Individual adolescents vary in the timing of pubertal onset, its duration or “tempo,” and its termination. In fact, very little is known about the “offset” mechanisms of puberty. There are a number of variables that may influence directly or indirectly when and how quickly one moves through puberty:
Health and well-being
Physical activity and fitness
Exposure to environmental toxins
It is unlikely that any one of these variables alone will delay or accelerate pubertal growth. Rather, it is the interaction among several of these variables that may affect maturation in complex ways. For example, since the turn of the 20th century, children in average economic conditions have increased in height approximately 1 to 2 cm per decade. Many sources report that this trend stabilized in industrialized countries in the mid-1900s. However, several recent comprehensive studies in the United States suggest that this secular growth trend is reoccurring (Freedman, Kahn, Serdula, Srinivasan, & Berenson, 2000; Herman-Giddens, Wang, & Koch, 2001). More specifically, in studies done on several U.S. populations, height gains were found to be significantly greater in 9- to 12-year-old children, with the largest height increases among African Americans and boys. The height gain was greater among younger adolescents compared to older adolescents, so the pattern points to earlier maturation rather than a difference in overall eventual adult height.
A similar secular trend has been observed in the onset of menstruation (Blythe & Rosenthal, 2000). It shows a marked decrease in the age of menses as well as breast and pubic hair development in industrialized countries over the last several decades. Most recently, a growth study in the Netherlands showed a 6-month decline in the age at menarche between 1955 and 1997 (Fredriks et al., 2000). Similarly, a U.S. study including both African American and Caucasian females showed that twice as many girls (in a 1992–1994 cohort) reached menarche before age 12 compared to girls from a 1978 to 1979 cohort (Wattigney, Srinivasan, Chen, Greenlund, & Berenson, 1999). Many explanations have been offered for these historical trends, including the reduction of growth-retarding illnesses and family size and changes in child labor, diets, housing, personal hygiene, health habits, medical care, exposure to sex steroids, and/or environmental estrogens (Susman, Dorn, & Schiefelbein, 2003).
Overnutrition or obesity, which is on the rise in this country, has been linked consistently to the precocious development of secondary sex characteristics (Wattigney et al., 1999; Adair, Gordon-Larsen, 2001). Recent findings suggest that obese children show higher levels of the hormone leptin, which is responsible for signaling to the brain information about sufficient fat stores (Clayton & Trueman, 2000). Leptin may spark the brain-hormone cycle; however, it is unclear whether leptin causes puberty or is merely present at higher levels when puberty begins. To further complicate matters, obesity is linked to early maturation in females only and early-maturing males in fact are skinnier (Wang, 2002)! More research is needed to understand how increased storage fat prompts early puberty.
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