Abstract
Individual variation in the age of pubertal onset is linked to physical and mental health, yet the factors underlying this variation are poorly understood. Life history theory predicts that individuals at higher risk of mortality due to extrinsic causes such as infectious disease should sexually mature and reproduce earlier, whereas those at lower risk can delay puberty and continue to invest resources in somatic growth. We examined relationships between a genetic predictor of infectious disease resistance, heterozygosity of the major histocompatibility complex (MHC), referred to as the human leukocyte antigen (HLA) gene in humans, and self-reported pubertal timing. In a combined sample of men from Canada (n = 137) and the United States (n = 43), MHC heterozygosity predicted later self-reported pubertal development. These findings suggest a genetic trade-off between immunocompetence and sexual maturation in human males.
Highlights
Individual variation in the age of pubertal onset is linked to physical and mental health, yet the factors underlying this variation are poorly understood
Because measures of major histocompatibility complex (MHC) heterozygosity varied across studies, they were standardized using a z-transformation prior to combining data sets, resulting in a sample of 180 young adult men (Sample 1: 137 Canadians and Sample 2: 43 Americans)
Controlling for sample origin, age, and ethnicity (Caucasian versus other), results revealed that MHC heterozygosity correlated with relative pubertal development, r(df = 175) = 0.22, p = 0.003, such that men who were more MHC heterozygous reported pubertal development that was later than men who were more MHC homozygous
Summary
Individual variation in the age of pubertal onset is linked to physical and mental health, yet the factors underlying this variation are poorly understood. Life history theory predicts that individuals at higher risk of mortality due to extrinsic causes such as infectious disease should sexually mature and reproduce earlier, whereas those at lower risk can delay puberty and continue to invest resources in somatic growth. We examined relationships between a genetic predictor of infectious disease resistance, heterozygosity of the major histocompatibility complex (MHC), referred to as the human leukocyte antigen (HLA) gene in humans, and self-reported pubertal timing. In a combined sample of men from Canada (n = 137) and the United States (n = 43), MHC heterozygosity predicted later self-reported pubertal development. These findings suggest a genetic trade-off between immunocompetence and sexual maturation in human males. According to the heterozygote advantage hypothesis, MHC heterozygosity confers enhanced resistance to pathogens due to the ability to recognize a greater number of pathogenic a ntigens[27]
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