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Rebuttal to popular press misconceptions about PNAS series of papers about seed consumption

African hominin stable isotopic data do not necessarily indicate grass consumption

Maelán Fontes-Villalba1, Pedro Carrera-Bastos1 and Loren Cordain2

1Faculty of Medicine, Center for Primary Health Care Research, Department of Clinical Sciences, Lund University, 205 02 Malmö, Sweden

2Department of Health and Exercise Science, Colorado State University, Fort Collins, CO



A series of three scientific papers was published in the Proceedings of the National Academy of Sciences (1-3) evaluating the diet of numerous species of fossilized hominins (bipedal or upright walking apes) who lived in Africa from 4.1 to 1.4 million years ago.  Additionally, the diet of a grass eating baboon was examined (4).  Many of the authors of these papers are friends and colleagues whose data contribute to our understanding of our remote African ancestors’ diets.  Collectively, the following hominin genus’s and the time frame they lived were examined: Australopithecus (circa 4 million years ago [MYA]), Kenyanthropus (circa 3-3.6 MYA), Paranthropus (circa 2.5-1.4 MYA), and early Homo (circa 2.3-1.5 MYA).    


Before I get into the details of these studies, let me first openly reprimand some of the popular press who have incorrectly interpreted these studies by suggesting that our distant ancestors were regular consumers of grass and grass seeds (cereal grains).  For instance, popular blogger Carrie Arnold, titles her write-up (5) of these three scientific studies as, “Even Our Ancestors Never Really Ate the “Paleo Diet”, and goes on to say, “Researchers are just beginning to understand what ancient humans ate, and these recent studies show that grasses and grains have been part of the human diet for millions of years.”  As I will shortly show you, this statement represents sensationalistic journalism and is patently false, as nowhere in any of these three papers (1-3) is this conclusion reached by any of the authors.


Another piece of inaccurate and hyped journalism (6) by author Chris Joyce at NPR labels his piece, “Grass: It’s What’s For Dinner (3.5 Million Years Ago)”.  Chris then tells us, “What the tale of the teeth reveals is this: About 3.5 million years ago, our ancestors started switching from the ape diet – leaves and fruit – to grasses and grass-like sedges.”  This statement is false and again nowhere in any of these three papers (1-3) is this assumption made by the scientists who wrote these manuscripts.  Chris finally gets it right in his following statement, “Now, one thing this carbon isotope technique can’t tell is whether Australopithecus just grazed like a bunch of antelope, or whether they ate the antelope that did the grazing”.  However, in his final paragraph his conclusion again is erroneous, when he tells us, “ So, what to make of this? Well, for one, those who favor a “Paleo diet” that resembles what our early ancestors lived on might consider investing in a lawn mower. After all, lawn grass is probably American’s largest un-harvested crop – there’s plenty to go around.  Why not go back to our roots?”


Catherine Griffin, a writer for Science World Reports obviously did not carefully read any of these three papers (1-3) because of incorrect statements she has made in her brief article (7), “Human Ancestors’ Ape-like Diet Changed 3.5 Million Years Ago to Grass”.  Catherine informs us, “Feel like eating some grass?  Didn’t think so – but our ancient ancestors did.  About 3.5 million years ago, our human forebears added tropical grasses and sedges to an ape—like diet of leaves and fruits from trees and shrubs”.  She goes on to make other statements like, “In the end, the scientists found a surprising increase in the consumption of grasses and sedges” and “The earliest ancestors that consumed substantial amounts of grass foods . . .” that were never made in the original scientific papers.


In science the devil is almost always in the details.  Accordingly, all three of these popular science writers have done their readers a disservice by inaccurately reporting the details of these three studies (1-3) and making assumptions about ancient hominin diets that the scientists themselves did not make. 


In all three papers the measurement of two stable isotopes of carbon (13C  and 12C) were made from samples of enamel in teeth of extinct hominins.  From the ratio 13C/12C a difference (delta) (?13C) is calculated relative to a standard value (8).  ?13C values can then be used to determine if the carbon isotopes in the enamel ultimately originated from plants using either the C3 or C4 photosynthesis pathways. 


In Africa and elsewhere, C4 plants include grasses and sedges and little else, whereas C3 plants include trees, shrubs, herbs and bushes.  C4 plants incorporate relatively more 13C into their tissues during photosynthesis than do C3 plants.  Hence, ?13C values extracted from enamel can reveal the dietary source of the isotopic signature, be it: 1) grasses and sedges, 2) trees, bushes, shrubs, herbs or 3) a combination of both categories of plants.


Unfortunately, a number of fundamental limitations exist with ?13C analysis to evaluate diet.  ?13C measurements cannot determine the exact species of either C3 or C4 plants that were consumed, but more importantly ?13C values cannot distinguish if the C3 or C4 signatures originated from the direct consumption of plants or from the indirect consumption of animals that consumed these plants. To emphasize this essential concept, I have bolded it.  In all three studies (1-3), this crucial point was brought out again and again by the authors.  Apparently, the popular science writers covering these papers missed it.  The data from all three papers (1-3) corroborates the increasing body of literature (8) demonstrating an increased C4 signature in the enamel of African hominins starting about 3.5 MYA, but whether or not it resulted from increased consumption of animal or plant foods or both is unknown.  The authors of one of these three scientific papers (1) put it best, “The 13C-enriched resources that hominins ate remain unknown and must await additional integration of existing paleodietary proxy data and new research on the distribution, abundance, nutrition and mechanical properties of C4 (and CAM) plants.


I would like to point out a number of logical shortcomings with any interpretation of the hominin C4 data suggesting that it originated primarily from increased consumption of either grass leaves, grass seeds (cereal grains) and sedges rather than from consumption of animals (grazers) that ate grasses and grains.  The point in time (~3.5 MYA) at which the C4 signature begins to increase occurs simultaneously with the earliest known use (before 3.39 MYA) of stone tools to cut flesh from animal carcasses and to extract marrow from their bones (9).  Such hominin dietary practices have also been documented by 2.5 MYA (10) and appear to be widely employed by 2.0 MYA (11) and by 1.5 MYA (12).  Hence  by triangulating these indisputable archaeological facts with stable carbon isotope data, it is virtually certain that ?13C values in hominin enamel were enriched partially or perhaps mainly from increasing consumption of  animals that ate C4 plants.


Other lines of evidence indicate that early African hominins were increasingly consuming more animal foods during the same time interval (3.5 MYA to 1.5 MYA) that ?13C had become enriched.  Aiello and Wheeler (13) have shown that the mass of the human gastrointestinal tract is only about 60% of that expected for a similar-sized primate. Consequently, the increase in brain size that occurred in hominins starting ~2.5 MYA was balanced by an almost identical reduction in the size of the gastrointestinal tract (13). The selective pressures that simultaneously allowed for both a reduction in gut size and an increase in brain size are attributed to an improvement in dietary quality (DQ) that occurred largely as a result of increased consumption of animal foods by Australopithecine species prior to the emergence of the first members of Homo (13-15). Because a diet with an increased DQ contains less structural plant parts and more animal material (16), its nutrient and energy density is greater.  Hence the greater DQ of animal foods permitted relaxation of the selective pressures in hominins that formerly selected for  a large, metabolically active gut necessary to process low DQ foods, which in turn permitted the natural selection of a large metabolically active brain (13, 14).  Grass leaves and seeds maintain a low DQ (15), and are high in fiber and cellulose and are indigestible in their raw, unprocessed state in modern humans (17).  Accordingly, the proposition that increased consumption of grass leaves and seeds were the C4 source in hominin enamel, is inconsistent with the evolutionary gut/brain metabolic tradeoff (13-15).  Selective pressures that reduce the size and metabolic activity of the gut require more energetically dense foods like meat and marrow – not energy poor, high cellulose and high fiber foods like grasses and sedges.


In addition to their low DQ, grass leaves and seeds are devoid of long chain fatty acids of both the omega 6 family (arachidonic acid, 20:4n6) and omega 3 family (docosahexanoic acid, 22:6n3), as are all plant foods (15).  These fatty acids are necessary structural elements required for the synthesis of brain and neural tissues and cannot be produced endogenously in sufficient quantities to relax the selective pressures normally constraining encephalization (brain volume expansion relative to body weight).  Therefore, exogenous sources of these two fatty acids must be obtained through diet in hominins to permit the evolution of large metabolically active brains (15, 18-21).  Likely candidate animal foods which simultaneously increased the DQ and provided arachidonic acid (AA) and docosahexanoic acid (DHA) were scavenged de-fleshed long bones (which contain marrow – a high fat food) and skulls (which contain brains – high in AA and DHA) from carnivore kills (15).   These foods along with meats from grazing animals likely represent the dominant dietary source for the increasing C4 signature in our African ancestors.


Another nutritional point lends little support to the notion that the increasing C4 signature in hominins starting 3.5 MYA resulted from direct consumption of grass leaves or seeds.  All great apes (chimps, gorillas, orangutans and gibbons) living in their native environment bear ?13C values indicative of near total reliance upon C3 plants.  Only a single higher primate (a baboon species, Theropithecus gelada) consumes grass leaves and seeds as their primary dietary source.  Accordingly, this baboon maintains a carbon isotopic signature that is nearly 100 % C4 derived (4). 


High reliance upon grass and grass seeds in Theropithecus gelada or in any hominin requires a number of evolutionary adaptations in the digestive tract to accommodate these low quality, high cellulose foods – none of which have been observed in contemporary humans.  All vertebrates lack the enzyme cellulase which is required to breakdown cellulose and hemicellulose found in grass leaves and seeds into glucose.  Mammals that rely heavily upon grass and grass seed consumption for their sustenance have evolved large caecums (hindguts) or a four compartment stomach (ruminants) containing enormous quantities of microflora which have the capacity to ferment and breakdown cellulose, hemicellulose, starches and proteins into simpler compounds which can then be assimilated and metabolized by the host animal.  In the case of Theropithecus gelada (the grass eating baboon), it has evolved a large hindgut where microbial fermentation of grass takes place (22).  In contemporary humans, and in the hominin line that led to Homo, there is no credible evidence that gut morphology became larger and more metabolically active to support fermentation of cellulose in the caecum, but rather the opposite (13, 14).  Hence, without the evolution of hindgut fermentation, efficient consumption of grass and grass seeds would have been impossible in any hominin species.


Other comparative physiological data between modern humans and the grass eating baboon (Theropithecus gelada) support the notion that the increasing C4 signature in evolving African hominins was not a result of grass or sedge consumption.  Dicots or C3 plants produce compounds called tannins which act as a chemical defense system that discourage animals from eating them.  Monocots or C4 plants (such as grass and sedges) do not synthesize tannins (23).  Over the course of evolution, mammals that consume tannin containing C3 plants have evolved measures to counter the adverse effects of tannins.  The most important of these mechanisms are salivary proteins that act as a defense against dietary tannins (24).  These proline rich salivary proteins (PRPs) bind tannins and form stable complexes which prevent tannins from producing adverse health effects (24-27).


Species that usually ingest tannin containing foods as part of their natural diets produce high levels of  PRPs, whereas species not exposed to tannins produce little or no PRPs (24).  In this regard, the saliva of the grass (C4) eating baboon (Theropithecus gelada) produces a saliva devoid of PRPs (23).  In contrast, modern humans synthesize a saliva containing abundant concentrations of PRPs (25-27) which have been suggested to result from the long evolutionary history of fruit and vegetable (C3 plants) consumption in human ancestors (25).  If ancestral African hominins had intensely exploited C4 plants (grasses and sedges) for millions of years, then it might be expected that the line of hominins that led to Homo and modern humans would also maintain low concentrations of salivary PRPs similar to Theropithecus gelada.  Data in contemporary Homo sapiens do not support this conclusion.


In summary, recent comprehensive analyses (1-3) of ?13C values in the enamel of African hominins from 4.1 to 1.5 MYA support the conclusion that plants of C4 origin were ultimately responsible for this isotopic signature.  Nevertheless, when the isotopic data is triangulated from archaeological, physiological and nutrition evidence, it is apparent that the C4 signature in ancestral African hominin enamel almost certainly is resultant from increased consumption of animals that consumed C4 plants.




1.         Matt Sponheimer, Zeresenay Alemseged, Thure E. Cerling, Frederick E. Grine, William H. Kimbel, Meave G. Leakey, Julia A. Lee-Thorp, Fredrick Kyalo Manthi, Kaye E. Reed, Bernard A. Wood, and Jonathan G. Wynn. Isotopic evidence of early hominin diets. PNAS 2013 : 1222579110v1-201222579.

2.         Jonathan G. Wynn, Matt Sponheimer, William H. Kimbel, Zeresenay Alemseged, Kaye Reed, Zelalem K. Bedaso, and Jessica N. Wilson. Diet of Australopithecus afarensis from the Pliocene Hadar Formation, Ethiopia. PNAS 2013 : 1222559110v1-201222559.

3.         Thure E. Cerling, Fredrick Kyalo Manthi, Emma N. Mbua, Louise N. Leakey, Meave G. Leakey, Richard E. Leakey, Francis H. Brown, Frederick E. Grine, John A. Hart, Prince Kaleme, Hélène Roche, Kevin T. Uno, and Bernard A. Wood. Stable isotope-based diet reconstructions of Turkana Basin hominins. PNAS 2013 : 1222568110v1-201222568

4.         Thure E. Cerling, Kendra L. Chritz, Nina G. Jablonski, Meave G. Leakey, and Fredrick Kyalo Manthi. Diet of Theropithecus from 4 to 1 Ma in Kenya. PNAS 2013 : 1222571110v1-201222571

5.         http://blogs.discovermagazine.com/crux/2013/06/03/even-our-ancestors-never-really-ate-the-paleo-diet/#.Ua31I0C1GYA

6.         http://www.npr.org/blogs/thesalt/2013/05/31/187559098/grass-it-s-what-s-for-dinner-3-5-million-years-ago

7.         http://www.scienceworldreport.com/articles/7290/20130604/human-ancestors-ape-diet-changed-3-5-million-years-ago.htm

8.         Lee-Thorp JA, Sponheimer M, Passey BH, de Ruiter DJ, Cerling TE.  Stable isotopes in fossil hominin tooth enamel suggest a fundamental dietary shift in the Pliocene. Phil. Trans. R. Soc. B (2010) 365, 3389–3396.

9.         McPherron SP, Alemseged Z, Marean CW, Wynn JG, Reed D, Geraads D, Bobe R, Béarat HA. Evidence for stone-tool-assisted consumption of animal tissues before 3.39 million years ago at Dikika, Ethiopia. Nature. 2010 Aug 12;466(7308):857-60

10.       de Heinzelin J, Clark JD, White T, Hart W, Renne P, WoldeGabriel G, Beyene Y, Vrba E. Environment and behavior of 2.5-million-year-old Bouri hominids. Science. 1999 Apr 23;284(5414):625-9.

11.       Ferraro JV, Plummer TW, Pobiner BL, Oliver JS, Bishop LC, Braun DR, Ditchfield PW, Seaman JW 3rd, Binetti KM, Seaman JW Jr, Hertel F, Potts R. Earliest archaeological evidence of persistent hominin carnivory. PLoS One. 2013 Apr 25;8(4):e62174.

12.       Pobiner BL, Rogers MJ, Monahan CM, Harris JW. New evidence for hominin carcass processing strategies at 1.5 Ma, Koobi Fora, Kenya. J Hum Evol. 2008 Jul;55(1):103-30.

13.       Aiello L, Wheeler P. The expensive tissue hypothesis. Curr Anthropol 1995;36:199-221.

14.       Leonard WR, Robertson ML: Evolutionary perspectives on human nutrition: the influence of brain and body size on diet and metabolism. Am J Hum Biol 1994;6:77–88.

15.       Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African hominids: evolutionary implications for human brain development. World Review of Nutrition and Dietetics, 2001, 90:144-161.

16.       Sailer LD, Gaulin SC, Boster JS, Kurland JA: Measuring the relationship between dietary quality and body size in primates. Primates 1985;26:14–27.

17.       Cordain L, (1999). Cereal grains: humanity’s double edged sword. World Review of Nutrition and Dietetics, 84: 19-73.

18.       Broadhurst CL, Cunnane SC, Crawford MA: Rift valley lake fish and shellfish provided brainspecific nutrition for early Homo. B J Nutr 1998;79:3–21.

19.       Crawford MA, Sinclair AJ: The long chain metabolites of linoleic and linolenic acids in liver and brains of herbivores and carnivores. Comp Biochem Physiol 1976;54B:395–401.

20.       Crawford MA, Bloom M, Broadhurst CL, Schmidt WF, Cunnane SC, Galli C, Gehbremeskel K, Linseisen F, Lloyd-Smith J, Parkington J: Evidence for the unique function of docosahexaenoic acid during the evolution of the modern hominid brain. Lipids 1999;34:s39–s47.

21.       Crawford MA: The role of dietary fatty acids in biology: Their place in the evolution of the human brain. Nutr Rev 1992;50:3–11.

22.       Mau M, Johann A, Sliwa A, Hummel J, Südekum KH. Morphological and physiological aspects of digestive processes in the graminivorous primate Theropithecus gelada-a preliminary study. Am J Primatol. 2011 May;73(5):449-57

23.       Mau M, Südekum KH, Johann A, Sliwa A, Kaiser TM. Saliva of the graminivorous Theropithecus gelada lacks proline-rich proteins and tannin-binding capacity.Am J Primatol. 2009 Aug;71(8):663-9

24.       Shimada T. Salivary proteins as a defense against dietary tannins. J Chem Ecol. 2006 Jun;32(6):1149-63

25.       Bennick A. Interaction of plant polyphenols with salivary proteins. Crit Rev Oral Biol Med. 2002;13(2):184-96

26.       Bacon JR, Rhodes MJ. Binding affinity of hydrolyzable tannins to parotid saliva and to proline-rich proteins derived from it. J Agric Food Chem. 2000 Mar;48(3):838-43.

27.       Yan Q, Bennick A. Identification of histatins as tannin-binding proteins in human saliva. Biochem J. 1995 Oct 1;311 ( Pt 1):341-7

Refutación Eroski Consumer

Postura de mi equipo científico acerca de la ciencia de la alimentación y las enfermedades de la civilización


Maelán Fontes Villalba, Óscar Picazo y Pedro Bastos


Habitualmente no suelo intervenir en intercambios de impresiones ante textos no escritos en revistas científicas por varias razones. Una de ellas es porque la mayoría de las veces no me siento identificado cuando se habla de paleodieta, como explicaré posteriormente, y la otra es que habitualmente se habla de temas que ya han sido ampliamente abordados en la literatura científica hace mucho tiempo (por ejemplo, que la esperanza de vida de los cazadores-recolectores no pasaba de los 20 años de edad), y que ya no hay lugar a la discusión. Casi todos, por no decir todos, los argumentos comentados en contra de la nutrición basada en la evolución, son conceptos básicos de biología (o mejor dicho, biología evolutiva) y que han sido tratados ampliamente en este libro de texto clásico1. También es sorprendente que John  Harvey Kellog (un vegetariano) tenga más influencia en la nutrición que Charles Darwin (Staffan Lindeberg). El libro “On the origins of species” fue publicado hace 153 años, que es el que sienta las bases de la biología evolutiva. Existen también muchos artículos que abordan la necesidad de tener conocimientos de biología evolutiva para la medicina del siglo XXI2-4. Pero esta vez parece que se solicita mi opinión al respecto de este texto aparecido recientemente en la red.



Aclarando conceptos


Cuando expreso que no me siento identificado muchas veces cuando se habla de paleodieta lo digo por diferentes motivos. Uno, el término paleolítico, quizás no sea el más adecuado para definir esa alimentación ya que insta a pensar que se trata de una dieta de hombres de las cavernas y de violentos con lanzas en la mano. De lo que se trata es de imitar en lo posible el patrón alimenticio que el ser humano ha tenido durante su evolución como especie, teniendo en cuenta que esta dieta variaba mucho dependiendo de la geografía, la estación del año, nicho ecológico o las glaciaciones5. Esto es lo que se conoce como nutrición basada en la evolución, que sigue los principios de la biología evolutiva, antes mencionada. Más adelante explico por qué deberíamos considerar la biología evolutiva en nutrición. Pero llamarla paleolítica o de las cavernas o de la edad de piedra no es lo importante, lo relevante es buscar un patrón dietético que se adapte lo mejor posible a nuestra especie, igual que un roedor se adaptará mejor a una dieta de semillas que a una dieta basada en alimentos de origen animal. La nutrigenética busca precisamente analizar el genoma bien de un individuo o de una población para conocer qué alimentos son los más propicios para la salud, en función de si se está o no adaptado a los mismos. 


Segundo, muchos defensores de la paleodieta proponen que es rica en grasas y proteína, y baja en hidratos de carbono, entre otras características. Incluso, algunas personas defienden una dieta muy baja en hidratos de carbono y cetogénica (Very Low Carb Ketogenic Diet-VLCKD). Estas dietas pueden ser útiles en ciertas circunstancias o ante ciertas patologías, pero de forma general, ese concepto es erróneo debido a que una dieta paleolítica no tiene que ser necesariamente baja en hidratos de carbono y rica en proteínas. Existen poblaciones de cazadores-recolectores que siguen una dieta rica en grasa y proteína y baja en hidratos de carbono, pero también existen otras que tienen una ingesta de hidratos de carbono moderada a alta63, 64, y no por eso son menos sanas. Y la idea de que una dieta rica en hidratos de carbono produce picos de glucosa y consecuentemente de insulina, y que si se repite en el tiempo da lugar a resistencia a la insulina y posteriormente a obesidad, enfermedades cardiovasculares, diabetes tipo 2 o hipertensión, no está clara, pues a pesar que existen algunos estudios de intervención en pacientes con Síndrome Metabólico, Diabetes Tipo II, acné y síndrome de ovarios poliquísticos (la resistencia a la insulina es una característica común66) donde que una dieta con restricción de hidratos de carbono o con bajo Índice Glucémico es superior a una dieta baja en grasa67-78, los estudios en individuos sanos no demuestran que una dieta rica en hidratos de carbono cause alteraciones metabólicas adversas y menos aún que lleve a la Obesidad, Síndrome Metabólico y Diabetes Tipo II 6-8, 13, 65. De forma importante, no está claro que el efecto de esos estudios con dietas con restricción de hidratos de carbono o bajo Índice Glucémico sea por los hidratos de carbono o Índice Glucémico en si, o por la restricción en compuestos bioactivos presentes en cereales79.


Existen además varias poblaciones tradicionales con un estilo de vida  no occidentalizado que consumen una dieta muy rica en hidratos de carbono, incluso hasta el 90% de la energía, pero tienen un estado de salud excepcional9-12. Cabe destacar que muchas personas que defienden la idea de que una dieta baja en carbohidratos suponga una ventaja metabólica, han encontrado en la paleodieta una especie de templo donde predicar su oración, debido a que existe el concepto erróneo que una dieta con restricción de cereales es necesariamente una dieta baja en hidratos de carbono; nada más lejos de la realidad13


Por todo lo anterior, una dieta paleolítica no tiene que ser necesariamente una dieta baja en hidratos de carbono y tampoco hay buena evidencia de que la simple restricción de carbohidratos sea mejor para la prevención y el tratamiento de las llamadas enfermedades de la civilización13. Es por tanto un error hablar de paleodieta y automáticamente decir que es peligrosa porque es hiperproteica y produce “daños irreparables”.  Recomiendo a los lectores los artículos de Sebastian et al.14 y de Eaton et al.15, para un mejor entendimiento del potencial acidificante de la dieta en la salud y el efecto de una dieta paleolítica en el equilibrio ácido/base. 


Primer gran error: meter en el mismo saco a la dieta VLCKD y a los que entendemos la nutrición desde una perspectiva evolutiva.



Hablando de macronutrientes


Si analizamos los estudios de intervención realizados con dieta paleolítica, comparada con la dieta mediterránea o de la American Diabetes Association (ADA), las diferencias son de 27.9% (dieta paleolítica) vs 20.5% (dieta mediterránea) y de 24% (dieta paleolítica) vs 20% (dieta ADA), respectivamente, en cuanto a porcentaje de calorías derivadas de proteínas16,17. Respecto a cantidad total de proteínas (sin tener en cuenta la ingesta energética total) no hubo ninguna diferencia, (90 gramos vs 89 gramos y 94 gramos vs 90 gramos, para la dieta paleolítica vs mediterránea y ADA, respectivamente). Además, en ninguno de los dos estudios la dieta paleolítica fue muy baja en hidratos de carbono, siendo los valores de 134 gramos17 y 125 gramos16. En el primer estudio la clasificaríamos de dieta normal en hidratos de carbono y en el segundo estudio de dieta moderada-baja en hidratos de carbono, pero no cetogénica. Es decir, aumentó el porcentaje de energía procedente de las proteínas sin aumentar la cantidad neta de proteína en la dieta, debido a la reducción en la ingesta calórica total en la paleodieta (a expensas de una reducción en la ingesta de carbohidratos frente a las dietas de referencia).


¿Proteínas peligrosas?


Aunque no defienda una dieta alta en proteínas como un requisito indispensable para hacer una alimentación sana, aprovecho para dejar claro un aspecto importante. Alrededor de las proteínas existen muchos mitos arraigados desde hace muchos años, probablemente iniciados tras un estudio publicado por Brenner et al. en la prestigiosa revista The New England Journal of Medicine18. Sus conclusiones fueron que en pacientes con enfermedad renal, ésta empeoraba si se aumentaba la ingesta de proteína. Ese es un hecho que ha sido demostrado muchas veces. No obstante, esos datos no se pueden extrapolar a pacientes sanos (del mismo modo que estudios con dietas bajas en carbohidratos hechos en pacientes con Síndrome Metabólico y/o Diabetes Tipo II tampoco se pueden extrapolar a personas sanas). En un estudio de intervención, se demostró que una ingesta de proteína de un 25% de la energía durante 6 meses no produjo alteraciones renales adversas, con una tasa de filtrado glomerular sin alteraciones y sin aumentar la albúmina urinaria19. En culturistas belgas, con una ingesta de proteínas de 2,8 gramos al día no hubo consecuencias adversas para la función renal20. En el conocido estudio observacional Nurse’s Health Study, los autores concluyeron que una ingesta elevada de proteínas no estaba asociada a un declive en la función renal en mujeres sin patología renal pre-existente21. En una excelente revisión sobre el tema, los autores concluyeron lo siguiente: “A pesar de que la restricción de proteína pueda ser apropiada en el tratamiento de patologías renales, no hemos encontrado evidencia de que una ingesta elevada de proteína afecte de forma negativa a la función renal de individuos sanos”22.

Interesantemente, algunos estudios han comparado el tipo frente a la cantidad de proteína en pacientes con enfermedad renal. En un estudio cruzado de 4 semanas de duración los investigadores probaron el efecto de dos fuentes de proteínas ingeridas en cantidades altas (1,35 gramos/kilo/día). Un grupo recibió proteína derivada de carne roja y el otro una combinación de proteínas derivadas de pescado y pollo. Los resultados fueron que al sustituir 1,35 g/kg/d de proteína de carne roja por la combinación de pescado/pollo en pacientes con diabetes tipo 2 y microalbuminuria patológica, se produjo una mayor reducción en la tasa de albuminuria incluso en comparación con una dieta baja en proteínas (0,62 g/kg/d)23. En otro estudio similar, los autores demostraron que una ingesta de proteínas normal, pero sustituyendo la carne roja por pollo y pescado, produce los mismos efectos favorables en la microalbuminuria que una dieta baja en proteínas (0,5 g/kg/d) en pacientes con diabetes tipo 124


En resumen, una dieta paleolítica no tiene que ser necesariamente alta en proteínas, pero además, la ingesta elevada de proteínas no compromete la función renal en pacientes sanos, y en pacientes con enfermedad renal, cambiar el tipo de proteína puede ser una intervención eficaz, más allá de la cantidad total.


La esperanza de vida


El siguiente mito que se repite continuamente en los comentarios acerca de la dieta paleolítica o nutrición evolutiva es que la esperanza de vida de nuestros antecesores no era mayor de 20 años, y que por lo tanto, esa es la razón por la que eran tan sanos (las enfermedades degenerativas no les alcanzaban en su corta existencia). El mismo argumento se esgrime a las poblaciones actuales de cazadores-recolectores u hortoculturistas. Este tema ya ha sido desmentido numerosas veces en la literatura científica hace muchos años25,26.


En primer lugar este comentario demuestra una confusión estadística notable. En una distribución normal de datos que se ajuste a la campana de Gauss, es lógico encontrar que la moda y la media se encuentren en valores próximos. En cambio, la distribución de la mortalidad en poblaciones de cazadores-recolectores y en poblaciones prehistóricas no se aproxima a la gaussiana, teniendo una forma en U, con un fuerte componente de la mortalidad infantil. Diversos estudios27-29 han demostrado que la mortalidad infantil en poblaciones contemporáneas de cazadores-recolectores es muy elevada, con un 30-40% de fallecimientos antes de los quince años de edad, la mayoría antes de los 5 años. Los estudios arqueológicos muestran que una vez superada esa edad de aproximadamente 15 años, la esperanza de vida era razonablemente elevada. Las tasas de mortalidad se elevaban a los 40 años, doblándose a los 60 y de nuevo a los 70. Gurven y Kaplan encontraron que la edad más probable de fallecimiento eran los 72 años. Es por ello que la esperanza de vida media no nos da ninguna indicación significativa sobre el modo de vida de estas poblaciones. En la isla de Kitava, estudiada por el Dr. Lindeberg, el 6% de una población de 2,300 habitantes, tenía entre 60 y 95 años de edad12,30. Además, las personas de avanzada edad no conocían la muerte por enfermedades de la civilización, alcanzando el final de su vida de forma natural.


Hay que destacar el hecho de que la esperanza de vida depende de los avances médicos, pero sobre todo de las medidas de salud pública y el estatus socioeconómico. La esperanza de vida de los humanos empezó a aumentar solo después del año 1800 y no desde el inicio de la revolución agrícola, como algunos opinan. La dieta poca influencia en la esperanza de vida, pero si tiene un rol fundamental en la calidad de la misma


La esperanza de vida en Londres en 1667 era menor de 18 años26. ¿La razón es que eran cazadores-recolectores o que las infecciones mermaban considerablemente la población infantil?; creo que la respuesta es clara. Se estima que la esperanza de vida desde la revolución agrícola (neolítico) nunca sobrepasó los 25 años de edad, e incluso el inicio de la revolución agrícola supuso un retroceso en la esperanza de vida25,26





Vamos a analizar datos de poblaciones actuales con un estilo de vida, y sobre todo una alimentación, parecida a la de nuestros antecesores, en concreto los habitantes de la isla de Kitava, en Papúa Nueva Guinea, ampliamente estudiados por el Dr. Lindeberg12,31. Si a la edad de 50 años un hombre o una mujer sueca tuvieran el índice de masa corporal de los habitantes de Kitava, pesarían 19 o 22 kilogramos menos de lo que pesan en realidad31. Si comparamos la glucosa en ayunas entre los habitantes de Kitava y habitantes suecos, ajustados por edad y sexo vemos que, incluso las personas de 65 a 90 años en Kitava, tienen niveles que confirman la ausencia de diabetes independientemente de la edad (figura 1)32. El mismo patrón se observa con el peso corporal (figura 2), la hipertensión arterial (figura 3), los infartos de miocardio o ictus cerebral12,30,31.

Figura 1

Glucosa Kitava

Figura 2

Peso kitava

Figura 3



Datos similares en otras poblaciones tradicionales fueron publicados por nuestro equipo de investigación en una revista científica “peer review”5, que pueden consultar aquí.



Si las momias hablasen


Si analizamos datos de poblaciones mediterráneas, incluida Creta (el modelo de la dieta mediterránea), la hipertensión y el ictus cerebral han sido prevalentes desde hace muchos años33,34. La aterosclerosis es la principal causa de las enfermedades cardiovasculares (ECV), en particular la angina de pecho e infarto de miocardio, pero también del ictus, fallo cardiaco y demencia. En los países occidentalizados, casi todas las personas de edad media y avanzada tienen aterosclerosis13. La cuestión es: ¿es normal que casi todas las personas en países occidentalizados tengan aterosclerosis?, ¿es un proceso normal de envejecimiento? o ¿es consecuencia de los hábitos alimenticios? Teniendo en cuenta que la dieta es uno de los principales factores desencadenantes, la aterosclerosis no es producida solamente por la introducción de la comida rápida, ya que existen datos de previos a la aparición de la comida rápida e incluso de la revolución industrial que demuestran la presencia de esta patología.


En un antiguo artículo publicado en la prestigiosa revista The Lancet en 1911, los autores indican tras analizar arterias de momias lo siguiente: “los antiguos egipcios sufrían con la misma frecuencia de lesiones arteriales idénticas a las que tenemos hoy en día. Además, cuando consideramos que pocas de las arterias estaban sanas, parece que esas lesiones eran tan frecuentes hace 3.000 años como lo son hoy en día”. Los autores destacan que el consumo de alcohol (no eran grandes bebedores de vino, y además en musulmanes también existe la aterosclerosis), la carne (era un lujo para ellos) o el estrés, no serían las posibles causas35. Por lo tanto, en una época totalmente libre de la influencia de los productos derivados de la revolución industrial, pero basada en alimentos derivados de la agricultura (principalmente cereales-trigo), las lesiones arteriales eran aparentemente tan frecuentes como en la actualidad, existiendo más datos que lo apoyan35-40


Afirmar que la prevalencia tan alta de enfermedades cardiovasculares es debida únicamente a los cambios de alimentación producidos por la comida rápida (Standard American Diet) y que alejarnos del patrón alimenticio mediterráneo es la causa de las ECV, es cuanto menos discutible, como mostraremos más adelante.


Hay que destacar que los egipcios comían cereales y no precisamente refinados. Otro aspecto muy importante a tener en cuenta para entender la nutrición desde una perspectiva evolutiva es, ¿qué es normal y qué no es normal? En este sentido, los estudios epidemiológicos se centran en comparar la incidencia o prevalencia de una enfermedad en comparación con lo normal. No obstante, lo normal en una población occidentalizada, puede que no sea lo normal en poblaciones de cazadores-recolectores donde la prevalencia de las enfermedades de la civilización es muy baja o cero5. Si el riesgo relativo “normal” es 1, alguien con un riesgo relativo de 0,75, tendría un riesgo bajo, y alguien con un riesgo relativo de 1,5 tendría un riesgo alto. Pero, ¿lo normal no sería tener un riesgo de 0 como ocurre en las poblaciones de cazadores-recolectores?, ¿quién quiere ser normal y tener un riesgo de ECV como la media?, ¡yo no! Este aspecto ha sido aclarado en este artículo del Dr. Lindeberg en la European Heart Journal41. Ver figura 4. Finalmente, ¿es posible que nadie siga las recomendaciones dietéticas?, porque casi nadie es capaz de mantener el perímetro de cintura como en las primera décadas de la vida, hecho que ocurre en casi todas las poblaciones tradicionales pre-agriculturales. Recordar que el ejercicio físico y la genética no explican completamente estos hechos, como analizaremos más tarde.

Figura 4



Más evidencia, por favor


El texto al que estamos dando respuesta indica que una dieta paleolítica va en contra de “lo propuesto por la totalidad de las autoridades sanitarias o entidades de referencia en nutrición humana y dietética, incluidas las especializadas en nutrición deportiva”. Hay que ser realistas y poner la ciencia encima de la mesa. El hecho de que esté propuesto por autoridades sanitarias no quiere decir que esté basado en la evidencia científica, y aclaro lo escrito: existen diferentes grados de evidencia científica que van desde “alta” a “muy baja” o de la A-E, dependiendo del tipo de estudios que existan sobre un tema (epidemiológicos, de intervención, randomizados o no, etc). Para más información visitar la web de GRADE Working Group. 


Las recomendaciones dietéticas actuales suelen hablar en estos términos: “se ha demostrado científicamente la asociación entre el consumo de grasas, especialmente las trans y las saturadas, con la tasa de mortalidad de la población por ECV”. 


Cuando se menciona la palabra asociación, se indica que los datos son derivados de estudios de observación, y no de intervención, con las limitaciones que ello implica, sobre todo que no se puede establecer relación de causa-efecto. Otros aspectos que limitan mucho los resultados de los estudios de observación son, por lo general, datos basados en cuestionarios de alimentos (muy imprecisos y sujetos a la memoria del paciente), factores de confusión, el factor de conciencia de salud (es poco probable que alguien que se cuide y coma cereales integrales y verduras, a la vez fume y beba mucho), y el hecho de que los datos son presentados como riesgos relativos, que al pasar a riesgos absolutos o Number Needed to Treat, se diluyen (para más información, lea este artículo co-escrito por mi). 


Que exista una asociación entre grasas saturadas y ECV no quiere decir que la causa sea la ingesta de grasas saturadas, por ejemplo. Y ya que tomamos este ejemplo, y que muchas recomendaciones están hechas en base a meta-análisis de estudios epidemiológicos, respecto a las grasas saturadas, en un meta-análisis de estudios prospectivos de cohorte publicado en la prestigiosa revista The American Journal of Clinical Nutrition, los autores no encontraron asociación entre el consumo de grasas saturadas y enfermedades cardiovasculares42. Sin embargo, las autoridades sanitarias siguen recomendando reducir la ingesta de estas grasas a menos de un 10% de la energía total, una incoherencia.


Volviendo al tema de las recomendaciones dietéticas actuales, la realidad es que no hay suficiente evidencia que apoye la pirámide de alimentación propuesta por muchas autoridades sanitarias. Y para matizar este tema, hay que hacer énfasis en que la máxima evidencia deriva de estudios de intervención, controlados y aleatorios, donde los datos son reproducibles y con consenso entre diferentes equipos de investigación. Voy a dar algunos ejemplos. 


Una revisión sistemática de Cochrane sobre cereales integrales y enfermedad de las arterias coronarias, concluye que aunque haya consenso, derivado de estudios de observación, que los cereales integrales están inversamente asociados con las enfermedades de las arterias coronarias, los resultados hay que interpretarlos con cautela ya que los estudios identificados son de corta duración, poca calidad e insuficiente poder estadístico. La mayoría de los estudios estaban financiados por compañías con intereses comerciales en cereales integrales (importante aspecto a la hora de conseguir financiación para un estudio con dieta). Finalmente, indican que hacen falta más estudios para obtener conclusiones definitivas43


En las recomendaciones dietéticas para la diabetes, otra revisión sistemática de Cochrane concluye que no hay datos de alta calidad sobre la eficacia de las intervenciones dietéticas para la prevención de la diabetes. Los autores también afirman que se necesitan más estudios para sacar conclusiones claras44. La misma ADA en un reciente estudio, indica que excepto para la pérdida de peso, no hay evidencia A de dieta para el tratamiento de la diabetes45. El consejo Sueco de valoración de salud y tecnología, publicó una revisión sistemática sobre el tratamiento dietético en la diabetes, la conclusión fue que no existen estudios de alta calidad para hacer recomendaciones dietéticas en tratamiento de la diabetes tipo 246


En cuanto al papel de los cereales integrales en la inflamación crónica, un estudio de revisión concluye que los datos derivados de estudios de observación no corroboran los estudios de intervención, ya que no se ha visto un efecto beneficioso de la ingesta de cereales integrales en marcadores de inflamación47.


Lo mismo ocurre para muchas otras recomendaciones dietéticas que se hacen como si hubiera suficiente evidencia científica, como es el caso de los aceites vegetales48, la grasa saturada42, el colesterol49 o la fibra dietética13. Referente a la recomendación de aumentar el consumo de aceites vegetales omega-6, respaldada por la American Heart Association (AHA), está basada en una revisión donde los autores concluyeron que el consumo de aceites vegetales omega-6 disminuye la incidencia de eventos cardiovasculares. Sin embargo, en una revisión de Ramsden et al.48, se observó que las conclusiones hechas por los autores del artículo estaban basadas en 5 estudios que mezclaron aceites omega-6 y omega-3, y otros 4 que usaron como intervención sólo aceites vegetales omega-6, lo cual impide concluir que el consumo específico de aceite vegetal omega-6 reduzca la incidencia de ECV. Es más, al analizar los datos objetivamente, en los estudios donde utilizaron solamente aceite vegetal omega-6, no solo no redujeron el riesgo CV sino que produjeron un ligero aumento estadísticamente no significativo (figura 5). Por lo tanto, la recomendación de aumentar el consumo de aceites vegetales omega-6 al menos a un 5-10% de la energía, no tiene suficiente evidencia. Acerca de la leche pueden encontrar más información aquí.

Figura 5




Quiero dejar clara la posición de mi grupo de investigación acerca de la evidencia sobre la nutrición. En ningún momento hemos afirmado que la dieta paleolítica esté “respaldada por miles de estudios clínicos de nutrición”. Precisamente, los que me conocen y siguen mi trabajo, saben que constantemente solicito que se hagan más estudios de calidad para poder establecer recomendaciones basadas en la evidencia.


También quisiera aclarar que existen estudios de intervención con dieta mediterránea mostrando eficacia en ECV50 y en la diabetes tipo 251. Pero debido a que estos estudios presentan importantes limitaciones, no podemos sacar conclusiones firmes. En el Lyon Diet Heart Study, hubo mayor educación al grupo de intervención por parte de los investigadores, frente al control, y además se redujo el consumo de ácido linoleico a menos de un 4% de la energía total, importantes factores de confusión50. En el estudio PREDIMED51, un estudio de intervención con dieta mediterránea en diabetes tipo 2, el grupo de control hizo una dieta baja en grasa, la cual se ha demostrado que es perjudicial en mujeres con enfermedad cardiovascular52. Por lo tanto, tener como grupo control una dieta low-fat, asegura resultados positivos. En este sentido, la dieta mediterránea es un paso en la dirección correcta si la comparamos con la dieta típica occidental o Standard American Diet, pero posiblemente no es la dieta ideal.


Especial mención merecen dos estudios de intervención de largo plazo estudiando algunas de las recomendaciones oficiales en la incidencia de infarto de miocardio y eventos cardiovasculares. El Diet and Reinfarction Trial (DART study) publicado en The Lancet en 1989, verificó el efecto de aumentar la ingesta de fibra de cereales, en pacientes que habían sufrido un infarto de miocardio. Al cabo de 700 días, el porcentaje de sobrevivientes a un segundo infarto de miocardio fue menor en el grupo que aumentó la ingesta de fibra de cereales, aunque la diferencia no llegó a ser significativa53 (figura 6). En el Women’s Health Initiative Study, los investigadores dividieron a casi 49.000 mujeres postmenopáusicas en dos grupos. En uno de ellos recomendaron ingerir 5 raciones de frutas y verduras al día, disminuir la grasa total a un 20% e ingerir al menos 6 raciones de cereales integrales al día. Al cabo de 6 años, en las mujeres que tenían enfermedades cardiovasculares al inicio del estudio, el riesgo aumentó en un 26% en el grupo de intervención54 (figura 7). En el mismo estudio, en las mujeres que tenían diabetes al inicio del estudio, el control de glucosa empeoró al cabo de 2 años en el grupo de intervención (>6 raciones al día de cereales, 5 raciones al día de frutas y verduras y <20% energía de grasa)55. Es destacable que estos trabajos no son mencionados habitualmente cuando se habla de recomendaciones dietéticas, siendo estudios de intervención, con muestras muy grandes y de larga duración.

Figura 6


Figura 7



En estudios de intervención aleatorios con grupo control, de corta duración (comento la limitación de una muestra pequeña), una dieta restringida en cereales, lácteos y aceites vegetales, es muy superior a la dieta mediterránea en pacientes con diabetes tipo 216,17 (figura 8, 9 y 10). Tampoco podemos obviar los resultados de estudios de intervención donde se compara un modelo dietético similar al que el ser humano tuvo durante su evolución con una dieta mediterránea o de la ADA, considerando que la mejoría en el control de glucosa fue mejor y estadísticamente significativa en la dieta paleolítica.

Figura 8


Figura 9


Figura 10



Recientemente el equipo de la Dra. Frassetto ha concluido otro estudio de intervención, de corta duración, en pacientes sanos sedentarios comparando los efectos de la dieta de la ADA con una dieta restringida en cereales y lácteos. Los alimentos fueron administrados por un comedor de un hospital y los investigadores se aseguraron de que no se producía pérdida de peso (importante ya que la ADA documenta que no hay evidencia A del efecto de la dieta en la diabetes más allá de la pérdida de peso)  y que la composición de macronutrientes (carbohidratos, proteínas y grasas) fuera la misma para los dos grupos—lo que indica que el efecto es producido por el “tipo” y no la proporción de macronutrientes o cantidad de alimentos. La dieta paleolítica produjo una reducción en la glucosa basal mucho mayor, y estadísticamente significativa, comparada con el grupo de la dieta de la ADA (datos no publicados). En la actualidad se está desarrollando un estudio de estas características en Suecia, pero con una muestra significativa y de larga duración. También está a punto de empezar otro estudio de larga duración en pacientes con diabetes tipo 2.



Haciendo tábula rasa


Llegados a este punto podemos decir que no hay suficiente evidencia para recomendar dietas bajas en grasa, dietas ricas en fibra, dieta mediterránea o dietas bajas en carbohidratos, entre otras13. Poniendo la ciencia por delante, tampoco hay evidencia suficiente (grado A) para recomendar una dieta restringida en cereales, lácteos, legumbres y aceites vegetales, sobre todo porque no hay estudios de larga duración con muestras con suficiente poder estadístico. Tampoco hay estudios que demuestren que son perjudiciales para la salud (no podemos asegurar lo mismo para dietas ricas en fibra de cereales y bajas en grasa), como se suele proclamar, entre otras cosas porque no son automáticamente dietas bajas en hidratos de carbono y cetogénicas16,17


La biología evolutiva aporta un paradigma del cual partir para realizar estudios con alimentación. En este sentido, como traté anteriormente, la epidemiología en poblaciones de cazadores-recolectores, comparada con otras poblaciones con hábitos alimenticios influidos por la revolución agrícola, es mucho más prometedora13, lo que se añade a los estudios de intervención cortos arriba citados. Todas las poblaciones que tienen una dieta adaptada a nuestro acervo evolutivo, tienen una prevalencia de síndrome metabólico mucho menor, o incluso inexistente13, que poblaciones como las mediterráneas. Y consistentemente, todas las poblaciones tradicionales que incorporan alimentos derivados de los cereales, aumentan la prevalencia de las enfermedades de la civilización, y la revierten volviendo a su estilo de vida tradicional56. Algunos argumentos que se suelen hacer para refutar estas observaciones, es argumentar que esas poblaciones tienen un factor de actividad física superior a los occidentales. Pero esa idea no es aplicable a todas las poblaciones y, por lo tanto, no parece ser la explicación. Por ejemplo, los habitantes de Kitava tienen una actividad física parecida a un obrero en Europa, pero el aspecto físico de un obrero a los 65 años en Kitava y en Europa es muy distinto31,57. Un reciente estudio en los Hadzabe de Tanzania también ha demostrado que realmente los cazadores-recolectores no tienen una actividad física más alta que en países occidentales58. Otro argumento muy frecuente es que tienen una cierta protección genética, pero la realidad es que estas poblaciones tienen una susceptibilidad genética aún mayor para sufrir las enfermedades de la civilización que los occidentalizados59,60.


Aprovecho para aclarar otro concepto acerca de la dieta paleolítica. Afirmar que debido a que nuestros antecesores no comían cereales, legumbres y lácteos, y que nuestro genoma no ha cambiado casi nada en los últimos 10,000 años (que si ha cambiado), y por tanto, no estamos adaptados a esos alimentos no es correcto científicamente, como podrán leer en nuestro artículo aquí. Lo correcto sería postular que probablemente, la mayoría de los seres humanos no estén completamente adaptados al consumo de los alimentos introducidos recientemente (a una escala evolutiva)5. Algunos ejemplos de adaptaciones a algunos alimentos neolíticos son la persistencia de la lactasa en adultos61 o el número de copias de genes de la amilasa salivar62.


Respecto a la afirmación hecha en el texto criticando a la dieta paleolítica, me gustaría hacer las siguientes reflexiones: se tacha de dieta mágica y de pseudociencia, o de dieta comúnmente propuesta por terapeutas alternativos, a un estilo de alimentación que nadie ha demostrado que sea perjudicial, del que existen estudios de observación (en los que se basan casi todas las recomendaciones de las autoridades sanitarias) demostrando una salud excepcional en poblaciones que la practican, y con estudios de intervención (de corta duración) que los comparan con las dietas aceptadas por la ortodoxia como sanas (en breve abordaré por qué es tan difícil hacer este tipo de estudios de intervención), donde se ha demostrado que es superior. 


En el artículo se llama ciencia a la idea de seguir lo que las recomendaciones de las autoridades sanitarias dictan sin pararse en ningún momento a poner en cuestión si esas recomendaciones están basadas en la evidencia o no. Recuerdo que los datos de estudios epidemiológicos no son evidencia A. ¿En qué lugar queda el razonamiento científico de dudar de una recomendación? ¿solo por el hecho de que sea lo recomendado significa que tiene evidencia?¿el hecho de que una hipótesis no esté respaldada por evidencia grado A (me refiero a estudios con alimentación basada en la evolución), sin haber estudios que demuestren que es falsa, significa que es errónea? Si usted fuera un paciente con diabetes tipo 2, viendo los resultados de las figuras 8-10, y teniendo en cuenta el efecto sobre el test de tolerancia oral a la glucosa, ¿qué intervención haría? (teniendo en cuenta la evidencia que existe en la actualidad). Cabe añadir, que uno de los autores de este artículo, tras solicitar a las autoridades el informe científico y referencias bibliográficas que apoyan a la pirámide nutricional recomendada en la actualidad, recibió por respuesta que “La Estrategia NAOS y la pirámide nutricional fueron desarrolladas por un grupo de expertos en nutrición y actividad física que contrató la AESAN tomando como referencias otras estrategias y pirámides nutricionales realizadas a nivel mundial y en otros países europeos”. Esta es toda la información que se recibió, sin ningún informe científico adicional o al menos un listado de referencias bibliográficas que consultar. Sería muy bueno, de cara a la transparencia frente a la sociedad y a la comunidad científica, poner a disposición el informe de investigación que apoya las recomendaciones, como hacen otras organizaciones gubernamentales a nivel internacional.



El pez que se muerde la cola


Una pregunta obligada es: ¿por qué no existen estudios de intervención de larga duración con alimentación basada en la evolución?. Una de las principales razones es que es muy difícil encontrar financiación para una dieta que restringe los cereales y los lácteos, dos grupos de alimentos que dan grandes beneficios a la industria alimentaria y otros negocios. Sin embargo, es relativamente fácil que una empresa de lácteos o de cereales integrales te financie un estudio, tal y como deja claro esta revisión sistemática de Cochrane43.


En cuanto a los comentarios acerca del U.S. News & World Report, precisamente mi equipo escribió un rebuttal que pueden leer aquí, y que aclara este tema. Para más información acerca de la evidencia de la nutrición y las enfermedades de la civilización, recomiendo este libro: Food and Western Diseases de Staffan Lindeberg. También recomiendo la lectura de nuestro artículo científico publicado en Research Reports in Clinical Cardiology: The Western Diet and Lifestyle and Diseases of Civilization




Como conclusión final, me gustaría resaltar algunos puntos acerca de mi visión, y la de mi equipo de investigación, sobre la ciencia de la nutrición:



Maelán Fontes Villalba, MS

Doctorando en Nutrición

Center for Primary Health Care Research, Faculty of Medicine, Lund University


Óscar Picazo, MS

Doctorando en Nutrición


Pedro Carrera Bastos, MS

Doctorando en Nutrición

Center for Primary Health Care Research, Faculty of Medicine, Lund University






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Red Meat Mortality Relative Risk



Meat intake and mortality

            Several recent epidemiological studies associated red meat and processed meat intakes to increased total mortality, heart failure, diabetes and cancer risks. Statements such as “men with the highest average intake of red meat (almost 10 servings per week) were at a 24 per cent higher risk of heart failure than men with the lowest average weekly intakes” make newspapers headlines everyday and make everyone aware of potential adverse health effects of red and/or processed meats. These apparently impressive results are often used by the media to scandalize the population, and to catch attention. However, several key points must be considered before making general population recommendations from these epidemiological studies.

            In one of these recent studies, the “Meat intake and mortality: a prospective study of over half a million people” (Sinha et al.) [1], the author’s main conclusion was that “red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality”. This was a prospective study of, as referred, more than half a million people, aged 50-71 years at baseline, followed from 1995 to 2005, where meat intake was estimated with a food frequency questionnaire according to quintiles of red meat, white meat and processed meat intakes. A casual look at this study leads one to believe that red meat was analyzed separately from the processed meat, but this is not the case. The red meat group also included processed red meats, from grain-fed animals.

            Red meat intake ranged from 9.3grs/1000kcal in the first quintile to 68.1grs/ 1000kcal in the fifth quintile. The multivariate model was adjusted for several food and lifestyle covariates, such as: age, education, marital status, family history of cancer, race, body mass index, 31-level smoking history, physical activity, energy intake, alcohol intake, vitamin supplement use, fruit consumption, vegetable consumption and menopausal hormonal therapy among women. Notice the authors assumed that saturated fat (SAFA) and cholesterol content in read meat would be responsible for the development of cardiovascular disease (CVD) and cancer, hence they might be biased in their hypothesis. These preconceived ideas frequently influence the selection of adjustment parameters, leaving other potentially more important factors ignored.

Relative and absolute risks

            The results of “Meat intake and mortality: a prospective study of over half a million people” (Sinha et al.) [1] showed namely that the maximum relative risk of increased all-cause mortality for men, that between the extreme quintiles of red meat intake, apparently is 31%. Also, according to [6], “if men and women in the studied age group (50-71) would reduce their intakes of red meat to that of the group with the lowest intake, then the mortality risk is expected to be reduced by 11% in men and 16% in women over the observed period of time. The portion of cardiovascular disease mortality of total mortality could be reduced by 11% for men and 21% for women. By reducing the intake of processed meat, the cardiovascular disease mortality for women over the period of study of 10 years could be reduced to 20%.”

            At first glance, all these statistical numbers look very impressive, and thus convincing, but they are quite similar to relative risks, which don’t take into account the size of the observed population. Actually, in this Sinha et al. study these ratios are actually hazard ratios estimated by Cox proportion. These are similar to relative risks, they also ignore the population size. Although ratio measures are commonly reported in the medical

literature, the underlying absolute risks are not. In a review of ratio measures in six major medical journals, Schwartz et. al. [12] found that “the underlying absolute risks were often difficult to access or were missing altogether”. These researches explain that “the lack of accessibility of these fundamental data may well lead journal readers (doctors, policy makers, journalists, and patients) to have exaggerated perceptions of the reported effect sizes”.

            Absolute risks and the so called “numbers needed to harm/treat” provide a much better picture of the (dis)advantages of a certain food intake and/or lifestyle change, in this case the red meat intake. When it is said that reducing red meat to that of the group with the lowest intake, the mortality (relative) risks would be reduced by 11% in men and 16% in women, we estimate that corresponding absolute risk reductions of such measures would be approximately 2.1% and 1.4%. On what concerts total mortality, we estimated that the equivalent absolute risk translates into about 4% from the lowest to highest quintile of red meat intake. In a similar way, the maximum absolute risks of cancer and CVD deaths were even smaller, probably close to 1.3% and 1.0% respectively. Also notice these are just statistical/observational associations, establishing causality requires that a plausible biological/biochemical mechanism is identified in carefully designed interventional studies. These causality proving studies against red meat intake simply don’t exist until now.

            Despite of these unfavorable statistical associations found for red meat intake and several unhealthy conditions that lead to increased mortality, even if direct biological causality existed, these results might still be not very relevant for most people, those in the many countries where their red meat intakes fall in the lower quintiles of this American study. For example, in the case of Germany, as discussed in a review of the Federal Institute for Risk Assessment, the average intake of red meat for men lies between the 2nd and 3rd quintile of the US data, and that of women between the 1st and 2nd quintile [6]. So the current, absolute amounts of red meat intake in each country should also be taken into account before assuming that recommending eating less red meat would provide any relevant mortality risk reductions.

Questionnaire inaccuracies

            According to Fraser [14], “the potential correlations between nutrients, and to a lesser extent foods, make it difficult to know whether the nominated variable is actually the active principle or whether there is some other dietary risk factor that is closely associated. It is not generally recognized that all traditional analyses of this sort are based on a powerful but incorrect assumption: that there are no errors in dietary assessment. If the incorrect assumption is not satisfied, relative risk estimates become distorted—reduced by one-half or more in some cases.”

C. Masterjohn text/ideas:

            According to Chris Masterjohn, a researcher affiliated with the Weston A. Price Foundation, because of important questionnaire inaccuracies, the Sinha et. al. study found “a correlation between increased mortality and a population's propensity to report eating meat, not a correlation between mortality and true meat intake”. In an extensive blog article, Masterjohn explains that the food frequency questionnaire (FFQ) contained 124 questions, each question about a particular type of food or group of food. Participants were asked how often they consumed those foods over the course of the previous year, giving them ten options. Then it asked how large of a serving size they consumed, giving them usually three or four options. Sometimes they were given additional instructions, like including sandwiches in some cases or excluding sandwiches in other cases.


            The problem is any individual trying to quantify his or her average intake of 124 foods over an entire year is going to have to engage in a lot of guess work. Even 24-hour recalls of what a person ate the day before are subject to a great deal of error. For this reason, researchers will commonly "validate" an FFQ or a 24-hour recall to test whether these accurately measure the intake of the foods of interest. In order to do this, they have the participants make a weighted dietary record where they meticulously weigh everything they eat with a dietetic scale and record it as they prepare each meal. Then the researchers compare the FFQ or 24-hour recall to the weighted dietary record, assuming that the weighted dietary record is the best indicator of true dietary intake.


            According to Masterjohn’s article, this type of validation was not applied and, instead, a 24-hour recall was used. With this simplified procedure, “the author's validation study found that the true intake of protein, carbohydrate, fat, cholesterol, fiber, vitamins, minerals, fruits, and vegetables could explain between 5 percent and 45 percent of the variation in the participants' answers on the FFQ, but they never validated the FFQ's ability to predict the true intake of meat”. When working with this type of questionnaires, other researchers found that FFQ predict true intake of some foods very well, and true intake of other foods very poorly. The ability of FFQ to predict true intake of meats is probably horrible. When some foods, in a certain cultural context, are socially and emotionally charged, participants are more likely to lie about their intake of those foods, or more likely to deceive themselves about how much of those foods they are really consuming.

            As an example of FFQ inevitable inaccuracies, consider what the researchers who validated the Nurses' Health Study FFQ had to say: “Focusing on the second questionnaire, we found that butter, whole milk, eggs, processed meat, and cold breakfast cereal were underestimated by 10 to 30% on the questionnaire. In contrast, a number of fruits and vegetables, yoghurt and fish were overestimated by at least 50%. These findings for specific foods suggest that participants over-reported consumption of foods often considered desirable or healthy, such as fruit and vegetables, and underestimated foods considered less desirable. This general tendency to over-report socially desirable foods, whether conscious or unconscious, will probably be difficult to eliminate by an alteration of questionnaire design.”

Confounding factors (and results)

            Should we consider these results meaningful enough to establish solid recommendations for the general population? Are all these epidemiological data sufficiently adjusted to the several lifestyle confounding factors that exist, and thus trustable? When dealing with large populations, it is difficult to control for all possible causing factors and, although results are adjusted for several factors, others cannot be ruled out, as the authors state. For example, the way meat is produced and cooked may affect the production of carcinogenic compounds such as heterocyclic amines, polycyclic aromatic hydrocarbons, nitrates, nitrites and N-nitroso compounds [15]. Other factors which could be involved in the potential disease promoting properties of meat, depending on the way it is produced and/or cooked [16], are the time meat stays in the intestines, fruit and vegetable consumption, hormone residues or salt.

            Individuals consuming red and processed meats also have lifestyle behaviors that may significantly affect mortality types, like education, physical activity, smoking, alcohol use, adiposity and fruit/vegetable intake. According to Mozaffarian [2], the model of Sinha et al. did not adjust for parameters like income, air pollution exposure, intake of high-glycemic index starches, sugars, and processed foods, and lower intake of dietary fiber, whole grains, and nuts, seeds, and legumes. Also there was no record about personal history of CVD, or related conditions like hypertension, diabetes, dyslipidemia, nor the use of medications, and such these factors were also not included in the multivariate analysis [4]. As referred above, the authors assumed that SAFA and cholesterol content in read meat would be related to CVD but, despite of this, they don’t inform of differences in saturated fat intake between quintiles or if this was included at all in the multivariate analysis.

            Given the known relationship between glycated hemoglobin (HbA1c), diabetes and heart disease, without the carbohydrate intake information (modern high-glycemic index starches and sugars tend to raise HbA1c) this study could not evaluate if it was the eventually higher amounts of carbohydrates, consumed along with the higher portions of meat, that raised the mortalities. Also, since high blood sugars tend to suppress the immune system and, at the same time, feed glucose to cancer cells, this might help explain the link found between increased cancer deaths and higher red meat intakes. Other similar observational studies, where meat intake was more accurately estimated, didn’t found such association.

            As Mozaffarian [2] refers in his comments, in such a large population, with broad social/economical, geographic, ethnic/cultural, and lifestyle diversity, adequate control for confounding factors assumer even higher importance. In fact, the small observed risk differences (eg, relative risks of 1.1-1.3), that are rendered statistically significant because of the large cohort, are those most susceptible to being due to bias. In these cases, the use of a “negative control”, for which an outcome for which the exposure would have no plausible mechanism, would be recommended. The multivariate model should be adjusted/calibrated until the association of observed variables with the negative control shows no effect. In the Sinha et al. study, such residual confounding actually exists, the “all other deaths” item. Since the association found of meat intake with this item was the strongest found in this study, this strongly suggests that insufficient adjustment for residual confounding variables is present.

Healthy cohort effect

            Regarding other factors involved in mortality associated to meat intake, it is noteworthy to mention that, in this Sinha et al. study, the participants in the top quintile of red meat consumption were 3 times more likely to smoke, half as likely to do regular exercise, much less likely to have a college degree, were substantially heavier and also had higher caloric intakes than low red-meat consumers [3].

             Furthermore, it is common that people who believe that red meat is not healthy tend to adopt other lifestyle factors that favor their health like doing more exercise, not smoking, not drinking alcohol, not frying and taking supplements. In summary, cause-effect cannot be deduced from observational studies as cancer or CVD are multifactorial diseases, in which several genetic and environmental factors are involved. If some relevant (unknown?) confounding factors are not adjusted in the multivariate model, then the risk factors are often overestimated. Large samples, such as this one, with different ethnic, socioeconomic, geographic, cultural and lifestyle need to be carefully controlled for many confounding factors.

            Also, when health authorities decide that a certain food and/or lifestyle behavior are healthy, from that point it becomes increasingly difficult to measure their impact on public health with epidemiological studies. This happens because health conscious people tend to gravitate toward the official, mainstream recommendations. As Dr. Stephan Guyenet, a researcher from University of Washington, explains in his blog Whole Health Source, “if a theory manages to become implanted early on, it will become a self-fulfilling prophecy as healthy, conscientious people adopt the behavior and are detected by subsequent observational studies. People who don't care about their health or aren't motivated enough to make a change will keep living how they used to, and that will also be detected”.


            Dr. Guyenet then adds that “you can't measure all the little things that accompany a health-conscious lifestyle. Do the participants take the stairs or the elevator? Do they take supplements, and if so, which ones? How much sunlight do they get? Do they have positive relationships with their friends and family? (…) What is the quality of the foods they buy? How often do they visit the doctor, and how often do they follow her advice? I believe there are too many confounds to measure and correct for. In my opinion, this means that observational data gathered from populations that already have opinions about the factor you're trying to study are unreliable and will tend to reinforce prevailing notions.

Evolutionary evidence above epidemiological uncertainties

            As a whole, epidemiological/observational studies can only provide statistical associations, but an epidemiological association does not equal causation and as we well know, very often, epidemiological studies show something and then randomized controlled trials show no association whatsoever, or even the opposite. They should not be completely worthless, but only by themselves we believe they are not sufficient to establish solid recommendations and dietary guidelines for the general population.

            Given all these epidemiological limitations, it is then worthwhile not forgetting the most powerful paradigm in human health: evolution. It is weird that a food which has been part of the human diet for 2.6 [17], or even 3.4 [18], million years is now responsible for the cause of CVD or cancer, among other diseases associated to meat intake [19]. Our genome was shaped during the long period of the paleolithic era with little change (0,005%) since the agricultural revolution, 10,000 years ago, despite an enormous change in human diet and other lifestyle factors.

            Nowadays, more than 70% (cereal grains, dairy products, refined vegetable oils and refined sugars) of the calories of the typical western diet come from foods unavailable for our ancestors during the paleolithic era. This discordance between our ancient, genetically determined biology and the nutritional characteristics of the actual diet may be the real cause of the so called diseases of civilization, including CVD and cancer [17].

Ricardo Carvalho and Maelán Fontes1

1. Center for Primary Health Care Research, Faculty of Medicine, Lund University


[1] Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: A prospective study of over half a million people. Arch Intern Med 2009;169:562-71.


[2] Meat intake and mortality: evidence for harm, no effect, or benefit? Mozaffarian D. Arch Intern Med. 2009 Sep 14;169(16):1537-8; author reply 1539.


[3] ACP Journal Club. High consumption of red meat and processed meat was associated with increased risk for mortality. Schectman J. Ann Intern Med. 2009 Jul 21;151(2):JC1-15.


[4] Higher red meat intake may be a marker of risk, not a risk factor itself. de Abreu Silva EO, Marcadenti A. Arch Intern Med. 2009 Sep 14;169(16):1538-9; author reply 1539.


[6] - Study on meat intake and mortality: BFR opinion. BfR - Federal Institute for Risk Assessment, Germany


[7] Stewart FH, Shields WC, Hwang AC. Presenting health risks honestly: Mifepristone, a case in point. Contraception 2004;69:177-8.


[8] Montori VM, Jaeschke R, Schunemann HJ, Bhandari M, Brozek JL, Devereaux PJ, Guyatt GH. Users' guide to detecting misleading claims in clinical research reports. BMJ 2004;329:1093-6.


[9] Felicia H. Stewart, Wayne C. Shields, Ann C. Hwang, MD. Presenting health risks honestly, mifepristone a case in point. Contraception 69 (2004) 177–178.


[10] Victor M Montori, Roman Jaeschke, Holger J Schünemann, Mohit Bhandari, Jan L Brozek,

P J Devereaux, Gordon H Guyatt. User’s guide to detecting misleading claims in clinical research reports. BMJ 2004;329:1093–6.


[11] Ratio measures in leading medical journals: structured review of accessibility of underlying absolute risks (BMJ)

Simple tools for understanding risks: from innumeracy to insight (BMJ)


[12] Edward F. Vonesh. Relatives risks can be risky. Peritoneal Dialysis International, Vol. 13, pp 59.


[13] Schwartz LM, Woloshin S, Dvorin EL, Welch HG. Ratio measures in leading medical journals: Structured review of accessibility of underlying absolute risks. BMJ 2006;333:1248.


[14] Gary E Fraser . A search for truth in dietary epidemiology. American Journal of Clinical Nutrition, Vol. 78, No. 3, 521S-525S, September 2003.


[15] Sugimura T. Nutrition and Dietary Carcinogens. Carcinogenesis. Vol. 1 Nº 3 pg 387-395. 2000


[16] Sinha, R., Rothman, N., Brown, E., Salmon, C., Knize, M., Swanson, C., Rossi, S., Mark, S., Levander, O., and Felton, J. 1995. High concentrations of the carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) occur in chicken but are dependent on the cooking method. Cancer Research 55(20): 4516-9.


[17] Cordain L. Et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 2005;81:341–54


[18] McPherron SP. Evidence for stone-tool-assisted consumption of animal tissues before 3.39 million years ago at Dikika, Ethiopia. Nature.  Vol. 466. 12 August. 2010


[19] Ashaye A. Red meat consumption and risk of heart failure in male physicians. Nutrition, Metabolism & Cardiovascular Diseases (2010).



Rebuttal to U.S. News







Rebuttal to U.S. News and World Top 20 Diets


Loren Cordain1, Ph.D., Maelán Fontes Villalba2 and Pedro Carrera Bastos2


  1. 1.Department of Health and Exercise Science. Colorado State University, Fort Collins, US
  2. 2.Center for Primary Health Care Research. Faculty of Medicine, at Lund University, Malmö, Sweden



The writer of this article suggests that the Paleo Diet has only been scientifically tested in “one tiny study”.  This quote is incorrect as five studies (1-7); four since 2007, have experimentally tested contemporary versions of ancestral human diets and have found them to be superior to Mediterranean diets, diabetic diets and typical western diets in regards to weight loss, cardiovascular disease risk factors and risk factors for type 2 diabetes.


The first study to experimentally test diets devoid of grains, dairy and processed foods was performed by Dr. Kerin O’Dea at the University of Melbourne and published in the Journal, Diabetes in 1984 (6).  In this study Dr. O’Dea gathered together 10 middle aged Australian Aborigines who had been born in the “Outback”.  They had lived their early days primarily as hunter gatherers until they had no choice but to finally settle into a rural community with access to western goods.  Predictably, all ten subjects eventually became overweight and developed type 2 diabetes as they adopted western sedentary lifestyles in the community of Mowwanjum in the northern Kimberley region of Western Australia.  However, inherent in their upbringing was the knowledge to live and survive in this seemingly desolate land without any of the trappings of the modern world.


Dr. O’Dea requested these 10 middle-aged subjects to revert to their former lives as hunter gatherers for a seven week period.  All agreed and traveled back into the isolated land from which they originated.  Their daily sustenance came only from native foods that could be foraged, hunted or gathered.  Instead of white bread, corn, sugar, powdered milk and canned foods, they began to eat the traditional fresh foods of their ancestral past: kangaroos, birds, crocodiles, turtles, shellfish, yams, figs, yabbies (freshwater crayfish), freshwater bream and bush honey.   At the experiment’s conclusion, the results were spectacular, but not altogether unexpected given what known about Paleo diets, even then.  The average weight loss in the group was 16.5 lbs; blood cholesterol dropped by 12 % and triglycerides were reduced by a whopping 72 %.  Insulin and glucose metabolism became normal, and their diabetes effectively disappeared.


The first recent study to experimentally test contemporary Paleo diets was published in 2007 (5). Dr. Lindeberg and associates placed 29 patients with type 2 diabetes and heart disease on either a Paleo diet or a Mediterranean diet based upon whole grains, low-fat dairy products, vegetables, fruits, fish, oils, and margarines.  Note that the Paleo diet excludes grains, dairy products and margarines while encouraging greater consumption of meat and fish.  After 12 weeks on either diet blood glucose tolerance (a risk factor for heart disease) improved in both groups, but was better in the Paleo dieters.  In a  2010 follow-up publication, of this same experiment the Paleo diet was shown to be more satiating on a calorie by calorie basis than the Mediterranean diet because it caused greater changes in leptin, a hormone which regulates appetite and body weight.


In the second modern study (2008) of Paleo Diets, Dr. Osterdahl and co-workers (7) put 14 healthy subjects on a Paleo diet.  After only three weeks the subjects lost weight, reduced their waist size and experienced significant reductions in blood pressure, and plasminogen activator inhibitor (a substance in blood which promotes clotting and accelerates artery clogging).  Because no control group was employed in this study, some scientists would argue that the beneficial changes might not necessarily be due to the Paleo diet.  However, a better controlled more recent experiments showed similar results.


In 2009, Dr. Frasetto and co-workers (1) put nine inactive subjects on a Paleo diet for just 10 days.  In this experiment, the Paleo diet was exactly matched in calories with the subjects’ usual diet.  Anytime people eat diets that are calorically reduced, no matter what foods are involved, they exhibit beneficial health effects.  So the beauty of this experiment was that any therapeutic changes in the subjects’ health could not be credited to reductions in calories, but rather to changes in the types of food eaten.  While on the Paleo diet either eight or all nine participants experienced improvements in blood pressure, arterial function, insulin, total cholesterol, LDL cholesterol and triglycerides.  What is striking about this experiment is how rapidly so many markers of health improved, and that they occurred in every single patient. 


In an even more convincing recent (2009) experiment, Dr. Lindeberg and colleagues (2) compared the effects of a Paleo diet to a diabetes diet generally recommended for patients with type 2 diabetes.  The diabetes diet was intended to reduce total fat by increasing whole grain bread and cereals, low fat dairy products, fruits and vegetables while restricting animal foods.   In contrast, the Paleo diet was lower in cereals, dairy products, potatoes, beans, and bakery foods but higher in fruits, vegetables, meat, and eggs compared to the diabetes diet.  The strength of this experiment was its cross over design in which all 13 diabetes patients first ate one diet for three months and then crossed over and ate the other diet for three months.  Compared to the diabetes diet, the Paleo diet resulted in improved weight loss, waist size, blood pressure, HDL cholesterol, triglycerides, blood glucose and hemoglobin A1c (a marker for long term blood glucose control).    This experiment represents the most powerful example to date of the Paleo diet’s effectiveness in treating people with serious health problems. 


So, now that I have summarized the experimental evidence supporting the health and weight loss benefits of Paleo Diets, I would like to directly respond to the errors in the U.S. News and World Report article.


1.         “Will you lose weight? No way to tell.”


Obviously, the author of this article did not read either the study by O’Dea (6) or the more powerful three month crossover experiment by Jonsson and colleagues (9) which demonstrated the superior weight loss potential of high protein, low glycemic load Paleo diets.  Similar results of high protein, low glycemic load diets have recently been reported in the largest randomized controlled trials ever undertaken in both adults and children.

A 2010 randomized trial involving 773 subjects and published in the New England Journal of Medicine (8) confirmed that high protein, low glycemic index diets were the most effective strategy to keep weight off.   The same beneficial effects of high protein, low glycemic index diets were dramatically demonstrated in largest nutritional trial, The DiOGenes Study (9), ever conducted in a sample of 827 children. Children assigned to low protein, high glycemic diets became significantly fatter over the 6 month experiment, whereas those overweight and obese children assigned to the high protein, low glycemic nutritional plan lost significant weight.


2.         “Does it have cardiovascular benefits? Unknown.” 


This comment shows just how uninformed this writer really is.  Clearly, this person hasn’t read the following papers (1 – 6), which unequivocally show the therapeutic effects of Paleo Diets upon cardiovascular risk factors. Moreover, as we have already reviewed elsewhere (10-12), high protein diets have been shown to improve dyslipidemia and insulin sensitivity, and are potential effective strategies for improving metabolic syndrome. Furthermore, mounting evidence suggests that a reduced-carbohydrate diet (which is obviously lower in sugars and cereal grains) may be superior to a western type low-fat, high-carbohydrate diet, especially in metabolic syndrome patients, because it may lead to better improvement in insulin resistance, postprandial lipemia, serum fasting triglycerides and HDL-C, total cholesterol/HDL-C ratio, LDL particle distribution, apo B/apo A-1 ratio, postprandial vascular function, and various inflammatory biomarkers (13, 14).


Finally, the evidence for recommending whole grains to reduce cardiovascular disease risk is based on epidemiological studies or intervention trials with soft end-points, while randomized controlled trials with hard end points do not seem to support it. For instance, the DART study, found a tendency towards increased cardiovascular mortality in the group advised to eat more fiber, the majority of which was derived from cereal grains (15). And of relevance, this non-significant effect became statistically significant, after adjustment for possible confounding factors, such as medication and health state (16).


            “And all that fat would worry most experts.” 

This statement represents a “scare tactic” unsubstantiated by the data.  As I, and almost the entire nutritional community, have previously pointed out, it is not the quantity of fat which increases the risk for cardiovascular disease or cancer, or any other health problem, but rather the quality.  Contemporary Paleo Diets contain high concentrations of healthful omega 3 fatty acids and monounsaturated fatty acids that actually reduce the risk for chronic disease (10-12, 17-22).


3.         “Can it prevent or control diabetes? Unknown.” 


Here is another example of irresponsible and biased journalism, which doesn’t let the facts speak for themselves.  Obviously, the author did not read the study by O’Dea (6) or Jonsson et al. (2), which showed dramatic improvements in type 2 diabetics consuming Paleo diets.


            “but most diabetes experts recommend a diet that includes whole grains and dairy products.” 

If the truth be known, in a randomized controlled trial, 24 8-y-old boys were asked to take 53 g of protein as milk or meat daily (23).  After only 7 days on the high milk diet, the boys became insulin resistant.  This is a condition that precedes the development of type 2 diabetes.  In contrast, in the meat-group, there was no increase in insulin and insulin resistance.  Furthermore, in the Jonsson et al. study (2) milk and grain free diets were shown to have superior results in improving disease symptoms in type 2 diabetics.

Finally, in an interventional study including 2263 postmenopausal women, participants were assigned to a low-fat (<20% en), high whole-grain fiber (>6 servings per day), high fruit (>5 per day) and high vegetable (>5 servings per day) diet or comparison group with no advice. After 6 years of follow-up, those women with diabetes at the start of the study, and allocated to the low-fat/high whole-grain fiber, actually worsened their glucose control (24). Notwithstanding, the majority of the evidence, supports the beneficial effect of soluble fiber, found mainly in vegetables and fruits, while the evidence supporting the beneficial effects of insoluble fiber, found in whole grains, seems less evident (25-28).


4.         “Are there health risks? Possibly. By shunning dairy and grains, you’re at risk of missing out on a lot of nutrients.”


 Once again, this statement shows the writer’s ignorance and blatant disregard for the facts.  Because contemporary ancestral diets exclude processed foods, dairy and grains, they are actually more nutrient (vitamins, minerals and phytochemicals) dense than government recommended diets such as the food pyramid.    I have pointed out these facts in a paper I published in the American Journal of Clinical Nutrition in 2005 (11) along with another paper in which I analyzed the nutrient content of modern day Paleo diets (19).  In addition, micronutrient analysis derived from the two studies performed by Lindeberg, et al. (5) and Jönsson et al. (2) shows that, except for calcium, a Paleolithic type diet, not only meets all of the micronutrients DRI, but in some cases exceeds that of the whole grain and dairy food diets. Regarding vitamin D, as we have already pointed out in a recent paper (12), except for fatty ocean fish, there is very little vitamin D in any commonly consumed natural (that is, not artificially fortified) food, and throughout history, almost all hominins (except for those living in the far North, such as the Inuit people) depended on the sun to satisfy their vitamin D requirements.


Moreover, most nutritionists are aware that processed foods made with refined grains, sugars and vegetable oils have low concentrations of vitamins and minerals, but not all have realized that dairy products and whole grains contain significantly lower concentrations of the 13 vitamins and minerals most lacking in the U.S. diet compared to lean meats, fish and fresh fruit and vegetables (11, 19). Interestingly, although micronutrient intake is important, intestinal absorption is even more impactful. It is widely known that some antinutrients contained in cereal grains, such as phytate, binds to divalent minerals (i.e., zinc, iron, calcium and magnesium) compromising their absorption (29).


Also, if you’re not careful about making lean meat choices, you’ll quickly ratchet up your risk for heart problems” .

 Actually, the most recent comprehensive meta-analyses and reviews do not show fresh meat consumption whether fat or lean to be a significant risk factor for cardiovascular disease (30-34), only processed meats such as salami, bologna, bacon and sausages (30).




1.         Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, Jr., Sebastian A: Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr 2009.


2.         Jönsson T, Granfeldt Y, Ahrén B, Branell UC, Pålsson G, Hansson A, Söderström M, Lindeberg S. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol. 2009;8:35


3.         Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahren B, Lindeberg S. A Paleolithic diet is more satiating per calorie than a Mediterranean-like diet in individuals with ischemic heart disease. Nutr Metab (Lond). 2010 Nov 30;7(1):85


4.         Jonsson T, Ahren B, Pacini G, Sundler F, Wierup N, Steen S, Sjoberg T, Ugander M, Frostegard J, Goransson Lindeberg S: A Paleolithic diet confers higher insulin sensitivity, lower C-reactive protein and lower blood pressure than a cereal-based diet in domestic pigs. Nutr Metab (Lond) 2006, 3:39.


5.         Lindeberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K, Ahren B: A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia 2007, 50(9):1795-1807.


6.         O'Dea K: Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes 1984, 33(6):596-603.


7.         Osterdahl M, Kocturk T, Koochek A, Wandell PE: Effects of a short-term intervention with a paleolithic diet in healthy volunteers. Eur J Clin Nutr 2008, 62(5):682-685.


8.         Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunešová M, Pihlsgård M, Stender S, Holst C, Saris WH, Astrup A; Diet, Obesity, and Genes (Diogenes) Project. Diets with high or low protein content and glycemic index for weight-loss maintenance. N Engl J Med. 2010 Nov 25;363(22):2102-13


9.         Papadaki A, Linardakis M, Larsen TM, van Baak MA, Lindroos AK, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunesová M, Holst C, Astrup A, Saris WH, Kafatos A; DiOGenes Study Group. The effect of protein and glycemic index on children's body composition: the DiOGenes randomized study. Pediatrics. 2010 Nov;126(5):e1143-52


10.       Cordain L, Eaton SB, Miller JB, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52


11.       Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O'Keefe JH, Brand-Miller J. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005 Feb;81(2):341-54.


12.       Carrera-Bastos P, Fontes Villalba M, O’Keefe JH, Lindeberg S, Cordain L. The western diet and lifestyle and diseases of civilization. Res Rep Clin Cardiol 2011; 2: 215-235.


13.       Westman EC, Feinman RD, Mavropoulos JC, et al. Low-carbohydrate nutrition and metabolism. Am J Clin Nutr. 2007 Aug;86(2):276-84.


14.       Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res. 2008; 47, 307–318.


15.       Fish and the heart. Lancet. 1989 Dec 16;2(8677):1450-2


16.       Ness AR, Hughes J, Elwood PC, Whitley E, Smith GD, Burr ML. The long-term effect of dietary advice in men with coronary disease: follow-up of the Diet and Reinfarction trial (DART). Eur J Clin Nutr. 2002 Jun;56(6):512-8


17.       Cordain L. Saturated fat consumption in ancestral human diets: implications for contemporary intakes.  In: Phytochemicals, Nutrient-Gene Interactions, Meskin MS, Bidlack WR, Randolph RK (Eds.), CRC Press (Taylor & Francis Group), 2006, pp. 115-126.


18.       Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000 Mar;71(3):682-92.


19.       Cordain L. The nutritional characteristics of a contemporary diet based upon Paleolithic food groups. J Am Nutraceut Assoc 2002; 5:15-24.


20.       Kuipers RS, Luxwolda MF, Dijck-Brouwer DA, Eaton SB, Crawford MA, Cordain L, Muskiet FA. Estimated macronutrient and fatty acid intakes from an East African Paleolithic diet. Br J Nutr. 2010 Dec;104(11):1666-87.


21.       Ramsden CE, Faurot KR, Carrera-Bastos P, Cordain L, De Lorgeril M, Sperling LS.Dietary fat quality and coronary heart disease prevention: a unified theory based on evolutionary, historical, global, and modern perspectives. Curr Treat Options Cardiovasc Med. 2009 Aug;11(4):289-301.


22.       Cordain L, Watkins BA, Florant GL, Kelher M, Rogers L, Li Y. Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr. 2002 Mar;56(3):181-91


23.       Hoppe C, Mølgaard C, Vaag A, Barkholt V, Michaelsen KF. High intakes of milk, but not meat, increase s-insulin and insulin resistance in 8-year-old boys. Eur J Clin Nutr. 2005 Mar;59(3):393-8.


24.       Shikany JM, Margolis KL, Pettinger M, Jackson RD, Limacher MC, Liu S, et al. Effects of a low-fat dietary intervention on glucose, insulin, and insulin resistance in the Women's Health Initiative (WHI) Dietary Modification trial. Am J Clin Nutr. 2011 May 11 [Epub ahead of print]


25.    Mann JI, De Leeuw I, Hermansen K, Karamanos B, Karlström B, Katsilambros N, et al. Evidence-based nutritional approaches to the treatment and prevention of diabetes mellitus. Nutr Metab Cardiovasc Dis. 2004 Dec.;14(6):373–394.

26.    Robertson MD, Bickerton AS, Dennis AL, Vidal H, Frayn KN. Insulin-sensitizing effects of dietary resistant starch and effects on skeletal muscle and adipose tissue metabolism. Am. J. Clin. Nutr. 2005 Sep.;82(3):559–567.

27.    Erkkilä AT, Lichtenstein AH. Fiber and cardiovascular disease risk: how strong is the evidence? J Cardiovasc Nurs. 2006;21(1):3–8.

28.    Chandalia M, Garg A, Lutjohann D, Bergmann von K, Grundy SM, Brinkley LJ. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N. Engl. J. Med. 2000 May 11;342(19):1392–1398.


29.       Cordain L. Cereal grains: humanity's double-edged sword. World Rev Nutr Diet. 1999;84:19-73.


30.       Micha R, Wallace SK, Mozaffarian D. Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Circulation. 2010 Jun 1;121(21):2271-83


31.       Micha R, Mozaffarian D. Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids. 2010 Oct;45(10):893-905. Epub 2010 Mar 31.


32.       Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep. 2010 Nov;12(6):384-90.


33.       Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):502-9


34.       Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46

The western diet and lifestyle and diseases of civilization

Authors: Pedro Carrera-Bastos, Maelan Fontes-Villalba, James H O’Keefe, et al

Published Date March 2011 Volume 2011:2 Pages 15 - 35

Pedro Carrera-Bastos1, Maelan Fontes-Villalba1, James H O’Keefe2, Staffan Lindeberg1, Loren Cordain3
1Center for Primary Health Care Research, Faculty of Medicine at Lund University, Malmö, Sweden; 2Mid America Heart and Vascular Institute/University of Missouri-Kansas City, Kansas City, Missouri, USA; 3Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, USA

Abstract: It is increasingly recognized that certain fundamental changes in diet and lifestyle that occurred after the Neolithic Revolution, and especially after the Industrial Revolution and the Modern Age, are too recent, on an evolutionary time scale, for the human genome to have completely adapted. This mismatch between our ancient physiology and the western diet and lifestyle underlies many so-called diseases of civilization, including coronary heart disease, obesity, hypertension, type 2 diabetes, epithelial cell cancers, autoimmune disease, and osteoporosis, which are rare or virtually absent in hunter–gatherers and other non-westernized populations. It is therefore proposed that the adoption of diet and lifestyle that mimic the beneficial characteristics of the preagricultural environment is an effective strategy to reduce the risk of chronic degenerative diseases.


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Algunas recomendaciones de alimentación están basadas en estudios observacionales y no siempre los datos de los estudios epidemiológicos se corroboran con estudios de intervención. Es decir, los datos de estudios observacionales establecen asociaciones, pero no causa-efecto, que permiten formular hipótesis para posteriormente testarlas con estudios de intervención.

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