Several recent studies suggest that the timing of the onset of puberty in girls has become earlier over the past 30 years, and there is strong evidence that the increasing rates of obesity in children over the same time period is a major factor. This article reviews studies from the United States that examined the age of menarche and the age of onset of breast development and pubic hair as a function of body mass index, which is a good surrogate measure of body fat. These studies are nearly all cross-sectional, so many questions remain unanswered. However, at least several studies show that girls who have relatively higher body mass index are more likely to have earlier menses, as well as a relationship between body mass index and other measures of pubertal onset. The evidence published to date suggests that obesity may be causally related to earlier puberty in girls rather than that earlier puberty causes an increase in body fat. In contrast, few studies have found a link between body fat and earlier puberty in boys. A growing body of evidence from both rodent and human studies suggests that leptin may be the critical link between body fat and earlier puberty. Leptin-deficient mice and humans fail to enter puberty unless leptin is administered, and rodent studies indicate that very low levels of leptin stimulate gonadotropin secretion both at the hypothalamic and the pituitary level. Current evidence indicates that leptin appears to play a permissive role rather than act as the critical metabolic signal initiating puberty. The linkage between body fat and the reproductive axis in girls may have evolved in mammals as a mechanism for ensuring that pregnancy will not occur unless there are adequate fat stores to sustain both the mother and the growing fetus.
Stephen Michael Kellat
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