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The Influence of Sedentism and Aggregation on Porotic Hyperostosis and Anaemia: A Case Study Author(s): Susan Kent Source: Man, New Series, Vol. 21, No. 4 (Dec., 1986), pp. 605-636 Published by: Royal Anthropological Institute of Great Britain and Ireland Stable URL: http://www.jstor.org/stable/2802900 Accessed: 09/12/2010 05:02

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http://www.jstor.org THE INFLUENCE OF SEDENTISM AND AGGREGATION ON POROTIC HYPEROSTOSIS AND ANAEMIA: A CASE STUDY

SUSAN KENT Old DominionUniversity Norfolk,Virginia

Porotichyperostosis and iron deficiencyanaemia are oftenthought to be thedirect result of a low irondiet, and by implication,a dietlow in meat. A case studyusing the prehistoric Anasazi fromthe North American Southwest, however, shows dietto be virtuallyinconsequential in the risein frequencyof porotic hyperostosis and chroniciron deficiency anaemia. Instead, it is shown thatthe effects of sedentismand aggregationresult in an increasein viral,bacterial and parasitic diseases, all of which can significantlycontribute to the incidenceof porotichyperostosis by causingchronic iron deficiency anaemia. The increasingfrequency of thistype of anaemiain the Southwestand elsewherethrough time is a directresult of the rise of sedentaryaggregated communities.

What do skeletalpopulations from the southwesternpart of the United States have in common with those fromSubsaharan Africa, , Greece, Qatal Hiiyiik in Turkey and the Yucatan Peninsula of Mexico? Each population containsskulls thatexhibit varying degrees of porotichyperostosis. Porotic hyperostosisis a descriptiveterm for the cranial lesions that are characterisedby a sieve-likeporosity involving parts of the outer skull (Moseley I965; I966: I2I). The explanationoften given forthe presenceof porotichyperostosis on skullsfrom Greece and the earlyNeolithic village of Catal Hiiyiik,Turkey is thalassaemia,one of thehereditary anaemias known to produceporotic hyper- ostosis(Angel I967: 387; I97 Ia: I I0; I97 Ib). That foundin Africais attributedto sickle cell anaemia (Steinbock I976: 235). Its high occurrencein prehistoric Mexican Mayans and southwesternNorth AmericanAnasazi populationsis explainedas the resultof a maize dependentdiet (firstsuggested by Hooton I 930: 3 I 7; later by Schuette I 979: 62; Ryan I 977; and others). Porotic hyperosto- sis is not restrictedto thesegeographical areas, but has been identifiedin skulls fromprehistoric Nubia (Carlson etal. I 974), Peru (HrdlickaI 9 I 4), and Mexico (Hooton I 940). It is also temporallywidespread, ranging from a few,extremely rareoccurrences in thePalaeolithic (Anderson I968), to theMesolithic (Janssens I970), to the (Angel I967), to theBronze Age (Cule & Evans I968), and up to the present(Powell et al. I965). It appearsto increasein frequency fromPalaeolithic and Mesolithicpopulations to modernones. There has been muchdebate over thecauses of porotichyperostosis (e.g., as

Man (N.S.) 21, 605-36 6o6 SUSAN KENT

early as in the I920'S, Williams I929: 852-5; also sometimes called cribia orbitaliaor symmetricalosteoporosis). Anaemia of varioustypes is most often cited as the causal agent. In the Mediterraneanregions and Africa, causal explanationsare relativelyeasy to posit-thalassaemia or sickle cell anaemia, dependingon thegeographical location. The above hereditaryanaemias do not always providesatisfying explanations, however, as in the case of prehistoric remainsfrom Italy where other factors are postulated(cf. Germana& Ascenzi I980). Most scientists,especially when describing New Worldmaterial, ascribe thecranial deformation to irondeficiency anaemia (cf. Huss-Ashmore et al. I982; Moseley I965; Saul I973), whichis attributedto nutritionaldeficiencies (e.g., El-Najar I977; Moodie I923a and b: I26; Pelto & Pelto I983: I77-82; and others). Chronic iron deficiencyanaemia in hospitalisedyoung childrenhas been documentedas causingporotic hyperostosis visible in roentgenogramsof eight- to twelve-monthold infants(Shahidi & Diamond I960). Porotichyperostosis was also visible in roentgenogramsof slightlyolder childrenwith iron de- ficiencyanaemia, specificallyin a I7-month-oldand I2-year-old,as well as others(Powell et al. I965). The assumedrelationship of dietarystress leading to irondeficiency anaemia producingporotic hyperostosis is a common one. For example,in prehistoric skeletalpopulations from the Isthmusof Panama which exhibitan increasein thefrequency of infections and porotic hyperostosis through time, 'The increase in porotichyperostosis can be relatedto the greaterdependence on a limited numberof dietary resources, primarily maize. The increasein infectionrate over time can, in the two agriculturalpopulations, be associated with a greater dependenceon fewerdietary resources and a resultingdecrease in thenutritional qualityof thediet' (Norr I984: 484). I propose that other factors specificallythe aggregationof people and sedentism-are responsiblefor the existenceof porotichyperostosis in many parts of the world. The following concentrateson a case study from the prehistoricsouthwestern region of the United States. In those areas of the Southwestoccupied by Anasazi (othergroups will not be examinedhere), iron deficiencyanaemia as theresult of a maize-dependentdiet has beenpostulated as the cause of porotic hyperostosisas exhibitedin skeletalpopulations (e.g., El-Najarn.d.; El-Najjar& RobertsonI976; Kelly I980; Ryan I977; and others). These authorssupport their contention by the factthat iron absorptionfrom maize is poor (e.g., El-Najjar I977; El-Najjar et al. I976). Studieshave focused on the increasedincidence of the disease throughtime, from Archaic hunting and gatheringpopulations to latermaize agriculturalAnasazi (see Kelley I980) and are based on thesupposition that later Anasazi consumed less meatthan did earlierones (e.g., Ryan I977). Using data fromthe Anasazi site of Arroyo Hondo in the Rio GrandeRiver Valley, New Mexico, Palkovich (I984: 436) statesthat the adoption of intensive led to marginal'diets in average years [that]were virtuallystarvation diets in droughtyears, which led to the ultimateabandonment of the [Arroyo Hondo] village.Thus, bufferingmechan- isms of settlementpatterns and agriculturalstrategies could not softenthe biologicalimpact of poor dietson theArroyo Hondo population.' SUSAN KENT 607 The followingshows thatspecifically maize, and dietin general,are at most onlyincidental causes of porotichyperostosis in theSouthwest region. In some areas, deficientdiets may exacerbatethe occurrenceof nutritionaliron defic- iencyanaemia, but an agriculturallydominant and low meatdiet was nota factor producingthe porotic hyperostosis found in southwesternskeletal populations. Instead,I proposethat the widespread prevalence of porotichyperostosis in the Southwestresults from population sedentism and aggregation.Aggregation is used here to mean hamlets or larger groupings.This is the common link between such geographicallyand temporallydisparate loci of the disease as prehistoricEgypt, Italy,Peru and the North Americanarctic, southwest and easternregions. The generalidea is not necessarilynovel (e.g., Armelagos& Dervey I970; Milner I983; Scrimshawet al. I968; Smithet al. I984: 20). That otherfactors than diet must be involved in producingthe porotic hyperostosisfound in prehistoricsouthwestern skeletal populations and its generalincrease through time has been noted by fewerauthors (for exceptions see Martinet al. I985; WeaverI985). Otheranthropologists (e.g., RyanI977: I98-200; KelleyI980: I74-8; Palkovich I98I: 8; Andrews I972), afteracknowledging additional, whatthey often consider to be secondaryfactors, believe that the ultimate prime mover behindthe increasein porotichyperostosis through time and between groupsin theNew Worldis theresult of an increasinglymaize-dependent diet. 'It is possiblethat the death rates are indicativeof an overalllow level of health caused mainly by malnutrition[at Oak Creek Pueblo, Arizona] . . . Their biggestproblem was anemiacaused by theirdependence on maize' (M. Taylor I985: II8). In easternNorth America,however, some anthropologistshave emphasisedthe synergisticinteraction between diet and infectiousdiseases (Lalo et al. I977: 478-9; also see Mensforthet al. I978: 47-8). Nevertheless, suchsynergistic interaction models are frequently ignored, or thedearth of meat intakepart overemphasisedin favourof the more commonly accepted diet model. For example,studies:

suggestfairly consistently that the adoption of farmingwas accompaniedby a decline in the overallquality of nutrition.The clearestindicator of thisis providedby theincidence of porotic hyperostosis. . . consideredindicative of anemia. Sixteenstudies . . . [in thebook] note ratesof porotic hyperostosisand most conclude that the lesions appear or increase with farming, suggestingthat anemia is primarilya diseaseof agriculturalgroups. (Such anemiais mostcommonly attributedtopoor nutrition but may also be geneticor parasite-related)(Cohen & ArmelagosI984: 587; myemphasis).

The aforementioneddiet-oriented explanation for the highinfant mortality rate and incidenceof porotichyperostosis at ArroyoHondo Pueblo, a large fourteenth-centuryRio Grandeaggregated Anasazi communityin the South- westmaintains that 'The malnutritionand relateddisease conditions themselves mayhave beenthe results of infant diet and feedingpractices, a generalemphasis on high-carbohydratefoods, and/orperiodic food shortagescaused by local drought'(Palkovich I980: 47). Others,such as El-Najar etal. (I976); El-Najjar & Robert(I976); Moodie (I923); Pelto& Pelto (I983); Ryan (I977) etc., concur. The beliefthat Anasazi had a low meat diet is revealed even in articleson 6o8 SUSAN KENT

differenttopics unrelated to Southwesternprehistory. One exampleof many is, 'The Eskimo with a high-meatdiet, exhibitedthe most frequenttype II remodeling,whereas the Pueblo, with a low-meatdiet, showed theleast' (Richman et al. I979: 209; my emphasis), and the authorscharacterise the Anasazi as 'vegetable-eatingPuebloans' (I979: 2I2). Anotherexample is thatin contrastto PlainsIndians, 'Southwestern groups continued to develop a specialiststrategy dependenton maize horticulturewith consequentbiological impacts to the populationsinvolved' (BumstedI980: 74). It is importantto note thatI am aware thatdiet can be one factorin iron deficiencyanaemia. I propose,however, that (i) theprehistoric Anasazi dietin thesouthwestern region of theUnited States was nutritionallyadequate and (2) otherfactors associated with sedentaryaggregations are the cause of porotic hyperostosisin Anasaziand otherpopulations. Both of thesepoints are assessed below.

How sedentaryis sedentism? How sedentarya group has to be in orderto be classifiedas sedentaryis an interestingand debatablequestion that is furtherput sued in Kentin pressb. The questionis, however,important enough to be at leastcursorily examined here, since sedentismis a major factorfor the nondiet-dependentmodel proposed below. I doubt thatmany proto- or prehistorictribal societies spent twelve monthsa yearseveral hundred decades at a timein one location-that is more commonin societiesin constrainedspace, suchas on islands,or in areasof high populationdensities, particularly urban centres. Even in contemporarysedentary urban Euroamerican society many families takeone monthor longervacations and thereforedo not spendevery month of theyear at thesame place. It has beensuggested that one out ofevery four North Americanswill move, althoughnot necessarilyout of a particularcity (Chuda- coffI972). In only a five-yearperiod between I970 and I975 in the United States,'44 per cent. of the nation'scivilian noninstitutional population over 4 yearsof age residedat a differentdwelling' (Berry & Dahmann I980: 26-8). Of all themoves withinthis short five-year span, I 5 percent. migrated to locations otherthan within the community of theoriginal residence (Berry & Dahmann I980: 28). The sedentaryZulu of South Africaoccupy theirhomesteads for fifteento thirtyyears and thenmove and builda new one; thuseach siteis rarely ifever occupied for more than one generation(Oswald I987). I suggestthat the factorsin operationin settlementsoccupied for more thana yearare similarto thoseoccupied fori00 or more years,and rangefrom constraints on sociopol- itical stratificationand organisationin terms of the necessityof a leader/ arbitrator,to refusedisposal patterning, disease epidemiology, and depending on the size of the aggregation,social integrativemechanisms. It is more productiveto view sedentismas a mobilitystrategy in whicha groupspends the major part of a year at one locus to which they returnafter a short,often seasonal, absence (Kent in press a; b). This would categorisethe Anasazi as sedentary. SUSAN KENT 609

Anasazi diet It is commonlyassumed that the earlierArchaic people emphasiseda hunting and gatheringsubsistence strategy in contrastto theAnasazi who increasingly throughtime relied more on agriculturefor their subsistence. Reconstructions of Anasazi subsistenceare usually based on threeassumptions-(I) that the numericaldecrease in faunalremains in relationto sitepopulation through time indicatesproportionately less hunting and consequentlyless meatconsumed; (2) thatthe larger and laterpueblos or villagesdepleted all potentialgame withinthe radius of space inhabitantswould be willing to exploit; and (3) that people would ratherdo withoutthan expend more calories or energyon a resourcethan theycould getby exploitingit. None of the above assumptionsis valid for the prehistoricSouthwest for several reasons. First,the fewerfaunal remains at many later sites probably indicatemore of a changein butcheringpatterns than in meat consumption. People who have to carrymeat a long distanceto theirsettlements often take onlythose heavy bones neededfor a particularpurpose, such as raw materialto manufacturespecific tools. Unnecessarybulk and weightare abandonedat the butcheringsite (examplesare presentin !Kung Basarwa [Bushmen]and other hunting-gatheringgroups). Once animalswere huntedout of the immediate area of a sedentaryvillage, people would be forcedto travelfurther to obtain them.This does not mean thatthey no longerate much meat; theysimply no longerbrought the bone refuseback to the site withthem. It is most unlikely thatpeople would carryheavy bones to a base camp onlyto discardthem there. So, one should anticipatea changein butcheringpatterns as a consequenceof sedentismand aggregationthat does not necessarilyreflect a changein diet. Secondly, contemporaryEuroamericans/Europeans who are used to pur- chasingmeat at a local marketmay feelthat a several-dayhike to obtainmeat was a rare occurrencefor prehistoricgroups. People withoutmotorised or animaltransportation, however, are accustomedto hikingdistances we might considerexcessive to procurea varietyof subsistence,ceremonial and social items. Examples fromthe Southwestinclude the Hopi salt trek.Meat can be preparedfor long distancetransport by drying,but the process resultsin the removalof bones at theprocessing locus, whichartificially lowers thenumber of faunalremains at a habitationsite. Bones broughtback are usuallyones used forfood, raw materialor fora specialceremonial/ritual or social purpose(e.g., theentire carcase from a boy's firstmajor kill; a variableCordell (I977) did not take into account in her otherwiseexcellent article on faunal remains and huntingat a Rio GrandeAnasazi pueblo). Thirdly,the Anasazi prehistoric intergroup and interpuebloexchange system could have included meat. This exchange networkis known throughthe extensivetrade of ceramicsand lithics.Many small to large siteshave at least some importednonlocal ,which atteststo the prevalenceof tradein Anasazi economy.' Moreover, recentwork from Chaco Canyon reveals a correlationbetween intra-Anasaziartefact exchange and artiodactylspecies frequencyat sites. For example,at Pueblo Alto, nonlocal deer replaceprong- horn as the primaryanimal resourceat the same time thereis an increasein 6io SUSAN KENT

ceramic temperingmaterials and WashingtonPass chertfrom the Chuska Mountainswhere deer would have been moreavailable (Akins I984). Analysisof faunalremains from the Gran Quivira pueblos indicatesthat the Anasazi didtrade for meat with nomadic hunters and gatherersof the adjacent Plainsculture area (Hayes etal. I98I: 2). Meat was probablytraded for ceramics and othergoods, and in fact,Cordell (I985: i8) has noted that'Rio Grande [Anasazi] glazes [pottery]were widelytraded not only in the Rio Grandearea itselfbut also to the adjacentPlains'. People fromthe northernPueblos also wentto thePlains to huntfor bison. Obsidian fromNew Mexico sourcesdated between A.D. goo and I400, in addition to Pueblo ceramics, have been recoveredat a numberof Plains sites (Spielmann I982: 3I I-I5). ProtohistoricallyPlains Indians and Navajos tradedmeat and skinsfor maize and otheragricultural products at 'tradefairs' at Taos and othernorthern New Mexican pueblos (GunnersonI956; etc.). Navajos historicallyalso tradedmeat and hides at the Hopi pueblos in Arizona (Dyk I938). That thisPueblo/Plains exchangeof cornfor meat was also a prehistoricphenomenon is supportedby the accountsof the firstexpeditions by Spanishexplorers, such as Coronado, and by slightlylater Spaniardswho also confirmedthe presenceof regular Pueblo/Plainsexchange (Spielmann I982: I28). Plains Indians barteredtheir bison meat, fat, and hides for Pueblo corn, cotton blankets,and ceramics (SpielmannI982: I28). It is doubtfulthat pre-horse Plains Indianswould have carriedentire carcasses to thePueblo area;instead meat probably was debonedat killor processingsites, dramatically raising the ratio of meatconsumed to bone refuseat thepueblos. The preparationofjerky was observedas occurringat the timeof initial butchering (Weltfish I965 as notedby SpielmannI982), and bone greasewas obtained'by smashingbones, boilingthem in water,and skimming offthe fat . . .' (SpielmannI982: I93). Both proceduresartificially lower the ratioof bones recoveredto actualmeat consumedat sites.Additionally, bison 'robes were observedto have been worn in thewinter by all Pecos males . . .' and were used in the interpuebloexchange network (Spielmann I982: 260). Nonlocal cornhas beenuncovered at a fewPlains archaeological sites, although Spielmann(I982: 296-7) suggeststhat much corn acquired from the pueblos in exchange for bison productsmay have been consumed while Plains Indians camped near the Pueblo villages. I suspectthat maize was carriedback to the Plains, but as archaeologicallyinvisible grounded flour,since the cobs are unnecessarybulk and weightfor pedestrian Plains peoples. Thereis otherconcurrence that the Anasazi were not as maize dependentas is oftenindicated by faunalassemblages. Turkeys were availableas a meatsource prehistorically,as evidencedby 'turkeypens' and consolidatedmasses of turkey droppingsfound at sites throughoutthe Anasazi occupied Southwest(Rohn I977: 86-7, and others);and aredescribed by earlyexplorers and ethnographers. Early historicsources oftenmention the procurementof bison meat and the consumptionof turkeys.Observed duringthe Rodriguezexpedition in A.D. I583, 'They [Rio GrandePuebloans] make tortillas and catoleswith buffalo meat and turkeys,because theyhave large numbersof the latter.There is not an Indian who does not have his corralin which he keeps his turkeys.Each one holds a flockof one hundredbirds' (Hammond & Rey I927: 26). Moreover,it SUSAN KENT 6ii

has been recordedthat protohistorically,both easternand westernPueblo Indians:

added to theirdiet by gatheringwild, edible plants and by organizingtribal hunts to gatherrabbits and othersmall game. Otherdelicacies were special species of wood rat,deer, and antelope.When theSpaniards first encountered the Pueblos, mostof thevillages kept vast flocks of turkeys,both forfood and feathers(Schroeder and Matson I965: I15). Periodictrips to thePlains countryto hunt buffaloare also well-rememberedactivities among old Pueblo residents.It is likely, however, thatbuffalo meat and skins were obtainedprimarily by tradeor giftexchange with friendlynomadic tribes (Dozier I970: I29).

Butcheringmarks on Canis spp. (probablydog) uncoveredfrom a small PuebloII, circaA.D. I030-I050, habitationsite in theMesa VerdeAnasazi regionsuggests an additionalavailable meat source not usually recognised (Kent in preparation).At the same site I3.55 per cent. of the faunal assemblage consistedof turkeybones, rabbitsmade up 44.06 per cent., rodents26.0I per cent.and dogs 2.26 per cent.Large and mediumsized mammalsmade up only i i.86 per cent.of theassemblage (Kent in preparation).When dog is identified at a site,their bones are oftennot carefullyinspected for butchering marks since it is assumed thatpeople would not eat 'man's best friend'.Even when such marksare noted,they are not always includedin thelist of domesticatedfood exploited,although this is changing(see Emslie I985). Dogs, then,might add anotherlocally available meat resource not commonlyacknowledged. Even in those areas wherethere was prehistoricallya relativelyhigh popu- lationdensity, meat was probablystill available. Perhaps turkey, rabbit, wood rat and othersmall animals were the meat staples of the Anasazi diet, with deer, bison, various birds,pronghorn antelope, dog and otheranimals being consumed less frequently.In fact, consumptionof meat sources typically consideredinedible by many Euroamericanarchaeologists but with high nu- trition,such as grasshoppers,are indicatedby coproliteanalysis. For example, coprolitesfrom Anasazi sites indicate that meat was consumedalong withbone cakes, rodentsand grasshoppers(Fry & Hall I975: 95). Furthermore,7I per cent. of the coprolitesidentified from Pueblo Alto in Chaco Canyon contain bonefragments (Clary I984). Out ofthirty-five samples, I,305 bonefragments were counted and most were deer mouse, prairiedog or cottontailrabbit remains(Clary I984: 269). That7I percent. of the coprolites from one Anasazi villagecontain bone fragmentsfrom species often considered intrusive to sites simplydoes notsupport the usual protrayalof the Anasazi diet as a primarily vegetarianone. Agriculturalfields actually promote the abundanceof certainanimal species and huntingthem is sometimesreferred to as 'garden hunting'.In addition, approximately67 to 76 per cent.of thelive weightof small mammals,such as rodents,is ediblemeat (Stahl I982: 823-7). Unfortunately,small animalbones are less visible archaeologicallyand more subject to carnivoreactivity and erosionalprocesses than large bones (Binford& Bertram1977). Archaeologists have oftendiscounted rodent bones as intrusivebecause rodentsare not an animalEuroamericans prefer to eat, unlessthey are starving.Even today,such animals are oftenconsidered to be 'starvationfood', since it is assumed that 6I2 SUSAN KENT

everygood Anasazi would preferthe meatfrom larger animals if available,an unwarrantedassumption. Some archaeologistshave arguedthat the low occurrenceof faunalremains coupledwith the small emphasis on huntingdescribed in Pueblo ethnographies indicatesa paucityof hunting,and by extension,of meatconsumed by pre-and protohistoricPuebloans. There are a numberof problemswith thisassertion, theleast ofwhich are the inherent problems ofusing the direct historical approach of ethnographicanalogy, as detailedin Kent I987. But evenmore problematical is thata morethorough study of Pueblo ethnographiesreveals that the analogue is incorrectethnographically and Puebloansdid huntsubstantially more than is commonly thought.There are tangiblereasons for the dearthof bones at historicsites. For example,the mythology of eastern Pueblos stronglysuggests thathunting formerly played a muchgreater part in theireconomy than is often recognised,the scarcity of faunalremains being the result of the modern Pueblo practiceof depositingbones at shrinesusually located outside the village (Ortiz I969: I76). Modern pueblos stilltoday performthe 'buffalo'dance in which bison and otheranimals are symbolicallyhunted by dancers.Furthermore, the Spaniardscaused the historic decline in Pueblo subsistencehunting by introduc- ing new crops, betteragricultural technology and animal husbandrythat depletedthe faunanear settlements,as well as more efficientweapons to hunt animals,an increasein thearea's population, new settlementsand appropriation of rangeland (Ortiz I 969: I 76-7). The above discussionof Anasazidiet negates many anthropologists' assump- tionsthat the Anasazi were singly dependent upon a maizediet. This is in contrast to, forexample, El-Naijar's (I977: 329) assertionthat 'Heavy dependenceon a single food item, such as maize, may have been responsiblefor the high incidence of [porotic hyperostosis] in the New World. . . . The nutritional propertiesof maizetogether with maize processing techniques are the two main factorsresponsible for porotic hyperostosisin groups whose diet consisted primarilyof maize.' Whilethis may be trueof a hypotheticalpopulation with a heavydependence on a singlefood item, especially maize, it is unlikelythat such populationsactually existed very oftenprehistorically. Such populationsare known historicallydue to thepresence of Europeansor Euroamericans,over- crowding and precipitouspopulation increasespartly a resultof improved healthcare, as well as over-exploitationof theland, etc. For evenif the Anasazi did not eat muchmeat (and thedata suggestotherwise), maize probably did not constitutethe 75 per cent.of theirdiet that has been claimed.Just one example can be seen in El-Najar and Robertson's(I976: I43) contentionthat 'Among inhabitants of environments similar to that of Canyon de Chelly . . . maize constitutedover 75 per cent. of the diet'. Beans and squash, as well as other plants,were also cultivated.

Twenty identifiedplant taxa have been recoveredto date [fromcoprolites at a large Anasazi pueblo] including the following common names: amaranth/pigweedseed, cactus family epidermis,chenopod/goosefoot seed, beeweed seed, squash seed and tissues,horsebrush stem, cotton seed and fiber,grass familyseed, sunflowerseed, pea familyseed, bean fragments, groundcherryseed, pine nut fragments,pine resin,purseland seed, squawbush seed, dropseed, and cornseed and tissue(Fry & Hall I975: 95; see also Williams-Dean& BryantI975). SUSAN KENT 6I3

Whereasmaize has a relativelylow iron absorptionrate (El-Najar I977), other Anasazi crops have higheriron absorptionvalues. Maize has an iron absorptionvalue in a normalaverage male of only o.9; however,black beans havean absorptionrate of I2, whichis higherthan that of either fish (2.8) or even veal (9.2; Layrisseet al. I969: 441). These values change when the items are consumed by an individualwith iron deficiencyanaemia: 'Normal subjects absorb 5 to IO% of dietaryiron, comparedwith about 20% in iron-deficient patients'(Lanzkowsky I980: 47). Also importantis thefact that plant and animal food,if eaten in combination,significantly increases the absorption of ironfrom vegetablesources, perhaps because'. . . severalof theamino acids, particularly cystine,lysine, and histidine,have been foundto be effectivein increasingthe absorptionof iron' (LanzkowskyI980: 46; also see HoffbrandI98I: 3 8-9). The consumptionof maize, beans and squash in the Southwest,augmented by various wild plants and meat fromsmall game and occasional large game, probablyproduced a nutritiousdiet adequate in iron.

Sedentismand aggregation: an alternativemodel If not a consequenceof diet, thenother causal agent(s) must account for the incidenceof porotic hyperostosisin the Southwest. In contrastto the diet model,I suggestthat the increase in porotichyperostosis can be betteraccounted forby theincrease in sedentismand aggregation(i. e., theoccupation of hamlets or largersettlements). Through timein the Southwest,as well as elsewhere, relianceon horticultureincreased. Also throughtime, however, settlements became moresedentary (using the definition presented earlier) and aggregated. In other words, thereis a correlationbetween an increasingagriculturally orientedAnasazi subsistencestrategy and an increasingsedentary aggregated settlementpattern as compared to the earlierArchaic. I have attemptedto demonstratethat Anasazi horticulturalistsdid not have chroniciron deficiency anaemiaresulting in porotichyperostosis as a resultof theirdiet. The following will demonstratethat sedentaryand aggregatedAnasazi did have chronic anaemiaas a resultof their demography. At differenttimes in differentbranches ofthe Anasazi, large sedentary villages of several hundred rooms were occupied (e.g., Pueblo II Chaco Anasazi and Pueblo III Mesa Verde Anasazi; see Cordell I985). The majorityof skeletonsdiscussed below are fromthe time periods of thelarge villages. From a sample of eighty-fourAnasazi skulls, rangingin time fromearly Basketmakerto Pueblo III, 24.7 per cent.exhibited porotic hyperostosis, most beingin immatureskeletons (Zaino I967: 42). It is importantthat infants from Alkali Ridge, Utah, and elsewherehad active cases of porotic hyperostosis, whereasadults had indicationsof healedmanifestations of thecondition (Brues I946: 328). Of 539 craniafrom various Anasazi large aggregated sites through- out the Southwest,34.3 per cent. exhibitedevidence of porotichyperostosis (El-Najar etal. I975). Children,as is typical,had a higherincidence than adults. Anasaziskeletons from Chaco Canyon,where very large sites occurred, had the highestpercentage of thedisease (7I.8 per cent.of 32 individuals)followed by 614 SUSAN KENT

InscriptionHouse (54.2 percent. of 24 individuals),Gran Quivira (I 5.3 percent. of I77 individuals)and Navajo Reservoirwhere there are no largevillages (I 3.0 per cent. of 92 individuals(El-Najar et al. 1976: 481-5). The earlierBasket- maker period skeletonsfrom Canyon de Chelly had 49.3 per cent. of I36 individualsaffected whereas the later Pueblo periodskeletons had 55. I percent. Of78 individualsaffected (El-Najjar et al. 1975: 922-3). The differencebetween early less horticulturallyoriented Basketmaker and latermore horticulturally oriented Pueblo skeletonsis only5.8 percent., casting some doubt on the magnitudeof differencein porotichyperostosis between a lesserand greateremphasis on a horticulturalsubsistence orientation, but not on theeffects of aggregationand sedentismsince some Basketmakervillages were large. It is also importantto takesample size into accountwhen viewingthese figures;for instance, disparate sample sizes froma poorlyknown or unknown universewere used to calculatethe aforementioned percentages. This does not howeverdeny the fact that porotic hyperostosis resulted from a fairlycommon malady among prehistoricgroups; nor does it mean thatone should simply discardthe data for fear of invalid conclusions resulting from potential sampling bias. It should, however,make one somewhatcautious, especially since more completeexcavations yielded lower percentagesof the affliction,as indicated below. Eighteen Pueblo III burials at Site 34 in Soda Canyon at Mesa Verde, Colorado, had porotichyperostosis, in additionto a fewskeletons with arthritic exostoses, cysts and mastoid abscesses togethercomprising one half of the skeletonsrecovered (Reed I965: 41). The WetherillMesa Project,Colorado, uncoveredan additionalI79 partialand completeburials with only six infant skullsfrom all threePueblo periodsdisplaying any evidence of porotic hyperos- tosis,in additionto fivedefinite and two probablecases of infections(mostly osteomyelitis)(Miles I966; I975). Of the 58I skeletons uncovered at the protohistoric/earlyhistoric Anasazi site of Pecos village, 3.27 per cent. had porotichyperostosis (Hooton I930: 320). Otherevidence of prehistorichealth problems includes a humanfluke infec- tion (digenetictrematoda of unknowngenus) discoveredin coprolitesfrom a late periodAnasazi site (A.D. I250-I300) in Glen Canyon, Utah (Moore etal. I974: I I 5-I 8). Many flukesthat invade humans can cause diarrhoea,as well as malnutritionby robbingtheir host's digested food, although species identifica- tionof thefluke is neededbefore its potential effects can be ascertained(Brown I975: 209-54). Otherevidence of parasites in theprehistoric Southwest includes eggs frompinworm (Enterobius vermicularis) found in fecalmaterial at sitesin Colorado (Samuels I965: I75-8), and Utah, and Arizona(Fry & Hall I975: 94). The factthat remains of parasiteshave been recoveredfrom prehistoric sites indicatesnot onlytheir presence, but their prevalence as well sincethe statistical odds of findingcoprolites with parasitesanalysed by people competentto identifythem is actuallyvery low. The previoussection elucidated the superficialcorrelation between Anasazi maize horticulture-whichactually always includedbeans, squash, some now wild plantsand meat-and porotichyperostosis. The misleadingcorrelation between agricultureand porotic hyperostosisis spurious,and otherfactors, SUSAN KENT 6I5

specificallysedentism and aggregation,also tendto go alongwith increases in an horticulturalsubsistence strategy. Because it is unlikelythat the Anasazi ever subsistedprimarily on maize, porotichyperostosis is more likelythe resultof the relationshipbetween anaemia and sedentaryaggregations, than between anaemia and diet. The ramificationsof sedentaryvillage life include increased bacterial,viral and parasiticinfections due to poor sanitaryconditions and contactwith potential hosts of carriersof infections.Those prehistoricsouth- western groups with lower incidences of porotic hyperostosislabelled 'non-maize dependentgroups' by El-Najar (I977), or in other words, less agriculturallydependent people suchas theNavajo Reservoirarea groups,were also less sedentaryand livedin smalleraggregations than the 'maize-dependent groups' (thelatter being inhabitants of Chaco Canyon, Canyon de Chelly,and InscriptionHouse sites).

Irondeficiency anaemia: causes and consequences Whatthen caused the incidence of porotic hyperostosis, and by implicationiron deficiencyanaemia, among theAnasazi? Iron deficiency anaemia is commonin humanstoday and,judging by the archaeologicalrecord, was common in the past. Currentlyiron deficiencyanaemia is widespreadthroughout the world. The impact of diarrhoealdiseases on an individual's health is not always recognised,since European/Euroamericans rarely have thefrequency or sever- ity of symptomsas have many non-Westernpeoples. Because of Western medicine(and sanitationstandards), the effects of diarrhoealdiseases often can be lessenedor eliminatedbefore they weaken or kill. Such medicineis scarcein some Third World nations and was not available prehistorically,although nativemedicine no doubt alleviatedsome symptoms.One can gain an appreci- ationof theprevalence and severityof these diseases that are oftenthought to be relativelybenign in contemporaryWestern societies by examiningthe health problemsrampant around the world. For example,a minimumof 35 per cent. of the deathsof Brazilianinfants in I958 was the resultof diarrhoealdiseases (Penido I959: 368). No lessimpressive is thefact that diarrhoeal diseases account for one halfof all hospitaladmissions for children under five yearsof age in Honduras(Kendall I98 i: i). In Venezuelaalone, almost 84 percent. of all deaths fromgastroenteritis occurred before a childwas two yearsold and betweenI950 and I954 diarrhoealdiseases accountedfor 6o per cent. of the deathsin rural towns withpopulations of fewerthan 5,000 people (Curiel & de Ochoa I959: 3 53-4). One studystates that 'diarrhea, as a cause of death,almost equals all the othercauses combined,even if respiratorytract infections are included. The World Health Organization. . . estimatesabout 750 millionepisodes of acute infectiousdiarrhea every year. . . . RecentWHO figuresfor worldwide mortal- ityfor young children with diarrheal diseases indicate 4.3 millionannual deaths, excludingChina' (FlewettI984: 343). Iron deficiencyanaemia is one of the most prevalentmodern deficiency diseases and its incidencevaries in differentcountries from 30 to 95 per cent. (Heilmeyer& HarwerthI970: 38I). In Europeit is presentin 25 percent. of post-pubertalfemales in (Halberg I970: 457), in I5 per cent.of females 6I6 SUSAN KENT

in the United Kingdom (KilpatrickI970: 443), in I3.9 per cent. of people in Germany(Seibold I970: 438) and in thelate I970'S, in I7-44 per cent.of North Americanchildren between six monthsand threeyears of age (Lanzkowsky I980: 57). A vegetariandiet, the cause usuallysuggested for historic cases of anaemiain and prehistoriccases of anaemiain theNew World, cannot alone accountfor these impressive statistics. Both aggregationand sedentism, however,can explain present and pastincidences of anaemia. Most ofthe archaeological examples of porotic hyperostosis are from children under the age of five, which is consistentwith the age of the most severe manifestationsof bacterial, viral and parasiticdiseases. The factorsinvolved will be detailedto demonstratetheir relationship in fosteringiron deficiency anaemia as a consequenceof people becomingmore sedentary and aggregated,a setting which createsmore person-to-personcontact and greateropportunity for the transmissionof gastrointestinaldiarrhoea-producing diseases.

Diet The most oftencited nutritional cause of iron deficiencyanaemia is a low iron or meat intake.In those partsof the world where meat is scarce, nutritional deficienciesplay an importantrole in causing and maintaininghigh levels of anaemia(Chandra I979; Baker I978; HummertI983); theprehistoric Southwest was not, however,such an area. In infancyand earlychildhood, when milkis themajor portion of the diet, it was and is stilloften thought that iron deficiency anaemia is a consequenceof the low iron contentof mother'sor cow's milk (Betke 1970; Palkovich I984, etc.). Nonetheless,prolonged lactation by itself does not oftenresult in anaemia,as severalrecent studies have shown, despite common beliefs otherwise. While I am not suggestingthat a completely iron-deficientdiet will not cause irondeficiency anaemia, I am suggestingthat theprevalence and severityof anaemiathat occurs in some youngchildren does so despitea dietadequate in ironand meat. The protectiveeffect of breast-feedingagainst infections has been recognised clinicallyfor decades, particularly in relationto diarrhoealdisease in conditions ofpoor hygiene(Jelliffe &Jelliffe I978: 5). Mother'smilk provides protection to vulnerableinfants from Escherichia coli, a diarrhoea-producingbacterium which is virtuallynonexistent in breast-fedyoung children in contrastto formula-fed children(Gryboski & Walker I983: 547). Furthermore,breast-fed infants, particularlyup to nine monthsof age, have a significantlyreduced risk of respiratoryinfection, including pneumonia, than have nonbreast-fedinfants (Forman et al. I984). Studies also indicatethat human milk protectsagainst Vibriocholerae, Shigella, Salmonella, rotavirus, and toxinsA and B of Clostridium difficle(Kim etal. I984; Hjelt etal. I985; Ryderet al. I985). Host resistancefactors in humanbreast-milk properties act mainlywithin the intestineand theactive anti-infective property of humanmilk is both humoral and cellular(Jelliffe &Jelliffe I978: 85). Lactoferrin,lysozyme, interferon and otherantibacterial and antiviralagents occur in human milk (Raiha I985) and new researchshows that exclusivelybreast-fed infants are generallymore healthythan nonbreast-fedones (cf. Forman et al. I984). In comparingfatal SUSAN KENT 6I7

versus nonfatalcases of acute diarrhoeain thirty-twoCuna Indian children underthe age offive from islands off the coast of Panama, all nonfatalcases were exclusivelybreast-fed at least duringthe first four months of lifein contrastto thefatal cases of diarrhoea in whichonly 62 percent. were exclusively breast-fed forthe firstfour months, 25 per cent. who were neverbreast fed, and I3 per cent.who wereintermittently breast-fed (Ryder et al. I985: 607). Breastfeeding reducesthe severity of theclinical manifestations of specificviral agents in cases where it does not actuallyprevent it (Duffyet al. I986). Most interestingin termsof this study is the suggestionthat because 'shigellosiscontinues to accountfor substantial morbidity and mortalityin children. . . the results[of our study]supports prolonged breastfeeding . . . [up to 35 months]'(Clemens etal. I986). I suggestthat the correlation between diet (mother's milk) and infantanaemia is actuallyspurious. Instead,I suggestthe anaemia noted in some breast-fed infantsis the consequence of maternallytransmitted viral, bacterialand/or parasiticinfections. Enterotoxigenic strains of staphylococci have beenfound in breastmilk of healthymothers whose childrenhave diarrhoea(Adekeye & AdesiynI984: 531). 'The factthat 7I.3% of breastmilk samples from 25I healthynursing mothers contained [ Staphylococcus]aureus is worrying,especial- ly as 48% of theisolates produced enterotoxins. The incidenceof enterotoxige- nicitymay even be higher,as we only looked forSEA, B and C' (Adekeye& Adesiyun I985: 536). The more frequentsuch infectionsare presentin the generalpopulation, as I suggestthey are in sedentaryaggregations, the more likelythe transmission of infectiousagents to an infantthrough mother's milk. Authorsfrom around the world have recentlynoted similar findings concerning the transmissionof diseasevectors through lactation. This seriouslyquestions the role of dietin causinganaemia in breast-fedinfants, and insteadimplicates bacterialand viralagents passed on to a childthrough mother's milk. Anaemia, in otherwords, is not solelydependent upon how muchiron is ingested,but on how much is absorbed by the body. These importantfactors are discussed below.

Infectionsand traumas Nongastrointestinalinfections or inflammatorystates of various types and traumassuch as fracturesare also potentialcauses of anaemia (referredto as anaemiaof chronic disease). By I952 itwas knownthat anaemia is mostlikely to developfrom (i) severerather than mild infections (i.e., io per cent.of patients in one study with moderatelysevere chronicinfections developed anaemia versus40 percent. of those with severe infections), (2) infectionslasting a month or longer, and (3) infectionsin infantsand young children(Cartwright & WintrobeI952: i68). Perhapsof more significancefor the present study is the factthat anaemia developed in infantsafter a seriesof infections, even though their dietswere unquestionablely adequate (May etal. I952). The typeof infection present is notas importantin causinganaemia as itsduration and severity(see de Gruchy I978: I97-9; ReizensteinI983: 92-4, the latterincludes a descriptionof the 6i8 SUSAN KENT severe anaemia resultingfrom pulmonarytuberculosis and rheumatoidar- thritis).This is particularlyinteresting when one considersthe frequencyof rheumatoidarthritis, osteomyelitis, tuberculosis and so on, in prehistoricseden- tarypopulations (cf. as identifiedby Hooton I930; I940; Fry I976; and others). Even with massive intravenoustherapy, and adequate dietaryiron intake, anaemia can resultas a consequenceof rheumatoidarthritis; although the link betweensuch chronicinflammatory diseases and anaemiais not yetknown, it maybe relatedto immunemechanisms (Hurley I983: I32; ReizensteinI983: 47; 70). Arthritis,though not always rheumatoid,is perhaps the single most common pathologyother than dental ones foundin prehistoricsouthwestern populations.2 Severalfactors implicated in thepathogenesis of theanaemia associated with chronicdiseases include (i) a decreasedproduction of red blood cells resulting fromrelative erythropoietic failure and a defectof iron mobilisationfrom the reticuloendothelialtissue, and (2) a shorterred blood cell lifesurvival from I20 daysto only6o to go days(Reizenstein I983: 42-4 and Zucker I980: 94). In other words, all thevariables are presentfor healthy haemoglobin/haematocrit levels but are not utilisedefficiently by people with chronicinfections or inflam- mations. In additionto these changesas a consequenceof chronicinfections or otherinflammatory processes, chronic anaemia can cause changes in the stomach-gastritisto gastricatrophy-in individualsof all ages. When in the small bowels of children,chronic anaemia can resultin occult blood loss in the stools among otherchanges (seeJacobs & Worwood I982: I76). This can perpetuatethe anaemia or increaseits severity. Also relevantto prehistoricpopulations is the fact that trauma such as fractures,contusions, or extensivelacerations can produceshort term anaemia duringthe first week or two followingan accident,potentially aggravating any underlyingproblems. This anaemiais not theresult of blood loss, infectionor hemolysis,but is, instead,the result of a disturbancein haemoglobinsynthesis. In fact,'Slight reductions [in the serumiron concentration]also are seen even afterthe most minimal trauma such as a smalloperation under local anaesthesia and a simplesmallpox revaccination . . .' (ReizensteinI983: 72). As Scrimshaw (I968: 708) has noted, 'Any cause of chronicbleeding will contributeto the developmentof iron-deficiencyanemia'.

Diarrhoealand othergastrointestinal diseases The prevalenceof a numberof diarrhoealand gastrointestinaldiseases increase in responseto sedentismand aggregation.Diarrhoeal diseases can cause iron deficiencyanaemia in two ways-by passingthe food through the intestines too rapidlyfor most of the nutrientsto be absorbed, or by actual blood loss, common to such diseases. In fact,nondiarrhoeal infections cause overt mal- nutritionas a resultof a possible increasein 'restingmetabolic expenditure duringinfection stress rather than the early fall in metabolicrate that character- izes starvationor underfeeding'and thiscauses a morerapid and severeweight loss than does starvationalone (Duggan et al. I986: 65). Specificallywith SUSAN KENT 6I9

gastrointestinalinfections, a sequence of hormonal,metabolic and immuno- logic eventscreate a precipitousnutritional cost (Santos I986). Fever,anorexia, vomitingand negativenitrogen catabolism associated with diarrhoearesult in food withdrawalin orderto restthe small intestineresulting in a 20 to 6o per cent.or more deprivationof a child'snormal caloric consumption (Kumate & Isibasi I986: 25). In general,both bacterial and viraldiarrhoea-causing infections have a higher frequencyin childrenthan adults and the symptomsare more severe and malabsorptionmore prevalent in children,especially the younger ones (Ackers I982: 422; Wilson etal. I98I: I3 I-2). A studyfrom Scotland revealed that the majority(83 per cent.) of rotavirusinfections appear in childrenunder five (Cash et al. I986). Specificallyin the cases of rotavirusand enterotoxigenic Escherichiacoli, two of themost common ailments, small children appear to lose a greaterproportion of theirtotal fluid volume duringdiarrhoea episodes and as a consequencehave a higherfrequency of severedehydration and death(Black etal. I984: 83). The averagediarrhoeal stool loss ratein infants is morethan twice that in adults with enterotoxigenicEscherichia coli (Black et al. I984: 87). A similarpattern has been associatedwith coronaviruslikeparticles (Rettig & AtlshulerI985). Weanlingdiarrhoea can cause anaemiaand deathand is linkedto weaninga childfrom mother's milk. For example,from I955 to I959 in India,22 percent. of all deathsduring infants' first year of life and 9 per cent. of all deaths of childrentwo to threeyears old were attributedto weanlingdiarrhoea (Gordon etal. I 963: 37 )O. Some ofthese deaths might not be associatedwith diet or wean- ing but were caused by increasedcontact with ill or asymptomaticcarriers of infectionsas a childbecame older and was in contactwith more people and/or sufferedthe loss of some of theimmunity afforded by mother'smilk. Whateverthe actualcause, abnormalsmall intestinallesions correlated with acute diarrhoea,especially during the firstyear of life,may contributeto the perpetuationof the diarrhoeaand be responsiblefor the lactase deficiencyand lactose intoleranceassociated with such diarrhoea(Fagundes-Neto et al. I984: 5I0, 5I4-I5). Another complication of acute gastroenteritis and protracted diarrhoeais monosaccharideintolerance associated with rotaviral infections but also presentin theirabsence, perhaps when multifactorialprotracted diarrhoea resultsin small intestinalmuscosal damage (Manuel et al. I984: 44; also see Brandt,et al. I985: 437-443). This conditionin infantsvaries in durationfrom 2.5 to 70 days in at least one study(Manuel etal. I984) and contributesto the length and severityof a diarrhoealdisease, potentiallymaking an infant vulnerableto otherdiseases present in thecommunity. Importantis thatmany of the bacterial, viral and parasitic infections that cause diarrhoeaactually increase as sanitationdecreases and are rampantin non- Westernpopulations settled in sedentaryaggregated groups which lack the amenitiescommon in Euroamerican/Europeansocieties. Sanitation decreases in such aggregations,usually as a resultof poor and contaminatedwater supplies, as well as beingassociated with certain practices. For instance, while conducting participant-observationfieldwork among Navajos in a remote part of the Reservation(Kent I984), I observed unrefrigeratedand unprocessed meat 620 SUSAN KENT cooked and eatenin midsummeras long as two weeks aftera sheep had been butchered.This custom no doubt enhances the chances of contractinga diarrhoealdisease. Drinkingand washingwater was hauled froma tribalwell several miles fromcamps and storedin open barrelswhere disease-carrying insectsand dirtwould gather.Outhouses were used at some camps, but were oftennot present at all, and whenabsent, an arroyoor gullywas used whichwas a potentialcontaminant of water sources over a wide area.Another example was theuse of thesame metalwash tub to wash dirtynappies and to clean dishesin cold water(cf. Kent i984). Obviously,this presented an excellentvehicle for the spreadof disease,especially since the infant and I both had diarrhoealdiseases -mine being diagnosed as a Shigellainfection-at the time. In developing nations,children under the age of fiveyears are ill on an averageof 34.2 to 35.2 percent. of thetime during an one and a halfyear period according to one study (McAuliffeet al. i985).

Bacterialand viral diseases Common bacterialdiarrhoeal diseases resulting in gastroenteritisare caused by Shigella,Salmonella and Escherichiacoli bacteria (Wadstrom I978; Levine & Hornicki98 I: 254, 256). All can be responsiblefor mild to severediarrhoea and all procreatein conditionsof sedentaryaggregations. Susceptibility of young childrento thesebacteria corresponds to the peak incidenceof porotichyper- ostosisfound in prehistoricinfants and youngchildren's skeletons. Most bacterialdiseases can be transmittedto humansby rabbits,ticks, deer flies,dogs, fleasand otheranimals. This is particularlysignificant when one realisesthat domesticated dogs and turkeyswere keptby the Anasazi and that the later archaeologicalrecord indicates an increasedreliance on rabbitsand othersmall animals for food. These bacterialdiseases are aggravatedby the sedentismand aggregationof people because of an increasein potentialvectors presentnear or in thehabitations. Diarrhoea, vomiting, and nausea character- istic of bacterialinfections can occur throughthe ingestionof contaminated meat or water,resulting in primarylesions in the gastrointestinaltract (Cluff ig80: 66i). For example,tularemia (rabbit fever) can be transmittedto humans frominfected rabbits, dogs, flies,and otheranimals with which the Anasazi were likely in contact (Cluff ig80: 66i). Viralgasteroenteritis is the second leading cause of illness in theUnited States, and no doubt caused illnessamong theprehistoric Anasazi. Currentlyparavo- virusesare responsiblefor diarrhoeal diseases in adultsand older childrenand rotavirusin young children.Rotavirus agents are the underlyingcauses of diarrhoeain many younger childrenand infantsbecause they have fewer antibodiesthan adults to protectthem against the virus (Lerner i980: 8I4). The linkbetween viral infections and haemolyticanaemia is well known, ifpoorly understood.The relationshiphas been suggestedto be connectedin some way to theautoimmune system as mentionedearlier (Lascari i984: i). Rotavirushas been diagnosedin childrenwith diarrhoea, vomiting, and in some cases limited gastrointestinalbleeding (Clemens et al. i983; Paniker et al. i982: I23-6; Stintzing et al. 198I: 67-7I). In summary: SUSAN KENT 62I

In developingcountries, where sanitationis generallyinadequate, young childrendevelop multipleepisodes of diarrhea(often four to eightper year) during the first 2 to 3 yearsof life.... Most of thesediarrheal episodes are mild,but some are life-threatening.All probablycontribute negativelyto thenutritional development of thechild (Carpenter & Sack I98 I: 2I3).

Parasiticinfections. The actualprevalence of parasites in theUnited Statesis quite variableand in theearly I900's, theirnumbers ranged from 93.9 per cent.of 83 ArapahoeNative Americansliving at a missionschool to 77.I per cent. of 83 childrenin an industrialschool, to 7I.0 per cent. of 42 orphansin Oregon to virtuallynonexistent in some Euroamericanpopulations (Owen et al. I934: 9I3-I5). A numberof protozoacan produceacute diarrhoea.3 Amoebic dysen- tery(Entamoeba histolytica) for example causes symptomsfrom chronic mild diarrhoeato fulminantdysentery with bloody stoolsand is stillfound on Native American Reservationsand anywherecrowding and poor sanitationexist (Brown & Neva I983: 30-3; Plorde I980: 863). Helminthparasites not onlyrob thebody of essentialnutrients, such as iron,but also can cause occultblood loss and/ordiarrhoea. Finally, fungal infections and chronicnonspecific diarrhoea syndromeor irritablecolon of childhood can also cause chronic diarrhoea (Gryboski& WalkerI983: 573-7), potentiallyleading to anaemia.

The epidemiologyofchronic gastrointestinal diseases Relativelylarge amounts of both rotavirusand Norwalk virus diarrhoea- producingagents have been detectedin untreatedand treated,including chlori- nated, drinkingwater in developed and undevelopedcountries (Cliver I984; HerbertI985; Zohar etal. I984; Goddard& Sellwood I984; Gerba I984). How theviruses enter water sources is notfully understood, although many probably do so frominfected faeces located near groundwater.A study fromAlaska indicatesthat viruses can contaminatesources as faras 3I7 km downstreamand live for at least 7. i days as theytravel that distance (Melnick I984: 6-7). In addition,infected wild animals,such as ducks with viralinfections, can con- taminatewater that is thenused by humans,beginning a cycleof chronic human infection(Melnick I984: 14). Blue herons,beavers, and muskratshave been implicatedin thespread of Giardiainfections (Georgi et al. I986) and chickensin the spreadof Campylobacter(Harris et al. I986). Virusesof varioustypes have been identifiedin a wide rangeof waterfowland otherbirds in NorthAmerica (Hinshaw etal. I985; Sacks etal. I986), in pigs and turkeysin (Aymard et al. I985), and in wild opossums in the Amazon region(Linhares et al. I986). There is additionallysome evidenceof certainrotaviral strains which may be transmittedby a respiratoryroute (Santosham et al. I985). Chronicinfections start through contaminated sources, but are maintained, even in a small hamletor aggregation,by therapid evolutionof some micro- organisms.These new strainscan infecteven thosewith antibodies against the originalstrain, as well as infectingthose without body defencesto resist.'The highmutation rate of RNA virusesmeans that mutants could possiblyemerge duringa singleinfection of an individualand, givena selectiveadvantage, such 622 SUSAN KENT

mutantscould predominatein the progenyvirus' (Oxford i985: I; see also Konno et al. I984; Nicolas et al. I984). A numberof RNA virusesincluding influenzacan have a rate of antigenicmutants in virus pools of one in ten (Oxford I985). The tendencyfor rapid evolution even withina singleepidemic negates some of theimmunity afforded by a previousexposure and infectionby rotavirusand Norwalk virus (cf. Oxford I985; Ryder et al. i985). Protectionby immune factorsproduced against rotavirus and Norwalk viralneonatal infections may not preventreinfection from the same virusbut oftencan lessenthe severity of thedisease the second timearound (Ryder et al. i985: I03). Even so, a studyof 369 childrenunder the age of 4. I7 years (S? months)in Bangladeshshowed 'that 46% of the childrendeveloped NW [Norwalk virus] infectionover a I2-monthsurveillance period. Adjustmentof our [own] seven-monthsurveil- lance ratesto an annualbasis forcomparison reveals that 63 % of San Blas Cuna Indianchildren [from Panama] less than 48 monthsold had NW [Norwalkviral] infection'(Ryder et al. i985: I04). Althoughperhaps immune to reinfection from the same identical strain,weakened individuals recoveringfrom an infectionmay be more vulnerableto differentstrains evolved duringa single epidemic. An epidemiologicalmodel forthe transmission and perpetuationof rotavirus has been proposed by Holdaway etal. (i985) whereinthose over fiftyyears of age act as a reservoirof rotavirusin a communitywhile rarelysuffering gastroenteritissymptoms themselves. The post-fifty-years-oldgroup then passes virusesto, and causesnew infectionsin, childrenunder ten years of age. They subsequentlyspread the virus to young adults between twentyand twenty-nineyears old, who areinvolved in thecare of thechildren. Support for thismodel comes fromobservations that the over fifty-years-oldgroup had a higherthan expected IgG antibodyresponse at all timesof theyear while at the same timehaving lower thanexpected levels of IgM in contrastto theone to ten and twentyto twenty-nine-year-oldgroups, both of which had highIgM levels (Holdaway et al. i985: 396). This is because IgM antibodiesare the first producedto an antigenicexposure, such as a bacterium,and thereforea higher titerimplies an acuteresponse to theantigen, while an IgG antibodyis produced laterin thesequence of immune response. All this is complicated by the presence of disease carriersin the most vulnerableage group, thoseunder the age of five,in additionto the older age group reservoir.According to Champsauret al. (i984b: 682), duringthe time when rotaviralinfection and diseaseare most common-that is, in theone to 24 monthsof age period-two out of ten childrenhospitalised had the actual rotaviraldisease (withserological response and diarrhoea),one had an asymp- tomaticrotaviral infection (with serologicalresponse and no diarrhoea),two were virus carriers(no serologicalresponse), and five were not affectedby rotavirus(Payne I984; also see Champsauret al. I984a). Faecal specimensfrom I,84I childrenunder the age of two withoutgastrointestinal symptoms yielded almost the same percentagesof salmonellae and shigellae as childrenwith diarrhoea(Ho & Wong i985: SS).Itis by maintaininga reservoirof disease, with organismsthat can mutateat rapidrates which are potentiallyable to reinfecta SUSAN KENT 623

'compromised'host, thata cycle of infectionscan be initiatedthat would be difficultto break without modern medicine, as is the case in developing countriesand was thecase prehistorically. Recent studiesstrongly indicate that primary viral infectionsincrease host susceptibilityto secondarymicrobial invasion and increasesusceptibility to opportunisticfungal and protozoal pathogensas well (Mills I984: 469-73). Although most studies have been restrictedto pulmonaryinfections, they provide a model forprobable gastrointestinal viral-bacterial synergistic inter- action. One mannerin which thisinteraction occurs is by viral depressionof normal neutrophiland macrophage activitythat would otherwisedestroy bacteria(Babiuk i984a: 43; i984b). Viralinfections can also impairchemotactic factorswhich are criticalto host defencein earlybacterial invasion (Mills I984: 473; Babiuk I984a: 436-7). Viral infectionsadditionally appear to enhance adherenceand colonisationof both gram-positiveand gram-negativebacteria by alteringcell surface,necessary for gastrointestinal tract infections which then allows bacteriato propagate withinthe intestinesrather than being flushed harmlesslythrough the system. This is accomplishedby reducingthe levels of fibronectinon thesurface of epithelialcells (by killingmature cells and increas- ing the numberof immatureones with less fibronection)and increasingcell surface proteases, therebyfavouring bacterial adherence and colonisation (Babiuk I984a and b). The link between primaryviral and secondarybacterial infections can be clearlydemonstrated in the respiratorytract. Bacterial adherence to epithelial cells, at least in the respiratorytract, is requiredfor bacterialinfections but requiresthe penetration of themucous layer that covers epithelial cells (Babiuk i984a and b; Mills I984). 'Viral infectionsmay be just thetrigger to increaseor decreasethe quantityas well as the qualityof thismucous layerand cause the epithelialdamage requiredfor the primary[bacterial] colonization' (Babiuk i984a: 434). Suppressedbactericidal activity from phagocytic cell dysfunction helps createthis situation. Further virus-induced immunosuppression includes the lymphocytesand specificallycytotoxic T (suppressor)cells (see Babiuk i984a: 432-8 for details). A similarcourse of events probablyexists in the interactionbetween viruses and bacteriain thegastrointestinal system, but has not yetbeen as well documented.

Discussion An epidemiologicalmodel can thusbe advancedwhich better accounts for the incidenceof porotichyperostosis among the Anasazi thanthe more common but simplisticmodel of a low meatdiet. A cycleof chronicviral, bacterial and parasiticinfections begins with the lack of sanitationthat often accompanies sedentaryaggregations. In thesesettings, waste accumulatesand is potentially introducedinto a communityvia contaminatedgroundwater used fordrinking and washingand/or contaminated animals such as dogs, rats,flies and toddlers. Diarrhoeal-producingviral infections are perpetuated within a sedentaryaggre- gatedcommunity by contactwith infected asymptomatic carriers who act as a 624 SUSAN KENT

reservoirfor maintaining disease withinthe community.Compromised indi- viduals,particularly those underthe age of fivewho are most vulnerableand most severelyaffected by diarrhoealdiseases, can be reinfectedby a mutant strainduring the same epidemic, as well as be predisposedto bacterialand parasiticsecondary infections. Chronic diarrhoea from chronic gastrointestinal infectionsleads to chroniciron deficiencyanaemia and to the distributionand frequencyof porotic hyperostosisvisible in prehistoricAnasazi skeletal populations. The precedingsections indicate the role of chronic bacterial, viral and parasitic infectionsin creatingand perpetuatingiron deficiencyanaemia,4 especially in childrenunder the age of five.A horticulturalist'sdiet need not be theprimary factorin explainingthe geographicaldistribution, frequency and age distribu- tionof porotichyperostosis and irondeficiency anaemia, since most prehistoric Southwesternpeople ate maize in combinationwith beans, squash, plantsnow wild, wild plantsand meat.This is notto denyany relationship between a solely vegetarian,and especiallymaize, dietand anaemiain thoseareas wheresuch a diet existed. One such area may have been the Valley of Mexico duringthe Classic and post-Classicperiods of highpopulation densities (Santley, personal communication).I believe,however, that the prehistoric Southwest was notone of thoseareas. The linkbetween diarrhoeal diseases and anaemiais throughthe nonabsorp- tionof all theavailable nutrients ingested and/or blood loss, usuallyin thestools. The causes of diarrhoealdiseases are thosethat are accentuatedand perpetuated in sedentaryaggregated settlements (Schliessmann I959: 38I). Althoughnot always recognisedin the prehistoricSouthwest, the effectsof sedentismand aggregationhave been postulatedas the impetus behind the frequencyof prehistoricdiseases in the restof the world (e.g., Polunin I967: 74-75). For instance,beginning with the earliest villages:

Certaincontagious diseases of man maintaintheir reservoir of infectionsolely by a continuous chain of contactbetween infectiveand susceptiblepersons. . . . Many of these viruses and pathogenshave shortpersistence outside the human body and it is, therefore,evident that a successfulchain of infectionmust depend to a largedegree on how close thesusceptible persons are to theinfected ones (Ipsen I959: I62; see also Cockburn I959; I971).

The aggregationand sedentismcharacteristic of theMesolithic and Neolithic in variousparts of theworld providednew breedingplaces formany forms of lifewhich harbour disease (Armelagos & Dervy I970: 273; also see Polgar I964). Although perhaps less a factor among the Anasazi, the general incidence of parasites also increases among sedentaryaggregated people. A study of nomadic Basarwa (Bushmen or San) shows that, with the exception of hookworm (Necatoramericanas), they are relativelyfree of parasitescompared to theirmore sedentaryand aggregatedBantu-speaking neighbours who are plagued by a numberof differentparasites including pinworm (Enterobius vermicularis), small tapeworms (Strongyloidesstercoralis), Hydatid cyst (Echinococcusgranulosum), largeroundworm (Ascaris lumbricoides), and whipworm(Trichocephalus trichura) (Heinz I96I: 209-I I). It is theBasarwa's nomadismand smallgroup sizes that helpdeter parasitic infections. Studies also show thatthe age rangeof the highest SUSAN KENT 625 incidence of porotic hyperostosisin archaeologicalskeletal populations is isomorphicwith the age range of the most susceptibleparasite hosts, thatis infantsand childrenunder ten years of age: 'It is well known thatjuveniles are above all endangeredby worm infestations.Thus forinstance in severalNorth African areas practicallyI00% of the childrensuffer from helminthiasis' (Hengen I97I: 68). Perhapsmost interesting and compatiblewith the proposed nondiet cause of porotichyperostosis in the prehistoricSouthwest is the factthat despite their high meat diet,Eskimo skeletalpopulations have high percentagesof porotic hyperostosisthat are sometimeseven higher than for some Southwesternhorti- culturalgroups. In one study,20.2 per cent.of ninetyEskimo craniaexhibited evidence of porotic hyperostosis(Nathan I966). Obviously a meat or iron deficientdiet cannot account for this relativelyhigh incidence of porotic hyperostosisamong Eskimos, since they are known for theirreliance on a meat-dominateddiet. The ramificationsof sedentismand aggregationcan, however,account for this high percentage, since Eskimos traditionally occupied seasonallysedentary winter villages. Parasiticinfections are known to afflict Eskimos, some of whichcould potentiallycause irondeficiency anaemia (e. g., Schiller I95I; see also Rausch I951: II4 for a discussionof the presenceof Echinococcusgranulosis,a small tapeworm). Bacillary infections producing diar- rhoea also are endemic to Eskimos. Such infectionsas Shigellaflexneri and Salmonellatyphosa which often cause diarrhoeaare commonin historicEskimo villages,some of whichhave as manyas one-thirdto one-halfof theoccupants ill with diarrhoeaat any one time duringthe year, with childrenthe most frequentvictims (Oswalt I967: 76-7). Furthermore,prehistoric marine- dependentCalifornian Indians had a similarfrequency of porotic hyperostosis to horticulturalistsdespite the former's heavy reliance on fish(Walker I986). It is informativeto compare in detail the semi-sedentaryor seasonally sedentaryEskimo huntersand gathererswith the nomadic !Kung Basarwa hunter-gatherers.The !Kung 'have an unusualsystem of sanitation.They live abouta milefrom their water and defecateinto the sand some distancefrom their camps' (SilberbauerI965). The feces,rapidly dried by thesun, are disposedof by dungbeetles. Furthermore, the San arenot crowdedand move camp several timesa year' (TrusNxrell& Hansen I976: I71). Significant,and I believe conse- quent, is the fact that the !Kung are rarelyanaemic, despite the occasional hookworm infectionevident in threeof eighteenfaecal samples (Truswell & Hansen I976). Anaemia was 'presentin only one sicklyinfant with malaria (anaemiacaused by a chronicdisease), one man out of 38 and one woman out of II3 nonpregnantfemales' (Truswell Hansen I976: I86). It is importantto note thatthe !Kung children'are not anemiceven thoughthey are breastfed until theyare three years old or older' (Truswell& Hansen I976: I93-I94); prolonged lactationoften being blamed for causing porotic hyperostosisin prehistoric populations (also questionableis how exclusivelybreast milk actuallywas in an Anasazi youngster'sdiet afterthe firstyear). Pygmies,another nomadic huntingand gatheringgroup, also show no signs of iron deficiencyanaemia (Truswell& Hansen I976: I92). Althougha highermortality rate from a varietyof causes was recordedfor the 626 SUSAN KENT nomadicversus the newly sedentary !Kung (Harpending& WandsmiderI982), sedentary!Kung tendto appear outwardlyless healthythan the stillnomadic ones (Harpending,personal communication). In fact,Hitchcock has notedthat:

Finally,some observationson thenutritional status of mobileand sedentaryBasarwa popula- tionsin easternBotswana revealthat nutritional problems are greaterin settledsituations.... Poor hygienicconditions and nutritionalproblems often correlate with high ratesof infective diseases (Robson and Wadsworth 1977: I96). Outbreaksof epidemic disease occurredin the Kalahariin I950-I and as recentlyasJuly I977. . . . In spiteof thetrend toward greater stature, boththe health and thenutritional statuses of settled Basarwa populationswere poorerthan those of mobileones. . . . (i982: 254-5)

AustralianAborigines in settledcommunities had irondeficiency anaemia IO to 20 timesmore often than non-Aborigine children in Australia(Taylor I977: I47).

The malnourishmentof infantsand children[in the settledcommunities] was not simplya matterof theirinadequate food intake.Intestinal malabsorption resulting from frequent bouts of infection.. . was also implicated.. . . [At thesettlement, children] acquired repeated respiratory and gastrointestinalinfections which, if theydid not prove to be fatal,may have impairedthe children'sability to absorbnutrients from the diet (Taylor I977: I47-8).

The presenceof Harris lines, transverse trabeculae or radio-opaquelines (Platt & StewartI962), is oftenattributed to dietarystress and used to furtherthe dietarymodel for the changesin porotichyperostosis frequencies (see Huss- Ashmoreet al. I982: 434-41). They can also occur,however, after the stress of a severeillness not relatedto a person'sdiet. Aftersuch an illness,regardless of the normaldiet, Harris lines can develop duringchildhood because therecuperating body requiresan increasein theamount of iron consumed, which usually occurs at a time when a person actuallydesires less nourishmentbecause of nausea. Other studiesalso indicatethat Harris lines do not develop only as theresult of chronicdietary deprivation (e.g., BuikstraI976: 356). In fact,Harris lines may be the resultof slightsubclinical infections and children'with no apparent history of severe illness may possess similar lineations . . . furtherindicating thata trivialcondition may motivatethe productionof a Harrisline' (Lobell I984: I io). The presenceof Harris lines can vary between observers,radio- graphictechniques used, skeletalelement observed, and age of sample (Good- man etal. I984: 24). In addition,new datareveal that there are 'low correlations between Harris lines and known stressorsin the clinical and experimental literatureas well as a seriesof inverserelationships between Harris lines and otherstress indicators in paleopathologicalstudies' (Goodman etal. I984: 24). Also, any stressfrom diarrhoeal infectious diseases can resultin stressof great enough magnitudepotentially to createHarris lines. Clearly more researchis needed. Althoughcombinations of diseasefactors have been suggestedas causingthe abandonmentof specificsites and of partsof the Southwestin general(e.g., Colton 1936; Kunitz & Euler 1972; Palkovich I984; Ryan 1977), thatis too simplistica model fora verycomplex phenomenon.I would concurthat the increasein chronicdiseases may have had some effect,but onlyin combination withsocial, political,economic, and in some areas,environmental changes and SUSAN KENT 627 stressesduring the later periods, which together resulted in theabandonment of largeparts of the Southwest region. That does notnegate the influence of disease in theprehistoric Anasazi and othergroups, but it does recognisethe limitations ofit as a primemover explanation. Certainly Europe, withits present-day high incidenceof diseases (specificallyanaemia) was not abandoned as a resultof massiveepidemics. While it is necessaryto recognisethe importance of disease, itis equallyimportant not to over-emphasiseits role in theculture history of any one area.

Conclusionsand summary The incidenceof porotic hyperostosis in NorthAmerican southwestern Anasazi populationshas in thepast been attributedto a maize-dependentdiet, which is one low in iron, althougha few anthropologistshave suggestedthat it was in combinationwith infectiousdiseases. This articlehas shown: (i) that the prehistoricAnasazi diet was not primarilydependent upon plant species- particularlymaize-and thatthis is probablytrue for many groups around the world priorto European/Euroamericanintervention; (2) thatthe Anasazi diet was probablynutritionally adequate and containedsufficient iron fornormal and healthypeople, the incidencesof porotichyperostosis being the resultof differentfactors; (3) thatAnasazi children were anaemic as a resultof the diseases thatgo alongwith sedentism and aggregation,the percentages not differing that muchfrom the percentages of anaemicchildren present in modernThird World countries;and (4) thatthese diseases include chronic bacterial, viral and parasitic infectionswhich cause chronicdiarrhoea and/or blood loss and lead to chronic irondeficiency anaemia. It is hoped thatthis articlewill raise serious questionsabout the common assertionthat the presenceof porotic hyperostosisin southwesternAnasazi skeletalpopulations is theresult of a nutritionallypoor diet,possibly aggravated by unspecifiedinfectious diseases. The ramificationsof sedentismand aggre- gation primarilyin terms of endemic chronic infectionsbest explain the distributionof anaemiaand porotichyperostosis in a numberof regions.When contrastedwith modern and otherprehistoric populations, the incidence of iron deficiencyanaemia among the Anasazi is not as high or unusual as one might firstsuspect. Such anaemiais present,sometimes at highlevels, in mostWestern Europeancountries, as well as in developingnations. To assumea prioriand uncriticallythat diet was always a causal factorto one degreeor anotherin irondeficiency anaemia is as carelessthinking as assuming withoutevidence that diet was nevera factor.It is now incumbentupon thediet model champions systematicallyto demonstratethat their position better accountsfor the observedpatterns of porotichyperostosis and betterexplains thedata thanthe sedentism-aggregation model in anyparticular area. Finally,if we areto see thesedentism and aggregationof people in theform of villages and townsas a growthin thecomplexity of human organisation, we mustalso view it as a growthin humanpestilence. We can now beginto formulatepredictive models for newly sedentary groups 628 SUSAN KENT such as the !Kung Basarwa and theirfuture, as well as to develop models that allow us to understandthe past more realisticallyand the processes that influencedit. Implicationsof thismodel reachfar beyond the health status of an ancientpopulation to questioncurrent priorities in some ThirdWorld countries' developmentfunding which is orientedtowards changing diet as partof some internationalhealth projects. It will be mostinteresting to notethe future effects of sedentismand aggregationon thenewly sedentary Basarwa and Aborigines aftera fewgenerations have passed. We shouldbe able to learnfrom the past, as well as thepresent, and modifyfunding programmes to emphasisethe eradica- tion of infectiousdiseases ratherthan concentrateso much on alteringfood consumptionand agriculturalpractices.

NOTES I shouldlike to thankMichael Whiteford, Norma Wolf,Sara Quandt, Carol Coe and mybrother, Steven Kent for editorialadvice and encouragement.I alone, however, am responsiblefor any shortcomingsin thearticle. An abbreviatedportion of the article was presentedin I 983 at theSociety forAmerican Archaeology Meetings in Pittsburgh,Pennsylvania. ' It is sometimesforgotten that humans do notalways make decisions based on calculationsof the amountof caloric energy expended compared to thatobtained from an activity.The effortplaced on the widespreadceramic exchange system operating throughout the Anasazi Southwestillustrates this, since with few exceptions,the inhabitantscould have expended energymore efficiently throughthe use of only locally producedplain pottery.Instead, they also made corrugatedand paintedwares and soughtothers from far and wide. Surelypeople todaydo nothave to be told that humansare not alwaysrational in theiractions nor do theyalways maximisethe most for the least effort,and tradeand/or long treksto obtain meat and otheritems was probablymore common prehistoricallythan is currentlyacknowledged. 2 I have admittedlynot dealt with the issue of dentition for reasons of space, even though Anasazi skeletonscontain various sorts of dental pathologies. Some ofthese were affected by theroughage of theirdiet, others by heredity(e.g., thehardness of theenamel), the use of theirteeth for tasks not connectedwith eating (e.g., chewinghides), the amountof intrusivenonedible particles uninten- tionallyadded to theirfood (e.g., sand and rock fromgrinding food on metates),the amountof fluorineand otherminerals in theirdrinking water, and thegeneral health of thepeople (e.g., sickly individualswith infections and anaemiawould probablybe moresusceptible to dentaldisease than healthypersons). 3 Diet can play a role in permittingthe infestation of certainprotozoa, such as amoebas, thatin high meat diets are unfavourable(Chandler & Reed I96I: 72). Althoughspeculative, nomadic Palaeo-Indiansmay not have sufferedas much fromamoebas or othersuch infections,whereas sedentaryand aggregatedpopulations, anaemic despite their diet due to bacterial,viral and parasitic infections,may have been more susceptibleto infestationbecause the iron ingestedwas not absorbed.This would have led to furthermalnutrition, regardless of dietand could have eventually led to prematuredeath. 4 According to Lee et al. (I980: Is5i), iron deficiencyanaemia can resultfrom a varietyof secondarycauses, includingmost importantlymenorrhagia and secondarilyulcers, neoplasm, haemorrholds,etc. (also see Madden& WilsonI980: 224-5; Rybo 1970: I69-70). Feversfrom infectionscan potentiallyaccelerate the loss ofiron through excessive sweating (Bothwell 1970: 156) and be a contributingfactor. Pregnancy also makesdemands on ironstores, especially during the latterhalf of term (Miale I982: 412; Duffy1980: I5), althoughthese tend to be either more minor or idiosyncraticcauses of irondeficiency anaemia. SUSAN KENT 629

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