Population-based trends and correlates of maternal overweight and obesity, Utah 1991-2001

Population-based trends and correlates of maternal overweight and obesity, Utah 1991-2001

American Journal of Obstetrics and Gynecology (2005) 192, 832–9 www.ajog.org Population-based trends and correlates of maternal overweight and obesi...

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American Journal of Obstetrics and Gynecology (2005) 192, 832–9

www.ajog.org

Population-based trends and correlates of maternal overweight and obesity, Utah 1991-2001 D. Yvette LaCoursiere, MD, MPH,a,* Lois Bloebaum, BSN,b Jeffrey D. Duncan, MS,b Michael W. Varner, MDc Department of Obstetrics and Gynecology, University of Utah Health Sciences Center,a Utah Department of Health,b Division of Maternal Fetal Medicine,c University of Utah Health Sciences Center, Salt Lake City, Utah Received for publication August 2, 2004; revised November 5, 2004; accepted November 15, 2004

KEY WORDS Maternal obesity Trends Cesarean section

Objective: This study aims to identify recent population-based trends in maternal overweight and obesity and adverse outcomes. Study design: Statewide retrospective cohort study of birth certificate data for live singleton births to women in Utah between 1991 and 2001. Results: Prepregnancy overweight and obesity increased from 25.1% in 1991 to 35.2% in 2001, a 40.2% increase (prevalence ratio [PR] 1.40 [1.37-1.43]), whereas maternal obesity at delivery rose 36.2% from 28.7% to 39.1% (PR 1.36 [1.33-1.39]). The attributable fraction of cesarean delivery in overweight and obese women was 0.388 (0.369-0.407). Statewide, among all women having a cesarean delivery in 2001, 1 in 7 is attributable to overweight and obesity. Conclusion: This is the first state-wide analysis of maternal obesity trends demonstrating a significant increase in maternal overweight and obesity. Overweight and obese women are at increased risk of cesarean delivery, preeclampsia, eclampsia, dystocia, and macrosomia, risks that increase as the body mass index rises. Ó 2005 Elsevier Inc. All rights reserved.

More than 127 million American adults are overweight (body mass index [BMI] O25), 60 million are obese (BMI O30), and 9 million are severely obese (BMI O40).1 In 1999 through 2000, 62% of women were overweight, 34% were obese, and 6% were severely obese, a significant increase when compared with the National Health and Nutrition Examination Survey (NHANES) data from 1988 to 1994.2,3 In Utah, 40% Supported by K12 Women’s Reproductive Health Research Scholar (D.Y.L.). * Reprint requests: D. Yvette LaCoursiere, MD, MPH, 30 N 1900 E, Suite 2B200, Salt Lake City, UT 84132. E-mail: [email protected] 0002-9378/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajog.2004.11.034

of women of all ages are overweight or obese.4 Despite the increasing prevalence of overweight and obesity in women in the United States,2,5,6 there has been less attention paid to the trends among pregnant women. National studies that identify trends in BMIs, including the NHANES and the Behavioral Risk Factor Surveillance System (BRFSS) systematically exclude pregnant women from their analyses.2,5 The 2 existing analyses of temporal trends in maternal obesity among American women report an increase in maternal obesity as defined as weight greater than 200 lb over the past 2 decades. These studies are limited to institutionally based samples with high proportions of African American women.7,8 Research suggests that

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African American women have higher BMIs, and thus these data may overestimate the prevalence of maternal obesity in other populations.2,7 There are no temporally based analyses that use maternal BMI to define maternal obesity. An analysis that uses BMI greater than 25 in lieu of absolute weight greater than 200 lb will include women previously excluded from trend studies. These women previously excluded may in fact have increased risks. Studies have shown that obese pregnant women are at increased risk for adverse pregnancy outcomes including diabetes, preeclampsia, preterm labor, induction, cesarean delivery, anesthetic complications, postpartum hemorrhage, maternal infection, macrosomia, fetal anomalies, intrauterine fetal demise, and early neonatal death.7-17 As obesity prevalence increases, the absolute number of patients affected by weight-related adverse pregnancy outcomes will also increase. The objectives of this study are to identify recent population-based trends in maternal overweight and obesity in Utah, both preconceptionally and at delivery, to describe the correlates associated with maternal overweight and obesity, and to estimate the impact on overall disease burden.

BMI and overweight obesity

Material and methods

Data analysis and statistical methods

Data source

Data analysis was performed with SPSS 12.0 (SPSS, Inc, Chicago, Ill). Extreme values were evaluated and erroneous weight and height data were excluded listwise. Trends in the prepregnancy and delivery BMI distributions were examined with the use of a percentile comparison plot. The slope of the line representing the aggregate overweight and/or obese was fit using the method of least squares. The trend analysis by year was performed with the c2 test for trend. The c2 analysis was used to compare the proportion of overweight and obese women in the first and last year of the study. An a priori list of independent and dependent variables were selected. For analyses of outcomes, only the first pregnancy for each woman delivering in the interval was included in the analyses to avoid the effect of repeat measures. For multiple logistic regression models, only data after 1997 were included, because UDOH began discriminating preexisting from gestational diabetes only after this date. Multiple logistic regression was used for analysis of BMI and outcomes. Ordinal scaled data were coded by using dummy variables. The variables were entered in block. Maternal age, parity, gestational age, and weight gain were included as continuous variables. Definitions of the variables include the following: parity was the number of prior deliveries over 20 weeks’ gestation, weight gain was included as number of pounds gained from preconception to delivery, preeclampsia was determined by provider documentation of disease that includes elevated blood pressure and proteinuria,

Institutional Review Board approval was obtained. Birth certificate information was collected and compiled into a computerized database by the Utah Department of Health (UDOH), Office of Vital Statistics. This solitary database contains demographic, antepartum, delivery, and postpartum information. All live singleton births between January 1991 and December 2001 were included in the primary analysis. The risk factor and outcome data were completed by the care provider and abstracted by a birth certificate specialist. The computerized birth certificate data undergo routine quality assessment by the UDOH. Each hospital contributing to the database is reviewed at least annually. A random sample of patients is selected. The medical record is compared with the information submitted on the birth record. UDOH data have not been published. Published data have revealed moderate-to-good concordance between the medical record and birth certificates on the following variables: race (k = 0.868), nulliparity (k = 0.969), gestational diabetes (k = 0.545), pregnancy-induced hypertension (k = 0.404), gestational age (k = 0.726), birth weight (k = 0.976), and delivery type (k = 0.963).18 Events with low prevalence were less likely to yield reliable results. Secondary to this finding, we have attempted to limit our analyses to include variables that have shown moderate-to-good correlation in the literature.

We determined the annual prevalence of maternal overweight and obesity using BMI (kg/m2). BMI was calculated by using height and weight data that were collected during postpartum hospitalization. Prepregnancy BMI was calculated by using self-reported height and prepregnancy weight, whereas delivery BMI was calculated by adding the self-reported prepregnancy weight to the pregnancy weight gain. With the use of prepregnancy and delivery BMI, each woman was stratified into a BMI category according to the International Obesity Task Force classification: underweight less than 19, normal weight 19 to 24.9, overweight 25 to 29.9, class I obesity 30 to 34.9, class II obesity 35 to 39.9, and class III obesity greater than 40.19 For analyses of prepregnancy BMI, we defined BMI 19 to 24.9 as normal when compared with those who have a BMI of greater than 25. However, the reference ‘‘normal’’ range for analyses of BMI at delivery was 19 to 29.9 (normal and overweight). This acknowledges that a normal weight woman who gains up to the recommended (Institute of Medicine) amount during pregnancy will have a BMI of up to 29.9.20

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Figure 1

Overweight and obesity before pregnancy, based on self-report of height and weight.

eclampsia was similarly determined by provider documentation of maternal seizure, and dystocia was characterized by labor progress that deviated from Friedman’s curve. Statistical hypotheses were tested with 2-tailed 95% CIs. There was similar cigarette use in the population and thus cigarette smoking was not included in the model (8.3% vs 9.5%, ns). The relative risk (RR) is needed to calculate the attributable fraction (AF) of disease. Multiple regression models yield adjusted odds ratios (OR). Thus, to calculate the AF of cesarean delivery we needed to convert the adjusted OR to adjusted RR. Currently, there is debate in the epidemiology literature regarding the most appropriate methods for estimating the RR from an OR. Adjusted RR of cesarean delivery was estimated by using 2 methods, the Zhang and Yu conversion and a modified Poisson regession.21,22 The attributable fraction in the exposed was then calculated.23 This fraction was applied to the percentage of women overweight and obese in 2001. In a similar fashion, we calculated the annual AF of preeclampsia across the study period.

Results Study population The trend analyses included 495,051 deliveries of liveborn singleton infants in Utah between 1991 and 2001.

Of the half million deliveries recorded in the database, 229,483 women had their first delivery in the interval and these women were included in the outcome analyses; of these, 168,051 were nulliparous. For multiple logistic regression models, data from 1997 to 2001 were included because before 1997 gestational diabetes was not recorded, therefore 93,294 women were included in the analysis. The cohort from 1997 through 2001 was included in its entirety to avoid selection bias. Height and weight data were available on 93.3% of women before pregnancy and 85.4% of women at delivery. The groups with missing data were similar overall to those with BMI data (specifically, maternal age, parity, gestational age, race, diabetes, hypertension, cesarean delivery, and macrosomia); however, women with missing data were less educated (P ! .0001). The percentage of women with prepregnancy overweight and obesity increased from 25.1% in 1991 to 35.2% in 2001, representing a 40.2% increase (prevalence ratio [PR] 1.40; 95% CI 1.37-1.40) (Figure 1). Average prepregnancy weight for all women increased 8.1 lb between 1991 and 2001, from 138.1 G 30.0 to 146.2 G 34.3. During the same period, maternal obesity at delivery increased 36.2% from 28.7% to 39.1% (PR 1.36; 95% CI 1.33-1.39). Figure 1 demonstrates the increasing rates of maternal BMI from 1991 through 2001. The proportion of overweight and obesity across all categories increased steadily throughout the interval. The coefficient of the slope of maternal overweight and

LaCoursiere et al Table I

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Characteristics of women with self-reported BMI O30 at the time of delivery, Utah 1991 and 2001 1991

2001

Characteristic

No.

% BMI R30

No.

% BMI R30

Percent change

Overall Race White Black Hispanic Native American Age (y) 12-19 20-29 30-39 40-49 Education !High school High school !4-y college R4-y college Parity Nulliparous Multiparous Grand multiparous (h/o R5 deliveries)

9933/34,552

28.7

17,407/44,509

39.1

10.4

8565 66 704 339

27.8 37.7 35.7 46.6

13,673 155 2486 368

37.8 44.2 43.8 61.1

10.0 6.5 8.1 14.5

839 5845 3069 179

22.4 27.6 33.4 39.4

1175 10,962 4928 336

31.8 38.2 43.2 49.1

9.4 10.6 9.8 9.7

1374 3791 3298 1391

29.0 31.1 29.3 22.8

2713 5906 5262 3349

41.2 42.6 40.0 31.9

12.2 11.5 10.7 9.1

3184 6061 677

25.8 29.6 40.4

5699 11,007 679

35.7 40.5 50.8

9.9 10.9 10.4

obesity prepregnancy was 0.95 and obesity at delivery was 1.02. Both of these trends were statistically significant. The maternal characteristics of obese women at delivery are described in Table I. Although all the BMI categories show an increase, there has been an approximate 2-fold increase in class III obesity in just 10 years (P ! .0001). In 2001, 2.7% of women before pregnancy and nearly 5% of women at delivery had a BMI greater than 40. There was an increase in the prevalence of obesity at delivery across all race, age, education, and parity groups. Similar to the general population, obesity was associated with nonwhite race, age, parity, and less education.9,24 In 2001, 61% of Native Americans, almost 50% of women older than 40 years, and 50% of grand multiparous women were obese at delivery. Among nulliparous women, different weight gain patterns had varying effects on cesarean delivery rates. Women who were overweight or greater before pregnancy and class I obesity or greater at delivery, conferred the greatest risk for primary cesarean delivery (26.3%). This risk was decreased in women who were not overweight before pregnancy and became obese during their pregnancy (22.0%) and was further attenuated in women who were overweight or obese before pregnancy who ultimately fell within normal range at delivery (16.8%). However, all these rates were increased compared with nulliparous women who were

normal weight before pregnancy and at delivery (13.3%). In nulliparous women without comorbid conditions, primary cesarean delivery rates rose with increasing prepregnancy BMI from 11.4% (underweight) to 42.6% (class III) (P ! .0001). Among nulliparous and multiparous women, preexisting and gestational diabetes and chronic hypertension (not including preeclampsia and pregnancy-induced hypertension) increased with rising BMI (data not shown). The proportion of cesarean delivery in class III obesity is 40.3% in women without risk factors, 43.8% with chronic hypertension, 49.2% in preexisting or gestational diabetics, and 58.8% with both hypertension and preexisting or gestational diabetes. After controlling for age, race/ethnicity, parity, gestational age, weight gain, diabetes, and hypertension, there was a statistically significant association between maternal overweight and obesity and cesarean delivery, preeclampsia, eclampsia, dystocia, and birth weight greater than 4000 g (Table II). We did not find an association between anesthesia complications or preterm labor. When using normal weight women as the reference group, a multiple regression model showed a stepwise increase in adjusted ORs of cesarean delivery as BMI increased (Table III). The model correctly predicted 82.7% of cesarean deliveries. The effect of maternal BMI on cesarean delivery was independent of neonatal macrosomia. When macrosomia (>4 kg birth weight) was added into the model, the effect on the adjusted

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Table II Adjusted ORs for various pregnancy outcomes for preconceptional overweight and obese women in Utah Preeclampsia Eclampsia Dystocia BW O4000 g Cesarean delivery PT delivery Anesthetic complications

Table III Multiple logistic regression model for risk of cesarean delivery by maternal BMI

OR (95% CI)

Prepregnancy BMI

OR (95% CI)

2.49 1.42 1.92 1.68 1.90 0.98 1.48

Normal weight (19-24.9) Underweight (!19) Overweight (25-29.9) Class I obesity (30-34.9) Class II obesity (35-39.9) Class III obesity (O40)

Reference 0.81 (0.76-0.86) 1.55 (1.48-1.63) 2.28 (2.13-2.45) 3.37 (3.04-3.73) 4.52 (3.93-5.20)

(2.35-2.64) (1.14-1.77) (1.82-2.03) (1.58-1.79) (1.82-1.98) (0.92-1.04) (0.85-2.58)

Controlling for maternal age, race, parity, gestational age (except for PT delivery), weight gain, diabetes, and hypertension. PT, Preterm.

ORs of BMI category decreased minimally (underweight 0.82, overweight 1.51, class I obesity 2.24, class II obesity 3.27, and class III obesity 4.20). The adjusted RR that was calculated varied insignificantly between methods: the model of Zhang and Yu yielded an adjusted RR of 1.664 (1.614-1.713)21 and the modified Poisson estimate was 1.633 (1.584-1.686).22 The most conservative estimate of RR yielded an attributable fraction of cesarean delivery in 2001 in the overweight and obese of 0.388 (0.369-0.407). The AF of preeclampsia secondary to prepregnancy BMI 25 or greater did not change across time, but the incidence of preeclampsia increased from 1991 to 2001 (Figure 2).

Comment Despite the increased awareness of obesity over the past decade, statewide prepregnancy overweight and obesity increased 40% in Utah, with a similar rise in obesity at delivery. A 2-fold increase in severe obesity has yielded a 5% proportion of women with a BMI of more than 40 at delivery. This increase in obesity has significant public health implications in pregnant women. In this large population-based study, we identified several adverse outcomes associated with increased BMI even when controlling for hypertension and diabetes, including cesarean delivery, preeclampsia, eclampsia, and fetal macrosomia. The odds of cesarean delivery increases stepwise with increasingly heavier strata of BMI.

National trends Nonpregnant women aged 20 to 39 years experienced a 37.9% increase in obesity (BMI O30) between NHANES III (1988-94) and NHANES data from 1999 to 2000 to 28.4%.2 In our analysis, the prevalence of preconceptional obesity (BMI O30) is less than those reported in this national sample of reproductive age women.2 We did, however, see temporal increases of similar magnitudes. In contrast, the prevalence of

Controlling for maternal age, race, parity, gestational age, weight gain, diabetes, hypertension, and macrosomia.

preconceptional severe obesity (BMI O40), which increased from 1% to 2% over the decade, was similar to national data of nonpregnant women.5 Strum et al6 saw a similar pattern when analyzing the BRFSS data from 1986 to 2000. The lower overall rates of preconceptional obesity in our population have several possible explanations. The population in Utah may be less obese than the general population, in part secondary to the white predominance in the state. This is supported in part by work by Mokdad et al.24 Although their data from the BRFSS include all adults of both genders, Utah ranked 33rd in the nation with respect to obesity, with 18.5% of adults having a BMI greater than 30.24 In Utah, we have fewer women with preconceptional BMI greater than 30 but similar rates of BMI greater than 40 compared with previously reported national data on nonpregnant women. Although this may reflect differences in the weight distribution in Utah compared with the nation, it may also reflect the differences in data collection between studies. The birth records depend on self-reported height and weight data. These data tend to inflate height and diminish weight,25 thus the bias exists to misclassify women to leaner strata. Our prevalence rates are consistent with the data of Freedman et al5 that were also obtained by self-report and are somewhat attenuated compared with the results obtained from Flegal et al2 that used actual BMI measurement. This observation supports the possibility that self-reported measurements downgrade the BMI strata to which women are assigned and may in part be responsible for the difference in obesity prevalence between our findings and that reported in a national sample of nonpregnant women of reproductive age.

Maternal trends Two studies in the obstetric literature that have characterized maternal obesity trends in Alabama and in Ohio used somewhat different inclusionary criteria and definitions. Both reported obesity increases similar to those seen in our report, but the actual percentage of women

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Figure 2 Incidence of preeclampsia, prevalence of prepregnancy BMI R25 and the attributable fraction of preeclampsia secondary to prepregnancy BMI R25, Utah 1991-2001.

who were obese was significantly larger. Most of the data from Alabama were evaluated by using absolute weights.7 However, of those subjects for whom they were able to calculate BMI, they described an increase from 25% to 36% in BMI 30 or greater at first prenatal visit. This is 3 times greater than our population and may be explained by the fact that their maternal sample consisted of nearly 70% black women. The mean gestational age at first prenatal visit of the women in this study, at first prenatal visit was 13 to 15 weeks and may slightly raise the BMI compared with prepregnancy. In an urban population in Ohio, 28% of women were more than 200 lbs at delivery.8 For average height women (5 ft 4 in), this is near a BMI of 34. Assuming that 28% of urban Ohio women have a BMI 34 or greater, this would represent a 2-fold greater prevalence than seen in Utah. Both of these studies were derived from single institutions in large cities in Alabama and

Ohio. Both states have a higher prevalence of obesity; Alabama ranked second in the country in the percentage of obese adults and Ohio 15th.24

Outcomes These data suggest that even moderate increases in body mass increase a woman’s risk of an adverse outcome even when controlling for diabetes and hypertension. Our data confirm previously reported associations between obesity and cesarean delivery, preeclampsia, eclampsia, and macrosomia.9,10,13-15,17,26 The importance of calculating adverse outcomes in a populationbased longitudinal study is the ability to estimate the overall disease burden related to the exposure. Although 1 study has previously calculated the AF of cesarean delivery caused by obesity as 11.6%, this estimate was based on a racially skewed sample and did not control for diabetes and hypertension.7 We compared 2 methods

838 for estimating the RR, the Zhang and Yu conversion and the modified Poisson regression of Zou.21,22 With our model, there were minimal differences between the 2 estimates. In 2001, more than 35% of women were preconceptionally overweight or obese. Given an attributable fraction of 0.38 for cesarean delivery in the overweight and obese, nearly 1 in 7 cesarean deliveries of singleton infants in our 2001 population was attributable to overweight and obesity. This result was obtained with conservative estimates, controlling for comorbid conditions, in a state that may be less obese than the nation as a whole. Although obesity is not the indication for delivery per se, it contributes to factors that increase the need for surgical intervention. Further research is urgently needed not only to confirm this observation but to explain the mechanism(s) responsible for the association and to develop clinical investigations (above and beyond preconceptional weight loss) to improve the likelihood of safe vaginal delivery for obese women. The incidence of preeclampsia appears to be increasing among nulliparous women delivering singletons. The AF of preeclampsia caused by BMI 25 or greater has not increased. Some of the excess cases could have resulted from a shift in maternal BMI. However, results from our study should be evaluated with caution given the suboptimal correlation between preeclampsia as documented in the medical record compared to the birth record. Additional prospective studies of preeclampsia trends may better describe this phenomenon. In summary, this is the first statewide populationbased analysis of pregnancy overweight and obesity trends. Not surprisingly, the epidemic of obesity spills into the pregnant population. Unlike previous trend studies in the obstetric literature, our dataset reported weight and height data and thus permitted calculation of BMI. It also includes overweight women who were previously excluded from other trend studies.2,3,5,6 There was an increase in overweight and obese women over the 12-year study period and even overweight women experienced increased adverse outcomes in proportion to their increasing BMI. We controlled for diabetes and hypertension to try to evaluate the impact of BMI itself. This may attenuate the ORs for cesarean delivery associated with overweight and obesity. Unlike other studies of outcomes, we included multiparous women to better characterize the overall trends and controlled for parity in the analyses.14 The study is limited by the selfreported data and may thus underestimate BMI. Also, the women who have missing data were less educated than those who reported height and weight. Although this represented 6% to 14% of the population and lower education was associated with increasing BMI, the absence of these women could reduce the trends and associations. All of these study limitations would impart a diminutive effect and underestimate the magnitude of the problem. However, an overweight and obesity

LaCoursiere et al problem even of the scale presented here warrants urgent attention.

References 1. American Obesity Association. Obesity in the U.S: AOA fact sheet. Available at http://www.obesity.org/subs/fastfacts. obesity_US.html. Accessed March 2004. 2. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002;288:1723-7. 3. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the United States: prevalence and trends, 1960-1994. Int J Obes Relat Metab Disord 1998;2:39-47. 4. The Henry J. Kaiser Family Foundation. Utah: overweight and obesity by gender, 2002. Available at http://www.statehealthfacts. kff.org. Accessed on October 2004. 5. Freedman DS, Khan LK, Serdula MK, Galuska DA, Dietz WH. Trends and correlates of class 3 obesity in the United States from 1990 through 2000. JAMA 2002;288:1758-61. 6. Strum R. Increases in clinically severe obesity in the United States, 1986-2000. Arch Intern Med 2003;163:2146-8. 7. Lu GC, Rouse DJ, DuBard M, Cliver S, Kimberlin D, Hauth JC. The effect of the increasing prevalence of maternal obesity on perinatal morbidity. Am J Obstet Gynecol 2001;185:845-9. 8. Ehrenberg HM, Dierker L, Milluzzi C, Mercer BM. Prevalence of maternal obesity in an urban center. Am J Obstet Gynecol 2002;187:1189-93. 9. Jensen DM, Damm P, Sø´renson B, Mø´lsted-Pedersen L, Westergaard JG, Ovesen P, et al. Pregnancy outcome and prepregnancy body mass index in 2459 glucose-tolerant Danish women. Am J Obstet Gynecol 2003;189:239-44. 10. Sebire NJ, Jolly M, Harris JP, Wadsworth J, Joffe M, Beard RW, et al. Maternal obesity and pregnancy outcome: a study of 287,213 pregnancies in London. Int J Obes Relat Metab Disord 2001;25:1175-82. 11. Cnattingius S, Bergstrom R, Lipworth L, Kramer MS. Prepregnancy weight and the risk of adverse pregnancy outcomes. N Engl J Med 1998;338:147-52. 12. Watkins ML, Rasmussen SA, Honein MA, Botto LD, Moore CA. Maternal obesity and risk for birth defects. Pediatrics 2003;111(Pt 2):1152-8. 13. Rosenberg TJ, Garbers S, Chavkin W, Chiasson MA. Prepregnancy weight and adverse perinatal outcomes in an ethnically diverse population. Obstet Gynecol 2003;102(Pt 1):1022-7. 14. Weiss JL, Malone FD, Emig D, Ball RH, Nyerg DA, Comstock CH, et al. Obesity, obstetric complications and cesarean deliveryda population-based screening study. Am J Obstet Gynecol 2004;190:1091-7. 15. Crane SS, Wojtowwycz MA, Dye TD, Aubry RH, Atral R. Association between pre-preganancy obesity and the risk of cesarean delivery. Obstet Gynecol 1997;89:213-6. 16. Baeten JM, Bukusi EA, Lambe M. Pregnancy complications and outcomes among overweight and obese nulliparous women. Am J Public Health 2001;91:436-40. 17. Cedergren MI. Maternal morbid obesity and the risk of adverse pregnancy outcomes. Obstet Gynecol 2004;103:219-24. 18. DiGiuseppe DL, Aron DC, Ranbom L, Harper DL, Rosenthal GE. Reliability of birth certificate data: a multi-hospital comparison to medical records information. Matern Child Health J 2002;6:169-79. 19. International Obesity Task Force. Managing the global epidemic of obesity: report of the WHO Consultation on Obesity. Geneva: World Health Organization; 1998. p. 1-276.

LaCoursiere et al 20. Institute of Medicine. Nutrition during pregnancy: part I, weight gain. Washington, DC: National Academy Press; 1990. p. 10. 21. Zhang J, Yu KF. What’s the relative risk? A method of correcting the odds ration in cohort studies of common outcomes. JAMA 1998;280:1690-1. 22. Zou GY. A modified Poisson regression approach to prospective studies with binary data. Am J Epidemiol 2004;159:702-6. 23. Rothman KJ. Epidemiology: an introduction. New York: Oxford University Press; 2002.

839 24. Mokdad AH, Bowman BA, Ford ES, Vinicor F, Marks JS, Koplan JP. The continuing epidemics of obesity and diabetes in the United States. JAMA 2001;286:1195-200. 25. Rowland ML. Self-reported weight and height. Am J Clin Nutr 1990;52:1125-33. 26. Weiss JL, Malone FD, Emig D, Ball RH, Nyberg DA, Comstock CH, et al, FASTER Research Consortium. Obesity, obstetric complications and cesarean delivery rateda population-based screening study. Am J Obstet Gynecol 2004;190:1091-7.