S P E C I A L
C l i n i c a l
F E A T U R E
R e v i e w
Constitutional Advancement of Growth, a.k.a. Early
Growth Acceleration, Predicts Early Puberty and
Childhood Obesity
Anastasios Papadimitriou, Polyxeni Nicolaidou, Andreas Fretzayas,
and George P. Chrousos
Third Department of Pediatrics (A.P., P.N., A.F.), University of Athens School of Medicine, “Attikon”
University Hospital; and Athens First Department of Pediatrics (G.P.C), University of Athens School of
Medicine, “Aghia Sophia” Children’s Hospital, Athens 124 64, Greece
Context: Constitutional advancement of growth (CAG), a.k.a. early growth acceleration, refers
to a growth pattern that is characterized by growth acceleration soon after birth, reaching a
zenith centile in the first 2 to 4 yr of life and followed by normalization of the growth rate until
the onset of puberty, which is usually early. CAG is the mirror image of the growth pattern of
constitutional delay of growth and puberty, which is characterized by growth deceleration in
the first years of life that is followed by normalization of the growth rate and late onset of
puberty. For a child to be considered as presenting CAG, other conditions that lead to early
growth acceleration, like genetic tall stature, infant overfeeding, and intrauterine growth
restraint, have to be excluded.
Evidence Acquisition: This review was based on our own data supplemented by relevant articles
identified by a PubMed search.
Evidence Synthesis: Girls with idiopathic precocious puberty almost invariably present the growth
pattern of CAG. Moreover, the growth pattern of growth acceleration in the first years of life, i.e.
CAG, is also present in children that become obese later in childhood; thus, it may be considered
a risk factor for childhood obesity.
Conclusions: Given the strong association between childhood obesity and early puberty, especially
in girls, infants that present the pattern of CAG have to be monitored for the development of early
puberty or/and obesity. (J Clin Endocrinol Metab 95: 4535– 4541, 2010)
T
he dramatic increase in the prevalence of childhood
overweight and obesity that has taken place in
industrialized as well as developing countries during
the last 30 yr is sending alarming signals to the health
authorities. Obesity is a risk factor for the development
of cardiovascular disease; hypertension; dyslipidemia;
diabetes mellitus; tumors such as breast, endometrial,
and colon cancer; and other diseases (1, 2). The risk
of death from all causes increases linearly with increasing adiposity for both men and women in all age groups
(3). This has led the World Health Organization (WHO)
to declare obesity as the major public health prob-
lem, with substantial impact on both morbidity and
mortality (4).
Adult obesity is often preceded by childhood obesity.
Most studies report a high percentage of childhood obesity
tracking into adulthood (⬃50 –70%) (5, 6). This suggests
that current measures in controlling the epidemic of childhood obesity are largely unsuccessful, and even more disappointing are the results of the treatment of obesity in
adults. Therefore, the medical community has to concentrate its efforts on prevention of childhood obesity.
Early puberty has been related to childhood obesity (7).
Although almost all studies report this association for
ISSN Print 0021-972X ISSN Online 1945-7197
Printed in U.S.A.
Copyright © 2010 by The Endocrine Society
doi: 10.1210/jc.2010-0895 Received April 19, 2010. Accepted June 15, 2010.
First Published Online July 7, 2010
Abbreviations: BMI, Body mass index; CAG, constitutional advancement of growth; CDG,
constitutional delay of growth; IPP, idiopathic precocious puberty; SGA, small for gestational age.
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
jcem.endojournals.org
4535
4536
Papadimitriou et al.
CAG Predicts Early Puberty and Obesity
girls, the results are contradictory for boys. There are reports showing a positive relation of obesity and early puberty, whereas others show a negative relation or a lack of
relation between early puberty and obesity.
In this review, we show that the growth pattern of early
acceleration, a pattern that we termed constitutional advancement of growth (CAG), may predict early puberty, at
least in girls, as well as childhood obesity.
The Growth Pattern of CAG
The term “constitutional advancement of growth” was
applied to a growth pattern that is the mirror image of the
well-known growth pattern of constitutional delay of
growth (CDG). CDG is characterized by growth deceleration in the first 2 to 3 yr of life, although birth length is
usually average (8). As a result of the growth deceleration,
the child’s height may fall to a nadir centile, which is at or
below the third centile, depending on parental height.
Then, growth resumes at a normal rate, and the child
grows along this centile until the onset of puberty, which
is usually delayed. In contrast, children with CAG present
growth acceleration soon after birth, reaching a zenith
centile in the first 2 to 4 yr of life; then the child grows
along this centile until the onset of puberty, which is usually early (9). In Fig. 1, the typical pattern of CAG is
shown.
For a child to be considered as presenting the growth
pattern of CAG, other conditions that lead to early growth
acceleration have to be excluded. These conditions are
genetic tall stature, overfeeding, and intrauterine growth
restraint.
In the first few years of life, children of tall parents
present with growth acceleration in an effort to reach their
genetic growth channel. These children are born with an
above average birth length that usually is within normal
limits. Growth is accelerated in early childhood, but a
normal rate is resumed at 4 –5 yr of age. In the following
prepubertal years, the growth curve parallels the 50th
centile (10).
According to the generally accepted ICP (infancy-childhood-puberty) growth model, growth in infancy is dependent on intrauterine growth factors (IGF-I, IGF-II, insulin)
and nutrition, and not on GH (11). Therefore, during this
period, underfeeding will result in reduced growth, and
overfeeding will induce growth acceleration.
Finally, intrauterine growth restraint may be compensated postnatally by a catch-up growth mechanism.
Catch-up growth is defined as a growth velocity that is
above the mean for age and sex. It is well known that
almost 90% of the small for gestational age (SGA) infants
present with postnatal catch-up growth (12), so by the age
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
of 3 yr their height usually is within the normal range of the
population.
Evidence for a Relation between
Childhood Obesity and Early Puberty
The improvements in socioeconomic conditions in the
20th century, in particular the improvements in nutrition
and hygienic conditions, have resulted in earlier pubertal
development of children. This can be clearly shown by the
fall in the age of menarche (13). It has been suggested that
the childhood obesity epidemic may influence the timing
of the onset of puberty in children. Furthermore, it has
been established that overweight girls tend to mature earlier than lean girls. In 1970, Frisch and Revelle (14) hypothesized that the degree of body fatness may trigger the
neuroendocrine events that lead to the onset of menses.
Since then, several researchers addressed the hypothesis
that increasing obesity may be a significant cause of earlier
onset of puberty.
The studies that examined the relationship of body
weight and timing of onset of puberty in girls are in line
with the notion that overweight girls tend to mature earlier
than girls of normal weight. Garn et al. (15) found that
menarcheal timing was a major determinant of weight and
fatness in early adulthood. In particular, they showed that
early maturers were 30% fatter than late maturers. Adair
and Gordon-Larsen (16) also examined the relation between the age at menarche and overweight in U.S. adolescents. Early maturing girls were twice as likely to be
overweight than average maturers, and this was true for all
racial/ethnic groups. Kaplowitz et al. (17) showed that in
6- to 9-yr-old U.S. girls, body mass index (BMI) Z-scores
were higher in pubertal than prepubertal white girls,
whereas in black girls the difference was significant only
for the 9-yr-old girls. However, in a study of AfricanAmerican girls, Himes et al. (18) showed that 8- to 10-yrold pubertal girls were more than six times as likely to be
classified as overweight and more than eight times as likely
to be obese than their prepubertal counterparts. Moreover, Lee et al. (19) examined the association between
weight status in early childhood and onset of puberty.
They determined BMI in 354 girls at the ages of 36 and 54
months and grades 1, 4, 5, and 6; pubertal stage was assessed by physical examination and maternal report in
grades 4 through 6 (19). The authors concluded that
higher BMI Z-score in girls as young as 36 months of age
and higher rate of change of BMI between 36 months of
age and grade 1, a period well before the onset of puberty,
are associated with earlier puberty.
However, the studies examining the subject of body
weight and sexual maturation in boys give contradictory
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
jcem.endojournals.org
4537
FIG. 1. The growth pattern of CAG in a girl with precocious puberty (onset of breast development was reported to be at the age of 7 yr). The
actual height of her parents is shown, as well as the target height (TH). Bone age is depicted by the orange square.
results. He and Karlberg (20), in a large longitudinal
growth study of Swedish children, found that increase in
BMI between the ages of 2 and 8 yr was related to early
puberty in both boys and girls; in particular, an increase of
1 BMI unit resulted in earlier peak height velocity (used as
an indirect way of determining onset of puberty) by 0.13
yr (20). Moreover, Ribeiro et al. (21) in their study of
Portuguese children reported that early maturation is as-
sociated with an increased risk for overweight or obesity
for boys and girls. However, Laron (22) reported no difference in sexual maturation between obese and normal
weight Israeli-born Jewish boys. In contrast, Wang (23),
who examined the relationship of body weight and sexual
maturation in 1520 boys (aged 8 –14 yr) that participated
in the Third National Health and Nutrition Examination
Survey (1988 –1994), showed that the prevalence of over-
4538
Papadimitriou et al.
CAG Predicts Early Puberty and Obesity
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
FIG. 2. The growth pattern of CAG in 47 girls with IPP. The girls presented growth acceleration soon after birth, reaching a zenith centile at the
age of 3 yr; then they grew along this centile until the onset of puberty, which occurred most commonly between the ages of 6 and 8 yr, and
manifested as a further growth acceleration. HSDS, Height SD score. [Adapted from Ref. 9.]
weight and obesity was lower in early-maturing boys. A
similar conclusion was also reached by Vizmanos and
Martí-Henneberg in Spanish boys (24).
Taken together, these data suggest that body fat and the
hormonal events that initiate puberty are in some way
related, at least in girls. Therefore, the question that arises
is what is the causal link between energy metabolism and
the GnRH secretory system. At present, the biological
mechanisms underlying the association between early
maturation and overweight are not well understood. It has
been suggested that caloric availability is the key element
determining reproduction; thus, fat deposition is a correlate of the positive energy balance rather than the causal
factor (25). Moreover, there is strong evidence that leptin,
an adipocyte protein and key regulator of body weight,
provides a permissive “gate” for puberty rather than a
causal “trigger” (26, 27).
CAG Predicts Early Puberty
Our group has shown that the growth pattern of CAG is
present in girls with idiopathic precocious puberty (IPP)
(9). Based on the observation that girls with precocious
puberty (i.e. with breast development before 8 yr of age)
are tall for age, even at the very early stages of pubertal
development, we examined the growth of 47 girls with IPP
from birth until diagnosis. The result was that the majority, i.e. 79%, of the girls with IPP manifested the growth
pattern of CAG (Fig. 2). Thus, we suggested that this pattern may be used as an additional clue to the differential
diagnosis of precocious puberty. We also observed a similar growth pattern in girls with early puberty, i.e. with
breast development at an age between 8 and 9 yr (our
unpublished data). Moreover, recently, early growth acceleration was reported in Finnish girls with premature
adrenarche, i.e. pubic or axillary hair development before
the age of 8 yr (28), which suggests that early growth
acceleration characterizes IPP and its variants in girls. It is
likely that the same growth pattern would be present in
boys.
There are several studies reporting a relation between
early sexual maturation and rapid growth in the early
years of life, although they did not attempt to correlate
growth in early life with a typical growth pattern like the
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
one we described as CAG. Analysis of the data of the 1946
British National Birth Cohort, in which height and weight
were measured prospectively from birth (for weight) or
age 2 yr (for height) throughout childhood (at ages 2, 4, 6,
7, 11, and 15 yr), showed a growth pattern that is similar
to CAG, i.e. women with earlier menarche presented rapid
growth in the first 2 yr of life and average growth rate
between the ages of 2 and 7 yr (29). Similarly, in a subcohort of the Avon Longitudinal Study of Parents and
Children, mother’s menarcheal age was inversely related
to her offspring’s height gain in the first 2 yr of life, but it
was unrelated to her offspring’s size at birth or later childhood growth rate (30), suggesting that maternal early age
at menarche may be a transgenerational marker of a faster
growth tempo during infancy, probably leading to earlier
maturation of the offspring.
Other conditions that may present growth acceleration, i.e. catch-up growth, which may be followed by early
puberty include intrauterine growth restraint and adoption of children from the Third World. In intrauterine
growth restraint girls, the age at both pubertal onset and
menarche are advanced by about 5–10 months, whereas in
boys pubertal onset usually occurs at an appropriate age
(31). Furthermore, early puberty may occur in adopted
girls from Third World countries. It has been suggested
that the catch-up growth that these children present may
trigger the onset of sexual maturation (32).
CAG Predicts Childhood Obesity
We have reported that growth acceleration in early life
may be a predictor for the development of obesity (33).
The study included 141 prepubertal obese children that
were classified as having early or late-onset obesity according to whether obesity developed before or after the
age of 3 yr, respectively. At the age of 2 yr, the children
with early-onset obesity were taller than controls, an expected finding given the dependence of growth during infancy to nutrition. Moreover, at 2 yr of age, the height of
the late-onset obese children, i.e. children of normal
weight who later became obese, was not significantly different than that of the early-obese children, and the lateonset obese children were significantly taller than controls
(Table 1). The birth weight and length of the late obese
children was average, and their target height was close to
zero; therefore, the tallness of these children could not be
attributed to genetic factors, and the accelerated growth in
early life could not be attributed to a catch-up process. We
suggested that growth acceleration in infancy induces programming of the hypothalamus to increased appetite,
which coupled to the obesogenic environment that modern children live in results in obesity during childhood.
jcem.endojournals.org
4539
TABLE 1. HSDS of children with early or late onset of
obesity and controls
n
Age (yr)
At onset of obesity
At presentation
HSDS
At age 2 yr
At presentation
Early
onset
48
Late
onset
93
2.2 (0.6)
9.2 (1.9)
5.1 (1.3)
9.5 (2.3)
9.1 (2.2)
1.3 (1.0)*&
1.1 (0.9)*#
0.9 (1.3)*
0.6 (1.0)*
0.4 (1.0)&
0.2 (0.8)#
Controls
72
HSDS, Height SD score. Adapted from Ref. 33.
Statistical significance between pairs in the same row bearing the same
symbol: *, P ⬍ 0.001; &, P ⬍ 0.005; and #, P ⬍ 0.001.
There is a growing body of evidence that accelerated
growth in childhood is related to development of obesity.
Recently, Buchan et al. (34) reported on the height and
BMI from a serial cross-sectional survey of 50,455 3-yrold children, performed from the years 1988 to 2003.
Overall, they found a slight increase in BMI during this
period; however, in the tallest 10% of children, the increase in BMI was 12 times greater than in the shortest
10% of children (34). Tallness could not be explained by
increased BMI because during the same period, mean
height fell by 0.5 cm. The authors concluded that the increase in BMI in tall children might be due to faster growth
and the resultant increase in appetite. Moreover, in a study
that was performed in Jamaican children, Walker et al.
(35) found that children stunted by age 2 yr were less likely
to be overweight than those who were never stunted, and
that among stunted children, greater linear growth during
mid to late childhood was associated with greater BMI at
age 17 yr. An association between early acceleration in
linear growth and increased weight for height at a later age
was also reported in Finnish girls with premature adrenarche (28).
Being born SGA is associated with increased risk of
developing metabolic syndrome later in life. It is of interest
that studies of SGA children have shown that insulin resistance is found only in children who achieve catch-up
growth, suggesting that rapid growth in infancy is implicated with the development of adverse metabolic consequences (36, 37).
Concluding Remarks
The data presented in this review suggest that CAG is the
mirror image of CDG. CAG may result in early puberty
and/or obesity, whereas it has been shown that CDG is
related to delayed puberty and underweight (38, 39).
Thus, what contrasts these two conditions is the post-
4540
Papadimitriou et al.
CAG Predicts Early Puberty and Obesity
natal height and weight gain, which are in the opposite
direction.
Moreover, pubertal delay predominantly affects boys,
whereas most children with idiopathic early puberty are
girls. Both conditions are influenced by genetics and, as we
have presented in this review, are characterized by a specific growth pattern. Thus, it would be important to examine whether more boys present the growth pattern of
CDG and more girls present with that of CAG. Data to
support this hypothesis come from a study on growth
tracks in infancy and early childhood (40); approximately
15% of girls and only 7% of boys had evidence of a mild
intermittent growth spurt at the end of infancy.
The mechanisms by which growth acceleration in the
first years of life result in early puberty and obesity are
largely unknown (41). Based on the fact that the growth
pattern of CAG has similarities to catch-up growth, we can
speculate that early GnRH neuron maturation in children
with CAG may be induced by factors implicated in
catch-up growth and early puberty and obesity in SGA
children (42, 43), i.e. increased IGF-I/insulin levels, and
possibly increased leptin levels early in life. However, the
involvement of the various neuroendocrine factors in
CAG and the subsequent early sexual maturation and/or
obesity need to be addressed in a prospective manner.
Acknowledgments
Address all correspondence and requests for reprints to:
Anastasios Papadimitriou, M.D., Third Department of Pediatrics, University of Athens School of Medicine, “Attikon”
University Hospital, Rimini 1 Street, Athens 124 64, Greece.
E-mail: [email protected].
Disclosure Summary: The authors have nothing to disclose.
References
1. Field AE, Coakley EH, Must A, Spadano JL, Laird N, Dietz WH,
Rimm E, Colditz GA 2001 Impact of overweight on the risk of
developing chronic diseases during a 10 year period. Arch Intern
Med 161:1581–1586
2. Pischon T, Lahmann PH, Boeing H, Friedenreich C, Norat T,
Tjønneland A, Halkjaer J, Overvad K, Clavel-Chapelon F,
Boutron-Ruault MC, Guernec G, Bergmann MM, Linseisen J,
Becker N, Trichopoulou A, Trichopoulos D, Sieri S, Palli D,
Tumino R, Vineis P, Panico S, Peeters PH, Bueno-de-Mesquita
HB, Boshuizen HC, Van Guelpen B, Palmqvist R, Berglund G,
Gonzalez CA, Dorronsoro M, Barricarte A, Navarro C, Martinez
C, Quirós JR, Roddam A, Allen N, Bingham S, Khaw KT, Ferrari
P, Kaaks R, Slimani N, Riboli E 2006 Body size and risk of colon
and rectal cancer in the European prospective investigation into
cancer and nutrition (EPIC). J Natl Cancer Inst 98:920 –931
3. Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath Jr CW 1999
Body mass index and mortality in a prospective cohort of US adults.
N Engl J Med 341:1097–1105
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
4. 1998 Obesity: preventing and managing the global epidemic. Report
of a WHO consultation on obesity. Technical Report Series, no. 894.
Geneva: World Health Organization
5. Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR,
Berenson GS 2005 Racial differences in the tracking of childhood
BMI to adulthood. Obes Res 13:928 –935
6. Deshmukh-Taskar P, Nicklas TA, Morales M, Yang SJ, Zakeri I,
Berenson GS 2006 Tracking of overweight status from childhood to
young adulthood: the Bogalusa Heart Study. Eur J Clin Nutr 60:
48 –57
7. Biro FM, Khoury P, Morrison JA 2006 Influence of obesity on timing of puberty. Int J Androl 29:272–277; discussion 286 –290
8. Wehkalampi K, Widén E, Laine T, Palotie A, Dunkel L 2008 Patterns of inheritance of constitutional delay of growth and puberty in
families of adolescent girls and boys referred to specialist pediatric
care. J Clin Endocrinol Metab 93:723–728
9. Papadimitriou A, Beri D, Tsialla A, Fretzayas A, Psychou F,
Nicolaidou P 2006 Early growth acceleration in girls with idiopathic precocious puberty. J Pediatr 149:43– 46
10. Dickerman Z, Loewinger J, Laron Z 1984 The pattern of growth in
children with constitutional tall stature from birth to age 9 years. A
longitudinal study. Acta Paediatr Scand 73:530 –536
11. Karlberg J, Engström I, Karlberg P, Fryer JG 1987 Analysis of linear
growth using a mathematical model. I. From birth to three years.
Acta Paediatr Scand 76:478 – 488
12. Saenger P, Czernichow P, Hughes I, Reiter EO 2007 Small for gestational age: short and beyond. Endocr Rev 28:219 –251
13. Rees M 1993 Menarche when and why? Lancet 342:1375–1376
14. Frisch RE, Revelle R 1970 Height and weight at menarche and a
hypothesis of critical body weights and adolescent events. Science
169:397–399
15. Garn SM, LaVelle M, Rosenberg KR, Hawthorne VM 1986 Maturational timing as a factor in female fatness and obesity. Am J Clin
Nutr 43:879 – 883
16. Adair LS, Gordon-Larsen P 2001 Maturational timing and overweight prevalence in US adolescent girls. Am J Public Health 91:
642– 644
17. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, HermanGiddens ME 2001 Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics 108:347–353
18. Himes JH, Obarzanek E, Baranowski T, Wilson DM, Rochon J,
McClanahan BS 2004 Early sexual maturation, body composition,
and obesity in African-American girls. Obes Res 12 Suppl:64S–72S
19. Lee JM, Appugliese D, Kaciroti N, Corwyn RF, Bradley RH,
Lumeng JC 2007 Weight status in young girls and the onset of puberty. Pediatrics 119:e624 – e630
20. He Q, Karlberg J 2001 BMI in childhood and its association with
height gain, timing of puberty, and final height. Pediatr Res 49:
244 –251
21. Ribeiro J, Santos P, Duarte J, Mota J 2006 Association between
overweight and early sexual maturation in Portuguese boys and
girls. Ann Hum Biol 33:55– 63
22. Laron Z 2004 Is obesity associated with early sexual maturation?
Pediatrics 113:171–172 [Letter]
23. Wang Y 2002 Is obesity associated with early sexual maturation? A
comparison of the association in American boys versus girls. Pediatrics 110:903–910
24. Vizmanos B, Martí-Henneberg C 2000 Puberty begins with a characteristic subcutaneous body fat mass in each sex. Eur J Clin Nutr
54:203–208
25. Schneider JE, Zhou D, Blum RM 2000 Leptin and metabolic control
of reproduction. Horm Behav 37:306 –326
26. Shalitin S, Phillip M 2003 Role of obesity and leptin in the pubertal
process and pubertal growth—a review. Int J Obes Relat Metab
Disord 27:869 – 874
27. Ebling FJP 2005 The neuroendocrine timing of puberty. Reproduction 129:675– 683
28. Utriainen P, Voutilainen R, Jääskeläinen J 2009 Girls with prema-
J Clin Endocrinol Metab, October 2010, 95(10):4535– 4541
29.
30.
31.
32.
33.
34.
35.
36.
ture adrenarche have accelerated early childhood growth. J Pediatr
154:882– 887
dos Santos Silva I, De Stavola BL, Mann V, Kuh D, Hardy R,
Wadsworth ME 2002 Prenatal factors, childhood growth trajectories and age at menarche. Int J Epidemiol 31:405– 412
Persson I, Ahlsson F, Ewald U, Tuvemo T, Qingyuan M, von Rosen
D, Proos L 1999 Influence of perinatal factors on the onset of puberty in boys and girls: implications for interpretation of link with
risk of long term diseases. Am J Epidemiol 150:747–755
Ong KK, Northstone K, Wells JC, Rubin C, Ness AR, Golding J,
Dunger DB 2007 Earlier mother’s age at menarche predicts rapid
infancy growth and childhood obesity. PLoS Med 4:e132
Virdis R, Street ME, Zampolli M, Radetti G, Pezzini B, Benelli M,
Ghizzoni L, Volta C 1998 Precocious puberty in girls adopted from
developing countries. Arch Dis Child 78:152–154
Papadimitriou A, Gousi T, Giannouli O, Nicolaidou P 2006 The
growth of children in relation to the timing of obesity development.
Obesity 14:2173–2176
Buchan IE, Bundred PE, Kitchiner DJ, Cole TJ 2007 Body mass
index has risen more steeply in tall than in short 3-year olds: serial
cross-sectional surveys 1988 –2003. Int J Obes (Lond) 31:23–29
Walker SP, Chang SM, Powell CA 2007 The association between
early childhood stunting and weight status in late adolescence. Int J
Obes (Lond) 31:347–352
Reilly JJ, Armstrong J, Dorosty AR, Emmett PM, Ness A, Rogers I,
Steer C, Sherriff A; Avon Longitudinal Study of Parents and Children
jcem.endojournals.org
37.
38.
39.
40.
41.
42.
43.
4541
Study Team 2005 Early life risk factors for obesity in childhood: cohort
study. BMJ 330:1357
Veening MA, Van Weissenbruch MM, Delemarre-Van De Waal HA
2002 Glucose tolerance, insulin sensitivity, and insulin secretion in
children born small for gestational age. J Clin Endocrinol Metab
87:4657– 4661
Sedlmeyer IL, Palmert MR 2002 Delayed puberty: analysis of a large
case series from an academic center. J Clin Endocrinol Metab 87:
1613–1620
Han JC, Balagopal P, Sweeten S, Darmaun D, Mauras N 2006 Evidence for hypermetabolism in boys with constitutional delay of
growth and maturation. J Clin Endocrinol Metab 91:2081–2086
Hermanussen M, Lange S, Grasedyck L 2001 Growth tracks in early
childhood. Acta Paediatr 90:381–386
Soto N, Bazaes RA, Peña V, Salazar T, Avila A, Iñiguez G, Ong KK,
Dunger DB, Mericq MV 2003 Insulin sensitivity and secretion are
related to catch-up growth in small-for-gestational-age infants at
age 1 year: results from a prospective cohort. J Clin Endocrinol
Metab 88:3645–3650
Iñiguez G, Ong K, Bazaes R, Avila A, Salazar T, Dunger D, Mericq
V 2006 Longitudinal changes in insulin-like growth factor-I, insulin
sensitivity, and secretion from birth to age three years in small-forgestational-age children. J Clin Endocrinol Metab 91:4645– 4649
Heger S, Partsch CJ, Peter M, Blum WF, Kiess W, Sippell WG 1999
Serum leptin levels in patients with progressive central precocious
puberty. Pediatr Res 46:71–75
Members can search for endocrinology
conferences, meetings and webinars on the
Worldwide Events Calendar.
www.endo-society.org/calendar