Several hypotheses that have been proposed that focus on environmental factors as an explanation for the earlier age of pubertal onset in girls. One such hypothesis is that exposure to environmental toxins may mimic estrogens in the body and thus stimulate pubertal development. Two epidemics of early puberty, one in Italy and the other in Puerto Rico, are suspected to have been caused by exposure to estrogens in food, specifically meat and poultry (Fara et al., 1979; Saenz de Rodriguez, Bongiovanni,
6 Conde de Borrego, 1985). However, no localized outbreaks of early breast development have been reported in the continental United States (Kaplowitz, 2004) and no published data provide evidence that an increased overall exposure to environmental estrogens leads to earlier puberty (Paretsch & Sippell, 2001). Another hypothesis is that manufactured compounds being released into the environment may interfere with the human endocrine system. Studies in this area are difficult because pubertal onset may occur many years after exposure to the chemical in question (Kaplowitz, 2004). Although a few studies have managed to collect data on exposure to environmental contaminants at the time of birth and relate it to growth and development (Colon, Caro, Bourdony, & Rosario, 2000; Gladen, Ragan, & Rogan, 2000; Krstevska-Komstantinova et al., 2001; Michels Blanck et al., 2000), the results do not provide enough compelling evidence that the overall trend for earlier puberty is linked with environmental contaminants. Hormone-containing hair products have been targeted as reason for earlier pubertal onset (Zimmerman, Francis, & Poth, 1995), but this hypothesis requires further examination.
Other hypotheses regarding the earlier onset of puberty focus on more intrinsic factors. For example, perinatal factors, such as birth weight, have been found to play a role in subsequent pubertal development. In one study, girls who were smaller at birth but had a rapid "catch-up" period of growth between birth and age 6 were earlier maturers (Persson et al., 1999). Mechanisms for this association are not clear, but it is likely that the prenatal environment may influence subsequent timing of onset of development, given that sex hormones are active prenatally in organizing the brain for subsequent pubertal development and reproductive functioning (Fechner, 2002). A more widely discussed hypothesis is that higher body fat is associated with earlier maturation. In general, overweight girls tend to mature earlier than girls of normal weight, and thin girls tend to mature later. Numerous studies have indicated that in the past thirty years, there is an increasing prevalence of obesity in both sexes, at all ages, and in all racial and ethnic groups. Since obesity is widespread and prevalent throughout all parts of the United States, it makes sense to examine obesity as a link to earlier pubertal onset. Kaplowitz and colleagues (2001) examined the role of body mass index (BMI) in earlier pubertal onset using data from the PROS study. BMI standard deviation scores (z scores) were computed in order to compare each girl's BMI with what was normal for her age. A key finding of the study was that 6- to 9-year-old girls with early breast development had significantly higher BMI scores than the girls of the same age and race who were prepubertal. When the difference in BMI z scores between African American and White girls was controlled, African American girls still had an earlier onset of puberty than did White girls. Furthermore, African American and White girls who had pubic hair but no breast development were also more overweight than prepubertal girls, even though hormonal regulation of pubic hair and breast development is quite different (Kaplowitz et al., 2001). The hormone leptin has been proposed as a mechanism linking body mass index with puberty (Clayton & Trueman, 2000). Leptin, a protein produced by fat cells, is involved in regulation of appetite and body composition. Evidence has accrued over the past 10 years that leptin also plays a role in the regulation of puberty (Barash et al., 1996). Leptin levels rise progressively during puberty in normal girls, beginning at age
7 to 8; their rise occurs before increases in LH and estradiol, which means that leptin could be a trigger for the production of puberty hormones (Ahmed et al., 1999; Blum et al., 1997; Garcia-Mayor, Andrade, Rios, Lage, Dieguez, & Casanueva, 1997).
A final hypothesis to be discussed is that psychosocial or environmental stress is associated with earlier puberty. In particular, stressful family situations have been linked to earlier onset of puberty
(Graber, Brooks-Gunn, & Warren, 1995; Moffitt, Caspi, Belsky, & Silva, 1992; Surbey, 1990). Lower warmth in parent-child relationships has been associated with earlier age at menarche after controlling for the effect of maternal age at menarche and level of breast development (Graber et al., 1995). Father's absence in the childhood years has been predictive of earlier maturation (Ellis & Garber, 2000; Surbey, 1990). In girls not living with their biological parents, the presence of a stepfather rather than the absence of a father was more strongly associated with earlier pubertal maturation (Ellis & Garber, 2000). A Polish study found that age of menarche in girls who experienced stressful family dysfunction was 0.4 years earlier than age of menarche in girls from families free of major trauma. Mechanisms for the relationship between family stress and early puberty are not clear. Estrogens may play a role, as there is an increasing body of evidence showing effects of stress on estrogen systems in adults (McEwen, 1994).
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