Considerable research has been conducted on the changes that take place during puberty. Among girls, psychiatric risks have been found to be associated with early onset. Hayward et al. (1997) associated early puberty with disturbed body image, scholastic underachievement, and high-risk behaviors, such as smoking, drinking, and sexual intercourse. They also indicated that these girls are at a higher risk for developing bulimia, phobic disorders, and depression during high school. Thus, from a public health standpoint, early sexual maturation needs to be addressed.
One of the theories that attempt to explain early onset of puberty points to chemical changes as the main reason. Biologists believe that greater exposure to estrogen in hair products, plastics, and insecticides may be implicated (Marshall, 1993; McKinney & Waller, 1994; Sharpe & Skappeback, 1993; Modica, 1997). Such chemicals are referred to as endocrine disrupters (Gillette, 1997).
Another explanation is based on the psychobiologic theory of stress (Goleman, 1991), which is rooted in Darwin's theory of evolution. According to this view, the time of puberty is not biologically fixed, rather it is influenced by experiences with one's environment (Belsky et al., 1991). Girls who are exposed to extremely stressful environments may reach sexual maturity earlier in order to ensure propagation.
Nutrition and changes in nutrition over time have also been theorized to be the cause of early puberty. According to this theory, the main factors that determine the age of menses are health and nutrition (Goleman, 1991). Gillette (1997) believes that estrogen-like growth hormones found in meat and milk provide the stimulus. Jennings (1997) reports that researchers suggest that the hormone leptin, produced by body fat, signals the brain to begin puberty. Thus, body fat percentage would determine when puberty would begin.
Researchers in general agree that this area of concern is particularly applicable to the African-American population. Herman-Giddens et al. (1997) indicated that for some reason early sexual maturation is more prevalent in the African-American population. Their study included 17,077 girls, ranging in age from 3 to 12. Complete physical exams were conducted and assessments of pubertal maturation were ascertained. Data analyses of the girls, of whom 9.6% were African-American and 90.4% Caucasian, indicated that at the age of 3, 3% of African-American and 1% of Caucasian girls showed breast and/or pubic hair development, with proportions increasing to 27.2% and 6.7%, respectively, at age 7. At age 8, 48.3% of African-American girls and 14.7% of Caucasian girls had begun sexual development. It was noted that at every age and for each characteristic, African-American girls were more advanced than Caucasians. Specifically, the mean ages of onset of breast development for African-American and Caucasian girls were 8 .87 years (SD 1.93) and 9.96 years (SD = 1.82), respectively; and for pubic hair development, 8.78 years (SD = 2.00) and 10.51 years (SD = 1.67), respectively. Menses occurred at 12.16 years (SD = 1.21) in African-American girls and 12.88 years (SD = 1.20) in Caucasian girls.
Preliminary findings of a study conducted at the USDA's Children's Nutrition Research Center at Baylor College of Medicine in Houston indicate that African-American girls tend to have more muscle and bone mass by age 6 than do Caucasian or Hispanic girls, a trend that progresses during puberty. A study of the changes in vertebral bone density at various stages of sexual development in African-American and Caucasian females indicated that the marked difference between them in vertebral bone density occurs during a relatively brief period late in puberty (Gilsanz et al., 1991). Further, cultural differences in bone mineral density (Wang, Aguirre, Bhudhikar, Kirshch, Marcus & Bachrach, 1997) have been found; greater femoral neck bone mineral apparent density (BMAD) was present in African-American than in white females at all pubertal stages. …