Stress, adaptation, and enamel developmental defects • 283 



No 

 Hypoplasias 



L.W. 



M.A.L.W. 



MM 



TOTAL 



Figure 2. Mean ages at death of Dickson Mounds adoles- 

 cents/adults by number of hypoplasias-stress periods be- 

 tween 3.5 and 7.0 years developmental age. LW = Late 

 Woodland, MALW = Mississippian Acculturated Late 

 Woodland, MM = Middle Mississippian. 



Finally, there is a significant decrease in longevity with 

 childhood stress periods in the total sample (Table 1 , Figure 

 2). The mean age at death of individuals without hypoplasias- 

 stress periods is 35.8 years, or 4.4 years greater than for those 

 with one hypoplasia-stress period (3 1 .4 years) and 10.2 years 

 greater than for those with two or more hypoplasia-stress 

 periods (25.6 years). The ANOVA yields a significant F-ratio 

 (4.99, p < .01 ) and all a priori contrasts are significant at the 

 . 10 level of confidence. Again, the most significant contrasts 

 are between the no-stress period group and the one or more 

 stress period and two or more stress period groups (t = 3.04 

 and 3.08, p< .01, < .01). 



At least three prior studies of archeological groups have 

 also noted an inverse relationship between the occurrence of 

 enamel hypoplasias and longevity. White (1978) assessed 

 hypoplasias on permanent maxillary first molars from South 

 African Plio-Pleistocene Australopithecines (ca. 1.5-3.0 

 M.Y.B.P.). He noted that individuals with maxillary first 

 molar hypoplasias from the Swartkrans site (n = 6) had 

 "lower-than-expected" ages at death. These individuals die 

 between 4 and 13 years of age, while individuals with non- 

 hypoplastic first molars (n = 1 10) die between 8 and 31 years 



of age. Goodman and Armelagos (1988) have calculated the 

 mean age at death of individuals in these groups as 7.8 and 

 19.6 years, respectively. While White's study sutfers from a 

 restricted sample size and lack of precision in assigning ages 

 of death to fragmentary palcontological materials, the data 

 nonetheless demonstrate a decrease in fitness associated with 

 hypoplasias. 



Cook and Buikstra ( 1979) compared the mean age at death 

 of infants and children with and without postnatal defects on 

 deciduous tooth crowns from Middle and Late Woodland 

 skeletal samples from Illinois. They conclude that postnatal 

 dental defects are associated with decreased longevity during 

 both the Middle and Late Woodland periods. 



Rose and co-workers (1978) studied areas of disturbed 

 enamel formation visible in thin-section (Wilson bands) in 

 Middle Woodland, Mississippian Acculturated Late Wood- 

 land, and Middle Mississippian samples from Illinois. They 

 found that individuals with Wilson bands died at an earlier 

 mean age at death in all samples. Overall, we calculated that 

 the average age at death of the 21 individuals with Wilson 

 bands to be 26.7 years, or 15.4 years less than the average 

 age of the 66 individuals without Wilson bands (42. 1 years). 

 In summary, these studies support our contention that dental 

 developmental defects may predispose to an earlier age at 

 death. 



There are at least three processes which may account for 

 the association between childhood stress and decreased life 

 expectancy. First, these data may result from differential life- 

 long patterns of biological susceptibility to physiological dis- 

 ruptions and their adverse effects. An increased suscep- 

 tibility to stress may be causative of both an increased 

 frequency of childhood hypoplasias and an earlier age at 

 death. That is, individuals who are ill during childhood may 

 continue to fall ill as adults due to a "weak constitution." 

 Second, individuals who were exposed to and survived a 

 period of severe childhood stress may suffer a loss in ability 

 to respond to other stresses. In a sense, these individuals are 

 "biologically damaged" by the early stress. The wear and tear 

 of stresses during development may render them less fit to 

 respond to and survive subsequent stresses. For example, 

 suboptimal early nutrition has been proposed as a mechanism 

 for later immune dysfunction (Chandra 1975; Miler 1982). 

 Third, these data may result from difTerential lifelong pat- 

 terns of behaviorally and culturally based exposure to 

 stressors. An increased lifelong potential for exposure to 

 stressors may be causative of both an increased frequency of 

 childhood stress and earlier ages at death. Barker and Os- 

 mond (1986a,b) have shown an association between poor 

 nutrition and respiratory infections in childhood and coron- 

 ary disease and chronic bronchitis in adulthood. They pro- 

 pose that this relationship is mainly due to social conditions 

 present in childhood, which are likely to persist into adult 

 life. 



Zagreb PaUopathotogy Symp. 1988 



