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Obesity in BioculturalPerspectiveStanley J. Ulijaszek and Hayley Lonk Institute of Social and Cultural Anthropology, University of Oxford,Oxford OX2 6PF, United Kingdom; email: [email protected],[email protected]

Annu. Rev. Anthropol. 2006. 35:33760

First published online as a Review in Advance on July 6, 2006

The Annual Review of Anthropology is onlineat anthro.annualreviews.org

This articles doi:10.1146/annurev.anthro.35.081705.123301

Copyright c 2006 by Annual Reviews. All rights reserved

0084-6570/06/1021-0337$20.00

Key Wordspopulation trends, socioeconomic status, nutrition transition,genetics, evolution, neurophysiology, food security

Abstract Obesity is new in human evolutionary history, having become psible at the population level with increased food security. Acrthe past 60 years, social, economic, and technological changes haltered patterns of life almost everywhere on Earth. In tandechanges in diet and physical activity patterns have been centrathe emergence of obesity among many of the worlds populatioincluding the developing world. Increasing global rates of obesare broadly attributed to environments that are obesogenic, againan evolutionary heritage that is maladaptive in these new contexObesity has been studied using genetic, physiological, psycholocal, behavioral, cultural, environmental, and economic framewor Although most obesity research is rmly embedded within displinaryboundaries, someconvergence between genetics,physioloand eating behavior has taken place recently. This chapter reviechanging patterns and understandings of obesity from these diveperspectives.

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Human genetics likely have undergone se-lection for traits that promote energy intakeand storage and minimize energy expendi-ture. Thus it is no surprise that there are agreat many obesity-related genotypes. Mod-els linking genetic susceptibilities with physi-ology and feeding behavior are emerging, and

although they only explain a small propor-tion of global obesity rates, might underliethe more-common and genetically complexforms of human obesity. Human physiology can only exert weak control on the reductionof food intake and the increase of energy ex-penditure when energy stores are replete andfood security is high, and obesity is almost aninevitable human biological outcome in theenvironments that have been constructed inindustrialized nations over the past 60 years

and that have emerged with modernizationelsewhere.

INTRODUCTION Obesity is the condition in which excess body fat has accumulated to a degree that healthand function are negatively affected. It isnew in human evolutionary history, havingbeen essentially nonexistent until approxi-mately 10,000 years ago (Brown 1991, Brown

& Krick 2001).Acrosshistory, individuals andgroups of privilege have been able to dis-play embodied wealth by above-average body size, including weight and fatness (Brown& Konner 1987, Brown 1991, de Garine &Pollock 1995). Obesity was known in ancient Greece (Bevegni & Adami 2003) and was acommon condition among the English upperclasses in the late eighteenth century (Trowell1975). It emerged more generally amongNorth American men in the nineteenth cen-tury (Kahn & Williamson 1994), increas-ing in successive surveys in both the UnitedStates and Britain across the twentieth cen-tury (Garrow 1978). Across the past 60 years,social, economic, and technological changeshave altered patterns of life worldwide. Dur-ing postWorld War II reconstruction, eco-nomic development grew on a more-global

scale, as colonial models of economic maagement fell from favor. In tandem, changin diet and activity patterns have been cetral to the emergence of obesity among manof the worlds populations, including poorones (Popkin & Doak 1998). In the vast m jority of nations for which comparative da

are available, rates of obesity are increasi(de Onis 2005, Nishida & Mucavele 2005)is estimated that over 300 million adults acurrently obese, as dened by having a bomass index (BMI) above 30 kg/m2. A furthe700millionpeople areconsidered overweigh with BMIs between 25 kg/m2 and 30 kg/m2

The prevalence of obesity among childrenalso rising.

Increasing rates of obesity across theworare broadly attributed to environments tha

are obesogenic (French et al. 2001, Brown2002, Hill et al. 2003), against an evolutioary heritage that is maladaptive in these necontexts (Neel 1962, Eaton et al. 1998, Neet al. 1998, Lev-Ran 2001). The term obesgenic environment was coined by Swinbuet al. (1999), who argued that the physiceconomic, social, and cultural environmenof the majority of industrialized nations ecourage positive energy balance in their poulations. A dominant explanatory framewo

for the emergence of obesogenic enviroments is that of nutrition transition (Popki2004), which relates globalization, urbaniztion, and westernization to changing fooenvironments across the populations of th world (Drewnowski & Popkin 1997, Grift& Bentley 2001, Contaldo & Pasanisi 2004Central to this transition are shifts in diet to ward increased consumption of energy-denfoods (Drewnowski & Popkin 1997) and dclines in physical activity (Erlichman et 2002). In this formulation, global food suppbecomes increasingly abundant, less expesive, and more-aggressively marketed; copled with declines in physical activity, this hled to higher prevalences of obesity (Nielset al. 2002, Drewnowski & Darmon 2005In addition, economic inequalities within anbetween nations have ensured food securi

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BMI range of 18.525 kg/m2 is likely to bemaintained in many populations by way of balancing selection. The BMI cut-offs areused to dene overweight and obesity inadults are 25 kg/m2 and 30 kg/m2, respec-tively (Shetty & James 1994). However, therelationship between BMI and fatness varies

across populations, as do relationships be-tween morbidity and BMI. In some Chinese(Li et al. 2002) and South Asian popula-tions (Gill 2001, Sullivan 2001, Wahlqvist 2001), increased chronic disease risk occursat lower BMIs than among European popu-lations (Li et al. 2002). The BMI does not give a measure of intra-abdominal (visceral)or lower-body fatness, however. High levelsof intra-abdominal fatness are independently associated with risk markers of cardiovascular

disease, NIDDM, and various cancers (WorldHealth Organization 2000). High lower-body fatness relative to waist size is associated withlower risk of the same disorders, and amongfemales it is important for buffering the en-ergetic stresses of pregnancy and lactation(Garaulet et al. 2000).

Classication of childhood obesity usingBMI is more problematic than for adults be-cause of the variability in the growth ratesof children both within and between popu-

lations. The BMI changes with age, and Coleet al. (2000) have proposed for internationaluse age-specic cut-offs for childhood overweight and obesity that pass through BMIsof 25 kg/m2 and 30 kg/m2, respectively, at the age of 18, using a normative distribu-tion that varies by age and sex. However, un-like in adults where it is possible to establishincreased health risks associated with an in-creased BMI, most healtheffects of childhoodobesity are manifested in adult life and not childhood, with the possible exception of risk markers for NIDDM.

POPULATION TRENDS IN OBESITY Obesity at thepopulation level waslargely un-known in the 1950s. However, by the 1990s,

33 nations had obesity rates exceeding 10of their adult populations (Figure 1 ) (Nishid& Mucavele 2005). Currently, obesity is moprevalent in some Pacic Island nations; tUnited States; most European, many Middle Eastern, and some Latin American ntions; and South Africa. Four Pacic Isla

nations (Nauru, Tonga, the Cook Islands, anFrench Polynesia) have the highest rates obesity in the world, in all cases exceedi40% of their adult populations. Obesity ratfor Bahrain and Kuwait lie close to that the United States, at a little below 30% the adult population. The rate for Canada approximately half that of the United StateFor the adult South African population, thrate is 22%, similar to Egypt, Turkey, Hungary, and Germany, the latter two having th

highest rates in Europe. The lowest rate iEurope, 5%, is among adults in Norway anSwitzerland. Of Latin American population Mexico, Uruguay, and Peru have rates that exceed 15%. Rates among wealthier Asian ntions vary from 6% in Singapore to 3% adult populations in Japan and South Krea. In the vast majority of nations, obesrates among females arehigher than formaleby an average of 5%. Obesity rates of males exceed those of males by more th

2% in 32 of the 66 nations for which daexist for both sexes, whereas obesity raof males exceed those of females in o4 nations.

Risingobesity rateshave variedindifferenations. In PacicIslandnations, ratesof obesity were already high by the 1960s and cotinued to increase dramatically into the 199(Ulijaszek 2005). The United States anCanada had similar rates of obesity 40 yeago, at approximately 10% of the adult poulation; subsequently, rates became higher the United States than in Canada (Nishida & Mucavele 2005). In the past 20 years, obesrates have risen in the majority ofnations witavailable data. Of 28 nations for which dareavailable, increasedobesity rateshave beobserved for adult males in20and for adult fmales in 19 (Nishida & Mucavele 2005). T

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fastest increases have taken place in Hungary,Russia, Ireland, Turkey, and Nauru. Of thenations with no increase or a decrease inobesity, three of them (France, Italy, and Japan) continued to have the low levelsof obesity they experienced approximately 20 years ago and are economically ad-

vanced nations with excellent food secu-rity. The extensive emergence and rise of obesity among most of the worlds popu-lations indicate that the ability to becomeobese is universal (Lev-Ran 2001). Further-more, the great variation in obesity ratesbetween nations in the same regions withdifferent economic standing supports the view that increasing food security is but one component of the recent emergence of obesity.

Although previously a condition pre-dominantly of the wealthy, the relationshipbetween social class and obesity has be-come inverted in wealthier and economi-cally emerging nations (Sobal & Stunkard1989, Kirchengast et al. 2004, Rennie & Jebb2005, Stamatakis et al. 2005). Similar inver-sions are also found in urban areas of less-developed countries (Monteiro et al. 2000,Pe na & Bacallao 2002), as increased foodsecurity and sedentization of life have in-

creasingly permeated poorer sectors of soci-ety, as well as wealthier ones. Within more-afuent nations, minority populations andrural communities show the highest ratesof obesity (Swinburn et al. 2004). For ex-ample, obesity rates among adult Pacic Is-landers living in New Zealand in the early 1990s were above 65% (Swinburn et al.2004), compared with nationwide values of 15%. In theUnited States, Native Americans, African Americans, Puerto Ricans, and Mex-ican Americans have higher body mass thanEuropean Americans (Denney et al. 2004).Nearly 40% of black non-Hispanic adultshave a BMI above 30 kg/m2, much higherthan obesity rates for Mexican American and white non-Hispanic adults, who have ratesof 35% and 29%, respectively (Flegal et al.2002).

FATNESS AND HUMAN EVOLUTION Larger body mass and increased ability to ac-cumulate fat relative to other nonhuman pri-mates in seasonal environments are two key adaptive features of human life history (Aiello& Wells 2002). The rapid brain evolutionobserved with the emergence of Homo erec-tus at approximately 1.61.8 million years agois likely associated with increased body fat-ness as well as diet quality (Leonard et al.2003), i.e., the greater availability of animalfat and cholesterol that would have come withincreased diet quality, possibly facilitatingencephalization (Horrobin 1999). WhereasCunnane & Crawford (2003) proposed that the modern human brain was an outcomeof earlier natural selection for greater fat-ness in neonates and infants, Kuzawa (1998)has argued that the two phenomena co-evolved in feedback with each other. Regard-less of whether fatness preceded encephal-ization, greater levels of body fatness andreduced levelsof musclemass relative to otherprimate species allow human infants to ac-commodate brain growth by having adequatestored energy for brain metabolism when in-takeislimitedandbyreducingthetotalenergy costs of the rest of the body (Aiello & Wells2002). Compared with apes, humans have asimilarproportionofmaternaldailynonmain-tenance energy budget invested in fetal tissue,but humans have a much higher diet quality. This allows both larger brain size and higherbody fatness at birth (Ulijaszek 2002a). En-ergy stored in adipose tissue buffers against mortality risk soon after birth and at weaning, when nutrition is often disrupted (Kuzawa1998).

Fatness in human females is linked tofertility (Brown & Konner 1987, Norgan1997), female ovarian function being partic-ularly sensitive to energy balance and en-ergy ux (Ellison 2003). At any BMI, femaleshave a greater proportion of body weight as fat than males. Furthermore, they havea greater proportion of lower-body fat than

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males. This has importance in reproductivefunction: Lower-body fat is less-readily avail-able for everyday energetic needs than upper-body or abdominal fat, but lower-body fat is mobilized during pregnancy and lactation(Garaulet et al. 2000). Reproductive ef-fort during pregnancy and lactation is thus

buffered from environmental energetic con-straints (Ellison 2003).Human genetics are likely to have under-

gone selection for traits that promote energy intake and storage and minimize energy ex-penditure(Rosenbaum & Leibel 1998).Thereis great diversity in obesity-related genotypes(Perusse et al. 2005). However, the vast majority of obesity is related to more than one lo-cus, each accounting for only part of the phe-notypic variance (Comuzzie 2002). Because

all aspects of metabolism are under geneticcontrol, and the expression of obesity phe-notypes is much more limited than the ex-pression of peptides that regulate metabolism,natural selection for the capacity to save andstore energy is likely to have taken place fordifferent genes with the same phenotypic re-sult (Lev-Ran2001),perhaps ultimately to de-fend the energy needs of large brain size. Neelet al. (1998) argued that many different genesunderwent such selection in different popula-

tionsand geographicareas andunderdifferent kinds of environmental pressure. Against thismicroevolutionary scenario, that most mam-mals are able to overeat to high levels of body fatness suggests the genetic basis for the majority of human obesity lies in deeper evolu-tionary time, although the greater normativelevel of body fatness of humans relative toother primates and most mammals is likely to have evolved with the encephalization that took place with H. erectus .

Seasonality of food availability likely wasa major environmental pressure, given that it occurred during hominid evolution (Foley 1993) and is common in primate (Hladik 1988) and human subsistence ecologies of all kinds (de Garine & Harrison 1988). Hu-man genotypes for obesity, however, are not incompatible with present environments of

good food security and sedentary lifestygiven that the almost-worldwide increasin survivorship and longevity have takplace often in tandem with the emergence obesity (Eaton et al. 1998).

Because energy stores arevital to survivoship and reproduction, the ability to con

serve energyasadipose tissuewould have coferred selective advantage to Homo sapieNeel (1962) suggested the existence of thrigenotypes that code for efcient and potentially excessiveenergy accumulation.Thisfomulation has undergone modication, witalternative terms proposed for conditionassociated with genes for diabetes, obesiand hypertension considered to have beeadaptive in the remote past but now compromised by changed environments. Thes

terms include syndromes of impaired genethomeostasis, civilization syndromes, and tered lifestyle syndromes (Neel et al. 199Genes corresponding to such syndromes mabe called stockpiling (Garrow 1993), greedor acquisitive instead because little obesitycaused by thrifty metabolism (Lev-Ran 2001

The biological drives of feeding, hungand the dietary regulation of macronutrienintake may have shared physiological and bhavioral bases with other animals (Ulijasz

2002b, Berthoud 2004). Various mammals asusceptible to overeating and increased bodfat deposition when presented with diets thare plentiful, palatable, and/or high in fat, idicating that the tendency to overeat in rsponse to food-portion size, palatability, eergy density and to overeat fat passively general mammalian evolutionary traits. Futhermore, social aspects of feeding are ffrom unique to humans; the social facilittion of food intake (in which social interation during eating increases food intake) hlong been known to take place among animafrom chickens to primates.

Body size in the genus Homo was greatthan that of most australopithecines, and athough meat and nutritionally dense planfoods were the major dietary componenmost likely to have fueled body-size incre

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and encephalization in Homo (Plummer2004), decreased taste sensitivities associated with greaterbody size would have also favoredincreased diet breadth. Low sweetness andbitterness sensitivities allow larger primatespecies to nd food sources of lower-energy density palatable and to eat them more fre-

quently than among primate species of smallbody size (Simmen & Hladik 1998). Fur-thermore, basal metabolic rate per unit of body mass scales negatively with body weight among primates (Martin 1993), making theenergy requirement per unit of body sizelower in large primates than in small ones.

Human eating behavior differs from othermammalian species in the extent to which(a) food availability is controlled, (b) socialand cultural norms of diet and eating exist,

and (c ) personal feeding constraints operate(Ulijaszek 2002b). Social and cultural normsof diet and eating are likely to have increasedin complexity only with the emergence of complex symbolic behavior among H. sapiens by75,000yearsago(Henshilwoodetal.2004). With cooking, the emergence of cuisine, andincreased complexity of food use, great diversity in the social patterning of feeding hastaken place. Social feeding may have been abehavioral adaptation of early Homo that has

continued to have implications for the energy balance of contemporary human populations.

GENETICS OF OBESITY Various types of evidence have been used toidentify genetic contributions to human obe-sity. These include (a) familial clustering of body fatness (Allison et al. 1996), (b) esti-mates of heritability for obesity and fatnessphenotypes in twin studies (Stunkard et al.1986, Keller et al. 2003), (c ) identication of monogenic severe early-onset obesity (Flier2004), and (d ) genotyping of polygenic obe-sity (Clement et al. 2002).

The heritability of human adiposity (es-timated in most studies from BMI, but alsofrom skinfolds) varies from 0.49 to 0.93(Keller et al. 2003). Heritability of food in-

take is lower, generally varying between 0.11to 0.65 (Keller et al. 2003). With respect toeating behaviors and styles, heritabilities of 0.44 and 0.65 have been reported for mealfrequency and size, respectively (de Castro1999), 0.40 and 0.45 for disinhibition (Nealeet al. 2003, de Castro & Lilenfeld 2005), 0.44

for cognitive restraint, and 0.24 for perceivedhunger (de Castro & Lilenfeld 2005).Over 600 genes, markers, and chromoso-

mal regions have been associated with humanobesity phenotypes (Perusse et al. 2005), andthe numbers continue to grow. By October2004, 173 human obesity cases owing tosingle-gene mutations in 10 different geneshad been reported, whereas 49 loci relatedto Mendelian syndromes relevant to humanobesity had been mapped to a genomic re-

gion, with causal genes or strong candidategenes identied for most of them. Further-more, 204 quantitative trait loci (single genes with large effects on a given quantitative trait)forobesity-related phenotypes had been iden-tied from 50 genome-wide scans (Perusseet al. 2005). Several single-point mutationshave also been associated with various obesity phenotypes (Bouatia-Naji et al. 2006, Wilsonet al. 2006). At the population level, obesity is mainly polygenic, with genetic variations

inuencing metabolism. There are interac-tions of different obesity genes, and gene-dosage effects in heterozygotes of obesity genotypes, such that intermediate phenotypesare less extreme than homozygotes (Chung &Leibel 2005). Success in the identication of polygenic determinants of obesity across hu-man populations has been limited (Comuzzie2002), although genome-wide scans in differ-ent populations have localized major obesity loci on chromosomes 2, 5, 10, 11, and 20(Clement et al. 2002). The study of polygenicobesity requires the analysis of genotype-phenotype associations while taking into ac-count the inuence of environmental factorssuch as diet and sedentary lifestyle (Clement 2005). However, such an integrated approachrequires large samples and the expansionof biocomputing tools for the analysis of


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Adiposetissue

Energyexpenditure

Appetite &energy intake

Leptin - MSH

Brain

Neuronsexpressing

MC4R

POMCneuronLeptin

receptor

NPY/AGRPneuron

PC1

NPY

AGRP

Reproduction

Figure 2Genetic regulationof energy balanceby way of leptinsignaling andagouti relatedprotein (AGRP). Modied from Mizuno et al. 2003and Flier 2004. -MSH, -melanocytestimulatinghormone; MC4R,melanocortin 4receptor; NPY,neuropeptide Y;PC1, prohormoneconvertase 1;POMC, pro-opiomelanocortin.

multiple interactions with no a priori hy-potheses (Clement 2005).

Forover 50 years,monogenicrodent mod-els of obesity have been used widely in at-tempts to understand body-weight regulationin humans. Linkages between the genetic andphysiological study of obesity became possi-ble with the identication of (a) the ob geneproduct leptin (Zhang etal. 1994) and the lep-

tin receptor (Tartaglia et al. 1995), and (b) theagouti gene andagouti related protein (AGRP)(Zemel et al. 1995, Mizuno et al. 2003). Lep-tin is a cytokine secreted from adipose tissueat a rate proportional to the size of body-fat stores and is the principal physiological indi-cator of nutritional state and fatness. AGRP,along with neuropeptide Y (NPY) and -melanocyte stimulating hormone ( -MSH),is a central mediator of leptin action. Themelanocortin4receptor(MC4-R)playsacen-tral regulatory role in the action of leptinand is inuenced by levels of -MSH, NPY,and AGRP. The signaling pathways involv-ing leptin and MC4-R inuence the regula-tion of all aspects of energy balance (Barsh& Schwartz 2002, Fan et al. 2005). Severaltypes of monogenic human obesity owingto genetic disruption of the leptin-signaling

pathway identied more recently include dciency syndromes of leptin, leptin recetor, pro-opiomelanocortin (POMC), MC4R, and prohormone convertase 1 (Farooqi ORahilly 2005). These peptides function a central nervous system pathway for energbalance regulation (Figure 2 ) (Mizuno et a2003, Flier 2004). Although the mechanis whereby MC4R inuences food intake is re

sonably elaborated, its inuence on energexpenditure is not. However, in the QuebeFamily Study, Loos et al. (2005) have idened a DNA-sequence variation at the MC4gene locus that may contribute to physical iactivity. Although the major leptin-regulatorarm of this model accounts for less than 4of severe early-onset obesity, quantitative dferences in the expression or function of thessame genes, either alone or in combinatio with one another, may underlie the morcommon and genetically complex forms human obesity (Flier 2004).

PHYSIOLOGY AND BEHAVIOR Physiologically, obesity can only developfood consumption is high and/or energy ependiture is low, resulting in positive energ

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balance across months or years. A positive en-ergy balance of10%can lead to approximately a13.5-kgincreaseinbodyweightwithinayear(Bray 1987). The increasing rates of obesity among adults in many industrialized popula-tions across the second half of the twentiethcentury are a result of a disregulation of en-

ergy balance of less than 1% per year. Thephysiology of energy accumulation is that of neuroendocrine, gut- and adipose-tissue reg-ulation of energy balance, the maintenanceof which involves coordinated and physi-ologically linked changes in energy intakeand expenditure (Moore 2000). Both leptin-and melanocortin-signaling pathways are up-stream of nervous systemeffector mecha-nisms that regulate both appetite and energy expenditure (Flier 2004).

Much less is known about the neurophys-iological mechanisms by which reduced en-ergy expenditure inuences energy balancethan about altered appetite and energy bal-ance (Flier2004). There is no dominant phys-iological pathway of the desire to eat in rela-tion to nutritional requirement or environ-mental constraint of intake through availabil-ity. Rather, a range of physiological signalsregulates intake. Over 60 obesity-related pep-tidesareknown,many identiedaseitherpro-

moting increased or decreased energy intake. Various models have been put forward that link energy-balanceendocrinology of the gut,pancreas, adipose tissue to the central nervous system and the brain (Tschop et al. 2000,Schwartz & Morton 2002, Flier 2004), andFigure 3 gives a simplied consensus view.

In the absence of food (Figure 3 a ), thereare falling levels of leptin from adipose tis-sue, insulin from the pancreas, and peptide YY-36 from the gut, as well as increasinglevels of ghrelin from the gut and upregu-lated NPY/AGRP neurons in the hypotha-lamus, the physiological system that linksthe nervous and endocrine systems. Upreg-ulated NPY/AGRP neurons cause the releaseof NPY and AGRP that inhibit downstreamneurons in the paraventricular nucleus of thehypothalamus and the ventromedial hypotha-

lamus (often thought of as the satiety centerof the brain), stimulating appetite. Stimula-tion ofNPY/AGRP neurons also causescellu-lar and tissue growth and appetite-stimulatingeffects in the lateral hypothalamus, which inturn upregulate energy intake and downreg-ulate energy expenditure. Decreasing leptin

and insulin concentrations also lead to re-duced stimulation of POMC neurons, re-sulting in lowered secretion of -MSH inthe pituitary. -MSH is a secondary peptideproduct of the POMC gene, one of eight yielded by differential processing of the pri-mary peptide product of this gene. This inturn lowers its stimulation of the downstreamneurons in the hypothalamus. Inhibition of these downstream neurons reduces metabolicbreakdown of larger molecules to smaller

ones. The NPY/AGRP neurons are stimu-lated by starvation but are not signicantly affected by overfeeding (Figure 3 b ), whereasPOMC neurons are affected by both starva-tion and overfeeding. Thus there would havebeen stronger natural selection against starva-tion than overfeeding.

Other gut peptides involved in appetiteregulation include cholecystokinin (CCK),glucagon-like peptide 1, and bombesin-likepeptides (similar in structure to a family

of short peptides widely distributed amongmammals with potentphysiological effects onfeeding and satiety). Bombesin-like peptidesinclude gastrin-releasing peptide, originally named so for its ability to release gastrin inthe gut but also expressed in the pituitary gland, and neuromedin B, whose physiolog-ical effects include the regulation of feeding,blood pressure, blood glucose, body tempera-ture, and cellular growth. CCK is involved inthe control of the amountof food eaten at any time and is released from the small intestineinto the circulation in response to nutrientsin the lumen of the gut, such as fatty acids(Moran 2000). Glucagon-like peptide 1 is re-leased after feeding and produces loss of ap-petite (Yamamoto etal. 2002).Aswellas its in- volvement in the regulationof energybalance, MC4R has been implicated in the regulation


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Environmental factors associated with mod-ernlife andgood food security createconstant pressures on food intake that are not compen-sated by equivalent increases in energy expen-diture, withsurplusenergy stored overwhelm-ingly in adipose tissue (Berthoud 2004). Thismodel is a partial one, however, because food

intakeisdrivenbyadditionalcognitiveanden- vironmental factors (Berthoud 2004). At thelow end of the BMI distribution, consider-able research has been conducted on low foodintake and adaptation to low energy intakes(Waterlow 1990, Shetty 1993), showing en-ergy balance at low intakes to be strongly defended. The major components are feed-forward mechanisms between the brain andgut that anticipate thenutritional needs of thebody (Myers & Sclafani 2003) by respond-

ing to the abundance of food cues in food-secure and socially enhanced environments(deCastro & Stroebele2002,Ulijaszek2002b,Rolls2003). Such cues include perceivedqual-ities of potential foods, including (a) smell;(b) associations with pleasure, displeasure,or disgust; (c ) expectations from foods; and(d ) sensory properties while eating. Thus theneuroendocrine pathways regulating energy balance must intersect with systems regulat-ing pleasure and reward (Saper et al. 2002).

Leptin is known to inhibit sweet-sensitivetaste cells in the tongue (Kawai et al. 2000). Thus, when leptin levels increase (as in over-feeding), perception of the sweetness of fooddeclines and with it the range of food intakebecause of the reduced palatability of foods with sweetness as a component of their avor.Furthermore, the gut peptide CCK is a phys-iological satiety factor in humans. However,little else is known of the links between thepathways for pleasure and reward and thoseregulating hunger and satiety (Flier 2004).

Food cues involve learning because thereare few unlearned sensory preferences forfoods and taste among humans (Mela & Catt 1996). Although infants have innate prefer-ences for sweetness in food and aversions tosour and bitter tastes, food preferences aremolded from birth, both culturally and be-

haviorally. At any given time they are highly stable but are heavily determined by socialcontexts of eating, in addition to expectationsfrom foods prior to eating (Mela 1999). Inthe absence of food limitation in either vol-ume, weight, or energy, the most-powerfulbehavioral inuences on the amounts of food

eaten by humans include (a) other individu-als at a meal (de Castro 1999, Bell & Pliner2003, Wansink 2004), (b) television viewing(Stroebele & de Castro 2004), (c ) the size of food packages and portion sizes (Rolls et al.2004, Wansink 2004), (d ) palatability (Spitzer& Rodin 1981), (e) the energy density of food(Stubbs 1998), and ( f ) the consumption of caloricbeverageswithameal(DellaValleetal.2005). In all cases, the greater the size or doseof the inuence, the more is eaten. Inuences

on the energy intake and density of food eatenin societies where there is food insecurity in-clude (a) economic constraints (Darmon et al.2002, 2003; Drewnowski & Darmon 2005),(b) consumption of energy-containing bever-ages (Bray et al. 2004), (c ) passive overcon-sumption of fat in high-fat diets (Blundell &Stubbs1997),and(d )socialandculturalmores(de Garine & Pollock 1995). There remains,however, great within-population variation infood-consumption behavior not explained by

these factors. Both food novelty andpalatabil-ity play to powerful behavioral inuences onthe size of food intake. Many industrial foodproducts appeal to the palate as well as beingenergy dense,whereas therange of novel fooditems marketed in the industrializedworld hasincreased dramatically in the past 20 years.Furthermore, technology in suchsocietieshasnow divorced the sensory and nutritional at-tributes of foods in a way that prevents learn-ing by associative conditioning of palatabil-ity, appetite, and satiety (Stubbs & Whybrow 2004). The extent to which this uncouplingbetween sensory and nutritional properties of food isresponsible foroverconsumption isnot known, however (Stubbs & Whybrow 2004).

Two theories have been proposed to ex-plain between-individual differences in foodconsumption behaviors and the tendency to


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between the two has yet to be demonstrated(Gorely et al. 2004).

Fast food has characteristics that favorthe development of obesity, including itshigh-energy density, fat, and fructose content (Isganaitis & Lustig 2005), and Jebb (2003)has proposed a possible mechanistic link be-

tween fast foods, energy density, and obe-sity. However, Bandini et al. (1999) foundthat obese adolescents in the United Stateseat no more fast food than nonobese adoles-cents, emphasizing that excess energy intakemay come from a variety of food sources andnot solely from energy-dense snack foods. Al-though the globalization of fast food is be-ginning to affect childrens eating patterns inmany countries undergoing nutrition transi-tion, the contribution of fast food and soft

drinks to childrens diet remains relatively small compared with the United States (Adair& Popkin 2005).

Increasing time constraints on home cook-ing in food-secure nations also likely con-tribute to obesity rates because of high femaleengagement in the workforce (St-Onge et al.2003). A consequence of this has been theemergence and rise in demand for prepack-aged convenience foods with short prepa-ration times (Schluter & Lee 1999) and of

food consumption away from the home (Linet al. 1996, McCrory et al. 1999, Frenchet al. 2001, Nielsen et al. 2002, Critser 2003,St-Onge et al. 2003). Both phenomena haveincreased dependence on industrialized foodin many countries. Other time-saving devices(includingdrive-through, 24-hour, take-away,and home-delivery food services) have helpedmake food ubiquitous in everyday life in theUnited States (Brownell 2002) and increas-ingly elsewhere.

In the United States, Sweden, UnitedKingdom, Poland, and other industrializednations, the inverse relationship between so-cioeconomic status and obesity has been ex-plainedby class differences inobesity-relevant healthbehaviors that have persisted, with peo-ple of higher social class eating diets withlower fat content, exercising more, and being

more likely to diet to control weight (Jeffrey et al.1991, Molarius 2003, Bielicki et al.2005,Stamatakis et al. 2005). It has also been linkedto dietary energy density and energy cost (Darmon et al. 2002, French 2003). In theUnited States, the price of fresh fruit and veg-etableshasincreasedasaproportionofdispos-

able income across time, whereas the price of rened grains, sugars, and fats has declined(Sturm 2005). Diets that are more energy-dense are associated with lower daily foodconsumption costs (Drewnowski & Darmon2005). However, they also have lower effectson satiety and can result in passive overeatingand weight gain (Prentice & Poppitt 1996).Obesity may thus be linked with disparitiesin food choice because affordability and ac-cessibility to foods recommended or seen as

healthymaybe limited by nancialconstraintsin low-income groups. In an ecological study of obesity in 21 developed nations, Pickett et al. (2005) found income inequality to bepositively associated with energy intake andobesity.

Low levels of physical activity are as-sociated with an increased risk of obesity (Erlichman et al. 2002), and obesogenicenvironments not only discourage physicalactivity but also encourage inactivity both oc-

cupationally and during leisure time (Hill &Peters 1998, Brownell 2002, Hill & Wyatt 2005). There has been a great decline in oc-cupationally related activity since the turn of the twentieth century (Popkin et al. 2005). Inindustrialized nations and urban areas of developing countries, jobs requiring heavy man-ual labor have been largely replaced by jobsin service and high-technology sectors, whichrequire minimal physical exertion (Frenchet al. 2001). The increased use of automo-biles and public-transportation systems en-courages inactivity, whereas increased timespent watching television, playing electronicgames, and/or using computers has increasedsedentarybehaviorof bothadults andchildren(Hill & Peters 1998, Jeffrey & French 1998,Brownell2002). Obesity is uncommonamongoccupational groups that undertake high


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levels of physical activity during workinghours. In one population with high levelsof obesity, Keighley et al. (2006) found that adults in American Samoa engaged in farm work had lower BMIs than those not en-gaged in such work. In the United States andelsewhere, children participate less in phys-

ical activity at school (Hill & Peters 1998), whereasunsafeneighborhoods and limitedac-cess to recreation areas in some urban environments discourage leisure-time physicalactivity (Pucher & Dijkstra 2003).

Cultural variations of appropriate andpreferable body image (de Garine & Pollock 1995) also may have contributed to obesity rates. In some societies, larger body size hastraditionally been seen as attractive and in-dicative of attributes such as health, fertility,

beauty, wealth, and power. In a cross-culturalcomparison of appropriate body size in differ-ent traditional societies, Brown (1991) foundthat the vast majority favored plumpness asbeing attractive. Such societies include onesin Nauru, Samoa, and Malaysia (de Garine& Pollock 1995). Various societies across the world practice or have practiced ritual fat-tening to promote fertility, marriageability,and embodied social status. These includegroups in Africa, Central and North America

(MexicanAmericansandAfricanAmericansinparticular), Japan, and the Pacic (de Garine& Pollock 1995). Among these, only popula-tionsin thePacic nowexperiencewidespreadobesity.

Relationships between obesity and per-ceived attractiveness vary among communi-ties and societies. African American womenpreferbody size that is larger, on average, thansimilar groups of European American women(Stevens et al. 1994, Flynn & Fitzgibbon1998, Becker et al. 1999, Fitzgibbon et al.2000). Furthermore, overweight and obese AfricanAmericanwomen perceive themselvesas healthier, more attractive, and more attrac-tive to the opposite sex than white womenof similar weight and age (Stevens et al.1994, Flynn & Fitzgibbon 1998, Becker et al.1999), whereas European Americans experi-

ence dissatisfaction with their own body siat lowerBMIs thaneitherHispanicAmericanor African Americans (Fitzgibbon et al. 2000

Studies showing an increasedvalueof thinness and increased awareness of the risk ftors associated with overweight and obesisuggest that sociocultural factors, such as p

ticipation in the global economy and expsure to western ideas, may inuence bodimage perceptions worldwide. A number communities and societies in which obesihas risen in recent decades and that prevously were shown to desire and/or accelarger bodies and obesity now prefer thinnbodies (Madrigal et al. 2000, Anderson et 2002, Tur et al. 2005). This has been observeamong African American girls (Katz et 2004) and women with diabetes (Anders

et al. 1997, Lieberman et al. 2003), BritiBangladeshis with diabetes (Greenhalgh et 2005), Turkish adolescents (Canpolat et a2005), Pacic Islanders (Wilkinson et 1994, Craig et al. 1996, Brewis et al. 199Becker et al. 2005), the Ojibway-Cree Canada (Gittelsohn et al. 1996), urban Nativ American youth (Rinderknecht & Smi2002), and Korean children (Lee et al. 2004 Among Europeans, the desire for thinnbody size is increasingly observed in childr

and adolescents and is not conned to fmales of upper-socioeconomic status (Stoet al. 1995, Katz et al. 2004, Lee et al. 200Canpolat et al. 2005). Although high cultur valuation of body fatness may contribute theemergence ofobesity, itmaypossiblyceato be an important contributor in subsequengenerations.

CONCLUSIONS

Increasing rates of obesity across the worare broadly attributed to environments thaare obesogenic, against an evolutionary heitagethatismaladaptiveinthesenewcontext The extensive emergence and rise of obesamong most of the worlds populations indcate that the ability to become obese is un versal, whereas great variation in obesity rat

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across geographical regions indicates possi-ble population differences in genetic suscep-tibility to obesity. Human genetics are likely to have undergone selection for traits that promote energy intake and storage and that minimize energy expenditure, and there area great many obesity-related genotypes. Cur-

rent models linking genotypes with physiol-ogy and feeding behavior are only able to ex-plain a small proportion ofallobesity, but they may underlie the more-common and geneti-cally complex forms of human obesity. Stud-ies of the regulation of energy balance show that human physiology exerts strong controlof feeding under conditions of fasting or foodshortage, but only weak control on reducingfoodintake andincreasing energy expenditureunder conditions of replete energy stores and

good food security. Thus it isalmostinevitablethat obesity should have emerged as a majorhuman biological phenomenon in the envi-ronments that have been constructed in in-dustrialized nations over the past 60 years andthat have been transferred across the world with modernization since.

Because of the diverse contexts in whichobesity has emerged and the complex envi-ronments in which it persists, a ubiquitous re- versal in the prevalence of obesity at any stage

is unlikely in the near future. Any ceiling onthe potential for obesity in the majority of the worlds populations is clearly far from beingreached. However, we should avoid the dan-ger of extrapolating from the recent past intothefuturebecausepresent obesity patternsareoutcomes of conjoining forces: (a) a contin-uing economic development with compara-

tively few serious setbacks; (b) an increasedfood security for much of the worlds popula-tions, yet unchanged or signicantly declinedfoodsecurityfortherest;(c ) thepenetration of the world food system into the remotest partsof the world; (d ) declining prices for energy-dense foods; (e) the progressive mechaniza-

tion of the vast majority of labor-intensivetasks; ( f ) the urbanization and sedentizationof work in the form of service-oriented jobsas replacements for labor-intensive produc-tion jobs; ( g ) the mechanization of transport;and (h) the sedentization of leisure time. That humans have biological tendencies to maxi-mize food intake and use it efciently is clearand increasingly elaborated by physiologists,but the picture is still far from complete. Thehuman tendency to minimize energy expen-

diture where possible is well-known but evenless well understood biologicallythan food in-take. However, many of the economic trajec-tories of the second half of the twentieth cen-tury may be environmentally unsustainable(Parker 1993, Kasun 1999, von Geibler et al.2004) because they rely on ever-increasingconsumption of global resources. Economicsystems create and respond to markets, andthese will change as sustainability issues be-come more important and new technologies

emerge. These undoubtedly will be reectedin changes in human body size andnutritionalstatus into the future. If food security con-tinues to improve across the twenty-rst cen-tury, obesity rates possibly may at least sta-bilize in the richer nations, while emergingand increasing at greater rates in nations that emerge economically.

LITERATURE CITED

Adair LS, Popkin BM. 2005. Are child eating patterns being transformed globally? Obes . Res.13:128199

Ahima RS, Prabakaran D, Mantzoros C, Qu D, Lowell B, et al. 1996. Role of leptin in theneuroendocrine response to fasting. Nature 382:25052

Aiello LC, Wells JCK. 2002. Energetics and the evolution of the genus Homo. Annu. Rev. Anthropol. 31:32338

Allison DB, Faith MS, Nathan JS. 1996. Rischs lambda values for human obesity. Int. J. Obes. Relat. Metab. Disord. 20:99099


A

U


16/30


17/30

Campbell P, Ulijaszek SJ. 1994. Relationships between anthropometry and retrospective mor-bidity in poor men in Calcutta, India. Eur. J. Clin. Nutr. 48:50712

Canpolat BI, Orsel S, Akdemir A, Ozbay MH. 2005. The relationship between dieting andbody image, body ideal, self-perception, and body mass index in Turkish adolescents. Int. J. Eat. Disord. 37:15055

Chung WK, Leibel RL. 2005. Molecular physiology of syndromic obesities in humans. Trends Endocrinol. Metab. 16:26772

Clegg DJ, Woods SC. 2004. The physiology of obesity. Clin. Obs. Gynecol. 47:96779Clement K. 2005. Genetics of human obesity. Proc. Nutr. Soc. 64:13342Clement K, Boutin P, Froguel P. 2002. Genetics of obesity. Am. J. Pharmacogenomics 2:17787Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. 2000. Establishing a standard denition for

child overweight and obesity world wide: international survey. Br. Med. J. 320:124043Comuzzie AG. 2002. The emerging pattern of the genetic contribution to human obesity. Best

Pract. Res. Clin. Endocrinol. Metab. 16:61121Contaldo F, Pasanisi F. 2004. Obesity epidemics: secular trend or globalization consequence?

Beyond the interaction of genetic and environmental factors. Clin. Nutr. 23:28991Craig P, Swinburn B, Matenga-Smith T, Matangi H, Vaughan F. 1996. Do Polynesians still

believe that big is beautiful? Comparison of body size perceptions andpreferences of Cook

Islands, Maori and Australians. N. Z. Med. J. 14:2003Critser G. 2003. Fat Land . New York: Houghton MifinCrooks DL. 2003. Trading nutrition for education: nutritional status and the sale of snack

foods in an eastern Kentucky school. Med. Anthropol. Q. 17:18299Cunnane SC, Crawford MA. 2003. Survival of the fattest: fat babies were the key to evolution

of the large human brain. Comp. Biochem. Physiol. A Physiol. 136:1726Darmon N, Ferguson EL, Briend A. 2002. A cost constraint alone has adverse effects on food

selection and nutrient density: an analysis of human diets by linear programming. J. Nutr.132:376471

Darmon N, Ferguson EL, Briend A. 2003. Do economic constraints encourage the selectionof energy dense diets? Appetite 41:31522

Decarli B, Cavadini C, Grin J, Blondel-Lubrano A, Narring F, Michaud PA. 2000. Food andnutrient intakes in a group of 11 to 16-year-old Swiss teenagers. Int. J. Vitam. Nutr. Res.70:13947

de Castro JM. 1999. Measuring real world eating behavior. Prog. Obes. Res. 8:21521de Castro JM. 2006. Heredity inuences the dietary energy density of free-living humans.

Physiol. Behav. 87:19298de Castro JM, Lilenfeld LR. 2005. Inuence of heredity on dietary restraint, disinhibition, and

perceived hunger in humans. Nutrition 21:44655de Castro JM, Stroebele N. 2002. Food intake in the real world: implications for nutrition and

aging. Clin. Geriatr. Med. 18:68597de Garine I, Harrison GA, eds. 1988. Coping with Uncertainty in Food Supply. Oxford, UK:

Oxford Univ. Pressde Garine I, Pollock NJ. 1995. Social Aspects of Obesity. Amsterdam: Gordon & BreachDella Valle DM, Roe LS, Rolls BJ. 2005. Does the consumption of caloric and noncaloric

beverages with a meal affect energy intake? Appetite 44:18793Del Toro W, Greenberg BS. 1989. Television commercials and food orientations among

teenagers in Puerto Rico. Hisp. J. Behav. Sci. 11:16877Denney JT, Krueger PM, Rogers RG, Boardman JD. 2004. Race/ethnic and sex differentials

in body mass among US adults. Ethn. Dis. 14:38998


A

U


18/30

de Onis M. 2005. The use of anthropometry in the prevention of childhood overweight aobesity. United Nations Syst. Standing Comm. Nutr. 29:512

Dietz WH, Gortmaker SL. 1985. Do we fatten our children at the television set? Obesity atelevision viewing in children and adolescents. Pediatrics 75:80712

Dilberti N, Bordi PL, Concklin MT, Roe LS, Rolls BJ. 2004. Increased portion size leadsincreased consumption in a restaurant meal. Obes. Res. 12:56268

Drewnowski A, DarmonN. 2005. Theeconomicsof obesity: dietary energy density andenerg

cost. Am. J. Clin. Nutr. 82:S26573Drewnowski A, Popkin BM. 1997. The nutrition transition: newtrends in the global diet. Nut Rev. 55:3143

Dyson T. 1996. Population and Food . London: RoutledgeEaton SB, Konner M, Shostak M. 1998. Stone agers in the fast lane: chronic degenerat

diseases in evolutionary perspective. Am. J. Med. 84:73949Ellison PT. 2003. Energetics and reproductive effort. Am. J. Hum. Biol. 15:34251Erlichman J, Kerbey AL, James WPT. 2002. Physical activity and its impact on health o

comes. Paper 2: Prevention of unhealthy weight gain and obesity by physical activityanalysis of the evidence. Obes. Rev. 3:27387

Fan W, Voss A, Cao WH, Morrison SF. 2005. Regulation of thermogenesis by the centr

melanocortin system. Peptides 26:180013Farooqi IS, ORahilly S. 2005. Monogenic obesity in humans. Annu. Rev. Med. 56:44358Fisher JO, Rolls BJ, Birch LL. 2003. Childrens bite size and intake of an entr ee are greate

with large portions than with age-appropriate or self-selected portions. Am. J. Clin. Nut77:116470

Fitzgibbon ML, Blackman LR, Avellone ME. 2000. The relationship between body imadiscrepancy and body mass index across ethnic groups. Obes. Res. 8:58289

Flegal KM, Carroll MD, Ogden CL, Johnson CL. 2002. Prevalence and trends in obesiamong US adults, 19992000. J. Am. Med. Assoc. 288:172327

Flier JS. 2004. Obesity wars: molecular progress confronts an expanding epidemic. Ce116:33750

Flynn KJ, Fitzgibbon M. 1998. Body images and obesity risk among black females: a reviethe literature. Annu. Behav. Med. 20:1324

Foley RA. 1993. The inuence of seasonality on hominid evolution. In Seasonality and Hum Ecology, ed. SJ Ulijaszek, SS Strickland, pp. 1737. Cambridge, UK: Cambridge UnPress

French SA. 2003. Pricing effects on food choice. J. Nutr. 133:S84143French SA, Story M, Jeffrey RW. 2001. Environmental inuences on eating and physi

activity. Annu. Rev. Public Health 22:30935Garaulet MP, P erez-Llamas F, Fuente T, Zamora S, Tebar FJ. 2000. Anthropometric, com

puter tomography and fat cell data in an obese population: relationship with insullepton, tumor necrosis factor- , sex hormone-binding globulin and sex hormones. Eur. J Endocrinol. 143:65766

GarciaM, Kennedy E.1994.Assessingthe linkages between lowbody mass index andmorbidin adults: evidence from four developing countries. Eur. J. Clin. Nutr. 48(Suppl.): S909

Garrow JS. 1978. Energy Balance and Obesity in Man. Amsterdam: Elsevier. 2nd ed.Garrow JS.1993. Thethrifty genotypeandnoninsulin dependentdiabetes. Br. Med.J.306:933

34Geliebter A, Aversa A. 2003. Emotional eating in overweight, normalweight, and underweig

individuals. Eat. Disord. Resour. 3:34147

354 Ulijaszek Lonk

A

U


19/30

Gill TP. 2001. Cardiovascular risk in the Asia-Pacic region from a nutrition and metabolicpoint of view: abdominal obesity. Asia Pac. J. Clin. Nutr. 10:8589

Gittelsohn J, Harris SB, Thorne-Lyman AL, Hanley AJ, Barnie A, Zinman B. 1996. Body image concepts differ by age and sex in an Ojibway-Cree community in Canada. J. Nutr.126:29903000

Gorely T, Marshall SJ, Biddle SJ. 2004. Couch kids: correlates of television viewing among youth. Int. J. Behav. Med. 11:15263

Greenhalgh T, Chowdhury M, Wood G. 2005. Big is beautiful? A survey of body imageperception and its relation to health in British Bangladeshis with diabetes. Psychol. Health Med. 10:12638

Grifths PL, Bentley ME. 2001. The nutrition transition is underway in India. J. Nutr.131:2692700

Harnack LJ, Jeffery RW, Boutelle KN. 2000. Temporal trends in energy intake in the UnitedStates: an ecologic perspective. Am. J. Clin. Nutr. 71:147884

Henshilwood C, dErrico F, Vanhaeren M, van Niekerk K, Jacobs Z. 2004. Middle stone ageshell beads from South Africa. Science 304:404

Herman CP, Mack D. 1975. Restrained and unrestrained eating. J. Personality 43:64760Hill JO, Peters JC. 1998. Environmental contributions to the obesity epidemic. Science

280:137174Hill JO, Wyatt HR. 2005. Role of physical activity in preventing and treating obesity. J. Appl.

Physiol. 99:76570Hill JO, Wyatt HR, Reed GW, Peters JC. 2003. Obesity and the environment: Where do we

go from here? Science 299:85355Hladik CM. 1988. Seasonal variations in food supply for wild primates. In Coping with Uncer-

tainty in Food Supply, ed. I de Garine, GA Harrison, pp. 125. Oxford, UK: Oxford Univ.Press

Horrobin DF. 1999. Lipid metabolism, human evolution and schizophrenia. Prostaglandins Leukot. Essent. Fatty Acids 60:43137

Isganaitis E, LustigRH. 2005.Fast food, central nervous system insulin resistance, andobesity. Arterioscler. Thromb. Vasc. Biol. 25:245162

Jahns L, Siega-Riz AM, Popkin BM. 2001. The increasing prevalence of snacking among USchildren from 1977 to 1996. J. Pediatr. 138:49398

Jebb SA. 2003. Fast foods, energy density and obesity: a possible mechanistic link. Obes. Rev.4:18794

JeffreyRE,FrenchSA. 1998.Epidemicobesity in the UnitedStates:Are fast foodsand television viewing contributing? Am. J. Public Health 88:27780

Jeffrey RW, French SA, Firster JL, Spry VM. 1991. Socioeconomic status differences in healthbehaviors related to obesitythe healthy worker project. Int. J. Obes. 15:68996

Kahn HS, Williamson DF. 1994. Abdominal obesity and mortality risk among men in nine-teenth century North America. Int. J. Obes. 18:68691

Kasun JR. 1999. Doomsday every day: sustainable economics, sustainable tyranny. Independent Rev. 4:91106

Katz ML, Gorden-Larsen P, Bentley ME, Kelsey K, Shields K, Ammerman A. 2004. Doesskinny mean healthy? Perceived ideal, current, and healthy body sizes among African- American girls and their female caregiver. Ethn. Dis. 14:53341

Kawai K, Sugimoto K, Nakashima K, Miura H, Ninomiya Y. 2000. Leptin as a modulator of sweet taste sensitivities in mice. Proc. Natl. Acad. Sci. USA 97:1104449

Keighley ED,McGarvey ST,Turituri P, VialS. 2006.Farming and adiposity in Samoan adults. Am. J. Hum. Biol. 18:11222


A

U


20/30

Keller KI, Pietrobelli, Faith MS. 2003. Genetics of food intake and body composition: lessfrom twin studies. Acta Diabetol. 40:S95100

Kirchengast S, Schober E, Waldhor T, Sefranek R. 2004. Regional and social differencesbody mass index, and the prevalence of overweight and obesity among 18-year-old min Austria between the years 1985 and 2000. Coll. Antropol. 28:54152

Kral TV, Rolls BJ. 2004. Energy density and portion size: their independent and combineffects on energy intake. Physiol. Behav. 82:13138

Kuzawa CW. 1998. Adipose tissue in human infancy and childhood: an evolutionary persptive. Am. J. Phys. Anthropol. 27(Suppl.):177209Lee K, Sohn H, Lee S, Lee J. 2004. Weight and BMI over 6 years in Korean children: re

tionships to body image and weight loss efforts. Obes. Res. 13:195966Leonard WR, Robertson ML, Snodgrass JJ, Kuzawa CW. 2003. Metabolic correlates of h

minid brain evolution. Comp. Biochem. Physiol. A Physiol. 136:515Levitsky DA,Obarzanek E,MrdjenovicG, StruppBJ.2005.Imprecisecontrol of energy intak

absence of a reduction in food intake followingoverfeeding in young adults. Physiol. Beh84:66975

Levitsky DA, Youn T. 2004. The more young adults are served, the more they overeat. J. Nutr134:254649

Lev-Ran A. 2001. Human obesity: an evolutionary approach to understanding our bulgi waistline. Diabetes Metab. Res. Rev. 17:34762Li G, Chen X, Jang Y, Wang J, Xing X, et al. 2002. Obesity, coronary heart disease risk fac

and diabetes in Chinese: an approach to the criteria of obesity in the Chinese populatiObes. Rev. 3:16772

Lieberman LS, Probart CK, Schoenberg NE. 2003. Body image among older, rural, Africa American women with type 2 diabetes. Coll. Antropol. 27:7986

Lin B, Guthrie J, Blaylock JR. 1996. The diets of Americas children: inuences on dining household characteristics, and nutritional knowledge. Agric. Econ. Rep. 746:137

Loos RJF, RankinenT,Tremblay A,Perusse L,ChagnonY, BouchardC. 2005.Melanocortin-4receptor gene and physical activity in the Quebec Family Study. Int. J. Obes. 29:42028

MadrigalH, Sanchez-Villegas A, Martinez-Gonzalez MA, Kearney J, Gibney MJ, Irala J. 200Underestimation of body mass index through perceived body image as compared to sreported body mass index in the European Union. Public Health 114:46873

Martin RD. 1993. Scaling. In The Cambridge Encyclopedia of Human Evolution, ed. S Jones, Martin, D Pilbeam, p. 42. Cambridge, UK: Cambridge Univ. Press

McConahy KL, Smiciklas-Wright H, Birch LL, Mitchell DC, Picciano MF. 2002. Food potions are positively related to energy intake and body weight in early childhood. J. Pediat140:34047

McConahy KL, Smiciklas-Wright H, Mitchell DC, Picciano MF. 2004. Portion size of common foods predicts energy intake among preschool-aged children. J. Am. Diet. Ass104:97579

McCrory MA, Fuss PJ, Hays NP, Vinken AG, Greenberg AS, Roberts SB. 1999. Overeatin America. Association between restaurant food consumption and body fatness in healtadult men and women ages 19 to 80. Obes. Res. 7:56471

Mela DJ. 1996. Eating behavior, food preferences and dietary intake in relation to obesity body-weight status. Proc. Nutr. Soc. 55:80316

Mela DJ. 1999. Food choice and intake: the human factor. Proc. Nutr. Soc. 58:51321 Mela DJ, Catt S. 1996. Ontogeny of human taste and smell preferences and their i

plications for food selection. In Long-Term Consequences of Early Environment: Gr

356 Ulijaszek Lonk

A

U


21/30

Development and the Lifespan Developmental Perspective, ed. CJK Henry, SJ Ulijaszek,pp. 13954. Cambridge, UK: Cambridge Univ. Press

Mizuno TM, Makimura H, Mobbs CV. 2003. The physiological function of the agouti-relatedpeptide gene: the control of weight and metabolic rate. Ann. Med. 35:42533

Molarius A. 2003. The contribution of lifestyle factors to socioeconomic differences in obesity in men and women: a population-based study in Sweden. Eur. J. Epidemiol. 18:22734

Monteiro CA, DA-Benicio MH, Conde WL, Popkin BM. 2000. Shifting obesity trends in

Brazil. Eur. J. Clin. Nutr. 54:34246 Moore MS. 2000. Interactions between physical activity and diet in the regulation of body weight. Proc. Nutr. Soc. 59:19398

Moran TH. 2000. Cholecystokinin and satiety: current perspectives. Nutrition 16:85865 Mrdjenovic G, Levitsky DA. 2005. Children eat what they are served: the imprecise regulation

of energy intake. Appetite 44:27382 Myers KP, Sclafani A. 2003. Conditioned acceptance and preference but not altered taste

reactivity responses to bitter and sour avors paired with intragastric glucose infusion. Physiol. Behav. 78:17383

Neale BM, Mazzeo SE, Bulik CM. 2003. A twin study of dietary restraint, disinhibition andhunger: an examination of the eating inventory (three factor eating questionnaire). Twin Res. 6:47178

Neel J. 1962. Diabetes mellitus: a thrifty genotype rendered detrimental by progress? Am. J. Hum. Genet. 14:35362

Neel JV, Weder AB, Julius S. 1998. Type II diabetes, essential hypertension, and obesity assyndromes of impaired genetic homeostasis: The thrifty genotype hypothesis entersthe 21st century. Perspect. Biol. Med. 42:4474

Nielsen SJ, Siega-riz AM, Popkin BM. 2002. Trends in energy intake in U.S. between 1977and 1996: Similar shifts seen across age groups. Obes. Res. 10:37078

Nishida C, Mucavele P. 2005. Monitoring the rapidly emerging public health problem of overweight and obesity: the WHO global database on body mass index. United Nations Syst. Standing Comm. Nutr. 29:512

Norgan NG. 1994a. Population differences in body composition in relation to the BMI. Eur. J. Clin. Nutr. 48(Suppl.):S1027

Norgan NG. 1994b. Relative sitting heightand the interpretation of thebody mass index. Ann. Hum. Biol. 21:7982

Norgan NG. 1997. The benecial effects of body fat and adipose tissue in humans. Int. J. Obes. Relat. Metab. Disord. 21:73846

Parker K. 1993. Economics, sustainable growth, and community. Environ. Values 2:23345Pe na M, Bacallao J. 2002. Malnutrition and poverty. Annu. Rev. Nutr. 22:24153Perusse L, Rankinen T, Zuberi A, Chagnon YC, Weisnagel SJ, et al. 2005. Human obesity

gene map: the 2004 update. Obes. Res. 13:381490Pickett KE, Kelly S, Brunner E, Lobstein T, Wilkinson RG. 2005. Wider income gaps, wider

waistbands? An ecological study of obesity and income inequality. J. Epidemiol. Comm. Health 59:67074

Plummer T. 2004. Flaked stones and old bones: biological and cultural evolution at the dawnof technology. Am. J. Phys. Anthropol. 125(Suppl.):11864

Popkin BM. 2004. The nutrition transition: an overview of world patterns of change. Nutr. Rev. 62:S14043

Popkin BM, Doak CM. 1998. Obesity is a worldwide phenomenon. Nutr. Rev. 56:10614Popkin BM, Duffey K, Gorden-Larsen P. 2005. Environmental inuences on food choice,

physical activity and energy balance. Physiol. Behav. 86:60313


A

U


22/30

PoskittEME.1995.Assessmentofbodycompositionintheobese.InBodyCompositionTechniin Health and Disease, ed. PSW Davies, TJ Cole, pp. 14655. Cambridge, UK: CambridUniv. Press

Prentice AM, Poppitt SD. 1996. Importance of ED and macronutrients in the regulation energy intake. Int. J. Obes. Metab. Disord. 20:S1823

Pucher J, Dijkstra L. 2003. Promoting safe walking and cycling improve public health: lessfrom The Netherlands and Germany. Am. J. Public Health 93:150916

Renders CM, Henneman L, Timmermans DR, Hirasing RA. 2004. Television watching ansome eating habits of 614 year-old children in Amsterdam, the Netherlands; a crsectional study. Ned. Tijdschr. Geneeskd. 148:207276

Rennie KL, Jebb SA. 2005. Prevalence of obesity in Great Britain. Obes. Rev. 6:1112Rinderknecht K,Smith C.2002.Body imageperceptionsamong urban NativeAmerican yout

Obes. Res. 10:31527Rolls BJ. 2003. The supersizing of America: portion size and the obesity epidemic. Nutr. Toda

38:4253RollsBJ,RoeLS,KralTV,MeengsJS,WallDE.2004.Increasingtheportionsizeofapackaged

snack increases energy intake in men and women. Appetite 42:6369Rosenbaum M, Leibel RL. 1998. The physiology of body weight regulation: relevance to

etiology of obesity in children. Pediatrics 101:52539Samuelson G. 2000. Dietary habits and nutritional status in adolescents over Europe. overview of current studies in the Nordic countries. Eur. J. Clin. Nutr. 54(Suppl. 1):S228

Saper CB, Chou TC, Elmquist JK. 2002. The need to feed: homeostatic and hedonic controf eating. Neuron 36:199211

Schachter S, Rodin J. 1974. Obese Humans and Rats . Washington, DC: Erlbaum/HalstedSchioth HB, Lagerstrom MC, Watanobe H, Jonsson L, Vergoni AV, et al. 2003. Functiona

role, structure, and evolution of the melanocortin-4 receptor. Ann. N.Y. Acad. Sci. 994:7483

Schluter G, Lee C. 1999. Changing good consumption patterns: their effects of the US fo

system, 197292. Food Rev. 22:3537Schwartz MW, Morton GJ. 2002. Obesity: keeping hunger at bay. Nature 418:59597Shetty PS. 1993. Chronic undernutrition and metabolic adaptation. Proc. Nutr. Soc. 52:2678Shetty PS, James WPT. 1994. Body Mass Index: A Measure of Chronic Energy Deciency in

Rome: Food Agric. Org.Shuldiner AR, Munir KM. 2003. Genetics of obesity: more complicated than initially thoug

Lipids 38:97101Simmen B, Hladik CM. 1998. Sweet and bitter taste discrimination in primates: scaling effe

across species. Folia Primatol. 69:12938Smiciklas-Wright H, Mitchell DC, Mickle SJ, Goldman JD, Cook A. 2003. Foods common

eaten in the United States, 19891991 and 19941996: Are portion sizes changing? J. AmDiet. Assoc. 103:4147

Sobal J, Stunkard AJ. 1989.Socioeconomic statusandobesity: a reviewof the literature. PsychBull. 105:26075

Spitzer L, Rodin J. 1981. Human eating behavior: a critical review of studies in normal weand overweight individuals. Appetite 2:293329

Stamatakis E, Primatesta P, Chinn S, Rona R, Falascheti E. 2005. Overweight and obestrends from 1974 to 2003 in English children: What is the role of socioeconomic facto Arch. Dis. Child. 90:9991004

358 Ulijaszek Lonk

A

U


23/30

Stevens J, Kumanyika SK, Keil JE. 1994. Attitudes toward body size and dieting: differencesbetween elderly black and white women. Am. J. Public Health. 84(8):132225

St-Onge M, Keller KL, Heymseld SB. 2003. Changes in childhood food consumption pat-terns:a cause forconcern in lightof increasing body weights. Am. J. Clin. Nutr. 78:106873

Story M, French SA, Resnick MD, Blum RW. 1995. Ethnic/racial and socioeconomic differ-ences in dieting behaviors and body image perceptions in adolescents. Int. J. Eat. Disord.18:17379

Stroebele N, de Castro JM. 2004. Television viewing is associated with an increase in mealfrequency in humans. Appetite 42:11113Stubbs RJ. 1998. Appetite feeding behavior and energy balance in human subjects. Nutr. Rev.

57:116Stubbs RJ, Whybrow S. 2004. Energy density, diet composition and palatability: inuences on

overall food energy intake in humans. Physiol. Behav. 81:75564Stunkard AJ, Fock TT, Hrubec Z. 1986. A twin study of human obesity. J. Am. Med. Assoc.

256:5154Sturm R. 2005. Childhood obesitywhat we can learn from existing data on societal trends,

part 2. Prev. Chronic Dis. 2:A20SullivanDR.2001.Cardiovascularrisk in theAsia-Pacicregion from a nutritionand metabolic

point of view: visceral obesity. Asia Pac. J. Clin. Nutr. 10:8284Swinburn BA, Caterson I, Seidell JC, James WPT. 2004. Diet, nutrition and prevention of

excess weight gain and obesity. Public Health Nutr. 7:12346Swinburn BA, Egger G, Raza F. 1999. Dissecting obesogenic environments: the development

and application of a framework for identifying and prioritizing environmental interven-tions for obesity. Prev. Med. 29:56370

Tartaglia LA, Dembski M, Weng X, Deng N, Culpepper J, et al. 1995. Identication andexpression cloning of a leptin receptor, OB-R. Cell 83:126371

Trowell H. 1975. Obesity in the Western world. Plant Foods Man 1:15765 Tschop M, Smiley DL, Heiman ML. 2000. Ghrelin induces adiposity in rodents. Nature

407:90813 Tucker LA, Bagwell MRN. 1991. Television viewing and obesity in adult females. Am. J. Public

Health 81:90811 Tucker LA, Friedman GM. 1989. Television viewing and obesity in adult males. Am. J. Public

Health 79:51618 Tur JA, Serra-Majem L, Romaguera D, Pons A. 2005. Prole of overweight and obese people

in a Mediterranean region. Obes. Res. 13:52736Ulijaszek SJ. 2002a. The comparative energetics of primate fetal growth. Am. J. Hum. Biol.

14:6038Ulijaszek SJ. 2002b. Human feeding from an evolutionary ecological perspective. Proc. Nutr.

Soc. 61:51726Ulijaszek SJ. 2005. Modernisation, migration, and nutritional health of Pacic Island popula-

tions. Environ. Sci. 12:16776 van den Bulck J, van Mierlo J. 2004. Energy intake associated with television viewing in ado-

lescents, a cross sectional study. Appetite 43:18184 von Geibler J, KuhndtM, SeifertE, LucasR, Lorek S, BleischwitzR. 2004.Sustainablebusiness

and consumption strategies. In Eco-Efciency, Regulation and Sustainable Business: Towards a Governance Structure for Sustainable Development , ed. R Bleischwitz, P Hennicke, pp.11664. ESRI Stud. Ser. Environ. Cheltenham, UK: Elgar

Wahlqvist ML. 2001. Nutrition and diabetes in the Asia-Pacic region with reference to car-diovascular disease. Asia Pac. J. Clin. Nutr. 10:9096


A

U


24/30

Wansink B. 2004. Environmentalfactors that increase the food intake and consumptionvolumof unknowing consumers. Annu. Rev. Nutr. 24:45579

Wansink B, Cheney MM. 2005. Super bowls: serving bowl size and food consumption. Obe Res. 293:172728

Waterlow JC. 1990. Mechanisms of adaptation to low energy intakes. In Diet and Disease, edGA Harrison, JC Waterlow, pp. 523. Cambridge, UK: Cambridge Univ. Press

Wilkinson J, Ben-Tovim D, Walker M. 1994. An insight into the personal signicance of weigh

and shape in large Samoan women. Int. J. Obes. Relat. Metab. Disord. 18:6026 Wilson SG, Adam G, Langdown M, Reneland R, Braun A, et al. 2006. Linkage and potenassociation of obesity-related phenotypes with two genes on chromosome 12q24 ifemale dizygous twin cohort. Eur. J. Hum. Genet. 14:34043

World Health Organization. 2000. Obesity: preventing and managing the global epidemWHO Tech. Rep. Ser., No. 894. Geneva

Yamamoto H, Lee CE, Marcus JN, Williams TD, Overton JM, et al. 2002. Glucagon-lipeptide-1 receptor stimulation increases blood pressure and heart rate and activates aunomic regulatory neurons. J. Clin. Invest. 110:4352

Young LR, Nestle M. 2002. The contribution of expanding portion sizes to the US obesepidemic. Am. J. Public Health 92:24649

Zemel MB, Kim JH, Woychik RP, Michaud EJ, Kadwell SH, et al. 1995. Agouti regulationintracellular calcium: role in the insulin resistance of viable yellow mice. Proc. Natl. AcSci. USA 92:473337

Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. 1994. Positional clonof the mouse obese gene and its human homologue. Nature 372:42532

Zizza C, Siega-Riz AM, Popkin BM. 2001. Signicant increase in young adults snackbetween 19771978 and 19941996 represents a cause for concern! Prev. Med. 32:3031

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Annual Review Anthropology

Volume 35, 20

Contents

Prefatory Chapter

On the Resilience of Anthropological Archaeology Kent V. Flannery 1

Archaeology

Archaeology of Overshoot and Collapse Joseph A. Tainter 59

Archaeology and Texts: Subservience or Enlightenment John Moreland 135

Alcohol: Anthropological/Archaeological Perspectives Michael Dietler 229

Early Mainland Southeast Asian Landscapes in the First Millennium a.d. Miriam T. Stark 407

The Maya CodicesGabrielle Vail 497

Biological Anthropology

What Cultural Primatology Can Tell Anthropologists about theEvolution of CultureSusan E. Perry 171

Diet in Early Homo: A Review of the Evidence and a New Model of Adaptive Versatility Peter S. Ungar, Frederick E. Grine, and Mark F. Teaford 209

Obesity in Biocultural PerspectiveStanley J. Ulijaszek and Hayley Lonk 337

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Evolution of the Size and Functional Areas of the Human Brain P. Thomas Schoenemann

Linguistics and Communicative Practices

Mayan Historical Linguistics and Epigraphy: A New Synthesis

Sren Wichmann Environmental Discourses

Peter M uhlh ausler and Adrian Peace

Old Wine, New Ethnographic Lexicography Michael Silverstein

International Anthropology and Regional Studies

The Ethnography of Finland Jukka Siikala

Sociocultural Anthropology

The Anthropology of Money Bill Maurer

Food and Globalization Lynne Phillips

The Research Program of Historical Ecology William Bale

Anthropology and International Law Sally Engle Merry

Institutional Failure in Resource Management James M. Acheson

Indigenous People and Environmental Politics Michael R. Dove

Parks and Peoples: The Social Impact of Protected Areas Paige West, James Igoe, and Dan Brockington

Sovereignty RevisitedThomas Blom Hansen and Finn Stepputat

Local Knowledge and Memory in Biodiversity ConservationVirginia D. Nazarea

x Contents

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Food and Memory Jon D. Holtzman 361

Creolization and Its DiscontentsStephan Palmi 433

Persistent Hunger: Perspectives on Vulnerability, Famine, and FoodSecurity in Sub-Saharan Africa Mamadou Baro and Tara F. Deubel 521

Theme 1: Environmental Conservation

Archaeology of Overshoot and Collapse Joseph A. Tainter 59

The Research Program of Historical Ecology William Bale 75

Institutional Failure in Resource Management James M. Acheson 117

Indigenous People and Environmental Politics Michael R. Dove 191

Parks and Peoples: The Social Impact of Protected Areas Paige West, James Igoe, and Dan Brockington 251

Local Knowledge and Memory in Biodiversity ConservationVirginia D. Nazarea 317

Environmental Discourses Peter Mhlhusler and Adrian Peace 457

Theme 2: Food

Food and Globalization Lynne Phillips 37

Diet in Early Homo: A Review of the Evidence and a New Model of Adaptive Versatility Peter S. Ungar, Frederick E. Grine, and Mark F. Teaford 209

Alcohol: Anthropological/Archaeological Perspectives Michael Dietler 229

Obesity in Biocultural PerspectiveStanley J. Ulijaszek and Hayley Lonk 337

Food and Memory Jon D. Holtzman 361

Contents x i

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Old Wine, New Ethnographic Lexicography Michael Silverstein

Persistent Hunger: Perspectives on Vulnerability, Famine, and FoodSecurity in Sub-Saharan Africa Mamadou Baro and Tara F. Deubel

Indexes

Subject Index

Cumulative Index of Contributing Authors, Volumes 2735

Cumulative Index of Chapter Titles, Volumes 2735

Errata

An online log of corrections to Annual Review of Anthropology chapters (if any, 1997the present) may be found at http://anthro.annualreviews.org/errata.shtml

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