CHAPTER 5 

Puberty
Its Role In Development
,>/
ELIZABETH J. SUSMAN AND LORAH D. DORN
~"
What is this mystical, dreaded, and shrouded
period of development, labeled puberty, that
is accompanied by rapid morphological body
changes, including physical growth and hormonal
changes as well as a myriad of psychological
and social contextual changes?
Puberty has intrigued scholars, altists, parents,
and adolescents alike fer centuries, and
cultures have ritualized puberty to varying
degrees. In some instances rituals feast the
reproductive transition of puberty, whereas in
other instances religious and social aspects of
puberty are celebrated. At its core, puberty is
the period of development through which its
passage endows an adolescent with reproductive
competence. At an even more basic analysis,
puberty is a brain-neuroendocrine process
that provides a stimulus for all the physical
changes and putative psychological changes
that accompany this period of development.
How, then, does a biologically based process
come to be so compacted with social and psychological
significance?
Puberty's significance likelyderives to some
extent from its mistaken identity and overlap
with the adolescent passage. Adolescence is
a wider concept that encompasses the time
and terrain that includes both puberty and the
social, emotional, and wider psychological
changes that characterize the chronological
transition from childhood to adulthood. The
primary functions of puberty and adolescence
are principally nonoverlapping; puberty entails
brain development consisting of neuroendocrine
changes, characterized by activation of
gonadotropin-releasing hormone (GnRH) and
elevated secretion of gonadotropins and sex
steroids, resulting in sexual maturation and
related physical growth changes (Rockett,
Lynch, & Buck, 2004; Sisk & Zehr, 2005).
Adolescence entails the acquisition of adult
cognition, emotions, and social roles that are
possible through maturation of brain functions
and dynamic interactions with varying family,
educational, and social contexts. How the biological
and psychological processes interact to
influence one another has been the challenge
to scientists for decades. The goal of this chapter
is to present a perspective on the neuroendocrinology
of puberty and the implications of
these brain changes for psychological development.
The chapter begins with a historical and
theoretical perspective on the role of puberty
in development followed by a review of the
major neuroendocrine changes that occur at
puberty and how these changes affect physical
morphological characteristics. Then, the
literature is condensed to present an overview
of the relations between pubertal status and
pubertal timing and psychological development.
Finally, we conclude with research and
intervention recommendations for the future.
HISTORICAL PERSPECTIVE
A classic perspective on adolescence is that it
is a period characterized by "storm and stress"
(Hall, 1904). This view portrays adolescents as
oppositional, emotionally labile, and in need
of constant monitoring so as to mold the adolescent's
developing character to prevent adult
116
psychopathology. The biological changes of
puberty were considered a major influence on
the storm and stress of adolescence (Freud,
1958). This viewpoint has been significantly
reconceptualized and now adolescents are
presented in a more balanced and positive
perspective. Adolescence now is viewed as
a transitional period that is characterized by
storm and stress for only a fraction of boys and
girls (Offer & Offer. 1975; Offer & SchonertReichl,
1992). If it even does exist, the storm
and stress of adolescence currently can be conand
ceptualized as neither a universal phenomenon
sex nor an exclusively biologically based aspect of
and development.
cett, Changes in this perspective on adolescence
05). evolved primarily from two distinct lines
dult of evidence. First, parents, teaehers, and othare
ers endowed with the responsibility to care
ions for youth were aware that all adolescents
lily, are not the stormy and stressed-out persons
biowho
were portrayed in the literature and past
:t to
popular press reports. Offer and Offer (1975)
cnge
published a seminal study showing that about
lap­
80% of adolescent boys remain well adjusted
lenduring
this transitional period. Adolescents do
s of
have problems, and multiple studies of men­
loptal
health problems have shown prevalence
and
rates of about 20% for mental health problems
~rty
(Costello et aI., 1996; Kashani, Orvaschel,
the 

r at Burk, & Reid, 1985; Offord et aI., 1987). 

Collectively, adolescence now seems to beysiviewed
as a more positive period of devel­the
opment, and newer research focuses on posi­iew
tive youth development (Catalano, Haggerty,and
Oesterle. Fleming, & Hawkins, 2004; Larson,op­

and 2000; Lerner, Brentano, Dowling, &Anderson, 

e. 	 2002) rather than the negative perspective in
past eras. In brief, adolescents are not consistently
characterized by emotional distress and
It it behavioral disruption and they are known to
ss" be competent to interact seamlessly with fam;
as ily, friends and others in their wider ecology.
~d The socially valuable movement toward posido­
tive youth development is designed to foster
lult growth potential along favorable directions.
Historical Perspective 117
Theories of Puberty and Psychological
Development 

Puberty as a biological process that determin­

istically influenced psychological functioning 

and social behavior was a view derived from 

evolutionary (Parker, 2000) and psychody­

namic theories (Bios, 1962; Freud, 1958; Freud, 

1998; Hall, 1904) that dominated the early
twentieth century. Sigmund and Anna Freud
were instrumental in advancing a perspective
that merged the biological-sexual and psychological
aspects of pubertal development. For
Sigmund Freud, the arrival of puberty signaled
the end of infantile sexual life and the beginning
of normal adult sexual life (Freud, 1998).
In infancy, the oral phase, the sexual instinct
was predominantly autoerotic; at puberty, the
genital phase, the search becomes for a sexual
object. The autoerotic zones of infancy become
subordinated to the genital zone. The two sexes
are considered to diverge as the basic anatomy
of sexuality is different between males and
females. Freud considered male sexuality as
straightforward and understandable, whereas
sexuality in females became a combination
of an affectional and a sensual current. The
sexual aim of males becomes discharge of the
sexual products, and the sexual aim is subordinate
to the reproductive function.
Anna Freud (1958) carried on and expanded
the traditional psychoanalytic perspective of
her father with regard to puberty and adolescence.
She developed the notion that defense
mechanisms are critical to understanding adolescent
adjustment. Defense mechanisms ward
off pregenital urges that are reawakened or
new urges arising from endogenous biological
changes. Unconsciously, adolescents call
on defense mechanisms to protect tl1e ego and
reduce anxiety.
After the analytically oriented era waned,
behavioral and contextually oriented models of
development became predominant in the mid to
late twentieth century. This period might aptly
be described as the dark ages ofempiricism with
regard to puberty and psychological development.
Skinnerian behaviorism (Skinner, 1953),
118 Puberty
social learning theory (e.g., Bandura, 1978),
ecological theories (Bronfenbrenner, 1979),
and life-course perspectives gave virtually no
attention to puberty or biology more broadly.
The rich inner psychological life and sexual
fantasies and urges of adolescents became as
repressed by late twentieth century scientists as
by the Victorian adolescent. However, a minority
perspective erupted in the 1980s that had
~
been brewing among developmental psychologists.
A foundation for the rise of a new era of
interdisciplinary models of the biological and
psychological aspects of puberty sprung out
of the now classic Petersen and Taylor (1980)
chapter on pubertal development in Adelson's
(1980) Handbook ofAdolescent Development.
Petersen and Taylor suggested that the biological
changes during puberty playa major role in
psychological development. Furthermore, they
suggested that being off time in pubertal development
was a risk for adjustment problems.
The publication was followed in the early
19808, parallel to the rise of the Society of
Research in Adolescence, by a movement
originating from a small group of scholars
(Jeanne Brooks-Gunn. Richard M. Lerner,
David Magnusson, Anne Petersen, Laurence
Steinberg, Elizabeth Susman, and others) who
put forth a paradigm that had parallels with
a phoenix rising from the ashes. Like the risen
phoenix. puberty and its psychological correlates
took on a new form as a period of development
characterized by integrated biological.
psychological, and contextual features. The
role of puberty in development then began to
receive moderate attention given its potential
as a mechanism involved in the etiology of
adolescent adjustment and psychopathological
problems. Several of these scholars began
or continued the first longitudinal studies that
focused on the integration of biopsychosocial
processes inherent in adolescent development.
The more integrated perspective became the
norm fOf considering puberty and psychological
development. This perspective is now
viewed as essential for understanding the
fragmented findings regarding the role of
puberty in psychological development.
It follows that the current chapter presents
a perspective on puberty as a biopsychosocial
transition that is initiated by major
neuroendocrine changes and is accompanied
by psychological and behavior changes that
simultaneously initiate changes in the social
contexts in which adolescents find themselves,
This theoretical approach is referred to as
dynamic integration and refers to the essential
and changing fusion of processes across psychological,
biological, and contextual levels of
analysis (Susman & Rogol, 2004). The neuroendocrine
changes that initiate and control the
progression of puberty now will be reviewed.
PUBERTY: A BRAINNEUROENDOCRINE
EVENT
Puberty consists of a coordinated series of hormone
and physical growth changes that form
the core of the transition from childhood to
adolescence. An increasing sophistication of
brain and neuroendocrine changes has led scientists
to consider the primacy of the neurobiological
basis of puberty. The brain undergoes
extensive remodeling at puberty and these
changes form the basis for reproductive maturation
(Sisk & Foster, 2004). These neurobiological
changes are responsible for both the
biological hormone and physical morphological
changes and likely contribute to the social,
cognitive, and emotional changes that occur
during puberty. The structural and functional
changes of the brain first will be considered,
followed by neuroendocrine changes responsible
for the onset and progression of puberty.
Structure and Function of Brain
Development
Coming to know the structure ofhuman brain during
adolescence is the result largely of the implementation
of new imaging technologies. Much
of what we know about adolescent brain development
is derived from studies using magnetic
resonance imaging (MRl) or functional MRI
(fMRI). The yield from imaging changes in the
brain is revolutionary as these studies show both
structural and functional changes during pUberty.
Much of the richest work has come from the
laboratories of Giedd (Giedd et al., 1999; Giedd,
2(08), Casey (Casey, Jones, & Hare, 2008) and
Paus (Paus, 2005). Importantly, some changes
in the brain occur prior to puberty, some during
puberty and some after puberty (Dahl, 2004).
Major changes in gray matter volume
develop in a U-shaped function (Giedd, 2004;
Gogtay et aI., 2004). Motor and sensory systems
mature earlier, in general, compared to the
higher order functions that are responsible for
associative areas of the cortex (Galvin et aI.,
2006; Gogtay et al.; Sowell, Thompson, &
Toga, 2004). Specifically, the limbic system is
proposed to develop earlier than the prefrontal
control areas of the brain. The prefrontal cortex
(PFC) is one of the last changes to occur
in brain development (Lewis, 1997). Based on
this model, the adolescent is considered to be
biased more toward functional limbic activity
relative to prefrontal control activity. With
advancing development there is a functional
connectivity between the limbic and prefrontal
regions. Nonetheless, Casey and colleagues
(Casey et a!., 2008) propose a model indicating
that bottom-up limbic and prefrontal top-down
control regions should be considered together,
even though they have different developmental
trajectories. In brief, findings to date are
interpreted to suggest differential development
of bottom-up limbic systems, which are
implicated in incentive and emotional processing,
and top-down control systems during
adolescence as compared to childhood and
adulthood. Adolescents are assumed to have a
heightened responsiveness to incentives and
socioemotional contexts simultaneous with the
period when impulse control is still relatively
immature. This perspective has direct implications
for social and emotional development and
behavior. The relatively late development
of the prefrontal cortex may be an underlying
process related to risk-taking behavior in
Puberty: A Brain-Neuroendocrine Event ]]9
adolescents (Steinberg, in press). In addition,
Casey et al. (2008) note that the sequence of
developmental events may be exacerbated
in adolescents prone to emotional reactivity,
increasing the likelihood of poor mental health
outcomes. Finally, given the major brain
changes at puberty, the adolescent brain may
be more vulnerable to the effects of substance
use and abuse or other environmental insults
that predispose youth to a trajectory of cognitive,
emotional, and behavioral problems.
Neuroendocrine Changes and
Reproduction
In spite of the new knowledge about the brain
presented earlier regarding the puberty-related
structural and functional aspects of brain
development, there is virtually no overlap
in the literature between this newly derived
knowledge and neuroendocrine, puberty-related
brain changes. The neuroendocrine changes
responsible for the onset and progression of
puberty consist of reactivation of the hypothalamic-pituitary-gonadal
(HPG) axis and
are referred to as gonadarche. Reactivation
of GnRH via the GnRH pulse generator is the
primary component of the neurobiology of
puberty. We refer to "reactivation" because the
initial activation of GnRH occurs in the fetal
and neonatal period.
GnRH is a decapeptide secreted in a pulsatile
fashion by specialized neurons in the
median eminence of the hypothalamus. GnRH
stimulates the pituitary to secrete gonadotropins,
luteinizing hormone (LH) and folliclestimulating
hormone (FSH). LH and FSH
travel via peripheral circulating blood to affect
target cells in the testes in males and ovaries
in females. Vital to reproduction, gonadal
hormones are stimulated by gonadotropins
and regulate ovulation and spermatogenesis
in females and males, respectively. Sisk and
Foster (2004) suggest that in the brain gonadal
steroids control GnRH secretion by way of
neuroendocrine feedback loops and facilitate
sexual behavior.
120 Puberty
Much of what we know about the GnRH
pulse generator and the onset of puberty
derives from animal models, primarily from
the rhesus monkey (see Plant, 2000; Knobil.
1988). The regulation of GnRH pulse frequency
is responsible for producing a pattern
of gonadotropin and steroid hormone secretion
that is necessary for gonadal function and
reproductive competence. The specific neural
~ mechanism regulating GnRH secretion is not
known in spite of decades of research. What
is known is that activation of the HPG axis
has a defined developmental history from the
prenatal period to midadolescence. In prenatal
and early postnatal life there is an increase in
gonadal steroids that is responsible for sexual
differentiation and organizing of the nervous
system. In early infancy, GnRH pulse frequency
declines and remains quiescent until
puberty. At that time, GnRH secretion gradually
increases and remains high, stimulating
gonadotropin and gonadal hormone secretion
during the reproductive years. In approximately
the third decade of life, testosterone
and estrogen begin to decline, reaching low but
detectable levels within the older adult. The
mUltiple species-specific signals for puberty
are integrated in such a way as to allow for the
increase in GnRH at pUberty. Sisk and Zehr
(2005) go on to suggest that permissive signals
cannot fully explain the onset of reproductive
competence, as such signals are not unique to
puberty. For instance, GnRH pulse frequency
goes from low to high in the resumption of fertility
after lactation. It was suggested that an
innate developmental clock senses the unfolding
of primary genetic programs that produce
signals that in turn determine responses to
endogenous and exogenous signals (e.g.• the
environment) that bring about high-frequency
GnRH pulses. There exists the notion that a
master regulatory gene allows for programming
of the multiple permissive genes, but to
date, this master gene remains elusive.
The trigger that determines the timing of
pubertal onset and the resurgence of GnRH
pulses is not known. The logical explanation
that a specific gene triggers the onset of
puberty has led to a search for a gene specific
to the initiation of puberty. The identification
of kisspeptin and its receptor, G protein coupled
receptor 54 (GPR54). held promise as the
gene responsible for the initiation of puberty
(Seminara, 2003). GPR54 is a promising candidate,
as the absence of this gene is associated
with the absence of GnRH activity at puberty.
But, to date, no single gene has been positively
identified as a precipitant for the initiation of
the complex pubertal process. Sisk and Foster
(2004) suggest that there are multiple permissive
signals rather than a singular cause of the
onset of puberty: melatonin. leptin, ghrelin,
body fat, and a complex of genes. Rather than
a single trigger, it is likely the case that multiple
triggers work in unison to bring about a
resurgence of GnRH secretion.
Sex Differences in Pubertal Triggers
Males and females differ in permissive signals
of puberty, and most of the triggers in women
are related to energy balance. Sex differences
likely stem from the different demands
involved in reproduction. The beginning of
the reproductive period is energy expensive for
both males and females, given the rapid physical
growth and metabolic changes that occur.
In subhuman primates, males and females
must defend the territory in which they will
rear their young. However, females bear the
added energy-intense period of pregnancy and
childbirth and then must lactate to feed and
rear offspring. Sisk and Foster (2004) suggest
that organisms must determine whether
growth is sufficient to reproduce (via metabolic
cues), relationships with possible mates
are possible (through social cues) and whether
the conditions are conducive to reproducing
(via environmental cues). In females, for
successful reproduction, there must be, for
example. insulin, glucose and leptin present
in quantities sufficient to support pregnancy
and lactation. Consider the case of leptin,
an adipocyte-derived hormone that has been
demonstrated to be a pivotal regulator for the
integration of energy homeostasis and reproduction
(Fernandez-Fernandez et aI., 2006).
Leptin is necessary, but not sufficient to trigger
the onset of puberty. When the permissive
signals collectively bring about metabolic and
growth conditions, reproduction becomes possible
and is partially observable in secondary
sexual characteristics.
Other Regulators ofthe Timing of
Puberty
Neurotransmitters also have an impact on
GnRH. For example, gamma-aminobutyric
acid (GABA) has primarily inhibitory control
on GnRH (McCarthy. Davis, & Mong, 1997)
and glutamate has excitatory control over
GnRH (Grumbach, 2002). The system and its
feedback loops are complex and are beyond
the scope of this chapter. The reader is referred
to Styne and Grumbach (2007). Figure 5.1
(Banerjee & Clayton, 2008) shows genetic and
neurobiological pathways and other factors
influencing puberty.
?
GABA
Glutamate
Puberty: A Brain-Neuroendocrine Event 121
Adrenarche
The neurobiological and peripheral processes
of gonadarche and the reproductive axis were
described above. Asecond componentofpuberty,
adrenarche, begins earlier than gonadarche at
around age 6-8 years ofage. Adrenarche reflects
maturation of the adrenal glands, although the
trigger for its initiation is unknown (Parker,
1991). Adrenal androgens such as dehydroepiandrosterone
(DHEA), its sulfate (DHEAS),
and androstenedione are products of the adrenal
glands whose concentrations begin to rise at
adrenarche and continue on an upward trajectory
through the third decade of life (Saenger &
Dimartino-Nardi, 2001). Adrenarche and gonadarche
are two independent, yet overlapping,
components of puberty.
Concentrations of adrenal androgens primarily
have an impact on the development of
axillary and pubic hair as well as acne and body
odor. However, these concentrations generally
are not high enough to act on peripheral target
tissues until later, often after gonadarche. Pubic
~ GPR54
o Kisspeptin
--l Likely inhibitory
1__ Likely excitatory i
o
~ X GnRH ne~rone
~ - ­ L..1_G_n_R_H_p_U_ls_e_s-,
/Multiple other factors
(e.g. IGF-1, teptin, FGF,
TGF-j3 and ?proteins
from clock genes)
~Aslroglial cells
FIGURE 5.1 Neurobiological pathways and other factors influencing the activity of gonadotropin-releasing
hormone neurons: Genetic variation in the components of these pathways and the other factors are likely to influence
the time of onset and tempo of human puberty. GnRH, gonadotropin-releasing hormone; IGF-I, insulin-like
growth factor-I: FGE fibroblast growth factor; TGF, transfoffi1ing growth factor. (Reprinted from Banerjee. I., &
Clayton, P. (2007). The genetic basis for the timing of human pUberty. Journal of Neuroendocrinoiog); 19(11),
831-838, with permission from Wiley-Blackwell Publishing Ltd.)
122 Puberty
hair generally is not evident at age 6 when adrenarche
alone has occurred. DHEA also serves as
a precursor for the development of other androgens
such as testosterone. In girls, much of the
exposure of androgens comes from DHEA or its
conversion. Concentrations of these hormones
also have been associated with behavior problems
aodmood disturbances (Goodyer, Herbert,
Tamplin, & Altham, 2000a, 2000b; Goodyer,
... Herbert, & Altham, 1998; Goodyer et a!., 1996;
Dom, Hitt, & Rotentstein, 1999; Dom et al.,
2008). It is yet to be identified whether adrenal
androgens have effects similar to testosterone
on aggressive or other behaviors.
A third axis, the growth axis, also is
involved in puberty. Growth, primarily linear
growth, also involves neuroendocrine changes.
Growth hormone (GH) increases, but there are
also other growth factors that are key contributors
to growth. Linear growth has been the
focus of the psychology of youth as changes in
linear growth, along with secondary sex characteristics,
constitute the signal for adolescents
themselves and others around them that the
adolescent years have arried.
Physical Changes at Puberty
External changes in height and weight and
secondary sexual characteristics provide visible
ways of marking the progress of pubertal
development. These growth changes include
increases in linear growth and body composition
and development of primary sexual
characteristics (ovaries, testes), as well as
secondary sexual characteristics (pubic hair,
genital and breast development). Collectively,
all the changes are a result of the neuroendocrine
development described earlier. Early
descriptions of growth and pubertal changes in
girls and boys were first described by Tanner
(Tanner, 1962; Marshall & Tanner, 1969,
1970). Generally, the height spurt begins earlier
in girls, at approximately age 12, than in
boys, at about age 14 (Marshall & Tanner 1969,
1970). In girls the earliest extemal change evident
at puberty is an increase in breast tissue
(Tanner & Whitehouse, 1976; Parent et aI.,
2003). Girls usually begin the development
of secondary sex characteristics with breast
development followed by pubic hair development,
whereas boys generally begin genital
growth with an increase in testicular volume
followed by appearance of pubic hair. Girls
tend to mature physically earlier than boys
by approximately 18-24 months (Patton &
Viner, 2007). Menarche is a reJatively late
event in the pubertal process, occurring after
the growth spurt and after breast development
and pubic hair growth has begun. The average
age of menarche for White, African American,
and Latino girls is: 12.6-12.9, 12.1-12.2, and
12.2-12.3 years, respectively (Wu, Mendola, &
Buck, 2002; Chumlea et a!., 2003). The rising
gonadal and adrenal hormone (DHEA,
DHEAS, and androstenedione) concentrations
as a result of GnRH secretion result in the
changes in primary and secondary sexual characteristics
previously described. These hormones
increase across puberty, but there are
large individual differences resulting in overlap
of hormones across adjacent stages of puberty
(Styne & Grumbach, 2008; Nottelmann et aI.,
1987). The result of wide individual variations
in hormone levels is that hormone levels cannot
be matched to a specific pubertal stage. It
follows that hormone levels to determine sexual
maturity stage is not an option in research
(See Dom, Dahl, Woodward, & Biro, 2006, for
further discussion).
Assessing Pubertal Maturation
Tanner and Marshall described methods of
quantifying breast and pubic hair development
for girls and genital and pubic hair for boys
(Tanner, 1962; Marshall & Tanner, 1969, 1970).
A five-stage rating sy~tem (1 = prepubertal to
5 =full maturation) was developed for each
secondary sex characteristic, and the characteristics
were originally adapted from Reynolds
and Wines (1948). Photographs are available of
these stages in endocrinology (e.g., Kronenberg,
Melmed, Polonsky, & Larsen, 2008) or adolescent
medicine textbooks (Neinstein, 2008), as
well as psychology-related textbooks focusing
adolescent development (Steinberg, 2007).
Additional photographs showing these same
stages were published later (van Wieringen,
& Wit. 1985) and most recently appear
in Biro and Dorn (2005). It is important to note
that Tanner criteria for assessing pubertal maturation
were developed from a relatively small
sample of boys and girls (less than 400) housed
in an institution in England. Thus, the sample is
representative neither of the United Kingdom
nor of other world populations. Further, the
sample included only Caucasians youth. To our
. knowledge there are no photographs describing
the stages in boys and girls of different ethnic
groups.
Components of Change
Three characteristics of changes in puberty
may have important implications for health
and development in adolescence and beyond.
These include timing, sequence, and tempo.
Timing refers to being earlier or later compared
to a normative age group. For example,
breast development at age 3 signals the need to
conduct an appropriate evaluation for precocious
puberty. Alternatively. a 14- or 15-yearold
boy with short stature (e.g., low percentile
in height compared to norms) signals the need
for an evaluation to determine a diagnosis of
delayed puberty. A critical question is whether
a developmental clock that determines the
.' timing of GnRH maturation also determines
gonadal maturation (Sisk & Foster, 2004). The
majority of psychological research on puberty
has focused on the importance of timing of
puberty. This literature is briefly reviewed
later in this chapter.
The sequence of pubertal components, that
is, the order in which growth or development
of secondary sex characteristic occurs, has
received little empirical attention. Generalities
ofthe sequence have been described by Tanner
(1962) and others showing that in girls, breast
development is often the first change, followed
by the height spurt and pubic hair growth.
Menarche is a relatively late event during the
pubertal process. If this sequence deviates
Puberty: A Brain-Neuroendocrine Event 123
substantially from the norm, it should set into
motion further concerns by a parent or health
care provider. For instance. early pubic hair
development in the absence of breast development
may reflect early adrenarche. In a recent
paper, Biro and colleagues (2003) reported that
most White girls with asynchronous maturation
were more likely to begin puberty with breast
development (thelarche) compared to initiation
with pubic hair (adrenarche). Of interest
is that the reported age of onset of puberty in
both groups was 10.7 years. Specifically, girls
in the thelarche pathway had a greater sum
of skin folds, percent body fat, waist-to-hip
ratio, and body mass index (BMI) at menarche,
andmany of these differences held across a
10-yearlongitudinal study. In this pathways
paper, Biro et al. proposed that the sequence
in which pubertal changes are experienced in
girls may have long-term ramifications for
health. For example, girls with breast development
first, stimulated by gonadal axis
activation, may be more at risk for obesity
and breast cancer than girls with pubic
hair development first. To our knowledge
there are no studies that examine the psychological
import of the sequence of pubertal
development.
Finally, the tempo of puberty, that is, the
rate of progression through puberty, also has
received little empirical attention from either
a medical or psychological perspective.
Nonetheless, there have been citations indicating
that the tempo of puberty has not really
changed in the last several decades (Reiter
& Lee, 200 I). The tempo of puberty varies
across adolescents, and differences in tempo
will determine the later progression through
puberty. For instance, at one time of measurement,
one adolescent may be more advanced
in physical maturation than another adolescent
who began puberty at the same time,
but one adolescent's maturational progression
may slow so that measurement at a second time
point finds the same adolescent as average in
terms of tempo. In African American children
aged 10-12 years old, Ge and colleagues (2003)
,; .~
...

124 Puberty
found that males who experienced accelerated 

pubertal maturation from the first to second 

assessment showed the highest increase in 

depressive symptoms. Does it follow then 

that a faster tempo constitutes a risk for 

depressive symptoms in males? The answer 

may be no. In a study of 327 male and female 

adolescents (aged 10-12 years at first assess­

ment and 12-14 years at second assessment). 

boys with accelerated pubertal matura­

tion had a lower isk of depression (Laitinen­

Krispijn. van der Ende, & Verhulst. 1999). 

An unanswered question is whether age of 

onset of puberty is correlated with tempo of 

puberty or age of menarche. It seems appro­

priate to suggest, given the opposing findings 

above, the need to consider pubertal tempo 

when examining pubertal int1uences and 

depressive affect. 

Timing of Puberty: Its Psychological 

Significance 

The biological changes of puberty are univer­

sal. but the timing and social significance of 

these changes to adolescents themselves, soci­

eties. and scientific inquiry vary across histori­

cal time, individuals and families, and cultures. 

The psychological significance of the timing of 

puberty is one of the most populartopics exam­

ined by scholars of adolescent development. 

Secular Trends in the Timing ofPuberty
The last decade evidenced a renewed interest in
secular changes in the timing of puberty (Buck
Louis et al., 2008; Euling et al., 2008; Golub
et aI., 2008; Kaplowitz, 2(08). The increase
in interest was sparked partially by a controversial
paper by Herman-Giddens et aJ. (1997)
showing that girls were entering puberty at
an earlier age than was the norm in U.S. girls.
Specifically, signs of pUberty were evident in
African American girls, on average. at age 7
and in Caucasian girls, on average, at age 9. The
study was conducted on more than 17,000 girls.
yet the report has been controversial based
primarily on methodological issues (see Emans
& Biro, 1998; Reiter & Lee, 200I; Rosenfield
et aI., 2(00). In another sample. Sun and colleagues
reported older ages of onset of puberty
based on breast development than did HermanGiddens
and colleagues (Sun et al.. 2(02).
Other studies of girls showing earlier maturation
(particularly by age at menarche) include
findings from the National Health Examination
Survey (Anderson. Dallal, & Must, 2(03). the
National Health and Nutrition Examinadon
Survey (Chumlea et al., 2(03). the Bogalusa
Heart Study (Freedman et aI., 2(02). and the
Fels Longitudinal Study (Demerath et ai., 2(04).
Importantly. age at menarche was not reported
to be earlier than in the past. Maturation in boys
also is reported to be earlier than in previously
described cohorts, as reported in a secondary
data analysis from a cross-sectional survey of
the National Health and Nutrition Examination
Survey (Herman-Giddens, Wang, & Koch,
2(01). The analysis included 2,114 boys who
were identified a" White. African American. or
Mexican American. In all racial groups, boys
matured earlier than reported in previous studies
based on Tanner criteria for genital and pubic
hair development. Further, African American
boys had the earliest age of onset ofpuberty (age
11.2 years; Tanner 2) based on pubic hair and
age 9.5 for genital development. The African
American sample also reached full maturity
of genital development (Tanner 5) at an earlier
age than the other groups. Importantly, age at
menarche, compared to age of onset of puberty,
has not varied in recent history. Nonetheless,
secular trends have shown dramatic differences
in timing of puberty across time (Gluckman &
Hanson, 2(06) and may be changing too "iowly
to show an evolutionary change in the time
period assessed (see Figure 5.21. In conclusion,
Biro and colleagues (Biro, Huang, et aI.. 2(06)
note that the correlation is low between age of
menarche and age of onset of puberty, and this
correlation has gotten progressively lower across
the decades. The divergence in the correlation
between age ofonset of puberty and age of menarche
may result from the increase in weight in
both boys and girls.
Puberty: A Brain-::'IIeuroendocrine Event 125
20
Menarche
}M;,matoh
~
(ll
Q)
b 10Q)
Ol
«
Industrial Social
revolution and complexity and
Agriculture social nutritional
settlement improvement overload
+ + +
20000 2000 200 Present
years years years
ago ago ago
TRENDS in Endocrinology and Metabolism
FIGURE 5.2 The relationship between the likely range of ages of menarche (light gray) and achievement of
psychosocial maturity (dark gray) from 20,000 years ago to the present day. The mismatch in timing between
these two processes is a novel phenomenon. (Reprinted from Gluckman, P. D., & Hanson, M. A. (2008).
Evolution. development and timing of puberty. Trends in Endocrinology & Metabolism, 17(1),7-12. with
permission from Elsevier.)
Not all recent findings support the divergence
of age of onset of puberty and age of
menarche. Current speculation is that secular
trends in the timing of puberty now may be
characterized by stability rather than change.
In Europe, Parent et al. (2003) reported that
the downward trend in age of maturation is
decreasing or is even slightly increasing in
some instances. Similarly. Sun et al. (2005)
noted no convincing evidence for earlier age
of pubertal maturation from 1966 to 1994.
Evidence to the contrary is that menarche, as
opposed to pubertal maturation, also is decreasing
in two longitudinal studies (Anderson &
Must, 2005). A recent panel concluded that
the findings for girls are sufficient to suggest
a secular trend toward an earlier age of onset
of breast development and age of menarche
(Euling et aI., 2(08). In contrast, the panelists
concluded that the data for boys were insufficient
to make a conclusion about a secular
trend in boys' development.
Recently, Biro (2006) raised the important
question, "Whither goest puberty?" And
what are the causes of the changes in timing
of puberty? Although the exact cause of early
timing of pUberty is unknown, there are several
plausible explanations. Several environmental
factors beyond heritability could influence the
earlier onset ofpuberty: nutritional status. chronic
diseases, migration to a healthy environment
infectious diseases, pollution and exposure to
environmental toxins (Delemarre-van de Waal,
2005). It is of note that we, and most of the literature
on timing of puberty, are referring to a
small variation in timing that is well within the
normal range of timing of puberty or menarche
from a health care perspective. Pediatric endocrinologists
would likely not see these smaller differences
as abnormal. Nonetheless. even minor
variations in the timing of puberty may have
implications for health and behavior. Following
is a discussion regarding endogenous and exogenous
influences on the timing of puberty.
126 Puberty
Obesity alld Timillg ojPuberty
Obesity as an initiator ofearly timing ofpuberty
is now a major concern given the epidemic of
obesity that is rampant in North America and is
spreading to other nations. The concern is that
the obesity observed during adolescence will
persist into adulthood. This concern was warranted
in a prospective study of boys and girls
(Bratberg, Nilsen, Holmen, & Vatten, 2007).
The study examined the influence of early sexual
maturation on subsequent overweight in late
adolescence and found that timing did relate to
later obesity, but this relation was modified by
central adiposity in early adolescence.
A question in the past was whether early
puberty initiates weight gain or whether heavier
weight is an initiator of earlier puberty. The
latter explanation has received recent support.
Girls who were heavier at age 5 had an earlier
timing of puberty based on both estradiol
levels and Tanner stage (Davison, Susman, &
Birch, 2003). In a similar vein, higher weight
status even in young children was related to
earlier timing of puberty (Lee et aI., 2007).
Surprisingly, infants' weight at 36 months
and higher rate of change in BMI between 36
months and grade 1, earlier age of mothers'
menarche, and non-White race each consistently
and positively was associated with an
earlier onset of puberty (Lee et al.). In a recent
review, Biro and colleagues reported relatively
consistent evidence for the relations of timing
of puberty and obesity (Biro, Khoury, &
Morrison, 2006) in older children and adolescents.
Kaplowitz (2008) suggests that obesity
may be causally related to earlier puberty in
girls rather than earlier puberty causing an
increase in body fat. Much of the research on
timing of puberty and obesity is in girls and
also shows that these relations are more evident
in Black compared to White girls (Biro et
aI., 2006). These relations do not hold in boys
for unknown reasons.
Endocrine Disruptors
One of the proposed mechanisms of earlier
timing of puberty focuses on endocrine
disruptors. Endocrine disruptors include a variety
of substances that could be natural or synthetic
environmental chemicals that disrupt or
change normal endocrine functions (Nebesio &
Pescovitz, 2007). Examples include such things
as harsh pesticides or chemicals that come
from industry processing or waste (e.g., polychlorinated
biphenyls [PCBs], phthalates) that
are converted to natural estrogens or phytoestrogens.
Etfects of these disruptors may be on
the HPG axis concurrently or may result from
accumulation over time, in turn contributing to
later reproduction problems. Examination of
the mechanisms involved in endocrine disruptors
and timing of puberty has been carried out
in both lower animal and human models.
There are extensive animal model studies
showing the impact of environmental chemicals
on pubertal timing, yet there is less empirical
evidence in human models (see review by
Buck Louis et aI., 2008). Some of these studies
report earlier timing of puberty as a result of
exposure to disruptors, whereas others report
later timing. It also seems that males may not be
as affected by endocrine disruptors as females.
Most of these studies using animals report on
development following a known exposure to a
chemical. Few studies of healthy children have
included measures of endocrine disruptors.
In studies that have found putative disruptor
effects on timing of puberty, speculation is
that endocrine disruptors may have played a
role. For example, one of the proposed mechanisms
involved in earlier puberty in African
Americans was the use of hair products containing
natural estrogens (Herman-Giddens
et aI., 1997). Exposure to specific chemicals
in hair products, however. was not measured.
In earlier reports, early puberty (precocious
puberty, premature thelarche, premature
adrenarche) in children in Puerto Rico was
thought to be related to significant amounts of
estrogen from the food supply (Bongiovanni,
1983; Comas, 1982; Saenz de Rodriguez,
Bongiovanni, & Conde de Borrego, 1985).
The amount of estrogen in the food supply was
not determined.
Caution is warranted regarding the potential
of these endocrine disruptors on health
well as on timing of puberty. Progress in
development of household and industrial
in our modern society, where there is
an increased use of household chemicals,
and plastics, may have a higher
,"""._np'nF'l'll ratio than in the past.
rlla.mr'ement ofPuberty: Pubertal 

and Pubertal Timing 

status and pubertal timing are key
in both biological and behavioral
. Whether puberty is considered a cause
iPfc)pn.ate method with respect to the research
cOuestlOn. Currently, the "gold standard" for
pubertal stage is by Tanner criteria
&Tanner, 1969, 1970) as assessed by
t'reommtly, psychosocial studies of adolescents
used self-report measure is the Petersen
Pubertal Development Scale (PDS; Petersen,
Crockett, Richards, & Boxer, 1988). Adolescents
report on specific puberty-related physical
or auditory changes (e.g., voice, skin
changes, body hair, linear growth). Other studies
have used photographs or line drawings
.' (Morris & Udry, 1980). Self-ratings are not
perfectly related to assessments by physical
examinations (i.e., by kappa coefficients) but
in some cases can be strongly correlated with
actual physical examinations. Although not
perfectly correlated, there are some instances
where self-report is an appropriate measure
of puberty. The measure of puberty should
match the research question. The reader is
. referred to a recent and more in-depth publication
outlining methods of measuring puberty
: and their respective strengths and limitations
Puberty: A Brain-Neuroendocrine Event 127
(Dorn et a!., 2006). In that report, the more frequently
used measures of pubertal status and
pubertal timing are evaluated for strengths and
weaknesses.
Age at menarche is another index frequently
used to reflect pubertal development. This measure
is most often obtained by self-report but
also has been obtained via parent report using
either a questionnaire or an interview. As mentioned
previously, menarche is a relatively late
event in the pubertal process. Thus, it can be
equated neither with "pre- versus postpubertal"
nor can it be used to detennine the exact stage
of pubertal development. Menarche does occur
when the majority of girls are Tanner 4 (nearly
two-thirds) but about 25% are Tanner 3, 5%
Tanner 2, and 10% Tanner 5 when becoming
menarcheal (Neinstein, 2008). Further, the consistency
of reporting age at menarche across
many years is not perfect. Correlations range
from 0.60 to 0.81 (Bergsten-Brucefors, 1976;
Casey et a!., 1991; Damon & Bajema, 1974;
Livson & McNeill, 1962; Must et a!., 2002). In
brief, age of menarche is an index ofjust thatage
of menarche; it reveals little about pubertal
maturation other than that gonadotropins and
sex steroids are at levels essential for the beginning
of the menstrual cycle.
The methods for estimating timing of
puberty are varied. In some instances, indices
of puberty are used to reflect adolescents as
early, on time, or late with respect to a sameage
cohort. Comparisons can be made to sexspecific
national norms or the peer group to
answer the question of whether a particular
adolescent is on time, early, or late. Frequently,
age at menarche or Tanner stage for age is categorized
in this manner. For example, distributions
of pubertal stage have been trichotomized
or cut points have been determined by a specified
number of standard deviations to estimate
timing of puberty. Importantly, one needs to
articulate the rationale for defining the method
of timing of puberty in each instance.
Other studies have used a pubertal status
(stage) measure to reflect pubertal timing as
a continuous measure. For example, pubertal
128 Puberty
stage has been regressed on chronological age
and the residuals then used in analyses as an
index of timing (Dorn, Ponirakis, & Susman,
2003; Ellis & Garber, 2000; Ellis et aI., 1999).
This methodology of considering the continuum
of timing of puberty tends to be useful for
smaller samples that are not population based.
The use of stage residual scores allows for
considering the relative age of pubertal stage
, or "earlier timing" rather than "early timing"
as defined by a categorical variable.
Does Pubertal Status or Timing
Make a Difference in Psychological
Development?
This section presents a brief review of major
findings on the relation between pubertal status
and pubertal timing and psychological
development. It first considers differences in
psychological parameters between adolescents
at different pubertal stages. Second, the section
discusses the relation between psychological
parameters and dming of puberty (earlier,
later, or on time).
Pubertal Status The relationship between
pubertal status and psychological functioning
has not been as thoroughly examined as timing
of puberty and psychological dimensions.
Noteworthy are three reports from the Great
Smokey Mountain longitudinal study that are
relevant to pubertal status and psychological
development (Costello et aI., 1996). First, after
the transition to midpuberty (Tanner Stage III
and above), girls were more likely than boys to
be depressed (Angold, Costello. & Worthman,
1998). Second. Angold, Costello, Erkanli, &
Worthman (1999) examined whether the morphological
changes associated with Tanner
stage or the hormonal changes were more
strongly associated with increased rates of
depression in adolescent girls. Models that
included testosterone and estradiol eliminated
the seemingly strong Tanner stage differences
and depression. The effect of testosterone on
depression was nonlinear. These findings were
interpreted as arguing against theories that
explain the emergence of the female excess of heal
depression in terms of changes in body mor­ eses
phology and resultant psychosocial effects on devi
social interactions and self-perception. The hype
authors conclude that causal explanations of late]
the increase in depression should focus on fac­ grov
tors associated with changes in androgen and adju
estrogen levels rather than the morphological ers 4
changes of puberty. Cas)
Third, a later report from the Great Smokey Tsd
Mountain study showed that after controlling opm
for age, Tanner stage predicted alcohol use and of tI
alcohol use disorder (AUD) in both boys and to c.
girls (Costello, Sung, Worthman, & Angold, is, iJ
2007). The effect of morphological develop­ reso
ment was strongest in early-maturing girls. yow
Early pubertal maturation predicted alcohol ratic
use in boys and girls and AUD in girls. The bea
highest level of excess risk for alcohol use was
in early-maturing youth with conduct disorder
and deviant peers. Lax supervision predicted
alcohol use in early-maturing girls. In contrast,
poverty and family problems predicted alcohol
use in early-maturing boys. The dearth ofrecent
studies on pubertal status differences in either
internalizing or externalizing behavior problems
prevents drawing definitive conclusions
about pubertal status differences and psychological
development. The need for assessment
of stage differences is especially acute in studies
that use sexual maturity ratings by a trained
health care provider.
Pubertal Timing Pubertal timing and its
connection to psychological adjustment has
received significantly more attention than
pubertal status. The literature on the psychological
significance of timing of puberty has
been extensively (See Alsaker, 1995) or partially
reviewed in various publications (Mendle,
Turkheimer, & Emery, 2007; Susman & Rogol.
2004). The next section presents representative
studies showing the association between timing
of puberty and internalizing and externalizing
behavior problems.
When scientists began to consider the timing
of the impact of physical maturation on mental
health and adjustment, primarily two hypotheses
were articulated. First, the maturational
deviance hypothesis, also coined the "off-time"
hypothesis, suggested that those either early or
late pubertal changes compared to same age peer
group will likely experience more stress and
adjustment difficulties than on-time developers
(Brooks-Gunn, Petersen, & Eichorn, 1985;
Caspi & Moffitt, 1991; Petersen & Taylor, 1980;
Tschann et aI., 1994). Off-time pubertal development
may be more difficult in the absence
of the necessary social support or resources
to eope with earlier or later maturation. That
is, if maturation is early, emotional and social
resources may not yet be in place for the
younger age adolescent. Alternatively, if maturation
is late, social and family resources might
be available but not at the time when they were
most needed by the adolescent. In turn, adjustment
problems may be more likely for either
the earlier or the later maturer. Few studies
focus on positive effects of either earlier or later
timing of puberty.
The second hypothesis is the earlymaturational
or early tlmmg hypothesis
(Brooks-Gunn et aI., 1985; Caspi & Moffitt,
1991; Petersen & Taylor. 1980; Tschann et aI.,
1994). This hypothesis suggests that early maturation,
particularly in girls, is a disadvantage
because girls bypassed the opportunity to complete
the normative tasks of development that
facilitate coping with the issues and problems
associated with puberty. Adding to the stress
of puberty, there are more advanced social
role expectations for early maturers since their
appearance is more physically mature, and in
tum they are expected to act more maturely.
Early-maturing girls also face more social
pressures at a time when they are cognitively
and emotionally unprepared to deal with
abstractions and complex emotional issues.
In brief, there is a mismatch between physical
development and cognitive and emotional
development. The findings from studies of timing
of puberty and adjustment are not consistent
in terms of whether earlier or later timing
ofpuberty is good or bad for boys or girls.
Puberty: A Brain-Neuroendocrine Event 129
Early Maturation and Internalizing
Problems
Early maturation for girls fairly consistently
is associated with negative psychological and
behavioral consequences (Ge, Brody, Conger,
Simons, & Murry, 2002; Ge, Conger, & Elder,
2001a, 2001b; Graber, Lewinsohn, Seeley, &
Brooks-Gunn, 1997; Hayward, Gotlib,
Schraedley, & Lin, 1999). Representative
findings are that early-maturing girls report
more negative emotions than on-time or later
maturing peers. For instance, Ge and colleagues
(2001a) report findings showing that
seventh-grade girls who experienced menarche
at younger ages subsequently experienced
a higher level of depressive symptoms than
on-time and later maturing peers. The gender
differences disappeared when pubertal transition
indices (pubertal status and menarche)
were included in the model. The finding is
important as it indicates that pubertal maturation
may explain the often reported gender difference
in depressive symptoms. The effects of
early maturation are true for boys as well as
for girls. Early-maturing boys reported more
hostile feelings and internalized distress symptoms
compared to on-time and later maturing
boys (Ge et aI., 2001b). The negative effects of
early maturation for boys are inconsistent with
the earlier findings reporting positive effects of
early timing of puberty on boys.
Early Maturation and Externalizing
Problems
The early-maturationalhypothesis suggests that
earlier maturing girls engage in more actingout
behavior than on-time or later maturing
peers (Ge et al.. 2001 a). Studies such as those
of Ge and colleagues do report that earlier
maturing girls tend to exhibit more behavior
problems and adjustment difficulties than
their on-time or later maturing peers. But the
relationship between earlier timing and externalizing
behavior problems can be moderated
by a history of vulnerability (Caspi & Moffitt,
1991). Early maturers with a history of behavior
problems later reported more behavior
130 Puberty
problems than on-time or later maturers without
a history of behavior problems. In addition,
earlier maturing girls with no history of
behavior problems experienced fewer behavior
problems than girls with a history of behavior
problems who matured on time.
A consistent finding related to pubertal timing
is the link between earlier maturation and substance
use. Substance use is more prevalent in
" 	 both earlier maturing boys and girls (Dick, Rose,
Kaprio, & Viken, 2000; Orr & Ingersoll, 1995;
van Jaarsveld, Fidler, Simon, & Wardle, 2007;
Wilson, Killen, & Hayward, 1994). Specifically,
early timing of maturation is linked to a higher
incidence of smoking (Martin et aI., 2001). Early
timing ofmaturation and substanceuse alsooccurs
across cultures. In East and West German youth,
earlier timing was associated with more frequent
cigarette and alcohol use (Wiesner & Ittel, 2002).
On-time and later maturation was not associated
with substance use. Similarly, in Norwegian and
Swedish youth, earlier pUberty was associated
with alcohol use, alcohol intoxication, drunkenness
onset, and number of units consumed
(Andersson & Magnusson, 1990; Wichstrpm,
2001). The mechanisms relating early timing of
puberty and substance use have received a moderate
amount of attention. Substance use may
lower resistance to peer pressure to use various
substances increasing both substance use and
other health-compromising behaviors, such as
risky sexual behavior. In brief, the growing body
of literature indicates that early pubertal maturation
in girls is generally associated with negative
psychological and health outcomes in Western
societies. The findings are strong enough at this
date to suggest to policy makers that programs
to reduce externalizing behavior, principally substance
use and risky behavior, should be initiated
earlier than in the past for adolescent girls who
exhibit early signs of puberty. The findings to
date are deemed insufficient to make a similar
recommendation for boys.
Timing ofPuberty and Health
A new set of findings shows that timing of
puberty has potentially serious implications
for health problems, either during adolescence
or later in the life span. Adolescents
with earlier puberty are at risk for accelerated
skeletal maturity and short adult height earlier
sexual debut, and a higher risk for sexual
abuse (Golub et aI., 2(08). An even more serious
implication of earlier timing of puberty is
its association with reproductive tract cancers
later in life. Earlier age of menarche is a risk
for breast cancer and lower age of puberty
in boys is associated with a higher incidence
of testicular cancer (Golub et aI., 2008). One
explanation for the link between earlier timing
of puberty and reproductive cancer is a longer
duration of exposure to estrogen in girls and
testosterone in boys. Estrogen and testosterone
are growth factors that putatively contribute to
reproductive cancer.
In the earlier discussion, the focus was on
timing of gonadarche and health risks. Early
adrenarche also carries a risk tor health problems
as well: metabolic syndrome or ovarian
hyperandrogenismJpolycystic ovarian syndrome
(PCOS) in adulthood (lbariez, Dimartino-Nardi,
Potau, & Saenger, 2000). PCOS is a disorder
characterized by infertility. hirsutism, obesity,
menstrual disorders, and ovarian atretic follicles.
These problems in turn put females at
risk for obesity, type 2 diabetes, cardiovascular
disease, and infertility (Golub et aI., 2008).
Obesity and reproductive problems additionally
are associated with mood and affect problems,
and there is speculation that depression and
mood problems may playa role in the onset of
these disorders. Premature adrenarche also is
associated with mood and behavioral problems
(Dorn, Hilt, & Rotenstein, 1999; Dorn, 2007).
Longitudinal studies to establish the connection
between timing of gonadarche and adrenarche
and metabolic and psychiatric disorders are not
yet available.
Earlier timing of puberty has negative
implications for lifestyle and health behaviors.
In addition to the well-known relationship
between earlier timing of puberty and smoking,
earlier maturers reported more sedentary
behavior, but earlier maturation was offset by
physical activity (van laarsveld et aI., 2007).
The same study also reported lower rates of
breakfast eating and higher reported stress,
especially among early-maturing girls. To
date, no policy recommendations are available
regarding education of adolescents and their
families regarding timing ofpuberty and health
risks.
Spermarche as an Index ofTiming of
Puberty
Spermarche (oigarche) is rarely used as an
index oftiming in boys compared to age ofmenarche
as an index of timing in girls. Reaching
spermarche at II years or younger was associated
with higher levels of depression (KaltialaHeino,
Marttunen, Rantanen, & Rimpela,
2003). But later timing of spermarche also was
associated with depression. A second paper
from the same sample yielded different results
as the adolescents were grouped based on age
at menarche or spermarche (10 or younger,
II years, 12 years, 13 years, 14 years, and 15
years or older) (Kaltiala-Heino, Kosunen, &
Rimpela, 2003). In boys, only early maturation
increased the risk of depression. It is not surprising
that spermarche is an infrequent index
of timing of puberty given that the presence
of sperm in urine is a preferred way to assess
spermarche. But urine is difficult to accurately
collect as it is an embarrassing and sensitive
procedure for some youth. Nonetheless, indices
of the timing of spermarche provide a
potentially valid and needed index of pubertal
maturation.
Family Influences on Timing ofPuberty
and Menarche
The evolution of puberty occurred so as to
maximize the probability for successful procreation.
Puberty-related mutations in successive
generations have favored biological qualities
fostering survival in particular geographic and
cultural settings. Draper & Harpending (1982)
proposed that individuals have evolved to be
sensitive to features of their early childhood
environment that may affect later reproductive
competence. Belsky, Steinberg, & Draper
Puberty: A Brdin-Neuroendocrine Event 131
(1991) extended this perspective to consider
family disruption/father absence and early timing
ofpuberty or menarche. Psychosocial acceleration
theory and life history theory have been
used to explain the unusual connection between
family disruption/father absence and timing of
puberty. The psychosocial acceleration theory
was proposed first by Belsky et al. to explain
the role of family disruption/father absence
and early timing of menarche. Specifically,
Belsky et a1. proposed an evolutionary function
of family ecology and psychosocial influences
to explain earlier timing of puberty. From an
early age, children are socialized to develop
an understanding of the availability and predictability
of resources, the trustworthiness of
meaningful others, and the enduring quality
of close relationships. In brief, individuals
are presumed to become sensitive to qualities
of the environment that enhance or suppress
reproductive tendencies. For instance, family
stressors create conditions that undermine
parental functioning, such as parental conflict,
and lower parental investment in girls. Girls
from families characterized by father absence
or discordant male-female relationships perceive
males as less salient to family relationships
and lack parental investment in offspring.
Given the perceived instability of relationships
with males, girls accelerate the timing of menarche
and subsequently engage in early sexual
activity and unstable pair bonding. Mendle et a1.
(2006) later similarly proposed that unstable
parental relationships subsequently lead girls
to believe that resources are limited, people are
untrustworthy, and relationships opportunistic.
Further, parents' mating reproductive behavior
characterized by multiple sexual partners and
erratic relationships contribute to a giri"s sense
of a transient family situation.
In a somewhat similar perspective to the
psychosocial acceleration theory, Ellis and
Essex (2007) proposed a life history theory
linking family structure and processes and timing
of puberty. They emphasize the importance
of life history traits, that is, the constellation of
maturational and reproductive characteristics
"
..
132 Puberty
that influence speed of reproduction and population
turnover. A key assumption of the life
history approach is that individuals make tradeoffs
in distribution of metabolic resources to
sustain vital functions: growth, reproduction,
and maintenance, given that resources are
finite and unpredictable. Individuals choose
evolutionarily relevant features of the environment
as a basis for altering the timing and
tempo of pubertal maturation (Ellis, 2(04). A
life history perspective asks questions about
when individuals should stop converting surplus
energy related to growth and begin to shift
resources to reproduction.
Published studies based on acceleration
and the life history perspectives show support
for the hypotheses regarding timing of puberty
or menarche and family structure or processes
(see also Ellis et aI., 2004). One notable and
consistent finding is that menarche occurs at an
earlier age among girls raised in stressful family
circumstances (Doughty & Rodgers, 2000;
Jones, Leeton, McLeod, & Wood, 1972; Kim &
Smith, 1998a, 1998b; Kim, Smith, & Palermiti,
1997; Moffitt, Caspi, Belsky, & Silva, 1992;
Surbey, 1990). The majority of the studies use
father absence as a marker of family disruption
in relation to timing of menarche. Other studies
assess father absence, family dysfunction,
or qualities of parenting (Belsky et aI., 2007;
Ellis & Essex. 2007; Surbey, 1998) or family
composition (e.g., stepbrothers) (Matchock &
Susman, 2006). Thus, it is difficult to separate
the effects of family disruption as indexed by
father absence and family disruption. Table
5.1 shows representative findings from father
absence and family disruption studies.
Father Absence
The absence of a biological figure and its
effects on timing of puberty or menarche was
the original focus of studies of the sociobiology
of puberty. The general conception was
that father absence or some permutation of
father absence (i.e., stepparent) was related to
earlier menarche in father-absent homes. For
instance, Surbey (1990) reported that girls
achieved earlier menarche in father-absent
homes than in father-present homes. The girls
in the survey who also experienced high levels
of stress also achieved earlier menarche. Since
the early Surbey (1990) study, more and more
family and contextual measures have been
added to the analyses of family structure and
function and timing of puberty or menarche
(See also Bogaert, 2008). The inclusion of
family functioning as in the case of parental
investment and early predictors of timing of
puberty (e.g., Belsky et ai.. 2007) has enriched
the wealth of findings on the sociobiology of
puberty. Nonetheless, specific mechanism and
pathways linking timing of puberty and menarche
to contextual and individual level variables
have not been identified.
Family stress or disruption refers to events
that are considered stressors in families and
include mental health problems of parents,
family conflict, and financial and employment
problems. The psychosocial acceleration
and life history evolution-based perspectives
propose that family disruption and father
absence playa causal role in early timing of
puberty (Belsky et aL, 1991). Girls in these
families engage in early sexual behavior and
early reproduction (Draper & Harpending,
1982; Ellis, 2004). In one of the first tests of
the psychosocial acceleration theory, Moffitt,
Caspi, Belsky, and Silva (1992) showed that
family conflict, divorce and father absence in
childhood predicted earlier age of menarche.
Weight also contributed to the influence on
earlier menarche. Similarly, in a retrospective
study of college age girls, earlier menarche
was related to family stress in later childhood
(age 7-11), conflict with mother and anxiousness
and internalizing symptoms (anxiousness!
depression) in early childhood (birth to age 6),
and earlier age at dating boys and more boyfriends
(Kim & Smith, 1998a). Other studies
report that greater marital and family conflict
is associated with primarily early timing of
puberty in girls (Ellis & Garber, 2000; Graber,
Brooks-Gunn, & Warren, 1995). Longer durations
of father absence also correlate with an
Table 5.1 Studies Examining Family Contextual Correlates of Pubertal Timing.
Authors Sample Puberty Measures Family/adolescent Characteristic Findings
Males l·'emales
Belsky, Steinberg. N =756 Tanner Stage Rearing experiences Pubertal onset was not significantly Mothers with earlier menarche had
Houts. Friedman, Boys and Girls Mother's age of menarche predicted by maternal age of daughters with earlier pUberty.
DeHart. Cauffman, Infant negative emotionality menarche, any rearing variables, or Insensitive parenting earlier in
Roisman, Halpern- Rearing by emotionally interaction by infant negativity. childhood, predicted earlier pubertal
Felsher, Susman, development.
NICHD Early Child Maternal harsh control predicted
Care Research earlier menarche
Network (2007).
Bogaert (2008). N = 5913 Menarche Father absence Earlier age of puberty was predicted
Girls Siblings hy father absence
Ellis & Essex N 756 Pubertal Timing Rearing experiences. Pubertal onset was not predicted by Mothers who reported an earlier age
(2007). Girls Menarche maternal age of menarche, rearing of menarche had daughters who
variables or infant negativity. reported earlier age of menarche and
initiated pubertal development earlier
than did girls whose mothers reported
later age of menarche. Infant negative
emotionality did not significantly
predict pubertal outcome.
Ellis, Bates. N 281 Pubertal Timing Father absence Greater exposure to father absence
Dodge, Fergusson, Girls Early sexual activity was strongly associated with elevated
Horwood. Pellit, & Teenage pregnancy risk for early sexual activity and
Woodward (2003). adolescent pregnancy. Elevated risk
was either not explained or only partly
explained by familial, ecological, and
personal disadvantages associated
with father absence. After controlling
fer covariates, there was stronger and
more consistent evidence of effects of
father absence on early sexual activity
and teenage pregnancy than on other
behavioral or mental health problems
or academic achievement.
Ellis, Bates,
Dodge, Fergusson,
Horwood, Pettit, &
Woodward (2003),
Ellis & Garber
(2000)
Ellis, McFadyenKetchum,
Dodge,
Peltit, & Bates
(1999),
Graber, BrooksGunn,
& Warren
(1995)
Kim & Smith
(1998a)
N =630
Girl:,
N =87
Girls
N 173
Girls
N =75 Girls
N =28
Daughters
N =21
Mothers
Petersen Development
Scale
Menarche
Pubertal timing
Pubertal Timing
Menarche
Menarche
Father absence 

Maternal psychopathology 

Discordant family relationships and father! 

stepfather absence, 

Stress in mothers' romantic relationships 

Negative-coercive parenting 

Heredity Transmission 

Weight and weight for height 

Stressful life events 

Family relationships 

Absence or present of an adult male 

Childhood slress 

Conflict in family environment 

Father absence was associated with
earlier sexual activity and teenage
pregnancy
Father absence earlier in the girl's life
was associated with sexual activity
and teenage pregnancy
History of mood disorders in mothers
predicted earlier pubertal timing in
daughters, Relation was mediated by
dyadic stress and biological fafher
absence; step father presence was
best accounted for earlier pubertal
maturation in girls
Negative-coercive (or less positiveharmonious)
family relationships
in carly childhood provoked earlier
puberty.
Fathers' presence in fhe home, more
time spent by fathers in child care,
greater supportiveness in the parental
dyad, more father-daughter affection,
and more mother-daughter affection,
prior to kindergarten, each predicted
later pubertal timing by daughters
Breast development, weight, family
relations, and depressive affect were
predictive of age at menarche; family
relations predicted age of menarche
above the influence of breast
development or weight
Earlier menarche correlated with
family stress at late childhood;
mOTe conflict with mother in early
childhood; more rejection from,
and less closeness to, mother
throughout childhood; more anxious
and internalizing symptoms in late
childhood; earlier age at dating boys
and more boyfriends.
(Continued)
Table 5.1 (Continued)
Authors Sample Puberty Measures :f<'amily/adolescent Characteristic Findings
Males Females
Kim & Smith
(l998b),
Kim, Smith, &
Palermiti (1997),
Matchock &
Susman (2006),
N =357 Age at Menarche and
Boys and girls Spermarche
N=380 Menarche and
Boys and Girls spermarche
N =1938 Menarche
Women
Early childhood stress or conflict in
the family environment
Absence of Biological Father
Presence of half or step-brothers
Living in an urban environment
Body weight
Race
Siblings
Earlier spermarche was associated
with father absence; more stress in
quality of family life, parental
marital unhappiness and parental
marital contlict in early childhood;
more independence from mother and
father in late childhood; earlier age at
dating women, more girlfriends, and
earlier age at sexual intercourse,
Earlier spermarche was associated
with more parental marital conflict,
less emotional closeness to father;
more aggressiveness, unruliness, and
externalizing symptoms in early or
late childhood,
Earlier spermarche was associated
with earlier age at dating women,
having more girlfriends, having had
intercourse and having more total
frequency of intercourse partners,
Earlier menarche was associated
with parental marital conflict in
early childhood; more parental
marital unhappiness throughout
childhood; more independence from
mother and father in late childhood;
less anxiousness or internalizing
symptoms (anxiousness/depression)
in late childhood; earlier age at dating
men and more boyfriends,
Earlier menarche was associated
with stress in quality of family life:
unhappiness in parental marital
relations during childhood: more
contlict with mother; less emotional
closeness to mother; and behavioral
independence from mother or father in
late childhood,
Earlier menarche was associated with
earlier age at dating men and older
age of first sexual intercourse partner
relative to own age at first intercourse,
Absence of the biological father,
prcsence of half or step-brothers and
living in an urban environment were
all predictors of earlier menarche.
Body weight and race were also
related to menarche timing, The
number of siblings and the birth order
had no effect on menarche. Although
presence of a sister showed delay in
menarche, especially if they were
older.
Mendle,
Turkheimer,
D'Onofrio. Lynch,
Emery, Slustke, &
Martin (2006).
Moffitt. Caspi &
Silva (1992).
Mustanski, Viken,
Kaprio. Pulkkinen.
& Rose (2004).
Romans, Martin,
Gendall. Herbison
(2003),
N =I284Girls Menarche
N 1037 Girls Menarche
N 1891 Pubertal Development
Boys and Girls Scale
N = 2225 Menarche
Girls
Childhood stress
Family Stress
Behavioral and Psychological Problems
Father absence
Environmental influences
Father absence
Family conflict
Genetic determination of early puberty
Genetic influences made the largest
contribution to variance common to
PDS items,
Genetic and non shared environmental
factors accounted for variation specific
to PDS items in boys. Genetic effects
were partially sex specific. Subsidiary
analyses found accelerated maturation
in boys who at age 14 were reared in
father-absent homes.
Within the discordant MZ twin pairs,
children raised by the twin providing
a stepfather had an age of menarche
slightly earlier than children raised by
the co twin without a stepfather. The
opposite pattern occurred in children
of the discordant DZ pairs.
Family conflict and father absence in
childhood predicted an earlier age of
menarche and these factors combined
with weight showed some evidence of
an additive influence on menarche.
Genetic influences made the largest
contribution 10 variance common
to PDS items, In girls. common
environmental influences were added
for growth spurt and menarcheal
status. For both common and itemspecific
variation. genetic effects
were partially sex specific, Subsidiary
analyses found accelerated maturation
in for girls who at age J4 were reared
in father-absent homes,
Early menarche was predicted by
low family socio-economic status,
absence of father, family conflict,
poor relationships between the girl
and eitherlhoth parents, a self-rated
childhood personality style as a loner,
and childhood physical and sexual
abuse,
(Continued)
Table 5.1 (Continued)
Authors Sample Puberty Measures Family/adolescent Characteristic Findings
Males J<'emales
Surbey (1998). N 1200 Pubertal Timing Father absence
Girls Menarche Heightened levels of childhood stress
Wierson, Long, & N = 71 Girls Menarche Divorced Families
Forehand (1993). Interparental Conflict
Wierson, Long, & N = 71 Girls Menarche Environmental Stress
Forehand (1993). Divorce
Interparcntal cont1iet
Menarche was earlier in gi rls from
father-absent households and those
reporting high levels of stress during
childhood. The mothers of the fatherabsent
girls also were early matures,
began dating early, tended to have
their first child al an earlier age and
have more children, and had more
negative attitudes toward males and
the family than mothers of father
present girls.
Earlier menarche in girls from
divorced families.Earlier menarche
in families with maternal reported
interparental conflict.
Compared to girls with intact families,
those from divorced families had
earlier onset of menarche.
Higher maternal reports of
interparental conllict were
significantly related to earlier
menarche in the total sample.
138 Puberty
earlier menarcheal onset (Motfitt et a1., 1992;
Romans, Martin, Gendall, & Herbison, 2003;
Surbey, 1990; Wierson. Long, & Forehand,
1993). Studies of family stress and timing of
puberty in males are more rare than studies of
girls.
Others have argued that the posited causal
relationship between family structure and functioning
and timing of puberty can be explained
by uncontrolled genetic and environmental
influences (Mendle et a1., 2006). Girls who
experience early menarche are more likely to
be from lower socioeconomic status (SES)
families, experience psychological difficulties,
and transmit the likelihood of earlier development
to children (e.g., Mustanski, Viken,
Kaprio, Pulkkinen, & Rose, 2004; Stattin &
Magnusson, 1990; Udry, 1979). These are
potential confounds that cannot be controlled
in research that compares age of menarche
among unrelated individuals. Mendle et al.
(2006) did a comparison of the stepparenting
effects in the children of monozygotic (MZ)
and dizygotic (DZ) twins and determined
that this design can potentially discriminate
whether confounds in the association between
stepfathering and menarche are mediated via
genetics or shared environment. A within-pair
difference between the daughters of discordant
DZ pairs but not between daughters of discordant
MZ pairs suggests that the confound
is primarily genetic. This is because DZ twins
differ in genetic endowment and shared environment,
whereas MZ twins differ only in
their shared environment. A comparison of the
stepparenting effects in the children of MZ and
DZ twins can potentially discriminate whether
confounds in the association between stepfathering
and menarche are mediated via genetics
or shared environment.
Variables indicative of stress were included
by Mendle and colleagues (2006): divorce,
being raised by both biological parents in
the household, presence of a stepfather in the
household, and absence of a biological father
in child rearing. Results show that girls reared
in families with stepfathers exhibit a significantly
earlier age of menarche than girls raised
without stepfathers. Of note is that the presence
of a step-uncle was as predictive of early
menarche as the presence of a stepfather. That
is, it was not necessary for a child to experience
the direct environmental influence of a
stepfather to experience an accelerated age of
menarche, if she is genetically related to someone
who does have a stepfather. In brief, in a
pair of twin mothers, of which only one raises
her children with a stepfather, the offspring of
both twins are equally likely to exhibit early
age of menarche. Mendle et al. conclude that
some genetic or shared environmental confound
accounts for the earlier menarche found
in female children living with stepfathers.
However, it is also possible that earlier menarche
results from some shared environmental
quality.
Parentallllvestment
Parental investment refers to the quantity and
quality of parenting of offspring. For example,
father investment as indexed by qualities of
parenting and timing of puberty was considered
(Moffitt et aI., 1992). Negative aspects of
family environment (family contlict, maternal
harsh control) and earlier timing of menarche
were related to timing ofpuberty. Recently, Ellis
and Essex (2007) used a life history approach
and proposed that humans have evolved to be
sensitive to specific features of early childhood
environments and that exposure to different
parental environments bias children
toward development of alternative reproductive
strategies, including differential pubertal
timing. Ellis (2004) extended the Belsky et al.
(1991) perspective to parental investment by
positing a unique and central role for fathers
in the regulation of female offspring sexual
development, separate from the etfects of
other dimensions of psychosocial stress and
family support in the child's ecology. Higher
quality parental investment in the preschool
years and greater parental supponiveness
predicted lower rates of evidence of adrenarche,
the early aspect of puberty, in boys and
girls in the first grade and less development
of secondary sexual characteristics in girls in
the fifth grade (Ellis & Essex, 2007). Higher
quality mother and father parental investment
and less father-reported maternal conflict or
depression predicted later adrenarche, the
early phase of puberty. Older age at menarche
in mothers, higher SES, greater mother-based
supportiveness, and lower third-grade body
mass index also uniquely and significantly
predicted later sexual maturity in daughters.
Ellis and Essex (2007) concluded that, consistent
with a life history perspective, quality
of parental investment emerged as a central
dimension of the proximal family environment
and pubertal timing.
These findings are consistent with the previous
Ellis et aL (1999) findings. Parental warmth.
positive family relationships, and paternal
involvement in child rearing were related to a
later age of menarche. The quality of the father's
investment in the family emerged as the most
importantfeature ofthe proximal family environment
as a correlate ofdaughters' pubertal timing.
Parenting qualities consisted of greater supportiveness
in the parental dyad, more time spent
by fathers in child care, more father-daughter
affection, and more mother-daughter affection.
Positive parenting characteristics, according to
the child development theory (COT), reap a longer
childhood (later sexual maturation and onset
of reproduction) and that high-investing family
contexts foster development ofsociocompetitive
competencies. In contrast, the costs of truncating
childhood are reduced in low-investing family
contexts that do not meaningfully facilitate
competitive competencies.
The argument proposed by Ellis and Essex
(2007) regarding early age at adrenarche
and family processes and the ecology of
development has good internal consistency.
Nonetheless, the logic is not consistent with the
biology of reproduction. Adrenarche is independent
of gonadarche; children can experience
gonadarche without adrenarche and children
Puberty: A Brain-Neuroendocrine Event 139
enter adrenarche in the absence of activation of
the GnRH system. Specifically, adrenarche is
not accompanied by increases in gonadal steroids,
testosterone and estradiol, hormones that
are essential for ovulation, spermatogenesis,
and reproduction. Thus, the evolutionary significance
of the timing of adrenarche is irrelevant
to reproduction. In brief, family environment
appears to affect a puberty-related event, adrenarche,
that is not related to reproduction suggesting
a reconsideration of the role of family
environment and early timing of puberty as a
reproductive strategy.
A limitation of many of the studies on
family and contextual influences on age of
onset of puberty or menarche is that they are
cross-sectional or short-term longitudinal.
Belsky et al. (2007) overcame this limitation by
capitalizing on a 12-year longitudinal design
to assess the effects of family intluences on
timing of puberty. Other major strengths of
the study were that it included boys and girls
and mothers and fathers, the adolescents had
annual repeated assessments of pubertal development
by trained nurses and physicians during
puberty, and both family structure and
process were considered. The results were
both consistent and inconsistent with earlier
findings. Rearing experiences predicted pubertal
timing among girls but not boys. There are
too few studies that included boys to know
how to evaluate the consistency of this finding.
Maternal age at menarche was a stronger
predictor of girls' pubertal development than
were early rearing conditions suggesting the
strength of the genetic influence on timing
of menarche. A unique finding was that early
maternal harsh control at 54 months and at first
and third grade predicted earlier menarche.
An additional novel finding was that negative
experiences with fathers and mothers predicted
earlier age of menarche. In summary, the study
yielded multiple novel findings supporting the
influence of parenting characteristics on timing
of puberty and menarche. A prominent
limitation of the study is the small effect size
and the limited number of significant findings.
140 Puberty
Nonetheless, it is noteworthy that any effects
emerged given the extended time frame of the
study and the major genetic influences on timing
of puberty.
Explanations are varied regarding the
mechanisms involved in father absence, fami
Iy disruption and timing of puberty. The studies
based on the evolutionary model imply a
causal relation between family disruption!
father absence and timing of age at menarche
or timing of puberty. One explanation is that
a stressful family environment characterized
by family conflict, absence of a biological
father. poverty, and accompanying low parental
investment creates an internalizing disorder
that lowers metabolism, thereby inciting a
weight gain that in turn accelerates menarche
(Belsky, et aI., 1991; Ellis & Essex, 2007).
Recent evidence raises questions regarding
mechanisms involved in weight and earlier
puberty. Heavier weight status even during the
preschool- and school-age period predicted
earlier timing of puberty (Davison et a1., 2003;
Lee et aI., 2007). The question, then, is: How
does this early weight gain affect timing of
puberty? To test the hypothesis that family
environment and weight status in combination
are mechanisms involved in early timing of
puberty, future studies need to be longitudinal
from infancy to the onset of puberty.
Family inl1uences on acceleration of timing
of puberty and menarche are based on the
assumption that the family environment is
stressful, likely arising from the unpredictability
of parental absence, psychopathology, and other
forms of family disruption. However. objectively
measured stress is not part of the design
of the studies, for the most part. Stress is merely
implied by family conflict, poverty, and father
absence or stepparenting. What is needed are
good measures of subjective aspects of stress as
well as the neuroendocrine indices of stress in
family members to establish the mechanisms
involved in stress and timing of puberty.
Noteworthy is that the acceleration and life
history perspectives on stress and reproduction
are at odds with the neuroendocrinology of
reproduction. Cortisol exerts inhibitory effects
on reproduction at the levels of the GnRH
neuron, the pituitary gonadotroph (responsible
for secreting LH and FSH), and the gonad itself,
thereby suppressing sex steroids (T and estrogen)
and delaying maturation of reproductive
function and physical growth (See Susman,
Reiter, Ford, & Dorn, 2002). That is, CRH,
ACTH, and cortisol suppress the reproductive
axis. In brief, theories regarding putative family
stress and timing of puberty or menarche
run counter to the well-known physiology of
stress and reproduction. The two sets of evidence
can be reconciled nonetheless. Although
acute stress may suppress reproductive functioning,
chronic stress may release gonadotropins
and sex steroids from the downregulating
effects of CRH, ACTH, and cortisol. Family
stress is likely to be of long duration, thus
attenuating the classic acute response to stress.
To advance the field, future studies would benefit
from including: (I) objective indices of
family stress, family structure and interactions,
and reliable and valid measures of timing of
puberty and menarche; and (2) longitudinal
assessment of early family adversity and the
neurobiology of stress and reproduction for
long periods prior to the onset of puberty.
Genetics can be an alternative explanation
to the evolutionary model of family relations
and timing of puberty (See Mendle et aI., 2006).
Girls who mature early tend to have earlier
sexual activity, and earlier age of first marriage
and tlrst birth, which increases the probability
of divorce and lower quality paternal investment.
Puberty, sexual, and reproductive timing
may be genetically programmed (Ellis et a1.,
1999). Mothers who are early maturers tend to
have daughters who are early maturers (BrooksGunn
& Warren, 1989), suggesting a genetic
linkage. In addition, the androgen receptor
(AR) gene has been used as an explanation of
the effect of father absence on age of menarche
(Comings, Muhleman, Johnson, & MacMurray,
2002). Shorter alleles of the X-linked AR gene
are associated with aggression, greater numbers
of sexual partners, impUlsivity, and divorce
in males, and with early age of menarche in
females (Comings et al.). The same genes may
predispose children to early timing and early
sexual activity. Comings et al. also reminded
the field that there are paternal as well as maternal
influences on age of menarche. The same
genetic factors that influence a man's likelihood
to abandon ma..rriages may also contribute to an
earlier age of menarche in female offspring.
Mendle et al. (2006) tested an alternative
hypothesis that nonrandom selection into stepfathering
families related to shared environmental
andior genetic predispositions leads to
a spurious relation between stepfathering and
earlier menarche (also discussed earlier in this
chapter). Using the controls for genetic and
shared environmental experiences offered by
the children-of-twins design, cousins discordant
for stepfathering were found not to differ in age
of menarche. Moreover, controlling for mother's
age of menarche eliminated differences in
menarcheal age associated with stepfathering
in unrelated girls. These findings strongly suggest
that selection and not causation accounts
for the relationship between stepfathering and
early menarche.
As an argument counter to genetic influences,
it could be proposed that the effect is
still there between family environmental factors
and timing of puberty when mothers' age
of menarche is controlled. Mothers' age of
menarche could be considered a poor control
for genetic influences. Age of menarche is a
broad proxy for a genetic influence, and there
is significant error of measurement in retrospective
recall of age of menarche. Molecular
genetics approaches yielding new genetic
markers will likely be illustrative of the complexity
of genetic influences on timing of
puberty in functional and disruptive families.
Mechanisms Involved in Timing or
Puberty and Adjustment
The mechanisms relating timing of puberty
and psychosocial adjustment, as discussed
here and elsewhere, remain an empirical largely
unknown. The findings are based on not
Puberty: A Brain-Neuroendocrine Event 141
well-articulated theories and few mechanisms
are proposed to explain the authenticated
connection between timing of puberty and a
diverse array of behaviors, emotions, and disorders
and family structure and functioning.
What then are the possible explanations for the
long-standing connection between timing of
puberty and psychological development? The
explanation can be separated into two broad
categories: social/contextual and brain development.
Social/contextual explanations include
peers, family, school, and the broader social
ecology of youth. A fairly consistent explanation
of earlier maturation and deviant behavior
is that early maturers tend to associate with older
and deviant peers. Older deviant peers may perceive
the early-maturing adolescent as older than
hislher stated age and include the early-maturing
adolescent in adult-like deviant behaviors that
include substance use and risky sexual activity.
In the case of sexually risky behaviors, earlymaturing
girls also may be preyed upon by
older boys and men, as these males perceive the
girls as inexperienced and vulnerable to sexual
coercion. Later maturing boys and girls may be
protected by their childish appearance and are
excluded by older, deviant peers.
Family members and teachers exert influences
on an off-time maturing adolescent via
expectations and social roles. The juvenile
appearance of a late-maturing adolescent can
lead to assigning less responsibility and independence
to the childlike-appearing adolescent
with the consequence to the adolescent
of not being allowed to participate in peer
activities that may lead to deviance or result
in fewer opportunities to develop competencies.
Similarly, institutions in the wider social
environment, such as church groups and clubs,
may assign less independent and challenging
tasks to the immature-appearing adolescents.
Therelationship between braindevelopment,
timing of puberty, and adjustment is now only
beginning to be considered. Briefly, the question
is whether there is asynchrony between
higher order functions like decision making
and impulse control and emotional areas of the
142 Puberty
brain and hypothalamic functioning and the
reactivation of the GnRH axis. Steinberg (in
press) suggests an explanation for the association
of brain development and risk taking that
can be applied to timing of puberty and risk
taking as well. As previously discussed, earlymaturing
adolescents may not have the social
decision-making skills and impulse control
required to avoid risky situations.
Puberty and Obesity
The higher weight status of early timing adolescents,
as previously discussed, has led to
the suggestion that the increase in obesity is
responsible for the earlier timing of puberty.
Adolescents worldwide are now considered
overweight or obese, and there is virtually no
evidence that the epidemic is subsiding, which
is an alarming trend, given the association of
obesity with cardiovascular disease and diabetes
and other chronic diseases (Dietz, 1998;
Katzmarzyk, Tremblay, Perusse, Despres, &
Bouchard, 2003). The increase in BMI in the
United States in particular may be related to
various eating behaviors characterized by highenergy
dense foods. For example, in a review
by Biro. Khoury, and Morrison (2006), calorie
consumption has increased across the last
three or so decades with high increases in soft
drinks and snacks that are salty and lower intake
of milk. Further, overweight adolescents seem to
be particularly vulnerable to consumeing more
in a fast-food setting. With respect to activity, the
Biro, Khoury et al. review also provides evidence
that physical activity decreases across adolescence,
and there is some evidence that the amount
oftelevision viewing and computer-related games
may have an impact on weight status.
Puberty is a sensitive period for the development
of overweight and obesity, since body
fat increases secondary to pubertal development
(Dietz, 1997). Early sexual maturation
is related to obesity and overweight in adolescence
and is carried over to the young adult
years (Bratberg et aI., 2007) and appears to
have a heritable intergenerational component
(Ong et aI., 2007). Environmental factors may
also playa role in weight status during puberty.
For example, Belsky et al. (1991) proposed
that a stressful family environment, characterized
by family conflict, absence of a biological
father, poverty, and resultant insufficient parenting,
predisposes girls to develop an internalizing
disorder that lowers metabolism, thereby
inciting weight gain that accelerates the timing
of menarche. Overall, the psychological consequences
of weight status are only beginning
to be addressed, but it is increasingly clear that
another negative consequence of early puberty
is overweight and obesity.
Puberty and Bone Health
In this section we provide an example of the
importance that puberty can have on accrual
of bone mineral density (BMD) or bone mineral
content (BMC) and, in turn, how depression
may playa role in bone health. Over 40%
of BMD is accrued in adolescence, with the
majority of accrual occurring in the two years
surrounding menarche (Glastre et aI., 1990).
During these two years, as much bone is laid
down as is lost in the last four decades of life
(Bailey, Mirwald, McKay, & Faulkner, 2000).
Thus, building an adequate store of bone mineral
is crucial during this period to decrease the
chance of becoming osteoporotic in the postmenopausal
years. Optimum accrual depends
on one's genetic and familial background, but
lifestyle and behavioral factors such as exercise,
nutrition, and smoking also influence
accrual. Timing of puberty has been shown to
have an impact on bone accrual. Later pubertal
timing (later menarche) girls had lower BMD
(Galuska & Sowers, 1999). The explanation
is that later maturing girls have less estrogen
exposure, and estrogen produces strong bones.
In brief, a later maturer has fewer ovulations
and menstrual cycles and in turn, less lifetime
estrogen exposure.
Where does depression fit into the pubertybone
density model? In the adult literature,
there is generally a strong association between
depression and BMD. Individuals with depression
or who report depressive symptoms are
more likely to have osteoporosis or lower
BMD (Eskandari et al., 2007; Jacka et aI.,
2005; Schweiger, Weber, Deuschle, & Heuser,
2000; Yazici, Akinci, Siit9ii, & OZ9akar, 2003;
Michelson et al., 1996). It is not known if this
relationship holds true in adolescents. If one
considers that rates of depression become
higher in girls during puberty (Costello,
Mustillo, Erkanli, Keeler, & Angold, 2003)
and that early maturers are more vulnerable
to depression (Hayward et aI., 1997; KaltialaHeino,
Marttunen, Rantanen, & Rimpela,
2003), early timing of puberty may also contribute
to bone density. Recognized is that
other factors may influence both bone health
and depression during puberty, and these
include smoking and change in exercise and
eating habits.
Puberty and Sleep
The media frequently describes findings on the
sequelae of lack of sleep in adolescents.
Factors responsible for this lack of sleep are
lack of parental monitoring, peer interactions
and influences, pervasive use of television and
communication media (cell phones and text
messaging), music devices, and Internet surfing.
Sleep characteristics of adolescence began
to receive systematic attention in the last two
decades. Carskadon, Acebo, & Jenni (2004)
have produced seminal work showing the systematic
changes that occur in the sleep patterns
of adolescents. This research showed that there
is a major shift in sleep characteristics during
the pubertal period. The total amount of sleep
decreases, and there is an increase in daytime
sleepiness (Carskadon & Acebo, 2002; Dahl &
Lewin, 2002). There is also a major shift in
time of onset of sleep and time of awakening,
referred to as phase delay. Phase delay
is related to stage of puberty independent of
age, suggesting that the biological changes
of puberty have links to changes in sleep patterns
(Carskadon, Vieira, & Acebo, 1993; see
also Carskadon et aI., 1997; Carskadon,
Wolfson, Acebo, Tzischinskky, & Seifer, 1998;
Carskadon & Acebo, 2002). The preference
Puberty: A Brain-Neuroendocrine Event 143
for later onset and offset of sleep and societal
demands for early school attendance results
in an asynchrony in the biological and social
needs of adolescents.
Changes in sleep quality and duration during
puberty can be justified based on biological and
social changes that occur at puberty. First, sleep
is associated with the same hormones involved
with endocrine changes of puberty (Knutson,
2005). For example, growth hormone-releasing
hormone that is produced in abundance during
puberty appears to be important in the regulation
of sleep (Steiger & Holsboer, 1997). Ghrelin
improves slow-wave sleep, which is the deeper
stages of non-rapid eye movement (REM) sleep
(Steiger, 2003). Sleep deprivation resulted in
a stronger increase of slow-wave activity in
Tanner 5 (39% above baseline) than in Tanner 1­
2 adolescents (18% above baseline). Additional
findings show that the buildup of homeostatic
sleep pressure during wakefulness was slower
in Tanner 5 adolescents compared with Tanner
Stage 1-2 children (8.9 +/- 1.2 hours) (Jenni,
Achermann, & Carskadon, 2005). The social
changes of adolescence, such as increasing
interaction with peers, have not been examined
in relation to the changes in sleep quality and
duration. An unfortunate side effect of lower
duration of sleep is its association with obesity.
Shorter sleep duration in third and sixth grade
was independently associated with obesity at
sixth grade (Lumeng et al., 2007).
A contributing factor to sleep problems during
adolescence is morningness/eveningness
(MIE) preference. MIE refers to a preference
for activities in the morning or evening.
Support was found for the hypothesis that trait
circadian preference mediates mood, daytime
functioning, and academic grades through
its effect on sleep variables at school time. It
was concluded that whereas the imposition of
school schedules negatively impacted mood
and daytime functioning for the sample as a
whole, evening-oriented adolescents were the
most vulnerable to poorer outcomes (Warner,
Murray, & Meyer, in press). Eveningness students
obtained poorer quality and less sleep
144 Puberty
than morning-oriented students and were
more likely to exhibit antisocial behavior
(Warner et aI., in press; Susman et aI., 2007).
The evening-preference adolescent gets less sleep
and. as a result, has difficulty concentrating and
controlling impulses.
What Do We Know for Sure About
Puberty and Development?
It is a given that puberty is an essential stage
ofreproductivedevelopmentthat haschallenged
scholars and scientists. communities and teachers,
as well as parents and adolescents themselves.
The degree to which adolescents
experience mood and behavior changes during
puberty varies considerably. Across time,
much has become known about both the biological
and psychological changes that occur
at puberty. First, in the past several decades,
discoveries have documented the neuroendocrine
processes of puberty due primarily
to technological advances in molecular biology
and other life sciences. hormone assay
development, and strong empirical studies in
lower animal models, as well as in studies of
humans. Second, in the psychosocial literature.
studies are relatively consistent in pointing
to early pubertal development as being
behaviorally and psychologically problematic,
primarily for girls. Such studies have generally
focused on negative outcomes related to mood
disturbances and risky behaviors and have
used timing of puberty variables in associative
or predictive models. Third, the measurement
of pubertal progression has been examined in
detail so that investigators now have access to
assessments of the appropriateness of different
measures of pubertal development, depending
on the research question. Fourth, research on
the psychological effects of pubertal development
has become based on more complex
theoretical and statistical models than in the
past. These complex models are characterized
by multiple levels of analysis that combine
"protein to popUlation" levels. Recent work
on identification of genes and proteins that are
responsible for the onset of puberty represent
the most basic level of analysis. At the population
level, the ADD Health study has produced
an abundance of information on sexual, psychological,
and social influences on the U.S.
population of adolescents. In addition, contextual
variables are now being examined as
mediators or moderators that may impact associations
of biological pubertal processes on
psychological outcomes. These multiple-level
studies offer a richness of detail that has never
before been available to scientists of adolescent
development.
What We Would Like to Know in the
Future and Some Conclusions
Although the knowledge regarding puberty
and its role in psychological development
has certainly expanded, much is left to be
uncovered. Puberty's "effects on health and
wellbeing are considered profound and paradoxical"
(Patton & Viner, 2007, p. 1130).
Thus, the topic warrants further attention as
a way of improving psychological and physical
health and developmental outcomes in
youth. Some of the gaps in the literature are
as follows:
I. 	 There is an asynchrony between medical
and psychological research with regard to
biological and psychological issues inherent
in the consequences of pubertal status
and pubertal timing. However. the medical
research community has identified
the significant impact of altered timing
of puberty (e.g., precocious puberty and
premature adrenarche) on current health
or later adult health problems (Golub
et aI., 2008; see review by Dorn, 2007).
For instance, there is now a growing recognition
of the association between timing
of puberty and adult disease, particularly
reproductive cancers. There is also growing
recognition in the medical community
that the downward secular trend in timing
of puberty may precipitate psychosocial
and health problems by compromising
growth, increasing the risk of early and
risky sexual actIvIty, potential sexual
abuse, and inappropriate expectation by
others (Golub et aL). What we would like
to know is whether these early psychosocial
problems have adult psychological
sequelae. As a beginning, basic knowledge
on the mechanisms involved in early
or late timing of puberty and psychosocial
functioning is needed. As an additional
issue, there is a continuing need for
health policy that continues surveillance of
human adolcscents to define and refine the
mechanisms of altered timing of puberty.
For instance, screening for exposure to
endocrine disruptors is a promising trend
for the future. There is also asynchrony
between the psychological and medical
community in the precision of measuring
puberty; its measurement has often lacked
rigor in psychological studies. Whether
puberty is a cause, correlate, or confound
of the outcomes of interest, it can playa
leading role in study outcomes and therefore
deserves scrutiny in both the medical
and psychological community.
2. 	 Health and developmental problems of
adolescence are complex and require ar:
interdisciplinary focus. The roots of psychological
and behavioral problems stem
from, or contribute to, brain-behavior
interactions, family dysfunction, reproduction
and physical morphological changes,
and peers. These inherent complex features
of puberty mandate that research
scientists are obligated to collaborate
across disciplinary lines. The richness
and expertise of each discipline in terms
of methods, measures, and theoretical and
empirical-statistical models could ultimately
lead to an empirically based body
of research to enhance prevention and
intervention efforts. An area of inquiry
with rich interdisciplinary attention is that
of brain development. Cognitive functioning
research from a neurobiological
perspective appears to be an area already
beginning to develop. Such functioning as
Puberty: A Brain-Neuroendocrine Event 145
assessed by neuropsychologists and functional
and structural brain imaging neuroscientists
and neurologists, in combination
with behavioral scientists, holds much
promise for understanding adolescent
behavior. A challenge for the scientific
community is to garner funding support
for such valuable interdisciplinary efforts.
3. 	 Longitudinal studies with rigorous methodology
for measuring puberty as well as
other biological and psychological parameters
are an additional necessary step
in solving complex research problems
encountered in pubertal-age adolescents.
Several sources have commented on
appropriate measures and methodologies
for studies of pubertal development (Dorn
et aI., 2006; Euling et aI., 2(08). Future longitudinal
studies will yield the most payoff
by beginning to assess the biological and
behavioral roots of pubertal processes by
beginning at an early age so as to capture
pubertal onset and the range of pubertal
changes through adrenarche and gonadarche.
Needed in these longitudinal assessments
are better biomarkers of onset and
progression of puberty, such as genomic
and hormone assay studies. A collateral
consideration is that to understand the role
of puberty on psychological development,
longer term perspectives are essential. We
do not know for certain whether the links
between internalizing and externalizing
behavior are a result of puberty per se or
whether they represent continuity from
earlier phases of development.
4. 	 Fourth, mechanisms impacting puberty
and, in tum, its effect on psychological
development need further examination. For
example, we know little about why pubertal
timing is early or late and whether timing
is a consequence of genetics, environmental
factors, other influences, or a combination
of these processes. In tum, we do not
know why early pubertal timing is generally
negative for girls but positive or neutral
for boys. Nor do we know why timing of
146 Puberty
puberty seems to have less of an impaet on
boys than on girls, at least in the psychosocial
arena. Importantly, there is a very small
amount ofknowledge on the positive effects
of puberty on development. The majority of
studies to date have focused on negative
outcomes of puberty with a minority
focused on positive youth development. For
some adolescents, pUberty is a positive sign
of emerging adolescence, adulthood, inde­...
pendence, and respect. For others, puberty
and its rapid physical growth may enhance
self-esteem and vigor and be a protective
influence for depression and anxiety.
5. 	 Much more research needs to be carried
out regarding structure and function of
brain development across puberty. Since
most studies have measured change only
across chronological age rather than pubertal
stage, appropriately little can be said
about neuroendocrine changes and brain
development as they relate to the external
manifestations of puberty. Briefly, we need
to know if pubertal status and pubertal timing
are related to brain structure and function
and, in turn, how those changes may
or may not be related to emotions and cognitions
as well as behavioral outcomes.
A concluding note is not complete without
mentioning the current state of prevention
and intervention to reduce problems of
youth and increase positive youth development.
The current state ofknowledge regarding
puberty and timing of puberty offers insights
into prevention and intervention efforts. One
issue is that most parents and school systems
have not caught up with the importance
of earlier timing of puberty in the health and
development of adolescents. As previously
indicated, earlier timing, especially for girls,
is associated with and predictive of internalizing
and externalizing problems, interactions
with older and perhaps deviant peers, and early
and risky sexual behavior. Thus, earlier maturing
adolescents require earlier risk education
efforts than their on-time peers on issues of
normal sexual development, risky behaviors,
relationships, and Internet safety. Parents, the
educational system, and health care providers
also are encouraged to undertake earlier health
promotion and disease prevention efforts with
the aim of assisting adolescents to cope with J
peer expectations, early sexual development,
and expectations for mature behavior.
It also may be advantageous to approach
adolescents in a more creative manner than in
educational programs that currently are available.
For instance, adolescents are likely to
be interested in new information about brain
development during puberty and adolescence,
especially if it is presented via the Internet.
Specifically, adolescents should be assured
that decision making will be difficult in some
instances as brain structures and functions
are still developing and adult decisions may
be beyond their grasp. Adolescents need to be
provided with the assurance that asking others
for help is healthy and expected. Within this
neurobiological approach, an aim could be to
familiarize the adolescent with the awareness
that since brains are still developing, they may
be highly vulnerable to insults (e.g., negative
effect of substance use) that have the potential
for affecting academic performance and
emotions later in life. In brief, an adolescentfriendly
approach that emphasizes the developing
brain and decision making is warranted.
The effort to mount such an approach is daunting
to consider but offers a novel approach to
adolescent health promotion.
Finally, scientists, clinicians, and policy
makers have not had an established venue for
sharing new scientific information that is relevant
to pubertal neurobiological processes and
the psychological, health, and societal implications
of timing of puberty and its wide-ranging
impact on development. Similarly, funding
agencies tend not to adopt an interdisciplinary
approach to basic science, health promotion,
or social policy regarding puberty and adolescence
more broadly. Conversations and formal
organizational struetures to guarantee cross discipline
and interagency eollaboration is most
assuredly guaranteed to improve the health and
development of adolescents and their families
in the next decade.
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HANDBOOK OF
ADOLESCENT PSYCHOLOGY
THIRD EDITION
Volume 1: Individual Bases of Adolescent
Development
Edited By
RICHARD M. LERNER 

LAURENCE STEINBERG 

@
WILEY 

John Wiley & Sons, Inc.