Origins and evolution of the Western diet: health implications for the21st century
Loren Cordain, S Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A Watkins, James H O’Keefe,and Janette Brand-Miller
There is growing awareness that the profound changes in the envi-ronment (eg, in diet and other lifestyle conditions) that began withtheintroductionofagricultureandanimalhusbandry
10 000yagooccurred too recently on an evolutionary time scale for the humangenome to adjust. In conjunction with this discordance between ourancient,geneticallydeterminedbiologyandthenutritional,cultural,andactivitypatternsofcontemporaryWesternpopulations,manyof the so-called diseases of civilization have emerged. In particular,food staples and food-processing procedures introduced during theNeolithic and Industrial Periods have fundamentally altered 7 cru-cial nutritional characteristics of ancestral hominin diets:
) glyce-mic load,
) fatty acid composition, 3) macronutrient composition,
) fiber content. The evolutionary collision of our ancientgenomewiththenutritionalqualitiesofrecentlyintroducedfoodsmayunderliemanyofthechronicdiseasesofWesterncivilization.
Am J Clin Nutr
Westernized diets, chronic disease, processedfoods, genetic discordance, hunter-gatherers, human evolution
Evolution acting through natural selection represents an on-goinginteractionbetweenaspecies’genomeanditsenvironmentover the course of multiple generations. Genetic traits may bepositively or negatively selected relative to their concordance ordiscordance with environmental selective pressures (1). Whenthe environment remains relatively constant, stabilizing selec-tion tends to maintain genetic traits that represent the optimalaverage for a population (2). When environmental conditionspermanently change, evolutionary discordance arises between aspecies’genomeanditsenvironment,andstabilizingselectionisreplacedbydirectionalselection,movingtheaveragepopulationgenome to a new set point (1, 2). Initially, when permanentenvironmental changes occur in a population, individuals bear-ing the previous average status quo genome experience evolu-tionary discordance (2, 3). In the affected genotype, this evolu-tionary discordance manifests itself phenotypically as disease,increased morbidity and mortality, and reduced reproductivesuccess (1–3).Similar to all species, contemporary humans are geneticallyadapted to the environment of their ancestors—that is, to theenvironment that their ancestors survived in and that conse-quently conditioned their genetic makeup (1–3). There is grow-ing awareness that the profound environmental changes (eg, indiet and other lifestyle conditions) that began with the introduc-tion of agriculture and animal husbandry
10 000 y ago oc-curred too recently on an evolutionary time scale for the humangenome to adapt (2–5). In conjunction with this discordancebetween our ancient, genetically determined biology and thenutritional,cultural,andactivitypatternsincontemporaryWest-ern populations, many of the so-called diseases of civilizationhave emerged (2–12).
CHRONIC DISEASE INCIDENCE
In the United States, chronic illnesses and health problemseither wholly or partially attributable to diet represent by far themost serious threat to public health. Sixty-five percent of adultsaged
20 y in the United States are either overweight or obese(13), and the estimated number of deaths ascribable to obesity is280 184peryear(14).Morethan64millionAmericanshaveoneormoretypesofcardiovasculardisease(CVD),whichrepresentstheleadingcauseofmortality(38.5%ofalldeaths)intheUnitedStates(15).FiftymillionAmericansarehypertensive;11millionhave type 2 diabetes, and 37 million adults maintain high-risk total cholesterol concentrations (
240 mg/dL) (15). In post-menopausal women aged
50 y, 7.2% have osteoporosis and39.6% have osteopenia (16). Osteoporotic hip fractures are as-sociated with a 20% excess mortality in the year after fracture
From the Department of Health and Exercise Science, Colorado StateUniversity, Fort Collins (LC); the Departments of Radiology and Anthro-pology, Emory University, Atlanta (SBE); the Department of Medicine andUCSF/Moffitt General Clinical Research Center, University of California,San Francisco (AS); the Department of Food Science, RMIT University,Melbourne, Australia (NM); the Department of Medicine, Lund University,Sweden (SL); the Department of Food Science, Lipid Chemistry and Mo-lecular Biology Laboratory, Purdue University, West Lafayette, IN (BAW);the Mid America Heart Institute, Cardiovascular Consultants, Kansas City,MO (JHO); and the Human Nutrition Unit, Department of Biochemistry,University of Sydney, Australia (JB-M).
Address reprint requests to L Cordain, Department of Health and Exer-cise Science, Colorado State University, Fort Collins, CO 80523. E-mail:firstname.lastname@example.org.Received June 17, 2004.Accepted for publication August 24, 2004.
Am J Clin Nutr
2005;81:341–54. Printed in USA. © 2005 American Society for Clinical Nutrition
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