Upward weight percentile crossing in infancy and early childhood
independently predicts fat mass in young adults: the Stockholm
Weight Development Study (SWEDES)13
Ulf Ekelund, Ken Ong, Yvonn Linn, Martin Neovius, Sren Brage, David B Dunger, Nicholas J Wareham, and
Stephan Rssner
ABSTRACT
Background: Rapid early postnatal weight gain predicts increased
subsequent obesity and related disease risks. However, the exact
timing of adverse rapid postnatal weight gain is unclear.
Objective: The objective was to examine the associations between
rapid weight gain in infancy and in early childhood in relation to
body composition at age 17 y.
Design: This prospective cohort study was conducted in 248 (103
males) singletons and their mothers. Height and weight were mea-
sured at birth, 6 mo, and 3 and 6 y. The rates of weight gain during
infancy (0 6 mo) and early childhood (3 6 y) were calculated as
changes in sex- and age-adjusted weight SD scores during these time
periods. At 17 y, body composition was measured by air-
displacement plethysmography.
Results: Increasing weight gain during infancy and early childhood
were both independently associated with larger body mass index, fat
mass, relative fat mass, fat-free mass, and waist circumference at
17 y (P 0.005 for all; adjusted for sex, birth weight, gestational age,
current height, maternal socioeconomic status, and maternal fat
mass). Rapid weight gain in infancy, but not in early childhood, also
predicted taller height at 17 y (P 0.001).
Conclusions: Rapid weight gain in both infancy and early childhood
is a risk factor for adult adiposity and obesity. Rapid weight gain in
infancy also predicted taller adult height. We hypothesize that rapid
weight gains in infancy and early childhood are different processes
and may allow separate opportunities for early intervention against
obesity risk later in life. Am J Clin Nutr 2006;83:324 30.
KEY WORDS Air-displacement plethysmography, catch-up
growth, weight gain, obesity, Stockholm Weight Development
Study
INTRODUCTION
Overweight and obesity in children and young people are
rapidly increasing in prevalence worldwide and are related to a
wide range of adverse outcomes (1). Perinatal life has been iden-
tified as a key period for the development of obesity (2). High
birth weight is associated with an increased risk of later obesity
(3). Conversely, lower birth weight and thinner size at birth have
been linked to increased central fat, impaired glucose tolerance,
and features of the metabolic syndrome later in life (4 7). Low-
birth-weight intrauterine growthrestricted infants usually com-
pensate by showing rapid catch-up growth during the first year of
324 Am J Clin Nutr 2006;83:324 30. Printed in USA. 2006 American Society for Nutrition
life. Postnatal rapid weight gain has been suggested to be a risk
factor for later obesity (8 12), elevated blood pressure in ado-
lescent males (13), impaired glucose tolerance in young adults
(14), and increased mortality from coronary heart disease (15).
However, the exact timing of rapid postnatal weight gain in
Downloaded from ajcn.nutrition.org by guest on July 16, 2015
relation to later obesity risk is unclear.
Rapid weight gain, or upward percentile crossing, during the
first 2 y of life has been linked to general and central adiposity at
age 5 y (9). More recently, rapid weight gain during the first week
or months of life was shown to be associated with an increased
risk of overweight and obesity, on the basis of body mass index
(BMI; in kg/m2), in childhood (10) and in young adulthood (11,
12). However, it has been debated whether rapid weight gain
during infancy or early childhood (the period of the adiposity
rebound at 3 6 y) may contribute to obesity and the adult
metabolic syndrome (16). Furthermore, it is unknown whether
rapid postnatal weight gain is associated with a general increase
in body size [ie, increase in fat mass (FM), fat-free mass (FFM),
and height] or a selective increase in these components of body
composition, because a detailed characterization of body com-
position was not available in previous studies (11, 12).
In a cohort of 17-y-old Swedish adolescents followed prospec-
tively from birth, we therefore examined whether rapid weight
gain during infancy or early childhood, or both, was associated
with FM, percentage FM, FFM, BMI, and waist circumference
later in life, after the adjustment for possible confounding factors.
1
From the Medical Research Council Epidemiology Unit, Cambridge,
United Kingdom (UE, SB, and NJW); the Department of Paediatrics, Uni-
versity of Cambridge, Addenbrookes Hospital, Cambridge, United King-
dom (KO and DBD); and the Obesity Unit, Karolinska Institutet, Karolinska
University Hospital, Stockholm, Sweden (YL, MN, and SR).
2
Supported by the European Commission, Quality of Life and Manage-
ment of Living Resources, Key action 1 Food, Nutrition and Health Pro-
gramme as part of the project entitled Dietary and genetic influences on
susceptibility or resistance to weight gain on a high fat diet (QLK1-2000-
00515). MN was supported by Arbetsmarknadens Frsakrings och Aktiebo-
lag.
3
Reprints not available. Address correspondence to U Ekelund, Medical
Research Council Epidemiology Unit, Elsie Widdowson Laboratory, Ful-
bourn Road, CB1 9NL, Cambridge, United Kingdom. E-mail: ue202@
medschl.cam.ac.uk.
Received August 30, 2005.
Accepted for publication October 17, 2005.
 EARLY POSTNATAL WEIGHT GAIN AND ADULT BODY FAT
SUBJECTS AND METHODS
Subjects
SWEDES is a prospective study of weight development in the
offspring of mothers participating in the Stockholm Weight and
Pregnancy Development Study (SPAWN) (17, 18). Briefly,
2342 mothers were invited to participate in 1984 1985 and were
followed during and after their pregnancies; 1423 of these moth-
ers completed the study at the 1-y follow-up, and 481 mothers
and their children participated in the follow-up study (SWEDES)
after 17 y. Of these participants, complete data (including weight
and height development during the first 6 y of life) were available
for 248 (103 males) singletons and constitutes the sample for the
present study.
A detailed dropout analysis between those mothers who were
initially invited but not participating in the present study (n
2094) and participants (n 248) showed no significant differ-
ences in the number of previous pregnancies, age, weight, height,
and BMI before pregnancy, total weight gain during pregnancy,
and BMI at 6 and at 12 mo after pregnancy (P 0.05 for all).
Birth weight (3461 494 compared with 3453 563 g) and
length of gestation (39.5 1.6 compared with 39.4 1.9 wk) did
not differ significantly between the groups of children (P
0.05).
Measurements in children
Birth weight and height were noted from hospital records. The
ponderal index was calculated as birth weight/length3 (kg/m3).
The heights and weights of the infants were measured by stan-
dard clinical procedures during routine visits at the child welfare
center 4 times during the first year (birth and 6, 9, and 12 mo) of
life and annually thereafter until age 6 y. Gestation was estimated
from the date of the last menstrual period reported by the moth-
ers; 242 infants were born full term (36 wk), and 9 children
were born preterm (3336 wk). Analysis of the data excluding
these 9 preterm individuals did not alter the results.
At follow-up, sexual maturity was assessed by using the
5-stage scale for breast development in females and for pubic hair
in males, according to Tanner (19). A dichotomous variable,
puberty passed (Tanner stage 5) or not passed (Tanner stage
5), was created.
Standing height was measured to the nearest 0.5 cm against a
wall-mounted stadiometer, and body weight was measured to the
nearest 0.1 kg with a BodPod scale (Life Measurement Instru-
ments, Concord, CA). BMI was determined as weight/height2
(kg/m2), and adolescents were classified as normal weight, over-
weight, and obese according to the age-adjusted cutoffs de-
scribed by Cole et al (20). Waist circumference was measured in
duplicate, at the minimum circumference between the iliac crest
and the rib cage, with subjects standing dressed in underwear and
rounded to the nearest 0.5 cm. Body volume was measured by
air-displacement plethysmography with the BodPod, after ad-
justments for predicted thoracic lung volume and estimated sur-
face area artifact (21). FM, relative FM, and FFM were calculated
according to the equation of Siri (22) by using the software
provided by the manufacturer. Body volume was measured in
duplicate or triplicate when the initial 2 measures differed by
150 mL. All subjects were measured while wearing tight-
fitting underwear, or a swimsuit, and a swim cap.
325
Measurements in mothers
Maternal birth weight, smoking during pregnancy, and breast-
feeding patterns were recorded on questionnaires during and
after pregnancy. At follow-up, maternal education, occupation
and monthly income were recorded on a questionnaire. Occupa-
tion was coded on a scale from 1 to 6 (according to Statistics
Sweden) and used as an indicator of socioeconomic status (SES)
(23). This variable is a commonly used indicator of SES in
Sweden and was recently used in the Health-related Habits of
Life report (23). Maternal body weight and weight development
during and 1 y after pregnancy were measured by using standard
clinical procedures (17). Standing height, body weight, waist
circumference, and body composition were measured by using
the same methods as described above. Mothers with a BMI 25
were considered overweight, and mothers with a BMI 30 were
considered obese. The same procedures were adopted for the
mothers and the study participants, and the mothers and their
children were measured on the same day at follow-up. The local
Ethical Committee of Huddinge University Hospital approved
the study, and informed consent was obtained from each mother
and each child.
Downloaded from ajcn.nutrition.org by guest on July 16, 2015
Calculations and statistical analyses
Using all recorded body weight data, we generated internal SD
scores, independent of sex and age, by subtracting the sample
mean from the individual mean and then dividing by the sample
SD for weight at birth, 6 mo, and 3 and 6 y. For an alternative
validation, we also generated SD scores by comparing them
against the Swedish growth reference (24). The rates of weight
gain during infancy (0 6 mo) and early childhood (3 6 y) were
calculated as changes in weight SD scores during these time
periods. The analyses were also performed with the rate of weight
gain stratified as rapid (gain in weight SD score 0.67),
slow (decrease in weight SD score 0.67), and no change
(SD change between 0.67 and 0.67). These groups are equiv-
alent to upward, downward, and average in weight per-
centile crossing, because an SD of 0.67 represents the distance
between each displayed percentile line on standard growth charts
(ie, 2nd, 9th, 25th, 50th, 75th, 91st, and 98th percentile lines) (9).
The values are reported are means SDs unless otherwise
stated. Differences between the sexes were tested by analysis of
variance. Relations between variables were assessed by correla-
tion and partial correlation coefficients. The independent asso-
ciations between weight gain during infancy and early childhood
and body-composition variables at age 17 y were tested by gen-
eral linear modeling (analysis of covariance) and adjusted for
sex, birth weight, gestational age, height, and maternal SES and
FM. When BMI was modeled as the outcome variable, height
was excluded as an exposure variable because height is one of the
components of BMI (outcome variable). Similarly, the indepen-
dent associations between weight gain and FFM or height were
tested by GLM. When FFM was modeled as the outcome vari-
able, adjustments were made for sex, birth weight, gestational
age, and maternal SES and FFM. When height was modeled as
the outcome variable, adjustments were made for sex, birth
length, gestational age, and maternal SES and height. Model
building was performed by first introducing infancy weight gain
and then early childhood weight gain and finally by testing the
interaction between weight gain during infancy and early child-
hood. We also analyzed our data by comparing groups of children
326 EKELUND ET AL

Table 1 had a slow weight gain during both periods. The exclusion of
Physical characteristics of the subjects at follow-up and size at birth1 these subjects from the analyses did not change the results.
Boys (n 103) Girls (n 145)
Body composition at age 17 y
Age (y) 16.8 0.4 16.8 0.4
Increasing rate of weight gain during infancy and early childhood
Weight (kg) 66.4 10.1 59.0 8.72
Height (cm) 179.8 6.3 167.0 6.02
(as continuous variables) were both significantly and independently
BMI (kg/m2) 20.5 2.6 21.2 2.7 (of each other) associated with larger FM, relative FM, FFM, waist
Waist circumference (cm) 73.5 6.6 70.9 6.23 circumference, and BMI at age 17 y (P 0.005 for all; adjusted for
Body fat (%) 14.8 5.8 28.9 6.22 sex, birth weight, gestational age, current height, and maternal FM
Fat mass (kg) 10.1 5.3 17.4 5.92 and SES; Table 2). Weight gain during infancy (P 0.0001), but
Relative fat mass (%) 14.9 5.8 29.0 6.22 not during early childhood (P 0.21), predicted taller stature at age
Fat-free mass (kg) 56.3 7.3 41.6 4.72 17 y; however, the effects of weight gain in infancy on later body
Birth weight (g) 3535 509 3409 4784 composition were independent of height.
Birth length (cm) 50.7 2.3 49.8 2.0 Weight gains (as FM, waist circumference, BMI, FFM, and
Ponderal index (kg/m3) 20.7 2.4 20.6 2.2
height) in infancy and early childhood, stratified as clinically
All values are x SD; n 248.
1
significant rapid, no change (or average), and slow, are
Significantly different from boys (ANOVA): 2P 0.0001, 3 P
2-4
shown in Figure 1. Rapid weight gain in infancy was associated
0.01, P 0.05.
4
with larger FM, waist circumference, BMI, FFM, and height at
age 17 y (P 0.001 for all). Rapid weight gain in early childhood
was associated with larger FM, waist circumference, BMI, and
who showed clinically significant rapid weight gain (ie, 0.67 FFM (P 0.001 for all) but not with height at age 17 y.

Downloaded from ajcn.nutrition.org by guest on July 16, 2015

SD) and average (no change) and decelerated weight gain (ie,
0.67 SD) during the 2 periods, with adjustment for the same
cofactors and with the use of the same model building as de-
scribed above. The statistical analysis was performed with the
use of SPSS for WINDOWS (version 11.0; SPSS Inc, Chicago,
IL), and a P value 0.05 denoted statistical significance.
RESULTS
The physical characteristics of the subjects are provided in
Table 1. Birth weight, BMI at birth, and BMI in the girls at age
17 y did not differ significantly from Swedish reference data (24,
25), whereas the BMI in the boys at age 17 y was slightly lower
than the Swedish reference data (20.5 2.5 compared with
21.3 2.6; P 0.002).
Weight gain in infancy (0 6 mo)
The gain in weight SD score in infancy (between 0 6 mo) was
inversely related to birth weight (partial r 0.48, P 0.001)
and ponderal index at birth (partial r 0.50; P 0.001;
adjusted for gestational age and maternal weight gain during
pregnancy). Overall, between 0 and 6 mo, 25.4% (n 63) of all
children showed rapid weight gain in infancy (0.67 SD scores),
whereas 24.2% (n 60) showed relatively slow weight gain (
0.67 SD scores).
Weight gain in early childhood (3 6 y)
The gain in weight SD score between 3 and 6 y was not
significantly associated with size at birth (not shown) but was
inversely related to body weight and BMI at age 3 y (r 0.28
and r 0.35, P 0.001). Only 8.8% (n 22) of all subjects
showed rapid weight gain during early childhood (0.67 SD
scores), and 8.5% (n 21) showed relatively slow weight gain
during this period.
Weight gain in infancy was inversely related to rapid weight
gain in early childhood (partial r 0.25, P 0.001), which
indicated that weight gain between 3 and 6 y tended to slow down
in those who showed rapid weight gain between 0 and 6 mo. Only
2 children had a rapid weight gain during both periods; one child
No significant interactions were observed between birth
weight and rapid weight gain in infancy and early childhood for
any of the models. The results were essentially unchanged after
further adjustment for sexual maturity (222 participants were
postpubertal and 26 were classified as Tanner stage 4). We there-
after reanalyzed all our data by using externally calculated SD
scores (24), and these results were also unchanged.
On the basis of recent international BMI standards (20), 10.5%
(26/248) of all subjects were overweight at age 17 y (of whom 3 were
obese). Fifty percent of these (n 13) subjects had clinically sig-
nificant rapid weight gain in infancy (n 10) or in early childhood
(n 5); 2 subjects had rapid weight gain during both periods). Thus,
15.9% (10/63) of the subjects with rapid weight gain in infancy
became overweight or obese at age 17 y (unadjusted relative risk:
1.8; 95% CI: 0.9, 3.8), and 22.7% (5/22) of the subjects with rapid
weight gain in early childhood became overweight or obese at age
17 y (unadjusted relative risk: 2.5; 95% CI: 1.0, 5.8).
DISCUSSION
In a healthy contemporary birth cohort, rapid weight gain during
both infancy (0 6 mo) and early childhood (3 6 y) were related to
long-term changes in body composition. A gain in weight of 1 SD
score in infancy and in early childhood was associated with an
increase in FM of 1.8 and 3.4 kg, respectively, and with an increase
in FFM of 1.0 and 1.4 kg, respectively, at age 17 y. Upward weight
percentile crossing at these early ages also predicted larger BMIs
and waist circumferences in young adulthood, whereas rapid weight
gain in infancy also predicted taller adult height.
Although the effect of weight gain in early childhood on obe-
sity risk appeared to be greater than that of weight gain in infancy,
rapid weight gain occurred more commonly during the shorter
infancy period (25.4%) than during early childhood (8.8%) in
keeping with other studies (9). Thus, the population attributable
risk (an estimate of the proportion of all overweight subjects that
could be prevented if each risk factor were removed) was slightly
higher for rapid weight gain in infancy (15.7%) than for rapid
weight gain in early childhood (11.7%).
A growing number of contemporary studies have linked rapid
weight gain in infancy to later obesity risk (8 12, 26, 27). The
 EARLY POSTNATAL WEIGHT GAIN AND ADULT BODY FAT 327
Table 2
Independent determinants of obesity indicators, fat-free mass (FFM), and height at age 17 y1

B coefficient (95% CI) P

BMI (kg/m2)
Weight gain in infancy (SD) 0.92 (0.534, 1.306) 0.0001
Weight gain in early childhood (SD) 1.507 (0.909, 2.106) 0.0001
Female sex 0.997 (0.325, 1.668) 0.004
Birth weight (kg) 0.00177 (0.00088, 0.00266) 0.0001
Gestational age (wk) 0.0433 (0.182, 0.269) 0.70
Maternal SES 0.159 (0.39, 0.0728) 0.178
Maternal BMI (kg/my2) 0.03 (0.115, 0.054) 0.478
Waist circumference (cm)
Weight gain in infancy (SD) 1.40 (0.448, 2.351) 0.004
Weight gain in early childhood (SD) 3.30 (1.873, 4.726) 0.0001
Female sex 0.578 (1.629, 2.786) 0.61
Current height (cm) 0.271 (0.0807, 0.353) 0.002
Birth weight (kg) 0.00267 (0.000283, 0.00506) 0.029
Gestational age (wk) 0.072 (0.624, 0.48) 0.80
Maternal SES 0.528 (1.087, 0.0216) 0.06
Maternal fat mass (kg) 0.06 (0.146, 0.024) 0.16
Relative fat mass (%)
Weight gain in infancy (SD) 1.701 (0.766, 2.636) 0.0001

Downloaded from ajcn.nutrition.org by guest on July 16, 2015

Weight gain in early childhood (SD) 3.069 (1.665, 4.472) 0.0001
Female sex 14.175 (12.0, 16.353) 0.0001
Current height (cm) 0.047 (0.182, 0.0884) 0.50
Birth weight (kg) 0.0037 (0.00135, 0.00608) 0.002
Gestational age (wk) 0.065 (0.606, 0.475) 0.81
Maternal SES 1.12 (1.918, 0.322) 0.006
Maternal fat mass (kg) 0.0216 (0.606, 0.475) 0.61
Fat mass (kg)
Weight gain in infancy (SD) 1.819 (0.977, 2.661) 0.0001
Weight gain in early childhood (SD) 3.366 (2.102, 4.63) 0.0001
Female sex 9.329 (7.367, 11.29) 0.0001
Current height (cm) 0.107 (0.0146, 0.229) 0.08
Birth weight (kg) 0.00404 (0.00192, 0.00615) 0.0001
Gestational age (wk) 0.064 (0.55, 0.423) 0.80
Maternal SES 1.098(1.817, 0.379) 0.003
Maternal fat mass (kg) 0.0071 (0.0824, 0.0682) 0.85
FFM (kg)
Weight gain in infancy (SD) 1.016 (0.28, 1.751) 0.007
Weight gain in early childhood (SD) 1.422 (0.323, 2.522) 0.011
Female sex 8.026 (9.779, 6.272) 0.0001
Current height (cm) 0.487 (0.374, 0.601) 0.0001
Birth weight (kg) 0.00165 (0.0002, 0.0035) 0.08
Gestational age (wk) 0.0787 (0.384, 0.505) 0.72
Maternal SES 0.225 (0.405, 0.855) 0.48
Maternal FFM (kg) 0.17 (0.0442, 0.297) 0.008
Height (cm)
Weight gain in infancy (SD) 2.698 (1.984, 3.412) 0.0001
Weight gain in early childhood (SD) 0.638 (0.373, 1.648) 0.21
Female sex 9.037 (10.235, 7.839) 0.0001
Birth length (cm) 1.712 (1.396, 2.029) 0.0001
Gestational age (wk) 0.534 (0.91, 0.158) 0.006
Maternal SES 0.0736 (0.525, 0.672) 0.81
Maternal height (cm) 0.39 (0.30, 0.481) 0.0001
1
n 248. Weight gains in infancy (0 6 mo) and in early childhood (3 6 y) were calculated as change in weight SD score and were entered as continuous
variables. Data for maternal socioeconomic status (SES) and body composition were collected at the same time as the 17-y follow-up. The associations between
weight gain during infancy and early childhood and body-composition variables were tested by general linear modeling (analysis of covariance).

major advantages of our study were the long-term follow-up and
the validated measure of body composition (ie, air-displacement
plethysmography), which allowed important discrimination be-
tween the effects of rapid weight gain on FM and FFM. However,
we cannot exclude the possibility that the entire childhood
period, from birth to 6 y of age, is a critical period for the
development of later obesity risk, as recently suggested (28).
Regardless, our data suggest that rapid weight gain in infancy
and early childhood are at least partly mediated by different
mechanisms, as indicated by their inverse interrelation and by
328 EKELUND ET AL

their differing effects on childhood height. Rapid weight gain in

infancy, or catch-up, is suggested to be a compensatory mech-
anism following intrauterine growth restraint (9, 29). Accord-
ingly, children who showed rapid weight gains in infancy were
shorter, lighter, and thinner at birth than were other children. In
contrast, children who had rapid weight gains in early childhood
did not differ in size at birth from other children. A previous study
suggested that rapid weight gain in infancy is mediated by de-
creased satiety (29), and another recent study reported that en-
ergy intake and sucking behavior, but not total and nonsleeping
energy expenditure, predict infancy weight gain (30). It has been
suggested that maternal prepregnant BMI and an interaction
between the duration of breastfeeding and the introduction of
complementary foods are associated with weight gain be-
tween birth and 1 y (31). In our study, maternal weight gain
during pregnancy, but not maternal BMIs before pregnancy,
was associated with weight gain in infancy; however, this
association disappeared after adjustment for gestational age
and birth weight (data not shown). Lower weight gain in
infancy may partly underlie the protective effects of breast-
feeding and of lower-nutrient milk formulas on later obesity

Downloaded from ajcn.nutrition.org by guest on July 16, 2015

and cardiovascular disease risk (32, 33). We did observe a
negative association between the degree of breastfeeding at
2.5 mo and infancy weight gain during the first 6 mo. How-
ever, the inclusion of breastfeeding to the models did not
substantially alter any of the other findings.
Rapid weight gain in infancy, but not in early childhood,
predicted an increase in height at age 17 y. Rapid weight gain in
infancy was shown to be associated with subsequent higher
insulin-like growth factor I concentrations (34), and this major
childhood growth factor could mediate the subsequent gains in
lean body mass and height. Considering its high prevalence,
rapid weight gain in infancy could have heterogeneous effects on
subsequent statural growth and body composition. We suggest
that interindividual differences in insulin-like growth factor I
secretion or activity could lead to variations in height and lean
mass gains and in disease risks in response to rapid weight gain
in infancy.
Rapid weight gain in early childhood was also consistently and
independently associated with an overall increase in FM and
FFM but not in height. The determinants of rapid weight gain
during early childhood are largely unproven. Compared with the
infancy period, different environmental factors are likely to be
important, including childhood food consumption patterns (35)
and a sedentary lifestyle (36). However, the causal associations
remain to be demonstrated.

FIGURE 1. Adjusted mean fat mass (FM), waist circumference, BMI,

fat-free mass (FFM), and height at age 17 y in the subjects, stratified accord-
ing to rapid (increase in SD score 0.67), no change (change in SD score
between 0.67 and 0.67), and slow (decrease in SD score 0.67) weight gain
during infancy (0-6 mo) and early childhood (3-6 y). Error bars indicate 95%
CIs. These stratifications are equivalent to upward, average, and downward
weight percentile crossings, respectively, on standard growth charts. Rapid
weight gain in infancy and in early childhood was associated with greater FM,
FFM, waist circumference, and BMI (P for trend 0.001 for all). Rapid
weight gain in infancy was associated with height (P for trend 0.005). Bars
with different lowercase letters are significantly different, P 0.05 (analysis
of covariance with Bonferroni adjustment for multiple comparisons). Data
were adjusted for sex, birth weight (or length), gestational age, maternal fat
mass (or BMI or height), and maternal socioeconomic status. Data for waist
circumference and FM were additionally adjusted for height.
 EARLY POSTNATAL WEIGHT GAIN AND ADULT BODY FAT
In a recent longitudinal study, physical activityrelated energy
expenditure, assessed by the doubly labeled water method, did
not predict future weight and FM gain in children (37). Future
studies using other robust methods of assessing physical activity
during daily living may help to clarify this issue. Food intake,
especially of energy-dense foods, may also contribute. For ex-
ample, the consumption of sugar-sweetened soft drinks among
children has more than doubled during recent decades (38).
Excessive intake of sweetened drinks is associated with
greater childhood weight gain (39), and the odds of becoming
obese may increase by as much as 60% with each additional
daily serving of sugar-sweetened drinks (40). Similar findings
were recently reported in adult women (41). Prospective stud-
ies incorporating careful characterization of childhood
growth, body composition, and endocrine-, metabolic-,
social-, nutritional-, and energy expenditurerelated factors
would advance our understanding of these complex associa-
tions. Identification of the mechanisms that underlie rapid
weight gain in early life is likely to be important to under-
standing how to prevent obesity throughout life.
As with any observational study, caution should be exercised
when inferring causality based on the findings. However, our
observations of independent associations between rapid weight
gain in infancy and childhood and body composition and height
at age 17 y were consistent in both continuous and stratified
analytic approaches. Our findings were consistent before and
after adjustment for potential confounding by most known vari-
ables that are plausibly associated with infancy and childhood
growth. Furthermore, all data were collected prospectively as
part of a study aimed at addressing weight development in off-
spring, which decreased the risk of recall bias or unreliable mea-
surements. Birth weight and body composition at age 17 y did not
differ significantly between our study sample and the larger
cohort on the basis of the availability of early growth measure-
ments. Furthermore, birth weight and BMI at birth and at age 17 y
in females were not significantly different from Swedish refer-
ence data (24, 25). Our relatively small sample size and the low
prevalence of obesity reduced the power to robustly predict over-
weight and obesity risk related to rapid weight gain. However,
the unadjusted relative risk of rapid weight gain in early child-
hood was significantly related to the risk in young adulthood, and
the relative risks were similar in size to those reported in earlier
larger studies (10, 27).
In conclusion, our data suggest that rapid weight gain, or
upward percentile crossing, in infancy and in early childhood
both predict increased adiposity and obesity risk in young adults.
We hypothesize that rapid weight gain in infancy and childhood
may be mediated by different factors and may provide separate
opportunities for targeted interventions to prevent the develop-
ment of obesity.
We are grateful to Prevnut, CNT, NOVUM, Stockholm, Sweden for sup-
port with the BodPod equipment.
UE conceived the hypothesis for this article and conducted the data anal-
yses. UE and KO were responsible for drafting the manuscript. YL and SR
were primarily responsible for developing the study design for SWEDES,
supervised the data collection, and provided critical input. MN, SB, NJW,
and DBD provided critical input on the data analyses and on all versions of
the manuscript. SR was the principal investigator, conceived the idea of the
Stockholm Pregnancy and Weight Development Study and of the SWEDES,
assisted with the study design, and provided critical input. All authors par-
ticipated in the interpretation of the results and approved the final version of
329
the manuscript. The sponsors had no role in the study design, data collection,
data analysis, data interpretation, or writing of the report. None of the authors
had any conflicts of interest.
REFERENCES
1. Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health
crisis, common sense cure. Lancet 2002;360:473 82.
2. Dietz WH. Critical periods in childhood for the development of obesity.
Am J Clin Nutr 1994;59:9559.
3. Oken E, Gillman MW. Fetal origins of obesity. Obes Res 2003;11:496
505.
4. Hales CN, Barker DJP, Clark PMS, et al. Fetal and infant growth and
impaired glucose intolerance at age 64. BMJ 1991;303:1019 22.
5. Phipps K, Barker DJP, Hales CN, Fall CHD, Osmond C, Clark PMS.
Fetal growth and impaired glucose intolerance in men and women.
Diabetologia 1993;36:225 8.
6. Barker DJP, Hales CN, Fall CHD, Osmond C, Phipps K, Clark PMS.
Type 2 (non-insulin dependent) diabetes mellitus, hypertension and hy-
perlipidemia (syndrome X): relation to reduced fetal growth. Diabeto-
logia 1993;36:627.
7. Lithell HO, McKeigue PM, Berglund L, Mohsen R, Lithell UB, Leon
DA. Relation of size at birth to non-insulin dependent diabetes and
Downloaded from ajcn.nutrition.org by guest on July 16, 2015
insulin concentrations in men age 50 60 years. BMJ 1996;312:406 10.
8. Eid EE. Follow-up study of physical growth of children who had exces-
sive weight gain in first six months of life. Br Med J 1970;2:74 6.
9. Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. Association
between postnatal catch-up growth and obesity in childhood: prospec-
tive cohort study. BMJ 2000;320:96771.
10. Stettler N, Zemel BS, Kumanyika S, Stallings VA. Infant weight gain
and childhood overweight status in a multicenter, cohort study. Pediat-
rics 2002;109:194 9.
11. Stettler N, Kumanyika SK, Katz SH, Zemel BS, Stallings VA. Rapid
weight gain during infancy and obesity in young adulthood in a cohort of
African Americans. Am J Clin Nutr 2003;77:1374 8.
12. Stettler N, Stallings VA, Troxel AB, et al. Weight gain in the first week
of life and overweight in adulthood: a cohort study of European Amer-
ican subjects fed infant formula. Circulation 2005;111:1897903.
13. Adair LS, Cole TJ. Rapid child growth raises blood pressure in adoles-
cent boys who were thin at birth. Hypertension 2003;41:451 6.
14. Bhargava SK, Sachdev HS, Fall CH, et al. Relation of serial changes in
childhood body-mass index to impaired glucose tolerance in young
adulthood. N Engl J Med 2004;350:86575.
15. Forsen T, Eriksson JG, Tuomilehto J, Osmond C, Barker DJ. Growth in
utero and during childhood among women who develop coronary heart
disease: longitudinal study. BMJ 1999;319:14037.
16. Dietz WH. Overweight in childhood and adolescence. N Engl J Med
2004;350:8557.
17. Rssner S, Ohlin A. Maternal body weight and relation to birth weight.
Acta Obstet Gynecol Scand 1990;69:475 8.
18. Ohlin A, Rssner S. Maternal body weight development after pregnancy.
Int J Obes 1990;14:159 73.
19. Tanner JM. Growth at adolescence. Oxford, United Kingdom: Black-
well, 1962.
20. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard
definition for child overweight and obesity worldwide: international
survey. BMJ 2000;320:1240 3.
21. Fields DA, Goran MI, McCrory MA. Body-composition assessment via
air-displacement plethysmography in adults and children: a review.
Am J Clin Nutr 2002;75:453 67.
22. Siri WE. Body composition from fluid spaces and density: analysis of
methods. 1961. Nutrition 1993;9:480 91.
23. Persson J, Sjberg I, Johansson S-E. Bruk och missbruk, vanor och
ovanor. (Health-related habits of life.) Stockholm, Sweden: Statistics
Sweden, 2004:1012. (Report no. 105.)
24. Albertsson-Wikland K, Karlberg J. Natural growth in children born
small for gestational age with and without catch-up growth. Acta Pae-
diatr 1994;399:S64 70.
25. He Q, Albertsson-Wikland K, Karlberg J. Population-based body mass
index reference values from Gteborg, Sweden: birth to 18 years of age.
Acta Paediatr 2000;89:58292.
330 EKELUND ET AL
26. Stettler N, Bovet P, Shamlaye H, Zemel BS, Stallings VA, Paccaud F.
Prevalence and risk factors for overweight and obesity in children from
Seychelles, a country in rapid transition: the importance of early growth.
Int J Obes Relat Metab Disord 2002;26:214 9.
27. Monteiro POA, Victora CG, Barros FC, Monteiro LMA. Birth size, early
childhood growth, and adolescent obesity in a Brazilian birth cohort. Int
J Obes Relat Metab Disord 2003;27:1274 82.
28. Cole T. Children grow and horses race: is the adiposity rebound a critical
period for later obesity? BMC Pediatrics [serial online] 2004;4:6. Inter-
net: http://www.biomedcentral.com/14712431/4/6 (accessed 30 No-
vember 2005).
29. Ounsted M, Sleigh G. The infants self-regulation of food intake and
weight gain. Difference in metabolic balance after growth constraint and
acceleration in utero. Lancet 1975;1(7922):13937.
30. Stunkard AJ, Berkowitz RI, Schoeller D, Maislin G, Stallings VA. Pre-
dictors of body size in the first y of life: a high-risk study of human
obesity. Int J Obes Relat Metab Disord 2004;28:50313.
31. Baker JL, Michaelsen KF, Rasmussen KM, Sorensen TI. Maternal
prepregnant body mass index, duration of breastfeeding, and timing of
complementary food introduction are associated with infant weight gain.
Am J Clin Nutr 2004;80:1579 88.
32. Gillman MW, Rifas-Shiman SL, Camargo CA Jr, et al. Risk of over-
weight among adolescents who were breastfed as infants. JAMA 2001;
285:24617.
33. Singhal A, Lucas A. Early origins of cardiovascular disease: is there a
unifying hypothesis? Lancet 2004;363:16425.
34. Ong K, Kratzsch J, Kiess W, Dunger D, ALSPAC Study Team. Circu-
lating IGF-I levels in childhood are related to both current body com-
position and early postnatal growth rate. J Clin Endocrinol Metab 2002;
87:1041 4.
35. St-Onge MP, Keller KL, Heymsfield SB. Changes in childhood food
consumption patterns: a cause for concern in light of increasing body
weights. Am J Clin Nutr 2003;78:1068 73.
36. Ekelund U, Sardhina L, Anderssen SA, et al. Associations between
objectively assessed physical activity and indicators of body fatness in 9-
to 10-y-old European children: a population-based study from 4 distinct
regions in Europe (the European Youth Heart Study). Am J Clin Nutr
2004;80:584 90.
37. Salbe AD, Weyer C, Harper I, Lindsay RS, Ravussin E, Tataranni PA.
Assessing risk factors for obesity between childhood and adolescence: II.
Energy metabolism and physical activity. Pediatrics 2002;110:30714.
38. Johnson RK, Frary C. Choose beverages and foods to moderate your
intake of sugars: the 2000 dietary guidelines for Americanswhats all
the fuss about? J Nutr 2001;131:S2766 71.
39. Mrdjenovic G, Levitsky DA. Nutritional and energetic consequences of
sweetened drink consumption in 6- to 13-year-old children. J Pediatr
2003;142:604 10.
40. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consump-
tion of sugar-sweetened drinks and childhood obesity: a prospective,
observational analysis. Lancet 2001;357:505 8.
41. Schulze MB, Manson JE, Ludwig DS, et al. Sugar-sweetened beverages,
Downloaded from ajcn.nutrition.org by guest on July 16, 2015
weight gain, and incidence of type 2 diabetes in young and middle-aged
women. JAMA 2004;292:97234.