Eur J Nutr 39 : 67–70 (2000)© Steinkopff Verlag 2000

Received: 24 February 2000Accepted: 20 March 2000

S. Boyd Eaton, MD (�) · S. Boyd Eaton IIIDept AnthropologyEmory University2887 Howell Mill RoadAtlanta GA 30327, USAe-mail: sboydeaton@aol.com

Summary The nutritional patternsof Paleolithic humans influenced ge-netic evolution during the time seg-ment within which defining charac-teristics of contemporary humanswere selected. Our genome can havechanged little since the beginnings ofagriculture, so, genetically, humansremain Stone Agers – adapted for aPaleolithic dietary regimen.

Such diets were based chiefly onwild game, fish and uncultivatedplant foods. They provided abundantprotein; a fat profile much differentfrom that of affluent Western nations;high fibre; carbohydrate from fruitsand vegetables (and some honey) butnot from cereals, refined sugars anddairy products; high levels of micro-nutrients and probably of phyto-chemicals as well.

Differences between contempo-

rary and ancestral diets have manypathophysiological implications. Thisreview addresses phytochemicals andcancer; calcium, physical exertion,bone mineral density and bone struc-tural geometry; dietary protein,potassium, renal acid secretion andurinary calcium loss; and finally sar-copenia, adiposity, insulin receptorsand insulin resistance.

While not, yet, a basis for formalrecommendations, awareness of Pale-olithic nutritional patterns shouldgenerate novel, testable hypothesesgrounded in evolutionary theory andit should dispel complacency regard-ing currently accepted nutritionaltenets.

Key words Paleolithic diet – insulin resistance – skeletal health –phytochemicals – type 2 diabetes

SPECIAL ISSUE

Stanley Boyd Eaton Stanley Boyd Eaton III

Paleolithic vs. modern diets – selectedpathophysiological implications

Introduction

The Paleolithic or Old Stone Age occupied nearly all thelast two million years of human evolutionary experience,an especially critical time segment during which the adap-tations that define our genus were selected: body mass andshape, locomotive capability, masticatory apparatus,growth/developmental schedule, relative (and absolute)brain size, resting metabolic rate, and daily foraging range[1]. Experiential changes associated with agriculture andindustry have been dramatic and might readily have influ-enced the human genome given sufficient time; however,the very rapidity of these innovations has almost totallyoverreached the capacity of genetic evolution to keep pace.

While there has clearly been some Holocene genetic adap-tation, primarily to infectious diseases (e. g. malaria), in-creasing population size and greater mobility have actuallyreduced the likelihood of genetic innovation in recent mil-lennia [2]. It is, therefore, not mere rhetorical hyperbole toassert that contemporary humans are, in the genetic sense,still Stone Agers and that, consequently, we remain adaptedfor a preagricultural nutritional pattern.

Paleolithic diets

There was no universal nutritional regimen for StoneAgers, but in terms of mathematical set theory, the super-

68 European Journal of Nutrition, Vol. 39, Number 2 (2000)© Steinkopf Verlag 2000

set believed to encompass Paleolithic dietary patterns (e. g.high latitude, arid lands, equatorial, coastal) and the super-set including contemporary ones (e. g. traditional EastAsian, Mediterranean, typical American, vegetarians) arelargely disjoint; they overlap surprisingly little. Preagricul-tural humans ate wild game, fish, uncultivated plant foodsand, when available, honey. Grains were for emergenciesand there were no dairy products, oils, salt, processedfoods, nor empty calories.

In almost all cases, Stone Agers consumed more animalprotein than do current Westerners (Tab. 1). Total fat con-sumption varied, chiefly with latitude, but intake of serum-cholesterol-raising fat was nearly always less than forAmericans and Europeans [3] while there was more di-etary long-chain (C20 and above) polyunsaturated fattyacid (LCPUFA) [4]. The preagricultural essential fatty acidratio (ω6:ω3) approached equality; for average Americansthis ratio is 10:1 or higher. Dietary cholesterol roughlyequated U. S. levels. Carbohydrate consumption also var-ied with latitude, but, in all cases, came chiefly from fruitsand vegetables, not from cereals, refined sugars, and dairyproducts. Compared with the Western European dietarypattern, Paleolithic foods provided much more fibre (bothsoluble and insoluble) and from two to ten times more mi-cronutrients (Table 2); there was probably a similar phyto-chemical discrepancy.

Evolution, nutrition, and pathophysiology

An appreciation of Paleolithic nutrient-nutrient interac-tions and of the relationships between diet and other as-pects of ancestral experience can enlighten topics of cur-rent interest and/or controversy. Three (of many possible)examples are phytochemicals, skeletal health and insulinresistance.

Phytochemicals

No free-living primates except humans consume cerealgrains, but from the emergence of agriculture, wheat, rice,corn, and their like have provided from 40 to 90% of ourenergy requirements. In so doing they have reduced thecontribution of fruits and vegetables, the major energysource for Stone Agers and their simian predecessors overthe preceding fifty million year evolutionary span. Recentepidemiological metaanalyses strongly suggest that fruitsand vegetables have far more cancer-preventive potentialthan do cereals [5], perhaps reflecting the phytochemicalcontent of non-cereal plant foods, phytochemicals to whichcurrent human biology became adapted through many mil-lion years of interrelationships. In contrast, the phyto-chemicals of grains have interacted with the humangenome for only 10,000 years. While it required epidemi-ology to demonstrate that fruits and vegetables have cancerpreventive-potential (and more such potential than docereals), evolutionary understanding suggests why this

Table 1 General paleolithic nutrition

Nutrient Typical Variation with Latitude

ProteinAnimal Very High PositiveVegetable Moderate Negative

FatTotal Moderate to High Positive

(~ Mediterranean vs.E. Asian)

C20 & Very High PositiveC22 LCPUFA1

n–6:n–3 Ratio ~1 PositiveSerum CholesterolRaising FA Low PositiveCholesterol High (~ US levels) Positive

CarbohydrateCereals None to Minimal NegativeVegetables & Fruits Very High NegativeDairy Foods None After Infancy –Refined Sugars None (Honey) –

Fibre Very High NegativeMicronutrients Very High NegativePhytochemicals (Probably High) (Probably Negative)

1long-chain polyunsaturated fatty acids

Table 2 Paleolithic nutrition

Paleolithic1 Current US2 Ratio

(mg/d) (mg/d)MINERALSCalcium 1622 920 1.8Copper 12.2 1.2 10.2Iron 87.4 10.5 8.3Magnesium 1223 320 3.8Manganese 13.3 3.0 4.4Phosphorus 3223 1510 2.1Potassium 10500 2500 4.2Sodium 768 4000 0.2Zinc 43.4 12.5 3.5VITAMINSAscorbate 604 93 6.5Folate 0.36 0.18 2.0Riboflavin 6.49 1.71 3.8Thiamin 3.91 1.42 2.8Vitamin A 17.2 7.8 2.2Vitamin E 32.8 8.5 3.91 based on 3000 kcal/d, 35 % animal: 65 % plant subsistence2 average of US men and women; Food and Nutrition Board, 1989

S. Boyd Eaton et al. 69Paleolithic vs. modern diets

should be so and also implies that the partial replacementof fruits and vegetables by cereals following the emergenceof agriculture probably increased our susceptibility to neo-plastic diseases.

Skeletal health

Despite their lack of dairy products, Paleolithic diets gen-erally provided more calcium than do the diets of Ameri-cans and Europeans. Wild plant foods often contain con-siderable calcium, the average for 119 such items being132.6 mg/100 g (vs. whole milk ~120 mg/100 mg) [6].However, in far northern latitudes, plant foods sometimesmade up only 5% of annual energy intake, so that low bonemineral density (osteoporosis) was common among StoneAgers living in such regions. Nevertheless, fractures wereinfrequent because a bone’s strength is determined not onlyby its mineral density, but also by its structural geometry,especially its diameter and cross-sectional configuration[7]. Structural geometry is affected by habitual physicalactivity which tends to increase bone diameter and createcross-sections more oval than round. Such bones resist me-chanical stresses effectively, even when osteoporotic. Thiseffect helps explain why Melanesians and black SouthAfricans, whose calcium intake is low, have far fewer age-related fractures than do black and white Americans whosecalcium intake is greater.

Diets high in protein have been positively correlatedwith hip fracture rates, presumably because protein in-creases urinary calcium loss. The mechanism involves en-dogenous acid production which is increased by metabo-lism of protein; renal acid secretion and urinary calciumloss are highly correlated. Conversely, dietary potassiumproduces a net alkalinising effect, opposite to that of pro-tein, and it appears that net endogenous acid production,which largely determines net renal acid excretion, can bepredicted by assessing the dietary protein (g/d) / potassium(mg/d) ratio, with lower values being protective [8]. Theextremely high potassium content of Paleolithic diets (e. g.10500 mg/d for a 3000 kcal, 35:65 animal:plant subsis-tence pattern vs. ~2500 mg/d in the average American diet)thus may have exerted a critically beneficial influence: aprotein / potassium ratio of 0.84 for typical Stone Agerscompared with an average value of 1.24 for 141 Americansubjects consuming 20 different contemporary diets.

Dietary sodium also increases urinary calcium loss [9];its effect is roughly similar in magnitude to that of protein.The typically low sodium intake of Stone Agers (~768mg/d vs. Americans ~4000 mg/d) would have exerted ad-ditional protective influence on Paleolithic skeletal health.

Insulin resistance

Insulin resistance and hyperinsulinaemia are increasinglythought of as central factors in the pathophysiology, notonly of type 2 diabetes, but also of hypertension and coro-nary heart disease. While it is clear that genetics, diet andexercise are all involved in the development of insulin re-sistance, the exact mechanism remains unclear. Since thefield remains open, perhaps an evolution-based hypothesismerits consideration.

The relationship between excess adiposity and insulinresistance is well recognised, but evolutionary considera-tions suggest a parallel linkage involving relative skeletalmuscle deficiency. Contemporary humans are distin-guished from their predecessors not just by hyperadiposity,but also by sarcopenia [10]. In addition, current physicalfitness levels are much below those typical in the past.These altered parameters distort the physiological milieufor insulin action from what it was when the genetic basesfor carbohydrate metabolic regulation was selected.

Gramme for gramme, insulin-stimulated muscle can ex-tract far more glucose from the blood than can insulin-stimulated adipose tissue and exercise-conditioned muscleextracts more than does non-conditioned muscle [11].Hence, a logical hypothesis is that functional insulin resis-tance, especially in its earliest stages, is directly propor-tional to body fat mass and inversely proportional to themass and metabolic activity of skeletal muscle. This rela-tionship might reflect competition between the insulin re-ceptors of myocytes and those of adipocytes for availableinsulin molecules. The initial effect would be repetitiveepisodes of transient hyperglycaemia and hyperinsuli-naemia. In genetically susceptible individuals, furthermetabolic deterioration could result from secondary down-regulation of insulin receptors, glucose transporters, andintracellular enzymatic sequences, leading ultimately toglucose intolerance and type 2 diabetes.

Conclusion

At one level the insights arising from these examples – eatmore fruits and vegetables, reduce sodium intake, and in-crease exercise – are banal. However, there are more pro-found implications. Basing the nutritional pyramid ongrains is wholly out of line with primate and hominid evo-lutionary experience. A Paleolithic model experimentaldiet – high protein, high fibre, minimal serum-cholesterolraising potential, balanced n–3:n–6 fatty acid ratios, highLCPUFA content, etc. – deserves investigative support.Micronutrient intake throughout evolutionary experienceexceeded current RDAs. The importance of bone structuralgeometry and possible myocyte-adipocyte insulin receptorcompetition both deserve study.

Paleolithic nutritional awareness is not, yet, a basis forformal recommendations, but it can generate testable hy-

70 European Journal of Nutrition, Vol. 39, Number 2 (2000)© Steinkopf Verlag 2000

potheses grounded in evolutionary theory. And it shoulddispel complacency regarding currently accepted nutri-tional tenets.

1. Wood B, Collard M (1999) The humangenus. Science 284: 65–71

2. Tattersall I (1998) Becoming Human.Evolution and Human Uniqueness. Har-court Brace, New York; pp 239.

3. Eaton SB, Eaton SB III, Konner MJ(1997) Paleolithic nutrition revisited: atwelve-year retrospective on its natureand implications. Eur J Clin Nutr 51:207–16

4. Eaton SB, Eaton SV III, Sinclair AJ, Cor-dain L, Mann NJ (1998) Dietary intake oflong-chain polyunsaturated fatty acidsduring the paleolithic. World Rev NutrDiet 83: 12–23

5. World Cancer Research Fund, AmericanInstitute for Cancer Research (1997)

Food, Nutrition and the Prevention ofCancer: a Global Perspective. AmericanInstitute for Cancer Research, Washing-ton D.C, pp 506–507

6. Eaton SB, Nelson DA (1997) Calcium inevolutionary perspective. Am J Clin Nutr54: 281S–2817S

7. Ruff CB (1992) Biomedical analyses ofarchaeological human material. In: Saun-ders SR, Katzenburg A (eds). The Skele-tal Biology of Past Peoples. Alan R Liss,New York, pp 41–62

8. Frassetto LA, Todd KM, Morris Jr RC,Sebastian A (1998) Estimation of net en-dogenous noncarbonic acid productionin humans from diet potassium and pro-

tein contents. Am J Clin Nutr 68:576–583

9. Devine A, Criddle RA, Dick IM, KerrDA, Prince RL (1995) A longitudinalstudy of the effect of sodium and calciumintakes on regional bone density in post-menopausal women. Am J Clin Nutr 62:740–745

10. Rode A, Shephard RJ (1994) The physi-ological consequences of acculturation: a20-year study in an Inuit community. EurJ Appl Physiol 69: 16–24

11. DeFronzo R (1997) Pathogenesis of type2 diabetes: metabolic & molecular impli-cations for identifying diabetes genes.Diabetes Rev 5: 177–269

References