Puberty, Sexuality, and Health Research Paper

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Puberty, the passage from childhood to adulthood, fascinates scientists, parents, and adolescents alike. This fascination originates from its complexity, rapid and pervasive physical growth, profound psychological changes, and sexual awakening. Puberty is perceived to contribute to the turbulence and stress experienced by some adolescents.

Fortunately, over the last few decades, the conception of adolescence as a period of storm and stress (Blos, 1962; Hall, 1904) is being replaced by a more balanced view of adolescence as a period when biological, cognitive, emotional, and social functioning becomes reorganized. The majority of adolescents are viewed as experiencing neither maladjustment nor grossly undesirable behaviors.

Along with the reconceptualization of adolescence great strides have been made in developing interdisciplinary models of puberty that realistically portray the diversity of pathways through which adolescents progress from childhood to adulthood. Because of the myriad biological and psychological changes that characterize it, puberty engenders scientific interests that span the social, behavioral, medical and life sciences. Research foci include the biological and social

mechanisms that initiate puberty, the timing of puberty, and the interactive influences among hormones, physical growth changes, emotions, problem behavior, cognition, and sexual activity. This research paper presents a summary of two predominant models of development at puberty as well as current perspectives on the biological processes of puberty, timing of puberty and psychological development, secular trends in timing of puberty, puberty and sexuality, and implications for theory, research, and social policy.

Theories and Models of Puberty and Adjustment

The biological processes of puberty historically were integrated with the psychological processes at a conceptual level. In fact, in the early twentieth century perspectives on adolescent development featured the centrality of biological processes in psychological development. In contrast, at an empirical level, research tended to focus either on biological and health issues or on social, emotional, and contextual processes in adolescent development but seldom on the interactions between biological, psychological, and contextual processes. Contextualism, behaviorism, and learning theory supplanted theories of development and evolution that dominated the early twentieth century (S. T. Parker, 2000). The empirical research reflected the predominant interest in contextual influences on development.

A turning point in the integration of puberty with biological, psychological, and contextual processes was the publication of Girls at Puberty (Brooks-Gunn & Petersen, 1983), followed shortly thereafter by models that incorporated the reciprocal interactions among biological, psychological, and contextual processes that contribute to the experience of puberty (Lerner & Foch, 1987; D. Magnusson, 1981; D. Magnusson, Stattin, & Allen, 1985). Subsequent to the articulation of these theories, empirical studies linking pubertyrelated hormones and psychological development began to appear in the literature. These studies addressed issues of aggressive behavior (Susman et al., 1985, 1987), adjustment (Nottelmann et al., 1987), depressed mood (Brooks-Gunn & Warren, 1989), and sexuality (Udry, Billy, & Morris, 1986; Udry, Billy, Morris, Groff, & Raj, 1985; Udry & Talbert, 1988). These studies integrated rather than compartmentalized psychological, biological, and contextual influences on development.

An early example of this integration was the recognition of the interdependence of family interactions and the adolescent’s stage of pubertal development (e.g., Steinberg, 1988; Steinberg & Hill, 1978). In later theoretical perspectives integrating biological and psychological processes, no single level of functioning is viewed as primary or as the ultimate causal influence on development. Rather, development is characterized by reciprocal interaction, bidirectionality, plasticity, and organization (Cairns, 1997; Cairns & Rodkin, 1998; Lerner, 1998; D. Magnusson & Stattin, 1998). Systems or configural views of development are considered paramount with processes from different levels viewed as equal forces in development (Ford & Lerner, 1992; Susman, 1998). Within this perspective, the physical maturational, hormonal, and psychological processes of puberty interact to create the diversity of changes at adolescence.

Two compatible and overlapping theoretical perspectives exemplify the integration of biological, psychological, and contextual influences on adolescent development: developmental contextualism and holistic interactionism.

Developmental Contextualism

The developmental contextualism model of adolescence, proposed by Lerner (1998), parallels modern life-span developmental theories. The life-span perspective is a set of ideas about the nature of human development and change from birth to death. This perspective is concerned with issues of the embeddedness of evolution and ontogeny, of consistency and change, of human plasticity, and of the role the developing person plays in his or her own development (Lerner, 1987). Within the developmental contextual perspective, individuals are viewed as producers of their own development (Brandtstaedter & Lerner, 1999): The theory embodies the notion of the dynamic interactions between individuals and the multiple contexts within which they live. With reference to adolescence, the biological changes of puberty both influence and reciprocally are influenced by psychological, behavioral, and social influences (Lerner, 1987; Lerner & Foch, 1987). Key concepts of the developmental contextualism perspective relevant to puberty are embeddedness, dynamic interactionism, and plasticity.

Embeddedness encompasses the notion that the phenomena of human life exist at multiple levels of being: inner-biological, individual-psychological, social network, community, societal, cultural, and the larger physical ecology and historical contexts. The biological, psychological, and social aspects of change are embedded in the contexts of development. Contexts of development include family, peers, and the multiple social institutions that surround the developing individual. The levels are not interdependent; rather, the processes at one level influence and are influenced by the processes at the other levels.

Dynamic interactionism refers to the dynamic interaction among the levels of analysis. This concept is especially central to integrating the biological and social contextual aspects of pubertal development. In contrast to a previous view that biological processes are deterministic or causal, dynamic interaction concepts embody the notion that biological processes and substances are dynamic and simultaneously influence and are influenced by the psychological and social contextual levels of analysis. For instance, genes no longer are considered purely deterministic influences on development. Instead, they are viewed as requiring a specific environment to be expressed. Furthermore, genetic influences are not static but shift with development (Rowe, 1999). Genes responsible for pubertal development, such as genes related to gonadotropin releasing hormone (GnRH), begin to express mRNAin late childhood, leading to a cascade of hormonal growth and psychological changes. Genes, the individual, and the environment consistently are in a state of dynamic interaction.

Plasticity evolves from the notion that the potential for change exists across the life span in the multiple levels of organization that characterize the developing human (Lerner, 1998). Contemporary theorists emphasize relative plasticity throughout the life span (Lerner, 1998). Relative plasticity implies that across the lifetime, intra-individual development is constrained.All developmental modifications are not possible, and all possible variations are not desirable (Brandtstaedter, 1998). Development and systematic change have constraints imposed both from endogenous (e.g., genetic) and exogenous (e.g., legal sanctions) constraints.

With regard to puberty, social and nutritional circumstances affect the timing of puberty, yet the normal age range for the onset of puberty is constrained by genetic influences. The normative current age range varies from 9 to 15 years for girls and 10 to 16 for boys, although this range may be broadening (see the section titled “Phases of Puberty: Adrenarche and Gonadarche”). Beyond this age range, plasticity in the timing of puberty becomes replaced by an abnormal or pathophysiological condition that requires evaluation and intervention. In brief, only a subset of variations in puberty is compatible with the natural laws of development.

Plasticity is influenced by the individual’s experiential history in interaction with the multiple contexts of development. Behaviors, social contexts, and nutrition are hypothesized to affect the relative plasticity of timing of puberty. For instance, boys with a history of aggressive, disruptive behavior with peers and family were later in their pubertal development and were lower on testosterone than were their nondisruptive peers (Schaal, Tremblay, Soussignan, & Susman, 1996). Overall, the study of plasticity involves scrutiny of the history of dynamic organism-context interactions or the fusion of nature and nurture (Lerner, 1998). Plasticity is a feature neither of nature nor of nurture but rather the fusion of the dynamic interactions between nature and nurture.

Viewed from the developmental contextualism perspective, development at puberty is the product of the dynamic interactions among psychological, biological, and contextual processes. These processes reciprocally and bidirectionally influence each other (Lerner & Foch, 1987). Processes at different levels of functioning are not independent but are merged throughout puberty. The physical and hormonal manifestations of puberty are a product of a species genotype. Yet the experiential history of adolescents and the contexts for social interactions can interact with genes to change the timing and tempo of puberty. Puberty is, then, a process of change and the product of a complex interaction among genotype, brain-behavior, and context. No one research project can test these multiple reciprocal influences on adolescent development. Rather, the developmental contextual model acts as a guide for selecting constructs and measures to be considered in the conceptual framework and design of a specific study.

Holistic Interactionism

A basic proposition of holistic interactionism’s theoretical framework is that the individual is an active, intentional part of an integrated complex, dynamic, and adaptive personenvironment system who develops in that context from the fetal period until death (D. Magnusson, 1999).The holistic interactionism model of development can be summarized in a set of fundamental principles (D. Magnusson & Cairns, 1996): An individual (a) develops as an integrated organism (b) in a dynamic, continuous, and reciprocal process of interaction with the environment. This functioning (c) depends on and influences the reciprocal interaction among subsystems within the individual (perceptual, cognitive, emotional, physiological, morphological, and neurobiological). (d) Novel patterns of functioning arise during ontogeny, and (e) differences in the rates of development, such as differences in timing of puberty, may produce differences in the organization and configuration of psychological functions that are (f) extremely sensitive to the environmental circumstances in which they are formed, particularly the environment as it is perceived and interpreted by the individual. It follows that an individual is viewed as an active, intentional part of an integrated complex, dynamic, and adaptive person-environment system.

Furthermore, within this person-environment system, the individual functions and develops as an integrated organism in which biological, psychological, and behavioral factors operate in reciprocal interaction and dependency within integrated multidetermined, dynamic, and adaptive processes (Magnusson, 1999). Each aspect of the structures and processes that are operating in the individual (perceptions, plans, values, goals, motives, biological factors, and conduct), as well as each aspect of the environment, takes on meaning from its role in the total functioning of the individual. A specific element derives its significance not from its structure or function per se, but from its role in the system of which it forms a part. From a holistic interactionism perspective, development at puberty takes on meaning not from physical change per se but from its meaning to the adolescent in relation to psychological attributes, experiences, the timing of the change relative to peers, and its role as a social signal. Physical development is a signal that a child is becoming an adolescent, and this new status implies new social roles and responsibilities in the societal and cultural system in which the individual develops.

The holistic nature of the functioning of the integrated organism is that normally a psychological-biological process cannot be determined by a single factor. As a consequence of the holistic nature of humans, the processes cannot be subdivided into independent parts in the analysis of the integrated organism’s way of functioning. To understand and explain the role of a specific element in the functioning and development of an individual, it has to be analyzed in the context of the relevant system to which it belongs. Applied to the current instance, psychological and behavioral processes at puberty (e.g., aggressive behavior) cannot be understood without an awareness of the biological and contextual processes that simultaneously influence the adolescent. These processes range from the molecular and cellular levels to the level of the individual as an active, intentional part of an integrated sociocultural person-environment system.

Within a holistic interactionist view, developmental processes are accessible to systematic, scientific inquiry because they occur in a specific way within organized structures and are guided by specific principles. The claim for a holistic view on individual development implies that any theoretical or empirical analysis of developmental processes has to be performed with reference to a complex set of phenomena. This view does not imply that all aspects of puberty need to be considered simultaneously. Rather, the interpretation of findings at one level of functioning should be made by integrating the findings to levels above and below the level of empirical verification. An investigation of hormones at the physiological level and emotions at the psychological level can more meaningfully be interpreted by simultaneously considering the social (peer or family) levels of analysis.

What Is Puberty?

Puberty encompasses a wide variety of phenomena, as reflected in the following definition: “Puberty is a transitional period between childhood and adulthood, during which a growth spurt occurs, secondary sexual characteristics appear, fertility is achieved, and profound psychological changes take place” (National Research Council, 1999, p. 1).

Phases of Puberty: Adrenarche and Gonadarche

Historically, puberty refers to the stage of development characterized by maturation of the reproductive system. Puberty now is considered to have two components, adrenarche and gonadarche, which are thought to be independent events controlled by separate mechanisms (Counts et al., 1987), although the mechanisms separating these periods remain controversial.

The first component of puberty, adrenarche (awakening of the adrenal glands), begins between the ages of 6 and 9 years. At adrenarche, the adrenal androgen concentrations begin to rise (Forest, 1989; Grumbach & Styne, 1992), but hormones of the hypothalamic-pituitary-gonadal (HPG) axis, testosterone and estrogen, are initially quiescent. The adrenal androgens continue to increase throughout gonadarche and include dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS) and androstenedione (∆4-A). The initial hormonal increases in adrenal androgen secretion occur prior to external physical changes, such as pubic hair development. The exact mechanism responsible for the onset of adrenarche is controversial, although recent evidence suggests that adrenocorticotropic hormone (ACTH; Weber, Clark, Perry, Honour, & Savage, 1997) or 3-hydroxysteroid dehydrogenase plays a significant role in the regulation of adrenarche (Gell et al., 1998). Adrenarche is severely understudied in relation to emotions and behavior change, an unfortunate happenstance given findings linking adrenarche and behavior (Brooks-Gunn & Warren, 1989; Susman et al., 1987). In addition, a recent study showed that premature-adrenarche children have significantly more behavior problems and psychopathology than do age-matched peers (Dorn, Hitt, & Rotenstein, 1999). (Findings relating adrenal androgens to behavior are discussed later.)

The second component of puberty, gonadarche, is the reactivation of the hypothalamic-pituitary gonadotropin-gonadal system, which initially had been activated during fetal and early infant development. Gonadarche begins at approximately age 9 to 10 years in White girls and at 8 to 9 years in African American girls (Herman-Giddens et al., 1997) and at 10 to 11 years in boys (Grumbach & Styne, 1992). Gonadarche is what most individuals refer to as “puberty” and entails sexual maturation and reproductive maturity. At gonadarche, HPG-axis activation and physical maturation result in the development of the primary sexual characteristics (testes and ovaries) and secondary sexual characteristics (pubic hair, body hair, and genital and breast growth). The culmination of gonadarche and reproductive function is menarche for girls and spermarche for boys.

Mechanisms Controlling the Onset of Puberty

Neural Control of Puberty

In the last two decades major advances have been made in explaining the physiology of puberty from the molecular level to the whole-organism level. Given that puberty (gonadarche) marks the development of reproductive capability, the physiology of puberty becomes synonymous with that of reproductive maturation. Gonadarche occurs when the GnRH pulse generator (neurons in the medial basal hypothalamus) is reactivated or reaugmented (Knobil, 1988; Medhamurthy, Gay, & Plant, 1990; Tersawa, Bridson, Nass, Noonan, & Dierschke, 1984) and gonadal sex steroid hormone secretion increases. The mechanism for understanding the control system that defines timing of puberty and the neurobiological basis of this reaugmentation of the GnRH pulse generator continues to be speculative (Plant, 1995; Suter, Pohl, & Plant, 1998). Much of what we do know about puberty is based on a nonhuman primate model. In humans, research on the onset of puberty is much more difficult to carry out because frequent serial sampling of blood at night in prepubertal children is required as gonadotropin pulsatile secretion first occurs at night. In addition, very sensitive assays are required for detection of low concentrations of gonadotropins and gonadal steroids. Thus, few human studies are available on the onset of puberty, and in those that do exist, the sample size is small and not likely to be representative of the general population.

Hormone and growth changes at puberty are the consequence of complicated neuroendocrine processes. In the early days of research on the endocrine component of puberty, the emphasis was on specific releasing hormones or specific hormones such as testosterone and estrogen. The emphasis now is on the neural (Plant, 1998) and genetic control of puberty. Specifically, the identification of specific genes and the expression of genes responsible for the onset and progression of puberty now are the focus of study. Given these advances, the most widely accepted explanation of the onset of puberty is the expression of genes controlling the GnRH pulse generator and the reactivation of the HPG axis. In addition, the cortex, limbic system, and neurotransmitter systems modulate hypothalamic function (Brooks-Gunn & Reiter, 1990) and thus puberty.

Weight, Body Fat, and the Onset of Puberty

Various theories posit additional factors contributing to the onset of puberty in combination with programmed genetic influences. One earlier theory posits that critical body mass must be attained before puberty (specifically, menarche as an index of puberty) will occur (Frisch, 1984). The findings indicated that menarche is dependent on the maintenance of a minimum weight for height, likely representing a critical fat storage level (Frisch & McArthur, 1974). Undernutrition also delays puberty in boys. Fat may influence reproductive ability in girls through two mechanisms: (a) Fat converts androgens to estrogens that are critical to regular menstrual cycles and the maintenance of pregnancy, and (b) relative fatness influences the direction of estrogen metabolism from its least to most potent form (Frisch, 1984). It was hypothesized that absolute and relative amounts of fat are important because the individual must be large enough to reproduce successfully. This theory largely fell from wide acceptance. Somatic growth and maturation at puberty are now considered to be influenced by several additional factors that act interdependently to influence the onset of puberty.

Leptin and Puberty

Discovery of the hormone leptin led to the theory that it may be a signal allowing for the initiation of and progression toward puberty (Mantzoros, Flier, & Rogol, 1997). An alternative perspective is that leptin is implicated in the onset of puberty but may not be the cause of the onset. Leptin is a 16-kDa adipocyte-secreted protein, a product of the obesity gene. Serum leptin levels reflect mainly the amount of energy stores but are also influenced by short-term energy imbalance as well as several cytokines (indexes of immune system function) and hormones (Mantzoros, 2000). Leptin is implicated in the initiation of puberty, energy expenditure, normal menstrual cycles, fertility, maintenance of pregnancy, and nutrition. Specifically, leptin may well be one of the messenger molecules signaling the adequacy of the fat stores for reproduction and maintenance of pregnancy at puberty (Kiess et al., 1999). The possible mechanism involves leptin as a hormone that serves to signal the brain with information on the critical amount of fat stores that are necessary for luteinizing hormone-releasing hormone (LHRH) secretion and activation of the hypothalamic-pituitary-adrenal (HPA) axis. Moreover, circadian and ultradian variations of leptin levels are also associated with minute-to-minute variations of LH and estradiol in normal women (Mantzoros, 2000). The mechanisms whereby leptin regulates body weight, adiposity, and the hormones that increase at puberty (e.g., testosterone and estrogen) are not yet known.

Controlling for adiposity, leptin is higher in girls than in boys (Blum et al., 1997). At the initiation of puberty, circulating leptin concentrations diverge in boys and girls. In boys leptin concentrations increase and then markedly decrease to prepubertal concentration levels in late puberty. In contrast, in girls there are increasing concentrations at puberty (Roemmich & Rogol, 1999). The increase in leptin is believed to result from alterations in the regional distribution of body fat in boys and girls at puberty. Overall, sex differences in leptin concentrations are accountable to differences in the amounts of subcutaneous fat in girls and greater androgen concentrations in boys (Roemmich et al., 1998).

The biological effects of leptin in adult humans are still to be determined, but reports show that congenital leptin deficiency leads to hyperphagia and excessive weight gain from early infancy onward as well as failure of pubertal onset in adolescence (Ong, Ahmed, & Dunger, 1999). Leptin concentrations also are higher in girls with premature adrenarche than in girls with on-time adrenarche (Cizza et al., 2001). Leptin concentrations have not yet been examined in relation to behavior changes at puberty, but leptin provides a promising biological probe for understanding physiological pubertal processes and issues of body image, self-esteem, and behavior at puberty.

Growth at Puberty

It is well known that pubertal growth includes a significant increase in height, or linear growth, as well as changes in body size and proportions. Puberty brings on the most rapid rate of linear growth since infancy (Rogol, Roemmich, & Clark, 1998). Rate of linear growth slows throughout childhood and reaches a low point just before the growth spurt (Tanner, 1989). The growth spurt refers to a rapid increase in linear growth at puberty. The timing and magnitude of the growth spurt is different for girls and boys. Girls grow an average of 25 cm with a peak rate of 9 cm per year at about age 12 (Marshall & Tanner, 1969). Boys grow more than girls, but their growth occurs later than in girls because they grow at an average of 28 cm with a peak rate of 10.3 cm per year at about age 14 (Marshall & Tanner, 1970). Tanner (1989) described much of what is known about growth and changes in physical proportions. The rapid increase in height in boys is largely due to faster growth in trunk length than in leg length, particularly since leg length peaks about 6 to 9 months before trunk length does (Tanner, 1989). However, the legs and trunk are not the only parts of the body that are growing. Adolescents show some increase in head diameter, an aspect of growth that has otherwise been basically dormant since the first few years of age. The skull bones also demonstrate an increase in thickness of about 15% (Tanner, 1989). Growth arrest occurs as a result of epiphyseal fusion (Cohen & Rosenfeld, 1996) or ossification (hardening) of the ends of long bones.

The main regulator of growth is growth hormone (GH), a hormone produced in the anterior pituitary. GH is secreted at puberty, first at night, followed by surges during the day in later stages of puberty. The hypothalamic hormones, growth hormone releasing hormone (GHRH) and somatostatin, stimulate and inhibit GH secretion, respectively (Cohen & Rosenfeld, 1996). The increase in GH at puberty parallels the growth spurt. Other endocrine factors influence growth, such as thyroid hormone and glucocorticoids. Sex steroids, primarily testosterone and estrogen, also facilitate growth at puberty. Many nonendocrine growth factors are implicated in growth, the largest of which are genetic influences that control the growth rate, age of puberty, and adult height (Cohen & Rosenfeld, 1996). Growth also can be affected by nutrition, physical activity, and stressors.

In addition to height and other linear measurements, body weight increases dramatically during puberty. Fifty percent of adult body weight is gained during adolescence (Rogol et al., 1998). As with height, girls reach their peak growth in weight earlier than boys, but boys show a greater increase in weight than girls. Girls’ average rate of weight gain peaks at 8.3 kg per year at about 12.5 years of age and about 6 months after their peak height increase (Barnes, 1975; Tanner, 1965). Boys’ peak weight gain of 9 kg per year occurs at about the same time (14 years) as their peak increase in height (Barnes, 1975; Tanner, 1965).

Along with the increase in body weight, body composition also changes at puberty. The changes in body composition are quite different for boys and girls. Girls reach the fat-free mass of a young woman by about 15 to 16 years of age (Rogol et al., 1998). Fat mass also increases by about 1.14 kg per year, and it increases to a greater extent than the fat-free mass, meaning that girls have a net increase in percentage of body fat (Rogol et al., 1998). Girls’ body fat is redistributed during puberty in a female-specific pattern. The deposition rate of subcutaneous fat on girls’ limbs decreases (Tanner, 1989), while estrogens promote fat deposition at the breasts, thighs, and buttocks (Sherwood, 1993). Another source of the body mass increase in girls is a deposition of skeletal minerals. Girls accumulate almost one third of their total bone mineral within 3 to 4 years after beginning puberty (Bonjour, Theintz, Buchs, Slosman, & Rizzoli, 1991; Slemeda et al., 1994). The importance of emphasizing good nutrition and exercise in fostering bone accretion during puberty has not been public health policy. Therefore, an important opportunity to prevent osteoporosis later in development may have been missed by many women.

Body composition in boys follows a very different pattern. Boys’fat-free mass increases faster and for a longer period of time than in girls, and boys reach the fat-free mass of a young man at about 19 to 20 years of age (Rogol et al., 1998). During this time of increase in fat-free mass, boys maintain a fairly constant fat mass, so they show a net decrease in percentage of body fat (Rogol et al., 1998). The skeletal mineral accumulation in boys also differs from that of girls. Boys accumulate bone mineral content for a longer period of time after the pubertal growth spurt, and they have substantial increases in mineralization between 15 and 18 years of age (Rogol et al., 1998), which may explain the lower incidence of osteoporosis in men than in women.

The sex differences in growth and especially in bodycomposition changes during puberty result in the typical female and male body types (Rogol et al., 1998). There are other sex differences in how body and facial structure change during puberty in addition to the previously discussed differences in height, weight, fat-free mass, body fat and its distribution, and skeletal mineralization. Adolescent girls experience a large spurt in hip width, a spurt that is quantitatively as great as boys’ growth even though girls’ growth is less in almost all other dimensions (Tanner, 1989). Boys demonstrate a large increase in shoulder width (Tanner, 1989). The differences in these body proportions are due to the responsiveness of cartilage cells in the hip to estrogens and of the shoulder cartilage cells to androgens, particularly testosterone (Tanner, 1989). Another sex difference is that the later growth spurt of boys results in the greater leg length typical of males (Tanner, 1989): boys’ legs grow for a longer period of time than do girls’. Finally, facial features change over the course of puberty, with the forehead becoming more prominent, the jaws growing forward, and facial muscles developing, although these changes tend to be much more pronounced in boys than in girls (Tanner, 1989). Facial structure in girls is rounder and softer than it is angular.

Secondary Sexual Characteristics

Secondary sexual characteristics refer to breast and pubic hair development in girls and genital and pubic hair development in boys. These changes have been carefully described and fall into five stages (Marshall & Tanner, 1969, 1970; pictures of these five stages appear in these references; see also Brooks-Gunn & Reiter, 1990). However, the description of stages of puberty has been done only for White adolescents; therefore, little information exists regarding pubertal changes in populations throughout the world. Adolescent, parent, or health-professional ratings of the five stages are frequently used in research assessing the relationship between pubertal development and psychological development, although the most well-accepted rating is that of a trained health care professional. Important to note is that there is wide variability in the timing and rate of pubertal development. This variability is normal yet may be distressful from the perspective of individual adolescents as their early or late maturation renders them different from same-age peers.

Pubertyand Changes in Emotions and Behavior

Puberty long has been considered a progenitor of changes in moods and behavior. Until the last two decades, studies of behavior change at puberty considered only physical morphological characteristics in assessing biological change. These physical changes were considered in relation to psychological processes and the various ecological contexts of development that included family, peers, neighborhood, and socioeconomic factors. This perspective now has been enriched by studies that include actual biological substances, such as hormones, that are essential for establishing the direct effects of biological changes at puberty, as well as physical characteristics and contextual factors in development. Overall, hormones have a stronger relationship to emotions and behavior than does pubertal stage.

Contemporary biopsychosocial theories reflect the theoretical perspectives discussed earlier: developmental contextualism and holistic interactionism. “A biobehavioral science recognizes that behaviors are simultaneously determined by processes within the individual, in the social ecology, and in interactions between the two. A focus on either social or biological factors can yield only part of the story of aggressive and violent behaviors: integrative investigations are essential to complete the picture” (Cairns & Stoff, 1996, p. 338). In the last decade the empirical research on hormones and behavior during adolescence reflects this integrated perspective.

Adolescent increases in depression, aggressive and delinquent behavior, and sexual activity have been attributed to changes in hormones and physical morphological changes, brain changes (Giedd et al., 1999; Lange, Giedd, Castellanos, Vaituzis, & Rapoport, 1997; Zijdenbos et al., 1999), altered reactivity to stressors (e.g., life events), and cognitive changes (Bebbington et al., 1998; Nolen-Hoeksema & Girgus, 1994). The links between the biological changes at puberty and changes in affective qualities and aggressive behavior have been extensively reviewed (Brain, 1994; Brain & Susman, 1997; Petersen, 1988; Susman & Finkelstein, 2001; Susman & Petersen, 1992). Given these comprehensive reviews, a brief summary of changes in behavior and affective qualities will be considered in relation to the two groups of hormones most often examined at puberty: sex steroids (testosterone and estrogen) and adrenal androgens (4-A, DHEA, and DHEAS).

Testosterone and Behavior

Products of the endocrine system, principally the steroid hormone testosterone, are implicated in physical aggression in animals and antisocial behavior in adolescents and adults, but the findings are not entirely consistent across human model studies (see Archer, 1991; Brain, 1994, for extensive reviews of both animal and human model studies). The effects of steroid hormones like testosterone on antisocial behavior are hypothesized to derive from the regulatory functions of hormones on brain development that occur during pre- and postnatal periods (organizational influences) as well as in later development (activational influences). Because males are exposed to higher concentrations of androgens than females during pre- and postnatal development and because males tend to express greater physical aggression, androgens are implicated in the higher incidence of physical aggression and dominance in boys than in girls. Because testosterone rises at puberty and antisocial behavior also rises at puberty, testosterone is assumed to affect antisocial behavior at puberty.

Evidence for the relationship between testosterone and aggressive behavior is derived from both correlational and experimental studies. Olweus, Mattson, Schalling, and Low (1988) examined the causal role of testosterone in older adolescents on provoked and unprovoked aggression. Based on path analysis, the findings showed that at Grade 9 testosterone exerts a direct causal influence on provoked aggressive behavior. Testosterone appeared to lower the boys’ frustration tolerance at Grade 9. Ahigher level of testosterone appears to lead to an increased readiness to respond with vigor and assertion to provocation and threat. For unprovoked aggressive behavior (starting fights and verbal aggression) at Grade 9, the findings were somewhat different. Testosterone had no direct effects on unprovoked aggressive behavior. There was an indirect effect of testosterone with low frustration tolerance as the mediating variable. The authors conclude that higher levels of testosterone made the boys more impatient and irritable, in turn increasing readiness to engage in unprovoked aggressive behavior. The findings of the Olweus et al. studies are consistent with a study of midadolescent boys. Adolescents higher in testosterone levels did exhibit behaviors that are distinguishable from behavior in boys with lower concentrations of testosterone. Adolescent boys’ perceptions of peer dominance were reflected in testosterone concentrations (Schaal et al., 1996; Tremblay et al., 1997). Testosterone was significantly higher in perceived leaders than in nonleaders.

Anegative relationship between testosterone and behavior problems was reported in healthy young boys (Susman et al., 1987). In contrast, there was no relationship between diagnoses of conduct disorder problems and testosterone (Constantino et al., 1993). The low concentration of testosterone in 4- to 10-year-old children in combination with the older relatively insensitive assays made the measurement of testosterone difficult in young boys.

In girls, testosterone was not related to aggressive behavior in two studies (Brooks-Gunn & Warren, 1989; Susman et al., 1987). Furthermore, testosterone was not related to dominance behaviors when young adolescent boys and girls interacted with their parents (Inoff-Germain et al., 1988). It is noteworthy that the associations between antisocial behavior and testosterone are less apparent in girls and in male children and younger adolescents (Brooks-Gunn & Warren, 1989; Constantino et al., 1993; Nottelmann et al., 1987) than in the associations in older adolescents (Olweus, 1986; Olweus et al., 1988) and adults (see review by Archer, 1991). These inconsistencies should be expected given the different constructs and measures used in the studies. Questionnaires that assess aggressive behavior may not have adequate sensitivity for capturing subtle differences in the behavior of adolescents that covary with testosterone levels. The developmental differences in findings between children, adolescents, and adults indicate that elevated testosterone and antisocial behavior may be a consequence as opposed to a cause of aggressive behavior during adulthood (Constantino et al., 1993; Susman, Worrall, Murowchick, Frobose, & Schwab, 1996). Boys who consistently displayed disruptive behavior problems across 6 years were significantly lower on testosterone than were boys who were not disruptive and who were later in pubertal maturation (Schaal et al., 1996). The effect of antisocial behavior on suppression of gonadal steroids may result from higher concentrations of stressrelated products of the HPA axis (corticotropin releasing hormone [CRH], ACTH, and cortisol; Susman, Nottelmann, Dorn, Gold & Chrousos, 1989).

Given the dynamic interactive process models discussed earlier, it is likely that biological characteristics, ongoing behaviors, and characteristics of the environment interact to predispose an individual toward certain levels of sex steroids. In an animal model, Sapolsky (1991) showed that the dynamic interactions between one’s place in the dominance hierarchy affected both cortisol and testosterone. As dominance increased, testosterone rose and cortisol decreased. In contrast, as dominance decreased, testosterone fell and cortisol increased, suggesting the importance of social interactions as influences on testosterone. High dominance was related to higher concentrations of testosterone, but this relationship was not stable over time. In an extensive review of the literature on testosterone and dominance, Mazur and Booth (1998) concluded that dominance is more closely linked to testosterone than is physical aggression. Dominance sometimes does entail physical aggression with the intent of inflicting harm on another person, but dominance also can be expressed nonaggressively such as in rebellion, competitiveness, and illegal behavior.

Testosterone is related to depression as well as to aggressive behavior at puberty. Earlier research assessed the indirect effect of hormone change on depression as reflected in the relationship between depression and pubertal stage. Transition to Tanner stage III was associated with a sharp increase in rates of unipolar depression (defined by the Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition) in girls, but neither the timing of puberty nor menarche had any effect on depression (Angold & Worthman, 1993). Tanner stage had a bigger effect on depression than did age, suggesting that biological change rather than merely a period in development had an effect on depression. A later study found an effect of Tanner stage on depression but a larger effect for testosterone (Angold, Costello, Erkanli, & Worthman, 1999). When Tanner stage and hormones were entered simultaneously, the effect for Tanner stage became nonsignificant, but the effect for testosterone and estradiol remained unchanged.

Experimental studies are the preferred method for establishing the cause-effect relationship between hormones and behavior at puberty. A unique experiment was carried out to examine this cause-effect relationship. Testosterone or estrogen was administered to boys and girls in a placebocontrolled, randomized, double-blind, cross-over design study. The boys and girls had delayed puberty and were being treated with physiological doses of testosterone (boys) or conjugated estrogens (girls; Finkelstein et al., 1997; Kulin et al., 1997; Susman et al., 1998). Each 3-month treatment period was preceded and followed by a 3-month placebo period. The doses of gonadal steroids were calculated to simulate the concentrations of gonadal steroids in blood in normal early (low dose), middle (middle dose), and late (high dose) pubertal adolescents. Aggressive behaviors, problem behavior, and sexual activity were measured by self-reports. In boys who were treated with testosterone, aggressive behaviors were measured by self-reports about physical and verbal aggression against peers and adults, aggressive impulses, and aggressive inhibitory behaviors. Significant increases in aggressive impulses and physical aggression against peers and adults were seen in boys but only at the middle dose. (Findings for estrogen are discussed later.) There were no effects for testosterone treatment on behavior problems (Susman et al., 1998). Administering midpubertal levels of testosterone to hypogonadal boys resulted in significantly increased self-reports of nocturnal emissions, touching girls, and being touched by girls (Finkelstein et al., 1998). (See also the section titled “Puberty and Sexual Activity.”) In brief, testosterone levels are related to aggressive behavior, but the results are not consistent across studies.

Estrogen and Behavior

The effects of estrogen, the other major sex steroid that increases rapidly at puberty, are less frequently examined in relation to behavior than is testosterone. In the few studies that have examined estrogens in relation to emotions and antisocial behavior, the relationship between estrogen and moods and behavior at puberty in girls may be as strong, or stronger in some instances, than the relationship between testosterone and moods and behavior in boys. The lack of progression of research on estrogen and behavior reflects two issues. First, only males are included in the majority of studies on hormones and antisocial behavior as physical aggression and violence occur more frequently in men and violence in women rarely comes to the attention of the judicial system or the media. Second, testosterone was considered the major hormone associated with antisocial behavior until recently.

The relationship between estrogen and behavior in girls may parallel that of testosterone in boys. In adolescents, correlational studies and a recent clinical trial study show a connection between estrogen and self-reports of aggressive tendencies. Of note is that in 9- to 14-year-olds, girls with higher concentrations of estradiol were more dominant while interacting with their parents than were girls with lower levels of estradiol (Inoff-Germain et al., 1988). In the same study, estrogen was not related to aggressive or delinquent behavior problems (Susman et al., 1987). In both sets of findings, pubertal stage did not contribute to the findings. In a parallel study girls were grouped by pubertal breast stages and four stages of estradiol secretion (Brooks-Gunn & Warren, 1985; Warren & Brooks-Gunn, 1989). No significant mood or behavior changes were reported as a function of pubertal stages. The hormonal stages revealed a significant curvilinear trend for depressive affect (increase, then decrease), impulse control (decrease, then increase), and psychopathology (increase, then decrease; Warren & Brooks-Gunn, 1989), indicating significant differences in these indexes during times of rapid increases in hormone levels.

In the placebo-controlled, randomized, double-blind, cross-over design study just described, girls with delayed puberty were treated with physiological doses of estrogen. Significant increases in self-reported aggressive impulses and in physical aggression against both peers and adults were seen in girls at the low and middle doses but not at the high dose (Finkelstein et al., 1997). In contrast, in boys, significant increases in aggressive impulses and physical aggression against peers and adults were seen but only at the middle dose of testosterone. Problem behaviors also were assessed using the Child Behavior Checklist (CBCL; Achenbach, 1991). In girls, only withdrawn behavior increased with estrogen treatment and only after the low dose (Susman et al., 1998). Unfortunately, there were no objective measures of reports (arrests, school or police reports) of dangerous behaviors in these adolescents.

In a recent study, the relationship between depression and estradiol was linear, with depression increasing with increases in estrogen (Angold et al., 1999) as opposed to the nonlinear relationship in the Warren and Brooks-Gunn study. Slight differences in the manner in which estradiol was categorized may have led to the different findings in these two studies. Collectively, these results demonstrate a clear relationship between estrogen and depression. Given the lack of relationships between physical maturation based on pubertal stage and emotions or behavior, hormonal changes appear to be more important than the physical changes as correlates of mood and behavior patterns at puberty.

Even though physical maturational changes at puberty were not directly related to depression, underlying hormone changes appear to have indirect effects on behavior, principally in girls. Stattin and Magnusson (1989) showed that morphological estrogen-related changes apparent in physical development, such as breast development, have life-long implications for development. Early maturation in girls was related to engaging in interactions with older peers and norm violation in midadolescence. In adulthood, the earlier maturers were likely to bear children earlier, have more children and more abortions, hold lower position employment, and have fewer years of education than were later maturers. In brief, the timing of physical maturational influences at puberty were potent predictors of later social development.

In summary, there is a significant relationship among sex roles, steroid hormones and depression symptoms, aggressive behavior, and mood in adolescents. Physical maturational status is related to emotions and aggressive behavior as well as to hormones. Adding hormones to a statistical model tends to account for variance above and beyond physical maturational status or to eliminate the relationship between physical maturation and behavior and emotions. Nonetheless, the relationships between physical maturation and adolescent behavior may be latent until adulthood, as evidenced by the outcome of early maturers (Stattin & Magnusson, 1989). When considering maturational influences, attention must be given to the contextual processes that may moderate or mediate maturation and emotions and behavior. Family and peer interactions are likely candidates as moderators of maturational effects as evidenced by the associations between high problem behavior and lack of parental monitoring and adolescent associations with deviant peers (Ary et al., 1999). In keeping with the developmental contextualism (Lerner, 1998) and holistic interaction (D. Magnusson, 1999) models described earlier, simultaneous consideration of emotions and individual behavior, biological influences, and the social context of development are essential for explaining individual development.

Adrenal Androgens

The adrenal androgens traditionally receive little attention in relation to behavior. The adrenal androgens are considered weak bonding androgens relative to testosterone (Bondy, 1985). Nonetheless, adrenal androgens are associated with aggressive behavior, affect, psychiatric disorder symptoms, and sexual behavior (Brooks-Gunn & Warren, 1989; Susman et al., 1987; Udry et al., 1985; Udry & Talbert, 1988). Higher levels of DHEAalso predicted the onset of the first episode of major depression (Goodyer, Herbert, Tamplin, & Altham, 2000).Adrenal androgen actions may parallel those of testosterone and behavior because one of the adrenal androgens, ∆4-A, is a precursor of both testosterone and estrogens. The rationale for examining the connections between behavior and adrenal androgens stems from findings from both animal and human model studies. In the female spotted hyena, the adrenal androgen ∆4-A is present in high concentrations, and the females of the species are highly aggressive and highly anatomically masculinized (Glickman, Frank, Davidson, Smith, & Siiteri, 1987). High ∆4-A concentrations during pregnancy may organize or activate sex-reversed traits in female spotted hyenas (Yalcinkaya et al., 1993). The roles of ∆4-Aand other adrenal androgens (DHEA, DHEAS) in humans are not as clear as in hyenas beyond their roles in the development of pubic hair, body odor, and acne during puberty.

In the last decade several studies of adolescents report relationships between adrenal androgens and antisocial behavior in adolescents. In healthy puberty-age girls (Brooks-Gunn & Warren, 1989), higher DHEAS correlated negatively with aggressive affect. The interaction between negative life events and DHEAS and aggressive affect also was significant. Girls with lower concentrations of DHEAS who experienced negative life events had more aggressive affect than did girls with fewer negative life events. The second study included 9- to 14-year-old healthy boys and girls. Reports from this study show a relatively consistent pattern of high adrenal androgens and low gonadal steroids associated with problem behaviors and negative affect (Nottelmann et al., 1987; Nottelmann, Inoff-Germain, Susman, & Chrousos, 1990; Susman et al., 1987; Susman, Dorn, & Chrousos, 1991). Adrenal androgens also correlate with dominance in interactions with parents (Inoff-Germain et al., 1988). This interaction supports the perspective of Raine, Brennan, and Farrington (1997) that biological factors interact with social factors to predispose an individual to antisocial behavior.

The third study demonstrates the contribution of adrenal androgens to sexual behavior and activities (Udry et al., 1985; Udry & Talbert, 1988).Afourth study with boys with conduct disorder reported significantly higher levels of DHEA and DHEAS and the intensity of aggression and delinquency (van Goozen, Matthys, Cohen-Kettenis, Thijssen, & van Engeland, 1998). Finally, DHEAS levels interact with timing of puberty and depression in girls. Girls with high levels of DHEAS and early maturation had the highest emotional arousalanddepressiveaffectscores(Graber,Brooks-Gunn,& Warren, in press). In brief, although adrenal androgens have a lower (weaker) binding affinity compared to testosterone, the relationship between adrenal androgens and antisocial behavior parallels the relationships between testosterone and antisocial behavior in adults.

Timing of Puberty and Psychosocial Development

Wide variation exists among individuals in the timing of the onset of activation of the HPG axis and pubertal growth spurt; therefore, there is a wide range of physiologic variations in sexual reproduction capability and normal growth at puberty. Thesevariationsarearesultofgeneticinfluencesandnutritional status, resulting from self-induced restriction of energy intake and heavy exercise training (Rogol, Clark, & Roemmich, 2000). The variation in timing of puberty and psychological development constitutes one of the most often examined topics in the entire field of adolescent development.

Early and Late Pubertal Timing

The classic studies of the effects of timing of puberty were first reported in the 1930s (H. E. Jones, 1938; M. C. Jones, 1958; M. C. Jones & Bayley, 1950). Psychological consequences of timing of puberty continue to be of sustained interest. In general, for boys in the early studies, early maturation tended to be advantageous, particularly with respect to social development. In contrast, early maturation for girls often tended to be disadvantageous (Faust, 1969; Jones, Bayley, & Jones, 1948; Stolz & Stolz, 1944), although the results were not always consistent across studies.

With the rise of interest in biobehavioral research, beginning in the 1980s, two predominant hypotheses were formulated to explain the influence of physical maturation on primarily negative psychological outcomes. First, the maturational deviance hypothesis (e.g., Brooks-Gunn, Petersen, & Eichorn, 1985; Caspi, Henry, McGee, Moffitt, & Silva, 1995; Caspi & Moffitt, 1991; Petersen & Taylor, 1980; Tschann et al., 1994; Williams & Dunlop, 1999) suggested that adolescents who are off time (earlier or later) in their pubertal development, with respect to peers, experience more stress than on-time adolescents. Being an off-time maturer may result in an adolescent’s lacking the usual coping resources and social support that characterize being on time in pubertal development. The added stress and lack of resources may increase vulnerability to adjustment problems. In brief, a maturational-deviance hypothesis predicts that early-maturing girls and late-maturing boys experience heightened emotional distress, which influences the initiation of antisocial behavior including use of illegal substances, sexual activity, and delinquent behavior.

The second hypothesis, the early-maturational or early timing hypothesis (e.g., Brooks-Gunn et al., 1985; Caspi & Moffit, 1991; Petersen & Taylor, 1980; Tschann et al., 1994) posited that being an early developer is especially disadvantageous for girls (Stattin & Magnusson, 1990). The disadvantage may result from the missed opportunity for completion of normal psychosocial developmental tasks of middle childhood (Brooks-Gunn et al., 1985). Early maturers may face greater social pressure to conform to adult norms and, importantly, to engage in adult behaviors. Earlier maturing adolescents look more physically mature than their chronological age, and hence society may view them as older and more socially, emotionally, and cognitively advanced (Brooks-Gunn et al., 1985; Caspi & Moffitt, 1991). However, the cognitive and social development of early maturers may lag far behind their seemingly adult status. With this mismatch, expectations are high for more adult-like behaviors and actions, yet the physically early maturing girls may not be ready for adult behaviors and roles. Thus, an early-maturation hypothesis predicts that early-maturing girls engage in more actingout behavior or negative emotions than all other groups, independent of emotional distress.

Although not always consistent, the results from the early timing of maturation studies report that early maturation for boys appears to be positive, particularly with respect to social development, whereas for girls early maturation is related to more negative moods and behaviors (Faust, 1969; Ge, Conger, & Elder, 2001a; Jones & Bayley, 1938; Stolz & Stolz, 1944). For instance, early-maturing girls experienced significantly higher levels of psychological distress and were more vulnerable to prior psychological problems, deviant peer pressures, and fathers’ hostile feelings when compared to on-time and late-maturing peers (Ge, Conger, & Elder, 1996). However, early-maturing boys also report more hostile feelings and internalizing behavior problems than do their later maturing peers (Ge, Conger, & Elder, 2001b). Other studies show that early timing is negative for both boys and girls. This finding was supported in studies of African American children as well (Ge, Brody, Conger, & Simons, in press). Tschann et al. (1994) reported that boys and girls who are earlier maturers reported more substance abuse compared to later maturers.

Earlier maturing boys and girls were more sexually active and participated in more antisocial behavior (Flannery, Row, & Gulley, 1993), and early-timing boys reported more antisocial behavior than on-time boys (Williams & Dunlop, 1999) compared to late maturers. Early-maturing boys also engaged in more health risk behaviors (Orr & Ingersoll, 1995). In other studies, early-maturing girls were least satisfied with their height and weight, had poorer body image, or were less happy (Blyth, Simmons, & Zakin, 1985; Brooks-Gunn et al., 1985; Brooks-Gunn & Warren, 1989; Duncan, Ritter, Dornbusch, Gross, & Carlsmith, 1985; Petersen & Crockett, 1985) and had more internalizing problems (Hayward et al., 1997), more behavioral and emotional problems (Caspi & Moffitt, 1991), and more interactions with peers who were deviant (Silbereisen, Petersen,Albrecht, & Kracke, 1989).

Timing of puberty is related to a variety of health and risk behaviors. Eating problems were reported by 9th-, 10th-, and 11th-grade girls who perceived their pubertal timing to be earlier than that of peers (Swarr & Richards, 1996). Moreover, they report that interactions between pubertal timing and various experiences or perceptions of parents are related to eating problems. Similarly, early-maturing girls engaged in risk behaviors such as drinking, smoking, and sexual activity at an earlier age (D. Magnusson et al., 1985). In another study, girls with earlier puberty had their first alcohol experience and drank moderate amounts of alcohol sooner than those with later pubertal timing did (Wilson et al., 1994). Finally, the perception of earlier pubertal timing was a statistical predictor for future suicide attempts in Norwegian adolescents, and this relationship was stronger in girls than in boys (Wichstrom, 2000).

Other studies show that early timing in girls and late timing in boys are related to affective and behavior problems. For example, early timing of puberty in girls and late timing in boys were related to a higher incidence of psychopathology and depressed mood (Graber, Lewisohn, Seeley, & Brooks-Gunn, 1997), and poor body image was evident in boys (Siegel, Yancey, Aneshensel, & Schuler, 1999). Similarly, Andersson and Magnusson (1990) reported that both early- and late-maturing boys may be more likely to be alcohol users. Using hormone concentrations standardized for age as an index of timing of puberty, earlier maturing adolescents, based on adrenal androgen levels, tended to have poor adjustment; however, the findings varied depending on the hormone under consideration (Susman et al., 1985). Later maturing adolescents, based on sex steroids, tended to have poorer adjustment. The findings were more pronounced for boys than for girls.

Later maturation is not as consistently related to negative emotions and behavior problems as is earlier maturation. Later maturation in boys was related to lower achievement (Dubas, Graber, & Petersen, 1991), lower self-esteem or confidence, and less happiness (Crockett & Petersen, 1987; Simmons, Blyth, Van Cleave, & Bush, 1979). Other studies showed no effects of pubertal timing, either earlier or later, in relation to mood and behavioral outcomes. For example, Brooks-Gunn and Warren (1989) reported no relationship between pubertal timing and negative emotions in girls, and Angold, Costello, and Worthman (1998) reported no relationship between pubertal timing and the rates of depression in boys and girls.

In summary, there is support for both the maturational deviance hypothesis and the early-maturational hypothesis. Adolescents who are off time in pubertal timing generally report more adjustment problems, supporting the maturational deviance hypothesis. Early timing of puberty does appear to be more disadvantageous for girls than for boys (the earlymaturational hypothesis), but boys are negatively affected by early timing as well. Nonetheless, there also is evidence that timing of puberty has no effect on adjustment and that earlier puberty is neither consistently disadvantageous for girls nor advantageous for boys. The effects of timing of puberty on adjustment and deviant behavior are made even more difficult to unravel by imprecise definitions and measurement of puberty and the inclusion of a wide age group of adolescents.

Theoretical and Methodological Issues

The studies just reviewed show both consistencies and major inconsistencies regarding the relationship among timing of puberty and behavior, adjustment, and psychopathology. Nonetheless, it is legitimate to conclude that both earlier and later timing of puberty has a major impact on multiple dimensions of psychological functioning in boys and girls. Of note is that timing of puberty has long-term implications. Later in adolescence or adulthood, early-maturing girls reported more psychopathology (Graber et al., 1997) and less educational achievement and career success than did later maturing girls (Stattin & Magnusson, 1990). The inconsistencies across studies of earlier and later puberty emerge from conceptual and methodological differences. The major theoretical interest appears to be on earlier timing of puberty given societal concerns regarding potential consequences of early maturation: precocious sexuality, substance use, and deviance. With some exceptions, few studies examine the longer term effects associated with earlier maturation. Earlier or later maturation has been theorized to be a stable characteristic of individuals rather than a dynamic concept that changes with changing age and contextual factors. The behaviors that are related to timing of puberty during adolescence, such as risky sexual behavior and other forms of externalizing problems, may disappear in late adolescence and adulthood. Nonetheless, the longer term implications of timing of puberty will emerge as transformed manifestations of these early behaviors as described by Stattin and Magnusson (1990). Specifically, early maturers may become affiliated with older and deviant peers for a limited time period and engage in deviant behaviors that cease in late adolescence. The expense of engaging in these behaviors is reduced achievement and educational and occupational success.

Although the findings regarding early and late puberty seem inconsistent, there is consistency across studies. The consistency of findings showing earlier maturation and problems in adjustment suggests that adolescents are exquisitely sensitive to their early pubertal status. Such is not the case for later maturers. The fewer findings relating later maturation and psychological functioning indicate the ability of adolescents to adapt to differences between themselves and same-age peers as puberty progresses. Less theorizing has taken place regarding developmental implications of later maturation.

Methodological differences also contribute to the inconsistencies in findings. The chronological age when adolescents are assessed for effects of timing, the measure of timing (age of menarche, pubertal stage, or other measure) and the construct assessed (antisocial behavior, depression, parentadolescent interactions) all may contribute to the discrepancies in how timing of puberty and psychological functioning co-occur. The method used to assess timing of puberty likely plays a major role in the discrepancies across studies. To a large degree, timing of puberty has been assessed utilizing a self-report measure of puberty (e.g., pubertal stage, age at menarche, appearance of body hair). Other studies use objective measures of physical development such as pubertal stage by physical examination (Tanner criteria; Marshall & Tanner, 1969, 1970) or hormone concentrations. The lack of reliability in self-reports of pubertal status (Dorn, Susman, Nottelmann, Inoff-Germain, & Chrousos, 1990) and age of menarche (Dorn et al., 1999) is likely a major source of error variance in assessing the multiple connections between timing of puberty and psychological functioning.

Puberty and Adolescent Health: Cultural Significance and Secular Change

Secular Changes in Timing of Puberty

Timing of puberty currently captures the interest of the public as well as the scientific community. Time (October 2000) magazine’s front cover and accompanying article featured the problem of early timing of puberty in girls. There has been a decrease in age of menarche over the last century (Blythe & Rosenthal, 2000; Gerver, De Bruin, & Drayer, 1994; Grumbach & Styne, 1992; Tanner & O’Keeffe, 1962; Wyshak & Frisch, 1982). The secular (generational) trend in age at menarche has been evident from at least the mid 1800s to currently when a decrease in the age of menarche was noted from 15 years to 12.7 years (Garn, 1992).Age at menarche decreased by approximately 1 year for those women born from 1900 to 1950. A decrease in the age of menarche also is evident in international studies.

In a nationwide growth study in the Netherlands, age of menarche was assessed in two cohorts. The first cohort was enrolled in 1952–1956, and the most recent cohort was enrolled in 1996–1997. Age at menarche decreased to 13.15 years, whichwasa6-monthdeclineoverfourdecades(Fredrikset al., 2000). Similarly, in two cohorts of American girls 14 years apart, age at menarche was found to decrease (Wattigney, Srinivasan, Chen, Greenlund, & Berenson, 1999). Cohort 1 included 1,190 girls (64% White) who were examined in 1978–1979. The second cohort was examined in 1992–1994 and included 1,164 girls (57% White). In Cohort 2 more than twice as many girls reachedmenarchebeforeage12yearsthan did in Cohort 1. Menarche occurred earlier in Cohort 2 for both Black andWhite girls. Furthermore, in both cohorts all of the obesity measures used in the study were correlated with age at menarche. The decrease in timing of menarche has generally been attributed to cultural factors, specifically, improved nutrition and socioeconomic conditions evident in the United States and numerous developing countries.

In 1997 a large-scale study of pubertal development in American girls received widespread attention in the media as well as in the health care and research arenas. Herman-Giddens et al. (1997) studied over 17,000 pre- and peripubertal-age girls (90.4% White) to determine age at onset of pubertal changes. They reported that African American girls began puberty on average between age 8 and 9 whereas White girls began puberty by age 10. For example, at age 9, 62.6% of African American girls had breast development at stage 2 or higher (indicative of puberty) compared to 32.1% of White girls. Similarly, age at menarche was 12.16 years for African American girls and 12.88 years for White girls (Herman-Giddens et al., 1997). In a follow-up article (Kaplowitz, Oberfield, & the Drug and Therapeutics and Executive Committees, 1999), based on the Herman-Giddens study, the suggestion was that breast or pubic hair development is not precocious unless under age 7 in White girls and 6 in African American girls. Thus, girls beginning puberty above that range need no medical follow-up. However, they further stress that no follow-up is needed only if other factors are not present (e.g., bone age >2 years ahead of chronological age and predicted height of 2 SD or more below target height or < 59 inches, underlying neurological finding, etc.; Kaplowitz et al., 1999). It appears prudent to seek medical advice in all instances of suspected early puberty.

Although, the Herman-Giddens et al. (1997) study is unique and important in that it includes a large number of girls, a number of important methodological considerations may have affected the findings and interpretations of secular trends in timing of puberty. These methodological considerations include the method of conducting the physical examination. Breast stage was determined by visual inspection and not palpation. Even with palpation conducted by an experienced clinician, it is difficult to distinguish between breasts and adipose tissue. Thus, some girls could have been classified as pubertal at Stage 2 when the actual cause of apparent breast development was obesity. Statistically controlling for body mass could have partially addressed the problem of overestimating the extent of breast development although the problem would not have been eliminated. Additionally, characteristics of the sample may have contributed to ratings of early puberty. Some of the girls in the sample likely were brought to their primary care provider for the evaluation of early pubertal development. In addition, nearly 7% of the sample had a chronic disease, and 3% were on medication. These percentages were higher in the African American sample. Finally, not all of the girls in the study had reached menarche (Emans & Biro, 1998), thereby possibly decreasing the average age of menarche. The authors are to be commended on the study, but the mean age of menarche reported may not truly be representative of the general population of adolescent girls. In spite of the earlier age of onset of puberty, there was little change in age at menarche noted in the Herman-Giddens et al. report compared to reports in the previous 25 years.

The report by Herman-Giddens et al. (1997) continues to remain controversial. In the fall of 2000, Rosenfield et al. (2000) emphasized that it is premature to state that puberty is occurring earlier in girls based on one study. Rosenfield et al. cited similar criticisms to those expressed earlier (e.g., stage of puberty was based on visual inspection versus palpation) but particularly emphasized the “fatal flaw” (p. 622) of utilizing a nonrandom sample. The authors concluded that regardless of race, when breast development or pubic hair appear before age 8 or 9 years, a diagnostic evaluation should be conducted for bone age and height prediction. Based on these results as well as the physical examination, decisions for further follow-up should then be made.

The exact decrease in the true onset of timing of puberty as opposed to the timing of menarche is difficult to assess as the timing of puberty is often indexed in girls by “age at menarche.” Age at menarche is a relatively easy marker to obtain by self-report or parental report but is not an accurate index of timing of onset of puberty. Variability in accuracy of reports of onset of menarche (Dorn et al., 1999) contributes to the difficulty of estimating secular trends in the onset of puberty. Unfortunately, the data on secular trends in onset of puberty in boys are much less complete than for girls. Theoretically, the first nocturnal emission or spermarche is a comparable timing measure for boys; however, information on spermarche is difficult to obtain. Sanders and Soares (1986) reported that many adult men either had difficulty recalling their first nocturnal emission or were hesitant to reveal the information. Few psychosocial studies include the concept of spermarche as an index of timing of puberty (for exceptions, see Downs & Fuller, 1991; Gaddis & Brooks-Gunn, 1985; Kim & Smith, 1998; Kim, Smith, & Palermiti, 1997). Information regarding secular trends in timing of puberty is not easily gleaned from these studies because they include a wide age range of subjects (up to age 62) or small sample sizes. None provided normative data regarding average age of spermarche or reliability of the measurement of spermarche. In an earlier study, Kulin, Fronera, Demers, Barthlomew, and Lloyd (1989) reported the average age of spermarche to be age 14, and at that age gonadotropins were at adult concentrations. To our knowledge, this is the only study that simultaneously assessed self-reported age at spermarche and gonadotropin levels. Given the lack of information regarding onset of puberty in boys, there is no valid method of estimating secular trends in the onset of puberty in boys. A study of boys that parallels the Herman-Giddens et al. (1997) study of girls in a randomly selected representative sample could make a significant contribution to the literature.

Puberty and Adolescent Health

Puberty implies that an adolescent is becoming an adult. Contemporary culture is ambivalent about the desirability of this transition. On the one hand, puberty implies independence and adult roles and the emergence of a physical morphology and reproductive capability characteristic of adults. On the other hand, for girls the thin prepubertal physique is valued, whereas fat deposition at puberty is viewed as a less desirable characteristic of female adults. These changes in physical size and proportions have definite negative social signaling value. As boys and girls progress in physical development there are societal expectations for moodiness and disruptive behavior and opportunities for risky sexual behavior. With the engagement in sexual activities, there is added risk for sexually transmitted diseases (STDs; e.g., HIV transmission) and teen pregnancy (Udry, 1979; Udry & Cliquet, 1982). Puberty, then, is a period of development ripe for the emergence of major health risk behaviors and health problems. Public health policies tend to focus on preventing the occurrence of the health problems (substance use, risky sex, and accidents) but at the same time ignore the role of puberty as a major factor affecting the onset and trajectory of risky health behaviors. The effects of timing of puberty on adult health are only now beginning to be identified.

Puberty and Adult Health

Health policies to reduce the risk of long-term implications of early timing of puberty are just beginning to be considered. This emphasis, based primarily on observational studies, regards the relationship between reported age of puberty and later health problems. Timing of puberty and later health have been understudied in males, so disorders linked with timing of puberty in males are yet to be identified. The lack of attention to long-term implications of pubertal processes (particularly, timing of puberty) represents a missed opportunity for possible public health prevention efforts.

Research on puberty and later health has focused primarily on cancer, obesity, and reproductive disorders. An increased risk of breast cancer is associated with early puberty based on age at menarche (Kampert, Whittemore, & Paffenbarger, 1988; C. M. Magnusson et al., 1999; Rockhill, Moorman, & Newman, 1998; Vihko & Apter, 1986; for a review, see Key, 1999). The increased risk of cancer in early maturers is attributed to the longer duration of exposure to circulating estrogens across the life span. Women who experience earlier menarche have higher levels of circulating free estrogen into at least the third decade of life compared to later maturers (Apter, Reinila, & Vikho, 1989). An additional indirect measure of estrogen, the timing of the pubertal growth spurt, is also associated with breast cancer risk. Women who attain their adult height at a later age have a lower risk of breast cancer, possibly due to their having lower levels of growth hormone (GH) and insulin-like growth factor (IGF1) during breast development (Li, Malone, White, & Daling, 1997). However, it is important to note that other studies do not show an increased risk of breast cancer with earlier menarche (e.g., R. G. Parker, Rees, Leung, & Legorreta, 1999) and that the cause of breast cancer is no doubt multifactorial.

Early maturing girls are at greater risk for obesity (Lovejoy, 1998; Ness, Laskarzewski, & Price, 1991). Obese girls also have an earlier timing of puberty, so the direction of the relationship between obesity and timing of puberty is unknown. Obesity in adolescence is related to major risk factors for cardiovascular disease (Morrison, Barton, Biro, Daniels, & Sprecher, 1999). In Black and White 10-to 15-year-olds, overweight status was related to lower high-density lipids and higherlow-densitylipids,arisk-profileforcardiovasculardisease. Obesity is also linked to the high incidence of Type II diabetes mellitus in adolescents.

Reproductive disorders related to timing of puberty are evident primarily in ovarian pathophysiology. Polycystic ovarian syndrome (PCOS) is a disorder in adulthood reported to be related to early puberty. PCOS is a heterogenous disorder characterized by oligo/amenorrhea (few or no menstrual periods), insulin resistance or high insulin, and hyperandrogenism, which is associated with an increased risk of developing impaired glucose tolerance and Type II diabetes (Ibáñez et al., 1993). PCOS is reported in 5% to 10% of women of reproductive age. PCOS can begin to express itself during puberty and continue into the adult reproductive years with ensuing infertility.

One possible mechanism linking PCOS and early puberty is premature adrenarche. During adrenarche the adrenal androgens, DHEA and DHEAS, and ∆-4A begin to rise. When adrenarche occurs prior to age 8 in girls and 9.5 in boys, it is considered premature (Siegel, Finegold, Urban, McVie, & Lee, 1992; Siegel & Lee, 1992; see Reiter & Saenger, 1997, for review). Premature adrenarche is characterized by high adrenal androgen concentrations and pubic hair development with no evidence of breast development. Off-time activation of the adrenal glands is presumed to be the cause of premature adrenarche. Premature adrenarche has been considered a benign condition (Kaplowitz, Cockerell, & Young, 1985) representing a variation of puberty; therefore, treatment was deemed unnecessary (Reiter & Saenger, 1997). Recent research suggests that children with premature adrenarche may have long-term sequelae such as PCOS, anovulation in late adolescence (and potentially infertility), and insulin resistance (Ibáñez, de Zegher, & Potau, 1999; Ibáñez et al., 1993; Ibáñez, Potau, Zampolli, Street, & Carrascosa, 1997; Oppenheimer, Linder, Saenger, & DiMartino-Nardi, 1995; Richards et al., 1985). In adulthood, women with PCOS have an increased risk for cardiovascular problems (Birdsall, Farquhar, & White, 1997; Talbott et al., 1995) and complications from diabetes mellitus (Dunaif, 1997, 1999; Dunaif, Futterweit, Segal, & Dobrijansky, 1989). Thus, women with early adrenarche may be at risk for PCOS, resulting in significant physical morbidity. It is unknown if there is continuity of adjustment problems observed in premature adrenarche (Dorn et al., 1999) and severe psychopathology observed in adult women with PCOS.

The timing of puberty is considered to have implication for brain development. Saugstad (1989b) pointed out that the “onset of puberty coincides with the last major step in brain development: the elimination of some 40% of the neuronal synapses” (p. 157) and postulated that synaptic loss may have implications for the development of manic-depressive psychosis and schizophrenia. Secular, social class, and geographic trends in body build and mental disorders suggest that early maturers may be more susceptible to manicdepressive psychosis and that late maturers may be more susceptible to schizophrenia (Saugstad, 1989a, 1989b). These hypotheses remain speculative until longitudinal studies provide more definitive findings.

Timing of Puberty and Stress

One of the most controversial issues regarding timing of puberty is whether stressors accelerate or delay the timing of puberty. Consistent with the theoretical perspectives discussed earlier, timing of puberty and behavior and experiences are considered dynamic and bidirectional processes (Susman, 1997). Experiences as well as genetic factors are speculative influences on the tremendous variations in the timing of puberty. Experiential-based sources of variation include disruptive behavior disorders (Schaal et al., 1996), family relationships (Steinberg, 1987, 1988), participation in intensive physical exercise such as ballet dancing (Warren et al., 1991), negative emotional states (Nottelmann et al., 1990; Susman et al., 1989), and family adversity (Belsky, Steinberg, & Draper, 1991). Interest in the mechanism for explaining the relationship between experience and timing of puberty began to emerge in the last decade.

The concept of stress is hypothesized to play a major role in timing of puberty. There are two opposing views on the relationship between stress and timing of puberty. The first perspective, advocated by Belsky et al. (1991), is based on an evolutionary model of psychosocial influences on the timing of puberty. The premise is that early on children develop an understanding of the availability of resources, the duration of close relationships, and the trustworthiness of adults. Exposure to these different types of resources and caretaking adults in the child’s environment are hypothesized to influence the child’s reproductive strategies. Environments characterized by stress are hypothesized to contribute to early reproductive development (Belsky et al., 1991). Three possible avenues are proposed whereby early stress accelerates reproductive development and subsequently earlier childbearing: (a) the stress of living in a conflicted family, (b) the stress of being reared in a single family home, especially with a single mother, and (c) exposure to the parental paramours if in a single parent home. Belsky et al. proposed that these early stressful experiences act by changing the child’s view of the world in general and the child’s view of relationships, in particular, as uncertain, unpredictable, and unstable. The uncertainty of living in a stressful environment has both psychological and physiological consequences. Early stress acts on psychological development via the individual’s having adopted a view of the world as being uncertain. If individuals view the world as uncertain, reproducing early, while they still can, is an adaptive strategy to counteract the uncertainty of the difficult family environment. Uncertainty also leads these individuals to not count on their partners for resources, thereby creating unstable pair bonds. Early stress is proposed to act on physiological systems to accelerate pubertal development, although the exact mechanisms involved in acceleration of puberty are not addressed.

The hypothesis has received mixed support. Conflict in the family at age 7 predicted earlier menarche (Moffitt, Caspi, Belsky, & Silva, 1992). Divorce as a stressor and as a context for girls being raised in father-absent versus fatherpresent homes also has been linked to timing of puberty. Girls in father-absent homes tend to reach puberty earlier than girls reared in father-present homes (Jones, Leeton, McLeod, & Wood, 1972; Moffitt et al., 1992; Surbey, 1990; Wierson, Long, & Forehand, 1993). The stress of living in a conflicted family has been extended to include having a father who is an alcoholic (Malo & Tremblay, 1997). Other studies show that greater marital and family conflict, as well as less marital and family harmony, are associated with pubertal timing in girls (Ellis & Garber, 2000; Ellis, McFadyen-Ketchum, Dodge, Pettit, & Bates, 1999; Graber, Brooks-Gunn, & Warren, 1995; Moffitt et al., 1992; Steinberg, 1988). Absence of positive parent-child relationships, rather than negative relationships, predicted early pubertal timing (Ellis et al., 1999). Positive interactions included greater supportiveness in the parental dyad and more father-daughter and mother-daughter affection.

Absence of positive parent-child relationships, rather than negative relationships, predicted early pubertal timing (Ellis et al., 1999). Positive relationships included greater supportiveness in the parental dyad and more father-daughter and mother-daughter affection. The quality of fathers’ investments in the family emerged as the most important feature of the proximal family environment. Presence of fathers in the home, more time spent by fathers in child care, greater supportiveness in the parental dyad, more father-daughter affection, and more mother-daughter affection, as assessed prior to kindergarten, each predicted later pubertal timing by daughters in seventh grade. The positive dimension of family relationships, rather than the negative dimension, accounted for these relations (Ellis et al., 1999). The interpretation was that the findings are consistent with the Belsky model because positive dimensions were related to later timing of puberty. The findings could also be interpreted as inconsistent with the Belsky model because it predicts that negative aspects of the family will predict earlier timing of puberty.

The mechanisms linking earlier onset of puberty and family stress are not articulated in the existing research. In contrast, the effect of father absence as a precipitant of earlier puberty is hypothesized to be mediated by endocrine mechanisms. Biological father absence frequently is replaced by a stepfather or mother’s boyfriend. Exposure to pheromones of unrelated males is hypothesized to lead to earlier onset of puberty. Exposure to chemosignals and pheromonal systems in a variety of species, including humans, leads to changes in menstrual cycles (McClintock, 1998; Stern & McClintock, 1998) and timing of puberty (Sanders & Reinisch, 1990). Pheromonal systems and chemosignals may function as modulators or signaling substances that precipitate the onset of puberty.

The relationship between family stress and timing of puberty, as well as the psychobiological perspective, in particular, has generated controversy regarding the validity of theoretical perspectives and the imprecision of defining and assessing family stress. A primary criticism of the stress and early timing hypothesis focuses on the logic of the argument that stress is responsible for early onset of puberty. The physiology of the stress system is such that stress should attenuate timing and progression of puberty. This perspective is based on the physiological principle of adaptation to stressors. Adaptation is accomplished at both the physiological and behavioral levels. At the neuroendocrine and peripheral levels CRH is secreted by the hypothalamus, ACTH by the pituitary, and cortisol from the adrenal glands (Chrousos & Gold, 1992; Stratakis & Chrousos, 1997). These components of the HPA stress system down-regulate the reproductive HPG axis at the level of the hypothalamus, pituitary, and gonads. For instance, cortisol exerts inhibitory effects at the levels of the LHRH neuron, the pituitary gonadotroph (responsible for secreting luteinizing hormone and follicle stimulating hormone), and the gonad itself, thereby suppressing sex steroids (testosterone and estrogen) and maturation of reproductive function. Down-regulation or attenuation of secretion of HPG-axis hormones is accomplished either directly or via endorphin. CRH suppresses the LHRH neuron in the hypothalamus. Adaptation at a behavioral level involves a delay or cessation of sexual reproduction activities to conserve vital metabolic resources (Chrousos, 1998). Based on these physiological and behavioral processes, the onset of reproductive capability will be attenuated in children reared in stressful environments (Nottelman et al., 1990; Susman et al., 1989). Conditions that are physically stressful, such as malnutrition and physical stressors (e.g., intense exercise), also suppress reproduction.

In young adolescents stress reflected in behavior problems and self-image problems was related to later maturation based on hormone levels and stage of pubertal development (Tanner criteria, Marshall & Tanner, 1969, 1970; Nottelmann et al., 1987; Susman et al., 1987). Family stressors related to paternal alcoholism led to a delay of male pubertal onset, supporting the hypothesis that stress activates the HPA axis and inhibits the HPG axis (Malo & Tremblay, 1997). Additional longitudinal studies that include actual indexes of stress hormones, as well as adolescent and family stressors, are needed to explain further the links between stress and timing of puberty.

A set of papers (Hinde, 1991; Maccoby, 1991) that accompanied the publication of Belsky et al. (1991) raised additional criticisms regarding the family stress and evolutionary theory of socialization. Maccoby (1991) evoked the concepts of quality and quantity to argue against the Belsky et al. perspective. The quantity argument based on the Belsky et al. perspective is that unstable rearing environments will lead to early maturation and sexual activity, and presumably earlier and more frequent childbearing. Maccoby proposed that if males invest less, females must invest more in rearing the young and that if the male is not available, she recruits investment from her mother and sisters. Her basic strategy should be to select a mate who has the resources and the motivation to be a quality parent rather than a quantity parent. Maccoby further suggested that it does not seem plausible that evolution would have shaped psychological and physiological maternal characteristics such that she would have more children in the absence of a supportive family environment as each additional child increases the difficulty of raising each child. Thus, skepticism is warranted regarding the claim that females have evolved so as to take up a quantity reproductive strategy in the face of instability in childhood relationships. Finally, Maccoby suggested that evolutionary concepts are not essential for explaining contemporaneous functioning. Social learning could explain the effects of family functioning on early sexual activity. Girls from disorganized families likely have less surveillance, are more aware of sexual activity (especially if the mother has multiple sexual partners), or have relationships with older men who are viewed as avenues for escaping dysfunctional homes.

The evolutionary approach to timing of maturation brings together rich perspectives on puberty from animal and human models of adaptation and change. Nonetheless, this perspective is at odds with the two predominant theories articulated at the beginning of the paper, developmental contextualism and holistic interactionism. Both perspectives acknowledge the importance of evolutionary and genetic contributions to development but include the contemporaneous dynamic interaction between psychological, biological, and contextual processes. Family context provides an arena within which parent-adolescent interactions evolve as a result of their past history together as well as current self-organizing properties.

Early maturation at puberty within these frameworks is a product of contextual factors (e.g., nutritional consumption and related obesity) and parent-adolescent interactions characterized by detachment or warmth. The relationship between timing of puberty and family processes is further clouded by the limited research on direction of relationships. Lewontin and Levins (2000) concurred with the contextualism and holistic interactionism developmental models in emphasizing that when considering systems of any complexity there are positive and negative feedback systems. Biological and psychological feedback loops at any time in development. Clear evidence based on models linking sequential and dynamic influences between family stability and instability and timing of puberty is essential to allow for an escape from current controversies regarding timing of puberty and family processes.

Puberty and Sexuality

One of the things that can be stated assuredly is that adolescence “is when most individuals first experience sexual intercourse” (Meschke, Zweig, Barger, & Eccles, 2000, p. 316). The Centers for Disease Control and Prevention (CDC; 1999) reported that in 1999 over 47% of the girls and 52% of the boys surveyed in grades 9 through 12 had had intercourse, and over one third of the sample had been sexually active in the previous three months; 4.4% of girls and 12.2% of boys reported experiencing intercourse before age 13. Trends in sexual activity vary by historical time. Singh and Darroch (1999) examined trends in sexual activity of American women across a 13-year period in three surveys. In the 1980s there was an increase in the proportion of adolescents who had ever had sexual intercourse, but by the mid-1980s and on into the 1990s this increased trajectory stabilized. On average, approximately 40% of adolescents in the 15- to 19-year-old age group had had sexual intercourse in the last three months. These percentages were equal across the three surveys. Kaufmann et al. (1998) reported similar trends.

There is some variation between subpopulations of adolescents. For example, Finkelstein et al. (1998) reported that delayed-puberty boys tended to engage in more advanced sexual behavior than did delayed girls of similar age. Halpern, Udry, and Suchindran (1997) found differences in the self-reported sexual behaviors of Black and White girls, with White girls more likely to report masturbation and Black girls more likely to report petting and coitus.

The influences on adolescent sexuality arise in many spheres: biological, psychological, social, and the media. Biologically, hormones are known to bring about sexual development at puberty and are also considered influences on adolescent sexual behavior. Hormones are thought to have both direct and indirect (e.g., via pubertal physical development) effects on sexuality (Halpern, Udry, & Suchindran, 1998). Androgens, in particular, are considered potent influences on sexuality in both boys and girls. The pubertal increase in male testosterone levels “is thought to provide a biological foundation for the increases in sexual interest and activity that occur during adolescence” (Halpern et al., 1998, p. 446). Studies have examined the relationship between testosterone and sexual activity using both randomized clinical trials and correlational and group difference designs. In a randomized clinical trial of sex hormone replacement therapy, intramuscular administration of midpubertal levels of testosterone to hypogonadal boys resulted in significantly increased self-reports of nocturnal emissions, touching girls, and being touched by girls (Finkelstein et al., 1998). Similarly, Halpern et al. (1998) found that adolescent boys with higher levels of salivary testosterone were more likely to initiate coitus and to participate in other partnered sexual behaviors. Within individuals, salivary testosterone increases were also associated with a greater likelihood of partnered sexual activity. Additionally, the study illustrated the importance of physical developmental influences on sexual activity. When the analysis of testosterone and partnered activity controlled for pubertal development, neither testosterone nor pubertal development reached statistical significance. These findings suggest that evaluations of the propensity to engage in sexual activity should consider multiple levels of influence by psychological, biological, and social functioning.

Testosterone and other androgens also have striking effects on sexuality in adolescent girls. Halpern et al. (1997) reviewed several lines of evidence for androgenic effects on female adolescent sexuality, including hormone replacement studies, female behavioral responsiveness to testosterone, and connections between testosterone levels and sexual activity during puberty (see also Hutchinson, 1995). Udry et al. (1986) reported that adolescent girls’ androgen levels, namely testosterone and the adrenal androgens DHEA, DHEAS, and ∆-4A, predicted the girls’anticipation of future sex. Halpern et al. examined within-individual changes as well as differences between girls and found that higher plasma testosterone levels were associated with a higher incidence of transition to coitus in both Black and White girls. Frequency of attendance at religious services operated as a social control factor among White females. Testosterone was concluded to be a causal factor in female sexual activity, but biological effects were moderated by relevant social variables. Processes at both the social and biological levels appear to interact to influence sexual activity.

Less research has examined the role of estrogens in adolescent sexuality, but there is some evidence for estrogenic effects on female adolescent sexual behavior. Finkelstein et al. (1998) found that administering oral conjugated estrogen to hypogonadal female adolescents resulted in significantly increased self-reports of necking behavior, but only at the highest dose used (intended to simulate the late stages of puberty). Of note is that when testosterone or estrogen is measured in blood or saliva and related to sexual activity, moods, or behavior, it is not known which of the hormones activates or is permissive of the expression of sexual behavior as testosterone can be converted to estrogen.

A plethora of nonhormonal factors also influences adolescent sexuality, but an additional factor is of note: body fat. Halpern, Udry, Campbell, and Suchindran (1999) examined the dating frequency and sexual behaviors of seventh- and eighth-grade girls in relation to measured body fat. Comparing girls with mean body fat levels to those 1 SD above or below showed that the lower body fat was associated with a greater chance of dating. This pattern was true for both Black and White girls, although the relationship was stronger for White girls. Additionally, this difference in dating frequency explained the relationship between higher body fat and lower incidence of coitus and petting. Halpern et al. warned, however, that these results must be taken in context because synchronous transitions (e.g., when dating begins at the same time as menarche and the transition to middle school) may exert unique pressures (as in Smolak, Levine, & Gralen, 1993). Other factors also influence dating such as late maturation in girls, with later maturers being less likely to date despite their lower levels of body fat.

Peer sexual activity is considered a potent influence on sexual activity. Udry et al. (1986) found that the strongest predictor of sexual behavior in pubertal girls was whether their close friends were sexually active. Meschke et al. (2000) supported these findings in a report showing that timing of first intercourse was associated with peer achievement levels and popularity for boys, along with “dating alone” and pubertal timing for girls. Siblings also influence sexual activity. Based on a social modeling theory, East and Shi (1997) proposed a sibling interaction hypothesis to explain sexual activity in pregnant or parenting teens and their younger sisters. Negative sibling relationship qualities, such as rivalry, competition, and conflict, were more closely related to younger sisters engaging in problem behavior and sexual behavior than were positive relationship qualities, such as warmth and closeness. Additionally, a shared friendship network with the older sister was found to be associated with extensive younger sister problem behavior and sexual behavior. Compared with the younger siblings of never-pregnant teenagers, the younger sisters of pregnant teenagers viewed school and career as less important, were more accepting of adolescent childbearing, perceived younger ages as appropriate for first intercourse, marriage, and childbearing, and engaged in more problem behavior (East, 1996). These attitudes are conducive to increasing the probability of early sexual activity and early childbearing. Collectively, these studies aptly demonstrate that a biopsychosocial model had greater statistical power for both boys and girls than do models that take fewer factors into account. In summary, hormones and pubertal development appear to impact strongly adolescents’ sexual development, but sexuality occurs within the context of the adolescent’s social development that incorporates peers and siblings.

Sexual Risk Taking

Sexual activity beginning sometime during puberty might be considered normative given the high number of adolescents engaging in early sexual activity. The danger inherent in considering sexual activity normative is that risky sexual behaviors are linked to high rates of morbidity and even mortality in adolescents. In a national survey of 10,645 youth, engaging in multiple health risk behaviors (including sexual behavior) increased across age in youth (Brener & Collins, 1998). For those in the 12–13 year age group, 1 in 12 engaged in two or more sexual behaviors, whereas one third of 14- to 17-year-olds and 50% of the 18- to 21-year-olds engaged in multiple sexual behaviors. There was a greater likelihood for males to engage in multiple health-risk behaviors. The predictive stability of early sexual behavior with regard to later mental and physical health problems is not well known. In one of the few longitudinal studies addressing this issue, women’s reproductive experiences during adolescence had repercussions in adult life with regard to sexuality, selfimage, and state of gynecological health (C. M. Magnusson et al., 1999). Women who had gynecological problems during adolescence experienced their adolescent sexual experiences as generally negative. In early adulthood these women had more recurrent and varied gynecological illnesses than did their comparison-group counterparts. Women’s early sexual experience was also linked to an increase in normbreaking behavior, lower educational attainment, and a younger age of adult responsibilities compared with the control women. These findings are unique in that they document long-term consequences of early sexual activity in diverse domains: health, adjustment, achievement, and socially sanctioned behavior. The lack of longitudinal information does not allow for sorting out whether early sexual activity is reflective of a constellation of behavior problems that persist over time or whether sexual activity, per se, leads to unique mental health and gynecological problems that persist into adulthood.

Limitations of self-report of sexual debut are acknowledged and likely result in an overestimate in the age of onset as well as the frequency of sexual activity during adolescence. In the NationalYouth Survey (Lauritsen & Swicegood, 1997) there were inconsistencies in age at first intercourse from reports as an adolescent to reports as an adult by 28% to 32% of subjects. Those most likely to have consistent reporting across time were females (70%), whereas only 27% of Black males were consistent in reporting. Given the seriousness of risky sexual behavior it seem prudent to continue to press for programs to reduce risky sexual behavior even in the absence of quality statistics on onset and progression of sexual activity during adolescence.

Implications for Research and Social Policy

The rapid increase in research findings in the last two decades relating puberty to various domains of functioning provides an exceptionally strong platform for planning interventions to improve the well-being of adolescents and to prevent problems. Findings from basic and applied research have implications for the content of prevention and intervention programs, the timing and type of interventions, and the modalities for delivering the program message. In addition, in the past several decades the importance of adolescence has been the focus of attention of various organized groups, which have, in turn, directed programs or policy issues toward that age group. For example, the American Academy of Pediatrics (www.aap.org) has a section on adolescent health, founded in 1978. Additionally, the Society of Adolescent Medicine offers specialized health services to adolescents (www.adolescenthealth.org). These services include not only the assessment of normal growth and physical health problems of adolescents but also psychosocial issues, health promotion, disease prevention, and anticipatory guidance. Unfortunately, the problem of maldistribution of health professionals specializing in adolescent health is significant. Many practitioners of adolescent health are in academic medical centers located in urban areas. Rural areas of the country continue to lack support services for adolescents. A parallel scenario is noted for psychiatrists specializing in adolescent development.

Policy-related goals for adolescent health and development also have been articulated. In 1998 Brindis et al. reviewed 36 national documents that emerged over the last decade and focused on or pertained to the health of adolescents. Through the synthesis of these documents, the committee determined the following six policy-related goals for the health of adolescents: (a) improve access to health care for adolescents, (b) improve the adolescent environment, (c) increase the role of schools in improving adolescent health, (d) promote positive adolescent health, (e) improve adolescent transitions to adulthood, and (f) improve collaborative relationships. In addition to the six policies, the committee also provided several cross-cutting themes that emerged from their recommendations. Most germane to this research paper is the theme that a “greater programmatic focus on primary prevention and early intervention, which is substantiated and shaped by rigorous research, is needed” (p. 183). Currently, adolescent health care focuses on secondary rather than primary prevention, and there is a dearth of research that characterizes the effect of providing counseling or anticipatory guidance services in the health care visits of youth or the effect of content and quality of primary care visits.

Content of Programs on Puberty

Public health policy lags behind the sophisticated knowledge that is accumulating regarding puberty, especially with regard to the notion that puberty signals the onset of reproductive competence, sexual activity, and risky sexual behavior. The majority of citizens in the United States are unaware of the recent advances in understanding the physiological aspects of puberty as well as the positive dimensions of psychological development during puberty. The sexual reproductive aspects of puberty receive disproportional attention compared to the normative and positive aspects of development during adolescence. The result is that normative health and developmental concerns receive little attention from major social institutions: health care, education, and family. A public health focus on puberty might profitably be based on the following questions: What do parents, educators, and the public need to know about puberty? What do adolescents want to know? Research initiatives and prevention programs arise almost exclusively from adults with virtually no consultation from adolescents. Therefore, a wide gap may exist between what information is presented to adolescents and what they want to know. In a rare study on what adolescents want to know, a majority of the questions reflected biological topics (88%), such as genital physiology (26%) and sexuality and reproduction (26%). Only 6% addressed psychosocial questions (Ryan, Millstein, & Irwin, 1996). Both females and Asians (compared with other ethnic or racial groups) expressed greater interest in the differences between male and female development. Prepubertal males were more concerned about general puberty than were boys in later Tanner stages.

In North America the study of puberty and reproduction is confused with sexual activity and the breaking of religious and social norms. Puberty and emerging sexuality take on negative societal connotations and thereby become shunned by the family and educational institutions. Adolescent sexuality is rarely viewed in the broader perspective as involving a social and cultural component. The interactions between boys and girls do not necessarily lead to sexual activity. Rather, these interactions reflect an arena whereby the socialand culture-based roles of males and females are learned and practiced.

Those entrusted with the care of adolescents should be cognizant of the broad range of emotional, behavioral, and even sexual activities that characterize the pubertal transition. Along with this awareness, those same persons should recognize that the diversity of acceptance or rejection of such functioning is often dictated by gender, ethnicity, age, and life history. Those involved in the health care system are in a prime position to educate the public and adolescents themselves about the range of new emotions and behaviors that will emerge by late puberty.

In addition to innovative content, positive attitudes about adolescents are critical elements of an effective program. Health care providers must recognize the specific challenges and rewards of providing services for adolescents. Quality care begins with the establishment of trust, respect, and confidentiality between the caregiver and the adolescent. Especially when providing care for the younger teen, caregivers must focus on involving a member of the family or another significant adult to provide needed support and guidance.

Anticipatory guidance for parents should focus on assessing their parenting styles and promoting supervision and monitoring. Although parents should strive to maintain open communication with their adolescents, they may estimate neither the depression and anxiety of their adolescents nor the sexual activity and the sexual risk experienced by their teenage children accurately. Most adolescents want to discuss sexual-related issues with health care providers and others and will welcome direct questions about sexual behaviors and possible risks when posed in a confidential and nonmoralistic manner. Discussion of the physical, emotional, familial, and social changes related to adolescence will encourage healthy sexual development.

Timing of Puberty and Prevention

A goal of prevention is to find a point in development when prevention efforts have some hope of success (Coie et al., 1993). With regard to puberty, the goal is to initiate interventions before or simultaneously with the biological changes. Puberty may be occurring at earlier ages than anticipated in girls (Herman-Giddens et al., 1997), which has important health care, educational, and social policy implications. Programs to improve adolescent mental and physical health problems should correspondingly begin earlier in ontogeny than in the past. All individuals responsible for any aspect of the well-being of adolescents—parents, teachers, and health system personnel—should be aware that puberty may be occurring earlier in American girls than it did a few decades ago. In earlier maturing adolescents, the effects of hormone changes can occur two to three years before they are anticipated by parents and teachers. Important to note is that much less is known about boys than girls and timing of puberty. Given that boys and girls find themselves together in multiple contexts, programs to prevent mental and physical health problems should be introduced simultaneously for boys and girls.

Prevention efforts to reduce early risky sexual behaviors and mental health problems, like depression, are likely to have a higher probability of success if initiated at a younger age than in the past, given the earlier age of puberty. Social policy with regard to the cognitive abilities of adolescents, parent training, and school health and sex education and guidance programs will need to be modified to take into account the early onset of puberty (Reider & Coupey, 1999). Body self-awareness and emotion recognition programs are especially important to implement early in gonadarche; otherwise, adolescents will be confused by body changes that accompany puberty. Similarly, parental monitoring in sexual possibility situations, as well as in other situations (e.g., when alcohol or drugs may be present), will need to occur earlier than in the past. In all cases, programs to prevent early sexual activity will present a challenge to program planners given the cognitive developmental status of the adolescents and the complexities of presenting information about the physiology and psychology of sexuality.

Research and Theory Development

Scholars of adolescent development have accepted the importance of the integration of biological, psychological, and contextual processes long before it was fashionable in other areas of developmental science. The theoretical frameworks discussed earlier (developmental contextualism and holistic interactionism) are hallmarks for the acknowledgment of the importance of integrated biological, psychological, and social perspectives on development. These theoretical perspectives are consistent with the emerging perspective that processes of development can only be understood by considering the multiple systems that function at multiple levels of development, from the genetic, molecular, and cellular levels to the societal level (Susman, 1998). Given these complexities, the following principles might guide research in the future.

First, models that consider multiple biological, psychological, and contextual levels of functioning will be interdisciplinary, bringing together the expertise of multiple professionals. An example of such interdisciplinary research in the future is that offered by the Human Genome Project, which offers a myriad of possibilities for linking individual genes or patterns of genes to specific behaviors in specific contexts. Given that experiences affect the timing of puberty and that genes are responsible for the initiation of puberty, future interdisciplinary studies have the potential of identifying genes that link experience and the onset of puberty.

Second, the complexity of integrating multiple levels of analysis necessarily implies that the scale and scope of investigations will be larger than in the past. Nonetheless, hypothesis-driven, small-scale studies at specific levels of analysis are critically important to continue as well. If studies focus on one level of analysis, such as the biological level, it is critical to acknowledge the contribution of mediators and moderators at other levels as well.

Third, methodological innovations and the integration of biology and behavior are possible given the advances in statistical models in the last decade. In addition, theoretical innovations act in concert with methodological innovations. This premise is nowhere more apparent than in the new methodologies for considering the dynamic interplay between hormones and behavior. The dynamic and changing nature of physical maturation, hormones, and psychological characteristics at puberty now can be captured in longitudinal statistical models using estimates of how changes in one domain (hormones) can lead to changes in another domain (behavior). Additionally, perspectives like the holistic interaction model proposed by D. Magnusson (1999) capture dynamic holistic processes through related methodological strategies (e.g., longitudinal cluster analysis) developed by Bergman and Magnusson (1997). These methodological strategies look for patterns or configurations in developmental processes.

Bibliography:

  1. Achenbach, T. M. (1991). Manual for Child Behavior Checklist/ 4-18 and 1991 Profile. Burlington: University of Vermont.
  2. Andersson, T., & Magnusson, D. (1990). Biological maturation in adolescence and the development of drinking habits and alcohol abuse among young males: A prospective longitudinal study. Journal of Youth and Adolescence, 19, 33–42.
  3. Angold, A., Costello, E. J., Erkanli, A., & Worthman, C. (1999). Pubertal changes in hormone levels and depression in girls. Psychological Medicine, 29, 1043–1053.
  4. Angold, A., Costello, E. J., & Worthman, C. M. (1998). Puberty and depression: The roles of age, pubertal status and pubertal timing. Psychological Medicine, 28, 51–61.
  5. Angold, A., & Worthman, C. (1993). Puberty onset of gender differences in rates of depression: A developmental, epidemiologic and neuroendocrine perspective. Journal of Affective Disorders, 29, 145–158.
  6. Apter, D., Reinila, M., & Vikho, R. (1989). Some endocrine characteristics of early menarche, a risk factor for breast cancer, are preserved into adulthood. International Journal of Cancer, 44, 783–787.
  7. Archer, J. (1991). The influence of testosterone on human aggression. British Journal of Psychology, 82, 1–28.
  8. Ary, D. V., Duncan, T. E., Biglan, A., Metzler, C. W., Noell, J. W., & Smolkowski, K. (1999). Development of adolescent problem behavior. Journal of Abnormal Child Psychology, 27, 141–150.
  9. Barnes, H. V. (1975). Physical growth and development during puberty. Medical Clinics of North America, 59, 1305–1317.
  10. Bebbington, P. E., Dunn, G., Jenkins, R., Lewis, G., Brugha, T., Farrell, M., & Meltzer, H. (1998). The influence of age and sex on the prevalence of depressive conditions: Report from the National Survey of Psychiatric Morbidity. Psychological Medicine, 28, 9–19.
  11. Belsky, J., Steinberg, L., & Draper, P. (1991). Childhood experience, interpersonal development, and reproductive strategy: An evolutionary theory of socialization. Child Development, 62, 647–670.
  12. Bergman, L. R., & Magnusson, D. (1997). A person-oriented approach in research on developmental psychopathology. Development and Psychopathology, 9, 291–319.
  13. Birdsall, M. A., Farquhar, C. M., & White, H. D. (1997). Association between polycystic ovaries and extent of coronary artery disease in women having cardiac catheterization. Annals of Internal Medicine, 126, 32–35.
  14. Blos, P. (1962). On adolescence: A psychoanalytical interpretation. New York: Free Press.
  15. Blum, W. F., Englaro, P., Hanitsch, S., Juul, A., Hertel, N. T., Muller, , Skakkebaek, M. L., Heinman, M., Birkett, A. M., Attanasio, W., Kiess, W., & Rascher, W. (1997). Plasma leptin levels in healthy children and adolescents: Dependence on body mass index, body fat mass, gender, pubertal stage, and testosterone. Journal of Clinical Endocrinology and Metabolism, 82, 2904– 2910.
  16. Blyth, D. A., Simmons, R. G., & Zakin, D. F. (1985). Satisfaction with body image for early adolescent females: The impact of pubertal timing within different school environments. Journal of Youth and Adolescence, 14, 207–225.
  17. Blythe, M. J., & Rosenthal, S. L. (2000). Female adolescent sexuality. Promoting healthy sexual development. Obstetrics and Gynecology in Clinics of North America, 27, 125–141.
  18. Bondy, P. K. (1985). Disorders of the adrenal cortex. In J. D. Wilson & D. W. Foster (Eds.), Williams textbook of endocrinology (pp. 816–890). Philadelphia: Saunders.
  19. Bonjour, J., Theintz, G., Buchs, B., Slosman, D., & Rizzoli, R. (1991). Critical years and stages of puberty for spinal and femoral bone mass accumulation during adolescence. Journal of Clinical Endocrinology and Metabolism, 73, 555–563.
  20. Brain, P. F. (1994). Hormonal aspects of aggression and violence. In A. J. Reiss Jr., K. A. Miczek, & J. I. Roth (Eds.), Understanding and preventing violence: Vol. 2. Biobehavioral influences (pp. 173–244). Washington, DC: National Academy Press.
  21. Brain, P. F., & Susman, E. J. (1997). Hormonal aspects of antisocial behavior and violence. In D. M. Stoff, J. Breiling, & J. Maser (Eds.), Handbook of antisocial behavior (pp. 314–323). New York: Wiley.
  22. Brandtstaedter, J. (1998). Action perspectives on human development. In W. Damon (Series Ed.) & R. M. Lerner (Vol. Ed.), Handbook of child psychology: Vol. 1. Theoretical models of human development (pp. 807–863). New York: Wiley.
  23. Brandstaedter, J., & Lerner, R. M. (1999). Action and selfdevelopment: Theory and research through the life span. Thousand Oaks, CA: Sage.
  24. Brener, N. D., & Collins, J. L. (1998). Co-occurrence of health-risk behaviors among adolescents in the United States. Journal of Adolescent Health, 22, 209–213.
  25. Brindis, C. D., Ozer, E. M., Handley, M., Knopf, D. K., Millstein, S. G., & Irwin, C. E. (1998). Improving adolescent health: An analysis and synthesis of health policy recommendations, full report. San Francisco: University of California, San Francisco.
  26. Brooks-Gunn, J., & Petersen, A. C. (1983). Girls at puberty: Biological and psychosocial perspectives. New York : Plenum Press.
  27. Brooks-Gunn, J., Petersen, A. C., & Eichorn, D. (1985). The study of maturational timing effects in adolescence [Special issue]. Journal of Youth and Adolescence, 14, 149–161.
  28. Brooks-Gunn, J., & Reiter, E. O. (1990). The role of pubertal processes. In S. S. Feldman & G. R. Elliott (Eds.), At the threshold: The developing adolescent (pp. 16–53). Cambridge, MA: Harvard University Press.
  29. Brooks-Gunn, J., & Warren, M. P. (1985). Measuring physical status and timing in early adolescence: A developmental perspective. Journal of Youth and Adolescence, 14, 163–189.
  30. Brooks-Gunn, J., & Warren, M. P. (1989). Biological and social contributions to negative affect in young adolescent girls. Child Development, 60, 40–55.
  31. Cairns, R. B. (1997). Socialization and sociogenesis. In D. Magnusson (Ed.), The lifespan development of individuals: Behavioral, neurobiological and psychosocial perspectives: A synthesis (pp. 277–295). NewYork: Cambridge University Press.
  32. Cairns, R. B., & Rodkin, P. C. (1998). Phenomena regained: From configurations to pathways. In R. B. Cairns & L. R. Bergman (Eds.), Methods and models for studying the individual (pp. 245– 265). Thousand Oaks, CA: Sage.
  33. Cairns, R. B., & Stoff, D. M. (1996). Conclusion: A synthesis of studies on the biology of aggression and violence. In D. M. Stoff & R. B. Cairns (Eds.), Aggression and violence: Genetic, neurobiological and biosocial perspectives. Mahwah, NJ: Erlbaum.
  34. Caspi, A., Henry, B., McGee, R. O., Moffitt, T. E., & Silva, P. A. (1995). Temperamental origins of child and adolescent behavior problems: From age three to fifteen. Child Development, 66, 55–68.
  35. Caspi, A., & Moffitt, T. E. (1991). Individual differences are accentuated during periods of social change: Sample case of girls at puberty. Journal of Personality and Social Psychology, 61, 157–168.
  36. Centers for Disease Control and Prevention (1999). Youth Risk Behavior Survey [On-line]. Available at www.cdc.gov/epo/ mmwr/preview/mmwr.html/ss4905a1.htm.
  37. Chrousos, G. P. (1998). Stressors, stress, and neuroendocrine integration of the adaptive response. Stress of Life: From Molecules to Man, Annals of the New York Academy of Sciences, 851, 311–335.
  38. Chrousos, G. P., & Gold, P. W. (1992). The concepts of stress and stress system disorders. Journal of the American Medical Association, 267, 244–1252.
  39. Cizza, G., Dorn, L. D., Lotsikas, A., Sereika, S., Rotenstein, D., & Chrousos, G. P. (2001). Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: Potential implications of preliminary study. Hormone and Metabolic Research, 33, 138–143.
  40. Cohen, R., & Rosenfeld, R. G. (1996). Growth regulation. In J. E. Griffin & S. R. Agate (Eds.), Textbook of endocrine physiology (pp. 244–259), New York: Oxford University Press.
  41. Coie, J. D., Watt, N. F., West, S. G., Hawkins, J. D., Asarnow, J. R., Marksman, H. J., Ramee, S. L., Shure, M. D., & Long, B. (1993). The science of prevention: A conceptual framework and some directions for a national research program. American Psychologist, 48, 1013–1022.
  42. Constantino, J. N., Grosz, D., Saenger, P., Chandler, D. W., Nardi, R., & Earls, F. J. (1993). Testosterone and aggression in children. Journal of the American Academy of Child and Adolescent Psychiatry, 32, 1217–1222.
  43. Counts, D. R., Pescovitz, O. H., Barnes, K. M., Hench, K. D., Chrousos, G. P., Sherins, R. J., Comite, F., Loriaux, D. L., & Cutler, G. B., Jr. (1987). Dissociation of adrenarche and gonadarche in precocious puberty and in isolated hypogonadotropic hypogonadism. Journal of Clinical Endocrinology and Metabolism, 64, 1174–1178.
  44. Crockett, L. J., & Petersen, A. C. (1987). Pubertal status and psychosocial development: Findings from the Early Adolescence Study. In R. M. Lerner & T. T. Foch (Eds.), Biologicalpsychosocial interactions in early adolescence: Child psychology (pp. 173–188). Hillsdale, NJ: Erlbaum.
  45. Dorn, L. D., Hitt, S., & Rotenstein, D. (1999). Psychological and cognitive differences in children with premature vs. on-time adrenarche. Archives of Pediatrics and Adolescent Medicine, 153, 137–145.
  46. Dorn, L. D., Susman, E. J., Nottelmann, E. D., Inoff-Germain, G., & Chrousos, G. P. (1990). Perceptions of puberty: Adolescent, parent, and health care personnel ratings of pubertal stage. Developmental Psychology, 28, 322–329.
  47. Downs, A., & Fuller, M. J. (1991). Recollections of spermarche: An exploratory investigation. Current Psychology: Research and Reviews, 10, 93–102.
  48. Dubas, J. S., Graber, J. A., & Petersen, A. C. (1991). The effects of pubertal development on achievement during adolescence. American Journal of Education, 99, 444–460.
  49. Dunaif, A. (1997). Insulin resistance and the polycystic ovary syndrome: Mechanism and implications for pathogenesis. Endocrine Review, 18, 774–800.
  50. Dunaif, A. (1999). Insulin action in the polycystic ovary syndrome. Endocrinology and Metabolism Clinics of North America, 28, 341–359.
  51. Dunaif, A., Futterweit, W., Segal, K. R., & Dobrijansky, A. (1989). Profound peripheral insulin resistance independent of obesity in the polycystic ovary syndrome. Diabetes, 38, 1165–1174.
  52. Duncan, P. D., Ritter, P. L., Dornbusch, S. M., Gross, R. T., & Carlsmith, J. M. (1985). The effects of pubertal timing on body image, school behavior, and deviance. Journal of Youth and Adolescence, 14, 227–235.
  53. East, P. L. (1996). The younger sisters of childbearing adolescents: Their attitudes, expectations, and behaviors. Child Development, 67, 267–282.
  54. East, P. L., & Shi, C. R. (1997). Pregnant and parenting adolescents and their younger sisters: The influence of relationship qualities for younger sister outcomes. Journal of Development and Behavioral Pediatrics, 18, 84–90.
  55. Ellis, B. J., & Garber, J. (2000). Psychosocial antecedents of variation in girls’ pubertal timing: Maternal depression, stepfather presence, and marital and family stress. Child Development, 71, 485–501.
  56. Ellis, B. J., McFadyen-Ketchum, S., Dodge, K. A., Pettit, G. S., & Bates, J. E. (1999). Quality of early family relationships and individual differences in the timing of pubertal maturation in girls: A longitudinal test of an evolutionary model. Journal of Personality and Social Psychology, 77, 387–401.
  57. Emans, S. J., & Biro, F. (1998). Secondary sexual characteristics and menses in young girls (Letter to the editor). Pediatrics, 101, 949–950.
  58. Faust, M. S. (1969). Developmental maturity as a determinant of prestige in adolescent girls. Child Development, 38, 1025– 1034.
  59. Finkelstein, J. W., Susman, E. J., Chinchilli, V., Kunselman, S. J., D’Arcangelo, M. R., Schwab, J., Demers, L. M., Liben, L., Lookingbill, M. S., & Kulin, H. E. (1997). Estrogen or testosterone increases self-reported aggressive behavior in hypogonadal adolescents. Journal of Clinical Endocrinology and Metabolism, 82, 2433–2438.
  60. Finkelstein, J. W., Susman, E. J., Chinchilli, V. M., D’Arcangelo, M. R., Kunselman, S. J., Schwab, J., Demers, L. M., Liben, L. S., & Kulin, H. E. (1998). Effects of estrogen or testosterone on selfreported sexual responses and behaviors in hypogonadal adolescents. Journal of Clinical Endocrinology and Metabolism, 83, 2281–2285.
  61. Flannery, D. J., Rowe, D. C., & Gulley, B. L. (1993). Impact of pubertal status, timing and age on adolescent sexual experience and delinquency. Journal of Adolescent Research, 8, 21–40.
  62. Ford, D. H., & Lerner, R. M. (1992). Developmental systems theory: An integrative approach. Newbury Park, CA: Sage.
  63. Forest, M. G. (1989). Physiological changes in circulating androgens. In M. G. Forest (Ed.), Androgens in childhood (pp. 104–129). Basel: Karger.
  64. Fredriks, A. M., Van Buuren, S., Burgmeijer, R. J. F., Muelmeester, J. F., Roelien, J., Brugman, E., Roede, M. J., VerlooveVanhorick, S. P., & Wit, J. M. (2000). Continuing positive secular growth change in the Netherlands 1955–1997. Pediatric Research, 47, 316–323.
  65. Frisch, R. E. (1984). Body fat, puberty and fertility. Biological Reviews of the Cambridge Philosophical Society, 59, 161–188.
  66. Frisch, R. E., & MacArthur, J. (1974). Menstrual cycles: Fatness as a determinant of minimum weight for height necessary for their maintenance or onset. Science, 185, 949–951.
  67. Gaddis, A., & Brooks-Gunn, J. (1985). The male experience of pubertal change. Journal of Youth and Adolescence, 14, 61–69.
  68. Garn, S. M. (1992). Physical growth and development. In S. B. Friedman, M. Fisher, & SK Schonberg (Eds.), Comprehensive adolescent health care (pp. 18–23). St. Louis, MO: Quality Medical.
  69. Ge, X., Brody, G. H., Conger, R. D., & Simons, R. L. (in press). Pubertal transition and African American children’s internalizing and externalizing symptoms. Journal of Youth and Adolescence.
  70. Ge, X., Conger, R. D., & Elder, G. H. (2001a). Pubertal transition, stressful life events, and the emergence of gender differences in adolescent depressive symptoms. Developmental Psychology, 37, 404–417.
  71. Ge, X., Conger, R. D., & Elder, G. H. (2001b). The relationship between pubertal status and psychological distress in adolescent boys. Journal of Research on Adolescence, 11, 49–70.
  72. Ge, X., Conger, R. D., & Elder, G. H., Jr. (1996). Coming of age too early: Pubertal influences on girls’vulnerability to psychological distress. Child Development, 67, 3386–3400.
  73. Gell, J. S., Carr, B. R., Sasano, I. I., Atkins, B., Margarf, L., Mason, J. I., & Rainey, W. E. (1998). Adrenarche results from development of a 3-beta-hydroxysteroid dehydrogenase-deficient adrenal reticularis. Journal of Clinical Endocrinology and Metabolism, 83, 3695–3701.
  74. Gerver, W. J., De Bruin, R., & Drayer, N. M. (1994). A persisting secular trend for body measurements in Dutch children: The Oosterwolde II Study. Acta Paediatrica, 83, 812–814.
  75. Giedd, J. N., Blumenthal, J., Jeffries, N. O., Rajapakse, J. C., Vaituzis, A. C., Liu, H., Berry, Y. C., Tobin, M., Nelson, J., & Castellanos, F. X. (1999). Development of the human corpus callosum during childhood and adolescence: Alongitudinal MRI study. Progress in Neuro-psychopharmacology and Biological Psychiatry, 21, 1185–1201.
  76. Glickman, S. E., Frank, L. G., Davidson, J. M., Smith, E. R., & Siiteri, P. K. (1987). Androstenedione may organize or activate sex-reversed traits in female spotted hyenas. Proceedings of the National Academy of Science, 84, 3444–3447.
  77. Goodyer, I. M., Herbert, J., Tamplin, A., & Altham, P. M. (2000). First-episode major depression in adolescents: Affective, cognitive and endocrine characteristics of risk status and predictors of onset. British Journal of Psychiatry, 176, 142–149.
  78. Graber, J. A., Brooks-Gunn, J., & Warren, M. P. (1995). The antecedents of menarcheal age: Heredity, family environment, and stressful life events. Child Development, 66, 346–359.
  79. Graber, J. A., Brooks-Gunn, J., & Warren, M. P. (in press). Pubertal effectsonadjustmentingirls:Movingfromdemonstratingeffects to identifying pathways. Journal of Youth and Adolescence.
  80. Graber, J. A., Lewisohn, P. M., Seeley, J. R., & Brooks-Gunn, J. (1997). Is psychopathology associated with the timing of pubertal development? Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1768–1776.
  81. Grumbach, M. M., & Styne, D. M. (1992). Puberty: Ontogeny, neuroendocrinology, physiology, and disorders. In J. D. Wilson & P. W. Foster (Eds.), Williams textbook of endocrinology (pp. 1139–1231). Philadelphia: Saunders.
  82. Hall, G. S. (1904). Adolescence. New York: Appleton.
  83. Halpern, C. T., Udry, J. R., & Suchindran, C. (1998). Monthly measures of salivary testosterone predict sexual activity in adolescent males. Archives of Sexual Behavior, 27, 445–465.
  84. Halpern, C. T., Udry, J. R., & Suchindran, C. (1997). Testosterone predicts initiation of coitus in adolescent females. Psychosomatic Medicine, 59, 161–171.
  85. Halpern, C. T., Udry, J. R., Campbell, B., & Suchindran, C. (1999). Effects of body fat on weight concerns, dating, and sexual activity: A longitudinal analysis of Black and White adolescent girls. Developmental Psychology, 35, 721–736.
  86. Hayward, C., Killen, J. D., Wilson, D. M., Hammer, L. D., Litt, I. F., Kraemer, H. C., Haydel, F., Varaday, A., & Taylor, C. B. (1997). Psychiatric risk associated with early puberty in adolescent girls. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 255–262.
  87. Herman-Giddens, M. E., Slora, E. J., Wasserman, R. C., Bourdony, C. J., Bhapkar, M. V., Koch, G. G., & Hasemeier, C. (1997). Secondary sexual characteristics and menses in young girls seen in office practice: A study from the Pediatric Research in Office Settings Network. Pediatrics, 99, 505–512.
  88. Hinde, R. A. (1991). When is an evolutionary approach useful? Child Development, 62, 671–675.
  89. Hutchinson, K. A. (1995). Androgens and sexuality. The American Journal of Medicine, 98, 111S–115S.
  90. Ibáñez, L., de Zegher, F., & Potau, N. (1999). Anovulation after precocious pubarche: Early markers and time course in adolescence. Journal of Clinical Endocrinology and Metabolism, 84, 2691–2695.
  91. Ibáñez, L., Potau, N., Virdis, R., Zampolli, M., Terzi, C., Gussinye, M., Carrascosa, A., & Vicens-Calvet, E. (1993). Postpubertal outcomes in girls diagnosed of premature pubarche during childhood: Increased frequency of functional ovarian hyperandrogenism. Journal of Clinical Endocrinology and Metabolism, 76, 1599–1603.
  92. Ibáñez, L., Potau, N., Zampolli, M., Street, M. E., & Carrascosa, A. (1997). Girls diagnosed with premature pubarche show an exaggerated ovarian androgen synthesis from the early stages of puberty: Evidence from gonadotropin-releasing hormone antagonist testing. Fertility and Sterility, 67, 849–855.
  93. Inoff-Germain, G., Arnold, G. S., Nottelmann, E. D., Susman, E. J., Cutler, G. B., Jr., & Chrousos, G. P. (1988). Relations between hormone levels and observational measures of aggressive behavior of early adolescents in family interactions. Developmental Psychology, 24, 129–139.
  94. Jones, B., Leeton, J., McLeod, I., & Wood, C. (1972). Factors influencing the age of menarche in a lower socio-economic group in Melbourne. Medical Journal of Australia, 2, 533–535.
  95. Jones, H. E. (1938). The California adolescent growth study. Journal of Educational Research, 31, 561–567.
  96. Jones, M. C. (1958). A study of socialization patterns at the high school level. Journal of Genetic Psychology, 92, 87–111.
  97. Jones, M. C., & Bayley, N. (1950). Physical maturing among boys as related to behavior. Journal of Educational Psychology, 41, 129–148.
  98. Jones, M. C., Bayley, N., & Jones, H. E. (1948). Physical maturing among boys as related to behavior. American Psychologist, 3,
  99. Kampert, J. B., Whittemore, A. S., & Paffenbarger, R. S., Jr. (1988). Combined effect of childbearing, menstrual events, and body size on age-specific breast cancer risk. American Journal of Epidemiology, 128, 962–979.
  100. Kaplowitz, P. B., Cockerell, J. L., & Young, R. B. (1985). Premature adrenarche. Clinical Pediatrics, 25, 28–34.
  101. Kaplowitz, P. B., Oberfield, S. E., and the Drug and Therapeutics and Executive Committees of the Lawson Wilkins Pediatric Endocrine Society. (1999). Reexamination of the age limit for defining when puberty is precocious in girls in the United States: Implications for evaluation and treatment. Pediatrics, 104, 936–941.
  102. Kaufmann, R. B., Spitz, A. M., Strauss, L. T., Morris, L., Santelli, J. S., Koonin, L. M., & Marks, J. S. (1998). The decline in US teen pregnancy rates, 1990–1995. Pediatrics, 102, 1141–1147.
  103. Key, T. J. (1999). Serum oestradiol and breast cancer risk. Endocrine-Related Cancer, 6, 175–180.
  104. Kiess, W., Reich, A., Meyer, K., Glasow, A., Deutscher, J., Klammt, J., Yang, Y., Muller, G., & Kratzsch, J. (1999). Arole for leptin in sexual maturation and puberty? Hormone Research, 51, 55–63.
  105. Kim, K., & Smith, P. K. (1998). Retrospective survey of parental marital relations and child reproductive development. International Journal of Behavioral Development, 22, 729–751.
  106. Kim, K., Smith, P. K., & Palermiti, A.-L. (1997). Conflict in childhood and reproductive development. Evolution and Human Behavior, 18, 109–142.
  107. Knobil, E. (1988). The hypothalamic gonadotrophic hormone releasing hormone (GnRH) pulse generator in the rhesus monkey and its neuroendocrine control. Human Reproduction, 3, 29–31.
  108. Kulin, H. E., Frontera, M. A., Demers, L. M., Barthlomew, M. J., & Lloyd, T. A. (1989). The onset of sperm production in pubertal boys: Relationship to gonadotropin excretion. American Journal of Diseases of Children, 143, 190–193.
  109. Kulin, H. E., Finkelstein, J. W., D’Arcangelo, R., Susman, E. J., Chinchilli, V., Kunselman, S., Schwab, J., Demers, L., Lookingbill, G. (1997). Diversity of pubertal testosterone changes in boys with constitutional delay in growth and/or adolescence. Journal of Child Clinical Endocrinology, 10, 1–6.
  110. Lange, N., Giedd, J. N., Castellanos, F. X., Vaituzis, A. C., & Rapoport, J. L. (1997). Variability of human brain structure size: Ages 4–20. Psychiatry Research, 74, 1–12.
  111. Lauritsen, J. L., & Swicegood, C. G. (1997). The consistency of self-reported initiation of sexual activity. Family Planning Perspectives, 29, 215–221.
  112. Lerner, R. M. (1987). A life-span perspective for early adolescence. In R. M. Lerner & T. T. Foch (Eds.), Biological-psychological interactions in early adolescence (pp. 1–34). Hillsdale, NJ: Erlbaum.
  113. Lerner, R. M. (1998). Theories of human development: Contemporary perspectives. In W. Damon (Series Ed.) & R. M. Lerner (Vol. Ed.), Handbook of child psychology: Vol. 1. Theoretical models of human development (pp. 1–24). New York: Wiley.
  114. Lerner, R. M., & Foch,T.T. (Eds.). (1987). Biological-psychological interactions in early adolescence. Hillsdale, NJ: Erlbaum.
  115. Lewontin, R., & Levins, R. (2000). Let the numbers speak. International Journal of Health Services, 30, 873–877.
  116. Li, C. I., Malone, K. E., White, E., & Daling, J. R. (1997). Age when maximum height is reached as a risk factor for breast cancer among U.S. women. Epidemiology, 8, 559–565.
  117. Lovejoy, J. C. (1998). The influence of sex hormones on obesity across the female life span. Journal of Women’s Health, 7, 1247–1256.
  118. Maccoby, E. E. (1991). Different reproductive strategies in males and females. Child Development, 62, 676–681.
  119. Magnusson, C. M., Persson, I. R., Baron, J. A., Ekbom, A., Bergstrom, R., & Adami, H. O. (1999). The role of reproductive factors and use of oral contraceptives in the aetiology of breast cancer in women aged 50 to 74 years. International Journal of Cancer, 80, 231–236.
  120. Magnusson, D. (1981). Toward a psychology of situations: An interactional perspective. Hillsdale, NJ: Erlbaum.
  121. Magnusson, D. (1999). Holistic interactionism: A perspective for research on personality development. In L. A. Pervin & O. P. John (Eds.), Handbook of personality: Theory and research (2nd ed., pp. 219–247). New York: Guilford Press.
  122. Magnusson, D., & Cairns, R. B. (1996). Developmental science: Toward a unified framework. In R. B. Cairns, G. Elder, & J. Costello (Eds.), Developmental science (pp. 7–30). New York: Cambridge University Press.
  123. Magnusson, D., & Stattin, H. (1998). Person-context interaction theories. In W. Damon (Series Ed.) & R. M. Lerner (Vol. Ed.), Handbook of child psychology: Vol. 1. Theoretical models of human development (pp. 685–759). New York: Wiley.
  124. Magnusson, D., Stattin, H., & Allen, V. (1985). Biological maturation and social development: A longitudinal study of some adjustment processes from mid-adolescence to adulthood. Journal of Youth and Adolescence, 14, 267–283.
  125. Malo, J., & Tremblay, R. E. (1997). The impact of paternal alcoholism and maternal social position on boys’ school adjustment, pubertal maturation and sexual behavior: A test of two competing hypotheses. Journal of Child Psychology and Psychiatry and Allied Disciplines, 38, 187–197.
  126. Mantzoros, C. S. (2000). Role of leptin in reproduction. Annals of the New York Academy of Sciences, 900, 174–183.
  127. Mantzoros, C. S., Flier, J. S., & Rogol, A. D. (1997). A longitudinal assessment of hormonal and physical alterations during normal puberty in boys: V. Rising leptin levels may signal the onset of puberty. Journal of Clinical Endocrinology and Metabolism, 82, 1066–1070.
  128. Marshall, W. A., & Tanner, J. M. (1969). Variations in patterns of pubertal change in girls. Archives of Disease in Childhood, 44, 291–303.
  129. Marshall, W. A., & Tanner, J. M. (1970). Variations in patterns of pubertal changes in boys. Archives of Disease in Childhood, 45, 15–23.
  130. Mazur, A., & Booth, A. (1998). Testosterone and dominance in men. Behavioral and Brain Sciences, 21, 353–397.
  131. McClintock, M. K. (1998). Whither menstrual synchrony? Annual Review of Sex Research, 9, 77–95.
  132. Medhamurthy, R., Gay, V. L., & Plant, T. M. (1990). The prepubertal hiatus in gonadotropin secretion in the male rhesus monkey (Macaca mulatta) does not appear to involve endogenous opioid peptide restraint of hypothalamic gonadotropin-releasing hormone release. Endocrinology, 126, 1036–1042.
  133. Meschke, L. L., Zweig, J. M., Barger, B. L., & Eccles, J. S. (2000). Demographic, biological, psychological, and social predictors of the timing of first intercourse. Journal of Research on Adolescence, 10, 315–338.
  134. Moffitt, T. E., Caspi, A., Belsky, J., & Silva, P. A. (1992). Childhood experience and the onset of menarche: Atest of a sociobiological model. Child Development, 63, 47–58.
  135. Morrison, J. A., Barton, B. A., Biro, F. M., Daniels, S. R., & Sprecher, D. L. (1999). Overweight, fat patterning, and cardiovascular disease risk factors in black and white boys. Journal of Pediatrics, 135, 451–457.
  136. National Research Council, Board on Children, Youth, and Families. (1999). Adolescent development and the biology of puberty. Washington: National Academy Press.
  137. Ness, R., Laskarzewski, P., & Price, R. A. (1991). Inheritance of extreme overweight in black families. Human Biology, 63, 39–52.
  138. Nolen-Hoeksema, S., & Girgus, J. S. (1994). The emergence of gender differences in depression during adolescence. Psychological Bulletin, 115, 424–443.
  139. Nottelmann, E. D., Inoff-Germain, G., Susman, E. J., & Chrousos, P. (1990). Hormones and behavior at puberty. In J. Bancroft & J. M. Reinisch (Eds.), Adolescence and puberty (pp. 88–123), New York: Oxford University Press.
  140. Nottelmann, E. D., Susman, E. J., Inoff-Germain, G. E., Cutler, G. B., Jr., Loriaux, D. L., & Chrousos, G. P. (1987). Developmental processes in American early adolescence: Relations between adolescent adjustment problems and chronologic age, pubertal stage and puberty-related serum hormone levels. Journal of Pediatrics, 110, 473–480.
  141. Olweus, D. (1986). Aggression and hormones: Behavioral relationships with testosterone and adrenaline. In D. Olweus, J. Block, & M. Radke-Yarrow (Eds.), Developmental of antisocial and prosocial behavior: Research, theories, and issues (pp. 51–72). Orlando, FL: Academic Press.
  142. Olweus, D., Mattson, A., Schalling, D., & Low, H. (1988). Circulating testosterone levels and aggression in adolescent males: A causal analysis. Psychosomatic Medicine, 50, 261–272.
  143. Ong, K. K., Ahmed, M. L., & Dunger, D. B. (1999). The role of leptin in human growth and puberty. Acta Paediatr Supplement, 88, 95–98.
  144. Oppenheimer, E., Linder, B., Saenger, P., & DiMartino-Nardi, J. (1995). Decreased insulin sensitivity in prepubertal girls with premature adrenarche and acanthosis nigricans. Journal of Clinical Endocrinology and Metabolism, 80, 614–618.
  145. Orr, D. P., & Ingersoll, G. M. (1995). The contribution of level of cognitive complexity and pubertal timing to behavioral risk in young adolescents. Pediatrics, 95, 528–533.
  146. Parker, R. G., Rees, K., Leung, K. M., & Legorreta, A. P. (1999). Expression of risk factors for breast cancer in women younger than 49. American Journal of Clinical Oncology, 22, 178–179.
  147. Parker, S. T. (2000). Comparative developmental evolutionary biology, anthropology, and psychology. In S. T. Parker, J. Langer, & L. M. McKinney (Eds.), Biology, brain, and behavior (pp. 1–24). Sante Fe, NM: Sar Press.
  148. Petersen, A. C. (1988). Adolescent development. Annual Review of Psychology, 39, 583–607.
  149. Petersen, A. C., & Crockett, L. (1985). Pubertal timing and grade effects on adjustment. Journal of Youth and Adolescence, 14, 191–206.
  150. Petersen, A. C., & Taylor, B. (1980). The biological approach to adolescence. In J. Adelson (Ed.), Handbook of adolescent psychology (pp. 117–155). New York: Wiley.
  151. Plant, T. M. (1995). Concluding remarks: Fourth international conference on the control of the onset of puberty. In T. M. Plant & P. A. Lee (Eds.), The neurobiology of puberty (pp. 337–342). Bristol: The Journal of Endocrinology Limited.
  152. Plant, T. M. (1998). The neurophysiology of puberty. Paper presented at Physical Development, Health Futures of Youth II: Pathways to Adolescent, Maternal, and Child Health Bureau, Annapolis, MD.
  153. Raine, A., Brennan, P. J., & Farrington, D. P. (1997). Biosocial bases of violence: Conceptual and theoretical issues. In A. Raine, D. Farrington, P. Brennan, & S. A. Mednick (Eds.), Unlocking crime: The biosocial key (pp. 1–20). New York: Plenum.
  154. Reider,J.,&Coupey,S.M.(1999).Updateonpubertaldevelopment. Current Opinion in Obstetrics and Gynecology, 11, 457–462.
  155. Reiter, E. O., & Saenger, P. (1997). Premature adrenarche. The Endocrinologist, 7, 85–88.
  156. Richards, G. E., Cavallo, A., Meyer, W. J., III, Prince, M. J., Peters, E. J., Stuart, C. A., & Smith, E. R. (1985). Obesity, acanthosis nigricans, insulin resistance, and hyperandrogenism: Pediatric perspective and natural history. Journal of Pediatrics, 107, 893–897.
  157. Rockhill, B., Moorman, P. G., & Newman, B. (1998). Age at menarche, time to regular cycling, and breast cancer. Cancer Causes and Control, 9, 447–453.
  158. Roemmich, J. N., Clark, P. A., Berr, S. S., Mai, V., Mantzoros, C. S., Flier, J. S., Weltman, A., & Rogol, A. D. (1998). Gender differences in leptin levels during puberty are related to the subcutaneous fat depot and sex steroids. American Journal of Physiology, 275, E543–E551.
  159. Roemmich, J. N., & Rogol, A. D. (1999). Role of leptin during childhood growth and development. Endocrinology and Metabolism Clinics of North America, 28, 749–764.
  160. Rogol, A. D., Clark, P. A., & Roemmich, J. N. (2000). Growth and pubertal development in children and adolescents: Effects of diet and physical activity. American Journal of Clinical Nutrition, 72, 521S–528S.
  161. Rogol, A. D., Roemmich, J. N., & Clark, P. A. (1998, September). Growth at puberty. Paper presented at a workshop, Physical Development, Health Futures of Youth II: Pathways to Adolescent health, Maternal and Child Health Bureau, Annapolis, MD.
  162. Rosenfield, R. L., Bachrach, L. K., Chernausek, S. D., Gertner, J. M., Gottschalk, M., Hardin, D. S., Pescovitz, O. H., & Saenger, P. (2000). Current age of onset of puberty (Letter to the editor). Pediatrics, 106,
  163. Rowe, D. (1999). Introduction to the special section on behavioural genetics. International Journal of Behavioral Development, 23, 289–292.
  164. Ryan, S. A., Millstein, S. G., & Irwin, C. E., Jr. (1996). Policy section: Puberty questions asked by early adolescents: What do they want to know? Adolescent Health, 19, 145–152.
  165. Sanders, S. A., & Reinisch, J. M. (1990). Biological and social influences on the endocrinology of puberty: Some additional considerations. In J. Bancroft & J. M. Reinisch (Eds.), Adolescence and puberty (pp. 50–62). New York: Oxford University Press.
  166. Sanders, B., & Soares, M. P. (1986). Sexual maturation and spatial ability in college students. Developmental Psychology, 22, 199–203.
  167. Sapolsky, R. M. (1991). Testicular function, social rank, and personality among wild baboons. Psychoneuroendocrinology, 16, 281–293.
  168. Saugstad, L. F. (1989a). Age at puberty and mental illness: Towards a neurodevelopmental aetiology of Kraepelin’s endogenous psychoses. British Journal of psychiatry, 155, 536–544.
  169. Saugstad, L. F. (1989b). Mental illness and cognition in relation to age at puberty: A hypothesis. Clinical Genetics, 36, 156–167.
  170. Schaal, B., Tremblay, R., Soussignan, B., & Susman, E. J. (1996). Male pubertal testosterone linked to high social dominance but low physical aggression: A 7 year longitudinal study. Journal of the American Academy of Child Psychiatry, 35, 1322–1330.
  171. Sherwood, L. (1993). Human physiology: From cells to systems. St. Paul, MN: West.
  172. Siegel, S. F., Finegold, D. N., Urban, M. D., McVie, R., Lee, P. A. (1992). Premature pubarche: Etiological heterogeneity. Journal of Clinical Endocrinology and Metabolism, 74, 239–247.
  173. Siegel, S., & Lee, P. (1992). Adrenal cortex and medulla. In W. Hung (Ed.), Clinical pediatric endocrinology (pp. 200–201). St. Louis, MO: Mosby.
  174. Siegel, J. M., Yancey, A. K., Aneshensel, C. S., & Schuler, R. (1999). Body image, perceived pubertal timing, and adolescent mental health. Journal of Adolescent Health, 25, 155–165.
  175. Silbereisen, R. K., Petersen, A. C., Albrecht, H. T., & Kracke, B. (1989). Maturational timing and the development of problem behavior: Longitudinal studies in adolescence. Journal of Early Adolescence, 9, 247–268.
  176. Simmons, R., Blyth, A., Van Cleave, E., & Bush, D. (1979). Entry into early adolescence: The impact of school structure, puberty, and early dating on self-esteem. American Sociological Review, 44, 948–967.
  177. Singh, S., & Darroch, J. E. (1999). Trends in sexual activity among adolescent American women: 1982–1995. Family Planning Perspectives, 31, 212–219.
  178. Slemeda, C. W., Reister, T. K., Hui, S. L., Miller, J. Z., Christian, J. C., & Johnston, C. C. (1994). Influence on skeletal mineralization in children and adolescents: Evidence for varying effects of sexual maturation and physical activity. Journal of Pediatrics, 125, 201–207.
  179. Smolak, L., Levine, M. P., & Gralen, S. (1993). The impact of puberty and dating on eating problems among middle school girls. Journal of Youth and Adolescence, 22, 355–368.
  180. Stattin, H., & Magnusson, D. (1989). The role of early aggressive behavior in the frequency, seriousness, and types of later crime. Journal of Consulting and Clinical Psychology, 57, 710–718.
  181. Stattin, H., & Magnusson, D. (1990). Pubertal maturation in female development. Hillsdale, NJ: Erlbaum.
  182. Steinberg, L. D. (1987). Single parents, stepparents, and the susceptibility of adolescents to antisocial peer pressure. Child Development, 58, 269–275.
  183. Steinberg, L. D. (1988). Reciprocal relations between parent-child distance and pubertal maturation. Developmental Psychology, 24, 122–128.
  184. Steinberg, L. D., & Hill, J. P. (1978). Patterns of family interaction as a function of age, the onset of puberty, and formal thinking. Developmental Psychology, 14, 683–684.
  185. Stern, K., & McClintock, M. K. (1998). Regulation of ovulation by human pheromones. Nature, 392, 177–179.
  186. Stolz, H. R., & Stolz, L. M. (1944). Adolescent problems related to somatic variations. Yearbook of the National Society for the Study of Education, 43, 80–99.
  187. Stratakis, C. A., & Chrousos, G. P. (1997). Neuroendocrinology and pathophysiology of the stress system. In G. P. Chrousos, R. McCarty, K. Pacák, G. Cizza, E. Sternberg, P. W. Gold, & R. Kvetn´ansky´ (Eds.), Stress: Basic mechanisms and clinical implications. Annals of the New York Academy of Sciences, 771, 1–18.
  188. Surbey, M. K. (1990). Family composition, stress, and the timing of human menarche. In T. E. Ziegler & F. B. Bercovitch (Eds.), Socioendocrinology of primate reproduction (pp. 11–32). New York: Wiley-Liss.
  189. Susman, E. J. (1997). Modeling developmental complexity in adolescence: Hormones and behavior in context. Journal of Research on Adolescence, 7, 283–306.
  190. Susman, E. J. (1998). Biobehavioural development: An integrative perspective. International Journal of Behavioral Development, 22, 671–679.
  191. Susman, E. J., Dorn, L. D., & Chrousos, G. P. (1991). Negative affect and hormone levels in young adolescents: Concurrent and longitudinal perspectives. Journal of Youth and Adolescence, 20, 167–190.
  192. Susman, E. J., & Finkelstein, J. W. (2001). Biology, development and dangerousness. In L. Pagani & G. F. Pinard (Eds.), Contributors of clinical assessment of dangerousness: Empirical contributions (pp. 23–46). New York: Cambridge University Press.
  193. Susman, E. J., Finkelstein, J. W., Chinchilli, V. M., Schwab, J., Liben, L. S., D’Arcangelo, M. R., Meinke, J., Demers, L. M., Lookingbill, G., & Kulin, H. E. (1998). The effect of sex hormone replacement therapy on behavior problems and moods in adolescents with delayed puberty. Journal of Pediatrics, 133(4), 521–525.
  194. Susman, E. J., Inoff-Germain, G., Nottelmann, E. D., Cutler, G. B., Loriaux, D. L., & Chrousos, G. P. (1987). Hormones, emotional dispositions, and aggressive attributes in early adolescents. Child Development, 58, 1114–1134.
  195. Susman, E. J., Nottelmann, E. D., Dorn, L. D., Gold, P. W., & Chrousos, G. P. (1989). The physiology of stress and behavioral development. In David S. Palermo (Ed.), Coping with uncertainty: Behavioral and developmental perspectives (pp. 17–37). Hillsdale, NJ: Erlbaum.
  196. Susman, E. J., Nottelmann, E. D., Inoff, G. E., Dorn, L. D., Cutler, G. B., Loriaux, D. L., & Chrousos, G. P. (1985). The relation of relative hormonal levels and social-emotional behavior in young adolescents. Journal of Youth and Adolescence, 14, 245–252.
  197. Susman, E. J., & Petersen, A. C. (1992). Hormones and behavior in adolescence. In E. R. McAnarney, R. E. Kreipe, D. P. Orr, & G. D. Comerci (Eds.), Textbook of adolescent medicine (pp. 125–130). New York: Saunders.
  198. Susman, E. J., Worrall, B., Murowchick, E., Frobose, C., & Schwab, J. (1996). Experience and neuroendocrine parameters of development: Aggressive behaviors and competencies. In D. Stoff & R. Cairns (Eds.), Neurobiological approaches to clinical aggression research (pp. 267–289). Hillsdale, NJ: Erlbaum.
  199. Suter, K. J., Pohl, C. R., & Plant, T. M. (1998). The pattern and tempo of the pubertal reaugmentation of open-loop pulsatile gonadotropin-releasing hormone release assessed indirectly in the male rhesus monkey (Macaca mulattta). Endocrinology, 139, 2447–2483.
  200. Swarr, A. E., & Richards, M. H. (1996). Longitudinal effects of adolescent girls’ pubertal development, perceptions of pubertal timing, and parental relations on eating problems. Developmental Psychology, 32, 636–646.
  201. Talbott,E.,Guzick,D.,Clerici,A.,Berga,S.,Detre,K.,Weimer,K.,& Kuller, L. (1995). Coronary heart disease risk factors in women with polycystic ovary syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology, 15, 821–826.
  202. Tanner, J. M. (1965). The relationship of puberty to other maturity indicators and body composition in man. Symposia of the Society for the Study of Human Biology, 6,
  203. Tanner, J. M. (1989). Foetus into man: Physical growth from conception to maturity. Cambridge, MA: Harvard University Press.
  204. Tanner, J. M., & O’Keeffe, B. (1962). Age at menarche in Nigerian school girls, with a note on their heights and weights from age 12 to 19. Human Biology, 34(3), 187–196.
  205. Tersawa, E., Bridson, W. E., Nass, T. E., Noonan, J. J., & Dierschke, D. J. (1984). Developmental changes in the luteinizing hormone secretory pattern in peripubertal female rhesus monkeys: Comparison between gonadally intact and ovariectomized animals. Endocrinology, 115, 2233–2240.
  206. Tremblay,R.E,Schaal,B.,Boulerice,B.,Arseneault,L.,Soussignan, R., & Perusse, D. (1997). Male physical aggression, social dominance, and testosterone levels at puberty: A developmental perspective. InA. Raine, D. Farrington, P. Brennan, & S.A. Mednick (Eds.), Biosocial bases of violence (pp. 271–291). New York: Plenum Press.
  207. Tschann, J. M., Adler, N. E., Irwin, C. E., Jr., Millstein, S. G., Turner, R. A., & Kegeles, S. M. (1994). Initiation of substance use in early adolescence: The roles of pubertal timing and emotional distress. Health Psychology, 13, 326–333.
  208. Udry, J. R. (1979). Age at menarche, at first intercourse, and at first pregnancy. Journal of Biosocial Science, 11(4), 433–441.
  209. Udry, J. R., Billy, J. O. G., & Morris, N. M. (1986). Biosocial foundation for adolescent female sexuality. Demography, 23, 217– 227.
  210. Udry, R. J., Billy, J. O. G., Morris, N. M., Groff, T. R., & Raj, M. H. (1985). Serum androgenic hormones motivate sexual behavior in adolescent boys. Fertility and Sterility, 43, 90–94.
  211. Udry, R., & Cliquet, R. L. (1982). A cross-cultural examination of the relationship between ages at menarche, marriage and first birth. Demography, 19, 53–63.
  212. Udry, R. J., & Talbert, L. M. (1988). Sex hormone effects on personality at puberty. Journal of Personality and Social Psychology, 54, 291–295.
  213. Van Goozen, S. H. M., Matthys, W., Cohen-Kettenis, P. T., Thijssen, J. H. H., & van Engeland, H. (1998). Adrenal androgens and aggression in conduct disorder prepubertal boys and normal controls. Biological Psychiatry, 43, 156–158.
  214. Vihko, R. K., & Apter, D. L. (1986). The epidemiology and endocrinology of the menarche in relation to breast cancer. Cancer Surveys, 5, 561–571.
  215. Warren, M. P., & Brooks-Gunn, J. J. (1989). Mood and behavior at adolescence: evidence for hormonal factors. Journal of Clinical Endocrinology and Metabolism, 69, 77–83.
  216. Warren, M. P., Brooks-Gunn, J., Fox, R. P., Lancelot, C., Newman, D., & Hamilton, W. G. (1991). Lack of bone accretion and amenorrhea: Evidence for a relative osteopenia in weight-bearing bones. Journal of Clinical Endocrinology and Metabolism, 72, 847–853.
  217. Wattigney, W. A., Srinivasan, S. R., Chen, W., Greenlund, K. J., & Berenson, G. S. (1999). Secular trend of earlier onset of menarche with increasing obesity in black and white girls: The Bogalusa Heart Study. Ethnicity and Disease, 9, 181–189.
  218. Weber, A., Clark, A. J. L., Perry, L. A., Honour, J. W., & Savage, M. O. (1997). Diminished adrenal androgen secretion in familial glucocorticoid deficiency implicates a significant role for ACTH in the induction of Adrenarche. Clinical Endocrinology, 46, 431–437.
  219. Wichstrom, L. (2000). Psychological and behavioral factors unpredictive of disordered eating: a prospective study of the general adolescent population in Norway. International Journal of Eating Disorders, 28, 33–42.
  220. Wierson, M., Long, P. J., & Forehand, R. L. (1993). Toward a new understanding of early menarche: The role of environmental stress in pubertal timing. Adolescence, 28, 913–924.
  221. Williams, J. M., & Dunlop, L. C. (1999). Pubertal timing and self-reported delinquency among male adolescents. Journal of Adolescence, 22, 157–171.
  222. Wilson, D. M., Killen, J. D., Hayward, C., Robinson, T. N., Hammer, L. D., Kraemer, H. C., Varady, A., & Taylor, C. B. (1994). Timing and rate of sexual maturation and the onset of cigarette and alcohol use among teenage girls. Archives of Pediatrics and Adolescent Medicine, 148, 789–795.
  223. Wyshak, G., & Frisch, R. E. (1982). Evidence for a secular trend in age of menarche. New England Journal of Medicine, 306, 1033–1035.
  224. Yalcinkaya, T. M., Siiteri, P. K., Vigne, J. L., Licht, P., Pavgi, S., Frank, L. G., & Glickman, S. E. (1993). A mechanism for virilization of female spotted hyenas in utero. Science, 260, 1929–1931.
  225. Zijdenbos, P. T., Worsley, A., Collins, K., Blumenthal, J., Giedd, J. N., Rapoport, J. L., & Evans, A. C. (1999). Structural maturation of neural pathways in children and adolescents. Science, 283, 1908–1911.
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