The Impact of Maternal Obesity on Maternal and Fetal Health

The increasing rate of maternal obesity provides a major challenge to obstetric practice. Maternal obesity can result in negative outcomes for both women and fetuses. The maternal risks during pregnancy include gestational diabetes and preeclampsia. The fetus is at risk for stillbirth and congenital anomalies. Obesity in pregnancy can also affect health later in life for both mother and child. For women, these risks include heart disease and hypertension. Children have a risk of future obesity and heart disease. Women and their offspring are at increased risk for diabetes. Obstetrician-gynecologists are well positioned to prevent and treat this epidemic.Key words: Obesity, Maternal health, Diabetes, Fetal health, Birth outcomesThe worldwide prevalence of obesity has increased substantially over the past few decades. Economic, technologic, and lifestyle changes have created an abundance of cheap, high-calorie food coupled with decreased required physical activity. We are eating more and moving less. There is evidence for metabolic dysregulation among obese individuals that has been linked with a number of possible environmental factors, including contaminants from modern industry. Obesity is a significant public health concern and is likely to remain so for the foreseeable future. Maternal obesity increases the risk of a number of pregnancy complications, including preeclampsia, gestational diabetes mellitus (GDM), and cesarean delivery (1 Excessive weight gain during pregnancy and postpartum retention of pregnancy weight gain are significant risk factors for later obesity in women.² Additionally, maternal health can have a significant impact on the in utero environment and, thus, on fetal development and the health of the child later in life (3

Table 1

Obstetric Complications in Obese Pregnant Women

Complication			OR (95% CI) or % vs Normal Weight	P
Early pregnancy
	Spontaneous abortion (miscarriage)
		After spontaneous conception	1.2 (1.1–1.5)	.04
		After IVF conception	1.8 (1.1–3.0)	< .05
	Recurrent miscarriage		3.5 (1.1–21.0)	.04
	Congenital anomalies
		Neural tube defects	1.8 (1.1–3.0)	< .05
		Spina bifida	2.6 (1.5–4.5)	< .05
		Congenital heart disease	1.2 (1.1–1.3)	< .05
		Omphalocele	3.3 (1.0–10.3)	< .05
Late pregnancy
	Hypertensive disorder of pregnancy
	Gestational nonproteinuric hypertension		2.5 (2.1–3.0)	< .0001
	Preeclampsia		3.2 (1.8–5.8)	.007
	Gestational diabetes mellitus		2.6 (2.1–3.4)	< .001
	Preterm birth		1.5 (1.1–2.1)	< .05
	Intrauterine fetal demise (stillbirth)		2.8 (1.9–4.7)	< .001
Peripartum
	Cesarean delivery		47.7% vs 20.7%	< .01
	Decreased VBAC success		84.7% vs 66%	.04
	Operative morbidity		33.8% vs 20.7%	< .05
		Anesthesia complications
		Excessive blood loss
		Postpartum endometritis
		Wound infection/breakdown
		Postpartum thrombophlebitis
Fetal/neonatal complications
	Fetal macrosomia (EFW ≥ 4500 g)		2.2 (1.6–3.1)	< .001
	Shoulder dystocia		3.6 (2.1–6.3)	< .001
	Birth weight < 4000 g		1.7 (1.4–2.0)	.0006
	Birth weight < 4500 g		2.0 (1.4–3.0)	< .0001
	Childhood obesity		2.3 (2.0-2.6)	< .05

Open in a separate window95% CI, 95% confidence interval; EFW, estimated fetal weight; IVF, in vitro fertilization; OR, odds ratio; VBAC, vaginal birth after cesarean.According to the in utero fetal programming hypothesis (Barker hypothesis), size at birth is related to the risk of developing disease later in life.⁴ Although the Barker hypothesis originally focused on low birth weight, there is evidence that high birth weight may have its own set of complications later in life. A link between maternal obesity in the first trimester and obesity in children has been demonstrated. Whitaker⁵ found that the relative risk of childhood obesity associated with maternal obesity in the first trimester of pregnancy was 2.0 (95% confidence interval [CI], 1.7–2.3) at 2 years of age, 2.3 (95% CI, 2.0–2.6) at 3 years of age, and 2.3 (95% CI, 2.0–2.6) at 4 years of age. Birth weight has also been shown to be directly correlated with body mass index (BMI) later in life.⁶One mechanism thought to underlie these relationships is in utero fetal programming by nutritional stimuli. Fetuses have to adapt to the supply of nutrients crossing the placenta whether a deficit or an overabundance, and these adaptations may permanently change their physiology and metabolism.³ These programmed changes may serve as the origins of a diverse array of diseases that arise later in life, including heart disease, hypertension, and non-insulindependent diabetes (Figure 1). Moreover, because of fetal programming, obesity may become a self-perpetuating problem. Daughters of obese women may themselves be vulnerable to becoming obese and more likely to have offspring who share this vulnerability.Open in a separate windowFigure 1The impact of malnutrition during early development.