No abstract

For nearly 500 years, scholars have argued about the origin and antiquity of syphilis. Did Columbus bring the disease from the New World to the Old World? Or did syphilis exist in the Old World before 1493? Here, we evaluate all 54 published reports of pre‐Columbian, Old World treponemal disease using a standardized, systematic approach. The certainty of diagnosis and dating of each case is considered, and novel information pertinent to the dating of these cases, including radiocarbon dates, is presented. Among the reports, we did not find a single case of Old World treponemal disease that has both a certain diagnosis and a secure pre‐Columbian date. We also demonstrate that many of the reports use nonspecific indicators to diagnose treponemal disease, do not provide adequate information about the methods used to date specimens, and do not include high‐quality photographs of the lesions of interest. Thus, despite an increasing number of published reports of pre‐Columbian treponemal infection, it appears that solid evidence supporting an Old World origin for the disease remains absent. Yrbk Phys Anthropol 54:99–133, 2011. © 2011 Wiley Periodicals, Inc.

BackgroundSince the first recorded epidemic of syphilis in 1495, controversy has surrounded the origins of the bacterium Treponema pallidum subsp. pallidum and its relationship to the pathogens responsible for the other treponemal diseases: yaws, endemic syphilis, and pinta. Some researchers have argued that the syphilis-causing bacterium, or its progenitor, was brought from the New World to Europe by Christopher Columbus and his men, while others maintain that the treponematoses, including syphilis, have a much longer history on the European continent.Methodology/Principal FindingsWe applied phylogenetics to this problem, using data from 21 genetic regions examined in 26 geographically disparate strains of pathogenic Treponema. Of all the strains examined, the venereal syphilis-causing strains originated most recently and were more closely related to yaws-causing strains from South America than to other non-venereal strains. Old World yaws-causing strains occupied a basal position on the tree, indicating that they arose first in human history, and a simian strain of T. pallidum was found to be indistinguishable from them.Conclusions/SignificanceOur results lend support to the Columbian theory of syphilis's origin while suggesting that the non-sexually transmitted subspecies arose earlier in the Old World. This study represents the first attempt to address the problem of the origin of syphilis using molecular genetics, as well as the first source of information regarding the genetic make-up of non-venereal strains from the Western hemisphere.

The Barker hypothesis asserts that stressful events early in the life history of an individual have negative health consequences later in adulthood. The hypothesis initially focused on prenatal stressors as indicated by birth weight and related outcomes. This initial concern with the fetal phase of development led to its description as the “fetal programming” or “fetal origins” hypothesis. The realization that stressors in the postnatal phase had similar impacts on adult health has led to its latest characterization as the Developmental Origins of Health and Disease Hypothesis (DOHaD). In this paper, we review the history and evidence in support of the DOHaD hypothesis. We then introduce an untapped source of information on early life stress: enamel hypoplasias and other developmental defects of enamel. Enamel defects are nearly indelible records of physiological perturbations, or stress, to developing ameloblasts (enamel‐forming cells). Furthermore, the location of the defects translates to specific periods of growth, providing a permanent temporal record of early life stressors from in utero to approximately twelve years of age. As we discuss, a handful of studies of different populations reveals that individuals with enamel defects that developed in utero and early in infant‐childhood development tend to be subject to earlier adolescent or adult mortality.