International Journal of Gynecology and Obstetrics 115 Suppl. 1 (2011) S6–S10

Contents lists available at ScienceDirect

International Journal of Gynecology and Obstetrics

j ourna l homepage: www.e lsev ie r.com/ locate / i jgo

ARTICLE

Maternal obesity: Implications for pregnancy outcome and long-term risks—a link to

maternal nutrition

Amir Aviram, Moshe Hod, Yariv Yogev *

Department of Obstetrics and Gynecology, Helen Schneider Hospital for Women, Rabin Medical Center, Petah Tiqva, Israel

a r t i c l e i n f o

Keywords:

Maternal nutrition

Obesity

Pregnancy

Pregnancy outcomes

Weight gain

a b s t r a c t

As obesity becomes a worldwide epidemic, its prevalence during reproductive age is also increased. Alarming

reports state that two-thirds of adults in the USA are overweight or obese, with half of them in the latter

category, and the rate of obese pregnant women is estimated at 18–38%. These women are of major concern

to women’s health providers because they encounter numerous pregnancy-related complications. Obesity-related

reproductive health complications range from infertility to a wide spectrum of diseases such as hypertensive

disorders, coagulopathies, gestational diabetes mellitus, respiratory complications, and fetal complications such as

large-for-gestational-age infants, congenital malformations, stillbirth, and shoulder dystocia. Recent reports suggest

that obesity during pregnancy can be a risk factor for developing obesity, diabetes, and cardiovascular diseases in

the newborn later in life. This review will address the implication of obesity on pregnancy and child health, and

explore recent literature on obesity during pregnancy.

© 2011 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

1. Introduction

Obesity has long been recognized as a global health concern, be it

among adults, adolescents, or children, of both sexes. The World

Health Organization’s (WHO) reports convey alarming figures

regarding this phenomenon, with up to 1.6 billion overweight

adults and 400 million obese adults in 2005 [1]. WHO and the

National Institutes of Health (NIH) define overweight as a body

mass index (BMI) of 25–29.9 and obesity as a BMI of 30 or greater.

Obesity is also subcategorized into 3 subgroups: Class I (BMI 30–

34.9), Class II (BMI 35–39.9), and Class III (BMI 40 or greater) [1].

Current predictions assess that by the year 2015, 2.3 billion adults

will be overweight and 700 million obese. Results from the United

States National Health and Nutrition Examination Survey (NHANES)

indicate that 66.3% of adults in the USA are either overweight or

obese, with half of them in the latter category.

As obesity becomes an ever-growing concern, the number of

women of reproductive age who are overweight or obese increases,

and the incidence of obesity among pregnant women is now

estimated at between 18.5% and 38.3% [2]. Maternal overweight

is now a known risk factor that affects the vast continuum

of pregnancy. Fertility and fecundity rates are lower among

overweight and obese women, in spontaneous conception as

well as in artificial reproductive techniques [2]. During pregnancy,

these women are more susceptible to pregnancy hypertensive

* Corresponding author. Yariv Yogev. Perinatal Division, Department of

Obstetrics and Gynecology, Helen Schneider Hospital for Women, Rabin

Medical Center, Beilinson Campus, Petah Tiqva 49100, Israel.

Tel.: +97239377400.

E-mail address: yarivyogev@hotmail.com (Y. Yogev).

disorders, gestational diabetes, respiratory complications, and

thromboembolic events [2–4]. As delivery approaches, overweight

women have a slower labor progression rate, higher rates

of cesarean deliveries, and more surgery-related complications

such as difficult spinal, epidural, or general anesthesia, wound

infection, and endometritis [2–4]. From the fetal and newborn

perspective, complications include congenital malformations, large-

for-gestational-age (LGA) infants, stillbirth, shoulder dystocia, and

adolescent complications such as obesity and diabetes [2–4].

2. Hypertensive disorders

Hypertensive disorders are associated with obesity in the pregnant

as well as the nonpregnant state. The risk of pregnancy-induced

hypertension or pre-eclampsia is significantly greater if the mother

is overweight as assessed by BMI in early pregnancy, with an

up to 2–3-fold increased risk for pre-eclampsia with a BMI

greater than 30 [5–7]. Epidemiological studies have shown a

relationship between pregnancies complicated by pre-eclampsia

and an increased risk of maternal coronary heart disease in later

life. The reported increase in the relative risk of death from ischemic

heart disease in association with a history of pre-eclampsia or

eclampsia is approximately 2-fold [8].

3. Gestational diabetes mellitus

The association between obesity, hypertension, and insulin

resistance in type 2 diabetes is well recognized. It has been shown

that even minor degrees of carbohydrate intolerance are related to

obesity and pregnancy outcome [9,10]. Prepregnancy overweight

and obesity were associated with adverse pregnancy outcome

0020-7292/$ – see front matter © 2011 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

A. Aviram et al. / International Journal of Gynecology and Obstetrics 115S1 (2011) S6–S10 S7

in glucose-tolerant women [9,10]. Several studies demonstrated

a 2–10-fold increase in the rate of gestational diabetes mellitus

(GDM) among obese patients [11–13]. A study of 6857 women

found a direct association between glucose screening categories,

obesity, and rate of GDM [14]. For patients with screening results

from 130–189mg/dL, the rate of obesity was approximately 24–30%.

Thereafter, this rate increased 2-fold. In contrast, for nonobese

women, the rate of GDM increased for each 10mg increment

in glucose screening. These data demonstrate that the rate of

obesity and glucose tolerance are both associated with the

development of GDM. Additionally, fetal size and cesarean section

rate are associated with the degree of carbohydrate intolerance as

represented by screening results. Furthermore, obesity remains a

significant contributor impacting fetal size [15].

To date, there is scant data on obesity and being overweight in

GDM. The few studies reporting obesity in GDM lack information

on the effect of achieving targeted levels of glycemic control

and treatment modalities on pregnancy outcome [16–18]. Leiken

et al. [16] demonstrated an independent risk for macrosomia

among obese women with GDM. They determined that GDM had

a frequency of macrosomia no different than that of nondiabetic

patients. Nonobese women with GDM and fasting hyperglycemia

treated with diet and insulin therapy also had a frequency of

macrosomia no different than that of nondiabetic women. However,

diet and insulin did not prevent excess macrosomia in women who

were obese.

These studies had small sample sizes, failed to provide

information on glycemic control, and only evaluated single outcome

variables. Maternal age, parity, and obesity are all over-represented

among women with GDM. These variables need to be controlled in

a study to draw accurate conclusions that also control confounding

effects. Therefore, it is not clear if obesity, level of glycemia, or

treatment modality is independently or cumulatively responsible

for fetal growth abnormalities.

Langer et al. [19] found that obese and overweight GDM patients

achieving established levels of glucose control with insulin therapy

showed no increased risk for composite outcome, macrosomia, and

LGA compared with normal weight GDM patients. In contrast, even

when diet-treated obese patients achieved good glycemic control,

there was no improvement in pregnancy outcome compared

with normal weight patients. Poorly-controlled overweight and

obese patients, regardless of treatment modality, had significantly

higher rates of composite outcome, metabolic complications,

macrosomia, and LGA. Although obesity in and of itself portends

potential adverse outcome in pregnancy, women with GDM treated

with insulin and possibly oral antidiabetic drugs who achieve

targeted levels of glycemic control will have pregnancy outcomes

comparable with those of normal weight women. The improved

outcome in the insulin-treated overweight and obese women may

be due to an unidentified effect of insulin itself on the fetus or

activation of other metabolic fuel pathways.

A recent study [20] concluded that a rise in BMI was translated

into an increased risk for GDM in consecutive pregnancy (OR 1.71

for gaining 1.0–1.9 BMI units, OR 2.46 for gaining 2.0–2.9 BMI units,

and OR 3.40 for gaining 3.0 or more BMI units), and that a decrease

in BMI was translated into lower risk for GDM in consecutive

pregnancy, but only in overweight or obese women (OR 0.26 for

losing at least 2.0 BMI units).

4. The impact of maternal weight change on pregnancy

outcome

The amount of weight gain recommended in pregnancy is

controversial. Historically, obstetricians used to restrict weight gain

of up to 15 lb (6.8 kg), regardless of race, ethnicity, or prepregnancy

weight. In the 1970s a more lax approach to weight gain was

followed, allowing weight gain of up to 20–27 lb (9.1–12.3 kg).

In 1990, the Institute of Medicine (IOM) published new guidelines

based on the effects of weight gain on fetal size. The new

recommendations were based on prepregnancy BMI: a weight gain

of 28–40 lb (12.7–18.2 kg) for a BMI of 19.8 and lower; 25–35 lb

(11.4–15.9 kg) for a BMI of 19.9–26; and 15–25 lb (6.8–11.4 kg)

for a BMI of 26.1 and greater. The IOM stated that the effect of

weight gain on fetal size diminishes as the mother’s prepregnancy

BMI increases [21]. This approach considered only immediate fetal

outcomes and disregarded long-term maternal and fetal effects.

This concept was challenged in the past 2 decades when studies

evaluated the association between maternal weight gain, obesity,

pregnancy outcome, and future development of diabetes in the

mother and the child.

Rooney et al. [22] evaluated a cohort of 540 women who

had documented weight over a 5-year postpartum period. They

concluded that excess weight gain and failure to lose weight after

pregnancy are important and identifiable predictors of long-term

obesity. Breastfeeding and exercise may be beneficial in controlling

long-term weight. Edwards et al. [23] found that obese patients

gained an average of 5 kg less during pregnancy and were more

likely to lose the weight or not gain weight at all. Obese women

who lost or did not gain any weight had lower mean birth weights of

infants and higher rates of small-for-gestational-age (SGA) infants

compared with obese women who gained 1 lb (0.45 kg) or more.

The incidence of macrosomic fetuses increased significantly only in

the group that gained 12kg or more. No weight gain and weight

gain up to 11.5 kg was associated with a macrosomia rate of 12.5–

13.3% with a background rate of 10% in nonobese women. Therefore,

they recommend weight gains of 15–25 lb (6.8–11.4 kg) for obese

women and 25–35 lb (11.4–15.9 kg) for normal weight women to

optimize fetal growth. Neonates of obese women who gained less

than 6.8 kg were 3 times more likely to be SGA than neonates

of obese women who gained at least 6.8 kg [24]. In addition, it

has also been reported that obese pregnant women who gained

at least 6.8 kg have been associated with increased frequency of

macrosomia [25].

Bianco et al. [13] reported that a weight gain of more than 25 lb

(11.4 kg) was strongly associated with the birth of LGA infants.

However, poor weight gain did not appear to increase the risk of

low birth weight infants. In contrast, Ratner et al. [26] found no

difference in fetal outcome in obese women when gaining more or

less than 10 lb (4.5 kg). They concluded that limited weight gain in

morbidly obese women does not adversely affect fetal outcome.

Luke et al. [27] reported that for every kilogram of gestational

weight gained, birth weight increased by 44.9 g for underweight

women, 22.9 g for normal weight women, and 11.9 g for overweight

women. For every kilogram of retained weight, birth weight was

increased by 35.6 g for underweight women, 15.9 g for normal

weight women, and 5.1 g for overweight women. These findings

suggest that beyond a certain level of weight gain, there is an

increase in birth weight at the expense of increasing maternal

postpartum obesity for the woman who has gained an excessive

amount of weight during pregnancy.

A systematic review published recently examined outcomes of

pregnancies according to the IOM 1990 guidelines in terms of

birth weight, fetal growth, and postpartum weight retention [28].

A strong correlation between weight gain below IOM recom-

mendations and lower birth weights was demonstrated; however,

only moderate correlation between weight gain in excess of

IOM recommendations and higher birth weights was found. As

expected, evidence suggested that weight gain in excess of IOM

recommendations, both total weight gain and weight gain rate, are

correlated with higher incidence of weight retention postpartum in

the short and long term.

S8 A. Aviram et al. / International Journal of Gynecology and Obstetrics 115S1 (2011) S6–S10

The IOM issued new guidelines for pregnancy weight gain in

2009, taking into account both maternal and fetal health [29]. For

underweight women (BMI < 18.5), a weight gain of 12.5–18kg at a

mean rate of 0.51 kg per week is considered adequate; for normal

weight women (BMI 18.5–24.9), 11.5–16kg at a mean rate of 0.42 kg

per week; for overweight women (BMI 25.0–29.9), 7–11.5 kg at a

mean rate of 0.28 kg per week; and for obese women (BMI 30 and

greater) 5–9kg with a mean rate of 0.22 kg per week. A recent study

examined whether differences exist in infant body composition

based on the new IOM guidelines [30]. It was found that infants

of obese mothers had a greater percentage of fat compared with

infants of normal weight and overweight mothers. Within the

excessive weight gain group, infants of normal weight mothers have

less fat percentage than infants of obese or overweight mothers.

Another study by Vesco et al. [31] found that obese women

gaining weight above the new IOM recommendations did not

decrease the risk for SGA but increased the risk for delivering LGA or

macrosomic infants, and that obese women gaining weight below

IOM recommendations had a higher risk for delivering SGA and a

lower risk for LGA infants.

Bondar et al. [32] demonstrated that the prevalence of excessive

gestational weight gain declined, and weight loss increased, as

obesity became more severe. Generally, weight loss was associated

with an elevated risk of SGA, medically indicated and spontaneous

preterm delivery, and high weight gain tended to increase the risk

of LGA and medically indicated preterm delivery. Hinkle et al. [33]

found that severity of obesity modified associations between

gestational weight gain and fetal growth. Compared with weight

gains of 5–9kg, weight loss in Class I obese women significantly

increased the odds of SGA, whereas a gestational weight gain of

0.1–4.9 kg was not associated with SGA and did not decrease the

odds of macrosomia. In Class II and III women, compared with

weight gains of 5–9kg, a gestational weight gain from −4.9 to

4.9 kg was not associated with SGA but did decrease the odds of

macrosomia.

In a population-based cohort, Blomberg [34] found that Class III

obese women who lost weight during pregnancy had a decreased

risk of cesarean delivery (OR 0.77; 95% CI, 0.60–0.99), LGA births

(OR 0.64; 95% CI, 0.46–0.90), and no significantly increased risk

for pre-eclampsia, excessive bleeding during delivery, instrumental

delivery, low Apgar score, or fetal distress compared with Class III

obese women gaining weight within the IOM recommendations.

There was an increased risk for SGA (OR 2.34; 95% CI, 1.15–4.76)

among Class III obese women losing weight, but there was no

significantly increased risk of SGA in the same group with low

weight gain.

Getahun et al. [35] looked at whether BMI changes between

2 consecutive pregnancies were associated with increased risk

for LGA in the second pregnancy. They found that overweight or

obese women in both pregnancies had an increased risk for LGA

infants, and that any decrease in BMI attenuated the risk. They also

concluded that 17.1% of LGA infants born to underweight mothers,

13.2% of LGA infants born to normal weight mothers, and 7.6% of

LGA infants born to overweight mothers could be prevented if BMI

had not increased between pregnancies.

Villamor and Cnattingius [36] found that compared with women

whose BMI changed between −1.0 and 0.9 units, women who gained

3 or more units had an increased risk of pre-eclampsia, gestational

hypertension, GDM, cesarean delivery, stillbirth, and LGA birth [36].

The associations were linearly related to weight change and were

also noted in women who had a healthy prepregnancy BMI for both

pregnancies.

Regarding bariatric surgery, Dell’Agnolo et al. [37] found that

women who underwent bariatric surgery had less obesity-related

comorbidities such as diabetes mellitus and hypertension, and less

pregnancy-related hypertensive disorders, but higher prevalence

of cesarean delivery and postoperative anemia. Their infants were

more likely to be appropriate-for-gestational-age (AGA) and be

born at term. Sheiner et al. [38] found that bariatric surgery was

associated with premature rupture of membranes, labor induction,

macrosomia, and obesity. No significant differences were noted

regarding pregnancy complications such as placental abruption,

labor dystocia, or perinatal complications. A systematic review by

Maggard et al. [39] included 75 articles, and concluded that fewer

maternal complications occurred following bariatric surgery (such

as GDM and pre-eclampsia), and that neonatal outcomes were

better than in obese controls.

5. Long-term fetal and neonatal issues

Both the Barker [40,41] and fetal insulin hypotheses [42] have

proposed that impaired adult cardiovascular health is programmed

in utero by poor fetal nutrition, or by genetically determined

reduction of insulin-mediated fetal growth, which results in the

birth of a small infant. Low birth weight may be a significant

variable for the development of the metabolic syndrome in

adulthood. Obesity was an independent risk factor in the diabetic

populations studied. Therefore, the emphasis today may need to

address sedentary lifestyle and issues related to obesity upon

fetal programming since undernutrition is now infrequent in high-

resource societies.

Another study [43] reported evidence of a link between maternal

obesity and cardiovascular disease in adult offspring, confirming

Barker’s hypothesis of higher adult death rates from coronary heart

disease in men who were classified as low birth weight. In addition,

they observed a positive association between the mother’s BMI

upon admission and future death rate from coronary heart disease

in male offspring. They concluded that the mother’s obesity may

be an independent yet additional contributing factor to infant low

birth weight. Fall et al. [44] reported higher adult rates of type 2

diabetes in the offspring of mothers who were above average weight

in pregnancy.

Therefore, there is an association between maternal (but not

paternal) obesity and insulin resistance and the risk for offspring

to develop cardiovascular disease in adulthood. In a further study,

high maternal weight or BMI accounted for the association between

birth weight and adult adiposity [45].

Lawlor et al. [46] found that maternal weight gain (MWG) was

associated with offspring BMI. In normal weight women, the

positive association between MWG and offspring BMI at age 18

years was driven largely by shared familial risk factors for BMI,

whereas in overweight or obese women the correlation seemed to

be through shared familial risk factors combined with intrauterine

mechanisms. In a review by Bouret [47], it is suggested that

maternal obesity and alterations in postnatal nutrition are related,

as determined by epidemiological and animal studies, to increased

risks of obesity, hypertension, and type 2 diabetes in offspring.

Furthermore, several mechanisms may be responsible for the

development of such diseases, such as developmental programming

of neuroendocrine systems by perinatal environment. As in GDM

or pregestational diabetes, maternal obesity can result in fetal

growth restriction or macrosomia. Paradoxically, both are related

to childhood metabolic syndrome [48].

Cho et al. [49] reported an association between maternal second

and third trimester free fatty acid (FFA) concentrations (which

increase with maternal obesity) and diastolic blood pressure in

the adolescent offspring. The majority of evidence suggests a

relationship between low birth weight and adult disease. However,

it is reasonable to speculate that overweight infants that are a

product of both genetic and environmental factors are programmed

in utero for the development of future diabetes, obesity, and

metabolic syndrome. Thus, diversity (accelerated and delayed) may

A. Aviram et al. / International Journal of Gynecology and Obstetrics 115S1 (2011) S6–S10 S9

be a source for adult disease already initiated in intrauterine

life. Given that obesity and maternal insulin resistance are not

only genetic but also acquired, improvement of periconceptional

maternal insulin sensitivity via exercise or diet, and controlling

the diabetes throughout pregnancy (improvement in intrauterine

environment), may impact not only the mother’s health, but also

the future cardiovascular risk for her child. Again, this hypothesis

remains speculative and further research is needed to address this

issue.

6. Potential management and intervention

In obese women, a modification of risk factors prior to or early in

pregnancy is recommended. Treatment options during pregnancy

using diet, pharmacological, or surgical means are contraindicated.

However, increased physical activity in women who are sedentary

and healthy food choices rather than fast foods may result

in a better pregnancy outcome for both mother and child. A

randomized trial of weight-bearing exercise (vs no exercise) from

8 weeks of pregnancy in women who did not normally exercise,

resulted in significantly higher birth weights in offspring of women

randomized to exercise [50]. In another study, exercise twice a

week or less was associated with low birth weight (adjusted odds

ratio 2.64; 95% CI, 1.29–5.39) relative to women who exercised

3–4 times per week after adjustment for potential confounders,

including social class [51]. Dye et al. [52] demonstrated that

women who were obese at the time of conception but exercised

regularly had lower rates of GDM. This has since been confirmed

by another group. Moderate exercise in pregnancy did not appear

to be harmful and there was no association with premature labor

or poor Apgar scores [53,54].

7. Summary

Obesity has implications for all aspects of maternal health

and outcome during pregnancy. Improved lifestyle changes can

mitigate pregnancy complications. Healthcare professionals and

social service providers need to actively promote a healthy lifestyle

to their patients and clients at every opportunity. Prepregnancy

clinics could provide education on healthy diet and exercise regimes

similar to those provided for women with diabetes.

Improving the health prospects of the mother during pregnancy

and the potential risk for developing complications later in life

should be the focus of care. A concerted effort by public policy

makers and the medical community could also effectively reduce

healthcare costs, including those for hospitalization resulting

from hypertensive disease, fetal anomalies, fetal assessment, costs

associated with the high rate of cesarean delivery, and postpartum

complications.

Conflict of interest statement

The authors report no potential conflicts of interest.

References

1. WHO. Obesity: preventing and managing the global epidemic. www.who.int.

http://whqlibdoc.who.int/trs/WHO_TRS_894.pdf. Published 2000.

2. Yogev Y, Catalano PM. Pregnancy and obesity. Obstet Gynecol Clin North Am

2009;36(2):285–300.

3. Reece EA. Perspectives on obesity, pregnancy and birth outcomes in the United

States: the scope of the problem. Am J Obstet Gynecol 2008;198(1):23–7.

4. Langer O. Management of obesity in GDM: old habits die hard. J Matern Fetal

Neonatal Med 2008;21(3):165–71.

5. Sibai BM, Gordon T, Thom E, Caritis SN, Klebanoff M, McNellis D, et al.

Risk factors for preeclampsia in healthy nulliparous women: a prospective

multicenter study. The National Institute of Child Health and Human

Development Network of Maternal-Fetal Medicine Units. Am J Obstet Gynecol

1995;172(2 Pt 1):642–8.

6. Sibai BM, Ewell M, Levine RJ, Klebanoff MA, Esterlitz J, Catalano PM, 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(5):1003–10.

7. Sattar N, Clark P, Holmes A, Lean ME, Walker I, Greer IA. Antenatal waist

circumference and hypertension risk. Obstet Gynecol 2001;97(2):268–71.

8. Sattar N, Greer IA. Pregnancy complications and maternal cardiovascular risk:

opportunities for intervention and screening? BMJ 2002;325(7356):157–60.

9. Sermer M, Naylor CD, Gare DJ, Kenshole AB, Ritchie JW, Farine D, et al. Impact of

increasing carbohydrate intolerance on maternal-fetal outcomes in 3637 women

without gestational diabetes. The Toronto Tri-Hospital Gestational Diabetes

Project. Am J Obstet Gynecol 1995;173(1):146–56.

10. Jensen DM, Damm P, Sørensen B, Mølsted-Pedersen L, Westergaard JG, Klebe J,

et al. Clinical impact of mild carbohydrate intolerance in pregnancy: a study

of 2904 nondiabetic Danish women with risk factors for gestational diabetes

mellitus. Am J Obstet Gynecol 2001;185(2):413–9.

11. Sebire NJ, Jolly M, Harris JP, Wadsworth J, Joffe M, Beard RW, et al. Maternal

obesity and pregnancy outcome: a study of 287,213 pregnancies in London. Int

J Obes Relat Metab Disord 2001;25(8):1175–82.

12. Kumari AS. Pregnancy outcome in women with morbid obesity. Int J Gynaecol

Obstet 2001;73(2):101–7.

13. Bianco AT, Smilen SW, Davis Y, Lopez S, Lapinski R, Lockwood CJ. Pregnancy

outcome and weight gain recommendations for the morbidly obese woman.

Obstet Gynecol 1998;91(1):97–102.

14. Yogev Y, Langer O, Xenakis EM, Rosenn B. Glucose screening in Mexican-

American women. Obstet Gynecol 2004;103(6):1241–5.

15. Yogev Y, Langer O, Xenakis EM, Rosenn B. The association between glucose

challenge test, obesity and pregnancy outcome in 6390 non-diabetic women.

J Matern Fetal Neonatal Med 2005;17(1):29–34.

16. Leikin E, Jenkins JH, Graves WL. Prophylactic insulin in gestational diabetes.

Obstet Gynecol 1987;70(4):587–92.

17. Lucas MJ, Lowe TW, Bowe L, McIntire DD. Class A1 gestational diabetes: a

meaningful diagnosis? Obstet Gynecol 1993;82(2):260–5.

18. Casey BM, Lucas MJ, Mcintire DD, Leveno KJ. Pregnancy outcomes in women

with gestational diabetes compared with the general obstetric population.

Obstet Gynecol 1997;90(6):869–73.

19. Langer O, Yogev Y, Xenakis EM, Brustman L. Overweight and obese in gestational

diabetes: the impact on pregnancy outcome. Am J Obstet Gynecol 2005;192(6):

1768–76.

20. Ehrlich SF, Hedderson MM, Feng J, Davenport ER, Gunderson EP, Ferrara A.

Change in body mass index between pregnancies and the risk of gestational

diabetes in a second pregnancy. Obstet Gynecol 2011;117(6):1323–30.

21. Committee on Nutritional Status During Pregnancy and Lactation, Institute of

Medicine. Nutrition during pregnancy: Part I: Weight Gain, Part II: Nutrient

Supplements. Washington, DC: National Academy Press; 1990.

22. Rooney BL, Schauberger CW. Excess pregnancy weight gain and long-term

obesity: one decade later. Obstet Gynecol 2002;100(2):245–52.

23. Edwards LE, Hellerstedt WL, Alton IR, Story M, Himes JH. Pregnancy

complications and birth outcomes in obese and normal-weight women: effects

of gestational weight change. Obstet Gynecol 1996;87(3):389–94.

24. Parker JD, Abrams B. Prenatal weight gain advice: an examination of the recent

prenatal weight gain recommendations of the Institute of Medicine. Obstet

Gynecol 1992;79(5):664–9.

25. Johnson JW, Longmate JA, Frentzen B. Excessive maternal weight and pregnancy

outcome. Am J Obstet Gynecol 1992;167(2):353–70.

26. Ratner RE, Hamner LH 3rd, Isada NB. Effects of gestational weight gain in

morbidly obese women: II: Fetal morbidity. Am J Perinatol 1990;7(4):295–9.

27. Luke B, Hediger ML, Scholl TO. Point of diminishing returns: when does

gestational weight gain cease benefiting birthweight and begin adding to

maternal obesity? J Matern Fetal Med 1996;5(4):168–73.

28. Siega-Riz AM, Viswanathan M, Moos MK, Deierlein A, Mumford S, Knaack J,

et al. A systematic review of outcomes of maternal weight gain according

to the Institute of Medicine recommendations: birthweight, fetal growth, and

postpartum weight retention. Am J Obstet Gynecol 2009;201(4):339.e1–14.

29. Rasmussen KM, Yaktine AM, Committee to Reexamine IOM Pregnancy Weight

Guidelines, Institute of Medicine, National Research Council. Weight Gain During

Pregnancy: Reexamining the Guidelines. Washington, DC: National Academy

Press; 2009.

30. Hull HR, Thornton JC, Ji Y, Paley C, Rosenn B, Mathews P, et al. Higher infant body

fat with excessive gestational weight gain in overweight women. Am J Obstet

Gynecol 2011. April 14 [Epub ahead of print].

31. Vesco KK, Sharma AJ, Dietz PM, Rizzo JH, Callaghan WM, England L, et al.

Newborn size among obese women with weight gain outside the 2009 Institute

of Medicine recommendation. Obstet Gynecol 2011;117(4):812–8.

32. Bodnar LM, Siega-Riz AM, Simhan HN, Himes KP, Abrams B. Severe obesity,

gestational weight gain, and adverse birth outcomes. Am J Clin Nutr 2010;91(6):

1642–8.

33. Hinkle SN, Sharma AJ, Dietz PM. Gestational weight gain in obese mothers and

associations with fetal growth. Am J Clin Nutr 2010;92(3):644–51.

34. Blomberg M. Maternal and neonatal outcomes among obese womenwith weight

S10 A. Aviram et al. / International Journal of Gynecology and Obstetrics 115S1 (2011) S6–S10

gain below the new Institute of Medicine recommendations. Obstet Gynecol

2011;117(5):1065–70.

35. Getahun D, Ananth CV, Peltier MR, Salihu HM, Scorza WE. 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(6):

530.e1–8.

36. Villamor E, Cnattingius S. Interpregnancy weight change and risk of adverse

pregnancy outcomes: a population-based study. Lancet 2006;368(9542):

1164–70.

37. Dell’Agnolo CM, Carvalho MD, Pelloso SM. Pregnancy after bariatric surgery:

implications for mother and newborn. Obes Surg 2011;21(6):699–706.

38. Sheiner E, Levy A, Silverberg D, Menes TS, Levy I, Katz M, et al. Pregnancy after

bariatric surgery is not associated with adverse perinatal outcome. Am J Obstet

Gynecol 2004;190(5):1335–40.

39. Maggard MA, Yermilov I, Li Z, Maglione M, Newberry S, Suttorp M, et al.

Pregnancy and fertility following bariatric surgery: a systematic review. JAMA

2008;300(19):2286–96.

40. Barker DJ, Gluckman PD, Godfrey KM, Harding JE, Owens JA, Robinson JS.

Fetal nutrition and cardiovascular disease in adult life. Lancet 1993;341(8850):

938–41.

41. Barker DJ, Osmond C, Simmonds SJ, Wield GA. The relation of small head

circumference and thinness at birth to death from cardiovascular disease in

adult life. BMJ 1993;306(6875):422–6.

42. Hattersley AT, Tooke JE. The fetal insulin hypothesis: an alternative explanation

of the association of low birthweight with diabetes and vascular disease. Lancet

1999;353(9166):1789–92.

43. Forsen T, Eriksson JG, Tuomilehto J, Teramo K, Osmond C, Barker DJ. Mother’s

weight in pregnancy and coronary heart disease in a cohort of Finnish men:

follow up study. BMJ 1997;315(7112):837–40.

44. Fall CH, Stein CE, Kumaran K, Cox V, Osmond C, Barker DJ, et al. Size at birth,

maternal weight, and type 2 diabetes in South India. Diabet Med 1998;15(3):

220–7.

45. Parsons TJ, Power C, Manor O. Fetal and early life growth and body mass index

from birth to early adulthood in 1958 British cohort: longitudinal study. BMJ

2001;323(7325):1331–5.

46. Lawlor DA, Lichtenstein P, Fraser A, Langstrom N. Does maternal weight gain

in pregnancy have long-term effects on offspring adiposity? A sibling study in

a prospective cohort of 146,894 men from 136,050 families. Am J Clin Nutr

2011;94(1):142–8.

47. Bouret SG. Early life origins of obesity: role of hypothalamic programming.

J Pediatr Gastroenterol Nutr 2009;48(Suppl 1):S31–8.

48. Ornoy A. Prenatal origin of obesity and their complications: Gestational diabetes,

maternal overweight and the paradoxical effects of fetal growth restriction and

macrosomia. Reprod Toxicol 2011;32(2):205–12.

49. Cho NH, Silverman BL, Rizzo TA, Metzger BE. Correlations between the

intrauterine metabolic environment and blood pressure in adolescent offspring

of diabetic mothers. J Pediatr 2000;136(5):587–92.

50. Clapp JF 3rd, Kim H, Burciu B, Lopez B. Beginning regular exercise in

early pregnancy: effect on fetoplacental growth. Am J Obstet Gynecol

2000;183(6):1484–8.

51. Campbell MK, Mottola MF. Recreational exercise and occupational activity

during pregnancy and birth weight: a case-control study. Am J Obstet Gynecol

2001;184(3):403–8.

52. Dye TD, Knox KL, Artal R, Aubry RH, Wojtowycz MA. Physical activity, obesity,

and diabetes in pregnancy. Am J Epidemiol 1997;146(11):961–5.

53. Carpenter MW. The role of exercise in pregnant women with diabetes mellitus.

Clin Obstet Gynecol 2000;43(1):56–64.

54. Kardel KR, Kase T. Training in pregnant women: effects on fetal development

and birth. Am J Obstet Gynecol 1998;178(2):280–6.