Minor sternum and vertebral column congenital defects in Lisbon Identified Skeletal Collection.

This study has mainly a descriptive aim, in which crude prevalence of minor skeletal congenital defects is calculated and sex differences are tested. Prevalence is compared with other studies to recognize regional patterns. Association with age-at-death and year-of-birth is tested to identify impact of environmental stress on minor congenital defects presence. Testing association between defects will identify defects with a probable identical etiology. Chi-square was used to identify sex differences, between studies differences, and to test relationships between defects and Spearman correlation to verify correlation intensity. T-test was used to test age-at-death and year-of-birth differences in defects prevalence. There were no statistically significant differences in prevalence of minor skeletal defects for sex and age-at-death. There were statistically significant differences in year-of-birth for sternal aperture and pectus excavatum (crude prevalence was higher for those who were born earlier). There was a statistical significant association between pectus excavatum and manubrium mesosternal joint and atlas posterior/lateral bridging and notochord defects. For most defects, this study has lower prevalence than other studies. From 18 minor axial skeletal congenital defects analyzed, prevalence ranges from absent to 26.3 (notochord defects). Pectus excavatum and manubrium mesosternal joint might have a similar etiology as well as atlas posterior/lateral bridging and notochord defects. This study has lower prevalence, for almost all defects, than other studies. None of the minor congenital defects tested might, at this time, be considered useful stress markers.

Can early-life growth disruptions predict longevity? Testing the association between vertebral neural canal (VNC) size and age-at-death.

This study tests the association of vertebral neural canal (VNC) size and age-at-death in a Portuguese skeletal collection from the 19th-20th century. If the plasticity and constraint model best explains this association, VNC size would be negatively related to mortality risk. If the predictive adaptive response (PAR) model is a better fit, no association can be inferred between VNC size and age-at-death. Ninety individuals were used in this study. The anteroposterior and transverse diameters of all vertebrae were measured. A Cox regression analysis was performed by sex to assess the effect of VNC size on age-at-death, after adjusting for the effects of year of birth and cause of death. Several measurements of VNC diameters have a statistically significant effect on age-at-death, but when the covariates were considered, this association became non-significant. The PAR model seems the best fit to explain the relation between VNC and age-at-death. Individuals who went through stressful events early in life were prepared to face a stressful environment later in life, allowing them to cope with adversity without affecting longevity. However, developmental plasticity may be buffered by maternal capital accumulated over several generations, and health hazards encountered throughout life can contribute to health outcomes and longevity.

Age at death and linear enamel hypoplasias: testing the effects of childhood stress and adult socioeconomic circumstances in premature mortality.

OBJECTIVE: The aim of this study was to test the association between linear enamel hypolasias and adult socioeconomic circumstances with age at death in a modern skeletal sample of known age. Specifically, this study wishes to test whether there is a relationship between early life stressors, environmental quality in adult life and premature mortality. METHODS: The presence/absence of LEH and the number of LEH episodes were recorded in 113 adult males from the Lisbon identified skeletal collection. The association between LEH and age was quantified using linear regression and binary logistic regression models, calculating crude and adjusted linear regression coefficients and odds ratios. The models were adjusted for year of birth, socioeconomic and migration status, and cause of death. RESULTS: The presence and number of LEH were related to premature mortality. Individuals expressing at least one enamel defect survived 9.0 years less or were 2.5 times more likely to die before 53 years of age compared to individuals with no LEH. However, when controlling for the confounding factors considered, the association between LEH and age became nonsignificant. CONCLUSIONS: The results indicate that although early life stressors, identified as LEH, seem strongly associated with premature mortality, adulthood socioeconomic circumstances accounts for most of the decreased longevity. This suggests that either macroscopically identified LEH in the permanent canine do not measure stressors early in life, or that a cumulative adversity model is a more adequate explanation.