management of obesity in pregnancy - acog

Clinical Expert Series

Management of Obesity in PregnancyPatrick M. Catalano, MD

Maternal pregravid obesity is a significant risk factor for adverse outcomes during pregnancy. Inearly pregnancy there is an increased risk of spontaneous abortion and congenital anomalies. Inlater gestation maternal metabolic manifestations of the metabolic syndrome, such as gestationalhypertensive disorders and diabetes, become clinically recognized because of the increasedinsulin resistance in obese compared with nonobese women. In women with pregestationalglucose intolerance, hypertension, central obesity, and lipid disorders, the physiologic changesin pregnancy increase the risk of problems previously not routinely encountered duringpregnancy. These include chronic cardiac dysfunction, proteinuria, sleep apnea, and nonalco-holic fatty liver disease. At parturition the obese patient is at an increased risk of cesareandelivery and associated complications of anesthesia, wound disruption, infection, and deepvenous thrombophlebitis. For the fetus there are short-term risks of fetal macrosomia, morespecifically obesity, and long-term risks of adolescent components of the metabolic syndrome.Although preliminary results of bariatric surgery are encouraging, the procedure is expensive andnot for all obese women, and we recognize that long-term follow-up data on offspring of obesewomen who have undergone bariatric surgery before pregnancy are lacking. In the interim, weneed to encourage obese women to lose weight before conception, using lifestyle changes ifpossible. During pregnancy, weight gain should be limited to Institute of Medicine guidelines(currently under review) and encouragement given for physical activity.(Obstet Gynecol 2007;109:419–33)

Obesity is an epidemic not only in the UnitedStates and developed countries but also in the

developing world. “Indeed, it is now so common thatit (obesity) is replacing the more traditional publichealthcare concerns including under-nutrition andinfectious disease as one of the most significant con-tributors to ill health.”1 The World Health Organiza-tion and the National Institutes of Health definenormal weight as a body mass index (BMI, weight[kg]/height [m]2) of 18.5–24.9, overweight as a BMI of25–29.9, and obesity as a BMI of 30 or greater.Obesity is further characterized by BMI into class I(30–34.9), class II (35–39.9), and class III (greater

than 40).1 In women of reproductive age in the UnitedStates, the prevalence of obesity was 30.2%, while theprevalence of overweight was 56.7% in the latestCenters for Disease Control and Prevention (CDC)reports. The problem of obesity is greatest amongnon-Hispanic black women (48.8%), as comparedwith Mexican-American (38.9%) and non-Hispanicwhite women (31.3%). Potentially more important,the prevalence of obesity in children as young as 2years old and adolescents has increased by 11.3%between 1994 and 2000.2 Again, the increased prev-alence has been especially notable among Mexican-American and non-Hispanic black adolescents.

The problems relating to the management ofobesity in pregnancy are many. There are both short-and long-term complications and implications forboth mother and fetus. This issue has recently beenaddressed in the American College of Obstetriciansand Gynecologists (ACOG) in Committee OpinionNo. 315, “Obesity in Pregnancy.”3 I will attempt tofirst comment on the Committee Opinion, and sec-ondarily discuss the potential implications of obesityfor the woman and her offspring.

From the Department of Reproductive Biology, Case Western Reserve Universityat MetroHealth Medical Center, Cleveland, Ohio.

Supported by National Institutes of Health grants HD-22968 and GCRCRR00080.

Corresponding author: Patrick M. Catalano, MD, 2500 MetroHealth Drive,Cleveland, OH 44109; e-mail: [email protected].

© 2007 by The American College of Obstetricians and Gynecologists. Publishedby Lippincott Williams & Wilkins.ISSN: 0029-7844/07

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Obesity is a risk factor for a number of pregnancycomplications. Therefore, as recommended by theACOG committee opinion, obese women should beencouraged to decrease weight before consideringpregnancy. Also recently, ACOG Committee Opin-ion No. 319, “The Role of the Obstetrician-Gynecol-ogist in the Assessment and Management of Obesity,”offers the obstetrician-gynecologist practical guide-lines on how to assess and manage obesity in thenonpregnant woman.4 Included are primers on theassessment of a patient’s readiness to make behavioralchanges. Lifestyle measures of calorie-restricted dietsand exercise, when employed together, are poten-tially more beneficial than either modality alone. Asnoted in Committee Opinion No. 319, fad diets, evenones with a potential physiological basis such aslow-glycemic diets, are controversial at best withrespect to long-term efficacy. Also included is infor-mation regarding approved weight-loss medicationsand guidelines for referral for bariatric surgery eval-uation, which will be discussed later.

Although preconceptual weight loss is certainly alaudable goal for the obese woman, many, if not most,pregnancies are unfortunately not planned. The lim-ited success in normalization of pregravid glucosecontrol in women with pregestational diabetes todecrease the risk of congenital malformations is ananalogous example of the limitation of preconceptualmanagement of lifestyle issues. Long-term publichealth programs addressing awareness of the prob-lems of obesity, like those programs in recent decadesthat promoted smoking cessation programs and leg-islation, hold promise for success in the future. In themeantime we need not give up hope, because someobese patients with the proper counseling can achievemeaningful weight loss before conception.

PREGRAVID OBESITY VERSUS WEIGHTGAIN IN PREGNANCYThe obstetric complications of maternal obesity aregenerally related to issues of maternal pregravidobesity rather than excessive weight gain duringgestation that results in a nonobese women becomingobese. Weight gain in pregnancy is generally consid-ered to be the difference between a woman’s weight atthe last antenatal visit and her pregravid weight or herweight at first antenatal visit. However, the concept of“net maternal weight gain” has gathered more inter-est, because this takes into account the fact that, onaverage, 4–5 kg of weight at term represents the fetus(3.5 kg), the placenta (0.5 kg), and amniotic fluid(0.5–1.0 kg). Therefore, one could easily express “netmaternal weight gain” as the difference between a

woman’s weight at her last antenatal visit minus thecombination of her pregravid weight and fetal weight.

The recommendations for weight gain in preg-nancy have been based on the Institute of Medicine(IOM) guidelines that were published in 1990.5 Thesuggested weight gains are a weight gain of 11.2–15.9kg (25–35 lb) for women with a normal BMI, 6.8–11.2kg (15–25 lb) for overweight women, and more than6.8 kg (15 lb) for obese women. These guidelines wereinitially intended to help decrease the risk of fetalgrowth restriction. In a report by Schieve et al6 fromthe CDC Pregnancy Nutrition Surveillance System, inover 266,000 women, the mean maternal weight gainand net weight gain, even when adjusted for week ofgestation, both decrease with increasing BMI. More-over, overweight and obese women had mean weightgains greater than the IOM guidelines. Based on thesedata and other data, including the increasing preva-lence of obesity in the population, the IOM currentlyis reviewing the recommendations for weight gain inpregnancy.

The components of weight gain have been previ-ously estimated by Hytten7 to be approximately 1 kgof protein and 4 kg of fat, with the remainder beingwater. In prospective studies initiated before preg-nancy in women with a wide range of BMIs, Butte etal8 reported a wide range of incremental accretion offat, depending on a subject’s pregravid BMI. The netaccrual of fat mass was 5.3 kg women with low BMI,4.6 kg in those with normal BMI, and 8.4 kg in thehigh BMI group. However, there was a wide range inincreased fat mass within each group. In our ownprospective studies, we found no significant differencein gain of fat mass in lean compared with obesewomen (4.7�3.2 kg versus 4.2�3.5 kg, P�.58), norlean body mass (7.6�3.9 kg versus 8.8�2.6 kg,P�.18) although the increase in percentage of bodyfat was significantly greater in the lean compared withthe obese women (3.3�3.8% versus 0.1�3.3%,P�.004).9 The increase in subcutaneous fat was in acentral distribution, ie, between the midthoraxthrough the upper thigh. Interestingly, there was nosignificant difference in accretion of fat mass inwomen with normal glucose tolerance compared withwomen with gestational diabetes mellitus (GDM)matched for pregravid body composition. There arelimited data about the relative changes in visceral fat,which potentially may be of more metabolic signifi-cance. Kinoshita and Itoh,10 reported an increase inboth preperitoneal and subcutaneous fat layers by thethird trimester of pregnancy, as well as an increase inthe ratio of peritoneal to subcutaneous fat, suggestingintra-abdominal fat increases during pregnancy.

420 Catalano Management of Obesity in Pregnancy OBSTETRICS & GYNECOLOGY

Hence, the accrual of fat mass in pregnancy is vari-able and may depend on a woman’s pregravid meta-bolic status and other lifestyle variables such as dietand physical activity.

OBSTETRIC RISKS ASSOCIATED WITHMATERNAL OBESITY: EARLY GESTATIONThe obese woman is at increased risk of a myriad ofobstetric problems in early pregnancy. There is anincreased risk of early miscarriage (odds ratio [OR]1.2, 95% confidence interval [CI] 1.01–1.46, P�.04)and recurrent miscarriage (OR 3.5, 95% CI 1.03–12.01, P�.04) in obese women compared with normalweight controls after natural conception.11 In over-weight women conceiving after in vitro fertilization orintracytoplasmic sperm injection, there was an in-crease in the abortion rate over the first 6 weeks (22%versus 12%) compared with lean or average weightwomen.12 The relative risk of spontaneous abortionwas 1.77 (95% CI 1.05–2.97). Therefore, particularlyin obese women considering assisted reproductivetherapy, weight loss before conception should bestrongly considered and measures initiated by thepatient’s health care provider.

As early as 1994, Waller et al13 suggested thatoffspring of obese women were at increased risk ofneural tube defects (OR 1.8, 95% CI 1.1–3.0), espe-cially spina bifida (OR 2.6, 95% CI 1.5–4.5). Theseresults have been confirmed in subsequent studiesand have also implicated maternal obesity with in-creased risks of heart defects (OR 1.18, 95% CI1.09–1.27)14 and omphalocele (OR 3.3, 95% CI 1.0–10.3).15 Because these types of congenital anomaliesare often seen with pregestational diabetes, someinvestigators have suggested that many of these obesewomen may have had undiagnosed type 2 diabetes.14

Additionally, because neural tube defects are associ-ated with folic acid deficiencies, Mojtabai16 reportedthat, after controlling for intake of folate in food andnutritional supplements, increased BMI was associ-ated with a lower serum folate concentrations(P�.001) and suggested that women with a BMIgreater than 30 would need to increase their folateconsumption by 350 mcg/d to achieve the same folatelevels as women with BMI less than 20. In contrast,Ray et al17 in a Canadian population estimatedwhether the risk of neural tube defects was lower afterflour was fortified with folic acid. Before fortificationof flour, increased maternal weight was associatedwith a modest increased risk of neural tube defects(OR 1.4, 95% CI 1.0–1.8); after flour fortification therisk actually increased (OR 2.8. 95% CI 1.2–6.6).Therefore, although the evidence implicated maternal

obesity with an increased risk of congenital anoma-lies, particularly neural tube defects, the mechanismsare not well understood. Practically, short of precon-ceptual weight loss in the management of obesepregnant women, one should consider glucose screen-ing of obese women in early pregnancy to rule outundiagnosed pregestational diabetes. Folate supple-mentation of cereal products was initiated in thiscountry in 1998, and whether additional folate sup-plementation should be offered to obese womenbefore conception or in early pregnancy is speculativeat this point. Obviously, more research must be done,but recognition of obesity as a risk factor for congen-ital anomalies remains an important factor for theclinician to consider in the management of the obesepregnant woman.

If, indeed, obese women are at increased risk ofneural tube defects and other congenital anomalies,how then does maternal obesity affect our diagnosticabilities in this population? There is a significantcorrelation between maternal serum alpha fetoprotein(AFP) and maternal weight (r�0.24, P�.001), withlighter women having greater maternal serum AFPthan heavier women.18 This is generally believed tobe a result of the proportionally greater plasma vol-ume in obese compared with nonobese women.Therefore, standard adjustments of maternal AFPvalues for maternal weights up to 200 lb have beenimplemented.19 Additionally, the use of cell-free DNAin the diagnosis of chromosomal abnormalities maybe affected by a woman’s degree of obesity. Wataga-nara et al20 reported that in the first trimester therewas no significant association between maternalweight and plasma-free DNA levels. However, in thesecond trimester there was a significant inverse cor-relation between maternal weight and serum-freeDNA (r� –0.26, P�.007), particularly if the womanweighed more than 170 lb.

The other modality commonly used in earlypregnancy to identify congenital anomalies is ultra-sonography. In 1990, Wolfe et al21 reported that therewas a significant impairment of adequate ultrasoundvisualization of fetal anatomy when BMI was greaterthan 36; visualization fell by 14.5%. A decrease invisualization was most marked for the fetal heart andspine. In 2004, Hendler et al22 reported that, in over11,000 pregnancies in which 38.6% of the patientswere obese, the rate of suboptimal visualization offetal anatomy was 37.3% in obese compared with18.7% in nonobese women (P�.001). Increased sever-ity of obesity was again noted for both cardiac andcraniospinal structures. The use of advanced ultra-sound equipment may be able to improve suboptimal

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visualization of the outflow tracts in obese womenafter 18 weeks of gestation but not of the four-chamber view.23

In summary, although obese women may be atincreased risk of neural tube defects, interpretation ofserum markers is more difficult because of thechanges in the volume of distribution of these mark-ers, and care needs to be taken so as not to increasethe number of false-negative results. The use ofpopulation-specific values may aid in the interpreta-tion of results. Similarly, the ability of ultrasonogra-phy to detect fetal cardiac and craniospinal abnormal-ities is significantly limited in obese women comparedwith nonobese women. The use of advanced ultra-sound equipment and delaying evaluation until after18 weeks may be of some value, although overallmaternal obesity still limits visibility of fetalstructures.

OBSTETRIC RISKS ASSOCIATED WITHMATERNAL OBESITY IN LATE GESTATION:MATERNAL PREGNANCY METABOLICDYSFUNCTIONThe obese nonpregnant woman is at significant riskfor what has variously been termed the metabolicsyndrome or insulin resistance syndrome. This syn-drome has as its metabolic core obesity, ie, centralobesity as estimated by an elevated waist-to-hip ratioand insulin resistance. The clinical manifestations ofthe metabolic syndrome include hypertension, glu-cose intolerance, and elevated cholesterol and triglyc-erides. Maternal obesity in pregnancy is also associ-ated with an increased risk of “metabolic syndrome-like complications” in late pregnancy, for example,gestational hypertension and preeclampsia. In retro-spective studies, Sibai et al24 have previously reporteda significant increase in the risk of preeclampsia inwomen with increased BMI. Based on a prospectivemulticenter study of 16,102 women, initially evalu-ated at 10–14 weeks, 85% were controls (BMI lessthan 30), 9% were obese (BMI 30–34.9), and 6% weremorbidly obese (BMI 35 or greater). Obese womenand morbidly obese women were 2.5 and 3.2 times,respectively, more likely to develop gestational hy-pertension than the control group. Similarly, pre-eclampsia was 1.6 and 3.3 times more likely todevelop in obese and morbidly obese women, respec-tively.25 The increase in preeclampsia in obese com-pared with average weight women extends to womenwith GDM as well. Yogev et al26 reported that, inwomen with well-controlled GDM, there is a signifi-cant increased risk of preeclampsia in obese (10.8%)compared with average BMI women (8.2%). The risk

of preeclampsia is also increased in obese womenwith GDM with poor control (14.9%). Furthermore,Crowther et al,27 in the Australian CarbohydrateIntolerance Study in Pregnant Women (ACHOIS),showed that the risk of preeclampsia in the interven-tion group for GDM was 12%, whereas in the routinecare group the risk was 18% (P�.02). In summary,although currently there are no known proven thera-pies to prevent the development of preeclampsia inobese women, for example, aspirin or calcium sup-plementation, there are data suggesting that tightglucose control in obese women with GDM maydecrease the risk. Additionally, the use of antioxidantsfor the prevention of preeclampsia in obese womenhas a theoretical benefit because of the increase inoxidative stress generated from maternal adiposetissue. Two recent randomized controlled trials, how-ever, have reported no benefit of antioxidants (1,000mg of vitamin C and 400 International Units ofvitamin E) in the reduction of preeclampsia in treat-ment compared with placebo-controlled groups.28,29

In the Vitamins in Preeclampsia trial, the investiga-tors examined the risk of preeclampsia in primiparouswomen with a BMI greater than 30 at enrollment. Inthe subgroup, there was no benefit of antioxidants indecreasing the risk of preeclampsia: risk ratio 0.87(95% CI 0.59–1.30). The Vitamins in Preeclampsiatrial also reported an increase in low birth weightbabies in the supplemented compared with the pla-cebo-control groups.29 Despite these data, after reviewby the data safety monitoring committee, the Mater-nal–Fetal Medicine Units network has decided tocontinue ongoing recruitment. To date, the results ofclinical trials of the use of antioxidants to preventpreeclampsia are not definitive as to their efficacy,and the Maternal–Fetal Medicine Units networkstudy is currently in progress.

Gestational diabetes mellitus is the clinical man-ifestation of glucose intolerance in pregnancy. Thepathophysiology of GDM involves both decreasedinsulin sensitivity and inadequate insulin response,resulting in hyperglycemia. In general, obese womenare more insulin resistant (or have decreased insulinsensitivity) compared with nonobese women, whetherpregravid or during pregnancy, when there are al-ready significant 50–60% decreases in maternal insu-lin sensitivity by the end of the third trimester.Decreased insulin sensitivity is the limited ability ofinsulin to transport glucose from the intravascular intothe peripheral tissues, primarily skeletal muscle.Therefore, it is not surprising that obese women arealso at significantly greater risk for the developmentof GDM, because they have decreased insulin sensi-


tivity compared with nonobese women (Figs. 1A andB). Weiss et al25 in the FASTER trial, after adjustingfor potential covariables, reported that the adjustedodds ratio for the risk of GDM was 2.6 (95% CI2.1–3.4, P�.001) for obese and 4.0 (95% CI 3.1–5.2,

P�.01) for morbidly obese women. Therefore, in themanagement of obese pregnant women, consider-ation should be given to early glucose screeningrather than waiting until the 24–28 week standardscreening period. This would be helpful in womenwith other risk factors for GDM, such as a previoushistory of GDM, a family history of type 2 diabetes(particularly maternal), or a history of a macrosomicfetus.

Increasing non–insulin-mediated glucose use is oftheoretical benefit in the prevention of GDM. There-fore, exercise with increased use of large skeletalmuscles, such as walking or swimming, may bebeneficial. Although the use of insulin sensitizers suchas metformin and thiazolidinediones may be theoret-ically useful to increase insulin sensitivity, theseagents cross the placenta and their fetal safety has notbeen documented. High fiber and complex carbohy-drate/low glycemic diets may decrease the need for alarge insulin response to a meal and theoreticallydecrease � cell failure, but the data on efficacy areagain controversial. Glyburide, which has recentlybeen introduced into the armamentarium of the treat-ment of GDM, helps restore euglycemia by enhanc-ing insulin response. Therefore, because obesewomen may have decreased insulin sensitivity rela-tive to nonobese women even in early gestation, inaddition to early testing for GDM, lifestyle measuressuch as moderate physical activity and nutritionalcounseling may be beneficial in the obese womenwith normal glucose tolerance.

Because obese women have an increased risk ofdeveloping or having preexisting manifestations ofthe metabolic syndrome in, for example, hyperten-sion, proteinuria, dyslipidemia, and diabetes, we arealso experiencing an increase in medical problemspreviously assumed to be diagnosed primarily in anolder nonpregnant population, for example, sleepapnea, nonalcoholic fatty liver disease, and chronicrenal and cardiac dysfunction. As such, considerationshould be given to obtaining data, for example, anelectrocardiogram to evaluate cardiac function andfurther cardiac evaluation, such as maternal echocar-diography, depending of clinical history and physicaland laboratory evaluation of obese women withchronic hypertension. Because these women are alsoat increased risk for the development of preeclampsia,obtaining an early evaluation of renal function anddegree of proteinuria in early gestation may assist indistinguishing the chronic renal dysfunction second-ary to maternal chronic hypertension and/or diabetesfrom pregnancy-associated hypertension, preeclamp-sia. Similarly, elevated liver function tests may be an

Fig. 1. A. The longitudinal changes in insulin sensitivity inwomen whose pregravid body mass index (BMI) was lessthan 25 (n�6) and in those with BMI of 25 or more (n�9)as estimated using the hyperinsulinemic-euglycemicclamp. There is a significant decrease in insulin sensitivityover time (P�.001) and between groups (P�.007). FFM,fat-free mass. B. The women with a BMI of 25 or morebefore conception were separated into BMI overweight(BMI 25–30, n�6) and obese (BMI 30 or more, n�3). Thereis a significant difference among groups (P�.001) and agroup/time interaction (P�.002). Reprinted from CatalanoPM, Ehrenberg HM. The short- and long-term implicationsof maternal obesity on the mother and her offspring. BJOG2006;113:1126–33. Copyright © 2006, with permissionfrom Blackwell Publishing Ltd.30

Catalano. Management of Obesity in Pregnancy. Obstet Gynecol2007.


indication of nonalcoholic fatty liver disease ratherthan a manifestation of severe preeclampsia. To date,there are no published studies evaluating the preva-lence of nonalcoholic fatty liver disease in pregnancy(PubMed research of the literature, English language,1990–2006, key words: “non-alcoholic steatohepati-tis,” “NASH,” “pregnancy”). We have seen an in-creasing number of obese women in pregnancy afterextensive workup in the past 5 years. This is notsurprising, given that obesity is recognized as the mostcommon factor associated with nonalcoholic fattyliver disease in the nonpregnant population. Othercommon risk factors, such as increased estrogenconcentrations, elevated lipids, and increased insulinresistance (all present in obese pregnant women),have been recognized as contributing factors.31 There-fore, as we have observed in our own population, weanticipate that the diagnosis of nonalcoholic fatty liverdisease will become a more common diagnosis inobese pregnant women with abnormal liver functionstudies. Unfortunately, there are no simple laboratorytests to screen for maternal sleep apnea. However, ahistory of daytime somnolence and a partner’s com-plaint of loud snoring should increase suspicion ofsleep apnea. Consideration of referral of these pa-tients to the appropriate pulmonary specialist to makethe diagnosis of obstructive sleep apnea and initiatetreatment, such as nighttime continuous positive air-way pressure, may be helpful because these womenwill have an increased risk of cesarean delivery.

PRETERM DELIVERYIn reviewing the literature relating preterm birth tomaternal pregravid BMI or weight gain during gesta-tion, most investigators have reported both low pre-gravid weight and poor weight gain in low BMIwomen as risk factors for preterm birth. Schieve et al32

reported that the greatest risk of a preterm deliverywas in women with a low pregravid BMI and weightgain less than 0.10 kg/wk. In a follow-up study, thesame investigators33 reported that, compared withwomen of average BMI and average pregnancyweight gain, the risk of preterm delivery increasedprogressively with decreasing pregravid BMI andweight gain of less than 0.5 lb/wk; BMI greater than26 (OR 1.6, 95% CI 0.7–3.5), BMI 19.8–26 (OR 3.6,95% CI 1.6–8.0), and BMI less than 19.8 (OR. 6.7,95% CI 1.1–40.6). Because as many as 25% of pre-term births are indicated because of maternal medicalor obstetric problems rather than the spontaneousbirths resulting from preterm labor or preterm rup-ture of the membranes, many of the preterm births inthe obese women may relate to indicated preterm

delivery because of underlying medical and or obstet-ric issues. Weiss et al25 reported that morbidly obesewomen had a significantly increased risk (OR 1.5,95% CI 1.1–2.1) of preterm delivery in comparisonwith a normal weight control group. Relative tomanagement, because the IOM guidelines for weightgain in pregnant women were initially aimed atdecreasing the risk of preterm and growth-restrictedneonates, the issue of weight gain among pregnantwomen relative to these issues is being reconsidered.

INTRAUTERINE FETAL DEATHThere has been an increasing awareness in the pastdecade of the role of maternal obesity in the risk ofunexplained antepartum fetal death. Huang et al,34 ina Canadian population, examined the factors relatedto 196 unexplained fetal deaths, 25% of the fetaldeaths in their population. The factor most stronglyassociated with unexplained fetal death was increasedprepregnancy weight. Maternal pregravid weightgreater than 68 kg increased the risk of unexplainedfetal death (OR 2.77, 95% CI 1.85–4.68), even afteradjusting for maternal age and excluding maternaldiabetes and hypertensive disorders. Factitious post-date pregnancies were eliminated because of earlyultrasound dating. Not unexpectedly, there was anincrease in unexplained fetal deaths when the birthweight ratios were greater than average, ie, more than1.15 (OR 2.36, 95% CI 1.26–4.44). These results wereconfirmed in a recent Danish National Birth Cohortstudy among 54,000 births from 1998 to 2001.35

Compared with normal weight women, the fetaldeath rate among obese women increased with in-creasing gestational age: from 28 to 36 weeks thehazard ratio (HR) was 2.1 (95% CI 1.0–4.4), 37–39weeks HR was 3.5 (95% CI 1.9–6.4), and at 40 weeksor more HR was 4.6 (95% CI 1.6–13.4). A similartrend was observed in overweight women. In contrastto the Canadian study, the birth weights of theunexplained fetal deaths among obese women werelower than the median birth weights of the live births,suggesting intrauterine growth restriction. Consistentwith this finding was the fact that obesity was associ-ated with a five-fold increase in the rate of stillbirthwith histological placental dysfunction.

At this time, we can only speculate as to thepathophysiology of unexplained intrauterine fetaldeath in obese women. However, because thesewomen are at increased risk for gestational hyperten-sive disorders and glucose intolerance, increased vig-ilance for these problems, known to be associatedwith increased perinatal mortality, is warranted.Given that maternal obesity may be associated with


an increased risk of stillbirth, how should we managethese pregnancies? Women with obesity-related prob-lems such as hypertension and diabetes need to bemonitored closely, as would nonobese women, in-cluding assessment of fetal well-being and growth,which is all the more difficult, however, as notedpreviously in obese women. In women without med-ical or obstetric complications, the increase in still-births in overweight women was twice that of normalweight women, whereas the increase in stillbirth inobese women was 240% greater than that in normalweight women.35 Certainly, close fetal monitoringwith assessments such as fetal kick counts in thesewomen is prudent, but the cost/potential benefit ofmore extensive evaluation is again speculative at thistime.

OBSTETRIC RISKS ASSOCIATED WITHMATERNAL OBESITY: PERIPARTUMIn addition to the increased risk of antenatal obstetri-cal problems in obese women, there is an increasedrisk of cesarean delivery and associated morbidities.Regional and general anesthesia both are concerns inthis population. There can be difficulty with place-ment of epidural or spinal anesthesia in obese women,requiring multiple attempts. Additionally, general an-esthesia carries the risk of difficult intubation, and theincreased incidence of sleep apnea post partum.Therefore obtaining an anesthesiology consult beforethe onset of labor should be encouraged. In themulticenter study of Weiss et al25 the cesarean deliv-ery rate for nulliparous women was 20.7% for womenwith a BMI of 29.9 or less, 33.8% for women with aBMI of 30–34.9 and 47.7% for women with a BMI of35–39.9. Similar data were reported by Durnwald etal36 in women attempting vaginal birth after 1 priorcesarean delivery (VBAC), of 510 women attemptinga trial of labor, 337 (66%) were successful and 173(34%) required repeat cesarean delivery. The greatestsuccess rate for VBAC was in underweight(BMI�19.8) women (84.7%) as compared with nor-mal weight (P�.04). Decreased VBAC success wasobserved in obese women (54.6%), but not in over-weight women (65.5%) compared with normal weightwomen (70.5%), P�.003 and P�.36, respectively.Additionally, normal weight women who gainedweight between pregnancies to become overweightduring their attempted VBAC had decreased successrates compared to those women whose BMI re-mained average, (56.6% versus 74.2%, P�.006). Un-fortunately, the converse was not true, in that weightloss resulting in a status change from overweight toaverage did not significantly improve their VBAC

success (64.0% versus 58.4%, P�.67). The increasedcesarean rate in overweight and obese women is alsoassociated with an increase in post operative compli-cations such as wound infection/breakdown, exces-sive blood loss deep venous thrombophlebitis andpostpartum endometritis. Therefore, if an obese pa-tient requires cesarean delivery she should receivepreoperative antibiotics even if the surgery is elective.

In obese women, there are no prospective trials todetermine the optimal type of skin incision (ie, verticalor horizontal) to decrease the risk of wound disruptionor infection. The vertical incision may afford greaterexposure and room to deliver a macrosomic fetus andavoid an incision in a thick pannus, but this incision mayresult in increased postoperative pain and risk of evis-ceration because of lateral tension. In contrast, thePfannenstiel incision may offer more postoperativecomfort. But, if there is a wound breakdown, manage-ment may be difficult because of exposure. Therefore,the type of incision at the time of cesarean in obesepatients will be made at the time of surgery based onmaternal anthropometry and the experience of theindividual surgeon. Because obese women are at in-creased risk for wound breakdown attempts to obviatethese complications have included closure of the subcu-taneous layers and/or placement of subcutaneousdrains. As noted in the Committee Opinion No. 315,suture closure of the subcutaneous layer after cesareandelivery may lead to a significant decrease in wounddisruption.3 However, the efficacy of subcutaneousdrains to prevent morbidity of wound breakdown is lessclear. Last, obese women are also at increased risk forpostoperative deep venous thrombosis (DVT). The useof early ambulation and compression stockings may beof benefit if used properly. The use of postoperativeheparin therapy is of value in the obese high risk patient,for e.g. with a previous history of DVT. The data on theuse of postoperative heparin in all obese women toprevent DVT are insufficient to make any generalrecommendations regarding risk benefit. In summary,overweight and obese women are at risk of increasedmedical and obstetrical problems in pregnancy, whichthen in turn increase their risk of preterm delivery,cesarean delivery, and attendant operative morbidities.

BARIATRIC SURGERY FOR OBESE WOMEN:GESTATIONAL CONSIDERATIONSAs discussed previously, the best way to decrease therisk of medical and obstetric problems in obesewomen planning pregnancy is weight loss beforeconception. Given that lifestyle measures and medicaltreatments have had limited long-term success to date,more obese women of reproductive age are seeking


bariatric surgery as an alternative. It is estimated thatthere are 150,000 bariatric surgical procedures per-formed in the United States each year. Bariatricsurgery may be considered in patients with class IIIobesity, ie, BMI greater than 40 or BMI greater than35 with comorbid conditions, if nonsurgical modali-ties have failed. Bariatric surgical procedures can becategorized into two primary types: 1) malabsorptiveprocedures such as Roux-en-Y gastric bypass, and 2)restrictive procedures such as laparoscopic adjustablegastric banding. The previously performed malab-sorptive procedures were associated with complica-tions during pregnancy, such as small bowel isch-emia,37 as well as nutrient deficiencies, such as iron,folate, and B12 deficiencies.38 There were also reportsof fetal abnormalities, small for gestational age infants,and premature births.39,40 In a report by Sheiner etal,41 298 patients became pregnant after bariatricsurgery including both malabsorptive or restrictiveprocedures. Compared with the general population,there was an increase in premature rupture of mem-branes (OR 1.4, 95% CI 1.3–2.7. P�.001), laborinduction (OR 2.1, 95% CI 1.6–2.7, P�.001), birthweight more than 4 kg (OR 2.1, 95% CI 1.4–3.0,P�.001), and cesarean delivery 25.2% versus 12.2%(OR 2.4, 95% CI 1.9–3.1, P�.001). The increased riskof cesarean delivery in women with previous bariatricsurgery remained significant after adjusting for possi-ble confounders. Of note, there were no significantdifferences between groups regarding other morbidi-ties such as placental abruption, placenta previa, labordystocia, or perinatal complications.

Although restrictive procedures including laparo-

scopic adjustable gastric banding are becoming morecommon, they are not without potential morbidity,including gastric ulcer perforation,42 intragastric bandmigration and balloon defect,43 and gastrointestinalhemorrhage resulting from erosion of a synthetic graftfrom a vertical banded gastroplasty.44 However, theearly reported results from laparoscopic adjustablegastric banding studies are encouraging. Dixon et al45

and Skull et al46 in two separate Australian studiesreported that maternal weight gain during pregnancywas significantly reduced in women who underwentlaparoscopic adjustable gastric banding in compari-son with control groups, without significant differ-ences in birth weights. The incidence of gestationaldiabetes and pregnancy hypertensive disorders werealso significantly reduced in women after laparo-scopic adjustable gastric banding (Table 1). In thereport of Dixon et al,45 there were no decreased folateor B12 levels in the women with laparoscopic adjust-able gastric banding, but some women who were nottaking multivitamins regularly had elevated homocys-teine concentrations.

Based on the available data, which does notinclude any randomized prospective trials or long-term follow-up of offspring of obese women whounderwent bariatric surgery before pregnancy(PubMed search, English language, 1990–2006, keywords: “bariatric surgery,” “pregnancy”), the follow-ing recommendations of ACOG Committee OpinionNo. 3153 are endorsed and expanded: 1) Patients withlaparoscopic adjustable gastric banding should beadvised that they are at risk of becoming pregnantunexpectedly after weight loss following surgery and

Table 1. Changes in Maternal Weight Gain, Birth Weight, and Obesity-Related Complications in ObeseWomen With Laparoscopic Adjustable Gastric Banding and Historical Controls

LAGP(n�79)

Control(n�79) P

Dixon et al45*Weight gain (kg) 9.6�9.0 15.5�9.0 .05Neonatal birth weight (g) 3,397�545 3,297�814 NSPregnancy-induced hypertension (%) 10 38 �.05Gestational diabetes (%) 6.3 19 �.05

Skull et all46†

Weight gain (kg) 3.7 (0.6–6.9) 15.6 (12.4–18.7) �.001Neonatal birth weight (kg) 3.31 (3.14–3.49) 3.53 (3.35–3.72) .19Diabetes mellitus (%) 8.2 25.8 .048Hypertension (%) 8 22.5 .06

LAGP, laparoscopic adjustable gastric banding; NS, not significant.Data for the Dixon et al45 study (LAGP: n�79; Control: n�79) are expressed as mean�standard deviation, and data for Skull et al46 study

(LAGP: n�49; Control: n�31) are expressed as mean (95% confidence interval), except where otherwise indicated.* Modified from Dixon JB, Dixon ME, O’Brien PE. Birth outcomes in obese women after laparoscopic adjustable gastric banding. Obstet

Gynecol 2005;106:965–72.† Modified from Skull AJ, Slater GH, Duncombe JE, Fielding GA. Laparoscopic adjustable banding in pregnancy: safety, patient tolerance

and effect on obesity-related pregnancy outcomes. Obes Surg 2004;14:230–5.


should use an appropriate contraceptive methods. 2)All patients undergoing laparoscopic adjustable gas-tric banding should delay pregnancy for 12–18months to avoid the rapid weight loss phase of theprocedure until their weight stabilizes and they are nolonger catabolic. This will allow for a greater weightloss before conception and possibly decrease the riskof pregnancy-related complications such as hyperten-sion and GDM. 3) Women with laparoscopic adjust-able gastric banding should be monitored by theirobstetrician and bariatric surgeon during pregnancy.Adjustments of gastric bands may reduce nausea andvomiting in pregnancy, but prophylactic removal orelimination of all the gastric band fluid may decreasethe effectiveness of the treatment and result in exces-sive weight gain. 4) All women should have adequatesupplementation of folate, calcium, and B12 after anybariatric surgical procedure because this may de-crease the risk of subclinical nutritional deficiencies.Additional nutritional supplementation and closemonitoring of fetal growth is necessary in women whohave undergone diversionary or malabsorptiveprocedures.

In women with pregestational glucose intoler-ance, hypertension, central obesity, and lipid disor-ders, the physiologic changes in pregnancy increasethe risk of problems previously not routinely encoun-tered during pregnancy.

FETAL GROWTHMaternal obesity is a well-recognized risk factor forfetal macrosomia, more specifically, obesity and long-term risks of adolescent components of the metabolicsyndrome. Weiss et al25 reported that the incidence offetal macrosomia, defined as birth weight greater than4,000 g, was 8.3% in the nonobese group, 13.3% in theobese women, and 14.6% in the infants of the mor-bidly obese women. However, just as there has beenan increase in obesity in the adult and adolescentpopulation in the past decade, neonatal birth weightshave increased significantly. Recent studies from bothNorth America and Europe have reported an increasein mean birth weights, particularly those infants eithergreater than the 90th percentile in weight for gesta-tional age (large for gestational age, LGA) or macro-somic (birth weight more than 4 kg).47,48 In Denmark,the percentage of macrosomic newborns increasedfrom 16.7% in 1990 to 20.0% in 1999.49 Factors suchas decreased maternal smoking, an increased inci-dence of diabetes, and increasing maternal BMI haveall been implicated.

In our own population, we have observed a meanincrease of 116 g in term singleton birth weight over

the last 30 years (Fig. 2). There was a mean 116-gincrease in birth weight at term (37–41 weeks) from1975 through 2003 (3,204�477 versus 3,320�488 g).The increase in birth weight was significant at the 5th,10th, 50th, 90th, and 95th percentiles (range 85–173g), with no significant difference among the percen-tiles (Fig. 3). From 1987 through 2003, the percentageof women who weighed less than 150 lb at deliverydecreased from 33% to 16%, and the percentage ofwomen who weighed more than 200 lb increasedfrom 17% to 34%, with no change in the groupbetween 150 and 200 lb (50%). Mean maternal ageincreased from 23.8 to 25.3 years. The percentage ofwhite women decreased from 49.4% to 39.1%, whilethe percentage of Hispanic (6.8–16.2%) and Asian(0.6–2.3%) women increased. The percentage ofwomen with diabetes increased from 4.0 to 5.7%,while the percent of women who smoked decreasedfrom 34.4% to 18.4%. There was no significant changein parity or gestational age at delivery. Using astepwise regression analysis, 8% of the variance in theincrease in birth weight was related to the increase inmaternal weight, while African-American race andfemale gender of the neonate accounted for an addi-tional negative 4% of the variance in birth weight.None of the remaining demographic variables thatwere considered were found to be significant contrib-utors to the change in birth weight.

Maternal anthropometric variables are importantfactors relating to fetal growth. Maternal pregravidweight has a very strong correlation with birthweight.50 Although maternal height is also associated

Fig. 2. Term singleton birth weight in grams from 37 to 41weeks from 1975 to 2003 at MetroHealth Medical Center,P�.001.Catalano. Management of Obesity in Pregnancy. Obstet Gynecol2007.


with an increase in birth weight, when adjusted forweight, there was no longer a significant correlationbetween maternal height and birth weight.51 Maternalweight gain during gestation is positively correlatedwith birth weight.52 The correlation is stronger innulliparous women (r�0.26) compared with parouswomen (r�0.16). The interaction of maternal pre-gravid weight and weight gain was examined byAbrams and Laros.53 There was a progressively stron-ger correlation between maternal weight gain andbirth weight in moderately overweight, ideal bodyweight, and underweight women. In women weighing135% of ideal weight for height before conception,there was no correlation between weight gain duringpregnancy and birth weight. Lastly, maternal age andparity have independently been reported to have apositive correlation with birth weight. However,McKeown and Gibson54 reported that when maternalage was adjusted for parity, there was no longer asignificant correlation between maternal age and birthweight. Parity has been shown by Thompson et al55 tobe associated with a mean 100–150 g increase in birthweight in subsequent pregnancies. However, the ad-ditional effect of parity on birth weight is diminishedwith increasing parity.

Relative to maternal factors, paternal anthropo-metric factors have limited impact on fetal growth.Morton56 reported that, in half-siblings with themother as the common parent, the correlation be-tween birth weight and the half siblings was r�0.58.In contrast, the correlation of birth weight in half-siblings with the father as the common parent wasonly r�0.10. Animal crossbreeding studies supportthese findings. Walton and Hammond57 crossbredShetland ponies with Shire horses. The size of thefoals was roughly the same as the foals of the maternal

pure breed. Thus, maternal regulation was moreimportant in determining intrauterine growth thanwere paternal factors. Klebanoff et al,58 using a Danishpopulation registry, reported that paternal birthweight, adult height, and adult weight together ex-plained approximately 3% of the variance in birthweight, compared with 9% for the correspondingmaternal factors. In summary, maternal factors, mostimportantly maternal pregravid weight, have thestrongest correlations with birth weight.

In our studies of fetal overgrowth and macroso-mia, we have elected to concentrate on measures ofbody composition, ie, fat and fat free or lean bodymass. The rationale for this approach stems fromwork done in the previous century. As early as 1923,research by Moulton59 described that the variability inweight within mammalian species was explained bythe amount of adipose tissue, whereas the amount oflean body mass was relatively constant and changedin a consistent manner over time. In the human fetus,Sparks60 used autopsy data and chemical analysis in169 stillborns, and described a relatively comparablerate of accretion of lean body mass in small forgestational age (SGA), average for gestational age(AGA), and LGA fetuses, but considerable variationin the accretion of fetal fat. Fat accretion in the SGAfetus was considerably less than in the AGA fetus,which in turn was less than that of the LGA fetus. Last,the term human fetus at birth has the greatest percent-age of body fat (approximately 12%) compared withother mammals.61 For these reasons we have electedto assess fetal growth in our studies using estimates ofbody composition. The methodologies we have em-ployed include anthropometric, stable isotope, andtotal body electrical conductivity. These methodshave been previously described.62–64

Fig. 3. Mean term singleton (37–41weeks) birth weight in grams for the5th, 10th, 50th, 90th, and 95th per-centiles from 1975 to 2003 at Metro-Health Medical Center.Catalano. Management of Obesity inPregnancy. Obstet Gynecol 2007.


The utility of using body composition in under-standing fetal growth is exemplified by a previous studyevaluating the proportion of the variance in birth weightexplained by body composition analysis of the fetus,and particularly fat and fat free mass. The mean birthweight of the population was 3,553�462 g and the meanpercentage of body fat was 13.7�4.2%. Fat free mass,which accounted for approximately 86% of mean birthweight, accounted for 83% of the variance in birthweight. In contrast, body fat, which accounted for onlyapproximately 14% of birth weight, explained 46% ofthe variance in birth weight.65

In an effort to better understand the potentialindependent effect of maternal obesity on fetal growthin infants of women with normal glucose tolerance,we performed a stepwise logistic regression analysis ofbody composition on 220 infants of women withnormal glucose tolerance (Table 2) previously pub-lished.66 Although maternal weight gain and heighthad the strongest correlations with birth weight andlean body mass, respectively, maternal pregravidweight had the strongest correlation with estimates ofneonatal fat and percentage of body fat. Similarly,Sewell et al,66 using the same data set, reported thatthe increase in birth weights between infants ofwomen with a BMI of 25 or greater, compared withthose having a BMI of less than 25, was explained byan increase in fat mass rather than lean body mass(Table 3). This was the case despite significantly lessweight gain (13.8�7.5 versus 15.2�5.3 lb, P�.001) inthe overweight/obese compared with lean/averageweight women.

What is the relative contribution of maternalobesity and GDM to the risk of fetal overgrowth inthe population? Ehrenberg et al67 reported that the

risk of having a LGA neonate was greatest for womenwith a history of diabetes (OR 4.4) when comparedwith maternal obesity (OR 1.6). However, there wasfour-fold greater number of LGA infants born ofobese women than women with diabetes because therelative prevalence of overweight and obesity todiabetes was 47% and 5%, respectively. Therefore, atleast in our population, maternal obesity and notdiabetes appears to be the more important factorcontributing to the population’s increase in meanbirth weight.

Relative to obstetric management, again a de-crease in maternal pregravid weight appears to be themost important factor relating to fetal overgrowth,defined as an increase in adipose tissue rather thanlean body mass. However, limiting weight gain inobese women may prove beneficial in the decreasedaccretion of fat mass in the infant of the overweightand obese women. In the study of Sewell et al,66

weight gain in overweight and obese women (BMI of25 or greater) had the strongest correlation withpercentage of body fat (r 2�0.13, P�.002), whereasweight gain was not significantly related to fat mass inthe lean and average weight women. However, opti-mal weight gain in average weight, let alone obese,women has yet to be defined. Obviously, total caloricintake is importantly related to fetal growth, but so isthe composition of the diet, ie, the percentage andtypes of fat as well as carbohydrate and protein. Theother end of the energy equation, of course, is energyexpenditure, ie, physical activity. A sedentary lifestyleonly increases the tendency for weight gain. There arenot enough evidence-based data, and it is beyond thescope of this review to speculate about the optimaldiet in pregnancy for obese women. However, theproblems related to maternal pregravid obesity andweight gain in pregnancy are not improving and willonly worsen unless appropriate research studies andtrials begin to address these issues because the conse-quences, as will be discussed, have far-reachingimplications.

LONG-TERM RISKS FOR THE FETUS OF THEOBESE MOTHERAlthough much has been written about the increasedrisk of the metabolic syndrome (obesity, hypertension,insulin resistance, and dyslipidemia) in infants bornsmall for gestational age (SGA), recent evidence pointstoward an increase in adolescent and adult obesity ininfants born either large for gestational age or macro-somic.68 There is abundant evidence linking higher birthweights to increased obesity in adolescents as well asadults for at least 25 years.69,70 Large cohort studies such

Table 2. Stepwise Regression Analysis of FactorsRelated to Body Composition ofNeonates (n�220) of Women WithNormal Glucose Tolerance

r 2 �r 2 P

Birth weightMaternal pregravid weight 0.029 — .01Maternal weight gain 0.07 0.041 �.001Maternal age 0.098 0.028 �.001

Lean body massMaternal height 0.025 — .02

Fat massMaternal weight gain 0.044 — .002Pregravid weight 0.10 0.056 �.001

Percentage of body fatMaternal weight gain 0.031 — .012Maternal pregravid weight 0.073 0.042 �.001


as the Nurses Health Study71 and the Health Profes-sional Follow-up Study72 report a J-shaped curve, ie, aslightly greater BMI among subjects born small but amuch greater prevalence of overweight and obesity inthose born large.73 The increased prevalence of adoles-cent obesity is related to an increased risk of themetabolic syndrome. The increased incidence of obesityaccounts for much of the 33% increase in type 2diabetes, particularly among the young. Fifty to ninetypercent of adolescents with type 2 diabetes have a BMIgreater than 27,74 and 25% of obese children 4–10 yearsof age have impaired glucose tolerance.75 Hence, theepidemic of obesity and subsequent risk of diabetes andcomponents of the metabolic syndrome may begin inutero with fetal overgrowth and adiposity rather thanundergrowth.

A recent retrospective cohort study by Whitaker76

in over 8,400 children in the United States in the early1990s reported that children who were born to obesemothers (based on BMI in the first trimester) weretwice as likely to be obese by 2 years of age. If awoman had a BMI of 30 or more in the first trimester,the prevalence of childhood obesity (BMI greaterthan the 95th percentile based on CDC criteria) atages 2, 3, and 4 years was 15.1%, 20.6%, and 24.1%,respectively. This was between 2.4 and 2.7 times theprevalence of obesity observed in children of motherswhose BMI was in the normal range (18.5–24.9). Thiseffect was only slightly modified by birth weight.

There is an independent effect of maternal pre-gravid weight and diabetes not only on birth weightbut also on the adolescent risk of obesity. Langer andcolleagues77 reported that, in obese women withGDM whose glucose was well controlled on dietalone, the odds of fetal macrosomia (birth weightgreater than 4,000 g) was significantly increased (OR2.12) compared with women with a well controlled(diet only) GDM with normal BMI. Similar results,were reported in women with GDM who were poorly

controlled on diet or insulin. In well-controlled insu-lin-requiring GDM, there was no significant increasedrisk of macrosomia with increasing pregravid BMI.Additionally, Dabelea et al78 also reported that themean adolescent BMI was 2.6 kg/m2 greater in siblingoffspring of diabetic pregnancies compared with theindex siblings born when the mother had previouslyhad normal glucose tolerance. Hence, both maternalpregravid obesity and the presence of maternal dia-betes may independently affect the risk of adolescentobesity in the offspring.

This risk of the developing the metabolic syn-drome in adolescents was recently addressed byBoney et al79 in a longitudinal cohort study of AGAand LGA infants of women with normal glucosetolerant and GDM. The metabolic syndrome wasdefined as the presence of two or more of thefollowing components: obesity, hypertension, glucoseintolerance, and dyslipidemia. Maternal obesity wasdefined as a pregravid BMI greater than 27.3. Chil-dren who were LGA at birth had an increased hazardratio for metabolic syndrome (2.19, 95% CI 1.25–3.82, P�.01) by 11 years of age, as did children ofobese women (1.81, 95% CI 1.03–3.19, P�.04). Thepresence of maternal GDM was not independentlysignificant, but the risk of the development of meta-bolic syndrome was significantly different betweenLGA and AGA offspring of women with GDM by age11 (relative risk 3.6).

CONCLUSIONThe primary objective in the management of obesityduring pregnancy is prevention. Having obesewomen lose weight with lifestyle changes and achievea normal BMI before conception would be the idealgoal, but realistically it is quite difficult to achieve.Once an obese woman does conceive, managementshould be directed at increased surveillance for theserisks: 1) in early gestation, the risks of spontaneous

Table 3. Neonatal Body Composition of Infants of Women With Pregravid Body Mass Index (BMI) LessThan 25 Compared With Those With BMI of 25 or More

Pregravid Body Mass Index

PLess Than 25 (n�144) 25 or More (n�76)

Birth weight (g) 3,284�534 3,436�567 .051Body composition (TOBEC) 2,951�406 3,023�410 .22Lean body mass (g)

Fat mass (g) 331�179 406�221 .008Body fat (%) 9.6�4.3 11�4.7 .006

TOBEC, total body electrical conductivity.Data are expressed as mean�standard deviation.Modified from Sewell, Huston-Presley L, Super DM, Catalano PM. Increased neonatal fat mass, and not lean body mass, is associated with

maternal obesity. Am J Obstet Gynecol 2006;195:1100–3.66 Copyright © 2006, with permission from Elsevier.


abortion and congenital anomalies, 2) in later gesta-tion, gestational hypertension and diabetes-relatedproblems, as well as the increased risk of unexplainedstillbirths, and 3) at parturition, the increased risk ofcesarean delivery and attendant complications ofanesthesia, wound disruption, infection, and deepvein thrombosis. Limiting weight gain in pregnancyto IOM guidelines (currently under review)5 and tightglucose control in women with GDM may improvematernal and neonatal outcomes. Therefore, preven-tion rather than treatment may offer the best hope ofbreaking the vicious cycle of obesity during preg-nancy. Until we attain a better understanding of theunderlying genetic predispositions, physiology, andmechanisms relating to maternal and feto-placentalinteractions and how these, in turn, relate to fetalgrowth and development, all treatments must, bynecessity, be empiric.

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Key Medical and Obstetric Complications inObese Pregnant Women

Early PregnancySpontaneous abortionCongenital anomalies

(Neural tube defects)Late Pregnancy

Gestational hypertension/preeclampsiaGestational diabetesPreterm delivery

(Related to maternal medical and obstetric con-ditions?)

Intrauterine fetal demisePeripartum

Cesarean deliveryFailed vaginal birth after cesarean delivery

Operative morbidities1) Anesthesia complications2) Postpartum endometritis3) Wound breakdown4) Postpartum thrombophlebitis

Fetus/neonateMacrosomiaFetal obesityChildhood obesity


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