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.

 

Selección_488

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.

 

imagen_0088

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

pone

 

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.

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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”?

imagen_1964

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:

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2 respuestas a “Guyenet and Hall demonstrate that what does happen cannot really happen

  1. — Stephan, I want to say that the CIM is not experimentally supported. What can I say to conclude that?
    — I don’t know, Kevin, give me a minute to think about it. I’ll think of something

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