Journal of Adolescent Health 47 (2010) 433439

Review article

The Timing of Puberty: Is It Changing? Does It Matter?

Emily C. Walvoord, M.D.*
Section of Endocrinology and Diabetology, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana
Manuscript received April 7, 2010; manuscript accepted May 21, 2010

Abstract Whether the secular trend of a decreasing age of puberty has continued over the past 50 years remains
controversial. Data that had been classically used to address this issue are reviewed and large
epidemiologic studies, which had not previously been included, are now considered to challenge
the conclusions of prior debates of this topic. The effect and timing of excessive weight gain are
discussed in detail and recent observations about the opposing effects of obesity on the pubertal timing
of girls versus boys are considered. The second half of the review examines both the causes and the
long-term health consequences of early puberty, touching on the possible effect of stress and
endocrine-disrupting chemicals along with the risks of reproductive cancers, metabolic syndrome,
and psychosocial consequences during adolescence and beyond. 2010 Society for Adolescent
Health and Medicine. All rights reserved.
Keywords: Puberty; Endocrine disrupting chemicals; Obesity; Secular trend; Menarche; breast cancer; Metabolic syndrome;
Pubertal onset; Testicular cancer; Children; Age of puberty

Over the past decade, significant concern has been raised
about children entering puberty at younger and younger ages
in the United States [1]. It has been well documented that the
age of puberty (as defined by the age of menarche) has
declined significantly since the 19th and early 20th centuries
[2,3], likely the result of improved nutrition and overall
public health. However, whether a continued downward
trend has persisted over the past 40 years, when arguably
public health conditions (with the notable exception of
dramatically increased rates of obesity), have changed
little, remains a significant area of debate [1,4]. Inherent in
the question of whether the timing of puberty is actually
changing are the issues of whether puberty is actually
starting earlier or if we are just measuring it differently;
whether the tempo of puberty has changed such that sexual
maturation (pubertal completeion) is being reached earlier;
and whether the timing of puberty has changed for both
boys and girls. Environmental factors, including obesity,
stress, and endocrine disruptors, that influence the timing
of puberty need to be considered, along with the long-term
*Address correspondence to: Emily C. Walvoord, M.D., Department of
Pediatrics, Indiana University School of Medicine, 702 Barnhill Dr. Room
5960, Indianapolis, IN 46202.
E-mail address: ewalvoor@iupui.edu
1054-139X/$ - see front matter 2010 Society for Adolescent Health and Medicine. All rights reserved.
doi:10.1016/j.jadohealth.2010.05.018
health and psychosocial implications of early pubertal devel-
opment, as all may be of considerable public health concern.
Is the Timing of Puberty Continuing to Change?
U.S. puberty timing data
Puberty data for U.S. boys and girls have been collected
from large national examination surveys over the past 40
years. However, rigorous comparisons between studies of
pubertal timing are fraught with complicating factors. Studies
have varied by design, population characteristics, ages of the
children included, methods of pubertal assessment, and
statistical analyses. This has led to difficulties and inconsis-
tencies in adequately comparing trends over time. Addition-
ally, Tanner staging is prone to between observer error,
particularly when done only by visual inspection and not
by palpation. No U.S. studies have systematically measured
sex steroid or gonadotropin levels, arguably the most accu-
rate way to determine activation of the hypothalamic pituitary
gonadal axis, although subject to diurnal variations in early
puberty and assay sensitivity issues.
Before the last 40 years, only relatively small studies had
been performed to determine the timing of puberty in U.S.
children. In the mid-1930s, the Guidance study started
434 E.C. Walvoord / Journal of Adolescent Health 47 (2010) 433439
collecting longitudinal pubertal data from nearly 200 chil-
dren living in California who were followed up from
21 months until 18 years of age [5]. Pubertal staging was
done by reviewing photographs. Longitudinal data were
similarly collected in Ohio from 49 girls in the 1940s [6,7].
The first national survey of U.S. children to acquire
pubertal data was the National Health Examination Survey
III (NHES III) and was conducted between 1966 and 1970,
collecting pubertal data from 3,130 children aged 1217
years [8,9]. Between 1988 and 1994 [1012], the National
Health and Nutrition Examination Survey (NHANES) part
III collected pubertal data from approximately 2,300
children aged 8 years. Both of these national surveys
used a complicated, multistage probability cluster design to
obtain representative national data. The Bogalusa Heart
Study, performed in rural Louisiana, included over 9,000
children aged 517 years. Menarchal and Tanner stage data
were collected from 19731974 [13] but only menarchal
data was obtained during the 19921994 follow-up study
[14]. Finally, the Pediatric Research in the Office Setting
(PROS) collected data from 1992 to 1993 [15] and included
17,077 girls aged between 3 and 12 years. All of the
preceding studies relied on trained observers to assess Tanner
staging, but this was done by visual assessment only, with the
exception that 39% of the subjects in the PROS study had
Tanner staging assessed by palpation [16]. Data from these
last four studies have been analyzed by multiple investiga-
tors, using many different statistical techniques, in an attempt
to determine whether the onset and pace of puberty has
changed in the United States over the past decade.
The main findings of the studies of puberty timing in girls
are summarized in Table 1. There does appear to be a down-
ward trend in the mean age of onset of Tanner II breast devel-
opment. However, the age of Tanner III breast development
may be a more accurate assessment of true puberty, as fat can
often be mistaken for early (Tanner II) breast development.
Interestingly, the mean age of Tanner III development has
not declined over time. Additionally, the age of menarche
also does not appear to have changed over the past half
century. The discrepancies in the findings from the PROS
and NHANES studies are notable because the data were
collected over the same period, although both studies show
a similar trend toward an earlier onset of puberty. The
Table 1
Studies of puberty timing in U.S. girls
Study Number of Ages of
subjects (N) subjects
Guidance Study 1930s1940s [5] 95 817 years
Fels Institute 1940s [6] 49 818 years
NHES III 19661970 [8] 3,100 1217 years
Bogalusa Heart Study
19731974 [13] 1,398 514 years
19921994 [14] 1,230 517 years
NHANES III 19881994 [1012] 2,300 818 years
PROS 19921993 [15] 17,077 312 years
differences may lie in the ages of the children studied, as
very young girls were included in the PROS study but not
in the NHANES III sampling. Very young girls with pubertal
development are more likely to have a pathologic condition
causing their early puberty and thus may not represent
a normal population shift.
There are obvious limitations to these analyses. Some
studies included children older than one would expect
puberty to start. For example, NHES III examined children
starting at age 12 years when 94% of girls and over 70% of
boys were already in puberty [17]. Thus, the median ages
for entry into a stage of puberty were not observed, but calcu-
lated using probit analysis, a type of regression analysis
which relies heavily on the assumption that the data are nor-
mally distributed, which influences predictions at the high
and low ends of the possible ages. This may make it difficult
to detect slight changes in the timing of pubertal onset over
time. Alternatively, the PROS study did not include girls
older than 12, with mean age of entry into any stage of
puberty also being calculated using probit analysis [15].
Differences in statistical analyses also make comparisons
difficult; for example, the PROS study reported mean age
at entry into a Tanner stage and age of the child in year incre-
ment, whereas the NHANES data was analyzed as median
age at entry into a Tanner stage and mid-point of a year for
age [10]. Additionally, comparative data for minority chil-
dren are lacking as only white children were studied in the
1930s and 1940s [57].
Interestingly, there are compelling menarche data which
have not been considered previously in the analyses exam-
ining the timing of puberty in U.S. girls over the past few
decades. In 2006, Nichols et al reported a reversal in the
downward trend of age of menarche over the last century
[18]. Data were collected during interviews of 22,066 women
in Massachusetts, New Hampshire, and Wisconsin, who
were born between 1910 and 1969. The mean age of
menarche declined from 13.1 to 12.7 years in women born
between 1910 and 1949 (p < .001) but then increased again
to 13 years for women born in the 1960s (p < .001).
Recently, Barsom et al reported very similar findings from
the TREMIN Research Program on Womens Health [19].
This longitudinal study reported the age of menarche for
4,444 women born between 1893 and 1991. The average
Age at Tanner II Age at Tanner III Age at menarche
breasts (white/black) breasts (white/black) (white/black)
10.6/ 11.2/ 12.8/
10.8/ 11.4/ 12.9/
12.8/12.5
10.4/10.2 11.7/11.0 12.7/12.8
12.5/12.1
10.4/9.5 11.8/10.8 12.6/12.1
9.9/8.9 11.3/10.2 12.9/12.2
 E.C. Walvoord / Journal of Adolescent Health 47 (2010) 433439 435

13.6 a year and a half earlier (10 years) than all other studies [12].
13.4
Age at Menarche

13.2
13
12.8
12.6
12.4
12.2
12
11.8
1900- 1910- 1920- 1930- 1940- 1950- 1960- 1970- 1973-
1909 1919 1929 1939 1949 1959 1969 1979 1984
Barsom [19] Nichols [18] Anderson NHANES III [10]
Figure 1. Mean age of menarche by decade of birth over the past century.
age of menarche decreased to a low of 12.45 years for the
cohort born in the 1930s and then increased again, peaking
at 13.37 years for women born in the 1960s and then declined
to a mean age to 12.83 for women born in the 1970s. Statis-
tical analyses in both studies indicated that age of menarche
varied significantly as a function of decade of birth. Figure 1
combines the data from these two studies as well as a repre-
sentation of the mean age of menarche for white girls as
found by Anderson et al in their analysis of the NHANES
III data [10]. A similar description of a reversal in the down-
ward trend in menarche age has been reported from England
[20], and Canadian women born in the 1960s also experi-
enced a later age of menarche when compared with those
born earlier in the century [21]. These data strongly suggest
that the timing of pubertal maturation, based on age of
menarche, has not been decreasing in a linear manner over
the past century, but instead suggest that variability between
decades is common.
Determining if the timing of puberty has changed for boys
over the past 80 years is even more challenging. Far fewer
studies have been performed in the United States. Most
studies used the highly subjective measure of visual genital
Tanner staging, with Tanner II being defined as reddening
and texture changes of the scrotal sac, without enlargement
of the penis. Findings are summarized in Table 2. A small,
but longitudinal, study done in the early 1970s found that
pubertal changes occurred at similar times in white boys as
was reported in the studies from the 1930s [22]. However,
the findings from the NHANES III survey differ dramatically
from the others, with the onset of puberty noted to be at least
The 2-year time span between the onset of puberty (Tanner II
genitals) and the visible signs of testosterone action (Tanner
II pubic hair) suggests that prepubertal boys were likely mis-
classified as having genital Tanner II development. These
NHANES III findings have also been subject to criticism
not only because of the subjective nature of the Tanner
staging, but also because the methodology allowed for
a one stage variance between the examiners assessment of
pubertal stage and the quality control standard [24]. The
study by Biro et al is the only study to use an increase in
testicular volume as the first sign of central puberty [23].
These investigators followed 515 fifth through eighth grade
white and black boys longitudinally. Because this study did
not include boys younger than approximately 10 years of
age, it is possible that some boys who had early puberty
were missed. Interestingly, on the basis of all of the data,
the timing of pubic hair development has not shown a linear
decrease over time, again speaking against a change in
puberty timing. Although usually linked to the timing of
central puberty in healthy children, pubic hair is admittedly
not always a reliable marker of true puberty as it may repre-
sent only isolated adrenarche. Therefore, it is difficult to draw
any firm conclusions from these studies about the changes in
the onset and duration of puberty in boys; hence, a further
study, using better markers of pubertal timing in boys, is
obviously needed.
Recent non-U.S. puberty timing data
Within the past year, two very interesting reports have
provided intriguing data about the change in pubertal timing
in Denmark [25,26]. These studies are of particular interest
because unlike any other study that has tried to measure
secular trends of puberty, these investigators not only
studied children from the same background 15 years apart,
but also used rigorous methods for pubertal assessment
(palpation of breast tissue in girls and testicular volume
measurements in boys) and obtained gonadotropin and sex
steroid levels in many of the subjects. These investigators
found that compared with girls studied in the early 1990s,
those studied 15 years later started puberty a full year
earlier, but attained menarche at similar ages. This held true

Table 2
Studies of puberty timing in US boys
Study Number of Ages of Tanner II genitals Tanner V genitals Tanner II pubic Tanner V pubic
subjects (N) subjects (white/black) (white/black) hair (white/black) hair (white/black)
Guidance Study 1930s1940s [5] 92 818 years 11.8/ 15.2/
Fels Institute 1940s [7] 59 921 years 11.5/ 17.3/ 12.2/ 16.1/
Lee Study 19691974 [22] 36 917 years 11.9/ 15.1/ 12.3/ 15.3/
Bogalusa Heart Study 19731974 [13] 1,829 514 years 11.8/11.2 12.5/11.7
NHANES III 19881994 [12] 1,333 819 years 10.0/9.2 16.0/15.0 12.0/11.2 15.7/15.3
Biro Study Late 1980s [23] 515 1018 years 12.2a (TV 3 cc) 12.8 15.2
TV testicular volume.
a
Genital staging done by testicular volume only.
436 E.C. Walvoord / Journal of Adolescent Health 47 (2010) 433439
even when the data were corrected for body mass index
(BMI). Interestingly, the estradiol levels were significantly
lower in girls aged 810 years studied between 2006 and
2008, whereas gonadotropin levels were the same between
the two cohorts. This suggests that the earlier breast
development seen in this more recent cohort may have
been stimulated by estradiol effects not mediated through
the hypothalamic-pituitary axis [25]. The findings for boys
were quite different, as puberty also started earlier in the
more recent group, but only by 3 months. This change was
not significant when corrected for BMI. However, unlike
what was found for girls, luteinizing hormone levels were
higher in the second half of the study, possibly signifying
effects of obesity and/or endocrine disruptors on pubertal
development and gonadotropin production in boys [26].
Does the Timing of Puberty Really Matter?
In contemplating the public health significance of puberty
shifting to an earlier age, there are two ways to think about the
issue. The first is to consider whether pressures causing this
change are of concern, and the second is to consider whether
there are worrisome long-term consequences of earlier
puberty.
Potential causes of earlier puberty
Obesity. Many studies have linked obesity with earlier
puberty and menarche in girls [14,27]. Analysis of the
PROS data revealed a significant positive correlation
between BMI and earlier entrance into puberty and higher
Tanner breast staging [28]. Similarly, when the NHANES
III data were analyzed, a BMI greater than the 85th
percentile was strongly associated with the occurrence of
breast development and menarche at younger ages [29].
Interestingly, the effect of excessive weight gain on
puberty timing seems to start very early in life. A relatively
small longitudinal study of 183 girls found that a higher
percent body fat at 5 years of age predicted early pubertal
development [30]. Another larger longitudinal study of 354
girls who were followed from 36 months through the 6th
grade revealed that a higher BMI z-score at 36 months of
age was associated with earlier puberty [31] However, the
most startling data comes from a study of over 2,700 girls
born in the United Kingdom and followed up
longitudinally. Excessive weight gain in the first 9 months
of life was a very strong predictor of early menarche [32].
Therefore, as the obesity epidemic in children continues to
worsen, we should not be surprised that girls will likely be
starting puberty at earlier ages. Interestingly, the opposite
effect of obesity on pubertal timing may occur in boys.
Analysis of the NHANES III data for boys has shown that
early maturing boys seem to have a lower rate of obesity
when compared with boys with normally or later timed
puberty [33]. Recently, a multicenter longitudinal study of
over 400 boys found that rapid weight gain during early
and middle childhood was associated with an increase risk
of being prepubertal at age 11.5 years [34]. This discordant
effect of obesity on pubertal timing in boys versus girls is
fascinating but yet unexplained.
Endocrine-disrupting chemicals. There has been growing
concern about the potential effects of endocrine-disrupting
chemicals (EDC) on the timing of puberty. EDC are
exogenous compounds that alter the production, action, or
metabolism of endogenous hormones. Although there is
convincing evidence that EDCs affect the pubertal timing of
animals, there is much less direct evidence linking specific
EDC exposure and alterations in the timing of puberty in
human beings (see comprehensive review [35]). This may be
due to the long latency between exposure and observed effect
as well as the large variety and combination of potential
EDCs to which human beings are exposed. Epidemiologic
studies in human beings have linked elevated phthalate levels
[36], phytoestrogens [37], serum polychlorinated biphenyls
[38], and dichlorodiphenyltrichloroethane/dichlorodiphenyl-
dichloroethylene [3941] with earlier puberty. However,
many studies report opposite effects of the same compounds
on puberty timing [38,4144]. Thus, more data are essential.
A more complete understanding of EDC effects on pubertal
timing will hopefully soon be possible as recruitment is
underway for the National Childrens Health Study [45],
which will examine the effects of a multitude of
environmental exposures from in utero to 21 years of age in
100,000 individuals.
Stress. In the early 1990s, the idea that chronic stress could
lead to early reproductive maturation was proposed [46] and
tested, showing that significant family conflict and the
absence of the father in the home lead to statistically earlier
menarche [47,48]. More recent longitudinal studies,
performed in lower-middle and middle-class families, have
supported these findings and also found that the presence
of a step-father or maternal boyfriend in the home [49],
maternal mood disorders, and a poor quality father
daughter relationship predict earlier pubertal developmental
[50,51]. Other stressful conditions as measured by the
Family Adversity Index, which assesses socioeconomic
status, family structure, parental education level, and
occupation, predict a younger age at menarche as well [52].
Interestingly, acute stressful events do not seem to result in
early pubertal development [52,53], and not surprisingly,
extreme stress accompanied by poor nutrition, such as
during times of war, results in pubertal delay [54,55].
Long-term effects of earlier puberty
Reproductive cancers. The possible link between early
puberty and an increase in the risk of breast cancer has been
widely studied. A report from the Breast Cancer Detection
and Demonstration Project published in 1989 put forth a breast
cancer prediction model, now widely known as the Gail
 E.C. Walvoord / Journal of Adolescent Health 47 (2010) 433439
model, which included the age of menarche as a significant
contributor to risk [56]. This study of 284,000 women, self-
enrolled in a breast cancer monitoring study, found a relative
risk of 1.21 for women who recalled having menarche
before age 12 when compared with women who had
menarche after age 14. However, a 2009 report from the
Nurses Health Study found a smaller increase in relative
risk of only 1.10 for women having menarche before age 12
[57]. This study did not suffer from the same potential bias
of enrolling higher risk women and thus may account for the
lower risk association. Finally, an analysis of the school
records of 141,000 women in the Danish Cancer registry
found an increased relative risk for women who had an
earlier age of peak growth, likely a marker for pubertal onset
(and the beginning of rapid growth of undifferentiated breast
cells), but no association with the age of menarche [58].
Thus, it appears that earlier puberty onset may increase the
risk for breast cancer. However, the risk seems to be quite
small, especially when compared with other modifiable risk
factors. Ovarian cancer risk seems to be increased with an
earlier age of menarche as well [59]. This risk has been
reported to be directly linked to the increased number of
ovulatory cycles, with each full year of ovulation increasing
ovarian cancer risk by 6% [60]. However, this association is
still considered controversial and the effect appears to be
weak and possibly only seen in white women [59,61,62].
The timing of puberty in boys has also been studied in rela-
tionship to the risk of testicular cancer, especially as the inci-
dence of testicular germ cell tumors is on the rise [63]. Older,
smaller studies seemed to suggest that earlier puberty
conferred an increase risk of testicular cancer [64], and a large
case-control study of 794 men in the United Kingdom in the
1980s found a trend toward an increased risk for testicular
cancer with earlier puberty [65]. However, a more recent,
very similar study of 767 U.S. men found no association
with the age of puberty [66], when adjusted for a family
history of testicular cancer which is one of the highest known
risk factors for testicular cancer. Thus, these disparate find-
ings of these two studies are likely due to the fact that the
UK study did not control for a positive family history, making
an association between puberty timing and testicular cancer
very unlikely.
Metabolic syndrome. As has become apparent, obesity is
a risk factor for early puberty in girls. However, in the past,
the converse was felt to be true that obesity later in life was
a consequence of early puberty. Although a report from the
Bogalusa Heart Study found that early puberty was associated
with obesity, increased insulin, and HOMA-IR levels in
adulthood, this analysis did not correct for childhood BMI
[67]. Additionally, an increased risk for type 2 diabetes in
women with a history of early puberty has been found, but
this association was not significant when adjusted for adult
BMI [68]. Two recent studies that controlled for childhood
BMI did not find early puberty to be a strong, independent
risk factor for adult obesity [69,70]. Of concern, however, is
437
a long-term, prospective study of over 61,000 Norwegian
women that found a strong inverse relationship between age
at menarche and total mortality, even when adjusted for
BMI throughout the study period [71]. The relationships
noted between very early weight gain and puberty, followed
by obesity, the metabolic syndrome, and an increase in
mortality all suggest a significant effect of rapid weight gain
during the infantile period that seems to result in
maladaptive hormonal or metabolic programming that
persists throughout life. Further study of these associations
should prove fascinating.
Psychological function. The psychological effects of early
puberty are also of concern. Numerous studies have shown
that girls with early puberty suffer from higher rates of depres-
sion [7276] and anxiety [77,78]. However, the data are more
controversial for boys, with some studies reporting that boys
with early puberty have higher rates of depression [73,79]
and anxiety [78], whereas others have found no such
association [72,74]. Both boys and girls with early pubertal
development seem to have increased rates of smoking [80],
delinquent behavior, and earlier sexual experiences [81,82].
Association with delinquent peers [83] and living in
a disadvantaged neighborhood [84] further increase the risk
for deviant behavior during adolescence. Although a few
smaller studies of adolescent girls have found that substance
abuse rates are higher in early maturing girls [75,85],
a study of more than 5,700 American and Australian
children aged 1015 years did not find a correlation
between early puberty and higher rates of substance abuse
when adjusted for current pubertal stage [86].
There is more controversy and less data as to whether
these problems persist into adulthood. Two large studies,
one from the United States [87] and one from Switzerland
[88], studied young adults in their late teens and early
twenties and reported the disturbing findings of lower
quality of life and higher rates of substance abuse and depres-
sion among those with early pubertal development. Another
study of U.S. undergraduate students found higher rates of
eating disorders and anxiety in early maturing men and
women [89]. Additionally, early maturing girls have been
reported to attain lower academic achievement [81,87].
Taken together, these data suggest that the biologic and
social transformations that accompany puberty make very
young adolescents more at risk for the development of
maladaptive coping mechanisms, presumably because they
are developmentally underprepared to effectively deal with
these changes.
In conclusion, puberty does seem to be starting earlier in
overweight girls, although obesity in boys seems to result
in the delay of pubertal onset. Earlier puberty in girls appears
to be directly linked to the long-term health consequences of
obesity and thus is a major public health concern. However,
the current data do not support that the timing of puberty has
changed for children who are not overweight, as the large
population studies of the age of menarche indicate that the
438 E.C. Walvoord / Journal of Adolescent Health 47 (2010) 433439
age of sexual maturation has not shown a linear decline over
the past century. The influence of stress on puberty timing is
fascinating, and more data about the effects of EDCs on
pubertal development in humans are critical. Finally, children
with early puberty are at considerable risk for subsequent
psychosocial difficulties during the adolescent years and
beyond, and should be monitored closely by their families
and primary care providers.
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