DOI: 10.1111/j.1471-0528.2011.03167.x www.bjog.

org

Epidemiology

Maternal waist to hip ratio is a risk factor for macrosomia

W Salem,a,b AI Adler,c C Lee,d GCS Smithe,f
Mayo Clinic College of Medicine, Rochester, Minnesota, USA b Institute of Public Health, Cambridge University, Cambridge, UK 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
c a

Accepted 24 August 2011. Published Online 18 October 2011.

Objective Fetal growth during pregnancy may be affected by the

Main outcome measures Macrosomia dened in three ways:

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.
Design Prospective historical cohort study. Setting The Avon Longitudinal Study of Parents and Children

birthweight 4000 g; birthweight 4500 g; large for gestational age (LGA: 95th percentile of birth weight adjusted for sex and gestational age).
Results Waist to hip ratios in the third and fourth quartiles were associated with a higher odds of delivering a macrosomic infant, dened 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 dened 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

(ALSPAC) prospective cohort study in Avon, UK.

Population A cohort of 3083 primiparous women with a term singleton delivery with expected dates of delivery from 1 April 1991 to 31 December 1992. Methods The distribution of WHR was categorised into quartiles.

We compared the second, third and fourth quartiles against the rst (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.

increased WHRs were signicantly more likely to give birth to macrosomic newborns.
Keywords Avon Longitudinal Study of Parents and Children, hip,

macrosomia, obesity, sensitivity, specicity, 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 consequences for both the mother and the infant. Stillbirth rates are higher in macrosomic infants than those of normal 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 macrosomic 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-gestational-age (LGA) infants has tripled since 1980.8 In the UK, 20% of women registering for maternity care are obese.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 modiable risk factor to reduce term LGA infants was to have a weight of <91 kg before pregnancy.12 A study based in Manchester, UK, found that morbidly obese women had a nearly ve-fold

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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 macrosomia,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 differences in 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 distribution 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 macrosomia 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 common measures: namely, birthweight 4000 g; birthweight 4500 g; and LGA (95th percentile, adjusted for sex and gestational age).

were included in the study. Among these, 3083 (45%) had valid measures for WHR assessment and analysis. Participants were asked to complete questionnaires at home in the prenatal period that addressed demographic and lifestyle factors. At enrolment in the ALSPAC study, participants 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 gestational age by ultrasound, if available. The inclusion criteria for the current study were nulliparous women, delivering a singleton liveborn infant in labour at term, who had documented WHR and infant birthweight. We used a database constructed from a previous study using the ALSPAC cohort with the addition of a WHR measure.27

Anthropometric measurements
Waist circumference was measured at home by the participant 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 buttocks.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 measurements in a rst-trimester questionnaire.

Exposure and outcome denitions

To investigate whether maternal WHR was associated with fetal macrosomia, we categorised the distribution of WHR into four quartiles using the rst quartile as the reference group. This allowed a comparison across quartiles using multivariate analysis while adjusting for possible confounding 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 <20, 2024, 2529 (reference), 30 34, 3539 and 40. BMI (kg/m2) was categorised as <20, 2024.9 (reference), 2529.9, 3034.9 and 35. Gestational age (in weeks) was categorised as 37, 38, 39, 40 (reference), 41, 42 and 43. We coded smoking as yes or no, and racial group as white or non-white. Data on blood glucose or gestational diabetes during pregnancy was not available, and therefore could not be included as a covariate. The outcomes of interest were described by three measures of macrosomia: birthweight 4000 g; birthweight 4500 g; and LGA (95th percentile for weight). We did not adjust for maternal height because it was highly correlated with maternal BMI (body weight/height squared).

Methods
Study population
The Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective population-based cohort study, enrolled pregnant women in Avon, UK, with expected dates 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 elsewhere.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 participants started as early in the antenatal period as possible. Of all eligible women, approximately 85% responded and

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Statistical analysis
We described the characteristics at baseline, stratied by quartiles of WHR, using medians and interquartile ranges for continuous variables and percentages for categorical variables. We used KruskallWallis and v2 tests to determine whether the continuous and categorical variables differed across quartiles of WHR. We used univariate and multivariate logistic regression analyses to explore the association 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% condence 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 values of each covariate by the median value of that variable. We reported the P value for a linear trend across quartiles of WHR. All statistical analyses were performed using stata 10.1 (Stata Corporation, College Station, TX, USA).

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 signicantly associated with a birthweight 4000 g in both unadjusted and adjusted analysis. In multivariate analysis, relative to the rst 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 2. Unadjusted and adjusted odds ratios for birthweight 4.0 kg Unadjusted OR (95% CI) Quartile of WHR 1 (referent) (1.0) 2 1.24 (0.851.80) 3 1.59 (1.122.26) 4 1.69 (1.182.42) Trend 1.20 (1.071.34) P Adjusted OR (95% CI) P

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.

0.26 <0.01 <0.01 <0.01

(1.0) 1.28 1.58 1.57 1.17

(0.871.87) (1.102.26) (1.072.30) (1.041.31)

0.21 0.01 0.02 0.01

Odds ratios and 95% condence intervals adjusted for maternal age, BMI, smoking status, ethnicity and gestational age.

Table 1. Characteristics of the cohort by WHR quartile Cohort n = 3083 1 (n = 805) WHR Age (years) Height (cm) BMI (kg/m2) Gestational age (weeks) Nonsmoker (%) Non-white ethnicity (%) Spontaneous birth (%) 0.68 28 165 21.5 40 86.1 1.6 77.6 (0.670.69) (2531) (160168) (20.022.7) (3941) WHR quartile 2 (n = 766) 0.71 28 165 21.5 40 87.6 2.9 78.7 (0.700.72) (2531) (160169) (20.222.7) (3941) 3 (n = 817) 0.75 28 165 21.7 40 86.8 2.7 75.8 (0.740.76) (2531) (160170) (20.523.3) (3941) 4 (n = 695) 0.81 26 165 22.2 40 80.9 2.3 77.3 (0.780.85) (2330) (160170) (20.724.6) (3941) P*

28 165 21.7 40 85.5 2.4 77.3

(2531) (160170) (20.323.4) (3941)

0.0001 0.71 0.0001 0.53 0.001 0.36 0.57

Data expressed as median (interquartile range), unless otherwise stated. *P value is for a linear trend across quartile of WHR.

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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 statistically signicant 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 birthweight 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 WHR was associated with a greater risk of macrosomia. The association maintained statistical signicance using three differ-

Table 3. Unadjusted and adjusted odds ratios for birthweight 4.5 kg Unadjusted OR (95% CI) Quartile of WHR 1 (referent) (1.0) 2 1.05 (0.34-3.27) 3 1.48 (0.534.19) 4 2.74 (1.057.16) Trend 1.44 (1.051.98) P Adjusted* OR (95% CI) P

0.93 0.46 0.04 0.02

(1.0) 1.20 1.64 2.63 1.40

(0.373.86) (0.564.78) (0.957.26) (1.011.93)

0.76 0.37 0.06 0.05

*Odds ratios and 95% condence 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) Quartile of WHR 1 (referent) (1.0) 2 1.37 (0.832.27) 3 1.77 (1.102.85) 4 1.78 (1.092.91) Trend 1.21 (1.051.41) P Adjusted* OR (95% CI) P

0.22 0.02 0.02 0.01

(1.0) 1.44 1.77 1.63 1.18

(0.862.42) (1.092.89) (0.972.73) (1.011.37)

0.17 0.02 0.06 0.04

*Odds ratios and 95% condence intervals adjusted for maternal age, BMI, smoking status, ethnicity, and gestational age.

ent denitions of macrosomia independently of other maternal characteristics. The nding was consistent with the only other known study that investigated the association 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 rst study, to our knowledge, to examine the relationship between WHR and macrosomia. Delivery 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 ndings 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 newborn 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 positive association between increasing BMI and an increased risk of a macrosomic newborn. Women with morbid obesity based on BMI have a signicantly increased risk of having 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 complications.14 A study of fetal macrosomia and maternal adiposity, as measured by magnetic resonance imaging (MRI), found an association between several metrics and macrosomia.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 measured 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 distribution 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 particular may be a major determinant of macrosomia. This study has some weaknesses inherent in the data collection of the ALSPAC cohort. The data set lacked information 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,

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previous population-based studies indicated that BMI was a more important determinant of macrosomia than gestational 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 ndings suggest that it is plausible that adjustment for gestational diabetes would not have signicantly 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%, suggesting that adjustment would have had little impact on the observed trends.39 As WHRs in this study were self-measured and selfreported, the possibility of the misclassication of exposure exists. Poor self-measurement of WHR would probably lead to noise in the data set rather than to bias. Selfreported 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. Improved techniques 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 factors may emerge during the rst trimester that may also affect WHR measurements. Overall, the rigorous study design of the ALSPAC cohort serves to minimise bias and misclassication whenever possible, and the large sample size allows for less chance variation in the demonstrated results. Our ndings suggest that the distribution of fat in pregnant 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 syndrome 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 leptin in cord blood have been associated with LGA infants. Hence, the mechanism that links increased WHR to macrosomia may be complex, and hyperglycaemia is just one of several factors that may explain the association. Future studies investigating the relationship between maternal adiposity 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 this work.

Contribution to authorship
All authors were involved in the writing and editing of this article. CL and WS carried out statistical analysis and data interpretation.

Details of ethics approval

The analysis is covered by the ALSPAC ethical approval, given by Bristol and Weston Health Authority (ref. E1808) on 28 November 1989.

Funding
The 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.

Acknowledgements
We 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, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. The UK Medical Research Council, the Wellcome Trust and the University of Bristol provided core support for ALSPAC. j

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