Optimizing weight for maternal and infant health: tenable, or too late?

Abstract

Obesity in pregnancy is the leading cause of maternal and fetal morbidity. Furthermore, gestational weight gain is one modifiable risk factor that improves pregnancy outcomes. Most pregnant women experience a weight increase that is higher than the 2009 Institute of Medicine recommendations, particularly with already overweight and obese women. Gestational weight gain less than the 2009 Institute of Medicine guidelines in obese women may improve pregnancy outcomes and reduce large-for-gestational-age infants, an independent risk factor for childhood obesity, without increasing small-for-gestational-age infants. Unfortunately, despite the fact that over 50 interventional trials designed to decrease excess gestational weight gain have been conducted, these interventions have only been modestly effective, and interventions designed to facilitate postpartum weight loss have also been disappointing. Successful interventions are of paramount importance not only to improve pregnancy outcomes but also for the future metabolic health of the mother and her infant, and may be key in attenuating the trans-generational risk on childhood obesity.

Keywords:

• childhood obesity
• diet
• fetal programming
• gestational weight gain
• Institute of Medicine guidelines
• interventions
• large for gestational age infants
• obesity
• physical activity
• postpartum weight loss
• pregnancy
• pregnancy outcomes

Financial & competing interests disclosure

This study was supported by the Division of General Internal Medicine and the Department of Medicine at the University of Colorado School of Medicine, and by NIH Grant BIRCWH K12 HD057022, which is funded to JM Nicklas. This study was supported by the Division of General Internal Medicine and the Department of Medicine at the University of Colorado School of Medicine, and by NIH Grant 5K12HD057022-08, Building Interdisciplinary Research Careers in Women's Health (JM Nicklas). This study is also supported through LA Barbour by NIH Grants R01DK078645, NIH R01 DK10165, and the American Diabetes Association/Glaxo Smith Kline Targeted Research Award.

Key issues

• Obesity in pregnancy has now been identified as the leading cause of maternal and perinatal morbidity, increasing the health care costs of pregnancy by up to 16-fold due to a striking increase in maternal medical and obstetric complications as well as major malformations, fetal loss, stillbirth and neonatal complications.

• Extensive animal data and accumulating human data support a ‘fetal programming’ paradigm that maternal obesity, excess gestational weight gain (GWG) and an abnormal intrauterine metabolic environment change organ development (pancreas, kidney, heart and liver), fat and muscle mass, and through epigenetic changes may affect appetite regulation, mitochondrial oxidative capacity, organ function and offspring behavior, resulting in an increased risk for childhood obesity, metabolic syndrome and diabetes.

• Maternal risks from excess GWG, especially in overweight and obese women, include a higher risk of gestational diabetes (GDM), pre-eclampsia or gestational hypertension, cesarean delivery and postpartum weight retention, which significantly increase the risk of maternal obesity, diabetes and cardiovascular disease and entering a subsequent pregnancy with these complications. Infant risks related to GWG include large-for-gestational-age (LGA) and increases in fat mass and childhood obesity risk.

• The ‘obligate’ amount of GWG needed to minimize maternal fat stores being used as an energy source is approximately 7.5 kg (17 lbs) to account for fetus, placenta, amniotic fluid and increases in breast and uterine tissue and plasma volume.

• Although underweight and normal weight women need to gain a sufficient amount of weight to minimize the risk of small-for-gestational age (SGA) infants, overweight and obese women who gain no weight on average deliver a normal weight infant. Obese women who deliver SGA infants commonly have other morbidities (e.g., chronic hypertension, renal disease) that place them at risk for placental insufficiency as the cause of the SGA.

• GWG, even when within the 2009 Institute of Medicine (IOM) guidelines, has been associated with an increase in the rate of LGA and childhood obesity in overweight and obese women.

• There is increasing evidence that to minimize both SGA and LGA risk and to decrease the risk of GDM, pre-eclampsia, cesarean delivery, postpartum weight retention and childhood obesity that normal weight and overweight women should gain at the lower limit of the IOM guidelines, women with class 1 obesity <5 kg, and increasing evidence that obese women with a BMI ≥ 35 do not need to gain any weight to have a normally grown infant.

• Women with GDM who are overweight or obese may benefit from weight gain less than that of the IOM recommendations, because minimal weight gain does not appreciably increase SGA but may decrease insulin requirements and LGA.

• Randomized controlled interventions to minimize excess GWG have been modestly successful with more intensive diet intervention studies tending to be the most successful. Multiple trials are ongoing.

• Postpartum weight loss interventions have been disappointing. Breastfeeding, especially for at least 6 months, may facilitate postpartum weight loss and appears to attenuate the risk for childhood obesity.

• If possible, targeted interventions, especially in overweight and obese women, should begin preconception due to the powerful influence of pre-pregnancy BMI on adverse pregnancy outcomes, continue during pregnancy to favorably affect diet and GWG, extend postpartum to facilitate weight loss, and follow through the interpregnancy period to optimize maternal health.

• Successful interventions to achieve healthy maternal weight antepartum, intrapartum and postpartum not only have the potential to favorably affect maternal health but also offspring health and decrease the intergenerational risk of obesity and diabetes on subsequent generations.