- Email: [email protected]
Obesity and implications for future generations
CAOG Papers
www. AJOG.org
PRESIDENTIAL ADDRESS
Obesity and implications for future generations Gayle Olson, MD
T
here is little debate that obesity has reached epidemic proportions. At last count, at least one-third of adults in the United States were obese, and all states, except Colorado, have experienced a doubling in obesity rates from 1980-2007.1 Should this upward spiral continue, projections for 2030 suggest 40% and 80% of the worldwide population will be obese or overweight, respectively.2 Several methods define obesity (skin fold, % of ideal body weight, waist: hip ratios, body mass index [BMI]); however, BMI (weight [kg]/height [m2]) is the most often used method, which defines a BMI of ⬎24.6 kg/m2 as overweight and of ⱖ30 kg/m2 as obese. To place this in perspective, a weight of 124154 lbs is a normal BMI for a woman who is 5 feet 6 inches tall. Remarkably, 30% of adult women are unable to maintain their weight within the range of a normal BMI.1
From the Department of Obstetrics and Gynecology, The University of Texas Medical Branch, Galveston, TX. The author reports no conflict of interest. Presidential address presented at the 78th Annual Meeting of the Central Association of Obstetricians and Gynecologists, Nassau, Bahamas, Oct. 26-29, Reprints: Gayle Olson, MD, Department of Obstetrics & Gynecology, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0587. [email protected]. 0002-9378/free © 2012 Published by Mosby, Inc. doi: 10.1016/j.ajog.2012.01.005
The prevalence of obesity during pregnancy has prompted the Institute of Medicine (IOM) to recommend new guidelines for gestational weight gain (GWG) during pregnancy.3 Nonetheless, obesity that is independent of GWG has been associated with adverse outcomes for both mother (miscarriage, thromboembolism, diabetes mellitus, preeclampsia, hemorrhage, cesarean section delivery, wound infection) and infant (congenital anomalies, stillbirth, neonatal death).4 Adherence to the IOM GWG guidelines, however, is difficult for many women. In a population-based study that assessed GWG, Chu et al5 demonstrated that approximately 40% of normal weight women and 60% of overweight women gained more weight during pregnancy than recommended. Obese women gained less weight as a group compared with the normal and overweight groups; however, approximately 25% still exceeded IOM recommendations. In addition, GWG was increased in women who were ⬍19 years old, white, or ⬎12 years of education. If pregnancy can be considered a window to future health, excessive GWG is a first glimpse at unhealthy trends that lead to adverse outcomes that are associated with obesity. An examination of the Danish National Birth Cohort by Nohr et al6 identified GWG as a determinant of long-term obesity. Obese women with GWG of ⬍10 kg were below their prepregnancy weight at 6 months after delivery
and were able to reduce their BMI; by contrast, 12% of overweight and 14% of obese women with excessive GWG, respectively, moved up a BMI category. Each successive pregnancy potentially allows for successive weight gain that perpetuates the obesity cycle and increases risks for cardiovascular disease, metabolic syndrome, and diabetes mellitus in later life. If the window during pregnancy provides a picture of adverse health consequences for mothers, what vision is revealed for the offspring? The increase in obesity of children mirrors the epidemic rise that is seen in adults. In adults, obesity is defined using a BMI cutoff of ⱖ30 kg/m2; the more acceptable definition of obesity for children is a BMI of ⱖ95th percentile, specific for age and gender. Overweight is defined as a BMI between the 85th and 95th percentiles.7 Data suggest that 37.1% of infants are overweight and that 16.9% of children and adolescents are obese.8 In addition, evidence suggests that the trend toward obesity starts as early as 6 weeks. Using a nested case control design, McCormick et al9 demonstrated a 16% prevalence of infant obesity and also noted children who were obese at age 24 months were more likely to have been obese at age 6 months (odds ratio, 13.3; 95% confidence interval, 4.50 – 39.53). Although additional evidence will be needed, this study suggests that interventions for obesity may need to be initiated early in infancy. The Bogalusa Heart Study included ⬎12,000 children. Eightyfour percent of obese children became
MARCH 2012 American Journal of Obstetrics & Gynecology
255
CAOG Papers
Presidential Address
obese as adults, and as adults, 65% of these had a BMI of ⱖ35 kg/m2.10 During childhood, they were likely to have cardiovascular risk factors, such as elevated lipid levels, insulin levels, or increased blood pressure. Skinfold-thickness measurements also confirmed evidence of excess adiposity. The prevalence of the aforementioned risks and measurementsincreasedexponentiallyasthe cutoff for BMI increased further from ⬎95th to ⬎99th percentile.10 Epidemiologic studies suggest a U-shaped relation between birthweight and adult manifestations of obesity, hypertension, and insulin resistence.11 Barker12 identified a portion of this U-shaped relationship when he investigated the effects of maternal malnutrition during the Dutch famine of 1944-45. Fetal growth restriction and low birthweight were associated with an increased incidence of diabetes mellitus, cardiovascular disease, and increased BMI in adult life. The other portion of the U-shaped relationship or “fetal over nutrition” is supported by several studies. In a retrospective cohort study of ⬎8400 children, Whitaker et al13 reported that children who were born to obese mothers (based on BMI in the first trimester) had double the rate of obeseity at age 2 years. In women with BMI ⱖ30 kg/m2, the prevalence of childhood obesity (BMI, ⬎95th percentile) at ages 2, 3, and 4 years was 15.1%, 20.6%, and 24.1%, respectively. The infants who were overweight at 3-5 years of age were 4.1-7.9 times more likely to be obese in young adulthood. Oken et al14 in the prospective study, Project Viva, studied 1000 predominantly non–low-income mothers and infants. The mothers had a rate of excessive GWG of 51%, which, after adjustment for covariates, was associated with an odds ratio of 4.35 (95% confidence interval, 1.69 –11.24) for obesity at 3 years of age (BMI, ⬎95th vs ⬍50th percentile). In addition, increased GWG was associated with higher offspring BMI z-score, triceps and subscapular skinfold thicknesses, and systolic blood pressure. In the Growing Up Today study that included nearly 12,000 participants, Oken15 found a strong, nearly linear, association between total maternal GWG and childhood obesity (BMI, ⬎95th vs ⬍85th percentile) at the ages of 9-14 years.15 256
There is some evidence to suggest that maternal obesity influences the in utero environment by altering the regulation of appetite, satiety, and adipocyte maturation. Fetal neuronal pathways that regulate appetite and satiety are functioning by the third trimester. Leptin, which is synthesized by adipose tissue and the placenta, promotes development of satiety pathways in the fetus, although appetite dysregulation may result in both deficient or high fatty nutrient environments, thus contributing to the obese phenotype in humans.11 In animal models, adipose tissue has been identified as a principal target of programming, although different mechanisms for hypertrophy and hyperplasia may be activiated under conditions of undernutrition vs overnutrition.11 Additional animal studies demonstrated that early postnatal alterations in feeding may be associated with alterations in the function of hypothalamic nuclei, which are influencial in appetite regulation. Also, postnatal hyperphagia has been noted in offspring of rats that were fed high-fat diets during pregnancy. These offspring also continued to consume more and maintain higher body weights than controls.16 Paradoxically, both growth restriction and macrosomia are associated with obesity and its complications later in life. Answers to this paradox will become evident only when we have studied all components of the puzzle: maternal contribution, in utero environmnent, fetal programming, and early postnatal development. Studies that will address the maternal component can take advantage of pregnancy as a teachable time-frame and involve education and lifestyle intervention, nutrition, and exercise. These are all components of firstline therapy for obesity. The characteristics of teachable moments include times when personal risk and the potential for adverse outcome are perceived as increased, when there is a strong emotional response, and when the environment promotes redefining self-concepts and social roles. Pregnancy provides a time-frame that incorporates all these characteristics and is therefore an excellent teachable moment in the lives of our patients.17 Only a few randomized trials that have focused on lifestyle intervention have been conducted, with varying results. A recent review and
American Journal of Obstetrics & Gynecology MARCH 2012
www.AJOG.org metaanalysis of available intervention trials suggested that dietary intervention, specifically targeted for the overweight and obese pregnant groups, resulted in GWG within the IOM recommended limits.18 This same analysis did not find an association with GWG and infant birthweight, which differs from other trials.18 Clearly well-designed trials are needed. Changing the course of the current obesity epidemic will have long-range implications for the health status of current and f future generations. REFERENCES 1. Centers for Disease Control and Prevention. Overweight and obesity. Available at: www.cdc. gov/nccdphp/dnpa/obesity. Accessed Feb. 25, 2011. 2. Catalano PM, Hauguel-De Mouzon S. Is it time to revisit the Pedersen hypothesis in the face of the obesity epidemic? Am J Obstet Gynecol 2011;204:479-87. 3. Institute of Medicine. Nutrition during pregnancy: weight gain. Washington, DC: National Academy Press;1990. 4. Olson G, Blackwell SC. Optimization of gestational weight gain in the obese gravida: a review. Obstet Gynecol Clin North Am 2011;38: 397-407. 5. Chu SY, Callaghan WM, Bish CL, D’Angelo D. Gestational weight gain by body mass index among US women delivering live births, 20042005: fueling future obesity. Am J Obstet Gynecol 2009;200:271.e1-7. 6. Nohr EA, Bech BH, Vaeth M, Rasmussen KM, Henriksen TB, Olsen J. Obesity, gestational weight gain and preterm birth: a study within the Danish National Birth Cohort. Paediatr Perinat Epidemiol 2007;21:5-14. 7. Barlow SE, the Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics 2007;120(suppl): S164-92. 8. Ogden CL, Carroll MD, Curtin LR, Lamb MM, Flegal KM. Prevalence of high body mass index in US children and adolescents, 2007 -2008. JAMA 2010;303:242-9. 9. McCormick DP, Sarpong K, Lindsay Jordan L, Ray L, Jain S. Infant obesity: are we ready to make this diagnosis? J Pediatr 2010;157:15-9. 10. Freedman DS, Mei Z, Srinivasan SR, Berenson GS, Dietz WH. Cardiovascular risk factors and excess adiposity among overweight children and adolescents: the Bogalusa Heart study. J Pediatr 2007;150:12-7. 11. Desai M, Ross MG. Fetal Programming of adipose tissue: effects of intrauterine growth restriction and maternal obesity/high-fat diet. Semin Reprod Med 2011;29:237-45.
CAOG Papers
www.AJOG.org 12. Barker DJ. Fetal origins of coronary heart disease. BMJ 1995;311:171-4. 13. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997;37:86973. 14. Oken E, Taveras EM, Kleinman KP, RichEdwards JW, Gillman MW. Gestational weight
gain and child adiposity at age 3 years. Am J Obstet Gynecol 2007;196:322.e1-8. 15. Oken E. Maternal and child obesity: the causal link. Obstet Gynecol Clin N Am 2009; 36:361-77. 16. Muhlhausler B, Ong Z. The fetal origins of obesity: early origins of altered food intake. Endocr Metab Immune Disord Drug Targets 2011;11:189-97.
17. Phelan S. Pregnancy: a “teachable moment” for weight control and obesity prevention. Am J Obstet Gynecol 2010;202:135.e1.8. 18. Quinlivan J, Julania S, Lam L. Antenatal dietary interventions in obese pregnant women to restrict gestational weight gain to Institute of Medicine recommendations: a meta-analysis. Obstet Gynecol 2011;118:1395-401.
Delivery of monochorionic twins in the absence of complications: analysis of neonatal outcomes and costs Amy Elizabeth Sullivan, MD; Paul Nathan Hopkins, MD, MSPH; Hsin-Yi Weng, MPH; Erick Henry, MPH; Jamie Oi-Ting Lo, MD; Michael Walter Varner, MD; Michael Sean Esplin, MD OBJECTIVE: We sought to estimate the optimal time to deliver uncom-
plicated monochorionic-diamnionic (MCDA) twins. STUDY DESIGN: Data were retrospectively obtained from twin pregnancies from 2000 through 2009. The gestational week–specific prospective perinatal mortality risk was calculated. A cohort of MCDA twins with nonindicated deliveries was analyzed separately. Neonatal outcomes and costs were compared between MCDA twins with nonindicated deliveries born at specific weeks of gestation, and those born the subsequent week. RESULTS: There were 5894 dichorionic-diamnionic twins and 1704 MCDA twins. After 28 weeks, the gestational week–specific prospec-
tive risk of perinatal mortality did not differ between groups. There were 948 MCDA twins with nonindicated deliveries. Until 37 weeks, the risk of severe neonatal morbidity, perinatal mortality, and hospital costs were greater for fetuses delivered compared to fetuses born in a subsequent week. CONCLUSION: To optimize neonatal outcome and decrease hospital costs, MCDA twins should not be delivered ⬍37 weeks unless medically indicated.
Cite this article as: Sullivan AE, Hopkins PN, Weng H-Y, et al. Delivery of monochorionic twins in the absence of complications: analysis of neonatal outcomes and costs. Am J Obstet Gynecol 2012;206:257.e1-7.
B ACKGROUND AND O BJECTIVE Monochorionicity has been associated with increased adverse perinatal outcomes when compared with dichorionicity.
From the Departments of Obstetrics and Gynecology (Drs Sullivan, Lo, Varner, and Esplin), Cardiovascular Genetics (Dr Hopkins), and Pediatrics (Ms Weng), University of Utah School of Medicine, and the Department of Obstetrics and Gynecology, Intermountain Health Care (Drs Sullivan, Varner, and Esplin and Mr Henry), Salt Lake City, UT. The authors report no conflict of interest. Presented orally, in part, at the 78th annual meeting of the Central Association of Obstetricians and Gynecologists, Nassau, Bahamas, Oct. 26-29, 2011. 0002-9378/free © 2012 Mosby, Inc. All rights reserved. doi: 10.1016/j.ajog.2011.12.016
For Editors’ Commentary, see Table of Contents
Many obstetricians now advocate iatrogenic preterm delivery of monochorionic twins to avoid potential perinatal complications such as stillbirth. Patients with monochorionic twins are more likely to develop complications, including twin-twin transfusion syndrome, fetal growth abnormalities, and severe preeclampsia–all of which warrant preterm delivery. However, the optimal timing of delivery for monochorionic twin pregnancies that do not have medical indications for delivery remains a subject of debate. The objective of this study was to estimate the optimal timing of delivery of monochorionic–diamnionic (MCDA) twins with no medical indications for delivery. We hypothesized that the morbidity and mortality rates of MCDA twins are similar to those of diamnionic twins, that the risk
for prematurity associated with elective delivery ⬍37 weeks’ gestation is greater than the risk for stillbirth, and therefore MCDA twins without medical indications for delivery do not warrant elective preterm delivery.
M ATERIALS AND M ETHODS Electronic data were obtained on patients with twin deliveries from January 2000 through December 2009 at 18 hospitals within the Intermountain Health Care medical system. Data from neonatal outcomes were collected and analyzed. We defined perinatal death as stillbirth (fetal death prior to delivery) or neonatal death (death of a liveborn infant by 28 days). We defined severe adverse perinatal events as stillbirth, neonatal death, bronchopulmonary dysplasia, grade ⬎3 intraventricular hemorrhage, necrotizing enterocolitis, or sepsis.
MARCH 2012 American Journal of Obstetrics & Gynecology
257
www. AJOG.org
PRESIDENTIAL ADDRESS
Obesity and implications for future generations Gayle Olson, MD
T
here is little debate that obesity has reached epidemic proportions. At last count, at least one-third of adults in the United States were obese, and all states, except Colorado, have experienced a doubling in obesity rates from 1980-2007.1 Should this upward spiral continue, projections for 2030 suggest 40% and 80% of the worldwide population will be obese or overweight, respectively.2 Several methods define obesity (skin fold, % of ideal body weight, waist: hip ratios, body mass index [BMI]); however, BMI (weight [kg]/height [m2]) is the most often used method, which defines a BMI of ⬎24.6 kg/m2 as overweight and of ⱖ30 kg/m2 as obese. To place this in perspective, a weight of 124154 lbs is a normal BMI for a woman who is 5 feet 6 inches tall. Remarkably, 30% of adult women are unable to maintain their weight within the range of a normal BMI.1
From the Department of Obstetrics and Gynecology, The University of Texas Medical Branch, Galveston, TX. The author reports no conflict of interest. Presidential address presented at the 78th Annual Meeting of the Central Association of Obstetricians and Gynecologists, Nassau, Bahamas, Oct. 26-29, Reprints: Gayle Olson, MD, Department of Obstetrics & Gynecology, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0587. [email protected]. 0002-9378/free © 2012 Published by Mosby, Inc. doi: 10.1016/j.ajog.2012.01.005
The prevalence of obesity during pregnancy has prompted the Institute of Medicine (IOM) to recommend new guidelines for gestational weight gain (GWG) during pregnancy.3 Nonetheless, obesity that is independent of GWG has been associated with adverse outcomes for both mother (miscarriage, thromboembolism, diabetes mellitus, preeclampsia, hemorrhage, cesarean section delivery, wound infection) and infant (congenital anomalies, stillbirth, neonatal death).4 Adherence to the IOM GWG guidelines, however, is difficult for many women. In a population-based study that assessed GWG, Chu et al5 demonstrated that approximately 40% of normal weight women and 60% of overweight women gained more weight during pregnancy than recommended. Obese women gained less weight as a group compared with the normal and overweight groups; however, approximately 25% still exceeded IOM recommendations. In addition, GWG was increased in women who were ⬍19 years old, white, or ⬎12 years of education. If pregnancy can be considered a window to future health, excessive GWG is a first glimpse at unhealthy trends that lead to adverse outcomes that are associated with obesity. An examination of the Danish National Birth Cohort by Nohr et al6 identified GWG as a determinant of long-term obesity. Obese women with GWG of ⬍10 kg were below their prepregnancy weight at 6 months after delivery
and were able to reduce their BMI; by contrast, 12% of overweight and 14% of obese women with excessive GWG, respectively, moved up a BMI category. Each successive pregnancy potentially allows for successive weight gain that perpetuates the obesity cycle and increases risks for cardiovascular disease, metabolic syndrome, and diabetes mellitus in later life. If the window during pregnancy provides a picture of adverse health consequences for mothers, what vision is revealed for the offspring? The increase in obesity of children mirrors the epidemic rise that is seen in adults. In adults, obesity is defined using a BMI cutoff of ⱖ30 kg/m2; the more acceptable definition of obesity for children is a BMI of ⱖ95th percentile, specific for age and gender. Overweight is defined as a BMI between the 85th and 95th percentiles.7 Data suggest that 37.1% of infants are overweight and that 16.9% of children and adolescents are obese.8 In addition, evidence suggests that the trend toward obesity starts as early as 6 weeks. Using a nested case control design, McCormick et al9 demonstrated a 16% prevalence of infant obesity and also noted children who were obese at age 24 months were more likely to have been obese at age 6 months (odds ratio, 13.3; 95% confidence interval, 4.50 – 39.53). Although additional evidence will be needed, this study suggests that interventions for obesity may need to be initiated early in infancy. The Bogalusa Heart Study included ⬎12,000 children. Eightyfour percent of obese children became
MARCH 2012 American Journal of Obstetrics & Gynecology
255
CAOG Papers
Presidential Address
obese as adults, and as adults, 65% of these had a BMI of ⱖ35 kg/m2.10 During childhood, they were likely to have cardiovascular risk factors, such as elevated lipid levels, insulin levels, or increased blood pressure. Skinfold-thickness measurements also confirmed evidence of excess adiposity. The prevalence of the aforementioned risks and measurementsincreasedexponentiallyasthe cutoff for BMI increased further from ⬎95th to ⬎99th percentile.10 Epidemiologic studies suggest a U-shaped relation between birthweight and adult manifestations of obesity, hypertension, and insulin resistence.11 Barker12 identified a portion of this U-shaped relationship when he investigated the effects of maternal malnutrition during the Dutch famine of 1944-45. Fetal growth restriction and low birthweight were associated with an increased incidence of diabetes mellitus, cardiovascular disease, and increased BMI in adult life. The other portion of the U-shaped relationship or “fetal over nutrition” is supported by several studies. In a retrospective cohort study of ⬎8400 children, Whitaker et al13 reported that children who were born to obese mothers (based on BMI in the first trimester) had double the rate of obeseity at age 2 years. In women with BMI ⱖ30 kg/m2, the prevalence of childhood obesity (BMI, ⬎95th percentile) at ages 2, 3, and 4 years was 15.1%, 20.6%, and 24.1%, respectively. The infants who were overweight at 3-5 years of age were 4.1-7.9 times more likely to be obese in young adulthood. Oken et al14 in the prospective study, Project Viva, studied 1000 predominantly non–low-income mothers and infants. The mothers had a rate of excessive GWG of 51%, which, after adjustment for covariates, was associated with an odds ratio of 4.35 (95% confidence interval, 1.69 –11.24) for obesity at 3 years of age (BMI, ⬎95th vs ⬍50th percentile). In addition, increased GWG was associated with higher offspring BMI z-score, triceps and subscapular skinfold thicknesses, and systolic blood pressure. In the Growing Up Today study that included nearly 12,000 participants, Oken15 found a strong, nearly linear, association between total maternal GWG and childhood obesity (BMI, ⬎95th vs ⬍85th percentile) at the ages of 9-14 years.15 256
There is some evidence to suggest that maternal obesity influences the in utero environment by altering the regulation of appetite, satiety, and adipocyte maturation. Fetal neuronal pathways that regulate appetite and satiety are functioning by the third trimester. Leptin, which is synthesized by adipose tissue and the placenta, promotes development of satiety pathways in the fetus, although appetite dysregulation may result in both deficient or high fatty nutrient environments, thus contributing to the obese phenotype in humans.11 In animal models, adipose tissue has been identified as a principal target of programming, although different mechanisms for hypertrophy and hyperplasia may be activiated under conditions of undernutrition vs overnutrition.11 Additional animal studies demonstrated that early postnatal alterations in feeding may be associated with alterations in the function of hypothalamic nuclei, which are influencial in appetite regulation. Also, postnatal hyperphagia has been noted in offspring of rats that were fed high-fat diets during pregnancy. These offspring also continued to consume more and maintain higher body weights than controls.16 Paradoxically, both growth restriction and macrosomia are associated with obesity and its complications later in life. Answers to this paradox will become evident only when we have studied all components of the puzzle: maternal contribution, in utero environmnent, fetal programming, and early postnatal development. Studies that will address the maternal component can take advantage of pregnancy as a teachable time-frame and involve education and lifestyle intervention, nutrition, and exercise. These are all components of firstline therapy for obesity. The characteristics of teachable moments include times when personal risk and the potential for adverse outcome are perceived as increased, when there is a strong emotional response, and when the environment promotes redefining self-concepts and social roles. Pregnancy provides a time-frame that incorporates all these characteristics and is therefore an excellent teachable moment in the lives of our patients.17 Only a few randomized trials that have focused on lifestyle intervention have been conducted, with varying results. A recent review and
American Journal of Obstetrics & Gynecology MARCH 2012
www.AJOG.org metaanalysis of available intervention trials suggested that dietary intervention, specifically targeted for the overweight and obese pregnant groups, resulted in GWG within the IOM recommended limits.18 This same analysis did not find an association with GWG and infant birthweight, which differs from other trials.18 Clearly well-designed trials are needed. Changing the course of the current obesity epidemic will have long-range implications for the health status of current and f future generations. REFERENCES 1. Centers for Disease Control and Prevention. Overweight and obesity. Available at: www.cdc. gov/nccdphp/dnpa/obesity. Accessed Feb. 25, 2011. 2. Catalano PM, Hauguel-De Mouzon S. Is it time to revisit the Pedersen hypothesis in the face of the obesity epidemic? Am J Obstet Gynecol 2011;204:479-87. 3. Institute of Medicine. Nutrition during pregnancy: weight gain. Washington, DC: National Academy Press;1990. 4. Olson G, Blackwell SC. Optimization of gestational weight gain in the obese gravida: a review. Obstet Gynecol Clin North Am 2011;38: 397-407. 5. Chu SY, Callaghan WM, Bish CL, D’Angelo D. Gestational weight gain by body mass index among US women delivering live births, 20042005: fueling future obesity. Am J Obstet Gynecol 2009;200:271.e1-7. 6. Nohr EA, Bech BH, Vaeth M, Rasmussen KM, Henriksen TB, Olsen J. Obesity, gestational weight gain and preterm birth: a study within the Danish National Birth Cohort. Paediatr Perinat Epidemiol 2007;21:5-14. 7. Barlow SE, the Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics 2007;120(suppl): S164-92. 8. Ogden CL, Carroll MD, Curtin LR, Lamb MM, Flegal KM. Prevalence of high body mass index in US children and adolescents, 2007 -2008. JAMA 2010;303:242-9. 9. McCormick DP, Sarpong K, Lindsay Jordan L, Ray L, Jain S. Infant obesity: are we ready to make this diagnosis? J Pediatr 2010;157:15-9. 10. Freedman DS, Mei Z, Srinivasan SR, Berenson GS, Dietz WH. Cardiovascular risk factors and excess adiposity among overweight children and adolescents: the Bogalusa Heart study. J Pediatr 2007;150:12-7. 11. Desai M, Ross MG. Fetal Programming of adipose tissue: effects of intrauterine growth restriction and maternal obesity/high-fat diet. Semin Reprod Med 2011;29:237-45.
CAOG Papers
www.AJOG.org 12. Barker DJ. Fetal origins of coronary heart disease. BMJ 1995;311:171-4. 13. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997;37:86973. 14. Oken E, Taveras EM, Kleinman KP, RichEdwards JW, Gillman MW. Gestational weight
gain and child adiposity at age 3 years. Am J Obstet Gynecol 2007;196:322.e1-8. 15. Oken E. Maternal and child obesity: the causal link. Obstet Gynecol Clin N Am 2009; 36:361-77. 16. Muhlhausler B, Ong Z. The fetal origins of obesity: early origins of altered food intake. Endocr Metab Immune Disord Drug Targets 2011;11:189-97.
17. Phelan S. Pregnancy: a “teachable moment” for weight control and obesity prevention. Am J Obstet Gynecol 2010;202:135.e1.8. 18. Quinlivan J, Julania S, Lam L. Antenatal dietary interventions in obese pregnant women to restrict gestational weight gain to Institute of Medicine recommendations: a meta-analysis. Obstet Gynecol 2011;118:1395-401.
Delivery of monochorionic twins in the absence of complications: analysis of neonatal outcomes and costs Amy Elizabeth Sullivan, MD; Paul Nathan Hopkins, MD, MSPH; Hsin-Yi Weng, MPH; Erick Henry, MPH; Jamie Oi-Ting Lo, MD; Michael Walter Varner, MD; Michael Sean Esplin, MD OBJECTIVE: We sought to estimate the optimal time to deliver uncom-
plicated monochorionic-diamnionic (MCDA) twins. STUDY DESIGN: Data were retrospectively obtained from twin pregnancies from 2000 through 2009. The gestational week–specific prospective perinatal mortality risk was calculated. A cohort of MCDA twins with nonindicated deliveries was analyzed separately. Neonatal outcomes and costs were compared between MCDA twins with nonindicated deliveries born at specific weeks of gestation, and those born the subsequent week. RESULTS: There were 5894 dichorionic-diamnionic twins and 1704 MCDA twins. After 28 weeks, the gestational week–specific prospec-
tive risk of perinatal mortality did not differ between groups. There were 948 MCDA twins with nonindicated deliveries. Until 37 weeks, the risk of severe neonatal morbidity, perinatal mortality, and hospital costs were greater for fetuses delivered compared to fetuses born in a subsequent week. CONCLUSION: To optimize neonatal outcome and decrease hospital costs, MCDA twins should not be delivered ⬍37 weeks unless medically indicated.
Cite this article as: Sullivan AE, Hopkins PN, Weng H-Y, et al. Delivery of monochorionic twins in the absence of complications: analysis of neonatal outcomes and costs. Am J Obstet Gynecol 2012;206:257.e1-7.
B ACKGROUND AND O BJECTIVE Monochorionicity has been associated with increased adverse perinatal outcomes when compared with dichorionicity.
From the Departments of Obstetrics and Gynecology (Drs Sullivan, Lo, Varner, and Esplin), Cardiovascular Genetics (Dr Hopkins), and Pediatrics (Ms Weng), University of Utah School of Medicine, and the Department of Obstetrics and Gynecology, Intermountain Health Care (Drs Sullivan, Varner, and Esplin and Mr Henry), Salt Lake City, UT. The authors report no conflict of interest. Presented orally, in part, at the 78th annual meeting of the Central Association of Obstetricians and Gynecologists, Nassau, Bahamas, Oct. 26-29, 2011. 0002-9378/free © 2012 Mosby, Inc. All rights reserved. doi: 10.1016/j.ajog.2011.12.016
For Editors’ Commentary, see Table of Contents
Many obstetricians now advocate iatrogenic preterm delivery of monochorionic twins to avoid potential perinatal complications such as stillbirth. Patients with monochorionic twins are more likely to develop complications, including twin-twin transfusion syndrome, fetal growth abnormalities, and severe preeclampsia–all of which warrant preterm delivery. However, the optimal timing of delivery for monochorionic twin pregnancies that do not have medical indications for delivery remains a subject of debate. The objective of this study was to estimate the optimal timing of delivery of monochorionic–diamnionic (MCDA) twins with no medical indications for delivery. We hypothesized that the morbidity and mortality rates of MCDA twins are similar to those of diamnionic twins, that the risk
for prematurity associated with elective delivery ⬍37 weeks’ gestation is greater than the risk for stillbirth, and therefore MCDA twins without medical indications for delivery do not warrant elective preterm delivery.
M ATERIALS AND M ETHODS Electronic data were obtained on patients with twin deliveries from January 2000 through December 2009 at 18 hospitals within the Intermountain Health Care medical system. Data from neonatal outcomes were collected and analyzed. We defined perinatal death as stillbirth (fetal death prior to delivery) or neonatal death (death of a liveborn infant by 28 days). We defined severe adverse perinatal events as stillbirth, neonatal death, bronchopulmonary dysplasia, grade ⬎3 intraventricular hemorrhage, necrotizing enterocolitis, or sepsis.
MARCH 2012 American Journal of Obstetrics & Gynecology
257