The onset of adolescence is considered a crucial developmental transition marked by a confluence of changes (Brooks-Gunn, 1984; Graber & Brooks-Gunn, 1996; Hamburg, 1974). In addition to the drastic physical changes that occur, the adolescent decade is defined by the restructuring of social roles, expectations, and relationships within the family, peer group and school environment (Feldman & Elliott, 1990; Graber & Brooks-Gunn, 1996). The pubertal transition is considered an impetus for some of the behavioral and social changes that occur during adolescence (Brooks-Gunn & Petersen, 1983; Graber & Brooks-Gunn, 2002). As individuals develop adult-like features during puberty, family, friends, and teachers may react to them differently and expectations of them may change. New behaviors related to sexual feelings and interest are emerging for the adolescent (Graber & Brooks-Gunn, 2002). Additionally, the internal changes of puberty, such as hormonal changes, have also been associated with variations in affect and behavior (Brooks-Gunn, Graber, & Paikoff, 1994; Buchanan, Eccles, & Becker, 1992; Susman, Dorn, & Chrousos, 1991). In other words, behavioral changes during adolescence may be influenced directly by physiological and physical changes, may be more generally related to the effects of age and grade in school, or may be linked to pubertal growth through social or contextual factors (Brooks-Gunn & Reiter, 1990). As such, interactive models have been developed in the field of puberty research to address the psychosocial implications of pubertal processes.
The timing of the transitions is salient for at least three reasons, the first having to do with level of development at the time of the transition, the second with the vulnerabilities of the psychological state at the time of change, and the third with social context (Rutter, 1989). These reasons have been illustrated using examples related to timing of puberty (Graber, Petersen, & Brooks-Gunn, 1996). First, any biological effects of the pubertal experience will differ depending on the level of development of the biological system at the time. For example, it has been suggested that puberty curtails lateraliza-tion of function between the two hemispheres of the brain, resulting in different cognitive abilities depending on timing of the pubertal transition (Waber, 1977). For the most part, research on pubertal timing effects on biological systems has been sparse. Second, any influences on the psychological state of the individual depend on the sensitivities and vulnerabilities of the psychological state at the time of change. For example, experiencing the pubertal transition earlier than others may not only result in being less prepared cognitively and emotionally, but also socially. This may make it more difficult for early maturers to successfully navigate the pubertal transition. Third, timing of puberty may interact with social context. Experiencing the pubertal transition either earlier or later than one's peers may have negative effects on the individual as he or she is perceived as deviating from normative development (Brooks-Gunn & Petersen, 1983; Neugarten, 1979). For example, earlier-maturing girls gain weight at a time when most girls still have childlike physical appearance, which may be one reason why early-maturing girls have reported poorer self-esteem especially related to their body image (Brooks-Gunn & Warren, 1985; Tobin-Richards, Boxer, Petersen, & Albrecht, 1990).
Before the 1980s, only two major studies were conducted on the effects of pubertal development—the California and the Fels Longitudinal Growth Studies. The 1970s were marked by two seminal works that described the lack of systematic study of pubertal development during adolescence (Hamburg, 1974; Lipsitz, 1977). Researchers were also reconsidering whether "storm and stress" was an appropriate characterization of the experience and behavior of young adolescents and whether alterations in self-image and emotionality during early adolescent transitions were influenced by context as well as pubertal changes (Nesselroade & Baltes, 1974; Offer, 1987). Pubertal processes became a subject of study in the 1980s, beginning in 1981 with a conference on girls at puberty (Brooks-Gunn & Petersen, 1983). The 1990s were marked by an increase in studies that address the psychosocial implications of pubertal changes (Alsaker, 1995, 1996; Brooks-Gunn, Graber et al., 1994; Brooks-Gunn, Petersen, & Compas, 1995; Brooks-Gunn & Reiter, 1990; Buchanan et al., 1992; Connolly, Paikoff, & Buchanan, 1996; Graber et al., 1996; R. L. Paikoff & Brooks-Gunn, 1991; Susman & Petersen, 1992; Susman & Ponirakis, 1997).
The current chapter will begin with a description of the biological aspects of pubertal development, with attention to the gender differences in development. Next, methods of measuring puberty, the age of pubertal onset, and the psychological correlates of pubertal development are addressed. In the third section, models linking pubertal development with psychosocial adjustment and the research supporting them are presented, along with proposed mechanisms underlying the models. Finally, we provide some suggestions for the next wave of research.
Pubertal development is a series of interrelated processes resulting in maturation and adult reproductive functioning. The physiological changes of puberty primarily involve the hypothalamic-pituitary-adrenal (HPA) axis and hypothalamic-pituitary-gonadal (HPG) axis. Pubertal development begins in middle childhood and takes five to six years for most adolescents to complete (Brooks-Gunn & Reiter, 1990; Petersen, 1987). A wide range of individual differences exists in the timing of onset and rate of puberty. The following sections describe the physiological, physical, and central nervous system changes of pubertal development, with attention to gender differences in development. An explanation of how the different aspects of pubertal development are measured is also provided.
Puberty is part of a continuum of events initiated at conception, mostly involving the hypothalamic-pituitary-gonadal (HPG) axis. The hypothalamic gonadotropin releasing hormone (GnRH) pulse generator, or "gonadostat" is active prenatally and during early infancy, suppressed during childhood, then reactivated at the onset of puberty (Fechner, 2003).1 In order for puberty to begin, the brain's sensitivity to the negative feedback of gonadal sex steroids (testosterone in males and estrogen in females) decreases, which then releases the HPA axis from inhibition. Puberty begins with the release of GnRH pulses, which activates pulsatile bursts of gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone (FSH), from the pituitary gland. The LH and FSH pulses secreted in response to the GnRH occur first at night and then during the day. Increases in LH and FSH are some of the earliest measurable hormonal indications of pubertal development, and they have been found to rise progressively during puberty (Reiter & Grumbach, 1982). Episodic nocturnal bursts of low-levels of LH are indicative of early pubertal stages (Grumbach & Styne, 1998). The gonads respond to LH and FSH by enlarging, maturing, and secreting increased amounts of gonadal sex steroids, androgens and estrogens.
Multiple gender differences in the mean levels and functions of hormone secretions are evident during the period of pubertal development. In females, the function of LH and FSH is to initiate follicular development in the ovaries, which stimulates them to produce estrogen. Estrogen sensitive tissues, such as the breasts and uterus, then respond to the increase (Fechner, 2003). In males, increased LH stimulates the testes to secrete testosterone, resulting in an increase in testicular size, and FSH stimulates spermatogenesis. LH levels increase in both girls and boys at puberty, while FSH is higher in girls than boys during the prepubertal and pubertal years. Increased FSH levels simulate the ovaries to produce estrogen. Whereas LH and FSH levels in both sexes are regulated by the negative feedback of the gonadal steroids and by the hormone inhibin, girls have a second control mechanism associated with their menstrual cycles which is under positive feedback and is cyclic. When estradiol level is high enough, it triggers an LH, and to a lesser extent, an FSH surge, each which lasts less than 2 days and stimulates ovulation. A corpus luteum forms from the ruptured follicle and begins to secrete progesterone. In the absence of pregnancy, the corpus luteum regresses and the progesterone and estrogen levels drop, triggering withdrawal bleeding and menstruation (Fechner, 2002).
Estrogen and testosterone levels also differ between the two sexes at puberty. Estradiol levels at puberty increase in females then remain elevated during periods of each menstrual cycle. In males, estradiol levels increase until their growth spurt (at midpuberty) then decrease again. On the other hand, while males experience substantial increases in testosterone and androstenedione (a weaker androgen than testosterone) at puberty, there is only a slight rise in females. The sexes also differ in their levels of dehydroepiandrosterone (DHEA) and DHEAS (sulfated form of DHEA), hormones which mark the beginning of adrenarche, the period of initial increases in adrenal androgen hormones, at 6 to 7 years of age in both sexes. Levels of DHEA and DHEAS are similar between the sexes until late puberty, when males begin to have higher levels than females. This difference persists into adulthood (Fechner, 2002).
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