Biomaterial Database

The long-term impact of developmental stress. Evidence from later medieval and post-medieval London (AD1117-1853). 2015

Rebecca Watts

University of Reading, Reading, Berkshire, RG6 6UR.

OBJECTIVE Episodes of ill-health in childhood can predispose affected individuals to further periods of illness and early adult mortality. This study uses nonspecific indicators of stress to examine how growth disruptions during infancy/early childhood, and late childhood/early adolescence affected adult longevity in later medieval and post-medieval London. METHODS Hazards analysis was used to evaluate the effect of linear enamel hypoplasia (LEH) and the size of the anteroposterior (AP) and transverse (TR) diameters of the vertebral neural canal (VNC) on adult age-at-death. This was applied to skeletal samples from later medieval (n = 461) and post-medieval (n = 480) London. RESULTS Growth disruptions during infancy/early childhood (LEH and AP VNC diameters) were not associated with longevity, or with impaired growth at later stages of development (TR VNC diameters). Growth disruptions during late childhood/early adolescence (TR VNC diameters) were associated with a significantly increased risk of adult mortality. CONCLUSIONS 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.

UI	MeSH Term	Description	Entries
D008131	London	The capital of the United Kingdom. It is located in England.
D008297	Male		Males
D008875	Middle Aged	An adult aged 45 - 64 years.	Middle Age
D009026	Mortality	All deaths reported in a given population.	CFR Case Fatality Rate,Crude Death Rate,Crude Mortality Rate,Death Rate,Age Specific Death Rate,Age-Specific Death Rate,Case Fatality Rate,Decline, Mortality,Determinants, Mortality,Differential Mortality,Excess Mortality,Mortality Decline,Mortality Determinants,Mortality Rate,Mortality, Differential,Mortality, Excess,Age-Specific Death Rates,Case Fatality Rates,Crude Death Rates,Crude Mortality Rates,Death Rate, Age-Specific,Death Rate, Crude,Death Rates,Determinant, Mortality,Differential Mortalities,Excess Mortalities,Mortalities,Mortality Declines,Mortality Determinant,Mortality Rate, Crude,Mortality Rates,Rate, Age-Specific Death,Rate, Case Fatality,Rate, Crude Death,Rate, Crude Mortality,Rate, Death,Rate, Mortality,Rates, Case Fatality
D002648	Child	A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL.	Children
D002657	Child Development	The continuous sequential physiological and psychological maturing of an individual from birth up to but not including ADOLESCENCE.	Infant Development,Development, Child,Development, Infant
D003744	Dental Enamel Hypoplasia	An acquired or hereditary condition due to deficiency in the formation of tooth enamel (AMELOGENESIS). It is usually characterized by defective, thin, or malformed DENTAL ENAMEL. Risk factors for enamel hypoplasia include gene mutations, nutritional deficiencies, diseases, and environmental factors.	Enamel Hypoplasia,Enamel Agenesis,Enamel Hypoplasia, Dental,Hypoplasia, Dental Enamel,Hypoplastic Enamel,Agenesis, Enamel,Enamel Ageneses,Enamel Hypoplasias,Enamel, Hypoplastic,Hypoplasia, Enamel
D005260	Female		Females
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000293	Adolescent	A person 13 to 18 years of age.	Adolescence,Youth,Adolescents,Adolescents, Female,Adolescents, Male,Teenagers,Teens,Adolescent, Female,Adolescent, Male,Female Adolescent,Female Adolescents,Male Adolescent,Male Adolescents,Teen,Teenager,Youths