Effects of gestational weight gain on pregnancy outcomes are well recognized, and over the past decades the guidelines for ideal weight gain have been periodically questioned and revised. Previous gestational weight gain guidelines were restrictive, reflecting concerns about preeclampsia, labor and delivery complications, and weight retention after pregnancy.1 Subsequent guidelines were revised upward to minimize mortality and morbidity risks for low birth weight (LBW) infants.2 The current guidelines provide gestational weight gain ranges based on prepregnancy body mass index (BMI) and were recommended by the Institute of Medicine (IOM) to again limit adverse pregnancy outcomes.1 However, the current IOM guidelines for obese women (prepregnancy BMI greater than or equal to 30.0 kg/m2) do not provide an upper limit on gestational weight gain, only advising women to gain at least 15 lb, and do not distinguish between the different levels of obesity as defined by the National Institutes of Health (NIH).3
Given the increasing prevalence of obesity among childbearing women,4 the tendency for postpartum weight retention,1 the high prevalence of perinatal complications in obese women,5–9 and the influence of pregnancy in the development of obesity later in life,10 reevaluation of the IOM gestational weight gain guidelines for obese women has important clinical and public health implications. Particularly, a distinction between the different levels of gestational weight change for women entering pregnancy as obese may lead to adequate gestational weight gain while maintaining optimal pregnancy and neonatal outcomes. The purpose of this study was to examine the relationship between gestational weight gain and pregnancy outcomes in obese women by using NIH obesity classifications.
MATERIALS AND METHODS
A population-based cohort study was conducted by using data from the Missouri linked birth-death certificate registry. The study population included all obese women residing in Missouri who delivered (at 37 or more weeks of gestation) liveborn, singleton infants during 1990–2001 (N=120,251). Prepregnancy BMI was calculated from self-reported prepregnancy weight and height recorded on the birth certificate. According to NIH guidelines, obesity was defined as class I (BMI 30.0–34.9 kg/m2), class II (BMI 35.0–39.9 kg/m2), and class III (BMI 40 kg/m2 or more).3
Gestational weight gain, which was abstracted from the mother's medical chart or provided by the physician, was divided into eight categories as follows: 10-lb or less loss, 2–9 lb loss, no weight change, 2–9 lb gain, 10–14 lb gain, 15–25 lb gain, 26–35 lb gain, and greater than 35 lb gain. The eight categories were selected to reflect levels at which weight gain or loss could become clinically relevant. Because the current guidelines encourage obese women to gain at least 15 lb, the 15–25 lb weight gain category was chosen as the referent group because this also represents the current recommendation for pregnant, overweight (BMI 25–29.9 kg/m2) women.
Pregnancy outcomes analyzed included preeclampsia, cesarean delivery, small for gestational age (SGA), and large for gestational age (LGA) infant. On Missouri birth certificates, preeclampsia is defined as pregnancy-associated hypertension after the 20th week of gestation that resulted in an increase in blood pressure of 30 mm Hg or more systolic or 15 mm Hg or more diastolic on two measurements taken 6 hours apart. Women who developed eclampsia were combined with preeclamptic women into a single group, hereafter referred to as preeclampsia. Cesarean delivery included all primary and repeat surgical procedures used to deliver the infant. Small for gestational age and LGA were defined as birth weight below the 10th percentile and above the 90th percentile, respectively, for gestational age and race or ethnicity.11
Potential confounders for this analysis included maternal age (younger than 26, 26–35, older than 35 years), race (non-Hispanic white, other), education (less than 12, 12, more than 12 years), and the dichotomous variables of poverty, tobacco use, parity (0, 1 or more prior live births), and chronic hypertension.10,12,13 Because income level was not captured on the birth certificate, enrollment in Medicaid, the Women, Infants, and Children public health program, or food stamp programs was used as a proxy measure for poverty.
The three classes of obese women were assessed for homogeneity with respect to demographic, lifestyle, and medical characteristics by using χ2 analysis. Within each obesity class, the absolute risk (or cumulative incidence) for each pregnancy outcome was computed as the percentage of all women with the specific outcome and was stratified by gestational weight gain category to assess the effect of gestational weight gain for each pregnancy outcome. Logistic regression was also used to examine the association between gestational weight gain and the four pregnancy outcomes. Odds ratios and 95% confidence intervals were estimated to determine the strength and precision of each association after adjusting for potential confounders. All analyses were performed with SPSS 12 (SPSS Inc, Chicago, IL) software.
This research was reviewed by the Saint Louis University institutional review board and classified as exempt from the U.S. Department of Health and Human Services regulations for the protection of human subjects. The exemption, 45 CFR 46.101(b)(4), permits epidemiologic research that uses existing publicly available data that are maintained in such a manner that subjects cannot be identified directly or through identifiers linked to the subjects.
A total of 120,170 women met the eligibility criteria, and 59% were class I obese, 25% were class II obese, and 16% were class III obese. Twenty-three percent of all obese women gained less than 15 lb during pregnancy, 31% gained 15–25 lb, and 46% gained more than 25 lb. All three obesity classes were similar with respect to maternal age, race, and education (Table 1). Class III obese women were more likely to live in poverty and to experience chronic hypertension, preeclampsia, cesarean delivery, and LGA births than class I or II obese women.
Figures 1–3 show the absolute risk of preeclampsia, cesarean delivery, LGA, and SGA by gestational weight gain category for each obesity class. All three figures show similar patterns of increasing risk of preeclampsia, cesarean delivery, and LGA birth and decreasing risk of SGA birth with increasing gestational weight gain. Collectively, the minimal risk for all four outcomes corresponds to the gestational weight gain categories where the risk of LGA and SGA births intersect. This equates to a gestational weight gain of 10–25 lb for class I obese women, a gain of 0–9 lb for class II obese women, and weight loss of 0–9 lb for class III obese women.
Figures 4–6 display the adjusted odds ratios and 95% confidence intervals for preeclampsia, cesarean delivery, SGA, and LGA by gestational weight gain category and obesity class. Compared with women who gained 15–25 lb during their pregnancies, those who gained less weight had significantly lower odds of preeclampsia, cesarean delivery, and LGA births, but higher odds for SGA births. Women who gained more than 25 lb had higher odds for the same three pregnancy outcomes and lower odds for SGA births. The magnitude of the association for each outcome differed by obesity classification, even after adjusting for known or suspected confounders.
Because gestational age is estimated by clinicians and these estimates can influence SGA and LGA status, the analysis was repeated using birth weight. Low birth weight (LBW) was defined as birth weight less than 2,500 g, and macrosomia was defined as birth weight greater than 4,000 g. As expected, the risk of LBW and macrosomia were lower than the risk estimates noted for SGA and LGA births, but the trends across gestational weight gain categories were very similar (data not shown).
The absolute effect of gestational weight gain expressed as the number needed to treat is displayed in Table 2. The number needed to treat represents the reciprocal of the absolute risk difference for women gaining less than the NIH-recommended 15 lb and those gaining 15 lb or more. With the exception of cesarean delivery, the number needed to treat for each outcome differed by obesity class and gestational weight gain category. To reduce the risk of preeclampsia for one patient, the clinician would need to counsel and monitor the gestational weight gain of 29 obesity class I women, 26 obesity class II women, and 20 obesity class III women. For SGA births, the number needed to treat ranges from 21 for class I women to 52 for class III women.
The results of this study are consistent with other studies showing the protective effect of reduced gestational weight gain on LGA births and cesarean delivery for obese women regardless of obesity class.1,2,5–7,9,10 Although previous studies have consistently identified prepregnancy BMI as a risk factor for the development of preeclampsia,2,5–7,9,12 less is known about the effect of gestational weight gain on preeclampsia occurrence. Our results suggest that reduced gestational weight gain is associated with decreased risk of developing preeclampsia. As expected, we observed reduced SGA risk with increasing gestational weight gain for all three obese classes. Our results suggest that SGA risk for class II and III obese women gaining less than 15 lb is minimal. These results are consistent with Bianco et al,7 who found that women with a prepregnancy BMI greater than 35 kg/m2 and poor gestational weight gain did not have a significant increase in SGA births.
Our results showed similar trends for the effect of gestational weight gain on all four pregnancy outcomes analyzed in all three obese classes. However, the amount of gestational weight gain associated with minimal risk for all four outcomes collectively is different for each obesity class. Our results suggest that this minimal risk may correspond to a weight gain of 10–25 lb for class I obese women, a weight gain of 0–9 lb for class II obese women, and a weigh loss of 0–9 lb for class III obese women. Treating each obesity class as a distinct obstetric population reflects the different magnitude of baseline and pregnancy-induced risks associated with each obesity class.
Like all observational studies, our study has its limitations. We used birth certificate data to identify a large cohort of pregnant, obese women. In Missouri, birth certificates are completed using data from patient medical records, although prepregnancy weights are often self-reported. We acknowledge that women may underestimate their prepregnancy weight, but believe that self-reported and clinically recorded weights are similar for nonpregnant and pregnant women as reported in other studies.14,15 For a 5 ft 5 in woman weighing 260 lb to be misclassified in our study, she would have to underestimate her prepregnancy weight by at least 20 lb and 50 lb to move from obesity class III to obesity class II and obesity class I, respectively. Furthermore, we were only able to use the pregnancy outcomes that were reliably reported on the birth certificate. An audit of Missouri birth certificate data (Schramm W. Data quality: new certificates. Proceedings of the AVRHS/VSCP Project Directors Meeting, San Francisco, 1991) reported that 85% of all preeclampsia cases were identified correctly on the birth certificate. We acknowledge that LGA and SGA status is dependent upon the accuracy of gestational ages that are routinely estimated by clinicians but noted similar risk patterns by gestational weight gain categories when we evaluated macrosomia and LBW as other measures of extreme fetal growth. We were unable to evaluate the effect of gestational weight gain on the risk of developing gestational diabetes because the Missouri birth certificate does not differentiate between type I, type II, and gestational diabetes. We chose to restrict our study population to full-term, singleton, live births among Missouri residents and acknowledge that our study results may not be generalized to other populations of pregnant, obese women. We used logistic regression analysis to adjust for known and suspected confounders, which did not affect the overall trends that were reported in our study. However, there may be other confounders that may explain the associations that we observed for all four pregnancy outcomes. We acknowledge that our study results show only statistical associations and do not imply causality. The latter can only be achieved by conducting a prospective randomized controlled trial of obese women to determine the effect of controlled gestational weight gain on specific pregnancy outcomes.
Our study suggests that appropriate gestational weight gain recommendations should be developed separately for each of the three NIH obesity classes, and an upper limit on gestational weight gain should be considered to prevent weight gain and comorbidities among obese women.
1. Schieve LA, Cogswell ME, Scanlon KS. An empiric evaluation of the Institute of Medicine's pregnancy weight gain guidelines by race. Obstet Gynecol 1998;91:878–84.
2. Ogunyemi D, Hullett S, Leeper J, Risk A. Prepregnancy body mass index, weight gain during pregnancy, and perinatal outcome in a rural black population. J Matern Fetal Med 1998;7:190–3.
3. National Institutes of Health, National Heart, Lung, and Blood Institute. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults [publication no. 98-4083]. Bethesda (MD): National Institutes of Health; 1998.
4. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002;288:1723–7.
5. Edwards LE, Hellerstedt WL, Alton IR, Story M, Himes JH. Pregnancy complications and birth outcomes in obese and normal-weight women: effects of gestational weight change. Obstet Gynecol 1996;87:389–94.
6. Kabiru W, Raynor BD. Obstetric outcomes associated with increase in BMI category during pregnancy. Am J Obstet Gynecol 2004;191:928–32.
7. Bianco AT, Smilen SW, Davis Y, Lopez S, Lapinski R, Lockwood CJ. Pregnancy outcome and weight gain recommendations for the morbidly obese woman. Obstet Gynecol 1998;91:97–102.
8. Abrams BF, Laros RK Jr. Prepregnancy weight, weight gain, and birth weight. Am J Obstet Gynecol 1986;154:503–9.
9. Caulfield LE, Stoltzfus RJ, Witter FR. Implications of the Institute of Medicine weight gain recommendations for preventing adverse pregnancy outcomes in black and white women. Am J Public Health 1998;88:1168–74.
10. Morin KH. Perinatal outcomes of obese women: a review of the literature. J Obstet Gynecol Neonatal Nurs 1998;27:431–40.
11. Alexander GR, Himes JH, Kaufman RB, Mor J, Kogan M. A United States national reference for fetal growth. Obstet Gynecol 1996;87:163–8.
12. O'Brien TE, Ray JG, Chan WS. Maternal body mass index and the risk of preeclampsia: a systematic overview. Epidemiology 2003;14:368–74.
13. Ray JG, Vermeulen MJ, Shapiro JL, Kenshole AB. Maternal and neonatal outcomes in pregestational and gestational diabetes mellitus, and the influence of maternal obesity and weight gain: The DEPOSIT study. Diabetes Endocrine Pregnancy Outcome Study in Toronto. QJM 2001;94:347–56.
14. Lederman SA, Paxton A. Maternal reporting of prepregnancy weight and birth outcome: consistency and completeness compared with the clinical record. Matern Child Health J 1998;2:123–6.
15. Rowland ML. Reporting bias in height and weight data. Stat Bull Metro Insur Co 1989;70:2–11.