All Content

January 2015 Volume 29, Issue 1, Pages 79–90

Obesity in obstetrics
Salzer Liat, MD
,
Luis Cabero, MD
,
Moshe Hod, MD
,
Yariv Yogev, MD
Published Online: August 15, 2014
DOI: http://dx.doi.org/10.1016/j.bpobgyn.2014.05.010
Article Info
 Abstract
 Full Text
 References

Article Outline
I. Obesity – introduction
II. Definitions
III. Scope of the problem
IV. International guidelines
V. Obstetrical management of the obese gravida
A. Prepregnancy consultation
1. Weight reduction
2. Consultation regarding risks and outcomes of obesity
3. Nutritional and exercise recommendations
B. Antenatal management
1. Care in the first trimester
2. Care in the second and third trimester
C. Labor, delivery, and post partum
D. Induction of labor
E. Protracted labor
F. Macrosomia and shoulder dystocia
G. Operative delivery
H. Cesarean section
I. Vaginal birth after cesarean section
VI. Long-term implications on the newborn – children of obese mothers
VII. Summary
VIII. Conflict of interest

Obesity is a rising global epidemic. Obesity during pregnancy is associated with increased
maternal and fetal risks, which is inversely correlated with the severity level of obesity. Other
comorbidities are common (diabetes mellitus, hypertensive disorders, etc.) and contribute to
an even increased risk. Maternal obesity during pregnancy contributes also to offspring
obesity and noncommunicable diseases later in life in a vicious cycle. Managing these
problems, and potentially reducing their risk, can pose a challenge in obstetric care. It is
important to provide preconception nutritional and exercise care, and guidance during
pregnancy and post pregnancy for appropriate weight loss.

Keywords:
obesity, overweight, noncommunicative disease, obstetric complications

Jump to Section

Obesity – introduction
A noncommunicative disease (NCD) is considered a medical condition, which by definition
is noninfectious and non-transmissible among people. The World Health Organization
(WHO) reports NCDs to be by far the leading cause of death in the western world [1].

We believe that obesity in general, and in obstetrics in particular, should be independently

considered one of the NCDs. Obesity is often accompanied by other chronic and obstetric
diseases; however, it is not always clear whether obesity is the direct cause of adverse
pregnancy outcomes by itself or only associated with pregnancy outcome The recent National
Health and Nutrition Examination Survey found that more than one-third of reproductive-
aged women were obese, and 7.6% of those women were extremely obese (body mass index
(BMI) ≥40 kg/m ) [2].
2

Jump to Section

Definitions
Overweight and obesity are defined as abnormal or excessive percent fat accumulation that
may impair health. The WHO and the National Institutes of Health define underweight as a
BMI of ≤18.5, normal weight as a BMI of 18.5–24.9, overweight as a BMI of 25–29.9, and
obesity as a BMI of ≥30. Obesity is further characterized by BMI into class I (30–34.9), class
II (35–39.9), and class III (>40) [3].

However, BMI by itself is a surrogate marker of adiposity and does not measure adipose
tissue directly. As a result, it has limitations and provides no information on fat distribution
[[4], [5]]. As a rule, women have more body fat than men, and it is widely agreed that women
with > 25% body fat are obese [3]. Moreover, much of the published research on obesity is
based on self-reporting of height and weight which has been shown to be unreliable [6].

Due to expected weight gain variability during pregnancy and the short interval of time, there
is no accepted definition for obesity during pregnancy. It is strongly recommended that in
pregnant women, BMI will be calculated at the first antenatal visit in the first trimester, as
during pregnancy the BMI is not recalculated. Some of the studies use other measures to
define obesity including weight at delivery [∗[7], [8], [9], [10]] and the waist to hip ratio
(WHR) [11].

Gestational weight gain is generally lower in obese women compared with normal-weight
women irrespective of any interventions [11]. There have also been inconsistencies in the
way gestational weight gain is measured [12]. In the United States, gestational weight gain is
measured during pregnancy. The US Institute of Medicine (IOM) guidelines [13], based on
observational data [14], stated that healthy women who are at a normal weight for their height
(BMI 18.5–24.9) should gain 11.5–16 kg (25–35 pounds) during pregnancy. As BMI
increases, gestational weight gain should be decreased (Table 1).

Table 1New American recommendations for total gestational weight gain (GWG) (Institute of
Medicine 2009) [13].

Prepregnancy BMI (kg/m ) 2

Range (kg) Range (lb)
Underweight (<18.5) 12.5–18.0 28–40

Normal weight (18.5–24.9) 11.5–16.0 25–35

Overweight (25.0–29.9) 7.0–11.5 15–25

Obese (>29.9) 5.0–9.0 11–20

The Society of Obstetricians and Gynecologists of Canada published in 2010 a clinical

practice guideline with roughly similar numbers. Overweight and obese women gaining
weight within IOM recommendations have less preeclampsia and emergency cesarean
sections; however, they continue to be at an increased risk of gestational diabetes, small for
gestational age, and preterm and perinatal mortality compared with those who gain less than
the IOM recommendations [15].

Weight gain above the IOM recommendations has been associated with poor maternal and
fetal outcomes independent of prepregnancy BMI. By contrast, Britain's National Institute for
Health and Clinical Excellence (NICE) [16] recommends that women should not be weighed
repeatedly during pregnancy as a matter of routine and only if weight has a clinical influence
or if nutrition is a concern.

Pregnancy is considered a window of opportunity for the promotion of healthy eating and
physical activity behavior among women [17].

Jump to Section

Scope of the problem

The latest reports of the WHO indicate that in 2008 approximately 1.4 billion adults were
overweight. Of these overweight adults, over 200 million men and nearly 300 million women
were obese. The WHO also projects that, by 2015, approximately 2.3 billion adults will be
overweight and >700 million will be obese [18].

Human pregnancy is an insulin-resistant condition by itself, potentially compounded by

increased pregravid insulin resistance in obese women. There is a 40–50% increase in insulin
resistance during pregnancy (from the pregravid condition) [[19], [20]].

Jump to Section

International guidelines
Worldwide, international committees addressed the issue of obesity in pregnancy and advise
an oriented weight surveillance approach [[16], ∗[21], [22], [24], [25], [26]].

The American College of Obstetricians and Gynecologists (ACOG), in their committee

opinion [21], strongly encourage preconception assessment and counseling for obese women
that should include the provision of specific information concerning the maternal and fetal
risks of obesity in pregnancy, as well as encouragement to undertake a weight-reduction
program including diet, exercise, and behavior modification. At the initial prenatal visit,
height and weight should be recorded for all women to allow calculation of BMI, and
recommendations for appropriate weight gain, guided by IOM recommendations, should be
reviewed both at the initial visit and periodically throughout pregnancy.

The Royal College of Obstetricians and Gynecologists (RCOG), in a joint guideline with the
Centre for Maternal and Child Enquiries (CMACE) [22], addressed the issues above and
emphasized that the management of women with obesity in pregnancy should be integrated
into all antenatal clinics, with available clear policies and guidelines for care. The guideline
also reinforced the need for dietary supplements (folic acid and vitamin D) during pregnancy.
Special attention was particularly given to the subclass of morbidly obese parturitions
(BMI ≥ 40) and a comprehensive approach was suggested that included an antenatal
consultation with an obstetric anesthetist and a documented assessment in the third trimester
of pregnancy to determine manual handling requirements for childbirth and consider tissue
viability issues.

The UK NICE also published guidance in 2010 regarding weight management before, during,
and after pregnancy [16]. The guidance recommends which actions should be taken in the
obese population in preparing for pregnancy, during pregnancy, and after childbirth with
respect to nutrition and physical activity.
The Society of Obstetricians and Gynaecologists of Canada published in 2010a clinical
practice about obesity in pregnancy [23] dealing with the issues above and also focused on
the preconception period and the opportunity for the gynecologist to raise the issue of weight
loss.

The Royal College of Physicians in Ireland and the Royal Australian and New Zealand
College of Obstetricians and Gynaecologists also published local guidelines dealing with
obesity in pregnancy [[24], [25]].

Jump to Section

Obstetrical management of the obese gravida

It is now universally acknowledged that maternal overweight and obesity are linked with
adverse pregnancy outcome. There are known higher infertility rates, maternal complications
including hypertension, diabetes, respiratory complications, (asthma and sleep apnea),
thromboembolic disease, more frequent intrapartum complications and cesarean delivery with
increased wound infection, endometritis, and anesthetic complications (mainly difficulties in
intubation and placement of regional anesthesia). Newborn complications include congenital
malformations, large-for-gestational-age infants, shoulder dystocia, and long-term adolescent
complications (obesity, diabetes, and possibly more). Class II and III obese women are prone
to an even increased rate of complications and adverse outcomes.

Jump to Section

Prepregnancy consultation
Jump to Section

Weight reduction
It is well established that the best management for obesity is prevention. Usually, by the time
of pregnancy diagnosis in the obese patient, the impaired organogenesis may have already
occurred [[26], [27]]. Thus, the ideal time for intervention is before conception and the
primary care services should ensure that all women of childbearing age have consultation on
how to optimize their weight prior to pregnancy. Interventions include behavioral
modification, dietary changes, exercise, pharmacotherapy, and surgical intervention of
bariatric surgery [28]. Inter-pregnancy weight reduction among women with obesity has been
shown to significantly reduce the risk of developing GDM [29]. An increase in pregravid
weight between the first and second pregnancies resulted in an increased risk of preeclampsia
(odds ratio (OR), 3.2; 95% confidence interval (CI), 2.5–4.2), whereas a decrease in
pregravid weight between the first and second pregnancies from obese to a normal BMI
decreased the risk of cesarean delivery and large-for-gestational-age infants [[30], [31], [32]].
 Jump to Section

Consultation regarding risks and outcomes of obesity

Women with a BMI ≥30 should receive information and advice about the risks of obesity
during pregnancy and childbirth, and they should be advised about the possible strategies to
minimize them prior to conception. Several studies have shown an increased risk of
anovulatory infertility in obese women (OR = 2–3) by mechanisms including
hyperandrogenism and polycystic ovary syndrome (PCOS), which share several
pathophysiological characteristics, namely insulin resistance [[33], [34], [35]]. Body fat
distribution in women of reproductive age seems to have more impact on fertility than age or
obesity itself; a 0.1-unit increase in waist–hip ratio led to a 30% decrease in probability of
conception per cycle (hazards ratio (HR) 0.7; 95% CI 0.5–0.8) [34]. If an in vitro fertilization
(IVF) treatment is needed, the patient should be aware of the possible association of obesity
with decreased chances of pregnancy (insufficient follicular development, lower oocyte
counts, poor oocyte quality, endometrial quality, or a combination of these factors)
[[36], [37],[38]]. In a systematic review and meta-analysis including 33 studies and almost
48,000 IVF/intra-cytoplasmatic sperm injection (ICSI) treatment cycles, women who were
overweight or obese (BMI ≥ 25 kg/m ) had a statistically significant small reduction in
2

clinical pregnancy rate (relative risk (RR) = 0.90) and live-birth rate (RR = 0.84) and a
significantly higher miscarriage rate (RR = 1.31) than normal-weight women
(BMI < 25 kg/m ) [38]. Some reports found that the outcomes were comparable to nonobese
2

women but needed higher doses of ovulation-inducing agents [[39], [40], ∗[41]].

Jump to Section

Nutritional and exercise recommendations

Nutrition consultation should be offered to all obese women, and they should be encouraged
to follow an exercise program [21]. The ACOG suggests a healthy diet that uses caloric
restriction in combination with daily aerobic exercise [28]. Nutritional recommendations
include a diet that is high in fiber with fresh fruits, vegetables, lean protein, and complex
carbohydrates while avoiding foods that contain large amounts of sugar, saturated fats, and
cholesterol. Few guidelines [[22], [25]] even advise taking 5 mg of folic acid due to the
higher risk of NTD in this population and evidence of lower serum folate levels even after
controlling for folate intake. Regular aerobic exercises such as brisk walking, stair climbing,
jogging, or swimming that use the larger skeletal muscles should be incorporated into weight
reduction programs.

There is also increasing evidence regarding the need for vitamin D supplementation during
pregnancy, especially in the obese women, as serum vitamin D levels are decreased in this
population. Cord serum vitamin D levels in neonates of obese women have also been found
to be lower than in babies born to nonobese women [42].
 Jump to Section

Antenatal management
Jump to Section

Care in the first trimester

 •
First antenatal visit – The goal of the first meeting is to learn the “medical baseline”
of the patient and to assess her level of risk for adverse maternal and perinatal
outcomes. Moreover, it is important to set goals for surveillance during pregnancy and
to give information and recommendations on how to minimize the risks. Special
attention should be given to detailed and thorough history and complete physical
examination. It is important to measure the patient's height and weight as this will
serve the physician to calculate the BMI. Questions should be oriented to the higher-
risk coexisting medical conditions. As the severity of obesity increases, these are more
prevalent and need closer monitoring. For pregnant women at the highest risk of
comorbidities (class III obesity), additional tests should be considered as a baseline:
laboratory tests (baseline chemistry and 24-h urine collection) as well as maternal
echocardiography [43]. Sleep disorder evaluation should be considered in symptomatic
patients as obesity is a strong risk factor for obstructive sleep apnea (OSA) which is
associated with a higher incidence of maternal (hypertension, stroke, and cardiac
dysfunction) and obstetric (hypertension disorders, GDM, and fetal growth retardation)
[[44], [45]] complications. Obese patients should receive dietary counseling to guide
them through the pregnancy with documented weight gain goals.
 •
Miscarriages – Patients should be aware of an increased risk of first-trimester
miscarriage, though data are not conclusive. Whereas several studies suggest that
obesity may increase the risk of miscarriage [[46], [47]] due to adverse influences on
the embryo, the endometrium, or both [[47], [48], [49]], others found no association
between miscarriage and obesity [[50], [51]]. These studies lack consistency, however,
mainly because of the use of different obesity classification systems that disregard the
WHO criteria.
 •
Early screening for diabetes – Because obesity is accompanied by insulin resistance
that is expected to increase during pregnancy, the obstetrician should consider an early
screening for preexisting diabetes mellitus. Women with severe obesity, personal
history of gestational diabetes mellitus (GDM) or delivery of large-for-gestational-age
infant, glycosuria, PCOS, or a strong family history of diabetes should be given a
higher degree of suspicion. A positive first-trimester diagnosis, especially with a high
value of glycosylated hemoglobin, is considered pregestational in nature and requires
 intensive surveillance and treatment [∗[21], [52], [53]]. If initially normal, a repeated
early third-trimester screening is obligatory.
Jump to Section

Care in the second and third trimester

Care in the second and third trimester should be aimed at early identification of fetal,
maternal, and placental pathologies. Additional goals of mid-trimester management include
ongoing counseling regarding appropriate weight gain and dietary recommendations and
maintenance and improvement of coexisting medical disorders.

 •
Diagnosis of congenital anomalies – Some malformations are found to be in higher
prevalence in the obese population [43] and the risk may increase with increasing
maternal weight [[54], [55]]. The malformations that are mostly connected with
obesity are neural tube defects and cardiac malformations, though additional
malformations are being associated with obesity such as diaphragmatic hernia,
hydrocephaly, hypospadias, cystic kidney, omphalocele, and more [[27], [56]].
Because these types of congenital anomalies are often seen with pregestational
diabetes, some investigators suggest that many of these obese women may have had
undiagnosed type 2 diabetes [56]. Apart from the increased prevalence of
malformations, there is also an increased risk of failure to detect these malformations
due to suboptimal visualization of fetal anatomy by ultrasound examination.
Approximately 15% of normally visible structures will be suboptimally seen in women
with a BMI above the 90th percentile [57].
 •
Gestational diabetes mellitus – Several studies demonstrated a two-to tenfold
increase in the rate of GDM among obese patients [∗[58], [59]]. The magnitude of this
risk is positively correlated with increases in maternal weight [∗[58], [60], [61]]. Post
partum, glucose intolerance associated with GDM generally resolves. However, obese
women with a history of GDM have a twofold increased prevalence of subsequent type
2 diabetes compared to lean women [62]. For those women whose first-trimester
screening test for GDM was normal, a repeat screening test between 24 and 28 weeks
with a 50-g 1-h oral glucose challenge is indicated [53]. As for later screening, though
few studies offered some advantages [[63], [64]], there is no current evidence to
support a significant clinical benefit.
 •
Pregnancy-associated hypertension – Obese women should be followed up closely
for the development of hypertensive disorders, and patients with chronic hypertension
should be followed up for the development of superimposed preeclampsia.
Hypertensive disorders during pregnancy have been consistently reported to be
 associated with obesity [∗[58], [65], ∗[66], [67]]. A systematic review of 13 cohort
studies comprising nearly 1/4 million women showed that the risk of preeclampsia
doubled with each 5–7 kg/m increase in prepregnancy BMI. This relation persisted in
2

studies that excluded women with chronic hypertension, diabetes mellitus, or multiple
gestations, and other confounders [66]. The mechanism for the association between
obesity and preeclampsia is not clear and perhaps related to pathophysiologic changes
such as insulin resistance, hyperlipidemia, and subclinical inflammation [[68], [69]].
Epidemiological studies have reported a relationship between pregnancies complicated
by preeclampsia and an increased risk of maternal coronary heart disease in later life
[66].
 •
Intrauterine fetal death – Obese pregnant women have been shown to have an
increased risk of intrauterine fetal death [[70], [71]]. A meta-analysis including nine
controlled studies showed that overweight and obese pregnant women experienced
significantly more stillbirths than normal-weight women (OR = 1.5–2), even after
controlling for other coexisting complications [72]. The risk of stillbirth increased in a
dose-dependent fashion with increase in BMI [71]. A meta-analysis found that
maternal overweight and obesity are the highest-ranking modifiable risk factor for
stillbirth in high-income populations, with a population-attributable risk of 8–18%
[73]. Maternal obesity is also associated with an increased overall risk of infant death,
mainly neonatal death [74].
 •
Fetal overgrowth – Obesity is a significant and independent contributor impacting
fetal growth [75]. Even after adjustment for GDM, there is approximately a twofold
RR for macrosomia [76]. Other coexisting diseases can restrict fetal growth [77].
Because body habitus in this population may limit the use of clinical fetal weight
estimation, serial ultrasound fetal weight estimation is recommended, especially near
term when the decision on the mode of delivery is impending.
 •
Timing of delivery – Obesity carries a higher risk of preterm delivery. Evidence
suggests that obesity may be associated with induced preterm delivery, but not
spontaneous preterm birth [[78], [79]]. Studies show that as the BMI increases, the risk
of spontaneous preterm labor decreases whereas the risk of requiring an elective
preterm delivery increased [80]. Most studies attribute the risk of induced preterm
delivery to obesity-related medical and obstetrical complications (diabetes mellitus,
hypertension, and preeclampsia). A recent population-based cohort study that included
>1.5 million singleton deliveries observed a dose-dependent relationship between
severity of obesity and the risk of spontaneous extremely preterm deliveries (22–27
 weeks of gestation) after adjustment of confounders. Inflammatory upregulation
mechanisms might be involved [81]. On the other hand, post-term deliveries are also
more common in an unknown mechanism. A few of the hypothesized explanations
include miscalculation of gestational age or hormonal changes associated with obesity
[[82], [83]].
Jump to Section

Labor, delivery, and post partum

Obesity can create significant challenges of intrapartum care due to difficulties in
examination and assessment of the mother and fetus. Additionally, obesity complicates the
management of labor by a proven association with macrosomia, shoulder dystocia,
cephalopelvic disproportion, and high incidence of operative delivery. Furthermore, morbidly
obese women also required more intervention, intense monitoring, and skilled clinical staff in
their intrapartum care. Obstetric units that care for extremely obese patients should also have
specialized equipment in the delivery room.

Jump to Section

Induction of labor
Obese women are more likely than normal-weight women to have an induction of labor
because of both an increased rate of obstetrical complications and a prolonged pregnancy in
an apparent dose-dependent manner with increasing class of obesity. The magnitude of this
risk ranges from a 1.6- to 2.2-fold increase [∗[58], [84]]. Induction of labor in the obese
patient, compared with the lean patient, is associated with longer induction to delivery time
with prostaglandins, higher requirements of oxytocin [[85], [86]], and higher chances of
failure and subsequent cesarean section (CS) [87]. Common indications for induction failure
and CS are fetal distress and arrested labor [88].

Jump to Section

Protracted labor
Observational studies on the progress of labor in the obese parturient have shown different
patterns of progress. Obese women are more likely to have an inadequate contraction pattern
during the first stage of labor and subsequently have a longer first stage [[89], [90]]. The
exact mechanism of dysfunctional labor in obese women is not completely understood.
Several authors have speculated that this dysfunction results from the added soft-tissue
deposits in the pelvis of the obese gravid [91]. Another explanation may be related to a
greater volume of distribution for ripening agents during the course of labor, making them
less effective. Increased levels of leptin, cholesterol, and apelin can also theoretically inhibit
uterine muscle contractility [92]. All these factors may contribute to increased rates of labor
induction, dysfunctional labor requiring intrapartum cesarean delivery, and postpartum
hemorrhage. The duration of the second stage of labor does not appear to be affected by an
increase in BMI [93].

Jump to Section

Macrosomia and shoulder dystocia

Maternal prepregnancy weight and decreased prepregnancy insulin sensitivity have been
shown to strongly correlate with fetal growth, especially on fetal fat mass accumulation and
distribution at birth [[94], [95]]. Obese women, even in the presence of normal glucose
tolerance, are almost twice as likely to have a macrosomic infant [96]. Clearly, this observed
increase in birth weight and macrosomia in this group can result in cephalopelvic
disproportion, shoulder dystocia and associated inherent birth trauma, perineal lacerations,
fetal injury, and postpartum hemorrhage. A study examining maternal anthropometric
parameters found that obesity is one of the strongest risk factors (2.7-fold risk) for shoulder
dystocia, even after adjustment for confounding factors such as macrosomia and diabetes
[97].

Jump to Section

Operative delivery
Obesity is associated with an increased risk of operative vaginal delivery (OVD), probably in
a dose-dependent matter [98]. OR may be up to 1.7 for OVD for women with class III obesity
in comparison to normal BMI patients [43]. Furthermore, not only does the obese gravida
carry a higher risk of operative delivery but also she is prone to fail when trying to. In a
population-based database of 60,167 deliveries, the OR for failed operative delivery was 1.75
in women of BMI ≥30 compared with women with BMI <30 [83]. The decision on an
attempt of operative delivery in obese patients should be carefully considered.

Jump to Section

Cesarean section
The incidence of cesarean delivery correlates with increased prepregnancy BMI [99] and also
with excessive gestational weight gain [∗[58], [100]]. For women without other
complications, the estimated adjusted RR is estimated to be 1.2–1.5 for overweight and obese
women and up to 3.1 for morbidly obese women [101]. This risk is further increased by other
obesity-related pregnancy complications [[102], [103]]. Unfortunately, obese women
undergoing CS experience more complications, including blood loss, increased operative
time, and the need for vertical skin incision [104]. After CS, the obese pregnant patient faces
a higher risk of wound infection and endometritis. Perioperative antibiotic prophylaxis to
protect against endometritis and surgical site infection may not be as effective in obese
patients in the accepted dose, due to different pharmacokinetics and pharmacodynamics
[105], and should be adjusted. An attempt to decrease the incidence of wound breakdown in
the obese patients after CS includes closure of the subcutaneous layer [106]. The placement
of a subcutaneous drain was not proven to be effective [107].

Jump to Section

Vaginal birth after cesarean section

The impact of morbid obesity on mode of delivery, particularly in those with a previous
cesarean, has only been examined in small populations and with disparate results, suggesting
a significantly lower success rate of trial of labor after cesarean delivery (TOLAC)
[[108], [109]]. Additionally, normal BMI women who became overweight before the second
pregnancy had also decreased vaginal birth after cesarean section (VBAC) rates [110]. In a
prospective multicenter study that included >4000 TOLAC attempts, the likelihood of VBAC
was related inversely to BMI. Normal-weight women had a VBAC failure rate of 15%,
compared with 39% for the morbidly obese (BMI > 40 kg/m ) group. A higher rate of uterine
2

scar dehiscence or rupture was noted for the morbidly obese group (2.1%), compared with the
overweight (1.4%) and normal-weight (0.9%) groups. Composite morbidity and neonatal
injury rates were found to be greater with increasing BMI [108].

Jump to Section

Long-term implications on the newborn – children of

obese mothers
The implications of maternal obesity far surpass intrauterine life, extending into infancy and
even adulthood with severe health repercussions. Maternal obesity long has been linked with
the delivery of a macrosomic infant. There is accumulating abundant evidence linking
macrosomia to increased overweight and obesity in adolescents as well as adults
[[111], [112]]. The prevalence of childhood obesity between 2.4 and 2.7 times higher in the
offspring of obese women was already reported in the early 1990s [111]. These findings
remained consistent even after controlling for additional risk factors including birth weight,
parity, weight gain, and smoking during pregnancy (RR 2.0; 95% CI: 1.7–2.3). This risk is
further increased with additive risk factors such as maternal diabetes during pregnancy.
Diabetes per se conveys a high risk of the development of diabetes and obesity in offspring in
excess of risk attributable to genetic factors alone [[113], [114], ∗[115]]. Thus, the epidemic
of obesity and subsequent risk of diabetes and components of the metabolic syndrome clearly
may begin in utero with fetal overgrowth and adiposity [116]. Maternal obesity is also
associated with cardiovascular disease in the adult offspring [117]. Therefore, there is an
association between maternal obesity (but not paternal) and insulin resistance on the risk of
offspring to develop obesity, diabetes, and cardiovascular disease in adulthood. Recently, a
population-based case–control study reported an association between maternal metabolic
conditions (including obesity) and neurodevelopmental problems in children (including
autism) [118]. Further studies are needed to support this observation.

Jump to Section

Summary
Obesity in pregnancy is a complex chronic disease. The primary objective in the management
of obesity is prevention as the obese woman enters the pregnancy with a baseline morbidity
that is exacerbated during pregnancy and influences pregnancy outcome. The worldwide
epidemic of adolescent and adult obesity may also be propagated and enhanced at an earlier
stage in life because of an abnormal metabolic milieu in utero during gestation. There are
both short- and long-term complications that accompany the pregnancy and almost all
pregnancy complications occur with greater frequency among the obese patients. Maternal
obesity during pregnancy also contributes to offspring obesity and noncommunicable
diseases later in life. Unfortunately, obesity, as an NCD, cannot be cured during pregnancy,
but rather be controlled carefully to the best possible ending – a healthy mother and child.
Treatment in these patients should be multidisciplinary and involve nutritionists, dietitians,
other internal medicine specialists, psychologists, and psychiatrists. Pregnancy of the obese
patient should be considered a high risk and thus be more closely monitored. The obstetrician
should inform the patients on the different risks and complications and keep them actively
involved in the treatment. Physician and patient cooperation and attention can lead to early
detection of complications and better fetal and maternal outcome. The obstetrician's role does
not end until after pregnancy, when every effort should be made to encourage weight
reduction and lifestyle modification in order to minimize the risks for the mother and her
future offspring. More studies are needed in order to attain a better understanding of the
underlying genetic predispositions, physiology, and mechanisms related to maternal and feto-
placental interactions.

Jump to Section

Conflict of interest
The authors report no conflict of interest.

+
Practice points

+
Research agenda

Jump to Section
 References
1. World Health Organization. Assessing national capacity for the prevention and control of noncommunicable diseases:
report of the 2010 global survey. World Health Organization, Geneva, Switzerland; 2012
o View in Article
2. Flegal, K.M., Carroll, M.D., Ogden, C.L. et al. Prevalence and trends in obesity among US adults, 1999–
2008.JAMA. 2010; 303: 235–241
o View in Article
3. World Health Organization. Obesity: preventing and managing the global epidemic. World Health
Organization,Geneva, Switzerland; 2000 (WHO technical report series 894)
o View in Article
4. Fattah, C., Farah, N., Barry, S. et al. Maternal weight and body composition in the first trimester of pregnancy. Acta
Obstet Gynecol Scand. 2010; 89: 952–955
o View in Article
5. Prentice, A.M. and Jebb, S.A. Beyond body mass index. Obes Rev. 2001; 2: 141–147
o View in Article
6. Niedhammer, I., Bugel, I., Bonenfant, S. et al. Validity of self-reported weight and height in the French GAZAL
cohort. Int J Obes Relat Metab Disord. 2000; 24: 1111–1118
o View in Article
7. Ben-Haroush, A., Hadar, E., Chen, R. et al. Maternal obesity is a major risk factor for large-for-gestational-infants in
pregnancies complicated by gestational diabetes. Arch Gynecol Obstet. 2009; 279: 539–543
o View in Article
8. Okun, N., Verma, A., Mitchell, B.F. et al. Relative importance of maternal constitutional factors and glucose
intolerance of pregnancy in the development of newborn macrosomia. J Matern Fetal Med. 1997; 6: 285–290
o View in Article
9. Jacobson, J.D. and Cousins, L. A population-based study of maternal and perinatal outcome in patients with
gestational diabetes. Am J Obstet Gynecol. 1989; 161: 981–986
o View in Article
10. Brown, J.E., Potter, J.D., Jacobs, D.R. et al. Maternal waist-to-hip ratio as a predictor of newborn size: results of the
Diana Project. Epidemiology. 1996; 7: 62–66
o View in Article
11. Farah, N., Stuart, B., Donnelly, V. et al. The influence of maternal body composition on birth weight. Eur J Obstet
Gynaecol. 2011; 157: 14–17
o View in Article
12. Turner, M.J. and Farah, N. Gestational weight gain and birth weight. Ir Med J. 2010; 103: 293–294
o View in Article
13. IOM (Institute of Medicine) (US). Weight gain during pregnancy; reexamining the guidelines. The National Academy
Press, Washington DC; 2009
o View in Article
14. Rasmussen, K.M., Catalano, P.M., and Yaktine, A.L. New guidelines for weight gain during pregnancy: what
obstetrician/gynecologists should know. Curr Opin Obstet Gynecol. 2009 Dec; 21: 521–526
o View in Article
15. Beyerlein, A., Lack, N., and von Kries, R. Within-population average ranges compared with Institute of Medicine
recommendations for gestational weight gain. Obstet Gynecol. 2010 Nov; 116: 1111–1118
o View in Article
16. National institute for health and care excellence (NICE), July 2010: Weight management before, during and after
pregnancy, NICE public health guidance 27, guidance.nice.org.uk/ph27.
o View in Article
17. Phelan, S. Pregnancy: a “teachable moment” for weight control and obesity prevention. Am J Obstet
Gynecol.2010; 202: 135.e1–135.e8
o View in Article
18. World health organization. Media centre. Obesity and overweight.
Factsheets.http://www.who.int/mediacentre/factsheets/fs311/en/.
o View in Article
19. Catalano, P.M., Tyzbir, E.D., Roman, N.M. et al. Longitudinal changes in insulin release and insulin resistance in non-
obese pregnant women. Am J Obstet Gynecol. 1991; 165: 1667–1672
o View in Article
20. Catalano, P. Editorial: obesity and pregnancy – the propagation of a viscous cycle?. J Clin Endocrinol
Metab.2003; 88: 3505–3506
o View in Article
21. American College of obstetricians and Gynecologists (ACOG). ACOG committee opinion no. 549: obesity in
pregnancy. Obstet Gynecol. 2013; 121: 213–217
o View in Article
22. CMACE/RCOG joint guideline: management of women with obesity in pregnancy. Centre for Maternal and Child
Enquiries and Royal College of Obstetricians and Gynecologists, London; 2010
o View in Article
23. Davies, G.A., Maxwell, C., McLeod, L. et al. SOGC clinical practice guidelines: obesity in pregnancy. No. 239,
February 2010. Int J Gynaecol Obstet. 2010 Aug; 110: 167–173
o View in Article
24. Institute of Obstetricians and Gynaecologists. Royal college of physicians of Ireland and clinical strategy and
programmes directorate, health service executive; obesity and pregnancy. Clinical Practice Guideline. June
2011; (revised June 2013)
o View in Article
25. The royal Australian and New Zealand college of obstetricians and gynecologists. College statement C-Obs 49;
Management of obesity in pregnancy. ; Sep 2013
o View in Article
26. Catalano, P.M., Presley, L., Minium, J. et al. Fetuses of obese mothers develop insulin resistance in utero.Diabetes
Care. 2009; 32: 1076–1080
o View in Article
27. Blomberg, M.I. and Kallen, B. Maternal obesity and morbid obesity: the risk for birth defects in the offspring. Birth
Defects Res A Clin Mol Teratol. 2010; 88: 35–40
o View in Article
28. American College of Obstetricians and Gynecologists (ACOG). ACOG committee opinion no. 319: the role of the
obstetrician gynecologist in the assessment and management of obesity. Obstet Gynecol. 2005; 106: 895–899
o View in Article
29. Glazer, N.L., Hendrickson, A.F., Schellenbaum, G.D. et al. Weight change and the risk of gestational diabetes in obese
women. Epidemiology. 2004; 15: 733–737
o View in Article
30. Getahun, D., Ananth, C.V., Oyelese, Y. et al. Primary preeclampsia in the second pregnancy: effects of changes in
prepregnancy body mass index between pregnancies. Obstet Gynecol. 2007; 110: 1319–1325
o View in Article
31. Getahun, D., Ananth, C.V., Peltier, M.R. et al. Changes in prepregnancy body mass index between the first and second
pregnancies and risk of large-for-gestational age birth. Am J Obstet Gynecol. 2007; 196: 530.e1–530.e8
o View in Article
32. Getahun, D., Kaminsky, L.M., Elsasser, D.A. et al. Changes in prepregnancy body mass index between pregnancies
and risk of primary cesarean delivery. Am J Obstet Gynecol. 2007; 197: 376.e1–376.e7
o View in Article
33. Grodstein, F., Goldman, M.B., and Cramer, D.W. Body mass index and ovulatory infertility. Epidemiology. 1994; 5:247–
250
o View in Article
34. Zaadstra, B.M., Seidell, J.C., Van Noord, P.A. et al. Fat and female fecundity: prospective study of effect of body fat
distribution on conception rates. BMJ. 1993; 306: 484–487
o View in Article
35. Metwally, M., Li, T.C., and Ledger, L. The impact of obesity on female reproductive function. Obesity
Rev. 2007; 8:515–523
o View in Article
36. Wang, J.X., Davies, M., and Norman, R.J. Body mass and probability of pregnancy during assisted reproduction
treatment: retrospective study. BMJ. 2000; 321: 1320
o View in Article
37. Petersen, G.L., Schmidt, L., Pinborg, A. et al. The influence of female and male body mass index on live births after
assisted reproductive technology treatment: a nationwide register-based cohort study. Fertil Steril. 2013; 99:1654
o View in Article
38. Rittenberg, V., Seshadri, S., Sunkara, S.K. et al. Effect of body mass index on IVF treatment outcome: an updated
systematic review and meta-analysis. Reprod Biomed Online. 2011; 23: 421
o View in Article
39. Maheshwari, A., Stofberg, L., and Bhattacharya, S. Effect of overweight and obesity on assisted reproductive
technology–a systematic review. Hum Reprod Update. 2007; 13: 433
o View in Article
40. Balen, A.H., Platteau, P., Andersen, A.N. et al. The influence of body weight on response to ovulation induction with
gonadotrophins in 335 women with World Health Organization group II anovulatory
infertility. BJOG. 2006; 113:1195
o View in Article
41. Souter, I., Baltagi, L.M., Kuleta, D. et al. Women, weight, and fertility: the effect of body mass index on the outcome of
superovulation/intrauterine insemination cycles. Fertil Steril. 2011; 95: 1042
o View in Article
42. Bodnar, L.M., Catov, J.M., Roberts, J.M. et al. Prepregnancy obesity predicts poor vitamin D status in mothers and
their neonates. J Nutr. 2007; 137: 2437–2442
o View in Article
43. Gunatilake, R.P. and Perlow, J.H. Obesity and pregnancy: clinical management of the obese gravida. Am J Obstet
Gynecol. 2011; 204: 106–119
o View in Article
44. Franklin, K.A., Holmgren, P.A., Jonsson, F. et al. Snoring, pregnancy-induced hypertension, and growth retardation of
the fetus. Chest. 2000; 117: 137–141
o View in Article
45. Olivarez, S.A., Ferres, M., Antony, K. et al. Obstructive sleep apnea screening in pregnancy, perinatal outcomes, and
impact of maternal obesity. Am J Perinatol. 2011; 28: 651–658
o View in Article
46. Lashen, H., Fear, K., and Sturdee, D.W. Obesity is associated with increased risk of first trimester and recurrent
miscarriage: matched case-control study. Hum Reprod. 2004; 19: 1644–1646
o View in Article
47. WanG, J.X., Davies, M.J., and Norman, R.J. Obesity increases the risk of spontaneous abortion during infertility
treatment. Obes Res. 2002; 10: 551–554
o View in Article
48. Metwally, M., Ong, K.J., Ledger, W.L. et al. Does high body mass index increase the risk of miscarriage after
spontaneous and assisted conception? A meta-analysis of the evidence. Fertil Steril. 2008; 90: 714–726
o View in Article
49. Bellver, J., Melo, M.A., Bosch, E. et al. Obesity and poor reproductive outcome: the potential role of the
endometrium. Fertil Steril. 2007; 88: 446–451
o View in Article
50. Lashen, H., Ledger, W., Bernal, A.L. et al. Extremes of body mass do not adversely affect the outcome of
superovulation and in-vitro fertilization. Hum Reprod. 1999; 14: 712–715
o View in Article
51. Roth, D., Grazi, R.V., and Lobel, S.M. Extremes of body mass index do not affect first-trimester pregnancy outcome
in patients with infertility. Am J Obstet Gynecol. 2003; 188: 1169–1170
o View in Article
52. American College of Obstetricians and Gynecologists (ACOG). ACOG practice bulletin no.137: gestational
diabetes. Obstet Gynecol. 2013; 122: 406–416
o View in Article
53. American Diabetes Association (ADA). Gestational diabetes mellitus. Diabetes Care. 2004; 27: 88–90
o View in Article
54. Stothard, K.J., Tennant, P.W., Bell, R. et al. Maternal overweight and obesity and the risk of congenital anomalies: a
systematic review and meta-analysis. JAMA. 2009; 301: 636
o View in Article
55. Gilboa, S.M., Correa, A., Botto, L.D. et al. Association between prepregnancy body mass index and congenital heart
defects. Am J Obstet Gynecol. 2010; 202: 51
o View in Article
56. Watkins, M.L., Rasmussen, S.A., Honein, M.A. et al. Maternal obesity and risk for birth
defects. Pediatrics. 2003;111: 1152–1158
o View in Article
57. Wolfe, H.M., Sokol, R.J., Martier, S.M. et al. Maternal obesity: a potential source of error in sonographic prenatal
diagnosis. Obstet Gynecol. 1990; 76: 339–342
o View in Article
58. Sebire, N.J., Jolly, M., Harris, J.P. et al. Maternal obesity and pregnancy outcome: a study of 287,213 pregnancies in
London. Int J Obes Relat Metab Disord. 2001; 25: 1175–1182
o View in Article
59. Kumari, A.S. Pregnancy outcome in women with morbid obesity. Int J Gynaecol Obstet. 2001; 73: 101–107
o View in Article
60. Torloni, M.R., Betrán, A.P., Horta, B.L. et al. Prepregnancy BMI and the risk of gestational diabetes: a systematic
review of the literature with meta-analysis. Obes Rev. 2009; 10: 194
o View in Article
61. Chu, S.Y., Callaghan, W.M., Kim, S.Y. et al. Maternal obesity and risk of gestational diabetes mellitus. Diabetes
Care. 2007; 30: 2070
o View in Article
62. O'Sullivan, J.B. Body weight and subsequent diabetes mellitus. JAMA. 1982; 248: 949
o View in Article
63. Virally, M., Laloi-Michelin, M., Meas, T. et al. Occurrence of gestational diabetes mellitus, maternal and fetal
outcomes beyond the 28th week of gestation in women at high risk of gestational diabetes. A prospective
study.Diabetes Metab. 2007; 33: 290–295
o View in Article
64. Kurtbas, H., Keskin, H.L., and Avsar, A.F. Effectiveness of screening for gestational diabetes during the late
gestational period among pregnant Turkish women. J Obstet Gynaecol Res. 2011; 37: 520–526
o View in Article
65. Sibai, B.M., Ewell, M., Levine, R.J. et al. Risk factors associated with preeclampsia in healthy nulliparous women.
The Calcium for Preeclampsia Prevention (CPEP) Study Group. Am J Obstet Gynecol. 1997; 177: 1003–1010
o View in Article
66. O'Brien, T.E., Ray, J.G., and Chan, W.S. Maternal body mass index and the risk of preeclampsia: a systematic
overview. Epidemiology. 2003; 14: 368
o View in Article
67. HAPO Study Cooperative Research Group. Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study:
associations with maternal body mass index. BJOG. 2010; 117: 575
o View in Article
68. Wolf, M., Kettyle, E., Sandler, L. et al. Obesity and preeclampsia: the potential role of inflammation. Obstet
Gynecol.2001; 98: 757
o View in Article
69. Bodnar, L.M., Ness, R.B., Harger, G.F. et al. Inflammation and triglycerides partially mediate the effect of
prepregnancy body mass index on the risk of preeclampsia. Am J Epidemiol. 2005; 162: 1198
o View in Article
70. Nohr, E.A., Bech, B.H., Davies, M.J. et al. Prepregnancy obesity and fetal death. Obstet Gynecol. 2005; 106: 250–259
o View in Article
71. Salihu, H.M., Dunlop, A., Hedayatzadeh, M. et al. Extreme obesity and risk of stillbirth among black and white
gravidas. Obstet Gynecol. 2007; 110: 552–557
o View in Article
72. Chu, S.Y., Kim, S.Y., Lau, J. et al. Maternal obesity and risk of stillbirth: a metaanalysis. Am J Obstet
Gynecol.2007; 197: 223
o View in Article
73. Flenady, V., Koopmans, L., Middleton, P. et al. Major risk factors for stillbirth in high-income countries: a systematic
review and meta-analysis. Lancet. 2011 16; 377: 1331–1340
o View in Article
74. Chen, A., Feresu, S.A., Fernandez, C. et al. Maternal obesity and the risk of infant death in the United
States.Epidemiology. 2009; 20: 74
o View in Article
75. Yogev, Y., Langer, O., Xenakis, E.M. et al. The association between glucose challenge test, obesity and pregnancy
outcome in 6390 non-diabetic women. J Matern Fetal Neonatal Med. 2005; 17: 29–34
o View in Article
76. Ehrenberg, H.M., Mercer, B.M., and Catalano, P.M. The influence of obesity and diabetes on the prevalence of
macrosomia. Am J Obstet Gynecol. 2004; 191: 964–968
o View in Article
77. Moynihan, A.T., Hehir, M.P., Glavey, S.V. et al. Inhibitory effect of leptin on human uterine contractility in vitro. Am
J Obstet Gynecol. 2006; 195: 504–509
o View in Article
78. McDonald, S.D., Han, Z., Mulla, S. et al. Overweight and obesity in mothers and risk of preterm birth and low birth
weight infants: systematic review and meta-analyses. BMJ. 2010; 341: c3428
o View in Article
79. Torloni, M.R., Betrán, A.P., Daher, S. et al. Maternal BMI and preterm birth: a systematic review of the literature
with meta-analysis. J Matern Fetal Neonatal Med. 2009; 22: 957
o View in Article
80. Smith, G.C.S., Shah, I., Pell, J.P. et al. Maternal obesity in early pregnancy and risk of spontaneous and elective
preterm deliveries: a retrospective cohort study. Am J Public Health. 2007; 97: 157–162
o View in Article
81. Cnattingius, S., Villamor, E., Johansson, S. et al. Maternal obesity and risk of preterm delivery. JAMA. 2013; 309:2362
o View in Article
82. Halloran, D.R., Cheng, Y.W., Wall, T.C. et al. Effect of maternal weight on postterm delivery. J Perinatol. 2012; 32:85
o View in Article
83. Usha Kiran, T.S., Hemmadi, S., Bethel, J. et al. Outcome of pregnancy in a woman with an increased body mass
index. BJOG. 2005; 112: 768
o View in Article
84. Jensen, D.M., Damm, P., Sørensen, B. et al. Pregnancy outcome and prepregnancy body mass index in 2459 glucose-
tolerant Danish women. Am J Obstet Gynecol. 2003; 189: 239
o View in Article
85. Pevzner, L., Powers, B.L., Rayburn, W.F. et al. Effects of maternal obesity on duration and outcomes of prostaglandin
cervical ripening and labor induction. Obstet Gynecol. 2009; 114: 1315–1321
o View in Article
86. Melamed, N., Ben-Haroush, A., Kremer, S. et al. Failure of cervical ripening with prostaglandin-E2 can it be
predicted?. J Matern Fetal Neonatal Med. 2010; 23: 536–540
o View in Article
87. Gauthier, T., Mazeau, S., Dalmay, F. et al. Obesity and cervical ripening failure risk. J Matern Fetal Neonatal
Med.2012; 25: 304–307
o View in Article
88. Cedergren, M.I. Non-elective caesarean delivery due to ineffective uterine contractility or due to obstructed labour in
relation to maternal body mass index. Eur J Obstet Gynecol Reprod Biol. 2009; 145: 163–166
o View in Article
89. Vahratian, A., Zhang, J., Troendle, J.F. et al. Maternal prepregnancy overweight and obesity and the pattern of labor
progression in term nulliparous women. Obstet Gynecol. 2004; 104: 943–951
o View in Article
90. Nuthalapaty, F.S., Rouse, D.J., Owen, J. et al. The association of maternal weight with cesarean risk, labor duration,
and cervical dilatation rate during labor induction. Obstet Gynecol. 2004; 103: 452–456
o View in Article
91. Ehrenberg, H.M., Huston-Presley, L., Catalano, P.M. et al. The influence of obesity and gestational diabetes mellitus on
accretion and the distribution of adipose tissue in pregnancy. Am J Obstet Gynecol. 2003; 189: 944–948
o View in Article
92. Hehir, M.P. and Morrison, J.J. The adipokine apelin and human uterine contractility. Am J Obstet Gynecol. 2012;206
o View in Article
93. Robinson, B.K., Mapp, D.C., Bloom, S.L. et al. Increasing maternal body mass index and characteristics of the second
stage of labor. Obstet Gynecol. 2011; 118: 1309
o View in Article
94. Sewell, M.F., Huston-Presley, L., Super, D.M. et al. Increased neonatal fat mass, not lean body mass, is associated with
maternal obesity. Am J Obstet Gynecol. 2006; 195: 1100–1103
o View in Article
95. Hull, H.R., Dinger, M.K., Knehans, A.W. et al. Impact of maternal body mass index on neonate birthweight and body
composition. Am J Obstet Gynecol. 2008; 198: 416.e1–416.e6
o View in Article
96. Sheiner, E., Levy, A., Menes, T.S. et al. Maternal obesity as an independent risk factor for caesarean delivery.Paediatr
Perinat Epidemiol. 2004; 18: 196–201
o View in Article
97. Mazouni, C., Porcu, G., Cohen-Solal, E. et al. Maternal and anthropomorphic risk factors for shoulder dystocia.Acta
Obstet Gynecol Scand. 2006; 85: 567–570
o View in Article
98. Yu, C.K., Teoh, T.G., and Robinson, S. Obesity in pregnancy. Br J Obstet Gynaecol. 2006; 113: 1117–1125
o View in Article
99. Weiss, J.L., Malone, F.D., Emig, D. et al. Obesity obstetric complications and cesarean delivery rate: a population-
based screening study. Am J Obstet Gynecol. 2004; 190: 1091–1097
o View in Article
100. Crane, S.S., Wojtowycz, M.A., Dye, T.D. et al. Association between pre-pregnancy obesity and the risk of cesarean
delivery. Obstet Gynecol. 1997; 89: 213–216
o View in Article
101. Dietz, P.M., Callaghan, W.M., Morrow, B. et al. Population-based assessment of the risk of primary cesarean delivery
due to excess prepregnancy weight among nulliparous women delivering term infants. Matern Child Health
J. 2005; 9: 237–244
o View in Article
102. LaCoursiere, D.Y., Bloebaum, L., Duncan, J.D. et al. Population-based trends and correlates of maternal overweight
and obesity, Utah 1991–2001. Am J Obstet Gynecol. 2005; 192: 832–839
o View in Article
103. Cedergren, M.I. Maternal morbid obesity and the risk of adverse pregnancy outcome. Obstet Gynecol. 2004; 103:219–
224
o View in Article
104. Wall, P.D., Deucy, E.E., Glantz, J.C. et al. Vertical skin incisions and wound complications in the obese
parturient.Obstet Gynecol. 2003; 102: 952–956
o View in Article
105. Edmiston, C.E., Krepel, C., Kelly, H. et al. Perioperative antibiotic prophylaxis in the gastric bypass patient: do we
achieve therapeutic levels?. Surgery. 2004; 136: 738–747
o View in Article
106. Chelmow, D., Rodriguez, E.J., and Sabatini, M.M. Suture closure of subcutaneous fat and wound disruption after
cesarean delivery: a meta-analysis. Obstet Gynecol. 2004; 103: 974–980
o View in Article
107. Hellums, E.K., Lin, M.G., and Ramsey, P.S. Prophylactic subcutaneous drainage for prevention of wound
complications after cesarean delivery-a metaanalysis. Am J Obstet Gynecol. 2007; 197: 229–235
o View in Article
108. Hibbard, J.U., Gilbert, S., Landon, M.B. et al. Trial of labor or repeat cesarean delivery in women with morbid obesity
and previous cesarean delivery. Obstet Gynecol. 2006; 108: 125–133
o View in Article
109. Carroll, C.S. Sr., Magann, E.F., Chauhan, S.P. et al. Vaginal birth after cesarean section versus elective repeat cesarean
delivery: weight-based outcomes. Am J Obstet Gynecol. 2003; 188: 1516–1522
o View in Article
110. Durnwald, C.P., Ehrenberg, H.M., and Mercer, B.M. The impact of maternal obesity and weight gain on vaginal birth
after cesarean section success. Am J Obstet Gynecol. 2004; 191: 954–957
o View in Article
111. Whitaker, R.C. Predicting preschooler obesity at birth: the role of maternal obesity in early
pregnancy. Pediatrics.2004; 114: e29–e36
o View in Article
112. Dyer, J.S. and Rosenfeld, C.R. Metabolic imprinting by prenatal, perinatal, and postnatal overnutrition: a
review.Semin Reprod Med. 2011; 29: 266–276
o View in Article
113. Dabelea, D., Hanson, R.L., Lindsay, R.S. et al. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and
obesity: a study of discordant sibships. Diabetes. 2000; 49: 2208–2211
o View in Article
114. Gillman, M.W., Rifas-Shiman, S., Berkey, C.S. et al. Maternal gestational diabetes, birth weight, and adolescent
obesity. Pediatrics. 2003; 111: e221–e226
o View in Article
115. Boney, C.M., Verma, A., Tucker, R. et al. Metabolic syndrome in childhood: association with birth weight, maternal
obesity, and gestational diabetes mellitus. Pediatrics. 2005; 115: e290–e296
o View in Article
116. Parsons, T.J., Power, C., and Manor, O. Fetal and early life growth and body mass index from birth to early adulthood
in 1958 British cohort: longitudinal study. Br Med J. 2001; 323: 1331–1335
o View in Article
117. Forsén, T., Eriksson, J.G., Tuomilehto, J. et al. Mother's weight in pregnancy and coronary heart disease in a cohort of
Finnish men: follow up study. Br Med J. 1997; 315: 837–840
o View in Article
118. Krakowiak, P., Walker, C.K., Bremer, A.A. et al. Maternal metabolic conditions and risk for autism and other
neurodevelopmental disorders. Pediatrics. 2012; 129: e1121
o View in Article

© 2014 Elsevier Ltd. Published by Elsevier Inc. All rights reserved.

Share on mendeley Share on facebook Share on twitter Share on email More Sharing
Services
Access this article on
ScienceDirect

Article Tools
 PDF (326 kB)

 Email Article
 Add to My Reading List
 Export Citation
 Create Citation Alert
 Cited by in Scopus (0)
 Request Permissions
 Order Reprints(100 minimum order)
 < Previous Article
Next Article >
January 2015 Volume 29, Issue 1, Pages 79–90
Copyright © 2014 Elsevier Inc. All rights reserved. | Privacy Policy | Terms & Conditions | About Us | Help & Contact
The content on this site is intended for health professionals.
Advertisements on this site do not constitute a guarantee or endorsement by the journal, Association, or publisher of the quality or
value of such product or of the claims made for it by its manufacturer.