Layne Norton, PhD analiza el debate Taubes-Guyenet (1/2)

Ya he hablado en el blog (ver) de Layne Norton, PhD, un defensor más de la pseudociencia del balance energético. Tras el debate Taubes-Guyenet, Norton publicó su análisis sobre el mismo. Voy a comentar algunos de sus argumentos. No he revisado ni todos argumentos ni todos los enlaces que pone Norton en su artículo. Sólo comento lo que he visto echando un vistazo por encima a su texto. No tengo tiempo para revisarlo todo, ni seguramente sirva para nada hacerlo. Si alguien lee su análisis completo y cree que hay algo de valor en alguno de los argumentos o de los enlaces que no comento en esta entrada, que lo diga.

Los tejidos hambrientos

Empiezo resaltando un hombre de paja que crea Norton hablando de las ideas de Taubes (mis negritas):

Their belief is that insulin, by way of inhibiting release of stored fat, causes the other tissues to sense an energy deficit (since the energy is “trapped” in adipose) and thus we overeat in order to provide fuel to the tissues that feel they are “starving.”

Su creencia es que la insulina, por medio de inhibir la liberación de grasa almacenada, causa un déficit de energía (ya que la energía está “atrapada” en el tejido adiposo) y, por lo tanto, comemos en exceso para proporcionar combustible a los tejidos que sienten que están “hambrientos”.

Es su interpretación —interesada— de lo que dice la hipótesis carbohidratos-insulina, no lo que dice esa hipótesis. La insulina no causa un déficit de nada, porque nada nos falta. Y tampoco lo hace actuando sobre la liberación de grasa: es un hecho perfectamente documentado que la insulina actúa tanto en la lipogénesis como en la lipólisis intracelular (ver).

Hablemos del orden de magnitud del problema, porque es muy relevante para entender la falsedad del hombre de paja de Norton. Simplemente para hacernos una idea de qué estamos hablando, supongamos que una persona acumula en un día 1 g de grasa corporal y hace 5 comidas. Por sencillez, podemos pensar que engordamos 0.2 g en cada una de esas 5 comida. Lo que plantea Norton es que si esos 0.2 g en concreto de todo lo que hemos comido en nuestra última comida quedan en sangre no pasamos hambre, pero si nuestro tejido adiposo los guarda, entonces nuestros tejidos se mueren de hambre y nuestro apetito nos obligará a comer para abastecer a esos tejidos que están a punto de morir de inanición. ¿Por 0.2 g? Pasará lo mismo entonces si un día ingieres 1 g menos que el día anterior, ¿no? El argumento es absurdo, pues ignora la magnitud del problema, ignora que nuestro gasto energético es variable y adaptativo a la ingesta (ver,ver,ver), e ignora que nuestros tejidos no se enteran de las variaciones leves en la ingesta, pues lo que realmente ven esos tejidos son niveles estables de glucosa en sangre que son regulados de forma exquisita por el hígado (fuente), y en el periodo postabsortivo también los niveles de ácidos grasos en sangre que pueden nutrir los tejidos son mantenidos estables (ver).

often plasma NEFA concentrations remain relatively stable as removal by muscle increases to match adipose tissue lipolysis (fuente)

a menudo las concentraciones de NEFA permanecen relativamente estables puesto que el músculo incrementa su retirada de ácidos grasos para equilibrar la tasa de lipólisis del tejido adiposo

Pensemos un poco. ¿De cuánto es la variación de la ingesta de un día al siguiente? ¿Consumimos todos los días exactamente la misma cantidad de comida, como un reloj suizo? ¿O más bien con total seguridad de un día a otro hay altibajos de decenas o incluso cientos de gramos? (fuente) Pero al parecer a nuestros tejidos que comamos más o menos les da igual: lo que les deja sin comida es si es específicamente el tejido adiposo el que almacena 1 ó 2 gramos de lo comido. ¡Eso nos crea un déficit de energía y nuestros tejidos se mueren de hambre! Es muy lógico, ¿verdad que sí?

Por otro lado, a diferencia de lo que afirma Norton, la hipótesis carbohidratos-insulina no dice que comamos “en exceso”, ni para satisfacer a los tejidos hambrientos (pobrecitos, tienen un gramo menos…) ni menciona el “exceso” por ninguna otra razón. Puedes seguir comiendo la misma cantidad y que cambie el aprovechamiento, la eficiencia. Exceso y sobreconsumo son términos del paradigma energético, no de la hipótesis carbohidratos-insulina. Lo que hace Norton es reinterpretar la hipótesis carbohidratos-insulina como le da la real gana.

No me enrollo más con esto y remito a un par de entradas del blog para quien quiera pensar más sobre ello (especialmente la primera que enlazo):

En cualquier caso, resalto que la interpretación que hace Norton, además de errónea por las razones que acabo de explicar, es coherente con sus creencias, no con la hipótesis que  supuestamente está explicando y que pretende refutar. Es un hombre de paja que le será útil para dar la impresión de que está rebatiendo los argumentos de sus oponentes. En realidad sólo va a vencer al falso argumento que está creando. Y lo hará con facilidad, como debe ser.

La hipótesis del azúcar

Otro detalle importante es qué piensa Taubes acerca de los efectos del azúcar. ¿Cree que estos efectos se manifiestan claramente a corto plazo, o cree por el contrario que hablamos de un producto cuyos efectos se manifiestan a largo plazo? Leamos su opinión (mis negritas):

It would indeed be nice if our bodies, both on a population-wide and individual basis, responded immediately to the removal of a toxic substance from the environment. But there are many reasons why they wouldn’t, among them being threshold effects, intergenerational effects (the passing down of a predisposition to become obese and diabetic from mother to child in the womb, as documented in the Pima population and discussed in my books) and an incubation period for development of the disease, of the kind that explains the smoking and lung cancer delay. Gary Taubes

De hecho, no estaría mal que nuestros cuerpos, tanto a nivel de la población como individual, respondieran de inmediato a la eliminación de una sustancia tóxica del medio ambiente. Pero hay muchas razones por las que no lo harían, entre ellos los efectos umbral, los efectos intergeneracionales (la transmisión de una predisposición a ser obesos y diabéticos de madre a hijo en el útero, como se documenta en la población de Pima y se discute en mis libros) y un período de incubación para el desarrollo de la enfermedad, del tipo que explica el hábito de fumar y el retraso del cáncer de pulmón.

Sugar and high-fructose corn syrup are not “acute toxins,” of the kind the FDA typically regulates, and the effects of which can be studied reasonably well over the course of days or months. The question is whether they’re chronic toxins, their effects accumulating over the course of many thousands of meals, not just a few. This means that what Tappy referred to as “intervention studies” have to go on for years or decades to be meaningful. Gary Taubes

El azúcar y el jarabe de maíz con alta fructosa no son “toxinas agudas”, del tipo que regula normalmente la FDA, y cuyos efectos pueden estudiarse razonablemente bien en el transcurso de días o meses. La pregunta es si son toxinas crónicas, cuyos efectos se acumulan a lo largo de miles de comidas, no solo unas pocas. Esto significa que lo que Tappy denomina “estudios de intervención” deben durar años o décadas para que aporten algo.

The hypothesis addressed in this book, for instance, is that sugar is the dietary trigger of obesity and diabetes and, if so, the diseases such as heart disease that associate with them. But this hypothesis is ultimately about what happens to us over decades—the time it takes chronic diseases to manifest themselves—and not months, as is the case, say, with vitamin-deficiency diseases like scurvy or beriberi. Gary Taubes

La hipótesis que se aborda en este libro, por ejemplo, es que el azúcar es el desencadenante dietético de la obesidad y la diabetes y, de ser así, también de las enfermedades asociadas a ellas. Pero esta hipótesis es en última instancia sobre lo que nos sucede durante décadas —el tiempo que le cuesta a las enfermedades crónicas manifestarse— y no meses, como es el caso, digamos, con enfermedades por deficiencia de vitaminas como el escorbuto o el beriberi.

Si, como es evidente a partir de las citas anteriores, Taubes postula que los efectos del azúcar pueden no manifestarse a corto plazo, siendo incluso en parte transmitidos de generación a generación en el útero, y dice textualmente que no es una cuestión de días ni de meses, sino de años o décadas, ¿encontrar experimentos científicos de unas pocas semanas o meses que no reporten un efecto claro del azúcar, refuta su hipótesis? Esto es importante, porque, como veremos, parte de los argumentos de Norton consisten en presentar experimentos a corto plazo y pretender que no encontrar un efecto refuta la hipótesis de Taubes. La realidad es que Norton sólo derrota a sus propios hombres de paja.

El mejor estudio que conoce Norton

La creencia de Norton es que a igualdad de calorías y de proteína, se pierde la misma cantidad de peso:

Further, numerous studies have shown that high carb diets and high fat diets produce the same weight loss between high carb and low-fat diets when calories are the same and protein is the same (it’s important to equate protein since it increases energy expenditure). Perhaps the most precisely controlled study on this topic is here: [1]

Además, numerosos estudios han demostrado que las dietas ricas en carbohidratos y las dietas ricas en grasas producen la misma pérdida de peso cuando las calorías son iguales y las proteínas son las mismas (es importante equiparar las proteínas ya que aumenta el gasto de energía). Quizás el estudio más precisamente controlado sobre este tema está aquí: [1]

Parece que la publicación de evidencia científica que refuta sus creencias no le hace cuestionarse sus creencias (ver).

La referencia que aporta como estudio muy controlado es un estudio piloto no aleatorizado y de muy corta duración, sólo 4 semanas. No es aleatorizado porque las dietas se prueban en un orden concreto en el que la dieta cetogénica es la segunda en ser usada. Es el estudio piloto de Kevin Hall que comenté en la cuarta parte de mi análisis del debate, sin ir más lejos. No aleatorizado, con los autores del mismo incapaces de mantener estable el peso de los participantes, lo que demuestra que tienen errores de base en sus creencias, para a partir de ahí comprobar el efecto de las dos dietas, y de tan sólo 4 semanas de duración,

Hagamos de pitonisos por unos minutos. ¿Cuál de las tres evoluciones que he dibujado en rojo en la siguiente gráfica será la que más se parecerá a la evolución de la grasa corporal en este experimento del que estamos hablando, de haber sido a más largo plazo?

¿No te atreves a hacer un pronóstico? ¿Por qué no? ¿No te parece bien inventarte el efecto a largo plazo de una dieta a partir de datos a corto plazo? Pues Guyenet, Hall y Norton sí creen en la futurología. Ellos pueden coger experimentos de unas pocas semanas de duración y sacar conclusiones para cualquier condición que se nos ocurra (ver). Seguramente es tener un doctorado lo que les faculta para adivinar el futuro.

Norton dice que no se encontraron diferencias entre dietas y que resaltar la corta duración del estudio es “mover los postes de la portería”:

Gary will say the study was too short (goal post moving) but if the CIM was correct, you would expect to see SOME difference, but you don’t.

Gary dirá que el estudio fue demasiado breve (mueve los postes de la portería) pero si la CIM fuera correcta, se esperaría ver ALGUNA diferencia, pero no se ve.

Como ya comenté (ver), la realidad es que sí encontraron diferencias entre dietas. Otra cosa es que a los autores no les hiciera gracia encontrar esas diferencias y que trataran de minimizar el daño que el resultado hacía a su pseudociencia. Hechos inconvenientes para Norton.

Por otro lado, resaltar la corta duración de los experimentos es molesto para los que engañan a la gente extrapolando a largo plazo resultados a corto plazo. ¿Es mover los palos de la portería? No lo es, si crees relevante el efecto a largo plazo de la dieta y lo crees diferente del efecto a corto plazo. Pero sí es un planteamiento molesto para los que ven el futuro mirando posos de té, porque delata las trampas en sus argumentos.

El clavo definitivo en el ataúd

Norton nos cuenta que si las calorías son las mismas y existe un incremento significativo de la insulina, deberíamos ver un incremento en la acumulación de grasa corporal, pero que hay un experimento que demuestra que no es así (mis negritas):

More to this end, if the CIM was valid, we would expect to see a large increase in fat deposition if calories remained the same and we significantly increased insulin, since calories aren’t what make us fat according to the CIM. However, the results of a trial with the drug Liraglutide absolutely put the nail in the coffin for this theory. Liraglutide (a GLP-1 mimetic) stimulates insulin release but it also reduces body weight and body fat and improves metabolic health. [7] This absolutely crushes the idea that insulin is the central player in the development of obesity and not energy balance.

Más a este respecto, si la CIM fuera válida, esperaríamos ver un gran aumento en la acumulación de grasa si las calorías permanecieran iguales y aumentáramos significativamente la insulina, ya que las calorías no son lo que nos hace engordar según la CIM. Sin embargo, los resultados de un ensayo con el medicamento Liraglutide pusieron el clavo en el ataúd para esta teoría. La liraglutida (un mimético de GLP-1) estimula la liberación de insulina, pero también reduce el peso corporal y la grasa corporal y mejora la salud metabólica. [7] Esto aplasta absolutamente la idea de que la insulina es el factor central en el desarrollo de la obesidad y no el equilibrio energético.

El artículo que referencia Norton es:

A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management

Este experimento está basado en el uso del fármaco liraglutide, que supuestamente actúa reduciendo el apetito y por tanto la ingesta energética:

Weight loss with liraglutide is dose-dependent up to 3.0 mg once daily and is mediated by reduced appetite and energy intake rather than by increased energy expenditure.

Como vemos en la gráfica, el grupo tratado con liraglutide (en azul) pierde unos 9.5 kg, frente al grupo placebo que pierde unos 3.5 kg (en gris).

¿Por qué ha perdido más peso el grupo tratado con liraglutide? Si, como hemos visto, el efecto del fármaco se produce actuando en la ingesta energética, supuestamente ese grupo ha consumido menos calorías que el otro. ¿Y Norton nos intenta colar este experimento como prueba de que a igualdad de calorías un incremento de la insulina no produce acumulación de grasa corporal? ¿Dónde ve Norton la igualdad de calorías en este experimento?

Norton dice que el liraglutide aumenta la secreción de insulina. ¿Fue así en este experimento? Por un lado, los autores dicen lo contrario que Norton: el grupo tratado con liraglutide tuvo menos insulina en ayunas:

There was a greater reduction in glycated hemoglobin, fasting glucose, and fasting insulin levels in the liraglutide group than in the placebo group

Y lo estamos interpretando correctamente, pues el dato está en la Tabla 2.

Pero la insulina en ayunas no es la insulina a lo largo de todo el día. ¿Qué se nos dice la insulina postprandial? El único dato que se da es una gráfica que demuestra una mayor secreción de insulina durante los primeros 100 minutos tras una carga oral de glucosa, es decir, ante un mismo estímulo.

Veo dos problemas:

  1. La respuesta ante una misma carga medida al final del experimento no es la respuesta durante el experimento, especialmente porque ambos grupos no han consumido la misma cantidad de comida: menos comida presumiblemente hace segregar menos insulina (al menos si no hay diferencias en la composición de la comida, como es el caso), lo que puede contrarrestar la supuesta tendencia a segregar más insulina del grupo liraglutide. Esta gráfica no demuestra, por tanto, que durante el experimento hubiera una menor secreción de insulina en el periodo postprandial.
  2. 100 minutos es muy poco tiempo. La elevada secreción de insulina por efecto del fármaco baja la glucemia antes (ver gráfica bajo estas líneas), por lo que cabe pensar que esa glucemia reducida va a dejar de estimular la secreción de insulina antes que en el grupo placebo. Si se vuelve a mirar la gráfica anterior, eso podría ser cierto (la secreción de insulina es mayor en el grupo liraglutide, pero en el minuto 100 deja de serlo). Ni siquiera sabemos si ante la misma cantidad de comida —que es el caso de la carga oral de glucosa pero que no es lo que ha sucedido durante este experimento—, la secreción de insulina postprandial ha sido realmente mayor en el grupo liraglutide que en el grupo placebo. Necesitaríamos datos durante las siguientes 4-5 horas para conocer la evolución real de la respuesta insulínica. No nos la podemos inventar.

En definitiva, la supuesta prueba de que a igualdad de calorías más insulina no significa más acumulación de grasa corporal, queda en que ni había igualdad de calorías ni sabemos si realmente había mayor secreción de insulina. ¡Y Norton hasta presume de que ésta es una evidencia tan contundente que es el clavo definitivo en el ataúd! Por este tipo de cosas es por lo que no hay que fiarse de nadie: da igual que presuman de citar mil estudios, da igual que proclamen arrogantemente haber refutado las hipótesis de sus oponentes, da igual que tengan un doctorado: cuando revisas los artículos que citan, muy a menudo estos no respaldan lo que ellos dicen. Si no consultas los datos y te dejas guiar por las apariencias, te van a engañar.

Esto aplasta absolutamente la idea de que la insulina es el factor central en el desarrollo de la obesidad y no el equilibrio energético.

Tampoco caigamos en la falacia de falsa dicotomía: aunque este experimento demostrara lo que Norton dice, y en absoluto lo hace, eso no demostraría correcta la pseudociencia del balance energético.

¿Qué es exactamente lo que demostraba este experimento?

El sinsentido

Norton vuelve a la carga con su hombre de paja, i.e. su tergiversación de lo que dice la hipótesis de la insulina para poder atacarla.

The idea that insulin traps free fatty acids in cells making the other tissues feel like they are “starving” has also been demonstrated to be incorrect. If this was correct, we would expect to see depleted levels of free fatty acids in blood during fasting in insulin resistant people. But we don’t. Obese people release MORE fatty acids from adipose, not less. [5]

Por lo tanto, se ha demostrado que la idea de que están “muriéndose de hambre” es incorrecta. Si esto fuera correcto, esperaríamos niveles mínimos de ácidos grasos libres en la sangre durante el ayuno en personas resistentes a la insulina. Pero no se ven. Las personas obesas liberan MÁS ácidos grasos de los adiposos, no menos.

Atentos al razonamiento: a partir de la idea que se ha inventado él de que los tejidos tienen que estar muriéndose de hambre por culpa de la acción de la insulina, se le ocurre (a saber por qué extraño razonamiento) que eso significa que en ayunas los niveles de ácidos grasos en plasma deberían estar por los suelos. Y dice que no es así porque el tejido adiposo de la gente que tiene obesidad libera más ácidos grasos, no menos. Pensémoslo un momento: ¿por qué el hecho de que nuestro tejido adiposo almacene un día 1g de grasa corporal debe hacer que en ayunas nuestros niveles de ácidos grasos estén por los suelos? ¡¡No tiene ningún sentido!! Pero aparentemente Norton cree estar planteando una idea inteligente.

En cualquier caso, la idea de que cuando hay resistencia a la insulina los adipocitos liberan más ácidos grasos de lo normal es sencillamente falaz. Lo cierto es que los adipocitos de la gente obesa tienen más dificultades tanto para incorporar ácidos grasos como para liberarlos. Pero como por definición hay mucha masa grasa, el efecto global es que una persona que sufre obesidad puede incluso liberar más ácidos grasos que una persona de peso normal (fuente). Pero hay patología en el tejido:

FFA release per unit of FM decreases in a curvilinear fashion with increasing body fat. Therefore, obesity is associated with a decrease in the rate of FFA release from adipose tissue. However, this downregulation in the rate of FFA release per unit of body fat does not completely compensate for the increase in total body fat, so total FFA Ra and FFA availability in relation to FFM are increased. (fuente)

La liberación de FFA por unidad de FM disminuye de forma curvilínea al aumentar la grasa corporal. Por lo tanto, la obesidad se asocia con una disminución en la tasa de liberación de FFA desde el tejido adiposo. Sin embargo, esta regulación a la baja en la tasa de liberación de FFA por unidad de grasa corporal no compensa completamente el aumento en la grasa corporal total, por lo que la disponibilidad total de FFA y y el FFA Ra total en relación con la FFM se incrementa.

Es decir, es como si Norton argumentara que los niños desnutridos o sin apenas masa muscular tienen la misma capacidad de realizar actividad física que niños correctamente alimentados y que hacen ejercicio físico. Y al comprobar sus fuentes lo que vemos es que se está comparando la acción de un niño normal levantando una pesa con la de tres niños desnutridos levantando ¡¡entre los tres!! esa misma pesa. Él nos diría que los niños desnutridos tienen incluso más fuerza, lo que demostraría, según él, que la desnutrición no sólo no debilita, sino que fortalece. Ése es su argumento, pero como digo, que sea falso el dato que aporta sólo es un elemento más en un argumento absurdo creado a partir de su hombre de paja. Pero si alguien entiende por qué tendríamos que tener carencia de ácidos grasos en plasma en ayunas porque nuestro tejido adiposo ha acumulado grasa corporal, que me lo explique. Y luego que me explique si va a pasar lo mismo con mis ácidos grasos en ayunas si hoy consumo 10 g de comida menos que ayer. Y que aporte evidencia científica de que eso sucede de verdad.

Nótese que esta misma falsedad ya se la hemos visto a Guyenet, PhD y a Danny Lennon. Uno la crea y el resto la repiten creyendo que dicen algo con sentido. Éste es el nivelazo que hay en el mundo de la nutrición.

Sigo en la segunda parte.

 

NOTA: a Layne Norton le gusta insultarnos a los que seguimos una dieta cetogénica o low-carb (ver). 

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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:

evolpeso2

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.

pastedimage

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:

image_3641

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.

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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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Debate Taubes-Guyenet. Mi análisis (II)

(English version: click here)

Mis notas del segundo segmento del debate (segunda media hora del mismo) y a continuación mis comentarios:

  • [SG 29m] El cerebro en realidad regula la grasa corporal. Esto no debería sorprender a nadie.
  • [GT 30m] Uno de los problemas es el “phase.lock intelectual” [una condición en la que las creencias dogmáticas evitan que se formulen ciertas preguntas]. La comunidad de investigación de la obesidad dejó de lado en sus investigaciones la endocrinología en la década de 1960, es decir, dejó de lado la regulación hormonal/metabólica de la grasa corporal, la oxidación, etc. Todo lo que han hecho desde entonces ha sido interpretar incorrectamente. La leptina es un buen ejemplo. Asumieron que lo que hace la leptina es controlar el cerebro, pero tal vez gran parte de lo que hace la leptina se hace en la periferia. En la búsqueda de genes asociados con el tipo de cuerpo, todos los genes actúan debajo del cuello (genes regulados por la insulina), pero con el exceso de grasa corporal decidieron que estaban en la cabeza. La cuestión es que cuando miran, están programados para pensar que la grasa corporal es causada por comer en exceso, por lo que buscan en el cerebro.
  • [SG 35m] No comienzan la búsqueda con ninguna suposición.
  • [GT 36m] Los genes pueden tener diferentes trabajos en diferentes células del cuerpo, pero si crees que el problema está en el cerebro, ahí es donde miras.
  • [GT 36m] Se supone que el libro de Stephan trata sobre la obesidad, pero en realidad nunca mencionas nada sobre la regulación hormonal de la acumulación de grasa. Simplemente no está ahí y tiene que estar ahí. [Podemos escuchar la risa de Guyenet mientras habla Taubes]
  • [GT 37m] Stephan es el defensor de la ortodoxia, y yo soy el que viene y dice: “hay psicólogos y psiquiatras a cargo de esta disciplina, mientras que los endocrinólogos lo resolvieron”.
  • [GT 37m] ¿Qué tiene que decir el cerebro sobre el hecho de que la grasa corporal se acumula en algunas partes del cuerpo y no en otras? [Nuevamente podemos escuchar a Guyenet riendo mientras habla Taubes]
  • [SG 38m] Cuando observamos los genes asociados con la grasa corporal total, lo que causa la obesidad, aparecen los genes relacionados con el cerebro, mientras que al buscar genes relacionados con la distribución de la grasa corporal, vemos genes relacionados con la insulina, por ejemplo en las personas que tienen grasa corporal alrededor de su cintura.
  • [SG 39m] [sarcasmo acerca de que Taubes habla de la leptina] “esto es bueno”, porque normalmente Gary no menciona la leptina. Los investigadores no hablan sobre las acciones periféricas de la leptina porque se ha demostrado que los efectos de la leptina son a través del cerebro, no porque usen anteojeras. [Guyenet habla sobre sí mismo como investigador: “NOSOTROS nos enfocamos”]. En los experimentos en los que los receptores de leptina se eliminan en el cerebro o en el hipotálamo, se produce obesidad, lo que demuestra que el cerebro es un sitio clave de acción.
  • [GT 40m] Un sitio clave de acción.
    [SG 41m] El cerebro es este sitio de acción que hace que esto suceda. Entendemos muy bien cómo funciona la leptina. Las personas con obesidad no consiguen perder grasa porque tienen un punto de ajuste más alto en su adipostato. Cuando una persona pierde peso, hay una reacción en los circuitos cerebrales que regulan la grasa corporal que provoca un aumento de sus antojos y hambre. Lo hace hasta que la grasa vuelve. La grasa corporal está regulada por un circuito de retroalimentación negativa que está controlado por la leptina.
  • [Joe Rogan 44m] Cuando comes una dieta azucarada, una dieta alta en calorías, tu cuerpo engordará, ¿verdad?
  • [SG 44m] Depende de cuántas calorías estés comiendo.
  • [GT 44m] La leptina no solo se produce en respuesta al tamaño del adipocito, sino también en respuesta a la entrada de glucosa en el adipocito, que está parcialmente mediada por la insulina.
  • [GT 45m] Todo lo que se dice tiene dos interpretaciones, dependiendo del paradigma que estés viendo. Y los paradigmas son esencialmente diferentes.
  • [GT 46m] Hace 8 años, Stephan y yo nos peleamos por primera vez cuando actué de manera inapropiada en el Simposio de Salud Ancestral.
  • [GT 46m] Saber que hay más personas entrando en una habitación que saliendo, no nos dice por qué la habitación está llena de gente. En la obesidad, la razón por la que se está engordando se ha dejado de lado y la gente decidió que comer en exceso era de alguna manera una explicación.
  • [GT 47m] Para saber cuál es la influencia del ambiente en la obesidad, debemos preguntarnos si podemos encontrar una epidemia de obesidad sin este “entorno alimentario moderno”. Y me enteré de los Pima en 1902: pobres, desnutridos, que habían sufrido hambruna durante 40 años, y sin embargo, las mujeres de la tribu, que hacen todo el trabajo duro, eran obesas. Luego podemos disociar la obesidad del “ambiente alimentario moderno” y los alimentos ultraprocesados. Tenemos obesidad a pesar de la existencia del hambre. [Oímos nuevamente las risas de Guyenet mientras Taubes habla]
  • [Joe Rogan 48m] ¿Cuál fue la causa de que las mujeres se volvieran obesas?
  • [GT 48m] Fueron convertidos en una “reserva” y comenzaron a comer alimentos occidentales. Puedes encontrar lo mismo en los sioux.
  • [GT 49m] Cualquier transición de una población a una dieta occidental o una dieta/estilo de vida occidental los vuelve obesos y hace que se desarrolle síndrome metabólico. La genética no es tan importante, lo importante es lo que la desencadena en el medio ambiente. Creo que son ciertos alimentos.
    [GT 50m] Doble carga de la obesidad: tenemos madres obesas con niños desnutridos. Y esto ocurre en poblaciones que no han podido “comer en exceso”. Y si hubieran podido comer más, ¿por qué se mueren de hambre sus hijos? ¿Cómo explicamos la obesidad en las madres sin suponer que las madres están comiendo en exceso?
  • [Joe Rogan 51m] Stephan, ¿existen poblaciones en el mundo que son obesas y que no consumen una dieta occidental, que no consumen productos azucarados?
  • [SG 51m] Probablemente no, porque una vez que tenga un sistema alimentario industrializado éste incluye azúcar. Pero hay poblaciones que comen mucha azúcar y no son obesas.
  • [SG 52m] Gary ha contado una historia, su versión de la historia de Pima. Déjame que te cuente la versión de la historia que aparece en la literatura científica. Eran una sociedad que dependía de la agricultura, pero con la llegada de los granjeros (pobladores de ascendencia europea), el río que los abastecía fue desviado y el gobierno comenzó a proporcionarles alimentos: alimentos refinados y ricos en calorías: harina, manteca y azúcar. Y se hicieron muy obesos. Otros Pima que, justo al otro lado de la frontera, mantenían su estilo de vida tradicional alto en carbohidratos y agrícola, eran mucho más delgados y saludables.
  • [SG 54m] Gary, parece que crees que las personas pueden aumentar de peso incluso si están comiendo muy pocas calorías …
  • [GT 54m] Sí
  • [SG 54m] Estas son observaciones muy informales, historietas. Cuando miras los datos, lo que ves es que las personas obesas consumen entre un 20 y un 35% más que las personas delgadas. Esos datos provienen de los métodos más precisos que tenemos. El modelo de Gary dice que es una consecuencia, un resultado, de ganar peso, mientras que mi modelo dice que eso es realmente un requisito para que se produzca engorde. ¿Qué sucede si reduce la ingesta de calorías en esa misma cantidad? No importa si lo haces restringiendo los carbohidratos o la grasa, estos experimentos se han hecho, y se pierde peso.
  • [Joe Rogan 56m] ¿Estás diciendo que al consumir bajas cantidades de calorías pero altas cantidades de azúcar, no tiene sentido que uno pueda volverse obeso de esa manera?
  • [SG 56m] Correcto
  • [GT 56m] Podemos encontrar casos en los que hay obesidad sin exceso de alimentos, como Trinidad en los años sesenta. Dos tercios de las mujeres adultas eran obesas, y había hambre, desnutrición y niños con crecimiento atrofiado. Los datos dicen que consumieron menos calorías que las recomendadas por la OMS para una dieta saludable. La hipótesis del cerebro no explica por qué una madre es obesa mientras sus hijos se mueren de hambre. Si tiene que comer calorías superfluas para engordar, como dice esa hipótesis, ¿por qué no le está dando esas calorías a sus hijos? Mi hipótesis es que la explicación es que es el contenido de macronutrientes de la dieta lo que desencadena la obesidad.
  • [GT 59m] Hay experimentos en los que los animales engordan incluso muriéndose de hambre.
  • [SG 59m] Son experimentos realizados en animales con mutaciones relacionadas con la leptina.
  • [GT 59m] La cuestión es que si mi cuerpo acumula grasa en los niveles de ingesta en los que una persona delgada no puede hacerlo, acumularé grasa corporal comiendo la misma cantidad que la persona delgada.
  • [SG 59m] Los datos de ingesta calórica para Trinidad no son fiables. No hay razón para creer que esas personas comían 1800 kcal/día y se volvían obesos. Las medidas precisas de ingesta calórica de personas que dicen que consumen 1200 kcal/d, dicen que consumen más calorías que las personas delgadas. Lo que Gary dice se observa solo cuando se utilizan métodos inferiores para medir la ingesta de calorías.
  • [GT 1h1m] Insisto en mi pregunta: madre obesa con un niño hambriento. La existencia de los niños desnutridos sugiere fuertemente que no hay mucha comida disponible. Y tenemos que explicar la obesidad en la madre.
  • [SG 1h1m] Hay muchas razones por las cuales un niño puede tener desnutrición en situaciones no industriales. No tengo una explicación, pero no es necesariamente por la razón que Taubes dice.

Depende de cuántas calorías consumas

Guyenet, PhD, la misma persona que unos minutos antes decía que una dieta con grasa y azúcar producía efectos que no se pueden replicar completamente con sólo azúcar o sólo grasa, ahora muestra fidelidad al dogma caloréxico:

[Joe Rogan 44m] Cuando comes una dieta azucarada, una dieta alta en calorías, tu cuerpo engordará, ¿verdad?

[SG 44m] Depende de cuántas calorías estés comiendo.

Es la misma persona que cree que el azúcar te puede engordar porque está bueno, al margen de cuántas calorías tenga. Pero cuando le interesa demostrar fidelidad a los dogmas oficiales, entonces afirma que las calorías son las que marcan si se engorda o no. Un gran campeón de la disonancia cognitiva. O un gran campeón en echarle cara y querer jugar a varias bandas al mismo tiempo.

No hay obesidad si no llega la comida occidental

Ambos están de acuerdo en eso. Está claro, añado yo, que no es una disfunción en el cerebro lo que causa obesidad. Podemos plantear como analogía, que si yo pincho a alguien con una aguja y sangra, la causa de que sangre no es la ausencia de una tirita: ha sido el pinchazo con la aguja lo que ha causado el sangrado. Aunque una venda pare el sangrado. Hablando de obesidad, si tu dotación genética es mejor que otra, a lo mejor te protege de una “comida” que no deberías estar comiendo, pero la causa de que otra persona sí engorde ante el mismo estímulo no está en su cerebro: la causa es el estímulo, es decir, lo que está comiendo y no debería estar comiendo.

Un ejemplo. Supongamos que tenemos dos personas (personas A y B) que son sometidas a dos condiciones ambientales diferentes (condiciones 1 y 2) durante un tiempo, con los siguientes resultados en términos de ganancia de peso corporal:

Persona\Entorno 1 2
A 0 kg +6 kg
B 0 kg +7 kg

Aunque existiera una relación entre genética y peso corporal que explicase la diferencia de +6 a +7 kg ganados, ¿cuál es la causa real de la ganancia de peso en este ejemplo? Sólo es un ejemplo, pero deja claro que aunque las diferencias entre personas pueden tener una explicación genética, no necesariamente eso nos habla de la causa de la obesidad.

Por otro lado, Guyenet argumenta que sí hay poblaciones que consumen mucho azúcar y no son obesas. Las enumerará en un segmento posterior. Lo que quiero resaltar es que su contraargumento no demuestra nada (en caso de que nos creamos los datos) sobre las razones por las que se engorda en el mundo occidental, pues no son las mismas condiciones. Por ejemplo, podría haber un efecto sinérgico del azúcar con los aceites de semillas (elevado omega-6) o con algún disruptor endocrino, y encontrar que en un pueblo que tiene un consumo elevado de azúcar, en ausencia de otros factores típicos del mundo occidental, no hay obesidad, no puede ser usado para exculpar al azúcar en sociedades en las que el azúcar coexiste con otros factores dietéticos y ambientales. O a lo mejor esos pueblos pasan mucho tiempo al aire libre (sol) y respetan los ritmos circadianos y eso les protege en cierta forma del azúcar, y ése no es nuestro caso. O quizá esas poblaciones siguen dietas muy bajas en grasa en las que el azúcar no es tan dañino para la salud. A saber.

Madre obesa e hijo desnutrido

La “doble carga de la obesidad y desnutrición” es la coexistencia de obesidad y desnutrición en una población (ver). Por ejemplo, en la siguiente gráfica vemos IMC (índice de masa corporal) en función de la edad, datos en campos de refugiados en el Sáhara Occidental. Como vemos, en todas las edades hay tanto personas con clara obesidad como personas con IMC bajísimo:

Y en este estudio una cuarta parte de las casas coexisten obesidad y desnutrición:

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.

Nuestros resultados demuestran que tanto el retraso en el crecimiento (en niños y mujeres) como la obesidad (en mujeres) son altamente prevalentes entre los refugiados saharauis, siendo la obesidad central aún más prevalente y apareciendo a una edad más joven en mujeres que la obesidad. En segundo lugar, más hogares se vieron afectados por el sobrepeso y la obesidad central que por la desnutrición, aunque estos últimos afectaron a más de un tercio de los hogares. En tercer lugar, una proporción importante de los hogares de refugiados, uno de cada cuatro, se ve afectada por la doble carga de la malnutrición.

¿Cómo se explica que haya una madre obesa que tiene un hijo desnutrido? Guyenet lo que hace es cuestionar los datos aportados por Taubes, es decir, cuestionar que una mujer pueda engordar consumiendo sólo 1800 kcal/d.

[SG 1h0m] Lo que Gary dice se observa solo cuando se utilizan métodos inferiores para medir la ingesta de calorías.

¿Es cierto lo que dice Guyenet? ¿Sólo sucede en esos casos? ¿La madre obesa come “de más” mientras su hijo se muere de hambre? Cuesta creerlo, la verdad.

[Joe Rogan 56m] ¿Estás diciendo que al consumir bajas cantidades de calorías pero altas cantidades de azúcar, no tiene sentido que uno pueda volverse obeso de esa manera?
[SG 56m] Correcto.

Vamos a recordar cuatro experimentos científicos comentados en el blog. En el primero (ver) tenemos un grupo de ratas, el grupo HS, que consume una dieta alta en azúcar. Como vemos en la tabla, consume unas 100 kcal/d, mientras que el grupo HF consume unas 200 kcal/d. Si nos fijamos en el peso corporal y en la grasa corporal, el grupo que consume 100 kcal/d acaba el experimento con más peso y más masa grasa que el que consume 200 kcal/d. ¿Se puede engordar comiendo muy poco? Sí, sí se puede. Diga lo que diga Guyenet.

Experimento en animales y por tanto, absolutamente controlado. No hay razones para poner en duda los datos de ingesta en experimentos con animales.

El segundo experimento (ver) lo que muestra es cómo la misma comida, con las mismas calorías, es mucho más engordante consumida en forma de polvo que consumida como bolas/píldoras. En la gráfica se muestra en rosa pálido la evolución del peso corporal de tres grupos dietarios que consumen muchas menos calorías que el grupo representado con círculos vacíos, y, sin embargo, la evolución del peso corporal es prácticamente la misma que en ese grupo:

Es decir, en este experimento, con mucha menos comida esos tres grupos de ratas están engordando lo mismo que ratas que consumen más comida. Insisto: en los experimentos con animales no se mide mal la ingesta. El truco de poner en cuestión los datos de ingesta aquí ya no vale.

En el tercer experimento (ver) el grupo de ratones que menos calorías consume (puntos huecos) es el que más peso y más grasa corporal gana:

En el cuarto experimento (ver), la dieta de las ratas es idéntica en términos de nutrientes y calorías, diferenciándose únicamente en el índice glucémico. Para evitar que las ratas de la dieta de alto índice glucémico subieran más de peso que el otro grupo, hubo que reducirles considerablemente la ingesta, tal y como se muestra en la parte superior de esta gráfica:

Y, pesar de la ingesta reducida respecto del otro grupo y de tener prácticamente el mismo peso, acabaron el experimento con un 71% más de grasa corporal: 98 g frente a 57 g. Comiendo claramente menos en términos de calorías, reitero:

 

[SG 54m] Gary, parece que crees que las personas pueden aumentar de peso incluso si están comiendo muy pocas calorías …

A lo mejor es que Taubes cree que es posible lo que estos cuatro experimentos científicos que acabamos de comentar demuestran que es posible. La pregunta es por qué Guyenet no lo cree posible. ¿Es que Guyenet desconoce lo que está publicado en la literatura científica?

De cualquier forma, creo que Guyenet está en su derecho de poner en duda que los datos sean correctos. Lo que es inaceptable es la arrogancia de calificar los argumentos de Taubes como historietas (story-telling) y presumir de que su opinión sí viene avalada por evidencia científica.

Gary ha contado una historia, su versión de la historia de Pima. Déjame que te cuente la versión de la historia que aparece en la literatura científica.

Como veremos en otros segmentos del debate, los casos “anecdóticos” que usará Guyenet (los Guna, crisis en Cuba o los Hadza) son observaciones totalmente equiparables a los casos de los Pima, Sioux o Trinidad citados por Taubes. Historietas o ciencia por igual en ambos casos, los ponga sobre la mesa uno o los ponga sobre la mesa el otro. Sobran los comentarios despectivos hacia los argumentos del interlocutor y sobra toda proclama de ser el defensor de lo que dice la evidencia. ¿Por qué Guyenet cree estar por encima de Taubes? Ni siquiera es investigador, como da a entender en el debate: es escritor y consultor científico. No sólo usa la falacia de autoridad, lo hace presumiendo de lo que no es.

La gente que sufre obesidad come “de más”

Junto en este último apartado de esta entrada tres argumentos de Guyenet:

  • la gente obesa consume entre un 20 y un 35% más que los delgados
  • en el modelo de Guyenet comer “de más” es un requisito para engordar
  • si reduces la ingesta en esa misma cantidad da igual que lo hagas restringiendo carbohidratos o grasa, los experimentos dicen que se pierde peso

El primer punto ya apareció en el primer segmento, pero insisto en él porque me parece interesante. Gary Taubes argumenta en el debate que para desarrollar obesidad basta con acumular 10 kcal/d, y que eso no se explica por un consumo “excesivo”, pues de esa ingesta “excesiva” que puede haber cada día sólo 10 kcal/d acaban siendo acumuladas. Como Guyenet no puede justificar hablar de “exceso” con 10 miserables kcal/d, lo que hace es redefinir “exceso” como lo que comes por encima de lo que come una persona delgada ¡¡cuando ya eres obeso!! Así convierte esas 10 kcal en una cantidad mucho mayor, lo que le permite seguir usando el término “exceso”. Es un truco retórico que le sirve para no responder a la cuestión. Y al hacerlo culpabiliza a la víctima por su problema de peso: si tienes obesidad pero mantienes el peso, para Guyenet sigues comiendo en “exceso” porque comes más que una persona delgada, aunque sea lo que tu cuerpo te pide o necesita para funcionar. No caigamos en la trampa tendida por Guyenet: no hablamos de la persona que ya tiene exceso de peso: el que está ganando peso lo hace a un ritmo de 10 kcal/d. ¿Se produce esa acumulación de energía porque consume esas calorías en exceso respecto de la persona que no engorda? Eso es a lo que Guyenet evita contestar. Porque nadie puede aceptar que 10 kcal/d puedan ser catalogadas de exceso. Y a lo mejor esa acumulación no la produce el “exceso”, sino la composición de la dieta. Guyenet tiene una creencia, pero es posible que esté equivocado.

Por otro lado, Guyenet usa este argumento como explicación para la “doble carga de la obesidad”, pero los datos que usa no están sacados de los casos que Taubes cita. No sabe si su explicación es aplicable a esas poblaciones.

El segundo argumento es que una ingesta aumentada es un requisito para engordar en su modelo de obesidad. Pues bien, hemos visto cuatro experimentos científicos que demuestran, en tal caso, que su modelo es erróneo. Y me parece muy interesante que use el término “requisito”, porque precisamente uno de los errores en los que se basa su pseudociencia es dar por supuesto que una ingesta aumentada respecto del gasto energético es un requisito para engordar. ¡¡No lo es!! Esa creencia nace de errores de razonamiento, y lo he explicado mil veces en el blog (y si nos descuidamos llegará un momento en el que decir mil veces no sea exagerar): ver, ver, ver, ver.

Por último, Guyenet dice que reduciendo la ingesta se pierde peso. Guyenet está engañando a los cientos de miles de personas que han visto el debate. Los experimentos científicos lo que dicen es que se pierde peso a corto plazo, pero se recupera a largo plazo, aunque se mantenga la restricción energética (ver,ver). Eso es lo que está publicado en la literatura científica, no lo que él afirma. Es más, que le pregunte a Kevin Hall, PhD qué sucede cuando intentas hacer adelgazar a alguien aplicando esa filosofía (ver,ver). Pero bueno, no es ninguna sorpresa que Guyenet engañe a la gente con argumentos claramente falsos. Tiene una explicación: es Guyenet, PhD.

A colación de esto, recordemos este otro experimento (ver,ver) en el que un grupo de ratones es obligado a consumir un 66% de las calorías que consumen el resto de ratones (que siguen diferentes dietas). Si nos fijamos en la evolución de su peso corporal, tras la bajada inicial se produce una recuperación del peso perdido.

¿Se han saltado la restricción calórica esos ratones? No. Han subido de peso comiendo poco.

NOTA: toda la terminología del paradigma energético está en entredicho. No es obvio que se pueda usar el término “exceso” (o “exceso calórico”) asociado al incremento de grasa corporal.

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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.

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

Further reading:

Debate Taubes-Guyenet. Mi análisis (I)

(English language version: click here)

Empiezo aclarando que hablar de quién ha ganado un debate me parece ridículo. Entiendo que es algo normal en política, donde lo único que importa a los que debaten y a sus respectivos partidos es vender imagen, pero en temas de nutrición/obesidad resumir un debate limitándonos a votar quién es el ganador no aporta nada. Sólo demuestra si los de un grupo de pensamiento son más o menos numerosos que los de otro grupo de pensamiento. Se puede hacer la votación antes de realizar el debate, y malicio que seguramente saldría el mismo resultado. Dejémonos de votaciones. Hablemos de qué argumentos han usado y hablemos de qué nos parecen esos argumentos. Si el único “argumento” que tenemos es buscar que el resto del grupo apoye nuestro grito de “ha ganado X”, siendo X nuestro “campeón del rey”, lo único que fomentamos es el sectarismo y mantener creencias que pueden ser erróneas.

¿Ganó Taubes? ¿Ganó Guyenet? Preguntas irrelevantes que llevan a respuestas irrelevantes.

Aclarado lo anterior, cuando la gente habla del ganador de un debate, no sólo habla de los argumentos racionales. Si leemos los comentarios en youtube de este debate, veremos claramente que es así. Muchísimas referencias son hacia la condescendencia (es decir, arrogancia y aires de superioridad) de uno de los participantes. Decir que A o B han perdido el debate porque son unos arrogantes insufribles no aporta nada. O, más bien, es la parte de “perder el debate” la que no aporta. Creo que sí es importante resaltar los argumentos ad hominem, el recurso a la falacia de autoridad o el comportamiento arrogante en general (como afirmar que las opiniones propias son ciencia, mientras que las del oponente son historietas). En esas actitudes no hay “argumento racional”, pero sí hay un intento de hacer parecer que se tiene razón y que el otro es un mindundi que no sabe de lo que habla. La humildad, por el contrario, es interpretada como falta de seguridad en las propias creencias. A mí la arrogancia no me transmite sensación de “competencia profesional”, igual que no lo hacen las letritas que ciertas personas ponen tras sus nombres. Me da igual que tengas un doctorado o cuatro, si tus argumentos son basura. Quizá en mis comentarios sí resalte esos comportamientos arrogantes, simplemente para señalar cómo se intentan usar esos argumentos no racionales para “ganar” la batalla de la imagen.

¿Ha sido interesante el debate? En mi opinión, sí lo ha sido. Desagradable de ver, pero interesante. No tiene que ver una cosa con la otra.

En esta primera parte voy a comentar la primera media hora de debate. Empiezo con mis notas sobre los temas tratados, indicando quién estaba hablando y en qué minuto.

  • SG [1m30] “Los circuitos cerebrales que regulan la grasa corporal”.
  • SG [3m30] Analogía extraterrestres, coche, ruedas, velocidad, cerebro.
  • SG [5m] El cerebro regula el tamaño de los adipocitos. Los adipocitos no regulan su propio tamaño.
  • SG [7m] En las personas que engordan hay un cambio en los mecanismos regulatorios. Una persona que engorda no es simplemente una persona delgada que come mucho.
  • SG [8m30] Los genes asociados con la obesidad son genes relacionados con el cerebro.
  • SG [10m] Fármacos aprobados para combatir la obesidad están basados en comer menos (reducir el apetito o reducir la absorción de nutrientes). Ninguna de las “effective fat loss drugs” actúa ni sobre la insulina ni en los adipocitos.
  • SG [11m30] Las mutaciones genéticas que causan obesidad lo hacen afectando a la señalización de la leptina. La leptina es la principal hormona reguladora de la grasa corporal.
  • SG [14m] El efecto de azúcar+grasa no se puede replicar completamente con sólo azúcar. Lo achaca a sabrosura.
  • SG [15m] No se puede conseguir, ni en animales ni en humanos, lo mismo aumentando la ingesta energética con azúcar y carbohidratos que si se hace con comida sabrosa que combina grasa y carbohidratos.
  • GT [17m] Ante la pregunta de si las calorías “importan”, contesta que es una forma equivocada de enfocar el problema.
  • GT [22m] La obesidad es un problema de acumulación de grasa, no de balance de energía.
  • SG [26m] Lo que diferencia una historia que es verdad de una que no lo es, es la evidencia. La propensión genética en la obesidad tiene que ver con el cerebro. El 75% de la diferencia en grasa corporal entre individuos es debida a diferencias genéticas entre ellos. El entorno es mucho menos importante.

Analogía del coche

Guyenet, PhD (omitiré el PhD de ahora en adelante por comodidad) ya desde el principio habla de “los circuitos cerebrales que regulan la grasa corporal”. No dice que influyen, dice que regulan. Recordemos que poco antes del debate Guyenet criticó a Taubes (ver) por creer que su hipótesis era la explicación principal de la obesidad, en lugar de estar abierto a que otros mecanismos sean importantes. Aquí vemos claramente la hipocresía de Guyenet, afirmando que la grasa corporal es regulada por circuitos cerebrales.

Bueno, la analogía que hace es que si unos extraterrestres observaran el comportamiento de los coches y quisieran entender por qué unos coches circulan a unas velocidades y otros a otras, si hicieran el análisis observando el comportamiento de las ruedas, no entenderían nada, porque la velocidad la determina el conductor, es decir, el cerebro. La analogía es, sencillamente, sorprendente, pues no aporta absolutamente nada. Ni es un contraejemplo de nada, ni ayuda a entender nada. Si la obesidad es controlada por nuestro cerebro, la analogía será adecuada, pero si tiene más que ver con las ideas de Taubes, sencillamente la analogía será errónea. Se la podía haber ahorrado.

Los adipocitos no regulan su propio tamaño

Argumento falaz, pues nadie dice que lo hagan. La hipótesis que defiende Taubes es más bien que es el estímulo que reciben los adipocitos (insulina), modulado por la respuesta de ciertos órganos a ese estímulo (resistencia a la insulina), lo que acabará determinando si hay acumulación neta de grasa corporal o no. La pregunta correcta es: ¿regulan los estímulos que reciben los adipocitos el tamaño de estos?

La genética de la obesidad tiene que ver con el cerebro, no tanto con el entorno

Entonces, ¿los pueblos del mundo que siguen sus dietas tradicionales, sin harina, sin azúcar, sin aceites de semillas, sin productos procesados, lo que tienen diferente que nosotros es el cerebro?

Se diría que el entorno, lo que comemos y como vivimos, es la causa principal de la obesidad, no cómo es nuestro cerebro ni qué genética tenemos. Hace 100 años teníamos los mismos genes, exactamente los mismos, pero no teníamos una epidemia de obesidad. ¿Es culpa de nuestros genes? Cuando un grupo de personas emigra desde una cultura no occidentalizada a una cultura occidentalizada, en general suben de peso. ¿Por su cerebro o por el cambio de entorno?

Por supuesto, ante los mismos estímulos unas dotaciones genéticas van a reaccionar mejor que otras, y dotaciones genéticas parecidas reaccionarán de forma parecida, pero eso no quita que la causa real del problema sea el estímulo improcedente, no la capacidad protectora de nuestra genética frente a ese insulto. ¿El 75% de la obesidad es de causa genética? No, el 100% parece ser de causa ambiental, pues la obesidad sólo aparece cuando el ambiente se occidentaliza.

No hay fármacos eficientes que actúen sobre la insulina o los adipocitos

La principal trampa en el argumento es asociar “FDA approved” con “eficiente”. No hay, que yo sepa, fármacos eficientes para tratar la obesidad. Hay pérdida de peso a corto plazo, como “comer poco”, pero no a largo plazo (ver,ver). Luego hablar de eficiencia es falaz, porque no la hay en los fármacos aprobados para su uso.

Por otro lado, Guyenet emplea la falacia de causa única, que es presuponer que una determinada condición (engordar o bajar de peso) tiene una única causa. Aunque los fármacos fueran eficientes haciendo perder peso, y no lo son, por hacer comer menos, eso no quiere decir que no sean posibles otras causas para el mismo resultado. Y un fármaco puede no ser viable no porque no funcione, sino por dificultades de otro tipo, como sus efectos secundarios o la dificultad de mantener el principio activo en condiciones óptimas hasta el día de su uso. Por ejemplo, que no existan fármacos que ayuden a adelgazar actuando sobre la leptina, ¿demuestra que la leptina no está implicada en la obesidad? Aplicando el argumento de Guyenet tendríamos que deducir exactamente eso, que la leptina no está implicada en la obesidad. Hasta que inventen la forma de producir un fármaco viable, en cuyo caso, mágicamente, sí estará implicada. Este argumento es un sinsentido.

Por otro lado, ¿experimentos con fármacos que reducen la insulina? Sí los hay: diazoxide, por ejemplo (ver).

Las mutaciones genéticas que causan obesidad lo hacen afectando a la señalización de la leptina

Falacia de causa única: que esa causa produzca el efecto, no quiere decir que otros factores no puedan causarlo. Por ejemplo, en los insulinomas suele haber una ganancia considerable de peso (ver) y se sabe que las inyecciones de insulina pueden causar acumulación local de grasa en las zonas de inyección (ver) y aumento de peso (ver).

El efecto de azúcar+grasa no se puede replicar completamente con sólo azúcar

Es, posiblemente, uno de los comentarios más interesantes por parte de Guyenet en este segmento. Lo que dice, textualmente, es que no se puede replicar completamente el resultado de consumir una dieta sabrosa que combina grasa y azúcares, empleando una dieta que sólo contiene azúcares (arroz y azúcar, por ejemplo). Dice “si incrementas el consumo de azúcar en animales o en humanos, haces que se gane peso corporal, pero éste es modesto, en comparación con lo que se consigue cuando se usa una dieta densa en calorías, sabrosa y que contiene tanto grasa como carbohidratos” y matiza, que eso demuestra que el azúcar y los carbohidratos no pueden explicar todo el efecto.

Yo creo que ese trozo del vídeo (min 13:00-17:30) hay que verlo, no escucharlo, y observar la cara de Guyenet. Me da la sensación de que Guyenet es incapaz de explicar lo que está diciendo exactamente. Especialmente porque parece claro que no quiere usar la palabra calorías. Y creo que no la usa, porque sería demasiado claro que está diciendo que, a igualdad de calorías, una dieta que contenga azúcar y grasa va a ser más engordante que una que contenga sólo azúcares. Porque si no está diciendo eso, nada de lo que dice tiene sentido, y, si todo fuera cuestión de calorías, sí sería posible replicar el resultado de una dieta con otra, simplemente haciendo que la ingesta energética fuera la misma. Pero no es eso lo que dice.

Yo estoy de acuerdo: una dieta con azúcar y grasa puede ser más engordante, al menos a corto plazo, que una dieta que sólo contenga azúcares. A igualdad de calorías.

¿Es que Guyenet sabe que a igualdad de calorías y de macronutrientes, una dieta puede ser más engordante que otra? Sí lo sabe, como podemos comprobar en este artículo suyo, que borró posteriormente pero del que hay copia en web.archive.

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 a 7.5% increase in total body weight, and the safflower group saw a 12.3% increase.

Encontré un estudio bien controlado en el que los investigadores pusieron ratas en tres dietas isocalóricas y con alto contenido de grasa. Cada una contenía una cantidad idéntica de grasa total, proteínas, carbohidratos, ácido omega-3 alfa-linolénico (de aceite de lino) y cantidades variables de ácido omega-6 linoleico.

Todas las ratas ganaron peso con la dieta alta en grasa, pero su composición de grasa corporal fue diferente. El tejido graso en el grupo de sebo fue 10,3% de ácido linoleico, 15,2% en el grupo de aceite de oliva y 54,5% en el grupo de cártamo. En relación con el grupo de sebo, las ratas en el grupo de aceite de oliva vieron un aumento del 7,5% en el peso corporal total, y el grupo de cártamo vio un aumento del 12,3%.

Entonces, si éstas son sus creencias, ¿cómo es posible que diga que es la ingesta energética la que determina los cambios en el peso/grasa corporal (ver)? Hay muchas preguntas que tienen una misma respuesta: es Guyenet, PhD, capaz de decir una cosa y la contraria y creer que tiene razón en ambos casos.

Para terminar esta primera entrega del análisis del debate, vamos a recordar un artículo de Guyenet en su blog (uno que todavía no ha borrado) que viene muy a cuento para entender sus creencias:

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

El grupo de investigación del Dr. Anthony Sclafani acaba de publicar un estudio que demuestra de manera definitiva que se requiere una alta sabrosura o que esté bueno para que el azúcar engorde en los ratones. 

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.

Los investigadores demostraron que los ratones que carecen de estas proteínas tienen una ingesta normal de alimentos y grasa corporal cuando se les alimenta con un chow estándar de laboratorio, pero a diferencia de los ratones normales, ambas cepas mutantes son casi completamente resistentes al aumento de grasa cuando se les da una solución de azúcar. Esto es a pesar del hecho de que bebieron una cantidad similar de azúcar que los ratones normales, que se volvieron obesos. Básicamente, bebían el agua azucarada pero ya no engordaba una vez que no tenía un sabor dulce

¿Lo estamos leyendo? Está diciendo que al margen de composición y calorías, si el azúcar no te sabe rico, no te engorda.

Vamos a ver los resultados de ese experimento, porque son interesantes.

En un primer experimento, a los ratones Task1r3 KO los sometemos a dos dietas: el grupo control consume chow normal (Con) y otro grupo (Suc) consume gran parte de las calorías en forma de azúcar. En la parte superior de la siguiente gráfica vemos la ingesta energética, donde la parte blanca de la barra representa la porción de las calorías procedentes de la solución azucarada. En resumen, el grupo Suc consume más calorías que el grupo Con. Pero, como vemos en las otras dos gráficas, ese grupo no gana ni más peso ni más grasa corporal que el Con.

Mayor ingesta energética, pero no hay diferencias en la grasa corporal acumulada. ¿No eran las calorías “extra” lo que nos engordaba, Guyenet? Pero lo bueno viene ahora.

En un segundo experimento, se añade una pequeña cantidad de emulsión de grasa a la dieta, haciéndola mucho más sabrosa. Y ahora esos mismos ratones que no habían engordado con la ingesta de una alta cantidad de azúcar y más calorías, ¡¡sí que engordan!! consumiendo esencialmente la misma comida que antes no les engordó. Y lo hacen sin apenas diferencias en la ingesta energética.

Los autores sugieren que para que los carbohidratos engorden, tienen que ser sabrosos, ¡¡no aportar calorías!! Y esto a Guyenet no sólo no le rechina, sino que lo celebra. Es como para recordarlo:

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.

Nuestros resultados sugieren que las soluciones nutritivas deben ser altamente sabrosas para causar obesidad inducida por carbohidratos en ratones, y que la palatabilidad produce este efecto en parte al mejorar la utilización de nutrientes.

Inesperadamente, la obesidad inducida por la dieta parece deberse en gran parte al aumento en el aprovechamiento de los carbohidratos y no a la ingesta calórica. Esto se ilustra más claramente en los ratones Tas1r3 KO, que mostraron una ingesta elevada de calorías, pero no un aumento de peso excesivo en la dieta de sacarosa en comparación con los ratones WT y Trpm5 KO. Sin embargo, cuando se les ofreció la solución de Suc+IL altamente sabrosa, el Tas1r3 KO ganó una cantidad significativa de peso aunque su ingesta calórica no fue elevada.

Quizá nos parezca un poco contradictorio que la misma persona que sabe que, a igualdad de calorías, una dieta puede ser más engordante que otra por tener una composición diferente (y acabamos de ver dos estudios citados por el propio Guyenet en su blog), lo acabe resumiendo todo como que los estudios científicos controlados demuestran que los cambios en el peso corporal sólo dependen de las calorías (ver). Pero estas contradicciones tienen una explicación: es Guyenet, PhD.

NOTA: en la parte final de este segmento Guyenet, PhD comenta que “lo que diferencia una historia que es verdad de una que no lo es, es la evidencia”. No nos dejemos engañar por la arrogancia. Guyenet, PhD presume de tener una opinión basada en evidencia, a diferencia de la de Taubes, a la que califica de “historietas”, pero sus proclamas sólo demuestran su falta de humildad. 

NOTA: respecto del valor de un doctorado, veamos un ejemplo práctico. El PhD nos cuenta lo siguiente (ver,ver):

Acerca de la “falacia lógica”, imagine un caso en el que A siempre activa B y D. Y B siempre activa C, pero D siempre suprime C. En esta situación, A siempre activa B, y B siempre activa C, pero A no activa C.

Por lo tanto, sólo porque A cause B, y B cause C, no implica que A cause C, incluso si esas afirmaciones son siempre ciertas.

Si A causa B y B causa C, con total seguridad A causa C. Diga lo que diga Guyenet. El error de este señor está en las premisas: no puede sostener simultáneamente que “B siempre activa C” y que “D siempre suprime C”. Porque como se produzcan simultáneamente B y D, una de las dos premisas es con seguridad falsa. En el momento en que corrija su error diciendo que “B activa C salvo en presencia de D”, la aparente paradoja desaparece. ¿Y este señor tiene un doctorado? Sí, tiene un doctorado. Y errores de lógica también los tiene. Y errores garrafales interpretando gráficas, como comentaré más adelante (ver).

NOTA: Guyenet publicó una página con comentarios y referencias bibliográficas para citarlas cómodamente durante el debate.

Ir a las conclusiones
Ir a la quinta entrega
Ir a la cuarta entrega
Ir a la tercera entrega
Ir a la segunda entrega
Ir a la primera entrega

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