International Journal of Obesity (2006) 30, S11–S17

& 2006 Nature Publishing Group All rights reserved 0307-0565/06 $30.00
www.nature.com/ijo

ORIGINAL ARTICLE
Early adiposity rebound: causes and consequences for
obesity in children and adults
MF Rolland-Cachera, M Deheeger, M Maillot, F Bellisle

Research Unit on Nutritional Epidemiology INSERM U557/INRA U1125/CNAM/PARIS 13, Human Nutrition Research
Center of Ile de France, Bobigny, France

Childhood obesity is an important public health problem, with a rapidly increasing frequency worldwide. Identification of critical
periods for the development of childhood and adolescent obesity could be very useful for targeting prevention measures.
Weight status in early childhood is a poor predictor of adult adiposity status, and most obese adults were not obese as children.
We first proposed to use the body mass index (BMI) charts to monitor individual BMI development. The adiposity rebound (AR)
corresponds to the second rise in BMI curve that occurs between ages 5 and 7 years. It is not as direct a measure as BMI at any
age, but because it involves the examination of several points during growth, and because it is identified at a time when
adiposity level clearly change directions, this method provides information that can help us understand individual changes and
the development of health risks. An early AR is associated with an increased risk of overweight. It is inversely associated with
bone age, and reflects accelerated growth. The early AR recorded in most obese subjects and the striking difference in the mean
age at AR between obese subjects (3 years) and non-obese subjects (6 years) suggest that factors have operated very early in life.
The typical pattern associated with an early AR is a low BMI followed by increased BMI level after the rebound. This pattern is
recorded in children of recent generations as compared to those of previous generations. This is owing to the trend of a steeper
increase of height as compared to weight in the first years of life. This typical BMI pattern (low, followed by high body fatness
level) is associated with metabolic diseases such as diabetes and coronary heart diseases. Low body fatness before the AR
suggests that an energy deficit had occurred at an early stage of growth. It can be attributable to the high-protein, low-fat diet
fed to infants at a time of high energy needs, the former triggering height velocity and the latter decreasing the energy density
of the diet and then reducing energy intake. The high-fat, low-protein content of human milk may contribute to its beneficial
effects on growth processes. Early (pre- and postnatal) life is a critical period during which environmental factors may
programme adaptive mechanisms that will persist in adulthood. Under-nutrition in fetal life or during the first years after birth
may programme a thrifty metabolism that will exert adverse effects later in life, especially if the growing child is exposed to
overnutrition. These observations stress the importance of an adequate nutritional status in childhood and the necessity to
provide nutritional intakes adapted to nutritional needs at various stages of growth. Because the AR reflects particular BMI
patterns, it is a useful tool for the paediatrician to monitor the child’s adiposity development and for researchers to investigate
the different developmental patterns leading to overweight. It contributes to the understanding of chronic disease
programming and suggests new approaches to obesity prevention.
International Journal of Obesity (2006) 30, S11–S17. doi:10.1038/sj.ijo.0803514

Keywords: adiposity rebound; growth; child nutrition; trends; metabolic diseases

Introduction occurring in early life could play a major role.1,2 Identifica-

Although obesity, particularly childhood obesity, is increa-
sing worldwide, no decisive evidence emerges to account
for this trend. Factors such as nutrition in childhood and
adulthood provide an inconclusive explanation for adult
health outcomes. By contrast, it seems that risk factors
Correspondence: Dr MF Rolland-Cachera, UMR 557 INSERM/U1125 INRA/
CNAM/Paris 13, SMBH – Université Paris 13, 74 rue Marcel Cachin-93017,
Bobigny cedex, France.
E-mail: mf.cachera@smbh.univ-paris13.fr
tion of early markers of adult body adiposity is useful for
clinicians to monitor the child fatness development and for
researchers to investigate the origin of obesity. Childhood
weight status is a poor predictor of adult adiposity and most
obese adults were not obese as children.3 Other anthropo-
metric parameters must be investigated. Age at adiposity
rebound (AR), recorded on individual BMI growth curves,
has been identified as an indicator predicting adult fatness.4
This indicator may help identify the critical periods of
adiposity development and the determinants of future
obesity and health risks.
 Early adiposity rebound
MF Rolland-Cachera et al
S12
Assessment of the age at adiposity rebound
Weight(kg)/Height2 (m)
31
Nutritional status during growth is currently assessed on the Overweight area Case 1
basis of weight and height. Weight for age and weight for 29 Girls
height are recommended for young children by the World
Health Organization.5 However, the first indicator ignores 27
97th
height and the second ignores age. Weight-for-height indices
according to age include the three parameters (weight, 25
Case 3 90th
height and age) simultaneously. As it is highly correlated
23
with weight and body fat, and weakly related to stature, the 75th

weight/(height)2, Quételet or body mass index (BMI) has

21 50th
been selected to predict adiposity in children.6 In the early
1980s, the first BMI distribution reference charts,6 revised 10 Case 2 25th
19
years later,7 were constructed for all ages throughout child-
hood (Figure 1) and adulthood.7 This method is now used 17
10th

worldwide. Case 4 3th

The development of the BMI during growth parallels the
development of more direct measures of body adiposity such
as skin folds. On the average, a rapid increase of the BMI
occurs during the first year of life. The BMI subsequently
declines and reaches a minimum around the age of 6 years,
before beginning a sustained increase up to the end of
growth. The point of minimal BMI value (the nadir of the
BMI curve) is the start of the AR.4,8
Different methods are used to assess age at AR. It was first
assessed by visual inspection.4,8 This involves identifying an
upward trend in the BMI after the nadir. In some cases, the
descending phase of BMI is followed by a plateau. In this
case, the age at AR corresponds to the start of the steep BMI
increase (e.g. 8 years in case 4; Figure 1). In order to identify
the upward trend in BMI, Dorosty et al.9 specified that all
consecutive measurements of the BMI after the nadir should
show an increase, and required that any increase in the BMI
after the nadir had to equal or exceed 0.1 kg/m2. Gasser
et al.10 determined the AR from the velocity curve of the
BMI. Age at AR corresponded to the point where the velocity
curve became positive after a fall of BMI in infancy and early
childhood. Polynomial models to describe the patterns of
change in BMI are also used.11–15 Age at minimum BMI is
derived from these models. Comparing different approaches,
a recent study15 concluded that estimating AR visually
appears to best reflect the physiological basis of the AR.
Using this method, mean age at AR in the French reference
population was 6.271.6 years.4,8 This is similar to the
generally reported mean values, varying between 5 and 7
years according to the population studied and the method
used.11–16
Prediction of adult fatness
AR and adult fatness
On average, AR takes place by the age of 6 years, but in
individual cases, as shown in Figure 1, it may occur earlier or
later.8 These individual BMI patterns explain why, before AR,
15
13
11
Underweight area
9
Age, years
0 1 3 5 7 9 11 13 15 17 19 21
6
Figure 1 BMI reference centiles for French girls. Four example of BMI
development plotted against the reference charts case no. 1, fat child at 1
year, remained fat after an early adiposity rebound (2 years); case no. 2, fat
child at 1 year, did not stay fat after a late adiposity rebound (8 years); case no.
3, lean child at 1 year, became fat after an early adiposity rebound (4.5 years);
case no. 4, lean child at 1 year, remained lean after a late adiposity rebound
(8 years) (after Rolland-Cachera et al.8).
the child’s BMI predicts adult fatness only poorly. Case 3 in
Figure 1 (a thin child at 4 years becoming overweight after an
early AR) points out that many cases of overweight that are
diagnosed at adolescence actually have their origin much
earlier in life. The BMI chart can be a very useful tool for the
paediatrician to monitor the BMI development in children.
Several studies have investigated the association between
the age at AR and adult adiposity.11–14,16–18 Using the French
sample6,19 of the International Growth Study,20 we estab-
lished that age at AR was significantly associated with BMI
level at later ages:4 the earlier the AR, the higher the BMI or
the subscapular skin fold at age 21 years.8 Regression analysis
performed on this sample indicated that each year decrease
in age at AR was associated with a 0.84 kg/m2 (0.82 in boys
and 0.85 in girls) increase in the predicted BMI level at age 21
years (Po0.001) (unpublished data). In a study conducted in
the US, each year decrease in age at AR was associated with a
2.5 kg/m2 increase in the predicted BMI level at age 19–23
years.17
Whether an early AR reflects increased fat or lean body
mass was questioned.21 A study following children between
5 and 9 years found that differences in BMI during the AR
period were caused specifically by alteration in body fat

International Journal of Obesity

 Early adiposity rebound
MF Rolland-Cachera et al
S13
assessed by dual X-ray absorptiometry (DXA) rather than by a 19
alteration in lean mass. Children undergoing early AR gained
fat at a faster rate than children who rebounded at a later 18
age.22 From this observation, it is justified to go on using the
term ‘Adiposity rebound’4 rather than using ‘BMI rebound’ 17
as proposed later on.17
We also investigated the association between AR and bone

BMI (Kg/m2)
16
age: an early AR was associated with advanced skeletal
maturity.4 This association, also reported by Williams et al.,13
15
is consistent with the association between rapid growth and
later high BMI23–26 and, as a rule, with the accelerated
14
growth of all body tissues observed in obese children.27
Accelerated growth is often reported in low birth weight
infants.23 Using the data of the French reference study,19 no 13

association was recorded between the age at AR and birth

BMI 6y Low High
weight (r ¼ 0.08; P ¼ 0.23) (unpublished data). An early AR 12
0 2 4 6 8 10
then reflects rapid post-natal growth, rather than catch up
AGE (years)
growth following low birth weight. In a study conducted in
New Zealand, AR arose earlier in children who were tall at b 19
3 years, and an early AR was associated with early menarche,
suggesting that the timing of rebound is an indicator of
18
physical maturity.28

17
BMI (Kg/m2)

Comparison between indicators predicting adult adiposity

It has been suggested that an early AR predicts later fatness 16
because it identifies children whose BMI is high21,29 and/or
crossing centiles upwards.29 BMI at the time of AR (5–7 years)
15
and BMI centile crossing were proposed as more direct
indicators than AR for predicting later fatness.3,10,13,17,21,29
Actually, different aspects must be considered. 14
A high BMI level at the age of 6 years is significantly
associated with later high BMI, but also with previous high 13
Adiposity rebound Early Late
BMI levels. In the Zurich study,10 the correlation between 0 2 4 6 8 10
BMI at 6 years and adult BMI was 0.60. It was of the same AGE (years)
magnitude (r ¼ 0.66) between the BMI at 6 years and the BMI Figure 2 Comparison between two indicators predicting adiposity deve-
at 1 year. Using the data of the French longitudinal study of lopment. Two subgroups are constituted on the basis of the median of the
nutrition and growth (ELANCE) described earlier,30,31 we distribution of each indicator converted into Z-scores: BMI at the age of 6
have compared the BMI patterns according to either BMI at 6 years (a) and age at AR (b) (n ¼ 104).

years or age at AR (Figure 2). Figure 2a shows that a high BMI

at the age of 6 years is associated with high BMIs at all ages,
starting from birth. By contrast, an early AR is associated
with a high BMI at adult age, but with normal or even low
BMI level before the rebound (Figure 2b). The association
between an early AR and low or average BMI before the AR
was reported in various studies.8,9,12,28 Consequently, as a
rule, a child fat at age 6 years is more likely to be always fat,
whereas a child with an early AR is more likely to have a
normal or even low adiposity level in early life and to
develop fatness only from the time of AR. The BMI trajectory
of subjects who were thin in infancy and thereafter put on
weight rapidly (Figure 2b) is associated with insulin resis-
tance and coronary heart diseases.32–34 In a study conducted
in India,33 despite an increase in BMI between the ages of 2
and 12 years, none of the subjects with impaired glucose
tolerance or diabetes were obese at the age of 12 years. The
mechanisms by which body fat is acquired seem to be at least
as important as the consequences of excess fat per se in the
pathogenesis of diabetes, hypertension and cardiovascular
diseases.35
Consequently, as compared with a high BMI at 6 years or
with centile crossing,29 the early AR, which is associated with
a particular BMI trajectory, has different implications and is
likely associated with different environmental factors.
BMI pattern in the obese
Mean age at AR in the obese generally occurs around the age
of 3 years compared to 6 years in reference populations. In a
study conducted in 62 obese children examined in a
department of paediatric endocrinology, mean age at AR

International Journal of Obesity

 Early adiposity rebound
MF Rolland-Cachera et al
S14
was 3.2 years.8 None of these children had an AR later than
the age of 6 years. Two children had their AR at the age of
6 years (i.e. average) and more than half of them (55%) had
an AR at, or before, the age of 3 years.8 These observations,
together with similar data reported elsewhere16,36 showing
that most obese subjects displayed an early AR, are in
contrast to the observation that most obese adults were not
obese as children. An early AR is a better indicator of the
timing of the origin of obesity than a high BMI, which may
only appear after a progressive increase over many years.37,38
The very early AR recorded in most obese subjects suggests
that factors promoting obesity have operated very early in
life and probably several years before the AR. This observa-
tion is consistent with studies showing that early (pre- and
post-natal) life is a ‘critical period’ for later risks.1,2
Secular trends in growth patterns
Childhood obesity is increasing but other growth parameters
are also changing. Secular trends to increasing adult height,
weight and BMI have been clearly documented. At birth,
weight trends are small.39 In childhood, height trends tend
to be greater than in adulthood, owing to the associated
advance in maturation. The increase in height from one
generation to the next occurs mainly in the first 2 years of
life. The adult height trend matches that at age 2 years, so
that the increment in adult height has already been achieved
by age 2 years.39 Similar trends are observed in France40
where two 20-year follow-up studies were conducted under
similar conditions 30 years apart.19,31 Weight, height and
BMI of subjects born in 1985 (ELANCE study) were converted
into Z-scores for each age and sex, in relation to the
population born in 1955 as the reference, using the LMS
method41 (Figure 3). At the end of growth, subjects born in
1985 are taller, heavier and fatter31 than those born in
1955.19 Over the 30 years period, subscapular skin fold
thickness at adult age increased from 8.8 to 14.2 mm in
males and from 9.9 to 17.3 mm in females. Height trend is
maximum between 4 and 10 years and decreases until
adulthood. As reported earlier,39 the adult height trend is
about the same as the trend at age 2 years. The decreased
height trend observed from the age of 10 years is accounted
for by the earlier growth cessation in children born in 1985,
owing to their advanced maturation.31 At the age of 20 years,
BMI is higher in the recent study, but this trend appears from
the age at AR only. Before the AR, BMI was lower in children
born in 1985, with a maximum trend at age 2 years. The
lower BMI in early life can be explained by the greater gain in
height as compared to weight. Mean age at AR occurred at
6.2 years in children born in 1955 and at 5.6 years in those
born in 1985. As compared to subjects born in 1955, the
growth pattern of subjects born 30 years later typically shows
a rapid height gain and a low BMI in early life, followed
by an early AR and subsequent high fatness.31 This BMI
International Journal of Obesity
1
0.8
Height
Weight
0.6
Born in 1985
Z-score
0.4
BMI
0.2
Reference population
(born in 1955)
0
0 2 4 6 8 10 12 14 16 18 20
-0.2
Age, years
-0.4
Figure 3 Trajectories of growth in two longitudinal studies carried out 30
years apart: mean Z-scores for height, weight and BMI in children born in
1985,31 compared to a mean value of zero for children of the French reference
population, born in 1955.19
trajectory during childhood is associated with insulin
resistance and coronary vascular diseases in later life.32–34
Similar secular trends are reported in other countries.
Anthropometric measurements recorded in a longitudinal
study conducted in German children from 197842 were
compared with more recent data recorded from 2001.43 At
the age of 2 years, BMI was lower in the second study
(Po0.034), which was due to a gain of height as compared to
the earlier study. In England, height increased in different
age groups between 1972 and 1994, weight for height also
showed a slight decline in the youngest (5- or 6-year-old)
children, it remained unchanged in the 7- and 8-year- old
and showed an increase in the 9- and 10-year- old.44
Factors associated with an early AR and increased
fatness
Positive energy balance results from high energy intake or
low physical activity. Results of a longitudinal study showed
an increased fatness development in children with a seden-
tary lifestyle. This increase appeared after an early AR.45
Nutritional studies have investigated the influence of early
nutrition on either later fatness development or on the age at
AR. The association between nutritional intakes at the age
of 2 years and fatness development was investigated in
our longitudinal study of nutrition and growth.30 Both high
protein (% energy) and high energy intakes were associated
with increased BMI at 8 years, but following different BMI
patterns. BMI values in subjects consuming a high-energy
diet at 2 years were high at all ages with average age at AR.
BMI values in subjects consuming a high-protein diet tended
to be lower in early ages and became higher after an early
AR occurred. The BMI pattern of subjects consuming a high-
energy diet is similar to the pattern in subjects with a high
BMI level at 6 years (Figure 2a), whereas the BMI pattern
of subjects consuming a high-protein diet is similar to the
pattern in subjects with an early AR (Figure 2b). No
association was found between the percentage of energy

from the other nutrients (fat and carbohydrates) and age at
AR or fatness level at 8 years. Other studies found an
association between high protein intake in infancy and later
high fatness,24,46 whereas others did not.9,47 A study
conducted in Danish children found an association with
measures of body size (weight and height) but not with body
fat.48
We previously proposed that the characteristics of child-
hood obesity, that is, increased stature and body mass (lean
and fat)27 were the consequence of high protein intakes
inducing changes in hormonal status.49,50 High plasma
insulin like growth factor-1 (IGF1) concentrations and
reduced growth hormone (GH) secretion (spontaneous or
in response to a wide variety of stimuli) are characteristic
features of children with simple obesity.51 Increased IGF1
could promote hyperplasia in all tissues, including adipose
tissue, and decreased GH levels could decrease lipolysis,
promoting the development and maintenance of large fat
stores. A study conducted in 2.5-year-old Danish children
found that animal protein (from milk but not from meat or
vegetables) was positively associated with serum IGF-1
concentrations and height.52
Our results regarding the association between nutritional
intakes in infancy and growth patterns have underlined the
inadequate nutrient balance of the infant diet in industria-
lized countries.50 By the age of 1 year, the infant diet is
characterized by high intake of protein (B4 g/kg body
weight or 16% of total energy) and low intake of fat
(B28%). Protein intake represents about 3–4 times the
protein needs. The nutrient imbalance is remarkable con-
sidering that human milk provides 6% of energy as proteins
and 52% as fat.53 The protective effect of human milk
reported in some studies could be explained by its low
protein and high fat content. Breast-fed infants have a slower
growth.23 A similar observation was recorded in our long-
itudinal study described earlier.30 Length increase between
birth and 2 years was 36.872.8 cm in breast-fed infants and
38.172.9 in those who were not breast fed (P ¼ 0.03)
(unpublished data). There is now increasing evidence that
a rapid growth (weight and/or length) in infancy or early
childhood can predispose to later risks.26 It is associated with
large subsequent weight gain17,23,24,54 and a central body fat
pattern23,25 and also with a risk of diabetes,55 cardiovascular
disease56 and cancer.57,58
Paradoxically, the proportion of fat in the infant diet is low
at a period of high energy needs. Subsequently, the
percentage of energy provided by fat increases. In our
longitudinal study of nutrition and growth,59,60 the percen-
tage of fat intake increased from the age of 10 months to 6
years (27.4 at 10 months, 32.6 at 2 years, 36.5 at 4 years and
37.3 at 6 years), then plateaued until 16 years and reached
38% at 20 years (Figure 4), whereas it should be high in early
infancy and should then gradually decrease during the first
years of life.53
Similar fat intake patterns were reported in other coun-
tries.53 The BMI pattern associated with an early AR (low BMI
Early adiposity rebound
MF Rolland-Cachera et al
S15
level followed by high BMI after the AR) can be the
consequence of reduced energy balance owing to high-
protein, low-fat intake in early life followed by increasing fat
intake with age. In the recent years, most studies report that
infants have been fed a diet with a higher proportion of
energy coming from protein and lower intakes of fat than
would have been the case in the past.61–65 These changes
could account for the secular trends of accelerated linear
growth and decreased BMI in the first 2 years of life as shown
in Figure 3. Decreased fat intake in French children was
mainly owing to a decreased consumption of whole milk,
compensated for by low-fat milk and dairy products.64 The
daily consumption of whole milk in 2-year-old children was
206 g in 1973 and 90 g in 1986, whereas the consumption
of low-fat milk (half skimmed and skimmed milk) was 44 g
in 1973 and 216 g in 1986. The decline in energy intake
in infants and children over the last decades is very likely the
consequence of the low-energy protein-rich diet they
currently consumed.50
Undernutrition at any time in early life (during fetal life as
reflected by low birth weight1 or before an early adiposity
rebound32–34) may predispose to later risks. A relative energy
deficit66 may programme ‘thrifty metabolism’ and mechan-
isms of adaptative thermogenesis.35 Lucas67 proposed the
term ‘programming’ for the process in which the program-
ming stimulus exerts long-term effects when applied at a
critical or sensitive period. Adaptation to low fat intake in
early life may have adverse effects when, later in life,
children will eat a more abundant high-fat diet. The low-
60
50
40
% Energy
30 % Protein
% Fat
% CHO
20
10
0
0 5 10 15 20
Age, years
Figure 4 Nutrient intake (percentage of energy) changes by age in subjects
followed longitudinally from early childhood to adulthood.59,60
International Journal of Obesity
 Early adiposity rebound
MF Rolland-Cachera et al
S16
fat diet given to infants may result from strategies to prevent
obesity or cardiovascular diseases in industrialized countries,
despite general agreement that dietary fat content should
not be reduced in early life,53,68 and from poor living
conditions in the developing world.
Conclusion
In order to prevent obesity, it is of great interest to identify
subjects at risk before adiposity reaches high levels. Age at AR
predicts later fatness, but because it involves the examina-
tion of several points during growth, the AR mainly reflects
the growth pattern rather than absolute fatness level.
Considering the age at AR allows a clear understanding of
changing BMI pattern in individuals. The early AR recorded
in most obese subjects suggests that determinants of obesity
have operated early in life. An early AR is associated with
low fatness before the rebound and high fatness after the
rebound. Similar BMI patterns are observed in relation with
various other situations (secular trends, sedentary life style,
high protein intake in early childhood). The pattern of low
fatness level followed by increased fat gain has important
health implications, as it is typically recorded in subjects
with diabetes or cardiovascular diseases. Low fatness before
the AR suggests that a period of energy deficit had occurred
at an early stage of life, which could have ‘programmed’
adaptive metabolism, becoming detrimental later on. These
observations stress the importance of an adequate nutri-
tional status in early childhood and the necessity to provide
nutritional intakes adapted at various stages of growth.
The AR seems to be a useful indicator to predict adiposity
for the use of paediatricians and researchers. The association
recorded between BMI patterns and various environmental
conditions suggests new approaches to investigate the origin
of obesity and metabolic diseases and to improve prevention
strategies starting from early life.
References
1 Barker DJP, Winter PD, Osmond C, Margetts B, Simmonds SJ.
Weight in infancy and death from ischaemic heart disease. Lancet
1989; 2: 577–580.
2 Lucas A. Programming by early nutrition in man. In: Bock GR,
Whelan J (eds). The Childhood Environment and Adult Diseases
CIBA Foundation Symposium 156. Wiley: Chichester, UK, 1991.
pp 38–55.
3 Power C, Lake JK, Cole TJ. Measurements and long-term health
risks of child and adolescent fatness. Int J Obes Relat Metab Disord
1997; 21: 507–526.
4 RollandCachera MF, Deheeger M, Bellisle F, Sempé M, Guilloud-
Bataille M, Patois E. Adiposity rebound in children: a simple
indicator for predicting obesity. Am J Clin Nutr 1984; 39: 129–135.
5 Report of a WHO Expert Committee. Physical status: the use and
interpretation of anthropometry. WHO: Geneva, 1995.
6 Rolland-Cachera MF, Sempé M, Guilloud-Bataille M, Patois E,
Péquignot-Guggenbuhl F, Fautrad V. Adiposity indices in chil-
dren. Am J Clin Nutr 1982; 36: 178–184.
International Journal of Obesity
7 Rolland-Cachera MF, Cole TJ, Sempé M, Tichet J, Rossignol C,
Charraud A. Body mass index variations: centiles from birth to 87
years. Eur J Clin Nutr 1991; 45: 13–21.
8 Rolland-Cachera MF, Deheeger M, Avons P, Guilloud-Bataille M,
Patois E, Sempé M. Tracking adiposity patterns from 1 month to
adulthood. Ann Hum Biol 1987; 14: 219–222.
9 Dorosty AR, Emmett PM, Cowin IS, Reilly JJ, the ALSPAC Study
team. Factors associated with early adiposity rebound. Pediatrics
2000; 105: 1115–1118.
10 Gasser TH, Ziegler P, Seifert B, Molinari L, Lardo R, Prader A.
Prediction of adult skinfolds and body mass from infancy
through adolescence. Ann Hum Biol 1995; 22: 217–233.
11 Siervogel RM, Roche AF, Guo S, Mukherjee D, Chumlea WC.
Patterns of change in weight/stature2 from 2 to 18 years:
findings from long-term serial data for children in the Fels
longitudinal growth study. Int J Obes Relat Metab Disord 1991; 15:
479–485.
12 Whitaker R, Pepe MS, Wright JA, Seidel KD, Dietz WH. Early
adiposity rebound and the risk of adult obesity. Pediatrics 1998;
101: e5.
13 Williams S, Davie G, Lam F. Predicting BMI in young adults from
childhood data using two approaches to modelling adiposity
rebound. Int J Obes Relat Metab Disord 1999; 23: 348–354.
14 Guo SS, Huang C, Maynard LM, Demerath E, Towne B, Chumlea
WC et al. Body mass index during childhood, adolescence and
young adulthood in relation to adult overweight and adiposity:
the fels longitudinal study. Int J Obes Relat Metab Disord 2000; 24:
1628–1635.
15 Kroke A, Hahn S, Buyken AE, Liese AD. A comparative evaluation
of two different approaches to estimating age at adiposity
rebound. Int J Obes (London) Relat Metab Disord 2006; 30:
261–266.
16 Prokopec M, Bellisle F. Adiposity in Czech children followed from
one month of age to adulthood: analysis of individual BMI
patterns. Ann Hum Biol 1993; 20: 51725.
17 Freedman DS, Kettel Khan L, Serdula MK, Srinivan SR, Berenson
GS. BMI rebound, childhood height and obesity among adults:
the Bogalusa Heart study. Int J Obes Relat Metab Disord 2001; 25:
543–549.
18 He Q, Karlberg J. Probability of adult overweight and risk change
during the BMI rebound period. Obes Res 2002; 10: 135–140.
19 Sempé M, Pédron G, Roy-Pernot MP. Auxologie, méthode et
sequences. Vol 1 Théraplix 1979. Paris, pp 1–205.
20 Falkner F, Hindley CB, Sénécal J, Dean RFA, Karlgerg P, Ferrel E.
Child development an international method of study. Med Probl
Pediatr Basel Karger Ed 1960; 5: 1–237.
21 Dietz WH. ‘Adiposity rebound’ reality or epiphenomenona?
Lancet 2000; 356: 2027–2028.
22 Taylor RW, Goulding A, Lewis-Barned NJ, Williams SM. Rate of fat
gain is faster in girls undergoing early adiposity rebound. Obes Res
2004; 12: 1228–1230.
23 Ong KK, Preece MA, Emmett PM, Ahmed ML, Dunger DB,
ALSPAC Study Team. Size at birth and early childhood growth in
relation to maternal smoking, parity and infant breast-feeding:
longitudinal birth cohort study and analysis. Pediatr Res 2002; 52:
863–867.
24 Gunnarsdottir I, Thorsdottir I. Relationship between growth and
feeding in infancy and body mass index at the age of 6 years. Int J
Obes Relat Metab Disord 2003; 27: 1523–1527.
25 Rolland-Cachera MF, Méance S, Deheeger M. Height gain in
infancy is associated with body fat and fat pattern at age 14 years.
Int J Obes Relat Metab Disord 2000; 24 (Suppl 1): S40.
26 Rolland-Cachera MF. Rate of growth in early life. A predictor of
later life? Adv Exp Med Biol 2005; 569: 35–39.
27 Knittle JL, Timmers K, Ginsberg-Fellner F, Brown RE, Katz DP. The
growth of adipose tissue in children and adolescents. Cross
sectional and longitudinal studies of adipose cell number and
size. J Clin Invest 1979; 63: 239–246.
28 Williams S, Dickson N. Early growth, menarche and adiposity
rebound. Lancet 2002; 359: 580–581.

29 Cole TJ. Children grow and horses race: is the adiposity rebound a
critical period for later obesity? BMC Pediatr 2004; 12: 4:6.
30 Rolland-Cachera MF, Deheeger M, Akrout M, Bellisle F. Influence
of macronutrients on adiposity development: a follow up study
of nutrition and growth from 10 months to 8 years of age. Int J
Obes Relat Metab Disord 1995; 19: 573–578.
31 Deheeger M, Rolland-Cachera MF. Longitudinal study of anthro-
pometric measurements in Parisian children aged 10 months to
18 years. Arch Pediatr 2004; 11: 1139–1144 (In French).
32 Eriksson JG, Forsen T, Tuomilehto J, Osmond C, Barker DJ. Early
adiposity rebound in childhood and risk of type 2 diabetes in
adult life. Diabetologia 2003; 46: 190–194.
33 Bhargava SK, Sachdev HS, Fall CH, Osmond C, Lakshmy R, Barker
DJ et al. Relation of serial changes in childhood body-mass index
to impaired glucose tolerance in young adulthood. N Engl J Med
2004; 350: 865–875.
34 Barker DJP, Osmond C, Forsen TJ, Kajantie E, Eriksson JG.
Trajectoires of growth among children who have coronary events
as adults. N Engl J Med 2005; 353: 1802–1809.
35 Dulloo AG, Jacquet J, Montani JP. Pathways from weight
fluctuations to metabolic diseases: focus on maladaptative
thermogenesis during catch-up fat. Int J Obes Relat Metab Disord
2002; 26: S46–S57.
36 Girardet JP, Tounian P, Le Bars MA, Boreux A. Obesité de l’enfant:
intérêt des indicateurs cliniques d’évaluation. Annal Pédiatr 1993;
40: 297–303.
37 Rolland-Cachera MF, Bellisle F. Timing weight-control measures
in obese children. The Lancet 1990; 335: 918.
38 Rolland-Cachera MF. Onset of Obesity assessed from the weight/
stature2 curve in children: the need for a clear definition. Int J
Obes Relat Metab Disord 1993; 17: 245–246.
39 Cole TJ. The secular trend in human physical growth: a biological
view. Econ Hum Biol 2003; 1: 161–168.
40 Akrout M, Deheeger M, Rolland-Cachera MF. Secular trends in
patterns of growth: comparison between two longitudinal studies
(2-to-8 years of age) of children born in 1955 and 1985. Int J Obes
Relat Metab Disord 1995; 19 (suppl 2): 51.
41 Cole TJ. The LMS method for constructing normalized growth
standards. Eur J Clin Nutr 1990; 44: 45–60.
42 Hesse V, Bernhardt I, Hofmann A, Kunath H, Hesse G. Jena
longitudinal study of growth of 0–3-year old children. 2:
percentile curves for body height, body weight, height related
weight and growth rate. Padiatr Grenzgeb 1991; 30: 22–35.
43 Ulmen U, Hesse V, Hinkel J, Beloudi P, Kabelitz M. Comparison of
length, height and body weight in two German longitudinal
studies in infants and toddlers with a time intervalle of more
than twenty years (1978 vs 2001). Monatsschrift Kinderheilkd 2005;
153: 1026.
44 Hughes JM, Li L, Chinn S, Rona RJ. Trends in growth in England
and Scotland, 1972 to 1994. Arch Dis Child 1997; 76: 182–189.
45 Deheeger M, Rolland-Cachera MF, Fontvieille AM. Physical
Activity and body composition in 10-year-old French children:
linkages with nutritional intake? Int J Obes Relat Metab Disord
1997; 21: 372–379.
46 Scaglioni S, Agostoni C, DeNotaris R, Radaelli G, Radice N,
Valenti M et al. Early macronutrient intake and overweight at 5
years of age. Int J Obes Relat Metab Disord 2000; 24: 777–781.
47 Magarey AM, Daniels LA, Boulton TJC, Cockington RA. Does fat
intake predict adiposity in healthy children and adolescents aged
2–15? A longitudinal analysis. Eur J Clin Nutr 2001; 55: 471–481.
48 Hoppe C, Molgaard C, Thomsen BL, Juul A, Michaelsen KF.
Protein intake at 9 months of age is associated with body size but
not with body fat in 10-y-old Danish children. Am J Clin Nutr
2004; 79: 494–501.
49 Rolland-Cachera MF. Prediction of adult body composition from
infant and childhood measurements. In: Davies PWS and Cole T
Early adiposity rebound
MF Rolland-Cachera et al
S17
(eds). Body Composition Techniques in Health and Disease. Cam-
bridge University Press: Cambridge, 1995. pp 100–145.
50 Rolland-Cachera MF, Deheeger M, Bellisle F. Increasing preva-
lence of obesity among 18-year-old males in Sweden: evidence for
early determinants. Acta Paediatr 1999; 88: 365–367.
51 Loche S, Cappa M, Borrelli A, Faedda A, Crino A, Cella SG et al.
Reduced growth hormone response to growth hormone-
releasing hormone in children with simple obesity: evidence for
somatomedin-C mediated inhibition. Clin Endocrinol 1987; 27:
145–153.
52 Hoppe C, Udam TR, Lauritzen L, Molgaard C, Juul A, Michaelsen
KF. Animal protein intake, serum insulin-like growth factor I, and
growth in healthy 2.5-y-old Danish children. Am J Clin Nutr 2004;
80: 447–452.
53 Michaelsen KF, Jorgensen MH. Dietary fat content and energy
density during infancy and childhood; the effect on energy
intake and growth. Eur J Clin Nutr 1995; 49: 467–483.
54 Stettler N, Stallings VA, Troxel AB, Zhao J, Schinnar R, Nelson SE
et al. Weight gain in the first week of life and overweight in
adulthood. A cohort study of European American subjects fed
infant formula. Circulation 2005; 111: 1897–1903.
55 Fewtrell MS, Doherty C, Cole TJ, Stafford M, Hales CN, Lucas A.
Effects of size at birth, gestational age and early growth in
preterm infants on glucose and insulin concentrations at 9–12
years. Diabetologia 2000; 43: 714–717.
56 Singhal A, Cole TJ, Fewtrell M, Deanfield J, Lucas A. Is slower
early growth beneficial for long-term cardiovascular health?
Circulation 2004; 109: 1108–1113.
57 Albanes D, Jones DY, Schatzkin A, Micozzi MS, Taylor PR. Adult
stature and risk of cancer. Cancer Res 1988; 48: 1658–1662.
58 Gunnell DJ, Davey Smith G, Holly JMP, Frankel S. Leg length
and risk of cancer in the Boyd Orr cohort. BMJ 1998; 317:
150–151.
59 Deheeger M, Rolland-Cachera MF, Labadie MD, Rossignol C.
Etude longitudinale de la croissance et de l’alimentation d’en-
fants examinés de l’âge de 10 mois à 8 ans. Cah Nut Diét 1994; 1:
16–23.
60 Deheeger M, Bellisle F, Rolland-Cachera MF. The French long-
itudinal study of growth and nutrition: data in adolescent males
and females. J Hum Nutr Dietetics 2002; 15: 429–438.
61 Gregory JR, Collins DL, Davies PSW, Hughes JM, Clarke PC.
National Diet and Nutrition Survey: Children Aged 15–45 Years.
HMSO: London, 1995; 391 p.
62 Alexy U, Sichert-Hellert W, Kersting M. Fifteen-year time trends
in energy d macronutrient intake in German children and
adolescents: results of the DONALD study. Br J Nutr 2002; 87:
595–604.
63 Noble S, Emmett, the ALSPAC Study team. Food and nutrient
intake in a cohort of 8-month-old infants in the south-west of
England in 1993. Eur J Clin Nutr 2001; 55: 689–707.
64 Deheeger M, Rolland-Cachera MF, Péquignot F, Labadie MC,
Rossignol C. Changes in food intake in two-year old children
between 1973 and 1986. Ann Nutr Metab 1991; 140: 132–146 (In
French).
65 Rolland-Cachera MF, Bellisle F. Nutrition. In: Burniat W, Lissau I
& Cole T (eds) The obese and overweight child. Cambridge
University Press: Cambridge, 2002. pp 69–92.
66 Rolland-Cachera MF, Maillot M, Deheeger M, Bellisle F. Nutri-
tional intakes in early life and adult adiposity; the ‘ELANCE’ two
decade follow-up study. Int J Obesity 2006; 30 (Suppl 2): S12.
67 Lucas A. Role of nutritional programming in determining adult
morbidity. Arch Dis Child 1994; 71: 288–290.
68 Prentice A, Branca F, Decsi T, Michaelsen KF, Fletcher RJ, Guesry P
et al. Energy and nutrient dietary reference values for children in
Europe: methodological approaches and current nutritional
recommendations. Br J Nutr 2004; 92 (Suppl 2): S83–S146.
International Journal of Obesity