The prevalence of obesity (body mass index [BMI, calculated as weight (kg)/[height (m)]2] 30 or greater) among women of reproductive age is increasing in most developed countries to worrying rates.1 In pregnant women, the prevalence of obesity varies between 1.8% and 25.3%.2 In Flanders, the northern part of Belgium, prepregnancy BMI and gestational weight gain have been systematically registered for all births since 2009 and a slight increase in the incidence of maternal obesity from 10.1% in 2009 to 10.7% in 2011 has been reported.3
Obese pregnant women and women with excessive gestational weight gain are estimated to carry a two- to fourfold increased risk for gestational diabetes mellitus (GDM), pregnancy-induced hypertension, and cesarean delivery compared with women with a normal BMI (18.5–24.9) and with those with an adequate gestational weight gain.2,4–11 Low and high birth weight neonates are also described more commonly in underweight and obese pregnant women, respectively.4,5 The cross-sectional design of most studies on the subject calls for caution when interpreting the results. Longitudinal data from large cohorts of pregnant women are needed to get stronger and valid estimates on the temporal and causal relation between maternal obesity and perinatal outcomes. This means that perinatal risks should also be analyzed against changes in maternal weight between two consecutive pregnancies.
Differences between pregnancy-related maternal weight retention and physiologic weight change in a woman's life cycle can be identified if we study interpregnancy weight changes in a relatively small interpregnancy time interval.12 Studies about interpregnancy weight changes and perinatal outcomes in the next pregnancy are rather scarce. Only one large Swedish study demonstrated an approximately twofold increased risk for pregnancy-induced hypertension, GDM, and large-for-gestational-age neonates if women gained 3 or more BMI units between the first and second pregnancy.13 Most studies took advantage of large interpregnancy time intervals and studied only one or two perinatal outcomes14–18 or had small sample sizes.19
We therefore examined associations between maternal weight changes between the start of the first and the second pregnancy and the risk for adverse perinatal outcomes in a regional representative cohort of women who had their first two consecutive singleton births in Belgium between 2009 and 2011.
MATERIALS AND METHODS
As from 1996, the Flemish Study Center for Perinatal Epidemiology routinely registers perinatal data from all deliveries in Flanders. Perinatal data from all maternity units are collated centrally, subjected to an error detection program, and checked for accuracy and completeness through feedback with the individual maternal units and reassessment of patient records, when needed.20 In case of extreme values (considered outliers) or missing values, the maternity units are contacted for confirmation or correction. All data refer to stillbirths or live births of neonates with a weight of 500 g or greater; the definitions used are in agreement with those from the World Health Organization and the Fédération Internationale de Gynécologie et d'Obstétrique.21 Data from the Study Center for Perinatal Epidemiology database contained information about maternal and gestational age (completed weeks) at delivery, maternal height and weight before pregnancy, and weight at delivery (since 2009), parity, pregnancy-induced hypertension, GDM, mode of delivery, birth weight, congenital malformations, and perinatal mortality.
For this analysis, data were linked by matching four key variables: parity, maternal date of birth, neonate date of birth, and maternity center. By merging the variables for the first and second delivery in the same mother, interpregnancy weight difference was calculated. Multiple pregnancies were excluded. In total 200, 706 singleton births occurred between January 2009 and December 2011. After exclusion of those with missing first date of birth in their second pregnancy data file (n=2,821) and missing maternal height or prepregnancy weight or weight at delivery (n=17,216), the data for 180,669 births remained. After merging women who had their first and second birth between 2009 and 2011 (n=8,792) and excluding those with differences in maternal height more than or equal to 5 cm between the two consecutive pregnancies (n=895), the final cohort for analysis consisted of 7,897 women. Ranges of maternal height (1.42–1.90 m), prepregnancy weight (35–144 kg), and weight at delivery (44–160 kg) were found to be acceptable to us.
The scientific committee of Study Center for Perinatal Epidemiology granted approval for the analysis of the deidentified data. This study was furthermore exempt from approval by an institutional review board because data were used for scientific purposes only.
Body mass index was categorized according to the World Health Organization in underweight (BMI less than 18.5, n=375), normal weight (BMI 18.5–24.9, n=5,517), overweight (BMI 25–29.9, n=1,444), and obese (BMI 30 or greater, n=561). Gestational weight gain was calculated by subtracting the maternal prepregnancy weight from the weight at delivery and was categorized as insufficient, adequate, or excessive in accordance with the 2009 Institute of Medicine guidelines for each BMI category.22 Prepregnancy weight and height were self-reported during pregnancy. Maternal weight at delivery was measured in the delivery room or, if not available, the weight at the last prenatal visit was used. Interpregnancy time interval was calculated as the number of completed weeks between the birth of the first and the second neonate minus the duration of the second pregnancy (weeks). Interpregnancy weight change was calculated as the difference between the prepregnancy BMI of the first pregnancy and the prepregnancy BMI of the second pregnancy. Besides analyzing it as a continuous variable, we categorized interpregnancy weight change into two different ways. First, we categorized the differences in BMI as less than −1 (BMI loss more than 1 unit), −1 to less than 1 (reference group), 1 to less than 2, 2 to less than 3, and 3 or more BMI units. This classification was also used in relevant earlier publications on the subject.13,23 Second, we categorized interpregnancy weight gain on the basis of a shift in BMI category from the first to the second pregnancy as previously used.14 For example, a woman who was overweight before her first pregnancy and obese before her second pregnancy was categorized as overweight–obese. This led to 14 categories as presented in Table 1. The latter was only used for descriptives.
We considered six main outcomes of interest: two complications related to the pregnancy (GDM and pregnancy-induced hypertension), one related to birth (cesarean delivery), and three related to the neonate (macrosomia [4,000 g or greater], low birth weight [less than 2,500 g], and congenital malformations). All of these outcomes were retrieved from the Study Center for Perinatal Epidemiology database.
The association between two continuous variables was investigated with Spearman's correlation coefficient. The association between two categorical variables was investigated with the likelihood ratio χ2. The association between a continuous and a categorical variable was investigated with the Kruskal-Wallis test. For each perinatal outcome variable (GDM, pregnancy-induced hypertension, cesarean delivery, macrosomia, and low birth weight), we built a logistic regression model with stepwise forward variable selection on the following variables: interpregnancy weight change as a categorical variable, prepregnancy BMI at the first pregnancy, interpregnancy time interval, gestational age at delivery in the first pregnancy, maternal age during the second pregnancy, gestational weight gain according to the Institute of Medicine recommendations, GDM, pregnancy-induced hypertension, induction of labor, cesarean delivery, macrosomia, low birth weight, major malformations, and perinatal mortality during the first pregnancy. The obtained variable selection was verified with backward selection of variables and assessment of the χ2 statistic score. We checked for outliers and the dfβ of the obtained variables coefficients. Because we found statistically significantly interactions between the prepregnancy BMI at first pregnancy and categorical BMI changes between pregnancies, we decided also to build logistic regression models for each outcome stratified by whether the woman's prepregnancy BMI at first pregnancy was below or above 25. All P values were two-sided and values <.05 were considered statistically significant. If we adjust for the multiplicity problem related to: 1) the six multiple outcomes; and 2) the different cutoffs for interpregnancy weight change (four cutoffs and one merged category), the statistical significance level then becomes .05/(6+4+1)=.05/11=.0045 (Bonferroni correction). This means that in the multivariate analysis, we will only consider variables with a P value <.005 as statistically significant. We are aware that Bonferroni is a rigorous method, and we therefore might have indicated clinically relevant variables as not statistically significant. SAS 9.3 was used for all analyses.
The mean prepregnancy BMI between the two consecutive pregnancies increased from 23.3 (standard deviation 4.1) to 23.9 (standard deviation 4.4) (P<.001); and we noticed an increase in the prevalence of overweight and obese women, from 25.4% to 31.4%. In the group of obese women at the onset of the first pregnancy, 28.7% gained 2 or more BMI units at the start of the second pregnancy compared with 15% in the normal-weight women (P<.001). The largest shifts occurred in the group of normal-weight women, of whom 8.6% shifted from normal weight to overweight (Table 1).
The proportion of women with excessive gestational weight gain was lower during the second pregnancy for all BMI categories; however, more than 50% of overweight and obese women gained more weight than recommended in both pregnancies. Excessive weight gain was present in 27% and 18% of the first and second pregnancies, respectively, in normal-weight women. Mean interpregnancy time lapse was 53.0 weeks (standard deviation 22.8). Weight retention between pregnancies decreased with maternal age and height, was lower with longer interpregnancy time interval, and was higher in cases of adverse outcome (pregnancy-induced hypertension, cesarean delivery, or macrosomia) during the first pregnancy (Table 2). The prevalence of GDM (from 1.9% to 2.3%; P=.001) and macrosomia (from 7.8% to 12.1%; P<.001) increased, whereas pregnancy-induced hypertension (from 5.5% to 2.4%; P<.001), cesarean delivery (from 15.8% to 14.7%; P<.001), and low birth weight (from 4.5% to 2.4%; P<.001) significantly decreased between the first and the second pregnancies.
Univariate associations between perinatal outcomes in the second pregnancy and changes in BMI between pregnancies showed that the prevalence of GDM, pregnancy-induced hypertension, cesarean delivery, and macrosomia increased with increasing interpregnancy weight change. The prevalence of low birth weight decreased with increasing interpregnancy weight change, but no association was observed between the prevalence of congenital malformations and interpregnancy weight change (Table 3). In the multivariate unstratified sample, women who lost more than 1 BMI unit between the first and second pregnancy, indicated a decreased risk of 30% (P=.003) for macrosomia, whereas the risk for low birth weight increased by 92% (P=.001; table not shown). The risk for pregnancy-induced hypertension increased by 80% (P=.02) and 76% (P=.01), respectively, for those who gained 2 and 3 or more BMI units between pregnancies compared with those with a BMI shift of less than 1 unit (reference group). The risk for cesarean delivery increased by 37% if women gained 3 or more BMI units between pregnancies (P=.02). After applying the Bonferroni correction for the multiplicity problem (six outcomes and different categories of interpregnancy weight), only P values <.005 were considered statistically significant. Interaction statistics between prepregnancy BMI and interpregnancy weight change indicated that the effect of interpregnancy weight change on perinatal outcomes was also influenced by the prepregnancy BMI. We therefore stratified our analysis in groups of women with prepregnancy BMI less than 25 (underweight and normal-weight women) and women with prepregnancy BMI of 25 or greater (overweight and obese women) at the beginning of the first pregnancy.
In the stratified analysis, we showed that the risk for GDM doubled with an interpregnancy weight gain of 2 or more BMI units. The risk for pregnancy-induced hypertension in the second pregnancy increased nearly fourfold with an increment of 3 or more BMI units between pregnancies, but both results were observed only in underweight and normal-weight women (Table 4). Their risk for macrosomia was halved and the risk for low birth weight doubled if the BMI decreased by more than 1 unit between pregnancies. Furthermore, in overweight and obese women, the risk for cesarean delivery doubled if the BMI increased by 2 units or more between the first and the second pregnancy. Overweight and obese women with excessive gestational weight gain during their first pregnancy showed a nearly threefold increased risk for GDM in the second pregnancy; but no effect was shown for interpregnancy weight change. Additionally, prepregnancy BMI before the first pregnancy remained significantly associated with the risk for GDM and pregnancy-induced hypertension in overweight and obese women only and was no longer statistically significant in underweight and normal-weight women after Bonferroni correction. In addition to the influence of interpregnancy weight change, the risk for all perinatal outcomes studied was positively influenced by their occurrence during the first pregnancy.
In this population-based cohort, we show that, in addition to the effect of prepregnancy BMI and excessive gestational weight gain, weight retention between the first and second pregnancy is associated with a significantly increased risk for GDM, pregnancy-induced hypertension, and cesarean delivery during the second pregnancy. More specifically, the increased risk for GDM and pregnancy-induced hypertension was only present in underweight and normal-weight women. If, for example, a normal-weight woman with a height of 1.65 m gains approximately 5.5 kg (1 unit BMI=2.7 kg) between pregnancies, her risk of developing GDM in the next pregnancy is more than doubled compared with her counterpart with a BMI shift of less than 1 unit (reference group). This shows that even a relatively small increase in BMI between pregnancies had an important effect on the risk of developing GDM in the next pregnancy in these women. On the other hand, the risk for cesarean delivery increased with interpregnancy weight retention, but only in overweight and obese women. This additional cesarean delivery risk related to interpregnancy weight retention is worrying in view of the already high and increasing cesarean delivery rates in Belgium and the rest of the world, especially in obese women.24 Concurrently, a high postpartum weight retention is an important contributor to long-term maternal obesity.25,26 Taken together, these results support the evidence for a more intensive follow-up of the postpartum period, a period that is not well studied at this moment.
The strength of this study is the large size and the longitudinal design of a population-based cohort looking at perinatal outcomes after a limited interpregnancy time interval. Conclusions about the effects of postpartum weight retention on relevant perinatal outcomes can be drawn, taking also into account the influence of gestational weight gain and prepregnancy BMI. Some limitations need consideration. The interpregnancy interval was short and did not exceed 2 years in our study. This may limit the generalizability of our findings but enables us to distinguish between the real postpartum-related weight and lifestyle-related weight fluctuation. We acknowledge the possible underestimation of self-reported prepregnancy weight and thus the underestimation of the BMI. No information on maternal education, ethnicity, and smoking behavior was available. We could only control for maternal age. Information on pregravid morbidity of hypertension or diabetes was also not available. The adjusted odds for congenital malformations of 2.35 in underweight and normal-weight women by interpregnancy weight retention between 1 and 2 BMI units must be interpreted with caution because of the small numbers involved (n=29). After applying the Bonferroni methods, only P values <.005 were considered statistical significant. The influence of weight changes before the first and after the second pregnancy was not studied. Consequently, effect sizes of interpregnancy weight loss within different categories of prepregnancy BMI on perinatal risks remain to be investigated. Few studies give support for lower perinatal risks with a loss of interpregnancy BMI units for the total group13 or for overweight and obese27,28 only.
Our results are in accordance with the scarce other studies examining interpregnancy weight changes and the risk of GDM, pregnancy-induced hypertension, and cesarean delivery.13,27,29 Villamor et al13 and Ehrlich et al27 reported stronger effects of interpregnancy weight gain and risk of pregnancy-induced hypertension and GDM in underweight and normal-weight women compared with those with BMI greater than 25. We additionally controlled and corrected for gestational weight gain and could find effects of interpregnancy weight gain on pregnancy-induced hypertension and GDM in underweight and normal-weight women only. From a clinical point of view, it could be important to distinguish between the influence of weight gain during pregnancy and the influence of interpregnancy weight change because interpregnancy weight retention is affected by gestational weight gain in the first pregnancy and weight change during the interpregnancy interval. Although no effect of interpregnancy weight retention is shown for risk of GDM in women with BMI 25 or greater, we show that excessive gestational weight gain during the first pregnancy is related to a nearly three times higher risk for GDM in the next pregnancy. Gestational weight gain during the first pregnancy is part of interpregnancy weight retention, and 61% of obese women in our cohort showed excessive gestational weight gain in their first pregnancy compared with 27% of normal-weight women. Therefore, one could question the Institute of Medicine-recommended weight gain ranges for overweight and obese women to obtain good perinatal outcomes not only for the current, but also for the subsequent pregnancy. The recommended ranges of 7–11.5 kg or 5–9 kg (Institute of Medicine) for overweight and obese women, respectively, may still be too high.30,31 A revision of guidelines on adequate gestational weight gain for obese pregnant women may lead to better perinatal outcomes in the subsequent pregnancy but awaits further confirmation.
Getahun et al29 also reported an association between an increased risk of cesarean delivery and interpregnancy weight retention; however, they did not distinguish between women with BMI less than or more than 25 and only used outcomes for primary cesarean delivery. They also showed that women who shifted to a lower BMI category had a cesarean delivery risk that was comparable to those with a normal BMI in both pregnancies. This was however not shown in our cohort, in which we did not distinguish between primary (elective) and secondary (emergency) cesarean delivery. It is known that the decision for cesarean delivery is also affected by maternal and physicians' preferences. Analyzing emergency cesarean delivery only would probably lead to a more risk-based insight.
An American study including more than 10,000 obese women28 found an increased risk for macrosomia in overweight and obese women with an interpregnancy weight retention of 2 or more BMI units. In contrast to our findings, they reported a lower risk for large-for-gestational-age neonates by an interpregnancy weight loss of 2 or more BMI units in obese women. We only found a lower risk of macrosomia in women with BMI less than 25 if they lost more than 1 BMI unit between the first and second pregnancy. We did, however, not differentiate between various weight loss categories in our multivariate analysis as was the case in the study by Jain.28
These results mean that for underweight and normal-weight women, the interpregnancy period should be an important window of opportunity for weight management and follow-up, especially if they plan a subsequent pregnancy. Routine visits with health care providers should focus on these “initial low-risk” women because they are usually not targeted for weight management and are often neglected in interventional programs. Although we could not find an association between interpregnancy weight loss and reduced risk of GDM as was the case in earlier studies,14,27 we should at least focus on stabilizing interpregnancy weight in this “initial low-risk” group. Motivation to return to prepregnancy BMI should be an important cue to action. Obesity at the onset of pregnancy is known to carry a high risk for both the mother and her child in the short and long term.2,4,5,32 This is supported in our study by the significant influence of the prepregnancy BMI at first pregnancy on perinatal risks. The preconceptional period before the first pregnancy therefore provides an important window of opportunity for motivational behavior coaching to strive for an optimal prepregnancy weight.33,34 Because the significant recurrence risks for perinatal complications in the second pregnancy are well demonstrated in this and other studies,27 the prevention of these complications in the first pregnancy should be an important target. Because most published intervention trials aimed at reducing gestational weight gain in obese women were not able to reduce their increased perinatal risks,35,36 the preconceptional period remains an important time to focus on for the prevention of an unhealthy maternal weight before the start of a pregnancy.
To conclude, we showed that weight retention between the first and second pregnancy increased the risk for GDM and pregnancy-induced hypertension in underweight and normal-weight women and for cesarean delivery in overweight and obese women. In underweight and normal-weight women, weight loss between the first and second pregnancy decreased macrosomia but at the expense of an increase in low-birth-weight neonates.
1. WHO Global Infobase data for saving lives 2012. Estimated obesity prevalence females aged 15+, 2010. Available at: https://apps.who.int/infobase
. Retrieved April 22, 2013.
2. Guelinckx I, Devlieger R, Beckers K, Vansant G. Maternal obesity: pregnancy complications, gestational weight gain and nutrition. Obes Rev 2008;9:140–50.
3. Bogaerts A. Obesity and pregnancy, an epidemiological and intervention study from a psychosocial perspective. Antwerp (Belgium): Garant Publishers; 2013.
4. Nohr EA, Vaeth M, Baker JL, Sorensen TI, Olsen J, Rasmussen KM. Combined associations of prepregnancy body mass index and gestational weight gain with the outcome of pregnancy. Am J Clin Nutr 2008;87:1750–9.
5. Heslehurst N, Simpson H, Ells LJ, Rankin J, Wilkinson J, Lang R, et al.. The impact of maternal BMI status on pregnancy outcomes with immediate short-term obstetric resource implications: a meta-analysis. Obes Rev 2008;9:635–83.
6. Madan J, Chen M, Goodman E, Davis J, Allan W, Dammann O. Maternal obesity, gestational hypertension, and preterm delivery. J Matern Fetal Neonatal Med 2010;23:82–8.
7. Mamun AA, Callaway LK, O'Callaghan MJ, Williams GM, Najman JM, Alati R, et al.. Associations of maternal pre-pregnancy obesity and excess pregnancy weight gains with adverse pregnancy outcomes and length of hospital stay. BMC Pregnancy Childbirth 2011;11:62.
8. Weiss JL, Malone FD, Emig D, Ball RH, Nyberg DA, Comstock CH, et al.. Obesity, obstetric complications and cesarean delivery rate—a population-based screening study. Am J Obstet Gynecol 2004;190:1091–7.
9. Yogev Y, Catalano PM. Pregnancy and obesity. Obstet Gynecol Clin North Am 2009;36:285–300, viii.
10. Sheiner E, Levy A, Menes TS, Silverberg D, Katz M, Mazor M. Maternal obesity as an independent risk factor for caesarean delivery. Paediatr Perinat Epidemiol 2004;18:196–201.
11. Torloni MR, Betran AP, Horta BL, Nakamura MU, Atallah AN, Moron AF, et al.. Prepregnancy BMI and the risk of gestational diabetes: a systematic review of the literature with meta-analysis. Obes Rev 2009;10:194–203.
12. Schmitt NM, Nicholson WK, Schmitt J. The association of pregnancy and the development of obesity—results of a systematic review and meta-analysis on the natural history of postpartum weight retention. Int J Obes (Lond) 2007;31:1642–51.
13. Villamor E, Cnattingius S. Interpregnancy weight change and risk of adverse pregnancy outcomes: a population-based study. Lancet 2006;368:1164–70.
14. Whiteman VE, Aliyu MH, August EM, McIntosh C, Duan J, Alio AP, et al.. Changes in prepregnancy body mass index between pregnancies and risk of gestational and type 2 diabetes. Arch Gynecol Obstet 2011;284:235–40.
15. Whiteman VE, Crisan L, McIntosh C, Alio AP, Duan J, Marty PJ, et al.. Interpregnancy body mass index changes and risk of stillbirth. Gynecol Obstet Invest 2011;72:192–5.
16. Mostello D, Jen Chang J, Allen J, Luehr L, Shyken J, Leet T. Recurrent preeclampsia: the effect of weight change between pregnancies. Obstet Gynecol 2010;116:667–72.
17. Paramsothy P, Lin YS, Kernic MA, Foster-Schubert KE. Interpregnancy weight gain and cesarean delivery risk in women with a history of gestational diabetes. Obstet Gynecol 2009;113:817–23.
18. Villamor E, Sparen P, Cnattingius S. Risk of oral clefts in relation to prepregnancy weight change and interpregnancy interval. Am J Epidemiol 2008;167:1305–11.
19. Chen A, Klebanoff MA, Basso O. Pre-pregnancy body mass index change between pregnancies and preterm birth in the following pregnancy. Paediatr Perinat Epidemiol 2009;23:207–15.
20. Cammu H, Martens G, Keirse MJ. Mothers' level of education and childbirth interventions: a population-based study in Flanders, Northern Belgium. Birth 2011;38:191–9.
21. Cammu H, Martens G, Martens E, Van Mol C, Defoort P. Perinatale activiteiten in vlaanderen 2009. Brussel (Belgium): SPE; 2010.
22. Institute of Medicine. Weight gain during pregnancy: re-examining the guidelines. Washington (DC): National Academy Press; 2009.
23. Nohr EA, Villamor E, Vaeth M, Olsen J, Cnattingius S. Mortality in infants of obese mothers: is risk modified by mode of delivery? Acta Obstet Gynecol Scand 2012;91:363–71.
24. Bogaerts A, Van den Bergh B, Nuyts E, Martens E, Witters I, Devlieger R. Socio-demographic and obstetrical correlates of pre-pregnancy body mass index and gestational weight gain. Clin Obes 2012;2:150–9.
25. Gore SA, Brown DM, West DS. The role of postpartum weight retention in obesity among women: a review of the evidence. Ann Behav Med 2003;26:149–59.
26. Gunderson EP. Childbearing and obesity in women: weight before, during, and after pregnancy. Obstet Gynecol Clin North Am 2009;36:317–32, ix.
27. Ehrlich SF, Hedderson MM, Feng J, Davenport ER, Gunderson EP, Ferrara A. Change in body mass index between pregnancies and the risk of gestational diabetes in a second pregnancy. Obstet Gynecol 2011;117:1323–30.
28. Jain AP, Gavard JA, Rice JJ, Catanzaro RB, Artal R, Hopkins SA. The impact of interpregnancy weight change on birthweight in obese women. Am J Obstet Gynecol 2013;208:205.e1–7.
29. Getahun D, Kaminsky LM, Elsasser DA, Kirby RS, Ananth CV, Vintzileos AM. Changes in prepregnancy body mass index between pregnancies and risk of primary cesarean delivery. Am J Obstet Gynecol 2007;197:376.e1–7.
30. Cedergren MI. Optimal gestational weight gain for body mass index categories. Obstet Gynecol 2007;110:759–64.
31. Potti S, Sliwinski CS, Jain NJ, Dandolu V. Obstetric outcomes in normal weight and obese women in relation to gestational weight gain: comparison between Institute of Medicine guidelines and Cedergren criteria. Am J Perinatol 2010;27:415–20.
32. Melzer K, Schutz Y. Pre-pregnancy and pregnancy predictors of obesity. Int J Obes (Lond) 2010;34(suppl 2):S44–52.
33. Heslehurst N, Rankin J, Wilkinson JR, Summerbell CD. A nationally representative study of maternal obesity in England, UK: trends in incidence and demographic inequalities in 619,323 births, 1989–2007. Int J Obes (Lond) 2010;34:420–8.
34. Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and trends in obesity among US adults, 1999–2008. JAMA 2010;303:235–41.
35. Bogaerts AF, Devlieger R, Nuyts E, Witters I, Gyselaers W, Van den Bergh BR. Effects of lifestyle intervention in obese pregnant women on gestational weight gain and mental health: a randomized controlled trial. Int J Obes (Lond) 2013;37:814–21.
© 2013 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.
36. Vinter CA, Jensen DM, Ovesen P, Beck-Nielsen H, Jorgensen JS. The LiP (Lifestyle in Pregnancy) study: a randomized controlled trial of lifestyle intervention in 360 obese pregnant women. Diabetes Care 2011;34:2502–7.