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

(Versión en español: pinchar aquí)

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

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

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

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

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

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

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

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

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

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

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

The conclusions from the authors are amazing:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Further reading:


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

(Versión en español: pinchar aquí)

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

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

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

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

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

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

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

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

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


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

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

The authors of the article apparently saw it differently:

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

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

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

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

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

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

Further reading:

¿Es esto adelgazar? (XXIX)

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

Experimento DIETFITS. 609 participantes inicialmente y 12 meses de duración. En este experimento se pretendía comparar dos dietas “saludables”, sin objetivo de calorías consumidas, una más alta en carbohidratos y una más baja en carbohidratos.

the reduction of edible oils, fatty meats, whole-fat dairy, and nuts was prioritized for the healthy low-fat group, whereas the reduction of cereals, grains, rice, starchy vegetables, and legumes was prioritized for the healthy low-carbohydrate group.

Both diet groups were instructed to (1) maximize vegetable intake; (2) minimize intake of added sugars, refined flours, and trans fats; and (3) focus on whole foods that were minimally processed, nutrient dense, and prepared at home whenever possible. Other components of the emphasis on high-quality food for both diet groups are described elsewhere

Ambos grupos dietarios fueron instruidos para (1) maximizar la ingesta de vegetales; (2) minimizar el consumo de azúcares agregados, harinas refinadas y grasas trans; y (3) centrarse en alimentos de verdad que fueran mínimamente procesados, ricos en nutrientes y preparados en casa siempre que sea posible. Otros componentes del énfasis en alimentos de alta calidad para ambos grupos de dieta se describen en otra parte

Los participantes perdieron 5.3 kg en un grupo y 6.0 kg en el otro. Eso, en un año de dieta, es igual que la media de estudios de pérdida de peso (ver).

 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]).

La diferencia entre grupos dietarios, en términos de peso corporal fue de 700 g al final del experimento, que no es nada, aunque sí lo sea en porcentaje respecto de los 5-6 kg perdidos en media.

Se nos dice que hubo una restricción calórica media de 500-600 kcal/d. Sin diferencias en la ingesta energética al comparar los dos grupos.

Despite not being instructed to follow a specific energy (kilocalorie) intake restriction, the mean reported energy intake reduction relative to baseline was approximately 500 to 600 kcal/d for both groups at each time point after randomization.

Según las cuentas de 3500 kcal por libra de grasa corporal, con 500 kcal/d de restricción calórica deberían haber perdido 23 kg por persona. Y, al menos según los datos del estudio, se trataba de gente que sí podía perder peso: mujeres de 90 kg, hombres de 105 kg.

Me gustaría ver la evolución del peso corporal, porque no es lo mismo perder 5 kg perdiendo 1 kg cada 2-3 meses que haber perdido todo en los primeros meses y luego estar recuperando o manteniendo esa pérdida. No he visto que den esos datos.

Edito: gráfica de evolución de pérdida de peso, retocada para que el eje horizontal tenga escala lineal y no se distorsione la evolución del peso corporal.


¿Qué conclusiones sacamos de este estudio? Fijémonos en estos dos artículos periodísticos: uno concluye que la proporción de macronutrientes no es relevante y el otro concluye que hay que fijarse más en la calidad que en la cantidad.

Low-carb vs. low-fat: New research says it doesn’t really matter (fuente)

The research lends strong support to the notion that diet quality, not quantity, is what helps people lose and manage their weight most easily in the long run (fuente)

¿Qué se puede deducir de un estudio en el que únicamente se han comparado dos “dietas saludables” concretas que han fracasado para hacer perder peso corporal? ¿Deducimos que una dieta que sí incluye azúcar, harinas, productos procesados y bebidas azucaradas es igual de buena para adelgazar que una basada en productos saludables? ¿Qué parte de este resultado nos indica eso? ¿Podemos deducir eso de un estudio en el que NO se ha usado una dieta plagada de productos basura? ¿Deducimos algo sobre una dieta más baja en carbohidratos que la empleada en este estudio? ¿Deducimos algo sobre qué es importante para adelgazar de un estudio que ha obtenido un fracaso en ese sentido? ¿Demuestra este experimento que la clave para adelgazar es la adhesión a la dieta?

No nos lo tomemos a broma: este tipo de resultados se cuentan de esa manera: se demuestra una vez más que la composición de la dieta no es demasiado importante y que lo más importante para adelgazar es la adhesión a la dieta (ejemplo). Ningún parecido con la realidad, pero eso no es un obstáculo para algunas personas.

Lo que veo en este estudio es:

  • Fracaso de los dos métodos de pérdida de peso concretos puestos a prueba: no se consigue una pérdida de peso significativa “a pesar de” una restricción calórica considerable. En este caso concreto el simple énfasis en “comer mejor”, interpretado según la definición de estos experimentadores, no ha dado resultado, aunque “se coma menos”.
  • Una dieta “saludable” con 100-130 g de carbohidratos es igual de mala para adelgazar que una dieta “saludable” baja en grasa.

Leer más:

“Pseudo-sciences do not talk about physiology”

(versión en español: pinchar aquí)

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

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

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

In obesity you have to talk about energy, not physiology

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

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

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

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

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

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

What are the physiologic mechanisms that detect a decrease in the energy intake and how is that information translated into the physiologic signals that produce the reduction of  the fat that is stored in the adipocytes? What explanation gives the energy balance theory on those physiologic mechanisms?

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

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

Further reading:

“La pseudomedicina rehúye hablar de los mecanismos fisiológicos”

(English language version: click here)

¿Cómo detectar una pseudomedicina? Es muy fácil: las pseudociencias no hablan de fisiología

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

Escribir sobre pseudomedicina es relativamente fácil. La mayoría de las pseudomedicinas son simples y autocontenidas. Manteniéndote en lo fundamentalmente ficticio, fuera de las complicaciones reales, no tienes que preocuparse demasiado por la fisiología, la anatomía y la plausibilidad y todos los otros aspectos de la medicina que hacen de ser un médico algo muy parecido a Barbie en una clase de matemáticas. Eso es duro.

¿Cómo dicen que podemos detectar una pseudociencia? Muy fácil: las pseudociencias no son capaces de dar explicaciones basadas en la fisiología o la anatomía y que puedan ser sometidas a verificación en experimentos científicos. Ejemplo de libro: la pseudociencia del balance energético. ¿Mecanismos fisiológicos que sustentan esa teoría? Ninguno: se basa en energías que entran y salen, y la fisiología es suplantada por una operación matemática sin ningún tipo de relación con el funcionamiento real de nuestros óganos y tejidos. Blanco y en botella: hemos detectado una pseudociencia.

En obesidad hay que hablar de energía, no de fisiología

Pero no. Aparentemente con la obesidad es al contrario: la pseudociencia es hablar de mecanismos fisiológicos, pues eso nos desvía de la causa real, que es “genética, ambiental y de conducta”. ¡Sin fisiología, por favor! Sin mundanos y sucios mecanismos fisiológicos, que esto va de energías porque sabemos muchísimo de física. Somos la repanocha en física.

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

Necesitamos entender por qué algunas personas ganan peso fácilmente y otras no. Taubes no tiene una respuesta para eso: su “causa” de la obesidad es tan sólo un “mecanismo” que realmente no explica las causas genéticas, ambientales y conductuales subyacentes. Mientras esperamos para entender eso, todavía tenemos el problema práctico de que las personas con sobrepeso necesitan perder peso ahora. Es innegable que si usted puede encontrar una manera de reducir la ingesta total de calorías suficientemente, perderá peso.

Tan sólo un mecanismo fisiológico que no es necesario entender para poder tratar la obesidad. Con la obesidad da igual tratar causas que síntomas (ver).

Las dos citas provienen de la misma web: Science Based Medicine. Tienen muy fácil ver que son ellos los que están divulgando patética pseudociencia: simplemente tienen que aplicar sus propios criterios de detección de pseudociencias. Poner a los héroes cara a cara con su verdadera identidad no es crueldad, es avanzar para que la obesidad deje de ser tratada con una teoría que es pura charlatanería (ver).

¿En qué mecanismos fisiológicos se basa la teoría del balance energético?

¿Cuáles son los mecanismos fisiológicos que relacionan nuestra ingesta energética con toda la energía almacenada en nuestro cuerpo, en todos sus formatos? ¿Cuáles son los mecanismos fisiológicos por los que funciona el “come menos (calorías)”?

¿Cuáles son los mecanismos fisiológicos que detectan la reducción de la ingesta energética y cómo se traducen en las señales fisiológicas que producen la reducción de la grasa acumulada en los adipocitos? ¿Qué explicación da la teoría del balance energético sobre esos mecanismos fisiológicos?

¿Por qué estos señores ignoran la reacción real de nuestro cuerpo, documentada en las revistas científicas, a la restricción de la comida y la sustituyen por fantasías falsamente basadas en una ley general de la física que nada tiene que ver con la fisiología?

NOTA: Me pregunto por qué ponen como ejemplo a Barbie de persona que tiene problemas con una clase de matemáticas… ¿Ken no tendría esos problemas? Creo que si ponemos a Ken en lugar de Barbie en la frase queda clarísimo lo que están diciendo.

Leer más:

“Sustituir azúcares simples por carbohidratos complejos NO produce una reducción en el peso corporal”


Vamos a echarle un vistazo a ese metaanálisis.

Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies

Metaanálisis que considera a) 19 estudios ad-libitum (no se pide control de la cantidad de comida) y b) 11 estudios isocalóricos.

a) Estudios ad-libitum

Se encontró una clara relación entre consumir menos azúcares y reducción en el peso corporal y también entre incrementar el consumo de azúcares y aumentar el peso corporal.

In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg, 0.30 to 1.19; P=0.001).

Es muy relevante que esa relación se vio mucho más claramente cuando los estudios tenían mayor duración. Un estudio de corta duración puede concluir que un efecto no es relevante por culpa de la corta duración del estudio, no porque el efecto no exista.

b) Estudios con sustitución isocalórica

En 8 de los 11 experimentos isocalóricos no se llega a los 2 meses de duración. 8 de los 11 están basados en participantes que sufren diabetes:

Como decía, únicamente 3 estudios tienen al menos 2 meses de duración. Esos 3 estudios son Grigoresco et al. 1988, Osei et al. 1989 y Santacroce et al. 1990. Como vemos en la Figura 5 del metaanálisis, resultado neutro para dos de ellos y contrario a los azúcares simples en el tercero:

De forma resumida, éstas son las características de esos tres estudios:

Participantes Azúcar usado Duración
Grigoresco et al. 8 (cruzado) T2D Fructosa (30g) 2 meses
Osei et al. 11 (cruzado) T2D Fructosa (60g) 6 meses
Santacroce et al. 12 (cruzado) T1D Sacarosa (30g) 2 meses

En total se trata de sólo 31 personas, la tercera parte de ellos diabéticos tipo 1. Dos de los estudios son de 2 meses de duración en los que tan sólo 30 g de azúcares simples son sustituidos por otro tipo de azúcares (pan en el de Santacroce). ¿Con esa duración, ese número de participantes y ese mínimo cambio en la dieta nos sorprendería no encontrar diferencias entre grupos? ¿Qué conclusiones se pueden sacar de experimentos de tan baja calidad?

Por otro lado, el estudio de Grigoresco et al. estaba basado en una dieta de unas 1500 kcal, lo que entra en contradicción con las bases de selección de artículos indicadas por los propios autores del metaanálisis, que aclaran que no quieren resultados de experimentos de pérdida de peso pues su objetivo es ayudar a crear recomendaciones para la población general, no dietas para gestionar la obesidad:

  • “Fructose could be taken at any time during the day as part of the 1400-1600 kcal allowed diet”
  • Interventions designed to achieve weight loss were excluded […] the ultimate aim of the review wasto facilitate the development of population based recommendations rather than nutritional recommendations for the management of obesity.

Es decir, que según su propio criterio ese experimento con dieta hipocalórica no debería ser sido incluido en la revisión. En cualquier caso, en ese experimento se está mezclando el efecto del cambio dietario con el efecto a corto plazo de la reducción en la cantidad de comida. Como ellos mismos argumentan, ¿van a sacar de ahí recomendaciones para la población que no está intentando perder peso? Son sus propios argumentos.

El estudio de Osei et al. es el único de 6 meses de duración y de los tres es el que sustituye una mayor cantidad de azúcares simples (60g en forma de fructosa). Es el único de los tres que encuentra diferencias en el peso corporal:

Como vemos los pesos corporales de partida no eran los mismos con ambas dietas por lo que es falso que la diferencia entre dietas sea de 2.5 kg: el cambio en el peso corporal fue de +1.8 kg con una dieta y -1.3 kg con la otra, es decir una diferencia de 3.1 kg.

Mean body weight did not change significantly during fructose supplementation (87.7 ± 7.6 vs 89.5 ± 5.0 kg) or on the normal diet (88.3 ± 5.8 vs 87.0 ± 6.0 kg) at month 0 vs 6, respectively. At 6 months, mean body weight was not significantly different between fructose and normal diet (89.5 ± 5.0 vs 87.0 -1- 6.0 kg).

Cabe plantearse qué tipo de científico se fija sólo en el peso final a la hora de extraer los datos para comparar grupos, sin tener en cuenta los pesos de partida (ver).

En cuanto al estudio de Santacroce et al., los participantes sufren diabetes tipo 1. ¿Qué sentido tiene incluir en este metaanálisis datos de personas en las que el efecto de la comida en el medio hormonal está absolutamente alterado por un páncreas disfuncional y el uso obligatorio de medicación? Los participantes se inyectaron la misma cantidad de insulina con ambas dietas y su peso fue el mismo con ambas dietas. ¿Cómo se puede atribuir el resultado a lo que están comiendo? ¿Cómo se pueden extrapolar este resultado con fructosa al consumo de sacarosa a largo plazo en personas que sí tienen un páncreas sano capaz de segregar insulina en respuesta a lo que comen?

Mean daily insulin dose (calculated as the mean of 7 days in each subject) was 42 ± 2 IU (SE) with the control diet and 43 ± 3 IU with the sucrose diet (p<0.5). Body weight was 64 ± 3 kg (SE) at the end of the control diet and 64 ± 4 kg at the end of sucrose diet (p>0.7).

Aparte del hecho de que 2 de los 3 estudios no deberían estar en el metaanálisis, llama muchísimo la atención el peso asignado a los mismos. Es habitual usar la inversa de la varianza como medida de fiabilidad y asignar un peso a los estudios proporcional a la inversa de la varianza. De esa forma los resultados de estudios con pocos participantes suelen tener menos peso en el total de un metaanálisis que estudios con más participantes. Parece razonable, ¿verdad? Pero en este metaanálisis el estudio de Grigoresco et al., con sólo 8 participantes, tiene asignado un peso 170 veces mayor que el de Osei et al., que tiene 13 participantes y tres veces más duración. ¡¡¡170 veces mayor!!! ¿Tan fiable es un estudio con sólo 8 participantes y dos meses de duración? Como consecuencia de estos sorprendentes pesos, el estudio de Osei et al. es, a efectos prácticos, como si no estuviera y el global de la comparación es básicamente como considerar sólo el de Grigoresco et al..

Las conclusiones de los autores

Las conclusiones de los autores del metaanálisis son que en dietas ad libitum el consumo de azúcares libres influye en el peso corporal, pero que como esa relación no la han visto cuando las dietas son isocalóricas entonces se deduce que probablemente el azúcar engorda porque hace comer “de más”:

Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.

Es decir, deducen que los azúcares simples sí engordan pero para ellos esos ocho experimentos que no llegan a los dos meses de duración junto con esos tres estudios que he comentado con algo de detalle, con unos pesos sorprendentes en el metaanálisis, permiten deducir que el azúcar engorda porque hace consumir más calorías, no por ser esencialmente engordante.

The most obvious mechanism by which increasing sugars might promote weight gain is by increasing energy consumption to an extent that exceeds energy output and distorts energy balance

El mecanismo más obvio por el cual aumentar los azúcares podría promover el aumento de peso es aumentando el consumo de energía en una medida que exceda la producción de energía y distorsione el equilibrio energético

Mis conclusiones

Muy lamentable. Esta patata de metaanálisis no permite concluir que el azúcar sea engordante por sus calorías. La ecuación matemática del balance energético NO es un “mecanismo” fisiológico sino simple charlatanería cuando se usa en el estudio de la obesidad, pues se inventa una causalidad en la primera ley de la termodinámica (ver,ver,ver,ver,ver). Esta chapuza no se hace con ningún otro crecimiento de un tejido en un ser vivo y la primera ley de la termodinámica SIEMPRE es aplicable (ver). Da que pensar, ¿no? Que se engorda por consumir más calorías de las que se gastan es tan obvio como que las pirámides egipcias las construyeron extraterrestres. Pero bueno, éste es el nivelazo que tienen los “científicos” en el área de la obesidad y la nutrición.

Noticia de última hora: un metaanálisis demuestra que experimentos que de forma aislada son muy malos pueden ser mezclados en un batido sospechoso que algunos podrían encontrar sabroso por error.


NOTA: la sustitución isocalórica de fructosa o sacarosa por otros azúcares no necesariamente reduce el índice glucémico.

NOTA: me parece cuestionable que se combinen en un mismo metaanálisis sustancias como la glucosa, sacarosa y fructosa que son procesadas de muy diferente forma por nuestro cuerpo. Es más razonable concluir que no hay datos para hacer un metaanálisis en condiciones, que extraer conclusiones de un conjunto de datos inadecuado por inconsistente. Parece que en temas de nutrición no hay ningún tipo de filtro a la hora de publicar: “a broken peer-review system”, que decía alguien por ahí, con toda la razón del mundo.

NOTA: uno de los autores del metaanálisis es Jim Mann (ver,ver).

Leer más: