infant growth is associated with parental education but not with parental adiposity - early...

REGULAR ARTICLE

Infant growth is associated with parental education but not with parentaladiposity – Early Stockholm Obesity Prevention ProjectV Svensson1*, A Ek ([email protected])1*, M Forss�en1, K Ekbom1, Y Cao1, M Ebrahim1, E Johansson1, H Nero2, M Hagstr€omer2, M Ekstedt3, P Nowicka1,C Marcus1

1.Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden2.Division of Physiotherapy, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden3.Division of Patient Safety, School of Technology and Health, Royal Institute of Technology, Stockholm, Sweden

KeywordsChildhood obesity, Infant growth, Parental adiposity,Parental education, Rapid weight gain

CorrespondenceA Ek, Karolinska University Hospital Huddinge, B62,SE-141 86 Stockholm, Sweden.Tel: +46 8 585 877 52 |Fax: +46 8 585 873 70 |Email: [email protected]

Received18 October 2013; revised 23 December 2013;accepted 2 January 2014.

DOI:10.1111/apa.12551

*Authors contributed equally to this work.

ABSTRACTAim: To explore the simultaneous impact of parental adiposity and education level on

infant growth from birth to 12 months, adjusting for known early-life risk factors for

subsequent childhood obesity.

Methods: Baseline data for 197 one-year-old children and their parents, participating in a

longitudinal obesity intervention, were used. Obesity risk groups, high/low, were defined

based on parental body mass index (n = 144/53) and parental education (n = 57/139).

Observational data on infant growth between 0 and 12 months were collected. The

children’s relative weight (body mass index standard deviation score) at 3, 6 and

12 months and rapid weight gain 0–6 months were analysed in regression models, with

obesity risk as primary exposure variables, adjusting for gestational weight gain, birth weight,

short exclusive breastfeeding and maternal smoking.

Results: Relative weight at 3, 6 and 12 months was associated with low parental education

but not with parental adiposity. No significant associations were observed with rapid weight

gain. None of the early-life factors could explain the association with parental education.

Conclusion: Low parental education level is independently associated with infant growth,

whereas parental obesity does not contribute to a higher weight or to rapid weight gain

during the first year.

INTRODUCTIONA high relative weight or a rapid weight gain in infancy hasbeen identified as a risk factor for subsequent obesity inchildren (1,2). How infant growth is associated with bothhereditary and socio-economic factors has been explored insome previous studies (3–5); however, the impact of bothparents’ weight status and educational level has not beenanalysed thoroughly. This study aimed to investigatewhether parental obesity and low education, two of thestrongest risk factors for child obesity (6,7), in combinationwould be associated with increased growth already duringthe first year of life, controlling for additional early-life riskfactors (gestational weight gain, birth weight, breast-feedingand maternal smoking) (8–10).

Parental obesity has been established as the strongestrisk factor for child obesity, likely operating throughgenes, epigenetics and lifestyle (6,11). Parental obesity

may interact with socio-economic status (SES), thuscontributing to an increased obesity risk in high-incomecountries (7,12). However, the evidence indicating whenthe impact of hereditary factors on children’s growthmanifested is conflicting. Twin studies have identified thatheritability is low at birth but higher already at 6 months(13) and similarly, genetic markers associated with adultobesity have been seen to increase weight during the firstmonths of life (14). Additionally, weak associationsbetween both parents’ and offspring’ body mass index

Abbreviations

BMI, Body mass index; BMI SDS, Body mass index standarddeviation score; CHC, Child health care; CI, Confidence interval;OR, Odds ratio; SD, Standard deviation; SES, Socio-economicstatus.

Key notes� Parental education level is associated with infant

growth during the first year independently of parentaladiposity, birth weight and other early-life factors.

� Parental adiposity does not have a significant impact oninfant growth up to 12 months.

� Parental socio-economic background is likely to affectchildren’s growth early in infancy through mechanismsother than parental adiposity. This emphasises theimportance of early support and education for parentswith poor socio-economic background.

418 ©2014 Foundation Acta Pædiatrica. Published by John Wiley & Sons Ltd 2014 103, pp. 418–425

Acta Pædiatrica ISSN 0803-5253

(BMI) have been identified in large population cohortsduring the first year, gradually growing stronger with age(15,16). In contrast, clinical relevant differences in growthwhen comparing samples of children at high and low riskof obesity have previously not been seen during the firstyears of life (17). Associations between low parental SESand high infant growth have been identified at 3 monthsin a British cohort (3) and at age 1 in a Dutch material(4), independently of parental BMI. These associations toparental education have been partly mediated by infantfeeding, smoking during pregnancy and maternal age(3,4).

The aim of this study was to compare infant growthduring the first year between children at high and low riskof developing obesity, based on both parents’ BMI andeducational level. A secondary aim was to examine whichearly-life factors may mediate the effects of parental BMIand education on infant growth. We hypothesised thatsimultaneous exposure to both high parental BMI and lowparental education would amplify the risk of a higherrelative weight and rapid weight gain during the first year oflife.

METHODSDesignThis study is based on the baseline data of the EarlyStockholm Obesity Prevention Project (Early STOPP),including longitudinal observational data on children’sgrowth between birth and 12 months. Early STOPP is acluster randomised controlled trial with a 5-year longitudi-nal design conducted in Stockholm County, Sweden(NCT01198847) (18). Ethical approval was granted by theStockholm Regional Ethical Review Board (2009/217–31).

PopulationThe Early STOPP intervention targets a high-risk popula-tion – children of overweight and obese parents – followedfrom 1 to 6 years. A separate group of children with parentsof normal weight is also observed as a low-risk group.Families were recruited during 2010–2013 through childhealthcare (CHC) centres. Inclusion criteria were parentalweight status (two overweight or at least one obese parentor two normal-weighted parents), the child’s age (<1 year)and parents’ ability to communicate in Swedish. For twinpairs, the firstborn twin was included. Children withchronic health problems likely to influence growth, physicalactivity or eating habits were excluded. Additionally, for thisstudy, preterm (gestational age <37 weeks) children wereexcluded. Data for the population reported in this studywere collected up to May 2012. The study populationconstituted 197 families.

Data collectionThe families completed one questionnaire for each parentand another for the child. Height was measured to 0.1 cm,horizontally for children (Seca 712; Seca, Hamburg, Ger-many) and using a fixed stadiometer for parents (Ulmer;

Busse Design Engineering, Elchinge, Germany). Children’sweight was measured to 0.1 kg without clothing using ababy scale (Seca 376); parents were weighed wearing lightclothing using a portable scale (HD-316; Tanita Corp,Tokyo, Japan). The means of three measurements werecalculated. For mothers pregnant at baseline (n = 9), theirreported inclusion weight was used instead of a baselineweight. BMI was calculated for children and parents. Bodymass index standard deviation score (BMI SDS) at12 months was derived from Swedish age- and sex-specificreference values (19).

Outcome variablesWe use the term ‘growth’ to denote both relative weight andrelative weight gain. Weight and height records measured atthe CHC centres between birth and 12 months were used tocalculate the children’s BMI SDS at 3 and 6 months,excluding records outside �2 weeks at 3 months and�4 weeks at 6 months. BMI SDS at 12 months wascalculated from the baseline measurements, includingrecords within �2 months. Rapid weight gain during0–6 months was defined as the weight SD gain between 0and 6 months >0.67 SD (1), where weight SD was calcu-lated based on Swedish growth reference data.

Exposure variablesThe primary growth exposure variables were (i) risk groupby parental BMI and (ii) risk group by parental education.Based on their BMI, parents were classified as normalweight, overweight or obese, according to WHO cut-offpoints (normal weight = 18–24.9, overweight = 25–29.9,obese ≥30). Parents who had undergone obesity surgerywere classified as obese regardless of current BMI. For therisk group based on parental BMI, families were classifiedas high risk if at least one parent was obese or if bothparents were overweight and as low risk if both parentswere normal-weighted. In comparison, maternal andpaternal BMI were used as continuous exposure variables.Educational level for each of the parents was combinedand dichotomised into ‘low parental education’/high riskif neither parent >12 years of school and low riskotherwise. An interaction term for the two risk variablesbased on parental BMI and education was created.Covariates used were previously identified early-life riskfactors for child obesity – maternal age, maternal gesta-tional weight gain, birth weight, short exclusive breast-feeding (0–2 months vs. >2 months), age at introduction ofsolid foods (in months) and maternal smoking habits(smoker/nonsmoker) – and additionally gestational ageand child’s gender.

Statistical analysisDescriptive statistics were expressed in terms of the mean,SD, numbers and percentages. Variables were checked fornormality through the visual inspection of histograms.Independent t-tests and chi-squared tests were used todetermine differences in the growth outcome variables andcovariates between the high- and low-risk groups. Linear

©2014 Foundation Acta Pædiatrica. Published by John Wiley & Sons Ltd 2014 103, pp. 418–425 419

Svensson et al. Parental adiposity and education and infant growth

and logistic regression analyses were applied with growthoutcome variables as dependent variables and with parentalBMI and education risk groups as primary exposurevariables, testing individual, additive and interaction effects,as well as the impact of the potential confounders/media-tors. All tests were two-sided, and p-values <0.05 wereregarded as statistically significant. Statistical analyses wereperformed using STATISTICA, version 10 (StatSoft, Inc.,Tulsa, OK, USA, http://www.statsoft.com) and SPSS Sta-tistics 20 (IBM, Armonk, NY, USA, http://www.ibm.com).

RESULTSThe study population, divided into low- and high-riskgroups, is described in Table 1.

Infant growth, unadjustedIn Table 2 the outcome and covariate variables aredescribed for low- and high-risk groups. BMI SDS at 3, 6and 12 months was reported for 181, 185 and 187 children,

respectively, and rapid weight gain for 180 children. Therewere no significant differences in BMI SDS at 3, 6 and12 months (p = 0.71; p = 0.42; p = 0.62) or in the preva-lence of rapid weight gain (p = 0.58) between the high- andlow-risk groups based on parental BMI. BMI SDS at 3, 6and 12 months was significantly higher in children with lowparental education (p = 0.03; p = 0.04; p = 0.03). Thedifference in the prevalence of rapid weight gain betweenchildren with low and high family education was notsignificant (p = 0.70).

Early-life risk factors, unadjustedShort exclusive breastfeeding was more common amonghigh-risk than among low-risk children determined byparental BMI (31% vs. 8%; p < 0.001). Significant differ-ences could be detected neither in birth weight nor ingestational weight gain between the risk groups defined byparental BMI. Gestational weight gain was significantlyhigher for mothers in families with low parental education(16.9 kg vs. 14.3 kg; p = 0.02).

Table 1 Characteristics of the study population, in high- and low-risk groups as determined by parental body mass index (BMI) and education

Parental BMI (n = 197)* Parental education (n = 196)†

High risk (n = 144) Low risk (n = 53) High risk (n = 57) Low risk (n = 139)

n (%) Mean (SD) n (%) Mean (SD) n (%) Mean (SD) n (%) Mean (SD)

Child characteristics at 12 months

Weight (kg) 143 10.3 (1.4) 52 10.0 (0.9) 57 10.3 (1.4) 137 10.2 (1.2)

Height (cm) 144 76.4 (3.1) 53 76.1 (3.0) 57 76.0 (3.1) 139 76.5 (3.1)

BMI 143 17.6 (1.6) 52 17.3 (1.2) 57 17.8 (1.7) 137 17.4 (1.4)

BMI SDS‡ 143 �0.37 (1.2) 52 �0.49 (0.9) 57 �0.16 (1.2) 137 �0.52 (1.1)

Sex, male 74 (51) 21 (40) 26 (46) 68 (49)

Parental characteristics

Mother

Age (years) 144 33.6 (4.3) 52 33.6 (4.9) 57 32.7 (5.3) 138 33.9 (4.0)

BMI (kg/m2)§ 144 32.0 (6.3) 52 22.0 (1.9) 57 32.2 (7.1) 138 28.2 (6.7)

Waist circumference (cm)§ 136 101.2 (15.9) 48 78.4 (6.7) 55 100.9 (17.6) 128 93.1 (16.7)

Father

Age (years) 135 35.9 (5.1) 51 36.1 (5.5) 51 35.6 (5.3) 133 36.0 (5.1)

BMI (kg/m2) 135 29.9 (4.9) 51 23.0 (1.5) 52 30.0 (5.7) 133 27.2 (4.8)

Waist circumference (cm) 134 103.6 (14.5) 51 85.0 (6.8) 51 102.3 (16.5) 133 97.0 (14.6)

Socio-demographic factors

Parental education

Mother low education 66 (46) 14 (26) (100) 23 (17)

Father low education 74 (51) 13 (25) (100) 37 (27)

Parental low education† 51 (35) 6 (11) (100) (0)

Ethnicity, other than Nordic

One parent 20 (14) 6 (11) 8 (14) 18 (13)

Two parents 7 (5) 1 (2) 4 (7) 4 (3)

Smoking habits

Mother smoker 8 (6) 3 (6) 4 (7) 7 (5)

Father smoker 8 (6) 5 (9) 6 (11) 7 (5)

*Parental BMI: High risk = at least one obese parent or two overweight parents; Low risk = two normal-weighted parents.†Parental education: High risk = Low parental education = both parents’ educational level <12 years; Low risk = High parental education = at least one parent’s

educational level ≥12 years.‡Body mass index standard deviation score.§For pregnant women, inclusion BMI is reported instead of baseline BMI and weight circumference is excluded (n = 9).


Parental adiposity and education and infant growth Svensson et al.

Table2

Outcomevariables

andcovariatesin

high-andlow-risk

groups,asdeterm

ined

byparentalbody

massindex(BMI)andeducation

ParentalBM

I*

p95%

CI‡

Parentaleducation†

p95%

CI‡

High

risk(n

=144)

Lowrisk(n

=53)

High

risk(n

=57)

Lowrisk(n

=139)

Mean(SD)

n(%

)Mean(SD)

n(%

)Mean(SD)

n(%

)Mean(SD)

n(%

)

Outcomevariables

BMISD

S

3months§

1.01(1.10)

0.95(1.02)

0.71

�0.29–0

.42

1.27(1.19)

0.88(1.02)

0.03

�0.73to

�0.03

BMISD

S

6months§

0.44(1.18)

0.30(0.84)

0.42

�0.21–0

.50

0.65(1.22)

0.29(1.03)

0.04

�0.71to

�0.01

BMISD

S

12months§

�0.40(1.15)

�0.49(0.90)

0.62

�0.26–0

.44

�0.16(1.18)

�0.54(1.03)

0.03

�0.72to

�0.04

Rap

id

weigh

tgain

0–6

months¶

32/1

28(25)

11/5

2(21)

0.58

13/5

0(26)

30/1

29(23)

0.70

Covariates

Sex,male

74(51)

21(40)

0.14

26(46)

68(49)

0.67

Maternal

smoking

8(6)

3(6)

0.98

4(7)

7(5)

0.58

Shortexclusive

breastfee

ding

44(31)

4(8)

<0.001

12(21)

36(26)

0.47

Maternal

age(years)

33.6

(4.3)

33.6

(4.9)

0.98

1.44–1

.41

32.7

(5.4)

33.9

(4.0)

0.08

�0.14–2

.61

Gestatio

nal

age(w

eeks)

39.8

(1.4)

39.9

(1.3)

0.66

�0.57–0

.36

39.8

(1.3)

39.9

(1.4)

0.68

�0.35–0

.55

Gestatio

nal

weigh

tgain

(kg)

14.7

(7.8)

15.6

(4.7)

0.33

�3.15–1

.40

16.9

(7.5)

14.3

(6.8)

0.02

�4.92to

�0.34

Birthweigh

t(g)

3751(589)

3631(431)

0.22

�0.66–2

87

3786(634)

3679(516)

0.23

�282–6

9

Introduction

ofsolid

foods(m

onths)

4.8

(1.0)

4.8

(0.8)

0.66

�0.36–0

.23

4.7

(0.9)

4.8

(0.9)

0.38

�0.16–0

.42

Antib

iotics

first

year

(days)

2.2

(5.9)

2.3

(5.9)

0.90

�1.97–1

.73

2.4

(6.3)

2.2

(5.6)

0.79

�2.05–1

.56

*Paren

talBMI:Highrisk=at

least1obeseparen

tortwooverweigh

tparen

ts;Low

risk=twonorm

al-weigh

tedparen

ts.

†Paren

taled

ucatio

n:Highrisk=Low

paren

taled

ucatio

n=both

paren

ts’ed

ucatio

nal

level<12years;

Low

risk=Highparen

taled

ucatio

n=at

leastoneparen

t’sed

ucatio

nal

level>12years.

‡CI:Confid

ence

interval

fordifferen

cebetwee

ngroups.

§Th

eBMISD

Svariablesarebased

onmeasuremen

trecordswith

in�2

wee

ksat

3months,�4

wee

ksat

6monthsan

d�2

monthsat

12months.

¶ Rap

idweigh

tgain

0–6

monthsisdefined

asweigh

tSD

gain

>0.67SD

,whereweigh

tSD

iscalculatedbased

ontheSw

edishgrowth

reference

(Albertsson-W

ikland1994).



Infant growth, adjustedThe results of three multivariate models are presented inTable 3. No association between the children’s growth andthe risk group by parental BMI could be statisticallydemonstrated, confirming the unadjusted results (model 1and 3). The same results were obtained using parental BMIas continuous variables (data not shown). The associationbetween the child’s BMI SDS and parental education wassignificant at 3 months (p = 0.02) and at 6 months(p = 0.04) and was statistically indicated at 12 months(p = 0.06) in model 3. In total, 18%, 14% and 11% of thevariance in BMI SDS at 3, 6 and 12 months, respectively,could be explained by the factors included in model 3. Noassociations could be seen between rapid weight gain andhigh/low obesity risk. A significant interaction effect of therisk exposures by parental BMI and education on infantgrowth could not be identified.

Birth weight was significantly and positively associatedwith BMI SDS at all ages (p < 0.0001 at 3 and 6 monthsand p < 0.01 at 12 months) and negatively associatedwith rapid weight gain (p < 0.001; OR = 0.86, 95% CI0.79–0.93). Birth weight contributed the most to thevariance in the outcome variables (data not shown).Maternal smoking was significantly and positively associ-ated with BMI SDS at 12 months. The variables notincluded in the final models did not affect the associa-tions between the outcome growth variables and theprimary risk variables.

DISCUSSIONIn a sample of almost 200 well-characterised 1-year-oldchildren, divided into groups at high and low risk of obesity,a higher relative weight during the first year was associatedwith low parental education level independently of parentalBMI and birth weight. High risk determined by parentalBMI did not have a significant impact on the children’sgrowth during the first year of life. None of the studiedenvironmental factors could explain the association withparental education.

The timing and effect sizes of hereditary and environ-mental impact on children’s growth are important toevaluate. Previous studies comparing children at high andlow risk for developing obesity support our results regardinga delayed impact of parental BMI (17). Additionally,infants’ growth curves across parental BMI categories arealmost identical between birth and 1.5 years of age (20).This also aligns with our previous study showing thatparental adiposity did not affect the age at onset of obesity,but influenced only the severity of obesity later in childhood(21). On the other hand, infant and parental BMI have beenweakly but statistically significantly associated alreadyduring the first year in large cohorts (15,16). In our study,the insignificant difference in BMI at 12 months betweenchildren with obese and lean parents was comparable to thesignificant difference in one population-based study (15),indicating that the clinical relevance of these associationsneeds to be clarified.

Our results confirm previous research reporting that theimpact of parental education on infant growth is indepen-dent of parental adiposity in infancy (3,4). Even though lowparental education was much more common in overweightand obese parents, we did not identify any additive orinteraction effects of parental obesity and education level aspreviously seen in older children (22); on the contrary, riskas defined by parental BMI weakened the multivariatemodels. This suggests a stronger gene–environment inter-action later in childhood.

Regarding the timing for the influence of parentaleducation on infant growth, two previous studies havereported positive associations of similar effect sizes as foundin our study between low SES and children’s weightdevelopment, the first study at 3 months (3) and the secondat age 1 (4). Our results extend the findings of theseprevious studies by accounting for both parent’s educa-tional level and by including several measures of children’sgrowth up to 12 months of age. By comparison, in theALSPAC longitudinal study, the socio-economic differ-ences associated with children’s BMI did not begin toemerge until the child reached 4 years of age (23). How-ever, the education levels in ALSPAC population weregenerally much lower than those in our population andthose in the previous British study (3), possibly explainingwhy no early differences were identified.

Another surprising result is that in contrast to theaforementioned studies (3,4), none of the previously iden-tified environmental determinants of childhood obesity(10,24,25) mediated the association with parental educa-tion and infant growth (4). In our study, the associationwith parental education was independent of birthweight,even though birthweight explained a large part of thevariation in infant growth. Only a weak mediating effect ofmaternal smoking on the association between growth andparental education was indicated at 12 months. Maternalsmoking during pregnancy has been associated with anincreased risk of overweight and obesity in later childhood(9,10), but the evidence for a mediating effect on theassociation between parental SES and infant growth isconflicting (3,4). Of note, in our sample, mothers in familieswith low education levels exhibited significantly highergestational weight gain than mothers in families with higheducation levels, but this factor could not explain theassociation between parental education and growth. Nordid feeding method influence the children’s growth incontrast to the findings of several previous studies (3–5,25).Thus, the mechanisms behind the ways parents’ educationlevels affect early weight gain remain uncertain. Futurestudies should also take into account other family factorswhen studying infant growth, such as parenting practices,income, work hours and social support (26,27).

One of this study’s limitations is that the sample sizelimits the possibility of identifying weaker associationsbetween weight gain and specific parental factors. We thusexpected to identify only the strong associations betweenobesity risk and child growth. It is possible that thenonsignificant results between children’s growth and



Table3

Estim

ates

from

linearregressio

nof

BMISDS

(bodymassindexstandard

deviationscore)

andfro

mlogisticregressio

nof

rapidweightgain,unadjusted

andadjusted

inthreemodels;model1with

riskexposure

determ

ined

byparentalbody

massindex(BMI),

model2with

riskexposure

determ

ined

byparentaleducationandmodel3with

both

exposure

variables

BMIS

DS3months

BMIS

DS6months

BMIS

DS12

months

Rapidweightg

ain0–6months

Unadjusted

associa

tions

bp

R2b

pR2

bp

R2OR

CIp

Highriskvs.low

risk–paren

talBMI

0.02

0.75

–0.06

0.42

–0.15

0.52

–1.24

0.57–2

.72

0.58

Highriskvs.low

risk–paren

taled

ucatio

n0.16

0.03

0.02

0.15

0.04

0.02

0.16

0.03

0.02

1.16

0.54–2

.47

0.70

Adjusted

associations

Model

1

Highriskvs.low

risk–paren

talBMI

�0.00

0.99

0.16

0.06

0.44

0.12

0.03

0.66

0.10

1.51

0.64–3

.59

0.34

Gen

der

�0.08

0.28

�0.04

0.56

�0.11

0.13

1.39

0.65–2

.96

0.39

Birthweigh

t(100g)

0.40

<0.0001

0.33

<0.0001

0.25

0.002

0.86

0.79–0

.93

<0.001

Gestatio

nal

weigh

tgain

(kg)

0.09

0.23

0.15

0.06

0.10

0.19

1.05

0.99–1

.11

0.08

Shortexclusive

breastfee

ding

0.04

0.60

0.05

0.49

0.03

0.69

0.97

0.40–2

.38

0.95

Maternal

smoking

0.06

0.39

�0.02

0.78

0.19

0.01

0.30

0.03–3

.25

0.32

Model

2

Highriskvs.low

risk–paren

taled

ucatio

n0.17

0.02

0.19

0.16

0.03

0.15

0.15

0.05

0.12

1.15

0.48–2

.73

0.75

Gen

der

�0.08

0.30

�0.05

0.47

�0.11

0.16

1.42

0.67–3

.01

0.36

Birthweigh

t(100g)

0.40

<0.0001

0.31

<0.0001

0.25

0.004

0.86

0.79–0

.93

<0.001

Gestatio

nal

weigh

tgain

(kg)

0.06

0.42

0.14

0.08

0.11

0.16

1.05

0.99–1

.11

0.11

Shortexclusive

breastfee

ding

0.03

0.64

0.06

0.38

0.04

0.59

1.10

0.47–2

.61

0.82

Maternal

smoking

0.06

0.40

0.05

0.49

0.18

0.01

0.27

0.03–2

.96

0.28

Model

3

Highriskvs.low

risk–paren

talBMI

�0.05

0.55

0.18

0.02

0.80

0.14

�0.00

0.96

0.11

1.50

0.62–3

.62

0.37

Highriskvs.low

risk–paren

taled

ucatio

n0.18

0.02

0.16

0.04

0.15

0.06

1.06

0.44–2

.56

0.90

Gen

der

�0.07

0.32

�0.05

0.46

�0.11

0.16

1.39

0.65–2

.97

0.39

Birthweigh

t(100g)

0.40

<0.0001

0.31

<0.0001

0.25

0.001

0.86

0.79–0

.93

<0.001

Gestatio

nal

weigh

tgain

(kg)

0.06

0.46

0.14

0.08

0.07

0.36

1.05

0.99–1

.11

0.10

Shortexclusive

breastfee

ding

0.05

0.54

0.06

0.44

0.04

0.60

0.98

0.40–2

.40

0.96

Maternal

smoking

0.06

0.41

0.06

0.49

0.18

0.01

0.30

0.03–3

.26

0.32



high/low obesity risk as determined by parental BMI is anoutcome of a low statistical power, but these associationsare weak and may not be clinically relevant. The homoge-neity in the studied sample with regard to participants’ethnic background is also a limitation, as children of non-Nordic background show higher rates of obesity (28).Additionally, weight and height for three of the outcomevariables were measured at CHC centres, and the quality ofthese measures could be questioned. However, CHC nursesare very experienced in measuring infants, and the scalesused at CHC centres are calibrated yearly. Another limita-tion is that data on smoking during pregnancy were notavailable. Instead, we used the mother’s smoking status atbaseline, as it is likely that mothers who were smokers whenthe child was 1 year old were also smokers during the firsttrimester of the pregnancy. It should also be acknowledgedthat infant feeding and breastfeeding can be measured inseveral ways, and the potential impact of bottle-feeding oninfant growth was not tested in this study. Informationregarding infant temperament and problematic behaviour,which have also been recognised as potential contributingfactors to childhood obesity (29), was not available at thispoint in the Early STOPP study. Finally, estimates ofnonpaternity were not taken into account in this study.

The strength of this study is its inclusion of manypreviously identified early-life factors that potentially influ-ence early growth and later obesity development. Anthro-pometric measurements of both parents and childrenstrengthen the results by removing reporting biases (30).This study will facilitate the tracking of multiple potentialcausal risk factors for the development of obesity duringpreschool years in future research on the Early STOPPcohort.

CONCLUSIONWe have identified that infant growth up to 12 months isassociated with low parental education independently ofparental BMI, breastfeeding, birth weight and other early-life factors. Risk as defined by both parents’ BMI did nothave an important influence on children’s growth duringthe first year. We conclude that socio-economic factors areof importance for children’s growth early in infancy,probably through mechanisms other than parental adipos-ity. This indicates that parental support and educationdirected to families with low education are of majorimportance for early obesity prevention.

ACKNOWLEDGEMENTSWe thank all the participating families, the child healthcarenurses and Jan Kowalski who advised us on the statisticalprocedures. This study was funded by the Swedish Councilfor Working Life and Social Research, the Jerring Founda-tion, the Swedish Heart-Lung Foundation, the StockholmFree Masons’ Foundation for Children’s Welfare, HRHCrown Princess Lovisa’s Foundation, Nestl�e Healthy KidsProgramme and the Karolinska Institutet.

CONFLICT OF INTERESTThe authors declare no conflict of interest.

References

1. Ong KK, Loos RJ. Rapid infancy weight gain and subsequentobesity: systematic reviews and hopeful suggestions. ActaPaediatr 2006; 95: 904–8.

2. Baird J, Fisher D, Lucas P, Kleijnen J, Roberts H, Law C. Beingbig or growing fast: systematic review of size and growth ininfancy and later obesity. BMJ 2005; 331: 929.

3. Wijlaars LP, Johnson L, van Jaarsveld CH, Wardle J.Socioeconomic status and weight gain in early infancy. IntJ Obes (Lond) 2011; 35: 963–70.

4. Van Den Berg G, Van Eijsden M, Galindo-Garre F, Vrijkotte T,Gemke R. Low maternal education is associated with increasedgrowth velocity in the first year of life and in early childhood:the ABCD study. Eur J Pediatr 2013; 172: 1451–7.

5. Mihrshahi S, Battistutta D, Magarey A, Daniels LA.Determinants of rapid weight gain during infancy: baselineresults from the NOURISH randomised controlled trial. BMCPediatr 2011; 11: 99.

6. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH.Predicting obesity in young adulthood from childhood andparental obesity. N Engl J Med 1997; 337: 869–73.

7. Shrewsbury V, Wardle J. Socioeconomic status and adiposity inchildhood: a systematic review of cross-sectional studies 1990–2005. Obesity (Silver Spring) 2008; 16: 275–84.

8. Ludwig DS, Rouse HL, Currie J. Pregnancy weight gain andchildhood body weight: a within-family comparison. PLoS Med2013; 10: e1001521.

9. Oken E, Levitan EB, Gillman MW. Maternal smoking duringpregnancy and child overweight: systematic review andmeta-analysis. Int J Obes (Lond) 2008; 32: 201–10.

10. Weng SF, Redsell SA, Swift JA, Yang M, Glazebrook CP.Systematic review and meta-analyses of risk factors forchildhood overweight identifiable during infancy. Arch DisChild 2012; 97: 1019–26.

11. Maffeis C. Aetiology of overweight and obesity in children andadolescents. Eur J Pediatr 2000; 159(Suppl 1): S35–44.

12. Lakshman R, Zhang J, Koch FS, Marcus C, Ludvigsson J, OngKK, et al. Higher maternal education is associated withfavourable growth of young children in different countries.J Epidemiol Community Health 2013; 67: 595–602.

13. Johnson L, Llewellyn CH, van Jaarsveld CH, Cole TJ, Wardle J.Genetic and environmental influences on infant growth:prospective analysis of the Gemini twin birth cohort. PLoS One2011; 6: e19918.

14. Elks CE, Loos RJ, Sharp SJ, Langenberg C, Ring SM, TimpsonNJ, et al. Genetic markers of adult obesity risk are associatedwith greater early infancy weight gain and growth. PLoS Med2010; 7: e1000284.

15. Durmus B, Arends LR, Ay L, Hokken-Koelega AC, Raat H,Hofman A, et al. Parental anthropometrics, early growth andthe risk of overweight in pre-school children: the Generation RStudy. Pediatr Obes 2013; 8: 339–50.

16. Fleten C, Nystad W, Stigum H, Skjaerven R, Lawlor DA, DaveySmith G, et al. Parent-offspring body mass index associationsin the Norwegian Mother and Child Cohort Study: afamily-based approach to studying the role of the intrauterineenvironment in childhood adiposity. Am J Epidemiol 2012;176: 83–92.

17. Berkowitz RI, Stallings VA, Maislin G, Stunkard AJ. Growth ofchildren at high risk of obesity during the first 6 y of life:implications for prevention. Am J Clin Nutr 2005; 81: 140–6.



18. Sobko T, Svensson V, Ek A, Ekstedt M, Karlsson H, JohanssonE, et al. A randomised controlled trial for overweight and obeseparents to prevent childhood obesity–Early STOPP(STockholm Obesity Prevention Program). BMC Public Health2011; 11: 336.

19. Karlberg J, Luo ZC, Albertsson-Wikland K. Body mass indexreference values (mean and SD) for Swedish children. ActaPaediatr 2001; 90: 1427–34.

20. Linabery AM, Nahhas RW, Johnson W, Choh AC, Towne B,Odegaard AO, et al. Stronger influence of maternal thanpaternal obesity on infant and early childhood bodymass index:the Fels Longitudinal Study. Pediatr Obes 2013; 8: 159–69.

21. Svensson V, Jacobsson JA, Fredriksson R, Danielsson P, SobkoT, Schioth HB, et al. Associations between severity of obesityin childhood and adolescence, obesity onset and parental BMI:a longitudinal cohort study. Int J Obes (Lond) 2011; 35: 46–52.

22. Semmler C, Ashcroft J, van Jaarsveld CH, Carnell S, Wardle J.Development of overweight in children in relation to parentalweight and socioeconomic status. Obesity (Silver Spring) 2009;17: 814–20.

23. Howe LD, Tilling K, Galobardes B, Smith GD, Ness AR, LawlorDA. Socioeconomic disparities in trajectories of adiposity acrosschildhood. Int J Pediatr Obes 2011; 6: e144–53.

24. Monte S, Valenti O, Giorgio E, Renda E, Hyseni E, Faraci M,et al. Maternal weight gain during pregnancy and neonatal

birth weight: a review of the literature. J Prenat Med 2011; 5:27–30.

25. Gunnarsdottir I, Schack-Nielsen L, Michaelsen KF, SorensenTI, Thorsdottir I. Infant weight gain, duration of exclusivebreast-feeding and childhood BMI – two similar follow-upcohorts. Public Health Nutr 2010; 13: 201–7.

26. Stenhammar C, Sarkadi A, Edlund B. The role of parents’educational background in healthy lifestyle practices andattitudes of their 6-year-old children. Public Health Nutr 2007;10: 1305–13.

27. Wen LM, Baur LA, Simpson JM, Rissel C, Wardle K, FloodVM. Effectiveness of home based early intervention onchildren’s BMI at age 2: randomised controlled trial. BMJ2012; 344: e3732.

28. Moraeus L, Lissner L, Yngve A, Poortvliet E, Al-Ansari U,Sjoberg A. Multi-level influences on childhood obesity inSweden: societal factors, parental determinants and child’slifestyle. Int J Obes (Lond) 2012; 36: 969–76.

29. Faith MS, Hittner JB. Infant temperament and eating stylepredict change in standardized weight status and obesity risk at6 years of age. Int J Obes (Lond) 2010; 34: 1515–23.

30. Connor Gorber S, Tremblay M, Moher D, Gorber B. Acomparison of direct vs. self-report measures for assessingheight, weight and body mass index: a systematic review. ObesRev 2007; 8: 307–26.



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