This research provides the first attempt to directly assess the age of pubertal development in adolescents during the 10th-17th centuries. Poor diet, infections, and physical exertion may have contributed to delayed development in the medieval adolescents, particularly for those living in the city of London. This study sheds new light on the nature of adolescence in the medieval period, highlighting an extended period of physical and social transition.
Adolescence is a unique period in human development encompassing sexual maturation (puberty) and the physical and psychological transition into adulthood. It is a crucial time for healthy development and any adverse environmental conditions, poor nutrition, or chronic infection can alter the timing of these physical changes; delaying menarche in girls or the age of peak height velocity in boys. This study explores the impact of chronic illness on the tempo of puberty in 607 adolescent skeletons from medieval England (AD 900-1550). A total of 135 (22.2%) adolescents showed some delay in their pubertal development, and this lag increased with age. Of those with a chronic condition, 40.0% (n=24/60) showed delay compared to only 20.3% (n=111/547) of the non-pathology group. This difference was statistically significant. A binary logistic regression model demonstrated a significant association between increasing delay in pubertal stage attainment with age in the pathology group. This is the first time that chronic conditions have been directly associated with a delay in maturation in the osteological record, using a new method to assess stages of puberty in skeletal remains.
Macroscopic hypoplasia represent short periods of stress during infancy/early childhood which did not disrupt future investments in growth or cause long-term damage to health. Small TR diameters represent chronic stress during late childhood/early adolescence which resulted in greater susceptibility to infections and increased risk of mortality. These interactions were influenced by sex and socioeconomic status, suggesting that socioeconomic circumstances in both childhood and adult life could influence exposure and resistance to stressors.
Selective mortality can occur towards individuals who survive episodes of physiological stress, such as disease and malnutrition, during development. The skeletal elements affected depend on the timing of these stressful episodes. Studying multiple non-specific indicators of stress can show which periods of development were affected and whether certain periods can be linked with selective mortality. To examine this method a preliminary study of 61 adult individuals from the Medieval population of Fishergate House, York was undertaken to examine small vertebral neural canal size and reduced adult stature. Previous studies have shown that selective mortality occurs towards individuals who display these non-specific indicators of stress. Statistical analysis showed that small transverse neural canal diameter was significantly associated with early adult mortality for males and females and there was evidence of selective mortality towards females with reduced stature. This suggests that individuals who died in early adulthood experienced health insults during late childhood which stunted VNC growth but males in particular were not significantly affected by health insults after this age as they achieved a normal adult stature. Therefore it appears that health insults which occurred during late childhood had a greater influence on adult health in the Fishergate House population. This method could be expanded to provide more detailed information by using a greater variety of non-specific indicators of stress which will allow more specific periods of development to be investigated.
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