Current Changes in Pubertal Timing: Revised Vision in Relation with Environmental Factors Including Endocrine Disruptors

Abstract

The aim of this chapter is to revise some common views on changes in pubertal timing. This revision is based on recent epidemiological findings on the clinical indicators of pubertal timing and data on environmental factor effects and underlying mechanisms. A current advancement in timing of female puberty is usually emphasized. It appears, however, that timing is also changing in males. Moreover, the changes are towards earliness for initial pubertal stages and towards lateness for final stages in both sexes. Such observations indicate the complexity of environmental influences on pubertal timing. The mechanisms of changes in pubertal timing may involve both the central neuroendocrine control and peripheral effects at tissues targeted by gonadal steroids. While sufficient energy availability is a clue to the mechanism of pubertal development, changes in the control of both energy balance and reproduction may vary under the influence of common determinants such as endocrine-disrupting chemicals (EDCs). These effects can take place right before puberty as well as much earlier, during fetal and neonatal life. Finally, environmental factors can interact with genetic factors in determining changes in pubertal timing. Therefore, the variance in pubertal timing is no longer to be considered under absolutely separate control by environmental and genetic determinants. Some recommendations are provided for evaluation of EDC impact in the management of pubertal disorders and for possible reduction of EDC exposure along the precautionary principle.

Development and validation of a method for precise dating of female puberty in laboratory rodents: The puberty ovarian maturation score (Pub-Score)

“…In the case in humans, pubertal maturation is scored on the basis of a combination of different indices, such as those assessing the initiation of breast growth (thelarche), the appearance of pubic hair (pubarche) and gonadal development, including the first menses in girls (menarche). Assessment of the chronology of these indices has permitted identification of intriguing (and worrying) trends for changes in the age of puberty, especially in girls, with a trend for earlier puberty onset (evidenced by earlier thelarche) but no clear anticipation of the age of menarche, which is the external sign of the first ovulation1920. Likewise, the non-invasive indices of puberty in rodents, as VO and FE, do provide valuable information on some aspects of the pubertal transition, such as the rise of ovarian estrogens that signals the onset of puberty, as it accompanies pre-pubertal follicular development leading to the first ovulation.…”

Persistent vs transient alteration of folliculogenesis and estrous cycle after neonatal vs adult exposure to Bisphenol A

“…Recent evidence suggests that exposure to BPA during this sensitive developmental period could have long-term impacts on reproductive function 9 . Early exposure to BPA affects puberty onset with effects depending markedly on the window and dose of exposure, and possible non-linear dose-response relationship [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] . Effects of neonatal exposure to BPA on estrous cyclicity have produced inconsistent results.…”

The tempo of puberty and its relationship to adolescent health and well‐being: A systematic review

“…There is a large body of evidence to show that earlier timing of onset and pubertal proxies predicts poorer physical and psychosocial health . Notably, such evidence is much stronger in females compared to males …”