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Maternal waist to hip ratio is a risk factor formacrosomiaW Salem,a,b AI Adler,c C Lee,d GCS Smithe,f

a Mayo Clinic College of Medicine, Rochester, Minnesota, USA b Institute of Public Health, Cambridge University, Cambridge, UKc Amanda I. Adler Institute of Metabolic Sciences and d Christine Lee Institute of Metabolic Sciences, Addenbrookes Hospital, Cambridge,

UK e Department of Obstetrics and Gynaecology, Cambridge University, Cambridge, UK f NIHR Cambridge Comprehensive

Biomedical Research Centre, Cambridge, UK

Correspondence:Prof GCS Smith, Department of Obstetrics and Gynaecology, Cambridge University, Rosie Maternity Hospital, Cambridge,

CB2 2SW, UK. Email gcss2@cam.ac.uk

Accepted 24 August 2011. Published Online 18 October 2011.

Objective Fetal growth during pregnancy may be affected by the

metabolic activity and distribution of fat stores in women. This

study investigates the association between waist to hip ratio

(WHR) as a measure of the distribution of adiposity in

primiparous mothers living in Avon, England, and macrosomia

in their offspring.

DesignProspective historical cohort study.

SettingThe Avon Longitudinal Study of Parents and Children

(ALSPAC) prospective cohort study in Avon, UK.

PopulationA cohort of 3083 primiparous women with a term

singleton delivery with expected dates of delivery from 1 April

1991 to 31 December 1992.

MethodsThe distribution of WHR was categorised into quartiles.

We compared the second, third and fourth quartiles against thefirst (reference) quartile with respect to whether the mother

delivered a macrosomic newborn. We controlled for maternal age,

gestational age, body mass index (BMI), marital status and racial

group using multivariate logistic regression.

Main outcome measures Macrosomia defined in three ways:

birthweight 4000 g; birthweight 4500 g; large for gestational

age (LGA: 95th percentile of birth weight adjusted for sex and

gestational age).

ResultsWaist to hip ratios in the third and fourth quartiles were

associated with a higher odds of delivering a macrosomic infant,

defined as a birthweight 4000 g (third quartile, OR 1.59, 95%

CI 1.122.26; fourth quartile, OR 1.69, 95% CI 1.182.42) or as LGA

(95th percentile of the cohort; third quartile, OR 1.77, 95% CI 1.10

2.85; fourth quartile, OR 1.78, 95% CI 1.092.91). When defined as a

birthweight 4500 g, the fourth quartile was associated with increased

odds of macrosomia (OR 2.74, 95% CI 1.057.16). Odds ratios after

adjustment for confounding factors followed a similar pattern.

Conclusion Independent of confounding factors, women with

increased WHRs were significantly more likely to give birth tomacrosomic newborns.

KeywordsAvon Longitudinal Study of Parents and Children, hip,

macrosomia, obesity, sensitivity, specificity, waist.

Please cite this paper as: Salem W, Adler A, Lee C, Smith G. Maternal waist to hip ratio is a risk factor for macrosomia. BJOG 2012;119:291297.

Introduction

The incidence of macrosomia is increasing, along with the

rising incidence of maternal obesity and overweight.1,2

Macrosomia leads to adverse clinical and social conse-quences for both the mother and the infant. Stillbirth

rates are higher in macrosomic infants than those of nor-

mal weight.3 Liveborn macrosomic newborns are at

increased risk of neonatal morbidity, most notably from

shoulder dystocia.46 Overall, macrosomic newborns are

more likely than normal weight newborns to be admitted

to the neonatal intensive care unit.7 Mothers of macro-

somic infants are more likely to deliver by caesarean

section, by an operative delivery and to suffer higher rates

of obstetric injury.

The contribution of obesity to the rates of large-for-ges-

tational-age (LGA) infants has tripled since 1980.8 In the

UK, 20% of women registering for maternity care areobese.911 The coexistent problem of maternal obesity and

macrosomia has stimulated a substantial body of research

addressing prenatal and early pregnancy predictors of fetal

macrosomia. A study of over 115 000 women in Alberta,

Canada, found that the most modifiable risk factor to

reduce term LGA infants was to have a weight of

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increased risk of a macrosomic birth in comparison with

women of normal weight.2 Pre-pregnancy obesity has been

found to be a risk factor for macrosomia in diabetic

women with treated euglycaemia during pregnancy. An

increased maternal body mass index (BMI) is associated

with an increase in fetal macrosomia.2,13,14 However, only

the extremes of BMI or large increases in BMI (>25%)

during pregnancy are strongly associated with macroso-

mia,15 suggesting that small deviations from an ideal BMI

have little consequence on fetal macrosomia. Although

maternal obesity, estimated by BMI, is the most widely

used indicator for the risk of fetal macrosomia, BMI does

not account for differences in bone density or capture

information on the distribution of adiposity, and increases

with parity.1618 These elements of BMI limit its utility as a

proxy measure of adiposity.

The waist to hip ratio (WHR), an alternative measure of

obesity, captures information about central adiposity, and

accounts for differences in the density and distribution of

lean versus adipose tissue. It also accommodates differencesin bone density and is minimally affected by parity.19

When compared with BMI, WHR is a better predictor of

other disorders related to obesity.2022 It is plausible that

WHR may be of particular value in obstetrics as the

increase in weight in early pregnancy affects WHR less than

it does BMI. WHR is largely unaffected until approximately

20 weeks of gestation, when the fundus reaches the level of

the umbilicus. Moreover, there is evidence that the distri-

bution of fat in pregnant women may differentially affect

intrauterine fetal growth independently of the total fat

mass.23,24 Despite this, there are no previous studies, to our

knowledge, that have compared the risk of fetal macroso-

mia in relation to maternal WHR. The aim of the present

study was to determine the relationship between maternal

WHR and the risk of fetal macrosomia using three com-

mon measures: namely, birthweight 4000 g; birth-

weight 4500 g; and LGA (95th percentile, adjusted for

sex and gestational age).

Methods

Study populationThe Avon Longitudinal Study of Parents and Children (AL-

SPAC), a prospective population-based cohort study,

enrolled pregnant women in Avon, UK, with expecteddates of delivery from 1 April 1991 to 31 December 1992.

This was a secondary analysis of the main cohort study.

The original study design is described in detail else-

where.25,26 Ethical approval for the study was obtained

from the ALPSAC Law and Ethics Committee and the local

research ethics committees. Enrolment of the study partici-

pants started as early in the antenatal period as possible.

Of all eligible women, approximately 85% responded and

were included in the study. Among these, 3083 (45%) had

valid measures for WHR assessment and analysis. Partici-

pants were asked to complete questionnaires at home in

the prenatal period that addressed demographic and life-

style factors. At enrolment in the ALSPAC study, partici-

pants answered a postal questionnaire including

information about racial group, pre-pregnancy weight,

height, waist circumference, hip circumference as well as

marital status, parity and smoking habits prior to their

pregnancy. Birth records provided the birth weights of

newborns. Gestational age was ascertained by using the last

menstrual period and then adjusted for estimation of gesta-

tional age by ultrasound, if available.

The inclusion criteria for the current study were nullipa-

rous women, delivering a singleton liveborn infant in

labour at term, who had documented WHR and infant

birthweight. We used a database constructed from a previ-

ous study using the ALSPAC cohort with the addition of a

WHR measure.27

Anthropometric measurementsWaist circumference was measured at home by the partici-

pant as the narrowest point around the waist between the

lower rib margin and the iliac crest. The hip circumference

was measured as the widest circumference around the but-

tocks.28 The unit-less WHR is the waist circumference

divided by the hip circumference. Participants were made

aware of the required measurements after initial enrolment,

and reported their pre-pregnancy waist and hip measure-

ments in a first-trimester questionnaire.

Exposure and outcome definitionsTo investigate whether maternal WHR was associated with

fetal macrosomia, we categorised the distribution of WHR

into four quartiles using the first quartile as the reference

group. This allowed a comparison across quartiles using

multivariate analysis while adjusting for possible confound-

ing factors. Potential confounding factors included age,

BMI, racial group, smoking status and gestational age.

We analysed all covariates as categorical variables. Age in

years was categorised as

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Statistical analysisWe described the characteristics at baseline, stratified by

quartiles of WHR, using medians and interquartile ranges

for continuous variables and percentages for categorical

variables. We used KruskallWallis and v2 tests to deter-

mine whether the continuous and categorical variables dif-

fered across quartiles of WHR. We used univariate and

multivariate logistic regression analyses to explore the asso-

ciation between WHR and three measures of macrosomia:

birthweight 4000 g; birthweight 4500 g; and LGA

(95th percentile for weight). Odds ratios (ORs), presented

with 95% confidence intervals (95% CIs), using the lowest

quartile of WHR as the reference category, were used to

investigate the association between WHR and the risk of

macrosomia. We included the covariates in multivariate

models if they were associated (P < 0.1) with the exposure

(WHR) and outcomes (measures of macrosomia) or if they

were of a priori clinical relevance. We replaced missing val-

ues of each covariate by the median value of that variable.

We reported the P value for a linear trend across quartilesof WHR. All statistical analyses were performed using

stata 10.1 (Stata Corporation, College Station, TX, USA).

Results

The ALSPAC study cohort comprised 14 541 pregnant

women who were enrolled by 19 July 1999. Of all singleton

term deliveries meeting the inclusion criteria for our study,

3083 (45%) had valid measures for WHR assessment and

analysis. Table 1 includes the descriptive characteristics of

the cohort. Women without WHR measures were found to

have similar characteristics as the cohort studied. The value

of WHR for each quartile was 0.68, 0.71, 0.75 and 0.81.

White participants constituted 97.6% of the cohort. Age,

BMI and smoking status differed across WHR quartiles.

Table 2 describes the relationship between the quartiles

of WHR and three different measures of macrosomia:

birthweight 4000 g; birthweight 4500 g; and LGA

(95th percentile of the cohort). An increasing WHR was

significantly associated with a birthweight 4000 g in both

unadjusted and adjusted analysis. In multivariate analysis,

relative to the first quartile, women in the third and fourth

quartile representing those with the largest WHRs were at

an increased risk (third quartile, OR 1.58, 95% CI 1.10

2.26, P= 0.02; fourth quartile, OR 1.57, 95% CI 1.072.30,

P= 0.01) of a macrosomic delivery, independent of age,

BMI, smoking status, racial group and gestational age. The

same comparison in a univariate analysis also yielded an

increased risk for a macrosomic delivery (third quartile,

OR 1.59, 95% CI 1.122.26, P< 0.01; fourth quartile,

OR 1.69, 95% CI 1.182.42, P< 0.01). We observed a

trend for increased odds of macrosomia with increasing

quartiles of WHR (OR 1.17, 95% CI 1.041.31, P= 0.01).

Table 1. Characteristics of the cohort by WHR quartile

Cohort

n = 3083

WHR quartile P*

1

(n= 805)

2

(n = 766)

3

(n= 817)

4

(n= 695)

WHR 0.68 (0.670.69) 0.71 (0.700.72) 0.75 (0.740.76) 0.81 (0.780.85)

Age (years) 28 (2531) 28 (2531) 28 (2531) 28 (2531) 26 (2330) 0.0001Height (cm) 165 (160170) 165 (160168) 165 (160169) 165 (160170) 165 (160170) 0.71

BMI (kg/m2) 21.7 (20.323.4) 21.5 (20.022.7) 21.5 (20.222.7) 21.7 (20.523.3) 22.2 (20.724.6) 0.0001

Gestational age (weeks) 40 (3941) 40 (3941) 40 (3941) 40 (3941) 40 (3941) 0.53

Nonsmoker (%) 85.5 86.1 87.6 86.8 80.9 0.001

Non-white ethnicity (%) 2.4 1.6 2.9 2.7 2.3 0.36

Spontaneous birth (%) 77.3 77.6 78.7 75.8 77.3 0.57

Data expressed as median (interquartile range), unless otherwise stated.

*Pvalue is for a linear trend across quartile of WHR.

Table 2. Unadjusted and adjusted odds ratios for birthweight

4.0 kg

Unadjusted

OR (95% CI)

P Adjusted

OR (95% CI)

P

Quartile of WHR

1 (referent) (1.0) (1.0)

2 1.24 (0.851.80) 0.26 1.28 (0.871.87) 0.21

3 1.59 (1.122.26)

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We noted that WHR was also independently associated

with a newborn weighing over 4.5 kg in unadjusted models

for the highest quartile of WHR (OR 2.74, 95% CI 1.05

7.16, P = 0.04; Table 3). This was supported by a statisti-

cally significant trend for an increased odds of macrosomia

with increasing WHR quartiles across unadjusted and

adjusted models (unadjusted OR 1.44, 95% CI 1.051.98,

P= 0.02; adjusted OR 1.40, 95% CI 1.011.93, P= 0.05).

When evaluating macrosomia based on a birth-

weight 95th percentile, we observed an increased odds of

delivering a macrosomic infant in the highest quartile in

the unadjusted analysis (OR 1.78, 95% CI 1.092.91,

P = 0.02), as can be seen in Table 4. We also observed an

increasing trend in both unadjusted and adjusted models

(unadjusted OR 1.21, 95% CI 1.051.41, P= 0.01; adjusted

OR 1.18, 95% CI 1.011.37, P= 0.04).

Discussion

This study demonstrated that an increasing maternal WHRwas associated with a greater risk of macrosomia. The asso-

ciation maintained statistical significance using three differ-

ent definitions of macrosomia independently of other

maternal characteristics. The finding was consistent with

the only other known study that investigated the associa-

tion between WHR and newborn size.29 Following 702

women, the study used multiple linear regression to assess

the effect of maternal WHR on birthweight. However, the

present study is the first study, to our knowledge, to exam-

ine the relationship between WHR and macrosomia. Deliv-

ery of a macrosomic infant is associated with an increased

chance of caesarean section and maternal injury during

labour.4,30 For the neonate, macrosomia is associated with

increased morbidity and mortality, in particular shoulder

dystocia and the need for resuscitation.7,31 The findings

from this study suggest that the distribution of adiposity in

the mother is an important determinant of macrosomia in

the infant. The precise aetiology of this relationship is

unknown, but this study proposes the notion that central

adiposity has a particular effect on the metabolic milieu in

pregnancy.

Studies relating maternal weight composition and new-born size go back to the Marseilles physician, Jean Vague,32

who in 1956 described macrosomia to be associated with

an android-type distribution of fat in the mother. Studies

using BMI as a measure of macrosomia have found a posi-

tive association between increasing BMI and an increased

risk of a macrosomic newborn. Women with morbid obes-

ity based on BMI have a significantly increased risk of hav-

ing a macrosomic infant (OR 4.78, 95% CI 3.865.92).2

Studies also indicate that based on BMI obese mothers are

more likely to have macrosomic infants that need higher

level nursery admissions and suffer from more complica-

tions.14 A study of fetal macrosomia and maternal adipos-

ity, as measured by magnetic resonance imaging (MRI),

found an association between several metrics and macroso-

mia.33 Maternal adiposity, measured by waist circumference

between 20 and 28 weeks of gestation, also predicted

macrosomia when the waist size exceeded 82 cm.34 Overall,

studies tend to indicate that severe obesity, generally mea-

sured by BMI, is predictive of macrosomia. Consequently,

it has been suggested that limited weight gain for pregnant

women who are obese may decrease macrosomia.35

We extend this previous work by showing that the distribu-

tion of fat is also predictive of macrosomia, having

accounted for total body fat as estimated by BMI. Our

study further suggests that central adiposity in particularmay be a major determinant of macrosomia.

This study has some weaknesses inherent in the data

collection of the ALSPAC cohort. The data set lacked infor-

mation on gestational diabetes, and thus it could not be

included in our multivariate models. Previous studies

addressing maternal obesity and macrosomia that were able

to control for gestational diabetes as a covariate observed

minimal confounding by gestational diabetes.24 Moreover,

Table 3. Unadjusted and adjusted odds ratios for birthweight

4.5 kg

Unadjusted

OR (95% CI)

P Adjusted*

OR (95% CI)

P

Quartile of WHR

1 (referent) (1.0) (1.0)

2 1.05 (0.34-3.27) 0.93 1.20 (0.373.86) 0.76

3 1.48 (0.534.19) 0.46 1.64 (0.564.78) 0.37

4 2.74 (1.057.16) 0.04 2.63 (0.957.26) 0.06

Trend 1.44 (1.051.98) 0.02 1.40 (1.011.93) 0.05

*Odds ratios and 95% confidence intervals adjusted for maternal

age, BMI, smoking status, ethnicity, and gestational age.

Table 4. Unadjusted and adjusted odds ratios for birthweight

95th percentile of cohort

Unadjusted

OR (95% CI)

P Adjusted*

OR (95% CI)

P

Quartile of WHR

1 (referent) (1.0) (1.0)

2 1.37 (0.832.27) 0.22 1.44 (0.862.42) 0.17

3 1.77 (1.102.85) 0.02 1.77 (1.092.89) 0.02

4 1.78 (1.092.91) 0.02 1.63 (0.972.73) 0.06

Trend 1.21 (1.051.41) 0.01 1.18 (1.011.37) 0.04

*Odds ratios and 95% confidence intervals adjusted for maternal

age, BMI, smoking status, ethnicity, and gestational age.

Salem et al.

294 2011 The Authors BJOG An International Journal of Obstetrics and Gynaecology 2011 RCOG

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previous population-based studies indicated that BMI was

a more important determinant of macrosomia than gesta-

tional diabetes.3638 In the study relating WHR to newborn

size, gestational diabetes was not predictive in any of the

regressions and was dropped from all models.29 These

findings suggest that it is plausible that adjustment for ges-

tational diabetes would not have significantly altered the

associations observed. A previous study demonstrated that

the incidence of gestational diabetes during pregnancy in

this population in Avon was approximately 0.5%, suggest-

ing that adjustment would have had little impact on the

observed trends.39

As WHRs in this study were self-measured and self-

reported, the possibility of the misclassification of exposure

exists. Poor self-measurement of WHR would probably

lead to noise in the data set rather than to bias. Self-

reported waist and hip measurements have been validated

for use in epidemiological studies.28 No values for WHR

were gross outliers, but we were unable to collect data on

women with unreported WHR measurements. Improvedtechniques and methods to assess body fat distribution

may be clinically more useful than BMI or self-reported

WHRs. It is also plausible that unknown uteroplacental fac-

tors may emerge during the first trimester that may also

affect WHR measurements. Overall, the rigorous study

design of the ALSPAC cohort serves to minimise bias and

misclassification whenever possible, and the large sample

size allows for less chance variation in the demonstrated

results.

Our findings suggest that the distribution of fat in preg-

nant woman may have an important role with relation to

the health of offspring. An excess of central fat is associated

with increased levels of triglycerides and free fatty acids in

the general population.4042 Central fat distribution is also

associated with decreased sensitivity to insulin and

increased fasting glucose levels.43 It has been previously

demonstrated that elevated triglyceride levels in pregnant

women, seen typically in individuals with metabolic

syndrome [high-density lipoprotein (HDL) cholesterol,

decreased HDL cholesterol and increased insulin, all

measured in plasma], were independent determinants of

macrosomia in the fetus.24 Individuals with metabolic syn-

drome tend to have an excess of central adiposity, and thus

an increased WHR. Moreover, fetal blood glucose and free

fatty acids increase with increases in maternal levels.44

Overweight and obese women have also been shown to

have higher serum levels of leptin.45 Increased levels of lep-

tin in cord blood have been associated with LGA infants.

Hence, the mechanism that links increased WHR to macro-

somia may be complex, and hyperglycaemia is just one of

several factors that may explain the association. Future

studies investigating the relationship between maternal adi-

posity and newborn macrosomia are necessary in order to

better understand the underlying mechanism, and to

decrease the associated morbidity and mortality to the

infant and mother. Prospective studies assessing WHR, and

other methods that better assess body fat distribution and

plasma levels of glucose and triglycerides, may be helpful

to evaluate the possible association and causative factors

linking central maternal adiposity and macrosomia.

Conclusion

This study found a strong association between WHR and

the delivery of a macrosomic newborn independent of

BMI. This association suggests that central adiposity may

be linked with the mechanism leading to macrosomia in

the newborn. This study establishes a basis for investigating

the metabolic aetiology of macrosomia in mothers who

have increased central adiposity.

Disclosure of interests

The authors have no competing interests in relation to thiswork.

Contribution to authorshipAll authors were involved in the writing and editing of this

article. CL and WS carried out statistical analysis and data

interpretation.

Details of ethics approvalThe analysis is covered by the ALSPAC ethical approval,

given by Bristol and Weston Health Authority (ref. E1808)

on 28 November 1989.

FundingThe data extraction and analysis were funded through

National Institute for Health Research (NIHR) Senior

Investigator funding to G.C.S.S. and through the NIHR

Cambridge Comprehensive Biomedical Research Centre.

AcknowledgementsWe are grateful to all the families who took part in this

study, the midwives for their help in recruiting and the

whole ALSPAC team, which includes interviewers, com-

puter and laboratory technicians, clerical workers, research

scientists, volunteers, managers, receptionists and nurses.

The UK Medical Research Council, the Wellcome Trustand the University of Bristol provided core support for

ALSPAC.j

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