| Abstract: |
The of this chapter was to present a model for the interpretation of skeletal indicators of stress and to provide an overview of the use and meaning of a series of commonly used indicators. The various indicators may have partially overlapping etiologies
but they are not identical or equally useful. This is why several indicators (and thereby multiple confirmations) of stress. By evaluating the pattern of stress within populations we may be able to better understand the conditions which are causative of the stress and evaluate likely responses to the stress. In Goodman et al's model, they make the basic assumption that if two different diseases are equal in the severity and duration of physiological disruption that they cause, the impact on the individual and the population should equal. Stree is a product of three sets of factors: 1) environmental constraints, 2) cultural systems, 3) host resistance. Environmental contraints include both limiting resources and stressors. These vary over space and time. Cultural systems may act to buffer the impact of environmental constraints, for example, technology. Intensification of cultural systems may allow for greater population density, may result in a lower quality of diet for each person and amplify interpersonal strife as access to quality nutrients is limited. Host resistance varies by age and sex. Genetic factors also play a role in resistance to certain diseases There are three indicators of stress: 1) cumulative stress, 2) episodic stress, 3) associated with specific diseases Cumulative stress provides a summation of the amount of stress over long periods of time. Indicators include mortality measures and growth assessments. Under stress an organism will either slow its growth or stop growing altogether. Since stress generally results in the realse of catbolic hormones (those which release energy) the anabolic process of growth is inhibited. Therefore, indicators of growth may be indicative of stress of a general nature. Episodic stress are more precise and confined in the time at which stress occurred. Two common examples are Harris lines (HL) and linear enamel hypoplasia (LEH). Mortality data is derived from the assessment of individual ages at death. From this, the direct estimation of life expectancy at birth or the construction of life tables are based. Life tables provides an estimation of life expectancy, probability of dying, and survivorship for all age classes. \uCriticisms of life tables\u 1) Assumes that a skeletal sample is truly representative of a real population 2) No population growth is occurring 3) There is little stochastic fluctuation in the population's size 4) Individual ages-at-death are accurately determined Growth Curves are a method used to make an assessments on the degree of environmental stress in prehistoric populations. The most valid use of prehistoric growth curves involves comparisons of curves from genetically similar populations. When studying long bone length and width curves it is important to keep in mind that length may be maintained at the expense of cortical thickness. \uCriticisms of growth curves\u 1) Prehistoric data are not strictly comparable to modern data 2) Age estimates for prehistoric individuals are based on developmental criteria (tooth eruption) whereas modern individuals are usually aged by the calendar 3) Prehistoric data are cross-sectional (different individuals dead in different age classes) rath than longitudinal (the same individuals progressing from age class to age class). \uCriticisms of adult long bone length and width\u Comparison across populations introduces problems in interpretation as it is difficult to estimate the degree of genetic involvement in size and shape differences. Size and shape differences in adult skeletons may be more easily related to environmental conditions and physiological disruption if there is relative genetic homogeneity in samples. The relative genetic continuity of successive samples involves the basis for the interpretation of recent secular increases in height within a country or define geographic area. The secular increases have most frequently been interpreted as being due to a decrease in infant-childhood disease and elimination of nutritional stresses. Similar interpretations may be applied to similar patterns in prehistory in genetic continued he can be isolated approved. While long bone length yields information on group adaptation, analysis of long bone thickness, with, and histological structure to reveal patterns of metabolic activity and physiological disruption adults. Because cortical bone is in a constant state of remodeling by resort in an deposition, introduction of any stress would seriously affect metabolism may alter the rate of remodeling. When rates of bone remodeling are in disequilibrium, bone can be lost instead of maintained. Conditions resulting osteoporosis (bone loss) include metabolic disturbances, systemic disease, a nutritional stress. Sexual dimorphism is compounded by potential genetic variation in the degree of dimorphism among populations in the likelihood that males are more protected from stress in many societies. Furthermore, in archaeological analysis the same traits which are used to determine sex are often used to access the degree of them organism, does engendering circularity. \bHarris Lines\b The mechanism by which Harris Lines are formed involves a reduction in the thickness of the epiphyseal cartilage plate with increased resistance of the immature cartilage cells to capillary and osteoblastic penetration. Once formed, Harris Lines may resort and disappear. There's little agreement on how, when, and where resort and occurs. Harris line frequencies have been used to measure gender differences and stress, interpopulation differences and stress, periodicity of stress, and the chronologies of stress during development. If Harris lines are invalid indicator of stress, then they're likely to indicate acute and episodic stress in contrast to the previously noted indicators of cumulative stress. \uCriticism of Harris Lines\u 1) differences in frequency may be interpreted as a function of variation in degree of episodic stress 2) there is a low correlation between Harris lines and then stress or in the clinical experimental literature as well as a series of inverse relationships between Harris lines and other stress indicators in paleopathology full studies 3) Harris line chronologies are dependent on one is faith in the meaning of lines as well as a consideration of age related host resistance and growth phenomena 4) evaluation of the frequency of Harris lines across studies is cautioned against because dated concerning Hearst lines are known to vary by Observer, radiographic material and method employed, long bone observed, and age of sample. \bEnamel Hypoplasia\b Enamel Hypoplasia is a deficiency in enamel thickness resulting from a cessation in amelogenesis. Enamel hypoplasias are visible on tooth crowned services as lines, bans, or pits of decreased enamel thickness. The usual method of analysis involves the recording defects on a single tooth, usually the canine. Enamel hypoplasias are a relatively valid and replicable indicator of infant-childhood stress. Further experimental work and more agreement on the of minimum requirement for scoring defects will benefit interpretation.
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