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Assessment and mechanism of variations in pubertal timing in internationally adopted children: a developmental hypothesis

Division of Pediatric Endocrinology and Adolescent Medicine, Department of Pediatrics, Center of Cellular and Molecular Neurobiology, University of Liège, University Hospital (CHU), B-4000 Liège (Sart-Tilman), Belgium

(Correspondence should be addressed to J-P Bourguignon; Email: jpbourguignon{at}ulg.ac.be)

Abstract

During the past decades, children migrating for international adoption have increased in number, creating an original condition of dramatic environmental change during development. In several countries, cohorts of these subjects have been shown to experience a global advancement in age at the onset of puberty, and sexual precocity is seen more frequently than in other conditions. Such early or precocious development has been assessed in relatively small cohorts or individual patients using well-defined physical indicators in comparison with updated references in the foster country. Family and adolescent evaluation of pubertal timing could allow for the study of large series of internationally adopted subjects. Also, this type of assessment integrates the physical changes of puberty with the adolescent changes in psychological and social functioning. The pathophysiological mechanisms leading to advancement of puberty in migrating children are still unclear and possibly involve several factors. In the present paper, we hypothesize that the sexual precocity in children migrating for international adoption could represent a developmentally programmed disorder resulting from cumulative anomalies in early remodeling of the central nervous system by communicational, social, nutritional, and hormonal inputs. There is some evidence that the deviations in those inputs can result in altered brain structure, particularly in the limbic system. We discuss the possible association with further disorders of developmental functions, such as cognitive, psychosocial, and sexual maturation. Along this hypothesis, some forms of idiopathic sexual precocity could result from dysfunction of one or several of the environmental programming factors, while other forms may involve predominantly genetic or familial factors.