The Osteological Paradox Reconsidered

Mark Nathan Cohen; James W. Wood; George R. Milner

Current Anthropology, Vol. 35, No. 5. (Dec., 1994), pp. 629-637.

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ter, and Sontz 1971; Gallagher 1977; Hayden 1977, 1979)
that the rules may be so lax [at least with regard to the
overall morphology of the lithic artifacts) that the ar-
chaeologist may be unable to ascertain from the lithics
that they were made according to such rules. I suspect
[although I do not speak as a lithics specialist) that we
recognize the symbolic nature of the archaeological rec-
ord of early Upper Paleolithic Europe more from its dec-
orative and representational art than from its lithics.
Nevertheless, I am in complete agreement with
Byers's interpretation of the Middle-to-Upper-Paleolithic
transition in Europe with the one exception that there
are more kinds or levels of symbolic behavior than he
mentions and that the origins of language are as impor-
tant to understand as the origins of symbolic culture.
., to see a scholar from outside
Above all. I am encouraged
Paleolithic archaeology taking a serious and anything
but naive interest in what archaeology has to offer. If
we archaeologists can return the compliment by taking
a serious and ideally not too naive interest in what other
disciplines have to tell us about the evolution of human
culture and of the human mind, our discipline will bene-
fit enormously.
References Cited
A X E L R O D , R. 1984 The evolution of cooperation. N e w York: Ba-
sic Books.
C H A S E , P. G . 1987 Specialisation de la chasse et transition vers
le Paleolithique superieur. L'Anthropologie 9 I : I 75-88.
-. 1988. "Scavenging and hunting i n the Middle Paleolithic:
T h e evidence from Europe," i n Upper Pleistocene prehistory of
Western Eurasia. Edited by H. L. Dibble and A. Montet-White,
pp. 226-32. Philadelphia: University Museum, University of
Pennsylvania.
-. 1989. "How different was Middle Paleolithic subsistence?
A zooarchaeological perspective on the Middle t o Upper Paleo-
lithic transition," i n The human revolution. Edited by P. R.
Mellars and C. Stringer, pp. 32 1-37. Edinburgh: Edinburgh Uni-
versity Press.
-. 1991. Symbols and Paleolithic artifacts: Style, standardiza-
tion, and the imposition of arbitrary form. Journal of Anthropo-
logical Archaeology 1o:193-214.
C H A S E , P . G . , A N D H A R O L D L. D I B B L E . 1992. Scientific archae-
ology and the origins o f symbolism: A reply t o Bednarik. Cam-
bridge Archaeological Iournal 2:42-5 I .
G A L L A G H E R , 7 . 1977. Contemporary stone tools i n Ethiopia: Im-
plications for archaeology. Journal of Field Archaeology 4:
407-14.
G A M B L E , C L I V E . I $182.Interaction and alliance i n Paleolithic so-
ciety. Man 17:92-102.
C O U L D , R . , D. K O S T E R , A N D A. S O N T Z . 1971. T h e lithic as-
semblage of the Western Desert Aborigines of Australia. Ameri-
can Antiquity 36:149-46.
H A M I L T O N , W . D. 1964. T h e genetical evolution of social behav-
ior. Iournal of Theoretical Biology 7:1-16.
H A Y D E N , B. 1977. "Stone tool functions i n the Western Desert,"
i n Stone tools as cultural markers: Change, evolution, and
complexity. Edited by R. V . S. Wright, pp. 178-88. Canberra:
Humanities Press.
-. 1979. Paleolithic reflections: Lithic technology and ethno-
graphic excavation among the Australian Aborigines. Atlantic
Highlands: Humanities Press.
S T R I N G E R , C . B . , A N D C . G A M B L E . 1993. In search of the Ne-
anderthals: Solving the puzzle of human origins. London:
Thames and Hudson.
W A A L , F . D E . 1989. Chimpanzee politics: Power and sex among
apes. Baltimore: Johns Hopkins University Press.
Volume 35, Number 5, December 1994 1 629
The Osteological Paradox
Reconsidered
MARK NATHAN COHEN
Department of Anthropology, State University of N e w
York College at Plattsburgh, Plattsburgh, N.Y. 12901,
U.S.A. 15 VII 94
In 1982 George Armelagos and I [Cohen and Armelagos
1984) collected studies of pathology from skeletons and
mummies of prehistoric hunter-gatherers and farmers
from every region of the world that had produced compa-
rable data. We found a number of fairly consistent
trends: [ I )that the frequency of nonspecific chronic in-
fection displayed by skeletons was commonly higher
among farmers than among earlier hunter-gatherers; ( 2 )
that the frequency of specific infections such as yaws
and tuberculosis or tuberculosis-like infection usually
increased as groups became larger and more sedentary;
13) that the frequency of intestinal infections and para-
sites increased with group size and sedentism when
mummies or feces were studied [see Allison 1984; see
also Reinhard, Hevly, and Anderson 1987); (4)that the
frequency of porotic hyperostosis, the skeletal lesion of
[childhood?)anemia, was almost always higher among
farmers than among earlier hunter-gatherers; ( 5 ) that
other signs of malnutrition [retarded growth and osteo-
porosis in children, premature adult osteoporosis, re-
duced tooth size, etc.) were more common among farm-
ers than earlier hunter-gatherers; (6) that the average
stature of measured adult individuals declined through-
out the Old World from the Paleolithic through the Neo-
lithic period; and (7)that signs of systemic stress visible
in teeth, including macroscopic enamel hypoplasia and
microscopic Wilson bands, were usually more frequent
and pronounced in farmers than among earlier hunter-
gatherers.
I have interpreted these data as supporting the conclu-
sion that biological stress increased with farming [Co-
hen 1989). I continue to interpret them this way, and I
note from at least two papers in the 1990s that Arme-
lagos and colleagues also continue to make this interpre-
tation [Armelagos 1990, Armelagos, Goodman, and Ja-
cobs 1991; see also Goodman 1993).This interpretation
makes the implicit assumption that skeletons in a cem-
etery, at least on the average, are reasonably representa-
tive of the living populations that produced them and
therefore that changes in skeletal assemblages reflect
real changes in the health of once-living populations.
This is an assumption made implicitly or explicitly,
with varying degrees of caution, by most quantitatively
oriented paleopathologists.
The skeletal data and our interoretation of them have
been challenged, however. In elaborating what they call
"the osteological paradox," Wood et al. [CA 33:343-70;
see also Harpending 1990) suggest that a number of fac-
tors including nonstationarity, hidden heterogeneity,
differential frailty, and selective mortality can bias the
630 I CURRENT ANTHROPOLOGY
sample of skeletons in a cemetery, making it an unrepre-
sentative sample of a once-living people and rendering
conclusions about the impact of economic change on
human health unreliable. The points that they raise
seem theoretically to be valid, and I note that they are
discussed positively by a number of my colleagues in
skeletal analysis with reference to the analysis of indi-
vidual populations (see CA* comments). However,
their theoretical arguments lead them to offer a reinter-
pretation of health trends associated with the origins of
agriculture which, from a broad geographic and temporal
perspective, 1 find untenable and refutable.
Wood et al. begin by conceding that Armelagos and I
may be correct in our interpretation of the consequences
of early farming, but they argue that other interpreta-
tions of the skeletal material are equally possible (and
equally difficult to prove or disprove). They argue, in
particular, that the apparent increase in pathology as-
sociated with early farming populations in fact could
reflect an improvement in health. They suggest that
farming populations may normally have been better-
nourished and longer-lived than their hunting-and-
gathering forebears and thus better able to record
stresses in their skeletons. By this interpretation, the
frequency of infection (or other pathology) did not in-
crease with farming, but its record was more fully pre-
served in the skeletons of better-nourished, more resil-
ient, longer-lived farming populations. The skeletons of
foragers were relatively pathology-free not because the
foragers were healthy but because they died of insults
before their skeletons could record them. Using this
logic, Wood et al. produce a reevaluation of the Dickson
Mounds archaeological sequence spanning the adoption
and intensification of agriculture in Illinois. They sug-
gest that low average ages at death and high frequencies
of dental enamel hypoplasia in the latest, fully agricul-
tural population, previously read as a record of declining
health and longevity (Goodman et al. 1984)~ might actu-
ally be indicative of increased fertility and biological
privilege.
I respectfully disagree. Various types of evidence sug-
gest that ours is the more probable interpretation. For
one thing, the conclusions from paleopathology, as I
have interpreted it, conform so closely to observations
of health from ethnography and predictions from epide-
miological theory that they should be taken as they ap-
pear. For example, epidemiological theory predicts an
increase in infection and parasite rates with sedentism
and larger group size, supporting the direct interpreta-
tion of this pattern of pathology in the skeletons. More-
over, the pattern of increasing infection and parasites
with group size and sedentism occurs repeatedly in com-
parisons of historical and modern populations (Cohen
1989). Similarly, modern hunter-gatherers display very
low rates of juvenile infection, malnutrition, and ane-
mia, just as their prehistoric counterparts display low
rates of porotic hyperostosis (see also Kent and Dunn's
[1993] discussion of hypoferremia in newly settled San
in the Kalahari). Contemporary hunter-gatherers also
display relatively low rates of weanling diarrhea,
thought to be a major contributor to enamel hypoplasia,
so the low rates of hypoplasia in prehistoric foragers
should not be surprising. Tuberculosis and related dis-
eases occur primarily in archaeological samples from re-
cent, relatively urban environments, mimicking the pat-
tern of the disease of the present day (Cohen 1989).
Goodman (1993) has pointed out, also, that enamel hy-
poplasia, one of the few skeletal pathologies that can
readily be seen in living individuals, has repeatedly been
found to occur among living people in the pattern that
our hypothesis predicts-it is regularly more common
in lower-class than in upper-class individuals, sug-
gesting that it reflects relative stress rather than relative
background nutrition or resilience. Can it really be mere
coincidence that our direct explanation of paleopatho-
logical data fits so well with these expectations?
Furthermore, it is arguable at best whether nutrition
and health improved with farming and sedentism among
prehistoric populations as Wood et al. assume or
whether survivorship was significantly greater in early
agricultural groups than in hunter-gatherers. Optimal
foraging data (reviewed in Cohen 1989; see also Simms
1987, Russell 1988) suggest that prehistoric hunter-
gatherers were in a position of descending to agriculture
as once-superior economic strategies had to be aban-
doned (see, in particular, Russell's description of the ef-
ficiency of harvesting wild and then domestic einkorn
wheat). Hunter-gatherers should typically have had bet-
ter background nutrition (as well as fewer background
infections) than farmers and should normally have been
the more resilient even though the stresses of mobility
itself might have worked against them.
The perspective of Wood et al, may be affected by their
(and our) familiarity with the !Kung San of the Kalahari,
whose caloric intake is marginal (at the low end of the
modern hunter-gatherer spectrum and undoubtedly well
below that of prehistoric hunter-gatherers [see Cohen
19891) and who gain weight and resilience when they
settle down under 20th-century conditions with 20th-
century benefits (Pennington 1992). Under these condi-
tions they attain a success at rearing their children that
should imply population growth rates greater than those
displayed by either prehistoric hunter-gatherers or pre-
historic farmers-so their use as an ethnographic anal-
ogy for prehistory may be limited.
In general, populations settling down under zoth-
century conditions often display either increased fertil-
ity or increased survivorship or both. However, neither
can have occurred to any significant degree with the be-
ginning of the Neolithic, as I will show. Perhaps more
to the point, neither fertility nor survivorship can have
changed very much at the Neolithic transition unless
the two changed in opposite directions. The best esti-
mates typically suggest that the rate of growth for our
species as a whole accelerated from an average of about
0.01% per year before the adoption of farming to only
about 0.1% after it (see, e.g., Hassan 1981, Bentley,
Goldberg, and Jasienska 1993). Even if we assume that
this entire acceleration resulted from increased survivor-
ship with no contribution from increased fertility, there
simply was not enough of an improvement in survivor-
ship on the average to account for the increase in visible

pathology. For the !Kung San, for example, an increase
from 44% to 45% of individuals surviving to the mean
age of maternity would suffice to explain the accelerated
Neolithic growth rate of 0.1%~but it alone could not
explain the apparent increase in pathology among early
farmers-especially because both ethnographic compar-
isons and some paleodemographic life tables suggest
that fertility often increased with farming, further reduc-
ing any possible average Neolithic increase in survivor-
ship (Cohen 1989, Buikstra, Konigsberg, and Bullington
1986, Wood et al.)
Further, re historic farmers also commonlv have
higher rates of dental caries than hunter-ga;herers.
Should we conclude, as almost all scholars do, that the
farmers' diet was more cariogenic than that of hunter-
gatherers, or should we conclude that hunter-gatherers
~ormally'alsosuffered but died of acute cariogeiesis be-
fore their teeth had had the chance to develop lesions
while farmers lived long enough to develop caries? Con-
versely, some prehistoric hunter-gatherers have greater
skeletal robusticity and more arthritis than farmers. Is
this simply because the hunter-gatherers lived long
enough to develop robusticity and arthritis but farmers
did not? We can reconcile these two contradictory pat-
terns only by recognizing that each pathology is telling
us something of its own character and the lifestvle of
its victims by its pattern in the skeletons. I submk that
caries and arthritis and also chronic afflictions like peri-
ostitis and porotic hyperostosis should be interpreted as
diseases whose skeletal pathology is fairly straightfor-
ward. Diseases like measles, which are known to kill
without scarring the skeleton, will unquestionably have
to be dealt with in a different manner.
Perhaps we can resolve our differences by pointing
out that heterogeneity, differential frailty, and selective
mortality, although real, do not play quantitatively as
important a selective role in the creation of cemetery
samples as Wood et al. imply.
If the individuals in a population were completely
equal in their risk of dying from all causes (or if all
causes of death were strictly accidental), we would ex-
pect a death cohort or a cemetery full of such cohorts
to be a random and usually representative sample of the
living group, as the our hypothesis assumes. As Wood
et al. point out, however, populations are in reality het-
erogeneous in various ways; individuals are not at equal
risk of dying from each cause, and death is selective.
But, as is true when we study natural selection and evo-
lution, that other domain of differential frailty and selec-
tive mortalitv, not all or even most deaths are necessar-
ily selected, ;or are they all selected for the one trait or
condition under consideration. For example, even in
that famous model of natural selection, the British pep-
pered moth whose color evolved to match the tree-
trunks, presumably only a fraction of the moths are ac-
tually eaten or spared because of their wing color.
Others presumably are eaten or escape being eaten de-
spite their color-get caught on the wing, hit the wind-
screens of fast-moving trucks, fly too close to hot lights,
get stepped on, starve to death, or suffocate in the smog
that is darkening the trees. The visible effect of natural
Volume 3 5 , Number 5, December 1994 / 631
selection for color in any one generation may be rather
small.
In fact, the sample of deaths in a population will al-
ways include both a selected and a random component.
I suggest that under most circumstances the effects of
selection will show up only as relatively minor statisti-
cal currents against the background of competing fac-
tors. I submit that, except under very extreme selective
conditions, the actual death cohort for a population for
any year will normally be a fairly good representation of
the living population from which it came because of
the random nature of the unselected deaths, with only
a small bias for each of various slight selective advan-
tages. In particular, most human deaths are probably
only weakly related to the chronic illnesses that human
skeletons display (or those pathologies make only a
small percentage contribution to the probability of dy-
ing), and skeletons may therefore be a relatively random
sample with regard to visible skeletal pathology in the
population. (In fact, accidents and zoonotic diseases [see
Fiennes 19781, significant causes of death among hunter-
gatherers and early farmers which tend to strike active
adults, would arguably kill those who were otherwise
the most fit and the least frail). In specific instances, of
course, severe selection or random statistical departure
from expected frequencies ("drift") may make any one
skeletal sample a misleading sample of the parent popu-
lation. I protect myself from this possibility by using
only trends that occur repeatedly in different popula-
tions.
One possible application of this reasoning is the
change in stature from the Paleolithic to the Neolithic
throughout the Old World. If we consider that only se-
lected mortality affects the distribution of heights in the
cemeteries, then, as Wood et al, claim, the declining
stature of Neolithic populations might represent the
overall good health and nutrition of the population from
which they come. However, if we allow that a signifi-
cant portion of the dead represent random deaths (with
regard to stature), as they certainly must, the implica-
tion is that the Neolithic skeletons represent a universe
of smaller people and therefore presumably a population
with declining nutrition-which is of course what the
optimal foraging data suggest we should find.
Although there is ample room for further discussion,
I suggest that for now, on the whole, the conclusions
of Cohen (1989) and Cohen and Armelagos (1984) can
stand.
JAMES W. W O O D A N D G E O R G E R. M I L N E R
Department of Anthropology, Pennsylvania State
University, University Park, Pa. 16802, U.S.A. 8 VIII
94
Several responses to our paper on "The Osteological Par-
adox" (CA 33:343-70) have now appeared in CURRENT
ANTHROPOLOGY, and this may be a good time to reply
to them all.' The commentators are evenly divided be-
tween those who heartily loathed the paper and those
who basically liked it but wanted to make additional
points or to suggest ways of tackling some of the prob-
lems we discussed. Since our intention was to spark
debate, we welcome all the comments, even those ac-
cusing us of scientific snobbery, nihilism, and aiding
and abetting sinister pro-state, pro-civilization forces-
although how we can be both nihilist and pro-civ-
ilization is something of a mystery to us.
Our paper highlighted several problems that can con-
found inferences drawn from skeletal s a m ~ l e about
s the
health of prehistoric populations. These iifficulties are
now widely recognized in epidemiology and demography
but have received insufficient attention in research on
skeletons from archaeological sites. As Goodman (CA
34:281-88) and Saunders and Hoppa (1993) point out,
and indeed as we pointed out ourselves, osteologists
have long acknowledged that they deal with samples
made up of life's failures at any particular age. But con-
trary to Goodman we see only limited progress being
made in the development of formal methods for building
this insight into the interpretation of skeletal lesions.
If problems of inference and interpretation have proven
difficult for researchers working with living popula-
tions, we cannot imagine that they can be any easier for
those dealing with bones dug up from cemeteries.
Most of the problems we discussed in our paper stem
from heterogeneous frailty and selective mortality, the
confounding effects of which can be illustrated with a
homely parable. Suppose that one of the four authors of
our original paper has grossly elevated serum cholesterol
levels, while the other three are normal, at least in that
respedt. In the population at large, s e r u i cholesterol has
a measurable, monotonic association with the risk of
death from coronarv heart disease. Thus, an individual's
serum cholesterol ievel can be considered a component
of frailty, and our tiny population of coauthors is het-
erogeneous for frailty. Now suppose that our high-
cholesterol colleague keels over dead one day on dis-
covering that he has been labeled a pro-civilization,
nihilistic, scientific snob in a major journal. An autopsy
reveals that this ill-starred anthropologist suffered a
myocardial infarction resulting from the plugging up of
his coronary arteries by atherosclerotic plaques, no
doubt aggravated by the arterial constriction that can
accompany acute psychological stress. In addition, mul-
tiple ischemic lesions are found on his heart, signs of
past cardiac "events." We now have a mortality sample
on our hands, albeit a small one. What can we infer
about the health status of the living population that
launched this lost soul on his journey across the Styx?
Obviously not much, except that it contained at least
one individual who was apparently at an elevated risk
I. Although this response is written by only two of the original resent the remaining frailty distribution among the liv-
coauthors, the other two have read and endorsed it. An additional
article focusing on the issues raised in our paper has appeared in the ing at whatever age the death occurs-except, of course,
Yearbook of Physical Anthropology [Saunders and Hoppa 1993). for the very last death, for that particular coauthor will
of death by cardiovascular disease. Because of selective
mortality, this one now-shattered vessel of clay, this
kicker of buckets, tells us little about the three individu-
als who did not die. And this sort of selective mortality
must occur whenever ( I )individuals differ in their bio-
logical (or even "lifestyle") characteristics and ( 2 ) those
characteristics bear some relationship to the likelihood
of death. Despite Cohen's assertion that deaths are es-
sentially random, we suggest (and we are by no means
the first to do so) that these two conditions are universal
in human populations.
This example allows us to lay to rest one point of
confusion in Goodman's comment (see his n. 7). Good-
man equates the words "biological" and "genetic" in a
way that we do not. Surely one's serum cholesterol level
is a biological characteristic. Yet our friend with the
clogged arteries may have had elevated serum choles-
terol because he had familial hypercholesterolemia (a
genetic condition) or because he habitually ate fried egg
sandwiches with pork drippings three times a day (the
ever-popular Elvis Diet). In either case, elevated serum
cholesterol is a frailty factor, and selective mortality will
act upon it. If serum cholesterol is at least partially heri-
table (as, in fact, it is), then selective mortality in the
demographic sense will also constitute natural selection
in the genetic sense. But demographic selectivity can
occur in the complete absence of natural selection.
There are other lessons to be drawn from this parable.
The fact is, the miserable corpse at our feet did not die
in childhood from diphtheria, typhus, or smallpox, and
he certainly did not die from marasmus precipitated by
weanling diarrhea. Thus, the fact that cardiovascular
disease is responsible for such a high fraction of the ob-
served deaths (IOO%in our sample so far) is partly attrib-
utable to the comparative unimportance of other dis-
eases in the population-the paradox of proportional
mortality. And the multiple ischemic scars on his now-
stilled heart suggest that he lived under conditions that
permitted him to survive with his disease for a consider-
able period before the fatal heart attack that left him
pining for the fjords. Indeed, had he died not from a heart
attack but from chronic congestive heart failure-had
he not perused the pages of CURRENT ANTHROPOLOGY
that sore and dreadful morn-he would have left behind
a heart in really terrible shape, and that hideous lump
of myocardial tissue would have been a sign, in all its
ugliness, that he had managed to live successfully for
many years despite his illness. The worse the condition
of the heart, the longer the inferred survival-a kind of
myocardial paradox.
This example can be criticized, most obviously be-
cause the sample is ludicrously small but more interest-
ingly because the other three coauthors will eventually
die, and we will then have an opportunity to bring their
blighted carcasses under the pathologist's knife. That,
one might think, would provide an unbiased view of the
entire population. But each and every death will misrep-
 Volume 3 5 , Number 5, December 1994 1 633

be perfectly representative of himself. Acquired condi- Pretending that it doesn't matter is precisely what Co-
tions, including those associated with aging, will partly hen [above)tries to do. As he remarks, his preferred in-
regenerate the upper tail of the frailty distribution terpretation of the paleodemographic and paleopatho-
among the survivors, so that selective mortality will al- logical evidence "makes the implicit assumption that
ways produce corpses that look terrible, no matter what skeletons in a cemetery, at least on the average, are rea-
the general health of the population. The fact that one sonably representative of the living populations that
in five Americans will eventually die of cancer does not produced them and therefore that changes in skeletal
mean that 20% of living Americans have cancer right assemblages reflect real changes in the health of once-
now. living populations. This is an assumption made implic-
Byers [CA 35:282-84) makes an interesting point in itly or explicitly, with varying degrees of caution, by
this connection. He suggests that it may be possible to most quantitatively oriented paleopathologists." That
assess the magnitude of the selective mortality acting was precisely the point of our paper: paleopathologists
on a trait such as stature by examining shifts in the do make this assumption, often without examining its
distribution of the trait among individuals who die at implications for their inferences. But according to Co-
later [presumably postselection) ages. The specific tests hen, the assumption that the dead are representative of
he advocates, however, are lacking in statistical power, the living is justifiable because mortality is largely ran-
as he is careful to point out; they also make a strong dom with respect to individual characteristics: "I sub-
presumption that the trait of interest is normally distrib- mit that, except under very extreme selective condi-
uted at the outset of the selection process, for otherwise tions, the actual death cohort for a population for any
measures of skew and kurtosis by themselves are unin- year will normally be a fairly good representation of
formative about selection. An assumption of normality the living population from which it came because of
may be approximately correct for stature but is unlikely the random nature of the unselected deaths." Frankly,
to hold for many frailty factors (see Schork, Welder, and we don't know whether to be terrified or relieved by
Schork 1990). Still, Byers's basic idea is sound. Here we this conclusion-terrified because even the healthiest
sketch an alternative approach to the same problem, an among us can drop dead tomorrow for no good reason,
approach that may be both more general and more pow- relieved because we can all stop worrying about diet,
erful. If z is a frailty factor, be it stature or whatever, exercise, and those annoying annual check-ups. We re-
then.the conditional distribution of z among survivors spectfully suggest that Cohen's assertion that mortality
at age t [i.e., among those whose life span T is greater is mostly random (nonselective)with respect to individ-
than t ) is ual characteristics is one of the most remarkable state-
ments in the history of population science. If it is true,
epidemiologists may as well retire, for no relative risk
will ever be distinguishable from I. And demographers
where f [ z )is the density function of frailty at the outset can pretty well close down shop too: life tables are un-
of the selection process and S(tl z ) is the survival func- necessary because mortality cannot be affected signifi-
tion conditional on z. Given appropriate specifications cantly by age, and sex-specific life tables are even more
of f [ z ) and S[tl z), the equation could be fitted to data of a waste of time because they foolishly assume that
on skeletal samples by straightforward maximum- one's sex may influence the risk of death. The claim
likelihood methods, thus providing a direct estimate of that mortality is largely random and nonselective is so
the effect of selective mortality on the trait. Of course, profound in its implications that it needs to be sup-
for a trait that changes with age, as does stature, we ported by evidence, not merely asserted. After all, the
would have to rescale the f [zl T > t ) function properly, entire insurance industry is founded on the premise that
perhaps by using the residuals from one of the Preece- the risk of death varies among individuals in a poten-
Baines model growth curves rather than raw stature it- tially predictable way.
self (see Preece and Baines 1978).But that is a secondary But we agree with Cohen that mortality has stochas-
point. We believe that Byers's suggestion has consider- tic [random) as well as deterministic [nonrandom) ele-
able merit and deserves further exploration. Inciden- ments. In fact, several of us have spent major portions of
tally, the equation tells us explicitly what we have to our professional lives formulating demographic models
worry about in this whole area of inquiry: how frailty that include both stochastic and deterministic compo-
varies, indicated by f [z),and how frailty affects mortal- nents [for a review, see Wood et al. 1992).With respect
ity, captured by S[tl z ) . to mortality, such models are consistent in showing the
The deeper problem, alluded to in our paper, is what following pattern: Within a given risk group, the vari-
to do when we don't have a readily measurable frailty ance in life span is typically large, and in that narrow
factor such as stature or when measurable variables do sense the random component of mortality can be consid-
not capture all the variation in frailty. As we tried to ered important [see Vaupel 1988 for an insightful discus-
convey in our paper, this is a tough nut but not, we sion of this point). When risk groups are pooled, how-
think, an uncrackable one (see the extended discussion ever, mortality at any given age will still be dominated
in Wood et al. 1992).But it can't be cracked by ignoring by those individuals of highest risk who survived to that
it, wishing it away, or pretending that it doesn't matter age [Manton, Stallard, and Vaupel I 986). In other words,
in the population of interest. demographic and epidemiological models make it clear
 634 1 CURRENT ANTHROPOLOGY
that substantial selective mortalitv can occur even in
the face of nontrivial stochastic variation in life span2
Cohen's claim that mortality was largely nonselective
in prehistoric societies appears to be based on his belief
that most deaths in such societies were accidental.
While reliable data on causes of death are notoriously
difficult to obtain from nonliterate people, such data as
exist suggest that the overwhelming majority of deaths
in all preindustrial populations are infectious in nature,
with undernutrition being a frequent contributary
cause. In our work with the Gainj, a population of swid-
den horticulturalists on the northern fringes of Papua
New Guinea's Central Highlands, we found that about
70% of deaths were from infectious causes, with diar-
rheal disease being more common in children and acute
respiratory infections somewhat more common in
adults; physical trauma accounted for only about 2% of
deaths (Wood 1980:122). Broadly similar patterns have
been reported for the !Kung [Howell 1979:69) and the
Aka Pygmies (Hewlett, van de Koppel, and van de Kop-
pel 1986:54-5 5). Infectious diseases are known to be
highly selective, especially with respect to nutritional
status and immune function. In a studv of the Turkana
of northern Kenya, one of the most traditional groups of
nomadic pastoralists in the world, Shell-Duncan (1993,
1994) has shown the overwhelming importance of gas-
trointestinal and respiratory tract infections in de-
termining patterns of morbidity and mortality (with
malaria running a somewhat distant third); more
important, she has shown that these diseases are power-
fully selective on nutritional status and immunocompe-
tence as assessed by delayed-type hypersensitivity tests.
In none of these studies or any others that we are aware
of have accidents been shown to be a leading cause of
death. It is all very well for Cohen to dismiss evidence
on the !Kung from the discussion, but the fact remains
that there are very few studies of anthropological popu-
lations that have yielded high-quality information on
causes of death, and none of them indicates that acci-
dents predominate. Perhaps people were clumsier in pre-
history, but we doubt it.
Besides, there is no reason to believe that accidents
are genuinely random: "accident-proneness" is a well-
established epidemiological phenomenon. Nor can we
assume that violent deaths as opposed to those from
illness or any of the other vicissitudes of life are ran-
domly distributed. The selectivity of violence can be
seen even in one of the very few osteological samples in
which a fairly large fraction (at least 16%) of individuals
died from being hit with clubs or shot with arrows (Mil-
ner, Anderson, and Smith 1991). In this skeletal collec-
tion from a cemetery geographically and temporally
close to Dickson Mounds, most of the people who had
been slaughtered were adults, presumably because their
daily activities put them at greater risk of being at-
tacked. Furthermore, many of these skeletons showed
2.For outstanding reviews of the relevant models, see Manton and
Stallard (1984: chap. 6; 19881, Mode (1985: chaps. 3 and 41, and
Namboodiri (1991: chap. 9).
signs of debilitating injuries or active infections that
would have reduced any chance they might have had to
fight or flee successfully. In this particular prehistoric
setting, then, violent death was not unrelated to an indi-
vidual's age, prior life history, or current health status.
In other words, even accidents and violence can be selec-
tive on individual characteristics.
Jackes (CA 34:434-3 9) notes, quite rightly, that there
are many serious problems that we did not highlight in
our original paper, including but not limited to age-
estimation and differential preservation. However, as we
pointed out, those issues have received far more atten-
tion in the literature than the ones we did raise.3 But
that does not mean that the issues we deemphasized
have all been settled. As long as we are enumerating
additional problems to worry about, we would mention
three more, without, however, meaning to imply that
this is an exhaustive list. First, as many osteologists
have noted, the disease processes that can leave ob-
servable skeletal lesions represent only a tiny fraction
of all the afflictions likely to be present in the living
population; focusing on them will almost necessarily
give a highly distorted view of overall health and disease
in the population. The second problem is differential
diagnosis-the difficulty of assigning a slzeletal lesion
unambiguously to a particular cause; because of errors
in differentiating diseases, skeletal lesions are often of
low specificity as diagnostic markers. The third problem
is that skeletal lesions usually occur only in rare, often
extreme, cases of the diseases that produce them; as a
result, such lesions are of low sensitivity as markers of
disease. As it happens, there are formal statistical meth-
ods for assessing both specificity and sensitivity (Kelsey,
Thompson, and Evans I 98 6:28 6). If such assessments
were done, we suspect that most skeletal lesions would
prove to be poor diagnostic markers.
A superficial reading of our paper might suggest that
we are being inconsistent on this point. Some of the
time we seem to be saying that mortality samples over-
estimate the prevalence of pathological conditions (be-
cause of selective mortality), and some of the time we
seem to be saying that mortality samples underestimate
the prevalence of pathological conditions (because of
low sensitivity). What we are actually saying is that
both biases are likely to be operating simultaneously,
and both make it difficult for us to link lesion frequen-
cies in skeletons with disease prevalence in the living
3. In fact, biases arising from the differential preservation of bones
in archaeological deposits were noted at least two centuries ago.
On digging a mound in Virginia in the 18th century, Thomas Jeffer-
son (1788:105)reflected that "the bones of infants being soft, they
probably decay sooner, which might be the cause so few were found
here." Observations on the differential preservation of soft tissue
are even older. When Hamlet asked the grave maker, "How long
will a man lie i'th'earth ere he rot!" he was told: "Faith, if 'a be
not rotten before 'a die-as we have many pocky corpses now-a-
days that will scarce hold the laying in-'a will last you some eight
year or nine year. A tanner will last you nine year" (Act 5, Scene
I ) . We only hope that these literary and antiquarian allusions are
not too pro-civilization for some of our readers' tastes (cf. Cohen,
CA 33:359).

population in any straightforward way. Although the
two biases operate in opposite directions, it would be
foolish to assume that they must exactly cancel each
other out for any disease.
In our view, a far more serious block to inference,
which none of our critics addresses, is the fact that le-
sion frequencies in the dead partly reflect proportional
mortality, which in turn reflects the whole spectrum of
conditions affecting the risk of death, not just those that
caused the particular lesion or lesions in question. This
problem is not solved by using Goodman's (p. 281) "mul-
tiple indicators of health," because the full set of lesions
potentially detectable in the skeleton still represents
only a small portion of that spectrum. Moreover, selec-
tive mortality may be operating on all the indicators
simultaneously, and to differing degrees.
According to Goodman (p. 282), "Wood et al. miss the
mark in their explication of the dynamics of selective
mortality partly because they are committed to the no-
tion that the goal of paleoepidemiology is understanding
cause of death. Paleoepidemiologists are in fact seldom
concerned with cause-of-death analysis, which is exceed-
ingly difficult for a number of reasons and is not at all es-
sential to saying something about health and adjustment
in past populations." Surely paleopathologists and espe-
cially paleodemographers are very interested indeed
in causes of death, at least part of the time. But that is
beside the point. If we want to say something about
health and adjustment on the basis of skeletal samples,
then we have to own up to the fact that we are looking
at samples of dead people, and presumably their reason
for dying had something to do with their health and
adjustment. We would never draw inferences about the
distribution of health characteristics in the general popu-
lation by exclusively examining hospital patients, among
whom serious disorders approach 100%. Serious disor-
ders are even more common among the dead: such disor-
ders are what most of them died of.
We cannot stress this point too much. If a skeletal
lesion-or the condition responsible for it, or a trait pre-
disposing to that condition, or another trait highly corre-
lated with that condition-has any relationship whatso-
ever to the risk of death, the skeletal collection must be
a biased sample for the living population. The bias
caused by selection may be large or small; it may be
positive or negativej but mathematically it must exist.
We would be more than happy to discover that the bias
is consistently small and, hence, untroubling, as Saun-
ders and Hoppa (1993) suggest for the special case of
staturee4But at present, we have neither theory nor em-
pirical evidence showing that the bias can always be
ignored. It will take a lot of hard work to develop the
4. Goodman (p. 283) argues that the linkage between short stature
and the risk of death is partly spurious, owing to the confounding
effects of "the causal link of both with impoverished and stressful
living conditions." Of course it is, and this fact reinforces our basic
point: mortality is selective not only for conditions that directly
cause death but also for any other traits (including socioeconomic
characteristics) that are consistently correlated with such condi-
tions, whatever the source of correlation.
Volume 3 5 , Number 5, December 1994 1 635
necessary theory and compile the necessary evidence;
bald assertions and appeals to conventional wisdom
won't take us very far in the right direction.
Readers of Goodman's comments might conclude that
we somehow missed the fact that skeletal lesions attrib-
utable to infection and malnutrition take some time to
develop, that people often live with those conditions for
extended periods, and that some fraction of them re-
cover from their illness. Yet it is precisely this variation
in experience that makes the interpretation of skeletal
lesions in mortality samples such a vexing topic-and,
if explored further, such a potentially enlightening one.
While it goes without saying that Goodman (p. 282) is
correct when he writes that there are many reasons to
investigate the "cultural and social repercussions" of
disease, it is difficult to see how morbidity and mortality
can be disassociated from one another in studies based
strictly on individuals of a particular age who failed to
survive. After all, the ability to live with a condition
causing a pathological bony response or to recover from
it, perhaps with an impaired ability to withstand further
illness, does not imply that the presence of these skele-
tal lesions is not in some way associated with an ele-
vated risk of death.
Goodman makes extended criticisms of several of our
illustrative exercises. In doing so, he misses the spirit of
those exercises, which was to illustrate potential prob-
lems and not to hold a mirror up to nature. (Having said
that, we would contend that the assumptions underly-
ing our illustrations are no less realistic than those made
by Goodman, Cohen, and others in their more "final"
analyses.) Goodman spends a long time on one espe-
cially simple-minded example that was merely intended
to introduce some of the problems; but by doing so, he
inadvertently uncovers one of the most fundamental dif-
ficulties in this area of study. In our example, we posited
three subgroups within a population and assumed that
those subgroups were exposed to low, moderate, and
high levels of "stress," respectively. Under not too unre-
alistic assumptions, we showed that the high- and low-
stress groups could display similar lesion frequencies
and thus be difficult to distinguish from one another
using skeletal samples alone. But Goodman says that
we willfully ignored an important piece of evidence: had
we examined the mortality patterns of the three groups,
they would have fallen out from each other unambig-
uously. This claim is unassailable-provided that we
know beforehand how many subgroups there are, are
able to assign skeletons to the subgroups without error,
and can reliably reconstruct the mortality patterns of
the subgroups. Otherwise we are presented with an un-
known number of risk groups, each of unknown size,
whose apparent pooled age-at-death distribution is con-
founded by heterogeneous frailty and demographic non-
stationarity. Alas, we fear that osteological samples
more often approximate the latter set of circumstances
than the former.
In his response to our alternative explanation for the
Dickson Mounds findings, - , Goodman criticizes the as-
sumptions of our model, dismissing many of them as
636 / CURRENT ANTHROPOLOGY
unrealistic. While the reasonableness of our assump-
tions is difficult to assess from the osteological evidence
available from Dickson Mounds (as Jackes so rightly em-
phasizes), this criticism again misses the point of the
exercise. Given the time, energy, and inclination, we
suspect that we could come up with a much more realis-
tic model (involving, for example, more than two sub-
groups or continuously distributed frailty). But that
would not alter our fundamental point: we can interpret
the osteological record meaningfully only if we do in-
deed have an explicit model for the formation of the
mortality sample we are working with. As we said re-
peatedly in our paper, the point is not that our model is
right and other models are wrong but that models are in
fact necessary and for the most part lacking.
It is clear from his very first sentence (p. 281) that
Goodman misunderstands our position: we emphati-
cally do not argue that "health inferences from paleode-
mographic and paleopathological data are impossible"
but merely suggest that such inferences are more diffi-
cult than we all originally believed, and also more inter-
esting. We are convinced that there are solutions to the
problems we raised, but finding the solutions will re-
quire some deep thinking about the processes linking
frailty, stress, disease, tissue responses, and the forma-
tion of mortality samples. It will also require formal
modeling of those processes. As Goodman (p. 282) notes,
"There is . . . a mathematical tethering of individual and
group frailty; if group frailty changes, then either the
size of subgroups or the frailty of one or more subgroups
must change. Furthermore, one can begin to interpret
the individual significance of aggregate frailty if one has
a theory about the distribution of frailty and some idea
of how groups might change in size and how exposures
might change subgroups' health risks-in short, contex-
tual information." Although apparently written in criti-
cism of us, this is in fact precisely our position. Indeed,
if one adds the further stipulation that we need models
of the linkage between frailty and the risk of death, then
Goodman's statement summarizes our view admirably.
We are pleased that Goodman underscores the impor-
tance of "cultural context" in the interpretation of skel-
etons from cemeteries; in doing so, he again reiterates
our position as expressed in the original paper. It is
strange, however, that the Dickson Mounds skeletons
continue to be misperceived by Goodman and others
(Goodman et al. 1984; Goodman and Armelagos 1985;
Cohen 1989: 121, 126) as somehow "spanning the adop-
tion and intensification of agriculture," to use Cohen's
phrase. The full course of changes in diets and lifeways
related to an increased reliance on cultivation actually
spanned a much longer period than the few centuries
when the Dickson Mounds burial ground was used, and
maize was a late addition to diets already based in large
part on several cultigens (see Smith 1989).To date, only
a few Dickson Mounds skeletons have been analyzed for
stable carbon isotopes-an indication of maize con-
sumption-but skeletons from throughout the cemetery
sequence yield figures that fall within the late prehis-
toric, or agriculturalist, range for eastern North America
(Buikstra and Milner 1991, Buikstra 1992).Thus, despite
~reviouscharacterizations of the Dickson Mounds sam-
ple, it does not encompass the full spectrum of changes
from hunting-gathering through intensified agriculture.
It is likewise difficult to argue from the available archae-
ological evidence that the latest Dickson Mounds people
were sick because they suffered the ill effects of an out-
flow of food to other places (Goodman et al. 1984, Good-
man and Armelagos 1985). At present, it is simply not
clear what the changes over time in skeletal lesion fre-
quencies observed at Dickson Mounds might mean and
what might have caused them.
In general, both Cohen and Goodman seem to want
to cast us as irredeemably opposed to the scientific posi-
tions they have staked out. This reaction is as surprising
as it is unwarranted. As we took pains to say, "It is
important to emphasize that our reinterpretation of the
health consequences of early agriculture is not necessar-
ily more correct than previous interpretations. And, in-
deed, we suspect that both interpretations may be cor-
rect for different periods and locations. The point,
however, is not that we are right and other authors are
wrong but that the data [by themselves, i.e., unaided by
models] support both interpretations equally well" (CA
3 3 :3 57). Cohen and Goodman also try to make us sound
more pessimistic than we actually are. We believe that
advances can be made, but we reiterate that a necessarv
precondition for advancement is the development of st;-
tistical models for the formation of mortality samples.
Although we do not underestimate the difficulties of
this work, we do not think they are insurmountable.
And we a;e pleased to acknowledge that the work has
already begun, thanks in part (we are gratified to say)
to our paper. Byers's idea on measuring selectivity, for
example, is a nice step in the right direction, as is the
more extended analysis of Saunders and Hoppa (1993).
While neither of these analyses can be considered the
final word on the subject, both at least show what can
be done if the issues are taken seriously. Jackes's (p.
435) trenchant comment is relevant here: "Despair
should arise only if osteologists are not intellectually
honest and able to withstand a reappraisal of their
methods."
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On the Emergence of
Agriculture in the New World
DOLORES R. P I P E R N O
Smithsonian Tropical Research Institute, Unit 0948,
Apartado 2070, Balboa, Panama. 15 VI 94
Fritz (CA 35:305-9) argues for a much younger chronol-
ogy for the emergence of agriculture in the New World
than is generally accepted. She suggests that the 5th-
millennium-B.P.radiocarbon dates obtained on the Te-
huacan maize cobs (Long et al. 1989) should cause schol-
ars to reevaluate the entire sequence of food production
and associated early settlement in both Central and
South America. I argue here that a major revision for
New World agricultural beginnings ( I ) is premature as
applied to Mesoamerica, ( 2 )does not fit the existing evi-
dence from lower Central America and northern South
America, and (3)fails to appreciate the plants and eco-
logical contexts around which New World tropical food
production emerged.
Fritz sets a beginning date on agriculture in Meso-
america no earlier than 6,ooo-5,ooo B.P., although ex-
perts agree that the maize, squash, and other domesti-
cates recovered from the Tehuacan Valley caves
underwent incipient domestication and genetic manipu-