Unjustified premises lead to fraudulent conclusions (II)

(versión en español: pinchar aquí)

How are the unjustified premises included in the CICO hypothesis?

The energy balance formula (EB), which is frequently used to explain how we should proceed in the case of wanting to lose, gain or maintain weight, is as simple as I quote below:

EB = caloric intake (CI) – caloric expenditure (CO).

The above equation is based on the Law of Thermodynamics

Alberto Hernández

I hope that at the end of this article we all will see in the previous quote the same deception that I see.

The conservation of energy principle

Well then, here we go. The conservation of energy principle: the energy present in the chemical links of the products that we eat (IC), either ends up being used by the body to generate movement/heat (CO), or ends up stored in a tissue/organ of the body (Adipose Tissue, GLycogen, Muscle Tissue, TUMor, etc.):

As an important note at this time, assuming a given energy intake, hypothetically the energy stored in the adipose tissue can change in response to the physiological/hormonal signals it receives, and that change, logically, would result in that either the energy expenditure would be affected or the energy stored in the rest of organs tissues would be affected. Nothing in the energy balance equation tells us this is impossible. Why do I say that it is important to highlight this possibility? Because one of the ideas that I want to explain with this article is how in the CICO hypothesis this possibility is “magically” eliminated. I will try to clarify in this article how this “magic” happens.

We make a definition

We define energy balance (EB) as calories IN (CI) minus calories OUT (CO):

And, once we have that definition we have two coupled expressions for EB, that is, two expressions that are dependent on each other:

The above equalities for EB are only correct when used together. Together they are the energy conservation equation. It is not possible to consider one of the equalities in isolation, because the other equality also contributes to establishing the correct values ​​of equality we select. With rigor, they can never be used separately.

What happens if we use only one of the two previous equalities? Please note that this is exactly what the quote at the beginning of this article does:

EB = caloric intake (CI) – caloric expenditure (CO).

If the first equality was used alone, we would arrive to a wrong conclusion, which is that EB is determined by the difference between CI and CO. Is it not what the equality says? No, it isn’t!!, because in that case the second equality is ignored! EB is not a “dead” term in this first equality, determined just by CI and CO: if we think about it for a moment, the reality is that the term EB could change because of changes in the second equality and CO could just reflect those changes. By ignoring the second equality and interpreting EB = CI-CO as the formula for calculating EB, we have arrived at the deceptive conclusion that CI and CO are the important terms for EB, the terms that “determine” it and, therefore, the only terms we have to look at. By using the first equality alone, a false causality has been created. And the important thing here is that we don’t see that we make a mistake!

The balance between calories IN and calories OUT determines our weight. Óscar Picazo

In summary: we erroneously interpret that EB is determined by CI and CO. Assuming that the intake is controllable, this points to the energy expenditure (CO) as the parameter responsible for establishing a value for the energy balance (EB).

Although we already know that we are making a mistake, I will go on with this reasoning in order to expose the conclusions it leads to. With a EB that has been (fraudulently) determined by CI and CO, now we use the second equality.

Once we have a EB term that has already been established by equality 1), another deception is created, which is to assume that the only energy in our body that can change is the one stored in the adipose tissue (AT). This is absolutely unwarranted and is deceptive (as proved if we just apply the same mistake to any other term of the second equality):

From this (false) second equality, it follows that the energy balance (EB) value established by CI and CO will command the adipose tissue to store or release energy. As I already anticipared that it would happen, by using the 2 equalities one after the other, instead of always using them together, an unjustified premise has been included in the argument: the possibility that the AT term changes by itself and the rest of terms adapt to that change has been removed. The chain of mistakes that have been made has turned the adipose tissue into a passive tissue: now it obeys what is commanded by the difference between the Calories IN and Calories OUT. This conclusion has not been reached because it is what physiology says, nor because it is what is inferred from the laws of thermodynamics, but as a result of the reasoning mistakes that have been made. Note that without deceptions and paralogisms that conclusion cannot be reached.

If we look again at the quote I presented at the beginning of the article, what do we see now?

How are the unjustified premises included in the CICO hypothesis?

The energy balance formula (EB), which is frequently used to explain how we should proceed in the case of wanting to lose, gain or maintain weight, is as simple as I quote below:

EB = caloric intake (CI) – caloric expenditure (CO).

The above equation is based on the Law of Thermodynamics

Alberto Hernández

If CI and CO determine EB, only one of the two equalities is used: the first one. And, as a result of that mistake, the adipose tissue is no longer a “living” tissue, capable of changing by itself while other terms adapt to its changes. Adipose tissue is not considered, because the adipose tissue is not explicitly included in the second equality. CI and CO determine EB, period. What terms are relevant in the computation of EB? If we only use one of the two equalities, only the terms included in that equality will matter. The whole approach to the treatment of obesity from this very moment is focused on CI and CO exclusively. And if it doesn’t work, then it is concluded that CI and CO are more complex than was previously thought. But, as we have seen, that one is not the error in the foundations of CICO.

It is very easy to understand what I am saying, if we start from the second equality (instead of using first one, which is what CICO does). If in the second equality we assume that AT changes by itself, that would lead us to the conclusion that AT determines the changes in EB:

And then from the first equality we would conclude that CI and CO are irrelevant. Can the second equality be used in isolation to calculate EB? It is not a rhetorical question. What is our answer?

The deception that I explain in this article is used in the arguments that defend the CICO hypothesis as the way in which our body behaves: in the speech a value for the energy expenditure is assumed and, therefore, for the energy balance, and then the second equality is used, to wrongly conclude that the adipose tissue is forced to adapt to an energy balance that has been established (by using fallacious arguments) without taking into account the adipose tissue. We clearly can see this in two quotes from Stephan Guyenet, PhD:

Any energy that’s left over after the body has used what it needs is stored as body fat. Stephan Guyenet, PhD

When calorie expenditure decreases and calorie intake increases, the energy balance equation leaves only one possible outcome: fat gain. We gained fat as we ate more calories than we needed to remain lean, given our physical activity level. In other words, we overate. Stephan Guyenet, PhD

I emphasize again how, in the behavior described in the two quotes above, it is not possible for the adipose tissue to change by itself and affect the energy balance (defined as CI-CO). As we have seen, this is possible in the correct equation, i.e. the energy conservation equation, but it is not possible in the CICO hypothesis.


The reasoning mistakes that I have explained in this article lead to the conclusion that the energy balance is established by the calorie intake (CI) minus the energy expenditure (CO). Once the energy balance term is established without taking into account the adipose tissue, this tissue is supposed to just obey the (false) energy conservation equation.

In short, with this long explanation what I try to make clear is that in the CICO hypothesis the adipose tissue is mistakenly turned into a passive tissue: from being a living tissue it is turned into a dead term, unable to change by itself. How is this fraudulent premise, which is a fundamental part of this hypothesis, introduced in CICO?That is what I have tried to explain in this article, although just to realize that it happens is a step forward in understanding the deception.

NOTE: if the 2 equalities are considered separately, to take into account many factors that affect the terms of the equalities doesn’t fix the reasoning mistakes that create CICO.

NOTE: EB=CI-CO is at the same time correct as an arbitrary definition and —for the reasons that I have explained in this article— wrong as the formula that allows the computation of EB. As we have seen, if that definition is used as an isolated formula, the principle of conservation of energy is being ignored.

Further reading:

Taubes-Guyenet debate. My analysis (IV)

(Versión en español: hacer click aquí)

My notes on the fourth segment of the debate (next-to-last) and my comments below them:

  • [GT 1h33m] The sugar hypothesis: you add something about a western diet/lifestyle to populations, you get explotions of obesity and diabetes. My hypothesis is that sugar is the something that has to be added. Maybe it is sugary beverages.
  • [SG 1h34m] It’s always possible to tell stories to salvage your hypothesis, but that does not necessarily make the story correct. We don’t have any evidence to support what Gary just said. Quote from Christopher Hitchens: “That which is asserted without evidence, can be dismissed without evidence”. And that’s the way I feel about this particular story.
  • [SG 1h35m] I am going to talk about three different cultures that eat a lot of sugar and don’t have obesity. The Hadza in Tanzania eat a lot of honey. 15% of their calorie intake comes from honey. This is as much as americans eat and they eat fruit on top of this. The pygmies in the Congo also eat a lot of honey. Up to 80% from calories can come from honey during the rainy season. And they are lean.
  • [SG 1h38m] If you eat a lot of sugar but everything else is in place, the sugar is not enough to make them fat. I am not saying it doesn’t contribute, I think sugar does contribute, but it is not singlehandedly responsible as Gary has argued. The Kuna of Panama is the 3d culture. They eat white sugar.
  • [Joe Rogan 1h39m] In non westernized-civilizations you burn off so many calories…
  • [SG 1h40m] I 100% agree with you.
  • [Joe Rogan 1h40m] The thing about burning off the calories is that in westernized lifestyles you are just existing, they are doing nothing to burn the shit off. I think what Gary is getting at is that if you have this lifestyle and then with that lifestyle consume sugar you are going to get fat. I don’t think you can compare that to athletes and I don’t think you can compare that to hunther-gatherers. I remember being working out 4h/day and eating everything I was in the mood (soda, cookies, etc.), and not gaining any weight other than muscle.
  • [SG 1h42m] I agree that it is not as simple as sugar, but Gary argues that sugar is the primary cause of obesity and that physical activity does not matter, calorie intake does not matter.
  • [GT 1h42m] When we talk about the cause of obesity, I don’t believe obese people become obese because they are sedentary.
  • [Joe Rogan 1h42m] Don’t you think that an athlete has a high sugar demand and will burn that off?
  • [GT 1h42m] Absolutely.
  • [GT 1h43m] Can I go back to the Kuna? Stephan calls my stories, stories, which they are, but he calls his “evidence”. About the Kuna [he reads a text from an e-mail exchange with Guyenet] they eat a low amount of sugar (32 pounds of sugar per year) and we don’t know how that amount has changed over the years. [Guyenet laughs out loudly while Taubes speaks] I also don’t believe the data from the urbanized Kuna, who apparently drink only 3 8-oz soda per week, and they consumed more sugar back where they used to live.
  • [GT 1h45m] Stephan is constantly citing studies which only speak about one hypothesis, like the overfeeding studies, or that are poorly constructed and poorly done. About the Hadza, I already told him that I don’t think it is a refutation of my hypothesis, since my hypothesis is that when you add sugar to the diet of any population you get obesity. May be the Hadza have been eating honey for 1000s of years. May be when they inmigrated to this area they had obesity then. I don’t think finding a hunter-gatherer population that eats honey and doesn’t have obesity is a refutation, Stephan does.
  • [GT 1h47m] My non-for-profit funded a study with 40 kids that had NFLD.They could eat fruit, as much as they wanted, but no added sugar and no sugary beverages. The fatty-liver disease resolved. We can’t talk about the mechanism. May be it was the weight loss.
  • [GT 1h48m] About the metaanálisis from Hall, it is putting together all the junk-science that has been done in the last 50 years, while ignoring any quality of the studies. And they did a poor job. In one study I checked, they even confused a 400 kJ decrease in energy expenditure with a 400 kcal decrease [N.T. 400kJ=95kcal].
  • [GT 1h49m] You have to do the right studies if you want to get the right answer.
  • [GT 1h50m] Stephan openly rejected this study that NuSi funded with 12 million dollars. There are basically 3 preople out there that are convinced that everything people like me are saying is wrong.  They keep coming over and over again. Kevin Hall claims that he has refuted the carbohydrate-insulin model. When his study comes out supporting it, he works to find out why the study is wrong. We all do the same thing. The goal is ultimately to do the right study, because we have to remember what is on the line here.
  • [GT 1h51m] For decades people have thought as Stephan does, and there is an alternative hypothesis and we have to find if it is true because people are dying out there.
  • [SG 1h51m]  This alternative explanation has been investigated extensively, included studies that were funded by his own organization, NuSi. 2 out of the 3 studies were a clear refutation of his hypothesis. There is a remarkable correlation between studies undermining your beliefs and you thinking those studies are garbage. [Guyenet smiles]
  • [SG 1h52m] About the Hill and Peters studies, if you can’t actually find specific problems with the studies, you can’t just dismissed them.
  • [GT 1h53m] I gave you a problem with the study: it was designed based on the assumption it was supposed to test.
  • [SG 1h52m] Ok, it wasn’t designed how Gary wanted it to be designed.
  • [SG 1h53m] The Kuna. The primary basis for Gary’s book is that when sugar comes into this cultures they become fat. I am pointing out 3 cultures that eat high levels of sugar and are not fat. In reference [22] we can see that in the Cuban economic crisis the intake of sugar went up, 28% of caloric intake, double what Americans eat. Their calorie intake went down and they had to walk a lot because of the lack of gasoline. If Gary is right and calories don’t matter, only refined carbohydrates and sugar, obesity should have gone through the roof. The prevalence of obesity declined by half: from 14% to 7%. The rate of underweight increased only slightly. As soon as they went back to their original diet, obesity went up.
  • [GT 1h57m] I would have to read the study to figure out what the problem is.
  • [Joe Rogan 1h57m] What about the NuSi studies?
  • [GT 1h57m] Well, this is a game people play. My issue with Stephan is that he speaks as if though he knows, with this authority.
  • [SG 1h58m] The 2 first studies refuted Gary’s hypothesis. Gary is about the only person who thinks they did not refute his beliefs. The scientific community is pretty unanimous.
  • [GT 1h59m] The first study was a pilot study that depends on what you look at, you can think it refutes a belief. Kevin Hall tends to believe that obesity is an energy balance problem, David Ludwig and his colleagues tend to believe what I believe. If you believe Kevin interpreted correctly his study (the one funded by NuSi), then it is not supportive of carbohydrates being responsible of driving insulin and insulin being driving fat accumulation. The David Ludwig’s study reported the opposite. David has critisized Kevin’s study and Kevin’s has critisized David’s study. The middle study was a free-living study done by Christopher Gardner. The low-carb diet was not a meaningful low-carb diet and they told both groups not to eat sugars and refined grains, which are by my hypothesis the most fattening carbohydrates. They tested two diets and neither of them had sugar nor white bread. It was a poorly done study, it didn’t answer the question.
  • [SG 2h3m] Caloric deficit was self reported, so it is not actually accurate.
  • [SG 2h4m] There was a 2-fold difference in carbohydrate intake.
  • [GT 2h4m] If you believe the food frequency questionares that you just said we don’t know whether can be believed.
  • [SG 2h4m] I agree with you that refined carbohydrates and sugar are the most fattening types of carbohydrates.
  • [Joe Rogan 2h5m] OMG, we can do an agreement?
  • [GT 2h5m] The question is why. Is it because people eat too much of them?
  • [SG 2h5m] If you believe Gary’s hypothesis, since any type of carbohydrate increases insulin levels more than fat does, if that matters for fat loss, these groups had a 2-fold difference in carbohydrate intake, even though it was predominantly healthy carbs. You should have seen something, not the same amount of weight loss in both groups.
  • [Joe Rogan 2h5m] But they are not high in sugar, right? Your argument has been always about sugar, right?
  • [GT 2h5m] Stephan is right: I defend my hypothesis. He does the same. We all do it. And every study ever done has plenty of reasons not to believe it. This is why independent replications is something you always want.

The ad populum fallacy

[SG 1h58m] The 2 first studies refuted Gary’s hypothesis. Gary is about the only person who thinks they did not refute his beliefs. The scientific community is pretty unanimous.

The ad populum fallacy is the appeal to the popularity of an opinion as a reason to accept it. The number of people who believe a claim is true is irrelevant in relation to whether it is correct or not. Taubes is aware that his ideas go against the prevailing opinions.

Guna, Cuba and Hadza

I think it would be a mistake to ignore the examples of the Guna, Hadza or the economic crisis in Cuba. Let’s see how they live and how healthy they are.

The Guna are presented by Guyenet as consumers of a large amount of white sugar. Actually, according to his calculations, the “high” consumption of white sugar (sucrose) is 36g/d. That amount includes 1/3 cup of sweetened drink per day. That is a consumption of a 12-oz soda per 4-5 days. According to this study, 23% of their calories come from dietary fat.

Is this an adequate example that you can consume a large amount of sugar and still not have obesity? In my opinion, this example tells us nothing about what happens in a Westernized culture. If, for example, they live on islands and due to their high fish intake they have a good omega-3 to omega-6 ratio, it is possible that this protects them from their —apparently very low— white sugar consumption.

The case of the Cuban economic crisis from 1989 to 2000 is another of the examples presented by Guyenet. As we can see in the graph below, which is included in the article linked by Guyenet, the energy intake was reduced around 750 kcal in the center years of the aforementioned period.

More data: the diet was very low in fat (13% of calories in 1993) and in protein, with only 46 g/d, only 10% of caloric intake (see):

The population had to walk or to use bicycles everywhere due to the lack of motorized transport (see):

Starting in 1990, this new situation, which produced changes in the nutritional status of some groups of the population, combined with a forced increase in the level of physical activity. As a result of the general scarcity of motorized transport, the population began to walk and use bicycles for their daily movements.

There was an increase in the cases of: anemia in pregnant women, chronic protein deficiency, underweight pregnant women, underweight births, etc. In other words, with a nutritionally-very poor diet, based on sugar and rice, when forced to exercise, and consuming much fewer calories than recommended, this population lost weight in the short term (see). And this happened despite consuming around 150g of sugar per day.

The prevalences of obesity in Havana were 11.9 percent, 5.4 percent, and 9.3 percent in 1982, 1994, and 1998, respectively.

As a summary, they lost weight transiently by being hungry with an unsustainable low-energy diet, that was nutritionally deficient and very low in fat, while they were forced to have more physical activity, just as if they were in a concentration camp. Under these conditions, sugar was not enough to produce obesity in the short term. Okay.

As for the Hadza, they apparently consume a large amount of honey during part of the year (source) and generally they do not have excess weight. Assuming that the food that is brought into their camps represents the foods that are available in each month of the year, the following graph would show that a high consumption of honey only happens during, approximatedly, half of the year.

It should be noted that what they consume is neither white sugar nor refined honey: it is honey with bee larvae, which contains more protein and fat than commercially processed honey:

Although only small amounts of protein (mainly free amino acids) are found in liquid honey (Bogdanov et al. 2008), wild honeys contain higher levels of protein and fat, most likely because they contain trace amounts of bee larvae, whereas cleaned and commercially processed honey does not (source)

On the other hand, the diet of the Hadza seems to be very low in dietary fat, with only 11% of the calories coming from fat (see). Could this be the key factor that makes honey not fattening for the Hadza? In any case, there may be other relevant factors, such as the speed of ingestion and honey’s texture, or low levels of omega-6 in their diet.

The Hadza’s story is an interesting one.

Do these stories refute the sugar hypothesis? If they do, we need a better hypothesis that is also based on physiology, not to go back to worship the energy balance pseudoscience.

And if the sugar hypothesis is unambiguously refuted, whatever hypothesis steps up as the next prime suspect has to be very carefully considered. (i.e., not the simplistic notion that people eat too much and move too little). We need a hypothesis that holds the promise of explaining the epidemics everywhere. Gary Taubes

The three studies that NuSI funded:

  • The pilot experiment (Kevin Hall)
  • DIETFITS experiment (Cristopher Gardner)
  • The weight maintenance experiment (David Ludwig)

As we have already discussed in the 3rd part of this analysis David Ludwig’s experiment, I focus on the other two.

” Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men “

In this 2016 video we have Kevin Hall bragging about refuting the carbohydrate-insulin model with a not-randomized pilot experiment!! (diets are applied in one sequence only and there is no control group) while on the background there is a poster whose title says the opposite of what he explains in the video (see): “Energy expenditure increases following an isocaloric ketogenic diet in overweight and obese men.”

The increase he found wasn’t enough for him, because he set a requirement as high as he liked so the difference between diets was reported as irrelevant (see): he demanded a difference of 300-600 kcal/d.

These data, although somewhat confounded by ongoing weight loss, suggest that large isocaloric changes in the proportion of dietary carbohydrate to fat transiently increase EE by only ∼100 kcal/d after adjusting for body weight and composition. […] the carbohydrate–insulin model predicts that the KD would lead to increased EE, thereby resulting in a metabolic advantage amounting to ∼300–600 kcal/d (21, 22). Our data do not support EE increases of that magnitude.

So, we see that Hall thinks of a 100 kcal/d difference between diets as small. It is awkward, though, because Hall believes that 10 kcal/d of caloric surplus explain the current obesity epidemic in the USA (see). In other words, he says a 100 kcal/d difference between diets is too little because he demands 300-600 kcal/day to the ketogenic diet, just because he wants to demand that. This is god-level zealotry. And he gets it published in a scientific journal!

We did not include a control group that did not receive the KD or a group that had the diets delivered in the reverse order.

The order of the diets can make, for example, the energy expenditure greater during the first diet, since no weight has yet been lost and there is more fat and non-fat mass. That’s why it was a pilot study, because it was non-randomized and not designed to detect differences between groups. It was not meant to draw conclusions, but rather to learn how to properly design a subsequent bigger study that would have enough statistical power (see). Did you say that the study has limitations? It doesn’t matter: when you think it can be useful to support your pseudoscience, you use the outcome as if it were a randomized experiment.

Moreover, in this experiment the authors (Kevin Hall among them) failed to keep the weight of the participants stable (see).

A major limitation of our study is the unintentional weight loss. Despite slight positive energy balance during the chamber days, the overall negative energy balance amounted to ~300 kcal/d and was likely due to greater spontaneous physical activity on nonchamber days.

It is an invaluable practical demonstration of the actual value of Hall’s ideas about how our body works. Bias? Cognitive dissonance? Zealotry? It’s Kevin Hall, PhD.

Guyenet summarizes this experiment saying that there are no differences. The article says the opposite of what Guyenet says, despite the limitations of the study, which probably played against the ketogenic diet:

The isocaloric KD was not accompanied by increased body fat loss but was associated with relatively small increases in EE that were near the limits of detection with the use of state-of-the-art technology.

“Was asociated.” Another inconvenient truth for Guyenet.

” Effect of Low-Fat vs. Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion “

This experiment, led by Christopher Gardner, is commented in this blog post. Since in that link we can read a detailed analysis, I go directly to the relevant facts. The  participants were supposedly doing a caloric restriction of 500 kcal/d. We see in the following figure the evolution of their body weight:


After 12 months, one group lost a mean of 5.3 kg while the other one lost a mean of 6.0 kg:

Weight change at 12 months was −5.3 kg for the HLF diet vs −6.0 kg for the HLC diet (mean between-group difference, 0.7 kg [95% CI, −0.2 to 1.6 kg]).

There was a difference between diets, but it didn’t reach statistical significance. But the important thing is that in the second half of the study both groups gained weight back. Why did they regain part of the lost weight? Is this what the CICO hypothesis predicts? The problem for Guyenet is as follows:

  • If he claims that the outcome shows no differences between diets, he has to assume that the intake data is reliable. Otherwise he doesn’t know if the caloric restriction was the same in both groups.
  • If he thinks that eating less is a valid weight loss strategy, he can’t accept the intake data as correct.

If he says that the intake data of this study are reliable, this experiment shows that the hypocaloric diet is a failure as a weight loss diet. That would be another refutation of Guyenet’s hypothesis. Are reliable the intake data from this study, Guyenet?

Taubes makes this point: “it’s the same data that you said that they were not reliable because they were self-reported”.

NOTE: Kevin Hall’s low level as a scientist and his lack of rigor are evident in his articles (seesee).

NOTE: it’s not obvious that nonindustrialized populations such as the Hadza have a high energy expenditure that allows them to eat as much as they want and not get fat (source).

Go to the conclusions
Go to the fifth part
Go to the fourth part
Go to the third part
Go to the second part
Go to the first part

Taubes-Guyenet debate. My analysis (III)

(Versión en español: hacer click aquí)

My notes on the 3rd segment of the debate and my comments below them:

  • [SG 1h2m] When you use accurate methods you find that people with magical metabolism, those who have obesity and don’t eat very much, seem to not exist any more.
  • [SG 1h3m] I want to talk about studies where they increase calorie intake. If we want to understand why people get fat, we can look at studies that overfed people on fat or carbohydrates exclusively. In one study they calculated the energy requirements and then they increased that by 50% with fat or carbohydrate. This is Horton’s study, reference [16]
  • [SG 1h4m] If Gary’s hypothesis is correct, these people should have gained fat in the carbohydrate overfeeding but not the fat overfeeding. These people were in a metabolic ward, so the researchers could monitor everything. No cheating. No inaccuracy.
  • [SG 1h6m] What they found is that at the end of a 2-week period of overfeeding, the carb and fat group gained exactly the same amount of body fat. In a 2nd study they did the same thing and found the same result. 3-week-long experiment. Different insulin responses, different amounts of carbohydrate and fat, exact same amount of fat gain. This demonstrates that insulin is not what gets fat into fat tissue. Calorie intake is what controls that.
  • [GT 1h7m] The paradigm you work in determines the questions you ask. This experiment assumes people get fat by overfeeding. They think they are just doing what happens naturally. They are answering the question of whether people can get fat by overfeeding. This experiment is built on the paradigm they want to test.
  • [GT 1h7m] [Comments about the relationship of Peters JC, Hill JO. with Olestra and the sugar industry]
  • [GT 1h10m] 10 kcal/d, less than a bite of food, explains obesity. How do we explain those 10 kcal/d? Is the brain somehow regulating that? Or is it due to a disregulation in the body that traps fat in the fat cells or prevents fat from being used for fuel? If someone drinks 5 beers a day, may be he/she only stores 10-20 kcal/d, how does that happen and why does it go here and not there?
  • [GT 1h12m] It is not that hard to imagine that someone during a relative famine can store 10 kcal/d. If they are only eating 1200, 10 get stuck in the fat cells and 1190 are excreted or expended. Nothing in the laws of physics says so. In animal models you can disassociate obesity from eating too much.
  • [Joe Rogan] In essence you’re saying that even if someone is consuming a lot or a few calories each day, 2000 kcal/d, if those calories are consumed in the form of sugar, the body will store part of them, even if the body is not receiving enough food, while if you consume protein, vegetables, etc. your body will not do that.
  • [GT 1h13m] This brings us to the subject of evidence and mechanism.
  • [Joe Rogan] But you’re saying that, right? If two people follow the same caloric intake, one of them with 2000 kcal/d of chicken, fish, vegetables, and the other one of 2000 kcal/d of milkshakes and sugary drinks, pasta and BS, that person is going to gain a certain amount of calories and put them to fat, regardless [of calories].
  • [GT 1h14m] Yes, that is the hypothesis. And that hypothesis can be tested. Stephan thinks it has been tested 80 times, I think they have done a bad job of testing it. And we both tend to reject the studies that we do not like, when we define “don’t like” as not having the answer that we think is correct.
  • [Joe Rogan] But You, Stephan, you think that this is not correct. You say that in the study where they add additional fat and additional carbohydrates, they both gain the same amount of weight.
  • [SG 1h14m] That’s right. If Gary’s hypothesis is correct, you have to see different levels of fat gain.
  • [Joe Rogan] It was a short term study?
  • [SG 1h14m] Yeah, it was a short-term study. 2 and 3 weeks. It is very short. But if insulin is the hormone that puts fat into fat cells, you should see any kind of difference, some kind of effect on fat gain.
  • [GT 1h15m] One problem with overfeeding studies is that one of the hypothesis says energy balance is dependent on the macronutrient content of the food. Therefore you are going to have different levels depending on what the macronutrient content is.
  • [GT 1h16m] Ludwig’s study is an example. They saw different levels of energy expenditure depending on the carbohydrate content of the diet. The lower the carbohydrate the higher the energy expenditure.
  • [GT 1h18m] Experiments should take into account all the competing hypothesis. If there is a threshold effect of insulin, which actually there is, you don’t actually expect to see any difference between groups, since they are both in the plateau of the insulin response. If it actually is activated in both groups, both hypothesis predict the same fat gain.
  • [GT 1h20m] Anecdote about an obese friend. My hypothesis is that he would have gained weight regardless of eating or not 300 kcal extra a day, because his insulin was elevated.
  • [SG 1h20m ] It is easy to tell stories, it is not easy to tell stories that are supported by scientific evidence.
  • [SG 1h20m ] 29 studies have measured energy expenditure on diets differing on carbohydrates and fat content. When you put all these studies together, it makes almost no difference in the metabolic rate if people are eating carbohydrates or fat. In fact, the very small difference favors high-carbohydrate diets.
  • [SG 1h21m] The study Gary says (Ludwig’s) is the one that reports the biggest difference among those 28+1 studies.
  • [SG 1h22m] In Ludwig’s study, some of the participant’s data are literally physically impossible. If you remove the clearly erroneous data, the study no longer reports a higher energy expenditure on a low-carbohydrate diet and is consistent with the previous 28 studies.
  • [SG 1h23m ] In regards of the 10 kcal/d, Gary, I continue to have the feeling that you don’t understand human energetics, because that is not how it works.
  • [GT 1h23m] You are insulting me, you have to stop doing that. You keep acting as if you think I am an idiot.
  • [SG 1h23m] It only takes a small amount of extra calories to make someone gain fat. As they get fat their calorie needs go up.
  • [GT 1h24m] How does the brain do that?
  • [SG 1h24m] I didn’t say the brain does that. The point is that by the time they have obesity, they are consuming 20-35% more calories than they were when they were lean. It is not one of 2 cokes a day that is allowing them to remain obese, they are consuming 20-35% more. It’s not 10 extra calories.
  • [SG 1h26m] If you eat 10 kcal more than you need, you store them.
  • [SG 1h27m] Sugar intake has been declining in the USA during the last 20 years, it peaked in 1999 and it is now 15-23% lower than it was in 1999. Obesity has increased during the last 20 years. The same in the UK.
  • [SG 1h29m] Taubes counterargument is that the amount of sugar we consumed 20 years ago may influence us today.

Arrogance is not the same as assertiveness

In this segment we have Guyenet again qualifying Taubes’ opinions as story-telling, presuming to defend an opinion based on scientific evidence and stating that his interlocutor does not understand the energetics of the human body. I insist on the warning that we should not take Guyenet’s arrogance as a symptom that he is right or that he knows what he is talking about. Arrogance is only a sign of arrogance, nothing else. And do not mistake arrogance for assertiveness.

Guyenet disinforms about sugar

I start with the end of the debate segment. Guyenet cites at 1h27m the fact that, in the USA and in the UK,  the rate of obesity continues to rise although sugar consumption has been declining in the last decades. The argument is inappropriate for a person with a college degree, specially if this person has a PhD. It doesn’t matter how arrogant he is: his argument is unquestionably stupid.

Why is it stupid? It is explained in these two articles:

In the following graph I show the annual sugar intake in the USA (blue curve) from 1980 to 2015 and the annual increment in the percentage of obese adults (orange curve):

As we see, there could be a causal relationship between sugar consumption and body weight, since changes in sugar consumption correlate with the growth rate of obesity. When the consumption of sugar goes up, obesity grows faster. And there is also a good correlation in the case of sugar-sweetened beverages. This is not proof of a cause-and-effect relationship, but a cause-effect relationship can’t be ruled out with these data.

Well, Guyenet, who has a Ph.D., assumes that if sugar is fattening there must be a direct relationship between sugar consumption (blue curve) and the integral of the orange curve (i.e. the accumulated value), something that does not make any sense when assuming that sugar is fattening, which is the hypothesis that he wants to refute. If he had just represented the data in another way, as we have seen in the graph above, he would have found that direct relationship that he believes does not exist.


And since he doesn’t find a direct relationship where nobody expects it to be, he assumes that sugar cannot be an important factor in the obesity epidemic. Regardless of whether this is true or not, regardless of the relevance of sugar in the obesity epidemic, Guyenet’s argument is blatantly wrong. For more detailed explanations of Guyenet’s mistake, I refer to the two blog posts (English language in both of them) I linked above.

Let’s not mistake arrogance for competence.

False dichotomy fallacy

[SG 1h6m] This demonstrates that insulin is not what gets fat into fat tissue. Calorie intake is what controls that.

Even if Guyenet were right about insulin, it doesn’t follow that calorie intake controls fat accumulation. He is using the false dichotomy fallacy. His claim that calorie intake is what controls body fat accumulation has to be proved.

Taubes’ arguments

Some of Taubes’ arguments seem remarkable to me:

  • 10 kcal/d, which is less than a mouthful of food, explains obesity. How do we explain those 10 kcal/d?
  • It is not so difficult to imagine that someone during a relative famine can store 10 kcal/d. If they are only eating 1200 kcal/d, 10 remain in the fat cells and 1190 are excreted or spent.
  • In animal models one can find the dissociation between obesity and eating too much.

Guyenet avoids addressing the first argument, as I explain below. Guyenet says that eating too little you cannot get fat, as we saw in part II of my analysis. In regards of the third one, and this is something we have seen in this blog, experiments with animals do show that they can gain body fat without an increased intake. How can Guyenet explain his irrational belief that overeating is a requirement for weight gain in humans?

Overconsumption experiments

This is one of the most interesting parts of the debate. Guyenet begins by citing the overconsumption experiment by Horton et al. 1995 in which extra food is given in the form of fat or in the form of carbohydrates. And Guyenet says, literally, that if the carbohydrate-insulin hypothesis were correct, differences between both diets should have come up, and he says that fat gain was the same in both groups.

We have already commented this experiment in the blog (see). Let’s watch again the graph of the fat balance (difference between ingested and oxidized fat) from this study:

As we can see, the first few days the 50% extra calories that are consumed as fat (black dots) are more fattening than when given in the form of carbohydrates (white dots). The two diets do not produce the same outcome, in contrast with what Guyenet says. This is very important, because anyone who hasn’t read this article and listens to Guyenet’s claims, is being deceived. Extra dietary fat makes you fatter than extra carbohydrates, at least in the two weeks of this experiment. And this is clearly stated by the authors of the experiment:

we find that for equivalent amounts of excessive energy, fat produces more accumulation of body fat than carbohydrates.

This is an inconvenient truth for Guyenet’s claims. And he hides this fact. He says that according to the carbohydrate-insulin hypothesis there should have been a difference between groups, and he says there is not. But the truth is that there are differences between groups, differences that refute Guyenet’s hypothesis, which is that the accumulation of body fat is determined by the caloric intake.

This demonstrates that insulin is not what gets fat into fat tissue. Calorie intake is what controls that. Stephan Guyenet, PhD

Guyenet uses this experiment as a refutation of Taubes’ hypothesis, but he hides that the experiment refutes his own hypothesis. It is not the calories in the diet what determines the accumulation of body fat. This experiment is very clear about this.

If we want to understand why people get fat, we can look at studies that overfed people […]

As I said, this is a very interesting part of the debate. And there are many clarifications I want to make. For example, that this type of experiments do not demonstrate that we gain fat because we eat more than we expend, which is Guyenet’s hypothesis. The overeating hypothesis is very complicated to test. How would it be tested? Imagine that we have two groups of participants to whom we give exactly the same food, but each day we give 10 kcal/d extra to one of the groups. As one group gets fatter than the other –if that actually happens— the intake would be adjusted to continue giving those 10 extra kcal/d that make them gain body fat. And, after 5 years, for example, that group would have gained 2.5 kg more than the other group, if the overeating hypothesis is correct. Of course, the experiment would have to be done with all kinds of diets, since checking the result only in one diet would not guarantee the same outcome with a different diet. I assume everybody can see the difficulty of carrying out this experiment with enough participants, for enough time, with enough control of the intake, testing a wide-enough set of diets and with enough control of the levels of physical activity to test this hypothesis. As the test cannot be performed under real conditions, what the overeating experiments do is change the conditions to achieve a much greater effect and much earlier. The experiment that Guyenet cites does something completely different from the situation of interest: they give 1000 or 1500 extra kcal/d each day on top of a specific diet, and, they assume that if that causes body fat accumulation, the mechanism by which people who do not force theirself to eat those extra 1000 kcal/d is the same as in that experiment, regardless of the diet composition. That approach is called the fallacy of a single cause, which is to suppose that when a cause of an effect has been found, that one is the only possible cause for that effect. The reason why a person gets fat when they are not forced to eat exorbitant amounts of food day after day may not have to do with the amount of food, but with its composition. That idea is what Taubes proposes. But that possibility is discarded without any further explanation by the advocates of the energy balance pseudoscience, like Guyenet. We can also interpret this error as a fallacy of continuum: although we do not know at which moment we are going to begin to gain weight “because of the excess” when we progressively increase the amount of food, something that will happen if you force yourself to eat much more than a normal person does, it does not follow that food ingestion in normal amounts and an abnormally high food intake are comparable situations. And these experiments claim that both situations are the same and aim to shed light on how obesity develops. And, as a matter of fact that is the way Guyenet introduces them: “if we want to understand why people get fat, we can look at studies that overfed people”.

The overeating experiments are the ones that can be done, and the ones that researchers can include in their CVs, but not necessarily those that bring light on the nature of obesity. Note, on the other hand, that those experiments do not test Taubes’ hypothesis: they do not change the composition of the food in order to produce a bigger or smaller insulin secretion. As Taubes says, these experiments assume that they are testing what happens naturally in the person who gains body fat. It is not necessarily true. They show that ONE WAY to gain body fat is to force an extreme food intake. One way, not necessarily the only one. This experiments do not show that this is the way in which those of us who do not force ourselves to eat exorbitant amounts of food gain weight.

Note from this experiment we only have fasting insulin data, not postprandial levels. Therefore, it is not possible to talk about relationships between fat accumulation and insulin levels. Guyenet assumes that for the high-carbohydrate extra load the secretion of insulin will be greater than for the high-fat extra load, but he does not know if it is true because that data is not in the article.

Another important aspect of this experiment is the time evolution of the outcome. At the very first days, the extra dietary load in the form of fat is more fattening than the dietary load in the form of carbohydrates, but as the days go by, the oxidation of fat is reduced in the high-carbohydrate-load diet, and after 14 days the two diets are almost equally fattening. What happens in the longer term? It is not tested, and we cannot make it up. In these unreal conditions, in the very short term, we know what happens, but in the long term we don’t know what will happen. We cannot draw conclusions about the effects of a diet from short-duration experiments, even if these experiments are the ones that can perform the best measures (see), because what they measure is irrelevant. The relevant outcome is the effect of a diet when it is followed for years.

Guyenet cites another overfeeding experiment (see), which, when examined in detail, doesn’t seem to prove anything. I analyzed it in a separate post, so the length of the present one was not increased. I just point out that the results in terms of body fat accumulation in that experiment are very unreliable and that Guyenet argues that there are different insulin responses in that experiment, when the authors actually said “no significant differences”. Another inconvenient fact that Guyenet misrepresents.

Hall and Guo’s meta-analysis

Guyenet mentions a meta-analysis by Hall and Guo that concludes that for any practical purpose, a calorie is a calorie.

In other words, for any practical purpose “a calorie is a calorie” when it comes to differences in body fat and energy expenditure between controlled isocaloric diets that differ in the ratio of carbohydrates to fat. Hall and Guo .

We have also seen that meta-analysis in the blog (see). As we have just seen, the effect of a diet changes over time, so I represented the duration of the experiments with the effect on body fat. As we see in the following graph, most of the experiments included in the meta-analysis are less than two weeks long, practically all of them reporting less accumulation of body fat with the diets that have more carbohydrates and less fat:

But, as we see in the graph above, for the experiments of greater duration (around a month and a half) the result is favorable in general to the diets that have less carbohydrates.

Hall and Guo don’t take into account the duration of the experiments, they put all together in a meta-analysis and they conclude that there is not a clear winner, so there is no effect of the diet composition! Well, that’s wrong, the composition does matter. If you follow the Western standard diet, with 50-60% carbohydrates, a sudden increase of dietary fat can cause you to accumulate body fat during the first days after the diet change, an effect that is biiger than if you increase carbohydrates and reduce fat. The composition of the diet does matter. But if you follow a diet for two months, it may be the other way around. If you have the “practical purpose” of living more than two months, this meta-analysis does not rule out the importance of the diet composition. We don’t know what happens in the long term and we can’t make it up.

Again, let’s notice that Guyenet says that this meta-analysis finds no differences between diets: it’s not true, and anyone who listens to him is being deceived. But to say the truth is inconvenient for the pseudoscience he defends. There are differences between diets and that fact refutes his hypothesis that body fat is determined by the calories in the diet . You always have to check the data and trust no one.

Ludwig’s experiment

This experiment is commented in this blog post, and one of the authors describes it here.

What happened with this experiment? The first reaction was to try to discredit the study by stating that the way of calculating the results had changed, because the outcome was not what the researchers wanted.

Is that true? According to David Ludwig (see), the protocol of the experiment was unusually detailed (unlike other experiments, in which the authors don’t give many details and then they do whatever they fancy) and was incorrectly stated. As the experiment progressed, they were fixing mistakes. And, when they realized that the measure of the energy expenditure was wrongly specified: they fixed the mistake. This happened BEFORE BREAKING THE BLIND in the experiment. I say this again: they fixed the mistake before breaking the blind.

The error was recognized and corrected a priori. We obtained IRB approval for our final analysis plan on 06 Sept 2017, before the blind was broken (and indeed, before measurement of the primary outcome had been completed by our collaborator Bill Wong in Houston). Similarly, we corrected the Clinical Trials registry prior to breaking the blind. We provide documentation of this timeline, and additional detail, in the Supplement Protocol section.

This is important: they fixed the error in the protocol without knowing if that correction would benefit one outcome or another. Therefore, to affirm that the protocol was changed because the data did not reflect what they wanted, is defamation. But, of course, the outcome of this experiment was inconvenient for Hall, Guyenet and their friends.

What has Hall done? With the unblinded data, which was provided by the authors of the experiment, he has looked for alternative ways to calculate an outcome so the statistical significance is reduced (see). For example, calculating the effect of different diets not from the moment they start to be different, but from before that, introducing noise in the measure:


I refer the interested reader to Petro’s analysis of Hall’s Hall’s jiggery-pokery:

Moreover, Guyenet says that there is dietary intake data for some participants that would violate the first law of thermodynamics, and that if the data from those participants is removed from the calculations the differences between diets disappear. This is not true. In this experiment we have both energy expenditure data and energy intake data, the latter being used as a corroboration of the former, since it is a fact that dietary intake data are inherently unreliable. As I understand it, Kevin Hall (see) decided to redo the analysis of the data by discarding the energy expenditure data of those participants whose energy intake data he thought was erroneous, a very questionable decision, since an error in the energy intake does not invalidate the corresponding energy expenditure data, which may still be correct. Even if the energy intake data is incorrect, the corresponding energy expenditure data is from of a person who maintains their body weight, and that’s what the experiment was about. By making that very debatable —-and convenient for him— reanalysis of the data, as the threshold for data elimination was lowered, the difference between groups was reduced, but the difference between groups was not eliminated as Guyenet claimed in the debate. In Hall’s words:

The intercept of the best fit line was 30 ± 3 kcal/d per 10% reduction in dietary carbohydrates and corresponds to the estimated dietary effect on TEE when all energy is accounted

A TEE increment by 30 kcal/d for every 10% reduction in the percentage of carbohydrates is a huge amount. An effect of that size can perfectly explain the difference between regaining the lost weight and keeping the lost weight. The difference between diets has not disappeared, it has only been reduced by this more than questionable data manipulation by Kevin Hall. Guyenet’s claim that there was no difference between diets is a lie.

It is Hall who has performed an alternative analysis of the data because the outcome of this experiment is inconvenient for the hypotheses on which he has based his career. And he has used unblinded data, knowing exactly what he had to change to achieve the desired result. Accuse the other side of what you are guilty.

Remember these actions by Hall and Guyenet, because later in the debate Guyenet will accuse Taubes of saying that experiments are garbage when they do not support his beliefs:

There is a remarkable correlation between studies undermining your beliefs and you thinking about those studies as garbage. Stephan Guyenet, PhD

Does he talk about Taubes or is he talking about Hall and himself? Huge hypocrisy!

10 kcal/d

Finally, we have the Guyenet’s insult to Taubes, saying that, in his opinion, he doesn’t understand human energetics (n.b. I didn’t know that there are special energetics for humans). Taubes asked him to stop treating him like he was an idiot. And Guyenet’s insult precedes him telling something that everyone knows, which is that when you get fat you usually have an increased energy intake and an increased energy expenditure. Is that what Taubes doesn’t understand? What a clarification from this energy genius named Guyenet.

But let’s not lose sight of Guyenet’s maneuver: as he cannot talk about “excess” in a person who accumulates 10 kcal/d and has still not gained weight, what he does to avoid explaining that situation is to talk about a situation that has nothing to do with it, which is that of a person who is already obese. Then he defines “excess” as the difference between what that person eats and what a lean person eats.  He says that people do not lose weight because they eat more than lean people. That is his belief, but he doesn’t know if it’s because of that or it isn’t. This is just his baseless belief. But he has avoided talking about the fattening process and has made it clear that, in his opinion, if you are overweight, you eat too much and that’s why you don’t lose your extra weight. This is a good trick, but the only thing that shows is his inability to answer Taubes question.

Taubes understands what Guyenet is explaining, but he doesn’t believe that body fat gain is caused by too much energy. And he believes that it is possible to gain weight without an increased intake, something that Guyenet believes is a requirement to gain weight. Guyenet insults him but he is not able to explain why Taubes’ view is wrong.

Go to the conclusions
Go to the fifth part
Go to the fourth part
Go to the third part
Go to the second part
Go to the first part

Taubes-Guyenet debate. My analysis (II)

(Versión en español: hacer click aquí)

My notes from the second segment of the debate (second half hour of it) and my comments below the notes:

  • [SG 29m] The brain actually regulates body fatness. No one should be surprised by this.
  • [GT 30m] One of the problems is “intellectual phase-lock” [a condition in which dogmatic beliefs prevent certain questions from being asked]. The obesity research community left out of its research endocronilogy in the 1960s, i.e. the hormonal/metabolic regulation of body fatness, oxidation, etc. Everything they have done since has been interpreted incorrectly. Leptin is a good example. They assumed what leptin does is control the brain, but perhaps a lot of what leptin does is done in the periphery. In the search for genes associated with body type all the genes act below the neck (insulin-regulated genes), but with excess body fat they decided they are in the head. The question is that when they look, they are programmed to think body fat is caused by overeating, so they look in the brain.  
  • [SG 35m] They don’t start with any assumption.
  • [GT 36m] Genes can have different jobs in different cells of the body, but if you think that the problem is in the brain, that’s where you look. 
  • [GT 36m] Stephan’s book is supposed to be about obesity, but in fact you never mention anything about the hormonal regulation of fat accumulation. It is just not there and it has to be there. [we can hear the laughter of Guyenet while Taubes speaks] 
  • [GT 37m] Stephan is the defender of the orthodoxy, and I’m the one who comes along and says “you have psychologists and psychiatrists running the field, while endocrinologists solved it”. 
  • [GT 37m] What has the brain to say about the fact that body fat accumulates in some parts of the body and not in others? [Again we can hear Guyenet laughing while Taubes speaks] 
  • [SG 38m] When looking at the genes associated with total body fatness, the thing that causes obesity, genes related to the brain pop up, whereas when looking for genes related to the body fat distribution, we see insulin-related genes, for example in the people who have body fat around their waist.
  • [SG 39m] [sarcasm about Taubes talking about leptin] “this is good”, because he does not normally mention leptin. Researchers do not talk about the peripheral actions of leptin because it has been shown that the effects of leptin are via the brain, not because they wear blinders . [Guyenet taks about himself as a researcher: “WE focus”]. In the experiments in which the leptin receptors are knocked-out in the brain or in the hypothalamus you get obesity, which shows that the brain is a key site of action.
  • [GT 40m] A key site of action. 
  • [SG 41m] The brain is this site of action that causes this to happen. We understand very well how leptin works. People with obesity don’t lose fat because they have a higher set point in their adipostat. When a person loses weight there is a reaction in the brain circuits that regulate body fatness that drives an increase in their cravings and hunger. It does that until the fat comes back. Body fat is regulated by a negatively feedback loop that is controlled by leptin.
  • [Joe Rogan 44m] When you are eating a sugary diet, a high-calorie diet, your body will get fatter, right? 
  • [SG 44m] It depends on how many calories you are eating.
  • [GT 44m] Leptin is not only produced in response to the size of the adipocyte, but also in response to the entry of glucose into the adipocyte, which is partly mediated by insulin. 
  • [GT 45m] Everything that is said has two interpretations, depending on which paradigm you are looking at. And the paradigms are essentially different. 
  • [GT 46m] 8 years ago Stephan and I first fell out when I acted inappropriately in the Ancestral Health Symposium. 
  • [GT 46m] Knowing that more people are entering a room than leaving does not tell us why the room is getting crowded. In obesity, why you are getting fatter has been left out and people decided that overeating was somehow an explanation. 
  • [GT 47m] To know what is the influence of the environment on obesity we must ask ourselves if  we can find an epidemic of obesity without this “modern food environment”. And I found out about the Pima in 1902: poor, malnourished, suffering through famine for 40 years, and yet the women of the tribe, who do all the hard work, were obese. We can then disassociate obesity from the “modern food environment” and the ultra-processed foods. We have obesity despite the existence of famine. [We hear Guyenet laughs]
  • [Joe Rogan 48m] What was the cause of the women becoming obese?
  • [GT 48m] They were “reservationized” and they began eating western foods. You can find the same in the Sioux.
  • [GT 49m] Any population transitions to a Western diet or western diet/lifestyle become obese and develop metabolic syndrome. Genetics aren’t that important thing, the important thing is what’s triggering it in the environment. I think it is certain foods. 
  • [GT 50m] Double burden of obesity: we have obese mothers with malnourished children. And this occurs in populations that have not been able to “overeat”. And if they could have eaten more, why are their children starving? How do we explain obesity in the mothers without assuming that the mothers are overeating? 
  • [Joe Rogan 51m] Stephan, are there populations in the world that are obese and that are not consuming a Western diet, that are not eating sugary products? 
  • [SG 51m] Probably not, because once you have an industrialized food system that is going to include sugar. But there are populations that eat a lot of sugar and are not obese.
  • [SG 52m] Gary has told a story, his version of the Pima story. Let me tell you the version of the story that appears in the scientific literature. They were a society that depended on agriculture, but with the arrival of farmers (settlers of european descent) the river that supplied them was diverted and the government began to provide them with food: calorie dense refined foods, flour, lard and sugar. And they became very obese. Other Pima who, right accross the border, maintained their traditional high-carbohydrate and agricultural lifestyle, were much leaner and healthier.
  • [SG 54m] Gary, you seem to believe that people can gain weight even if they are eating too few calories …
  • [GT 54m] Yes 
  • [SG 54m] These are very casual observations, story-telling. When you look at the data, what you see obese people consume between 20 and 35% higher than people who are lean. Those data come from the most accurate methods that we have. Gary’s model says that is a consequence, a result, of gaining weight, while my model says that that is actually required for the fattening effect to occur. What happens if you reduce the calorie intake by that same amount? It does not matter if you do it by restricting carbohydrates or fat, these experiments have been done, they lose weight.
  • [Joe Rogan 56m] You’re saying that by consuming low amounts of calories but high amounts of sugar, it does not make sense that one can become obese that way. 
  • [SG 56m] Right.
  • [GT 56m] We can find cases where there is obesity without excess food, such as Trinidad in the 1960s. Two thirds of adult women were obese, and there was famine, malnutrition and stunted children. Data say that they consumed fewer calories than those recommended by the WHO for a healthy diet. The brain hypothesis does not explain why a mother is obese while her children are starving. If she has to eat superfluous calories to get fat, which is what that hypothesis says, why isn’t she giving those calories to her children? My hypothesis is that the explanation is that it is the macronutrient content of the diet what triggers obesity. 
  • [GT 59m] There are experiments on which the animals get fat even if they are starving. 
  • [SG 59m] They are experiments done on animals with mutations related to leptin.
  • [GT 59m] The point is that if my body accumulates fat at intake levels at which a thin person can’t, I will gain fat eating the same amount. 
  • [SG 59m] The caloric intake data for Trinidad are not reliable. There is no reason to believe that people were eating 1800 kcal/d and becoming obese. Accurate measures of caloric intake from people who say that they are consuming 1200 kcal / d, say that they consume more calories than thin people. What Gary says is only observed when inferior methods are used to measure calorie intake.
  • [GT 1h1m] I insist on my question: obese mother with starving children. The existence of the starving children strongly suggests that there is not a lot of food available. And we have to explain the obesity in the mother. 
  • [SG 1h1m] There are many reasons why a child may have malnutrition in a non-industrial situations. I don’t have an explanation but it is not necessarily for the reason that Taubes says.

It depends on how many calories you are eating

Guyenet, PhD, the same guy who just a few minutes earlier said that a diet with fat and sugar produced effects that cannot be completely replicated with only sugar or only fat, now worships the energy-balance dogma:

  • [Joe Rogan 44m] When you are eating a sugary diet, a high-calorie diet, your body will get fatter, right? 
  • [SG 44m] It depends on how many calories you are eating.

This is the same guy who believes that sugar can make you fat because it is palatable, regardless of how many calories it has. But when he is interested in showing support to the official dogmas, then he says that calories are what makes us gain fat. Guyenet is a master of cognitive dissonance. Or a master of decepcion who is betting to two horses at the same time.

There is no obesity if westernized food is not present

They both agree on that. It is clear, I would add, that it is not a dysfunction in the brain what causes obesity. An analogy can make this clear: if I prick someone with a needle and that person bleeds, the cause of the bleeding is not the lack of a band-aid: it’s been the needle prick what has caused the bleeding. Even if we know that a band-aid stops the bleeding. Speaking of obesity, if your genetic endowment is better than that from other people, maybe it protects you from “food” that you shouldn’t be eating, but what causes obesity in those other people is the insult, not their faulty brain: the cause is the stimulus, that is, what they are eating and they shouldn’t be eating.

Let’s see an example. Suppose we have two people (person A and person B) who are exposed to two different environmental conditions (conditions 1 and 2) for a time, with the following results in terms of body weight gain:

Person \ Environment  1 two
A 0 kg +6 kg
B 0 kg +7 kg

Even if we found a relationship between genetics and weight gain that explained the difference between those +6 and +7 kg, what is the real cause of the weight gain in this example? It is only an example, but it makes clear that although the differences between people’s fat mass under environment #2 can have a genetic explanation, not necessarily that fact tells us anything meaningful about the actual cause of their obesity.

On the other hand, Guyenet argues that there are populations that consume a lot of sugar and they are not obese. He will give details later in the debate. What I want to emphasize is that his counterargument does not prove anything about the reasons why we get fat in the western world, not even in case we believe the data of those populations are reliable. They just don’t live under the same conditions we do. For example, there could be a synergistic effect of sugar with seed oils (high omega-6) or with some endocrine disruptor, and finding out a population that has a high consumption of sugar and no obesity, in the absence of other factors typical of the western world, cannot be used to exonerate sugar in societies in which sugar coexists with a different set of dietary and environmental factors. Or maybe these people spend a lot of time outdoors (under the sun) and respect their circadian rhythms and that fact protects them in a certain way from sugar, and that is not our case. Or maybe those populations follow very low-fat diets in which sugar is not so harmful to their health. Who knows.

Obese mothers and undernourished children

The “double burden of obesity” is the coexistence of obesity and undernutrition in a population (see). For example, in the following graph we have BMI (body mass index) versus age in refugee camps in Western Sahara. As we can see, in all ages there are both people with clear obesity and people with very low BMI:

And in this study in a quarter of the households coexist obesity and malnutrition:

Our results demonstrate that both stunting (in children and women) and obesity (in women) are highly prevalent among Sahrawi refugees, with central obesity being even more prevalent and appearing at a younger age in women than obesity. Second, more households were affected by overweight and central obesity than by under-nutrition, although the latter affected over one-third of households. Third, an important proportion of refugee households, one in four, are affected by the double burden of malnutrition.

How do you explain that there is an obese mother who has an undernourished child? Guyenet puts into question the data provided by Taubes, that is, he says that a woman cannot gain weight by consuming only 1800 kcal/d.

[SG 1h0m] What Gary says is only observed when inferior methods are used to measure calorie intake

Is that so? Does the obese mother overeat while her child is starving? This is hard to believe.

[Joe Rogan 56m] You’re saying that by consuming low amounts of calories but high amounts of sugar, it does not make sense that one can become obese that way. 
[SG 56m] Correct.

Let’s mention four scientific experiments I have already commented in the blog. In the first one (see), we have a group of rats, the HS group that consumes a diet high in sugar. As we can see in the table below these lines, this groups consumes about 100 kcal/d, while the HF group consumes about 200 kcal/d. The body weight and body fat data tell us that the group that consumes 100 kcal/d finishes the experiment with more weight and more fat mass than the one that consumes 200 kcal/d. Can you get fat while eating too little? Yes, you can.

This is an experiment in animals and, therefore, absolutely controlled. There are no reasons to doubt caloric intake data in animal experiments.

The second experiment (see) shows that the same food, and therefore with the same calories, is much more fattening when consumed as powder than when consumed as pellets. The graph shows in pale pink the evolution of the body weight of three dietary groups that consume much fewer calories than the group represented with empty circles, and yet, the evolution of their body weight is practically the same as in that group:

This means that in this experiment, while eating much less food, those three groups of rats are gaining weight at the same rate as rats that consume more calories. I insist: in the experiments with animals the caloric intake is not poorly measured. The trick of questioning the reliability of the caloric intake is unwarranted here.

In the third experiment ( see ) the group of mice that eats the lowest amount of calories (white points) is the one that gains more weight and more body fat:

In the fourth experiment (see), the diet of the rats is identical in terms of nutrients and calories, differing only in their glycemic index. To prevent rats in the high-glycemic-index diet from gaining more weight than the other group, their intake had to be considerably reduced, as shown in the graph a the top:

Despite the reduced intake compared to the other group and despite having practically the same weight as they have, the high-glycemic group finished the experiment with 71% more body fat: 98 g vs 57 g. And they are eating less food:

[SG 54m] Gary, you seem to believe that people can gain weight even if they are eating too few calories …

Gary Taubes believes that it is possible what the  four scientific experiments above show is possible. The question is why Guyenet doesn’t think it is possible. Doesn’t Guyenet know what has been published in the scientific literature?

Anyway, I think Guyenet is entitled to doubt the data. What is unacceptable is the arrogance of saying that Taubes’ arguments are story-telling and of presuming that his own opinion is supported by scientific evidence.

Gary has told a story, his version of the Pima story. Let me tell you the version of the story that appears in the scientific literature.

As we will see in other segments of the debate, the “anecdotes” that Guyenet will use (the Kuna, the Cuban economic crisis or the Hadza) are observations that are quite similar to the cases explained by Taubes, i.e. the Pima, the Sioux and Trinidad. Story-telling or science in both cases, no matter who puts them on the table. Guyenet uses plenty of derogatory comments towards the Taubes’ arguments and presumes of being the defender of what the scientific evidence says. Why does Guyenet think he is better than Taubes? He is not even a researcher any more, in contrast with what he implies in the debate: he is a writer and a scientific consultant. Not only does he use the fallacy of authority, he does it by bragging about being what he isn’t.

People who suffer from obesity eat too much

I put together here three of Guyenet’s arguments:

  • obese people eat between 20 and 35% more calories than lean people
  • in the Guyenet model eating a lot is a requirement to gain weight
  • if you reduce the intake in that same amount it does not matter if you do it by restricting carbohydrates or fat, the experiments say that you lose weight

The first point already appeared in the first segment, but I insist on it because I find it interesting. Gary Taubes argues in the debate that to develop obesity it is enough to accumulate 10 kcal/d, and that this is not explained by an “excessive” consumption, because of that “excessive” intake that there may be every day only 10 kcal/d end up being storead as body fat. As Guyenet cannot justify saying 10 ridiculous kcal/d are an “excess”, what he does is redefine “excess” as the difference between what you eat when you are already obese and what a lean person eats. With this trick he converts those 10 kcal into a much larger amount, and this allows him to go on using the term “excess”. In any case it is a rhetorical trick that he uses to avoid answering the question. And in doing so, he blames the victim for his weight problem: if you have obesity Guyenet says that you overeat even if you maintain your weight, even if you eat what your body asks or needs to function. We should not fall in his trap: we are not talking about the person who already has excess weight: the one who is gaining weight does so at a rate of 10 kcal/d. Does this accumulation of energy occur because this person eats 10 excess kcal/d compared to the person who does not gain fat? That is the question that Guyenet avoids to answer. Because nobody can accept that 10 kcal/d are an “excess”. And maybe that fat accumulation is not produced by the “excess”, but instead by the composition of the diet. Guyenet has beliefs, but he may be wrong in his beliefs.

Moreover, Guyenet uses this argument as an explanation for the “dual burden of obesity”, but he is not using data from the populations cited by Taubes. He doesn’t know if that is the case of those populations.

The second argument is that an increased intake is a requirement to gain weight in Guyenet’s obesity model. Well, we have seen four scientific experiments that show that, in such a case, his model is wrong. And I find it very interesting that he uses the term “requirement”, because precisely one of the errors on which his pseudoscience is based is to assume that an increased intake with respect to the energy expenditure is a requirement to gain weight. It is not!! That belief is based on errors of reasoning, and I have explained thousands of times in the blog (and we are near the point where saying a thousand times is not an exaggeration): see, seeseesee.

Finally, Guyenet says that by reducing the caloric intake people lose weight. Guyenet is deceiving the hundreds of thousands of people who have seen this debate.The scientific experiments show that people lose weight in the short term, but the lost weight is almost always regained in the long term, even when the energy restriction is maintained (see, see). That’s what the scientific evidence shows, not what Guyenet is telling. What’s more, he could ask Kevin Hall, PhD what happens when you try to make someone lose weight by applying that method (seesee). But hey, it’s no surprise that Guyenet deceives people with clearly wrong arguments. This has an explanation: this guy is Guyenet, PhD.

In regard to this, let’s remember an experiment (see , see) in which a group of mice is forced to eat only 66% of the calories consumed by the rest of the mice (who follow different diets). As we can see, after the initial drop in their body weight they gain weight.

Have those mice lost adherence to the caloric restriction? No. They have gained weight while eating a small amount of food.

NOTE: all the terminology of the energy paradigm is in question. It is not obvious that the term “excess” (or “caloric excess”) can be used associated to body fat gain .

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Taubes-Guyenet debate. My analysis (I)

(versión en español: pinchar aquí)

To talk about who won a debate seems ridiculous to me. I understand why this happens in politics, where the only thing that matters to those who debate and to their respective parties is to sell an impression, an image, but in matters of nutrition/obesity to summarize a debate with a poll that determines who is the winner is useless. It only shows which thought group has more followers. You can launch the poll before the debate, and you will probably get the same result. Let’s forget polls. Let’s talk about what arguments they have used and let’s talk about what we think about their arguments. If the only “argument” we have is to make the rest of our group shout “X won”, where X is our “king’s champion”, what we promote is sectarianism and the defense of beliefs that may be wrong.

Did Taubes win? Did Guyenet win? Irrelevant questions that lead to irrelevant answers.

Moreover, when people talk about who won a debate, they go beyond who has better rational arguments. If we read the comments on youtube in regards of this debate, we will clearly see that there are a lot of references to the condescendence (i.e., arrogance and air of superiority) of one of the participants. To say that A or B have lost the debate because they are insufferably arrogant is useless. Or, rather, it is the part of “losing the debate” that is useless. I think it is important to highlight the ad hominem arguments, the use to the argument from authority or the arrogant manners (like affirming that one’s opinions are science, while those of the opponent are story-telling). In these attitudes there is no “rational argument”, but there is an attempt to convey that you are right and that your oponent is a moron who does not know what he is talking about. Humility, on the other hand, is interpreted as a lack of faith in one’s beliefs. Arrogance does not convey to me a sense of “professional competence”, and neither do these letters that certain people write after their names. I do not care if you have one or four PhDs, if your arguments are garbage. I will probably comment these arrogant behaviors, just to highlight how these non-rational arguments are used to “win” the image battle.

Was it an interesting debate? In my opinion, it was. Unpleasant to watch, but interesting. One thing has nothing to do with the other.

Please note that even when some of the hyperlinks I use in this article lead to Spanish-language blog posts, the titles of the scientific articles I comment in those posts are always clearly visible.

In this first part I comment the first half hour of debate. I start with my notes on the topics covered, indicating who was talking and when.

  • SG [1m30] “The brain circuits that regulate body fatness”.
  • SG [3m30] Aliens analogy, car, wheels, speed, brain.
  • SG [5m] The brain regulates the size of adipocytes. Adipocytes do not regulate their own size.
  • SG [7m] In people who get fat there is a change in the regulatory mechanisms. A person who gets fat is not simply a thin person who eats a lot.
  • SG [8m30] The genes associated with obesity are genes related to the brain. 
  • SG [10m] Drugs approved to fight obesity are based on eating less (reducing appetite or reducing nutrient absorption). No “effective fat loss drugs” targets either insulin or adipocytes.
  • SG [11m30] Genetic mutations that cause obesity do so by affecting the signaling of leptin. Leptin is the main hormone that regulates body fat.
  • SG [14m] The effect of sugar + fat cannot be completely replicated with only sugar. Guyenet attributes it to palatability.
  • SG [15m] It is not possible to obtain, either in animals or in humans, the same increase in energy intake with sugar and carbohydrates than with tasty food that combines fat and carbohydrates.
  • GT [17m] When asked if calories “matter”, he answers that it is the wrong way of thinking about the obesity problem.
  • GT [22m] Obesity is a problem of fat accumulation, not an energy balance problem.
  • SG [26m] What differentiates a story that is true from one that is not, is the evidence. The genetic propensity in obesity has to do with the brain. 75% of the difference in body fat between individuals is due to genetic differences between them. The environment is much less important.

The Car Analogy

Guyenet, PhD (I will omit the PhD from now on for conciseness and readability reasons) from the beginning talks about “the brain circuits that regulate body fatness”. He does not say that they influence, he says that they regulate. Recall that shortly before the debate Guyenet criticized Taubes (see) by saying that he believes that his hypothesis was the “primary” mechanism that caused obesity, instead of being open to other mechanisms being important. Here we see clearly Guynet’s hypocrisy, when he says on his part that body fat is regulated by brain circuits.

The analogy he uses is that of some aliens who observe the behavior of cars and try to understand why some cars go faster than others. He says that if they did the analysis observing the behavior of the wheels, they would not understand anything, because the speed is determined by the driver, that is, by the brain. The analogy is just surprising, since it does not contribute anything at all to our understanding of the problem. If obesity is regulated by our brain, the analogy will be adequate, but if it has more to do with Taubes’ ideas, the analogy will be simply wrong. This analogy is a waste of our time.

Adipocytes do not regulate their own size

The argument is a fallacy because nobody says they do. The hypothesis that Taubes defends is rather that it is the stimulus received by the adipocytes (insulin), modulated by the response of certain organs to that stimulus (insulin resistance), which will ultimately determine whether there is a net accumulation of body fat or there is not. The correct question is: do the stimuli that the adipocytes receive regulate their size?

The genetics of obesity have to do with the brain, not so much with the environment

So, the populations that follow their ancestral diets (no flour, no sugar, no seed oils, no processed products, etc.) have a brain that is different from ours?

It seems to me that the environment (i.e. what we eat and how we live), is the #1 cause of obesity, neither our brain nor our genes. 100 years ago we had the same genes, exactly the same ones, but we did not have an obesity epidemic. Is it our genes’ fault? When a group of people migrate from a non-westernized culture to a westernized culture, in general these people gain weight. Do they gain weight because of their brain or is it because of the environment change?

Of course, when exposed to the same stimuli some genetic dotations will react better than others, and similar genetic dotations will react in a similar way, but the real cause of the problem is the inappropriate stimuli, not the protective capacity of our genes to cope with that insult. Is obesity 75% genetic? No, 100% seems to be caused by environmental factors, as demonstrated by the fact that obesity only appears when the environment becomes westernized.

There are no efficient drugs that act on insulin or adipocytes

On the one hand, it is a fallacy to associate “FDA approved” with “effective”. There are not, to the best of my knowledge, effective weight-loss drugs. They produce weight loss in the short term, just as “eating less” does, but they don’t work in the long term (see, see). To use the word “effective” is fallacious, because  those drugs approved for use by the FDA are not effective.

On the other hand, Guyenet uses the fallacy of the single cause, which is to assume that a certain condition (weight gain or loss) has a single cause. Even if the approved weight-loss drugs were effective at making people lose weight by making them eat less, and they are not, that does not mean that other causes for the same outcome are not possible. And a drug may not be viable not because it does not work, but because of other difficulties, such as its side effects or the difficulty of keeping the active principle in optimal conditions until the day it is used. For example, the fact  there are no effective weight-loss drugs that target leptin, is a demonstration that leptin is not involved in obesity? Applying Guyenet’s reasoning we would have to conclude exactly that, that leptin is not involved in obesity. Until the day someone comes up with a way to produce a viable drug that targets leptin, in which case, magically, leptin will be involved in obesity. Guyenet’s argument is nonsense.

On the other hand, are there experiments with drugs that reduce insulin? Yes, there are: diazoxide (see), for example (see).

Genetic mutations that cause obesity do so by affecting leptin signaling

Again, fallacy of the single cause: the fact that a cause produces the effect, does not mean that other factors cannot cause it too. For example, in insulinomas there is usually a considerable weight gain (see) and it is known that insulin injections can cause accumulation of fat at the injection sites (see) and also weight gain (see).

The effect of sugar + fat cannot be completely replicated with only sugar

It is possibly one of the most interesting comments from Guyenet in this debate segment. What he says is that you cannot completely replicate the result of consuming a tasty diet that combines fat and sugars, using a diet that mainly contains sugars (rice and sugar, for example). He says that if you increase the consumption of sugar in animals or in humans, you make them gain body weight, but this gain is modest, in comparison with what you get when you use a diet dense in calories, tasty and that contains both fat and carbohydrates, and, according to him this result shows that sugar and carbohydrates cannot explain the full effect.

I think that piece of the video (min 13:00-17:30) must be watched, not listened, so you can observe Guyenet’s face. I get the feeling that Guyenet is unable to explain exactly what he is saying. Especially because it seems clear that he does not want to use the word “calories”. And I think he does not use it, because it would be too clear that he is saying that, for the same amount of calories, a diet that contains sugar and fat will be more fattening than one containing only sugars. Because if he’s not saying that, nothing he is saying makes sense. If it were all a matter of calories, it would be possible to replicate the result of one diet with the other one, just by making the diets isocaloric. But that’s not what he says.

I agree: a diet with sugar and fat can be more fattening, at least in the short term, than a diet that only contains sugars. Even when calories are the same.

Does Guyenet know that with the same amount of calories and the same macronutrients, one diet can be more fattening than another? Yes he knows that, as we can see in a blog post he published, which he later deleted (but we can still read the copy in archive.org). My bolds:

I found a well-controlled study in which investigators put rats on three different isocaloric high-fat diets. Each one contained an identical amount of total fat, protein, carbohydrate, omega-3 alpha-linolenic acid (from flax oil), and variable amounts of omega-6 linoleic acid

All rats gained weight on the high-fat diet, but their body fat composition differed. Fat tissue in the tallow group was 10.3% linoleic acid, 15.2% in the olive oil group and 54.5% in the safflower group. Relative to the tallow group, rats in the olive oil group saw to 7.5% increase in total body weight, and the safflower group saw to 12.3% increase.

So, if these are his beliefs, how can he say that it is the caloric intake what determines the changes in body weight/fat (see)? There are many questions that have the same answer: this is Guyenet, PhD, a guy that can say one thing and the opposite and behave as if he is right in both cases (see Note #2 below).

To finish this first part of my analysis of the debate, I want to review an article published by Guyenet on his blog (one article that he has not yet deleted) that can help us understand his beliefs (my bolds):

Dr. Anthony Sclafani’s research group just published a study definitively demonstrating that high palatability, or pleasantness of taste, is required for sugar to be fattening in mice

The investigators showed that mice lacking these proteins have a normal food intake and body fatness when fed standard lab chow, but unlike normal mice both mutant strains are almost completely resistant to fat gain when given a sugar solution. This is despite the fact that they drank a similar amount of sugar as the normal mice, which became obese. Basically, they drank the sugar water but it was no longer fattening once it didn’t taste sweet.

Are we paying attention to this? He is saying that regardless of its composition and its calories, if the sugar does not taste sweet, it does not make you fat. Let’s see the results of that experiment, because they are interesting. In a first experiment, the Task1r3 KO mice follow two different diets: the control group consumes chow (Con) and another group (Suc) consumes a large part of the calories as sugar. In the upper part of the following graph we see the energy intake of both groups, where the white part of the bar represents the fraction of calories that come from the sugar solution. In summary, the group Suc consumes more calories than the group Con. But, as we see in the other two graphs, that group does not gain more weight nor more body fat than the Con group.

Higher energy intake, but there are no differences in the body fat that is gained. Are not the “extra” calories what makes us fat, Guyenet? But there is more good stuff here.

In a second experiment, a small amount of fat emulsion is added to the diet, making it much tastier. And now those same mice that didn’t gain body fat while ingesting a high amount of sugar and more calories, now they do get fat!! by consuming essentially the same food that was not fattening for them in the previous experiment. And now they gain considerably more body fat with little difference between groups in the energy intake.

The authors suggest that for carbohydrates to induce obesity, they have to be palatable, not provide calories!! Guyenet not only doesn’t say this is impossible, but he welcomes this result. It’s something to remember:

Our results suggest that nutritive solutions must be highly palatable to cause carbohydrate-induced obesity in mice, and that palatability produces this effect in part by enhancing nutrient utilization.

Unexpectedly, the diet-induced obesity appeared to be due in large part to increases in carbohydrate utilization not caloric intake. This is illustrated most clearly in Tas1r3 KO mice, which exhibited elevated caloric intake but no excess weight gain on the Sucrose diet compared to WT and Trpm5 KO mice. However, when offered the highly palatable Suc+IL solution, the Tas1r3 KO gained a significant amount of weight although their caloric intake was not elevated.

Perhaps it seems a little contradictory that the same guy who knows that, with the same amount of calories, one diet can be more fattening than another because it has a different composition (and we have just seen two studies cited by Guyenet himself on his blog), ends up saying that controlled scientific studies show that changes in body weight depend only on calories (see). But these contradictions have an explanation: this guy is Guyenet, PhD.

NOTE #1: In the final part of this segment, Guyenet, PhD comments that “what differentiates a story that is true from one that is not, is the evidence”. Let’s not be fooled by the arrogance. Guyenet, PhD presumes to have an opinion based on evidence, unlike Taubes’ opinion, which he describes as “story-telling”, but his proclamations just show his lack of humility.

NOTE #2: regarding the actual value of a PhD degree, let’s see a practical example. Guyenet, PhD gives the following explanation (see, see):

About the ‘logical fallacy’, imagine a case where A always activates B as well as D. B always activates C, but D always suppresses C. In this situation, A always activates B, and B always activates C, but A does not activate C.

Therefore, just because A causes B, and B causes C, does not imply that A causes C, even if those statements are always true.

If A causes B and B causes C, for sure A causes C. Whatever Guyenet says. This guy’s mistake lies is in the premises: he cannot simultaneously hold that “B always activates C” and that “D always suppresses C”. Because when B and D occur simultaneously, one of the two premises must be false for sure. When his error is fixed by saying that “B activates C except in the presence of D”, the apparent paradox is no longer a paradox. And this guy has a PhD? Yes, he has a PhD. And he also has logic mistakes. And he also makes blatant errors interpreting data, as I will comment soon (see).

NOTE #3: Guyenet posted a document with comments and bibliographical references in order to cite them easily during the debate.

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Further reading:

Guyenet in his labyrinth

The CICO hypothesis says, in a nutshell, that when our energy intake is greater than our energy needs, the excess energy is accumulated as body fat (see, see).

The carbohydrate-insulin hypothesis says, in a nutshell, that an abnormal insulin secretion can directly affect the “entrapment” of fatty acids in our adipose tissue, in which case the changes in the energy expenditure and/or energy intake are not the cause of the accumulation, but just a possible (not necessary) consequence of the accumulation (see, see).

The graph below make it clear that both hypotheses propose opposite causalities:

Is it possible that sometimes our body behaves as the CICO hypothesis predicts, but sometimes its behaviour is more like what the carbohydrate-insulin hypothesis predicts? I think so, but let’s not fall into a false dichotomy between these two hypotheses: sometimes the behavior resembles what CICO predicts, but it is possible that other times the loss or accumulation of body fat is caused by the changes in the adipose tissue itself, perhaps caused by insulin, but perhaps caused or affected by physiological factors different from insulin. In this second option, changes in both the energy intake and the energy expenditure are, as we have seen in the previous graph, possible consequences, not causes, of gaining or losing body fat (see).

Let’s consider the following argument:

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

“It really is as simple as that”

Would you say that the author of that argument is explaining the mechanism by which, according to him, we accumulate body fat? He is considering only one mechamism for the accumulation of body fat, right?

Let’s consider another argument:

for insulin to cause fat gain, it must either increase energy intake, decrease energy expenditure, or both

According to the argument above, the only mechanism the author allows for insulin to be fattening is to work according to the CICO hypothesis. This argument says that insulin can not make you gain body fat by acting directly on your adipose tissue, as the carbohydrate-insulin hypothesis proposes. That option is not even discussed.

OK then, the two previous quotes are from Stephan Guyenet, PhD: one taken from his blog and another taken from his book. Would you say that he defends the CICO hypothesis as THE mechanism that explains why we get fat? If that is the case, you are probably mistaking him with another gentleman who is also called Stephan Guyenet, PhD, because Stephan Guyenet, PhD is against proposing hypotheses that explain why we get fat, without considering that other mechanisms may be relevant :

— Stephan, are both hypothesis 100% mutually exclusive?

— They are mutually exclusive, but only because Gary believes that his mechanism is the “primary” cause of obesity and other mechanisms are basically irrelevant.

So the gentleman who wrote a book that explains why we eat “too much”, not how insulin makes us fat by affecting directly our fat tissue, actually believes that it is inappropriate to defend hypotheses as the primary explanation for why we accumulate fat . He would never do that. As a proof that he would never do that, here we have a third argument where he does that again:

When calorie expenditure decreases and calorie intake increases, the energy balance equation leaves only one possible outcome: fat gain. We gained fat as we ate more calories than we needed to remain lean, given our physical activity level. In other words, we overate.. Stephan Guyenet, PhD

And this is the same gentleman who wrote an article arguing that the causality of the carbohydrate-insulin hypothesis is not possible! (see). Now he says that it is possible, and compatible with his ideology, because he is not dogmatic like others. What is your true opinion, then or now?

Let’s see another argument from Guyenet in which he makes clear that he believes insulin is irrelevant and calories are what matter:

So even though insulin temporarily suppresses fat burning and the release of fat from fat cells when you eat carbohydrate, at the end of the day if you ate the same number of calories you end up with the same amount of fat in your fat cells either way. You now know more about insulin than many popular diet gurus. Stephan Guyenet, PhD

And we know that Stephan Guyenet, PhD has always appreciated the carbohydrate-insulin hypothesis:

the insulin hypothesis is not consistent with basic thermodynamics. Stephan Guyenet, PhD

Cynicism: lie and/or defense of the indefensible with absolute impudence.

What hypothesis has been used for almost a century in a hegemonic way to treat obesity, using the fraudulent argument that it is an indisputable idea that drinks from the udders of the almighty laws of physics? But Guyenet, PhD, is against hypotheses that are proposed as the “primary” explanation for why we get fat if other possible mechanisms are regarded as irrelevant. An advocate of CICO would never do that. Guyenet’s nerve redefines cynicism.

A word of warning for CICO believers: Guyenet, PhD, does not defend CICO with arguments and, instead of that, he moves the goalposts , by accusing Gary Taubes of promoting an alternative hypotheses as the “primary” explanation for obesity. Is that really all he can say to defend the hypothesis that has been imposed on all of us dogmatically accross the world for the last 80-100 years?

I already warned those who believe that CICO is a law of physics that they have run out of gurus to follow. Please, walk on the catwalk to reach phase 2 of CICO beliefs. Do not stop and do not get close to the borders.

A warning for the CICO believers: the guru has left you in the lurch!!

Let’s see more examples of people who say that the energy balance is important but the physiology of the adipose tissue is irrelevant. I am quite sure these opinions upset Stephan Guyenet, PhD. Any time soon he will criticise phase-1 CICO believers.

1. “As long as there is an energy deficit, macronutrients play a secondary role”

2. “The insulin response will NEVER supersede the overall caloric balance of a diet”
3. “THE TRICK in the scientific studies of the Ketogenic, Paleolithic, Zone, or whatever, is to create an energy deficit to make the diet work. In order to deceive people, fad diets divert attention to “metabolic distractions,” such as hormones, insulin, glycemic index, macro-nutrient proportions, etc “

4. “The balance calories ingested minus energy expenditure determines your body weight”

5. “Hormones influence hunger & energy intake. The foods you eat influence hormones”

6. “A ketogenic or low-carb approach does not work because it creates metabolic magic or the ketones give you superpowers, it often works because it decreases your appetite”

7. “for reasons that are backed up by observation, inference, logical fallacy and straw men, apparently he’s decided that living creatures are magical beings that live independently of the laws of physics and thermodynamics.” Yoni Freedhoff

Yoni Freedhoff says that to talk about causalities different from CICO’s is to pretend that we are “magical beings that live independently of the laws of physics and thermodynamics”. It seems to me that Freedhoff doesn’t consider other mechanisms different from CICO’s. For sure Guyenet is not happy about Freedhoff’s opinion.

8. “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.”Kevin Hall, PhD

Kevin Hall, PhD has created mathematical models of obesity that are 100% CICO. His computer models consider de facto that the physiology of the adipose tissue is irrelevant (see, see, see, see, see, see). Is this the peaceful and positive coexistence of hypotheses that Stephan Guyenet, PhD defends? Moreover, when Kevin Hall, PhD says that “regain occurs only because interventions wane over time” (see), it does not sound like Kevin Hall, PhD is open to the idea of mechanisms other than CICO being relevant. Does he?

But, uh, Guyenet says that the extremist is Taubes because he claims that his hypothesis is the hypothesis that explains everything. CICO believers like Guyenet, PhD would never do that. They would never do that for a whole century. They would never do that for a whole century defending an erroneous hypothesis that leaves no room for other hypotheses because we have been tricked into believing that CICO is an indisputable law of physics. They would never be doing that right now accross the world. What are you telling me, Guyenet? What a magnificent straw man you have created, Guyenet. What a magnificent medal of moderation you gave yourself, Guyenet. This guy is the dictator who, from his throne, claims that the opposition parties, which have never been allowed to be legal parties, what they really want is to impose a dictatorship in the country. This is impudence and cynicism.

For the most clueless people, I insist that what Stephan Guyenet, PhD is saying is that he does not believe that CICO’s causality is indisputable. He explicitly admits that behaviors that don’t follow CICO are possible. He even criticises those who only contemplate one mechanism as possible. And he does not dare to defend CICO by mentioning the First Law of Thermodynamics.

NOTE: there is a long list of BS arguments used by Stephan Guyenet, PhD to make people believe that insulin is not fattening by acting directly on the adipose tissue (example, example, example, example, example, example). But now he presumes to be an open-minded person who believes that the insulin effects that he has systematically denied are indeed possible and can be accepted and coexist with his beliefs. Can you guess who has claimed over and over again to put the “final nail in the coffin of the carbohydrate-insulin hypothesis” (example)? Well then, now we find out that Guyenet was all this time a fan of the carbohydrate-insulin model. I am not sure I can believe him. 

NOTE: “Accuse the other side of what you are guilty of” is a well-known disinformation strategy. It is often attributed to Joseph Goebbels, but I am not sure that this attribution is correct (source).

Further reading:

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: