Paradox and promise: Research on the role of recent advances in paleodemography and paleoepidemiology to the study of “health” in Precolumbian societies

Bioarcheology has made tremendous strides since the subdiscipline's inception, subsequent syntheses, the standardization of data collection methods, and analytical advances ranging from molecular analyses through age-estimation and biodistance. Concurrently, health and the adaptive success of past populations have remained primary concerns. However, questions are routinely raised about lesions and whether or not changing frequencies are synonymous with increases or decreases in stress, morbidity, and overall health. These include how and why healed lesions can simultaneously represent stress and survival, demanding that researchers understand how population dynamics influence skeletal sample formation. In this study, methods to analyze age- and sex-specific mortality patterns prior to, and in conjunction with, the analysis of linear enamel hypoplasias are demonstrated. Paleodemographic and paleoepidemiological models are presented for late Pre-Columbian skeletal samples from the Eastern Woodlands. Results of hazard modeling demonstrate that elevated mortality rates were commonplace during the latter half of the Mississippian period (AD 1200–1450) with reproductive-age females experiencing high age-specific risk of death attributed to the development of fortified villages and novel environments for increased pathogen loads. Corollary results are presented for the age-specificity of linear enamel hypoplasias in the central Illinois River valley. The epidemiological models demonstrate that the relationship between adult mortality and early childhood stress varied through space, culture, and time. These findings highlight the need to effectively operationalize measurements related to health and stress in past populations and support the adoption of selective mortality and heterogeneity in frailty as key concepts in bioarcheological research. Am J Phys Anthropol 155:268–280, 2014. © 2014 Wiley Periodicals, Inc.     

A comparison of dental enamel defects in Christian and Meroitic populations from Geili,central Sudan

El Geili, located in the region of the Middle Nile, was occupied successively by Neolithic, Meroitic, and Christian populations at betweenn 3,500 BC and 1,500 AD. The scant archaeological evidence suggests that the Meroitic and Christian populations at Geili were patoral nomads. Dental enamel hypoplasias, indicators of general stress (malnutrition/disease), were studied in order to characterize and compare the health of these groups. A total of 130 individuals comprise the skeletal populations examined, from which a variety of appropriate sub-samples were analysed for defect presence, type, and age of occurence. Permanent incisors and canines represent the period of enamel development between birth and 6.5 years of age. Sample consisting of sets of incisors and canines (n=29) showed a negligibile difference of 77,8% vs. 81.8% in the Meroitic and Christian groups, respectively. Frequency differences by hypoplasia type reveal no obvious consistencies. Chronological analyses show chronic stress between 1 and 6 years of age. The research was supported by the Italian Ministery of Education (M.P.I. quota 40%) and the Italian Council of Research C.N.R. grant n. 89.00902.15).     

Under restrictive conditions,can the widths of linear enamel hypoplasias be used as relative indicators of stress episode duration?

Linear enamel hypoplasia (LEH), a type of enamel defect reflecting nonspecific physiological stress, has traditionally been used by bioarchaeologists to assess human health. Initially, measurements of defect width were used to estimate the duration of stress episodes. More recently, methods of counting within-defect perikymata (enamel growth increments) were developed to more accurately assess duration. Because perikymata are often not continuously visible within defects, while widths can usually be measured, the primary purpose of this article was to determine if, under restrictive conditions, the widths of LEH defects might be used as relative indicators of stress episode duration. Using a set of dental replicas from the prehistoric Irene Mound (1150-1400 A.D.), this study also investigated potential sources of variation in defect widths and how often defect widths could be measured and within-defect perikymata counted. Of 120 defects, only 47 contained both measurable defect widths and total within-defect perikymata, while 79 had measurable defect widths. Regression analysis revealed that, for these 47 defects, defect widths were more strongly related to the total number of within-defect perikymata than they were to crown region or tooth type. Although wide prediction intervals indicated that a defect's width could not be used to predict the number of within-defect perikymata for an individual, narrower confidence intervals associated with hypothetical mean population widths suggested that mean defect widths might be used to rank populations in terms of relative average stress episode duration.     

“Missing perikymata”—fact or fiction? A study on chimpanzee (Pan troglodytes verus) canines

Recently, a lower than expected number of perikymata between repetitive furrow‐type hypoplastic defects has been reported in chimpanzee canines from the Fongoli site, Senegal (Skinner and Pruetz: Am J Phys Anthropol 149 (2012) 468–482). Based on an observation in a localized enamel fracture surface of a canine of a chimpanzee from the Taï Forest (Ivory Coast), these authors inferred that a nonemergence of striae of Retzius could be the cause for the “missing perikymata” phenomenon in the Fongoli chimpanzees. To check this inference, we analyzed the structure of outer enamel in three chimpanzee canines. The teeth were studied using light‐microscopic and scanning‐electron microscopic techniques. Our analysis of the specimen upon which Skinner and Pruetz (Am J Phys Anthropol 149 (2012) 468–482) had made their original observation does not support their hypothesis. We demonstrate that the enamel morphology described by them is not caused by a nonemergence of striae of Retzius but can be attributed to structural variations in outer enamel that result in a differential fracture behavior. Although rejecting the presumed existence of nonemergent striae of Retzius, our study provided evidence that, in furrow‐type hypoplastic defects, a pronounced tapering of Retzius increments can occur, with the striae of Retzius forming acute angles with the outer enamel surface. We suggest that in such cases the outcrop of some striae of Retzius is essentially unobservable at the enamel surface, causing too low perikymata counts. The pronounced tapering of Retzius increments in outer enamel presumably reflects a mild to moderate disturbance of the function of late secretory ameloblasts. Am J Phys Anthropol 157:276–283, 2015. © 2015 Wiley Periodicals, Inc.     

Association of prostate cancer susceptibility variant (MSMB) rs10993994 with risk of spermatogenic failure

β-Microseminoprotein (MSMB) is one of the most abundant proteins in human seminal plasma. It has been identified that MSMB increased significantly in oligoasthenoteratozoospermic patients compared with fertile controls. We hypothesized that the functional polymorphism (rs10993994) of MSMB gene could be a risk factor for spermatogenic failure. For this study, 338 patients with idiopathic oligozoospermia or azoospermia and 382 fertile controls were recruited from an infertility clinic. Semen analysis was performed by computer-assisted semen analysis system. The functional polymorphism of MSMB gene was genotyped using TaqMan method. Sixty three seminal plasma samples were used to test the expression of MSMB by enzyme-linked immunosorbent assay (ELISA). The TT genotype and T allele were associated with an increased risk of idiopathic infertility with azoospermia (TT genotype: OR, 1.75; 95% CI, 1.03–2.95; T allele: OR, 1.34; 95% CI, 1.03–1.75). However, no differences were found in risk for the TT genotype or T allele among men with oligozoospermia. In addition, idiopathic infertile males have significantly higher MSMB expression levels than fertile controls. We present the first epidemiologic evidence supporting the involvement of common genetic polymorphism in MSMB gene in spermatogenic failure. These results suggest that men carrying the variant have an increased risk of spermatogenic failure associated with male infertility. Further studies are needed to confirm the roles of the polymorphism in idiopathic azoospermia and investigate the biological mechanism of elevated MSMB expression in infertile males.