are true for a normal diet, not one that absurdly forces an excess of food:

  • In the short term, during the first week or the first two weeks after a dietary change, a low fat diet makes you lose more weight than a high-fat diet.
  • As time goes by, a physiologic adaptation happens and the roles of the diets are exchanged, being on average the low-carbohydrate diet better for body fat loss.

I am not saying that the premises are true, I only ask that we assume for now that they are true.

In this situation a person who I will call John decides to do a meta-analysis of weight loss studies and puts together in the same meta-analysis a) a dozen studies with a duration no longer than a week that mostly show a favorable effect for low-fat diets, and b) a few studies that are a little bit longer, a couple of months at most, which show a favorable effect for low-carbohydrate diets.

John mixes all the studies in the same meta-analysis and concludes that since no diet is clearly the best one, the composition of the diet is not that relevant and that what really matters are the calories! a conclusion that is actually in contradiction with each and every one of the individual studies. How do you feel? In this hypothetical situation that I am proposing, the composition of the diet would be key in the long term and the meta-analysis would have reached just the opposite conclusion, generating noise. A person who wanted or needed to lose weight and keep the reduced weight in the long-term would have to choose the right composition of the diet to achieve that goal.

Does anyone believe that the long-term effects of a diet can be inferred from experiments that are shorter than a week? Does anyone believe that the behavior of our body after months of losing weight has anything to do, anything at all, with what happens in the first three days of following that same diet? (see)

Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition

I this article from 2017 its authors present a compilation of around twenty dietary studies. Table 2B shows us data on changes in body fat for these studies and concludes that, on average, low-fat diets help people to lose more body fat than low-carb diets do:

What are not shown in the previous graph are the durations of those studies. I copied the data from the ES column of the graph above (just as shown in that table, without checking the original articles) and I represented those values as a function of the amount of days the participants followed the diet. As we can see in the graph below, in half of the studies the diet was followed for one week or less. The duration of the study in days is represented on the horizontal axis.

Moreover, those studies with a longer duration, those where the diets are followed at least for a month, are favorable to low-carb diets (the one with the longest duration in the compilation did not use a low-carb diet, as I comment below, but two diets very high in carbohydrates):

The conclusions from the authors are amazing:

In other words, for all practical purposes “a calorie is a calorie” when it comes to body fat and energy expenditure differences between controlled isocaloric diets varying in the ratio of carbohydrate to fat.

Can you really deduce that from very short-term diet studies? It is enough for the believers in the energy balance pseudo-science, who, undoubtedly, use this type of articles to prop up their ideology, but for rest of us it is impossible to draw relevant, general or useful conclusions from this collection of experiments.

First, because of their duration: what is relevant is whether there are differences between diets in the long term, and in this compilation of studies no diet has been followed for more than two months. As a matter of fact, half of the experiments are no longer than a week. Do we want to know which diet is more effective in the long term? Let’s do the experiment, instead of making up a result from short-term data.

Secondly, the fact that some studies favor low-carbohydrate diets and some favor low-fat diets does not mean there are no differences between diets. At the beginning of this text I explained that if the differences were due to the duration of the experiment, by combining experiments of different durations in the same data pool the actual effect of the composition of the diet would be obscured in the average, when the reality would be that the composition of the diet would be key in the long-term effect of the diet. As I have said before in this blog, meta-analysis are another way of lying (see,see,see).

Thirdly, because all kinds of diets are being mixed in the comparison, from ketogenic diets maintained for a few days to diets that are simultaneously high in fat and carbohydrates that have absolutely nothing to do with healthy low-carbohydrate diets. For example, in the experiment from Rumpler et al. de 1991, the longest of all those considered in the compilation (see the last graph above), the high-fat diet was also very high in carbohydrates: 46% carbohydrates and 40% fat.

Can we infer from that result anything about a low-carbohydrate diet? Would the result have been the same if the diet had been ketogenic? The authors of the meta-analysis want us to believe that it would, but by including experiments like the one I am commenting in a meta-analysis, all they do is create misinformation.

Fourth, based on short-term studies, the authors of the meta-analysis reach conclusions that contradict the results of studies with longer durations (see). Are most of the long-term studies poorly done and their data is not reliable? Can we deduce that from 4-day long studies that have nothing to do with the long-term effects of the diets? Shall we ignore all the scientific evidence and replace it with the imagination/ideology of the authors of this meta-analysis?

Note, on the other hand, that not even the authors of the meta-analysis believe what they are doing. They downplay their own result by saying that a difference in fat accumulation of 16 g/d is “physiologically meaningless”.

Figure 2B shows differences in the rate of body fat change between diets with the pooled weighted mean difference of 16 g/d (P < .0001) greater body fat loss in favor of the lower fat diets (P < .0001). These results are in the opposite direction
to the predictions of the carbohydrate-insulin model, but the effect sizes are so small as to be physiologically meaningless.

But an energy imbalance equivalent to only 1 g d of dietary fat could explain the current obesity epidemic.

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)

Yes, this last statement comes too from one of the authors of the meta-analysis, Kevin Hall. He should explain why 16 g/d of difference between diets is “physiologically irrelevant”, as he says, but an imbalance of 1 g/d could explain the obesity epidemic, as he also says. They simply downplay their own result because it is so unbelievable, in the bad sense of the term, so erroneous, that it gives away that something is not right in its origin. Extrapolating this result to the long term makes it obvious that it is wrong. But, if it is not extrapolated to the long term, the authors of the article cannot conclude that “a calorie is a calorie”.

It is not the first time that Kevin Hall interprets very short-term results as a demonstration of long-term behavior (see).

What are the postulates of the energy balance pseudo-science?

We should notice that the energy balance pseudo-science is never explicitly and rigorously formulated in a way that its postulates could be falsified. Other theories are criticized and the followers of this pseudo-science argue that, as the other theories do not seem correct, “then a calorie is a calorie” (see). This is exactly what the authors of this meta-analysis do. It is typical of pseudo-sciences to avoid formulating their postulates so that they can be subjected to falsification. With the energy balance theory the absence of well-defined dogmas allows the coexistence within this pseudo-science of factions that defend postulates that are incoherent among them (see).

The consequences of all this charlatanism are very serious: public-health dietary recommendations are still based on the stupid energy balance pseudo-science, weight loss methods that have never been proved to work are still the official treatment for obesity and we continue to blame the victims for their failure to lose weight, arguing that they are not lean because they do not show enough adherence to the diet (see,see).

As a final note, the fact that something could only be accurately measured in specific conditions, does not mean that what we measure in those conditions is useful. Maybe only weight loss studies that last three days are really reliable, because you have the participants locked in a facility and you have absolute control about what they eat and what they do. You measure everything very well and you control everything very well, but the data that you measure is rubbish because the failure of the diets is a problem that happens after following the diet for several months (see).

Further reading:

The short-term effect of a diet may have nothing to do with its long-term effect (1 of 2)

(Versión en español: pinchar aquí)

One of the main dogmas of the energy balance pseudo-science is that when two diets have the same amount of calories and the same amount of protein, in that case they are equal for the control of our body weight (example). We are told that this idea derives from the First Law of Thermodynamics and that, therefore, to deny this dogma is to deny unbreakable laws of physics.

Let’s imagine that we do an experiment in which two groups of people are given much more food for a week than they would normally consume. Both groups receive the same amount of calories: one group receives 50% extra food in the form of carbohydrates and the other group 50% extra food in the form of fat. The same energy intake and the same percentage of protein. On the 7th day we measure how much body fat these two groups of people have gained that day. Should we get the same result from both dietary groups?

Is it possible, according to the energy balance pseudo-science, a result like the one I show in the graph below, where one of the diets produces more body fat accumulation than the other one?

No. It would not be possible according to that theory. This result would be in contradiction with the idea that our body weight is determined by the calories of the diet: the two dietary groups ingested the same amount of food in terms of calories!

How would the energy balance pseudo-science explain this result? It could not explain it and the reason is that that theory is nothing but charlatanism.

It is a real result, obtained from the following article.

Fat and carbohydrate overfeeding in humans: different effects on energy storage

For 14 days, 9 lean people and 7 obese people are given 50% more calories than the amount that is considered necessary for each participant. Each participant receives two types of extra food: one based on carbohydrates and one based on fat. The authors do not give details about the base diet nor about what the composition of the excess food is.

The evolution with time of the fat balance (difference between fat that is ingested and fat that is oxidized) is very interesting. Very interesting indeed.


As we can see, the result of this experiment shows that in those participants in the very first first days the “extra” dietary fat is much more fattening than the “extra” carbohydrates. But can we forecast, based on the previous figure, what will happen after day #14 (which is the day this experiment ends)?

It is impossible to ignore what we see in the figure above: not only the outcome is not determined by the calories of the diet —which is what the CICO theory postulates as obvious—in those participants (the result is a function of the composition of the diet), but we also found that it is irrelevant to know what happens in the first few days to know what will happen in the long term. We see what happens in the first 14 days of the experiment and we have no idea how the accumulation of fat would evolve from that moment on. We do not even know in what type of participants a diet can be more fattening than the other one in the long term.

The authors of the article apparently saw it differently:

we found that for equivalent amounts of excess energy, fat leads to more body fat accumulation than does carbohydrate.

Please note that they confirm that the CICO theory is dead.

But what I am most interested in is that this is a very short-term result, for all-male participants, for participants that are used to follow a high-carbohydrate diet and that are forced to eat a lot of extra food, extra food that is based on food products with a single macronutrient, not natural foods, etc. It seems to me that some people have serious problems limiting their conclusions to the conditions in which data have been obtained.

Do we extrapolate this result to people who follow a low-carbohydrate diet, who do not force themselves to consume more food than what their appetites demand, who do strength training, who follow a diet for years —instead of two weeks— and who consume real food, instead of half of their food in the form of a product that is 100% fat? Making that extrapolation is barbaric. In this article I want to talk about “scientists” who do that extrapolation.

This experiment is absolutely irrelevant for practical purposes, since it has nothing to do with the conditions in which a person would follow a diet high in fat and low in carbohydrates. Nobody defends a diet that is simultaneously high in carbohydrates and high in fat, such as the one that is used in this experiment. Moreover, in this experiment people are forced to eat in excess. But this experiment is useful a) as one evidence more of the falsity of the CICO theory and b) to demonstrate that short-term data are irrelevant for understanding long-term weight loss or gain.

The other major barrier to understanding is the focus on short-term studies. Obesity usually takes decades to fully develop. Yet we often rely on information about it from studies that are only of several weeks’ duration. If we study how rust develops, we would need to observe metal over a period of weeks to months, not hours. Obesity, similarly, is a long-term disease. Short-term studies may not be informative. Jason Fung

Further reading:

“Pseudo-sciences do not talk about physiology”

(versión en español: pinchar aquí)

How to detect a pseudo-medicine? It’s very easy: pseudo-sciences do not talk about physiology

Writing about pseudo-medicine is relatively easy. Most pseudo-medicines are simple and self-contained. Being fundamentally fictional, outside of real complications, you do not have to fret overmuch about physiology and anatomy and plausibility and all the other aspects of medicine that make being a doctor a lot like Barbie in a math class. It’s tough. (source)

How do they say we can detect a pseudo-science? It is quite simple: pseudo-sciences are unable to give explanations based on physiology or anatomy that can be verified in scientific experiments. We have a textbook example: the energy balance pseudoscience. Are there any physiologic mechanisms that support this theory? None: it is based on “energies that enter” and “energies that leave”, and physiology is replaced by a mathematical operation that lacks a plausible link with the actual function of our organs and tissues. Clear as day: we have found a pseudo-science.

In obesity you have to talk about energy, not physiology

But, apparently, with obesity it is the opposite: pseudoscience is talking about physiologic mechanisms, because that distracts our attention away from the actual cause, which is “genetic, environmental and behavioral.” No physiology, please! Without mundane and dirty physiologic mechanisms, because we know a lot about physics laws and this is an energy problem. We are damn good at physics.

We need to understand why some people gain weight easily and others don’t. Taubes doesn’t have an answer for that: his “cause” of obesity is more of a “mechanism” that doesn’t really get at the underlying genetic, environmental, and behavioral causes. While we are waiting to understand that, we still have the practical problem that overweight people need to lose weight now. It is undeniable that if you can find a way to reduce total calorie intake sufficiently, you will lose weight. (source)

Just a physiologic mechanism that is irrelevant in order to treat obesity. In obesity it does not matter if we treat causes or symptoms (see).

The two quotes above come from the same website: Science Based Medicine. They can easily see that they are the ones who defend pathetic pseudo-science: they simply have to apply their own detection criteria for pseudo-sciences. To put heroes face to face with their true identity is not cruelty: it is to move forward so that obesity stops being treated with a theory that is pure charlatanism (see).

What are the physiologic mechanisms that support the energy balance theory?

What are the physiologic mechanisms that link our energy intake with all the energy stored in our body, in all its formats? What are the physiologic mechanisms by which “eat less (calories)” works?

What are the physiologic mechanisms that detect a decrease in the energy intake, and how is that information translated into the physiologic signals that reduce the fat that is stored in the adipocytes? What explanation does the energy balance theory give on those physiologic mechanisms?

Why do these people ignore the actual reaction of our body, as can be found in scientific journals, to food restriction and replace it with fantasies falsely based on a general law of physics that has nothing to do with our physiology?

NOTE: I wonder why they use Barbie as an example of someone who has problems with a math class … Are they saying that Ken would not have those problems? I think it’s obviously clear what they’re saying.

Further reading: