| Abstract: |
Concede that Armelagos and Cohen may be corrent in their interpretation of the observed patterns, but they argue that other interpretations are equally possible and equally difficult to prove or disprove because hidden problems in the analysis of skeletal cemetery populations (nonstationary, heterogeneity, differential frailty, selective mortality) complicate the interpretation by making a cemetery a potentially biased sample of the once-living population. Wood and colleagues said that becuase individuals with and without pathology were not at equal or random risk of dying, the proportion of the dead in a skeletal population exhibiting pathology was not necessarily an accurate gide to community health
and they said following Sattenspiel and Harpending (1983), that becuase a population might have been growing or declining irregularly or being affected by in- and out- migration at the time a cemetery was formed, the distribution of ages-at-death in the cemetery had not fixed relationship to the real life expectancy of the once-living population. <p> Explores models for inferring health in archaeological human populations. Three important conceptual issues are addressed: demographic nonstationarity, selective mortality, and hidden heterogeneity in risks. <u>Demographic nonstationarity</u> refers to the departure of a population from the stationary state- a state characterized by closure to migration, constant age-specific fertility and mortality, zero growth rate, and an equilibrium age distribution. Thus is a population is not stationary then small variations in fertility have large effects on its age-at-death distribution, while quite large modifications or mortality have virtually none. (Life expectancy or the mean age at death are often effectively measures of fertility rather than mortality. <u>Selective morality</u> simply is the problem that we never have a sample of all the individuals who were at risk of disease or death at a given age (problem of sample bias of representation). <u>Hidden heterogeneity</u> states that a skeletal series is made up of a mixture of individuals who varied in susceptibility to illness, disease, and death. As a result, aggregate-level age specific mortality rates in terms of individual risks of death are impossible to determine. <p> All these problems reflect two unavoidable facts. First, it is impossible to obtain direct estimates of demographic or epidemiological rates from archaeological samples. Second, although "health" (however defined) is a biological characteristic of the individual, inferences about it must be based on aggregate- or population-level statistics. <p> Several diseases can potentially affect the skeleton in similar ways and some diseases will leave no mark on the bone. Infectious disease may be acute (rapidly resolved or leading to death) or chronic (a recurring condition that may lead to bone change). In spite of problem of the "invisible" nature of many of the infectious diseases, either because they do not manifest themselves in the skeleton or because they kill the person before bone change occurs, the presence of lesions associated with infectious diseases provides useful data on how people adapted to the environment in which they lived. <p> One of the major problems confronting researchers is that the male:female ratio of the sample may not be representative of the original population. However, this is usually hard to determine (Waldron 1994). The fact is, most biological anthropologists working on past populations have to cope with fragmented and incomplete data. Careful consideration of the biases and problems inherent to the study of human skeletal material is thus critical if researchers hope to understand patterns of health and disease in past populations <p> pg. 351</br> There are numerous studies which use stature as an indicator of the overall health of the population. It is commonly assumed that shorter long bone length are consistent with increased stress. However, it does not take into account that the differences in stature are observed strictly in individuals who died at each age. Basic assumptions used: <p> 1) distribution of stature among living children at a given age is absolutely invariant between two populations or time spans, that is, that there is no differnetial, stress-related stunting between these two groups.</br> 2) mortality is selective with respect to the distribution of stature- in particular, shorter children are at higher risk of death. <p> *The correct way to interpret:</br> When mortality is high, a larger fraction of the entire distribution of stature is represented among dead individuals
as a result, dead individuals are comparatively tall on average. If mortality slackens, only the most frail (i.e., short individuals) die. Periods of low mortality are therefore characterized by comparatively low mean stature among the dead. In general, the frequency of apparent "stunting" among the dead is uninformative about the distribution of stature or relative health among the living unless the level of mortality and the relationship between stature and frailty are known. One again, proportional mortality is a poor guide to population prevalence. <p> pg 352</br> Mortality may signal either an improvement or a deterioration in the population's health. <p> pg 353</br> Periostitis is a lesion of infectious origin, while cribra orbitalia and porotic hyperostosis reflect synergistic interactions of infection and nutrition. Thus, the presence of healed periostital lesiond may sometimes indicate a state of comparatively good overal health. As cribra and hyperostosis, it is possible that all children survive to recover and for their lesions to heal, unless they happen to die from some other unrelated cause. <p> pg 354</br> Goodman and Armelagos (1988 AA 90:936-944) suggest 3 hypotheses to account for the lower age at death in individuals with enamel hypoplasia: <p> 1) enamel defects may represent frailty, or the constitutional susceptibility to stress.</br> 2) childhood stress resulted in a lack or adequate immuno-physiological response to mount an effective biological repsonse to later stress which led to premature death later in time.</br> 3) social inequality led to higher incidences of stress among certain groups in the population at-large which led to greater premature mortality.</br> 4) [suggested by Wood et al. 1992] suggests that enamel hypoplasia does not occur unless the child survives the period of stress and resumes normal enamel formation. Thus individuals with observable lesions were principally from the less frail (i.e., advantaged) group, and they had a lower mean age at death than the disadvantaged group because of higher fertility, not because of poor survival. <p> pg. 356</br> **In sum, a significant health advantage is reflected in a lower mean age at death and a higher frequency of skeletal lesions. Better health makes for worse skeletons. Thus the real question is "Do skeletal lesions accurately reflect the prevalence of a disease in a living population,or are they representive of the survivors of a disease who lived long enough to manifest them? So if interpreted properly, according to Wood et al (1992), skeletal lesions usually indicate that the individual survived a disease expereicne or stress episode, and that individual is obviously healthier than someone who died from the ame disease experience without having had an opportunity to leave its mark on the skeleton. <p> <u>Transition to Agriculture</u> [reviews Cohen and Armelagos 1984 <u>Paleopathology at the Origins of Agriculture</u> and Cohen 1989 <u>Health and the Rise of Civilization</u>]</br> Currently the data is interpreted as indicating that increased stress and reduced survival at various ages, both signs of apparent deterioration in general health among the early agriculturalists. It is plausible that the shift in mean age at death reflects an increase in fertility rather than an increase in mortality associated with a deterioration in general health. Such an elevation in fertility, if it occurred, might have reflected greater availability of digestible weaning foods and, hence, shorter periods of lactional infecundability among th early agriculturalists. It is further by Woods et al. that higher frequencies of skeletal lesions observed in early agricultural samples could reflect an enhanced ability to survive episodes of illness and stress or an amelioration of other, competing and perhaps unobservable causes of death. <p> pg 364</br> The existence of a group of weaning-age skeletons may suggest increased failty relative to weanling diarrhea, but this same group also provides evidence - by its very existence - of low fraility relative to neonatal and infant mortality. <p> <i>Frailty</i> defined, refers to individual biological characteristics associated with persistent differences among individuals in susceptibility, propensity, or relative risk with respect to disease or death.
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