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tlr lr: lilrli, (, o ) 6 o o o o d : a. n ) : C :. *, (. :) b o g @ C o a o f -n o 5 C s -O N O k t \J $ s a, L t-;; r I'84' Maternal body weight and pregnancy outcomel'2 Richard L Naeye ABSTRACI Pregnancies that produced 56 857 children were analyzed to eYaluate the relationship olthe mothers' rela- tive pregravid body weight to pregnancy outcome. Perinatal mortatiiy rales proBressively increased from 37 of 1000 in off' springofthin subjects to l2l of 1000 in the offspring ofobese subjects (p < 0.001). Nearly half of this mortality increase was due to preterm deliveries, pa(icularly before 3 i wk of gesta- tion. More than half o[ the increase in preterm births was caused by acute chorioamnionitis. Other factors that made ma' jor contributions to the overall mortality increase were rises 1n the lrequencies of older gravidas (ages 35-50 y)' gravidas who had diabetes mellitus, children who had major congenital malformations, and dizygous twins, Am J Clin trrrlr 1990; 52:773-9. KEY WORDS Fatness, obesity. perinatal mortality, preg nancy outcome, preteffn birth. twins Introduction Obese women have long been known to have more stillbirths and children who die as neonates than do nonobese women, The usual explanations are that ob€se women more often have diabetes mellitus, hypertension' twins' and infants who are prone to birth trauma because they are macrosomic ( l-6). Un' til recently no consideration was Siven to the possibility that the greater perinatal mortality might be systematically related to the whole spectrum of maternal body composition, lrom thin 10 obese, rather than just at the extreme represented by obesity. A large British study recently raised this possibiliry when it found that increased perinatal mortality lor preterm infants was not limited to offspring of obese women but stafied with offspring olthin women and progressively increased with increasing matemal body weight to reach its peak for offspring ofobese women (7), That study did not take antenatal and neo' natal disorders or demographic and liflestyle factors into con- sideration, so its frndings could be due to factors unrelated to maternal weight. If increasing pcrinatal mortality has a system' atic relationship to increasing maternal weight, there is a need to identify the responsible mechanisms' We used data lrorn a large $rospective study to determine the changes that take place in perinatal mortality rates as relative maternal body weight increases. The analyses cover the entire spectrum of relative maternal body weight from thin to obese and include the risks associated with antenatal and neonatal disorden as well as de' mographic and lilestyle factors. Subjects and methods Data lor the analyses came from the Collaborative Perinatal Study (CPS) of the National Institute of Neurological and Communicative Disorders and Stroke (8- l0)' The CPS was set up to identify antepartum and subsequent events that affect children's morbidity. mortality, and development' It prospec' tively followed the course of58 957 children from before birth to aje 7 y in l2 medical school-affiliated hospitals in different regions of the United States between 1959 and l966 Data from z ioO oftne 58 957 childrcn could not be analyzed because their mothers delivered at a non-CPS hospital. leaving 56 857 avail- able lor the current analyses. These children were the products of 55 665 singleton gestations and 598 pregnancies that pro- duced twins^ The CPS recorded events ofgestation, labor, de- livery, and neonatal periods as well as children's subsequent groMh and psychomotor and sensory development' Detaited descriptions of the sampling methods, definitions' and study procedures have been published (8-10). Data from the CPS are still being analyzed because they are the largest set o[prospec- tive information ever gathered to study pregnancy and its out' come. The current anatyses locus on the relationship olrelative maternal pregravid body weight to pregnancy outcome' Quetelet's index [pregravid weight (kg)/ht (m'?)] was used to measure relative weieht (?), Maternal heights were obtained by measurement and maternal pregravid weights by interview at the first clinic visit for antenatal medical care. Mothers wel:e divided into four categories according to Quetelet's index val- ues: < 20 (thin), 20-24 (normal), 25-30 (mildly overweight)' and > 30 (obese). Those in the 25-30 category presumably in- cluded women who had a large lean body mass flor height in addition to those who were slightly obese, and that is why women in this category were designated as slightly overweight rather than slightly obese. Maternal pregnancy risk factors ana- lyzed included age, parity, cigarette smoking' weight gain' the presence or absence of diabetes mellitus, and hypertensive dis- orders. Age groups analyzed as potentially high risk were teen' agers (10-18 y) and advanced age (35-50 v) (8). The diabetes rietlitus category included both women who developed the dis- i I liirrt, ni ll I From the Depanment of Pathology' MS Hershey Medical Center' Pennsylvania State University College of Medicine, Hershey' PA' : Addres reprint requesls to RL Naeye. MS Hershey Medical Cen- ter. Pennsylvania State University College ol Medicine, Hershcy' PA l 7033. Received July 3, 1989. Accepted for publication September 20. I 989. ..tm J Clin,\,rrrr !990:52:273-9. Pnnted in USA. rO 1990 Amencan Society forClinical Nutntton 273 l l I ili lilllllii, il lt' ' ,,,

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    Maternal body weight and pregnancy outcomel'2Richard L Naeye

    ABSTRACI Pregnancies that produced 56 857 childrenwere analyzed to eYaluate the relationship olthe mothers' rela-tive pregravid body weight to pregnancy outcome. Perinatalmortatiiy rales proBressively increased from 37 of 1000 in off'springofthin subjects to l2l of 1000 in the offspring ofobesesubjects (p < 0.001). Nearly half of this mortality increase wasdue to preterm deliveries, pa(icularly before 3 i wk of gesta-tion. More than half o[ the increase in preterm births wascaused by acute chorioamnionitis. Other factors that made ma'jor contributions to the overall mortality increase were rises1n the lrequencies of older gravidas (ages 35-50 y)' gravidaswho had diabetes mellitus, children who had major congenitalmalformations, and dizygous twins, Am J Clin trrrlr 1990;52:773-9.

    KEY WORDS Fatness, obesity. perinatal mortality, pregnancy outcome, preteffn birth. twins

    Introduction

    Obese women have long been known to have more stillbirthsand children who die as neonates than do nonobese women,The usual explanations are that obse women more often havediabetes mellitus, hypertension' twins' and infants who areprone to birth trauma because they are macrosomic ( l-6). Un'til recently no consideration was Siven to the possibility thatthe greater perinatal mortality might be systematically relatedto the whole spectrum of maternal body composition, lromthin 10 obese, rather than just at the extreme represented byobesity. A large British study recently raised this possibilirywhen it found that increased perinatal mortality lor preterminfants was not limited to offspring of obese women but stafiedwith offspring olthin women and progressively increased withincreasing matemal body weight to reach its peak for offspringofobese women (7), That study did not take antenatal and neo'natal disorders or demographic and liflestyle factors into con-sideration, so its frndings could be due to factors unrelated tomaternal weight. If increasing pcrinatal mortality has a system'atic relationship to increasing maternal weight, there is a needto identify the responsible mechanisms' We used data lrorn alarge $rospective study to determine the changes that take placein perinatal mortality rates as relative maternal body weightincreases. The analyses cover the entire spectrum of relativematernal body weight from thin to obese and include the risksassociated with antenatal and neonatal disorden as well as de'mographic and lilestyle factors.

    Subjects and methods

    Data lor the analyses came from the Collaborative PerinatalStudy (CPS) of the National Institute of Neurological andCommunicative Disorders and Stroke (8- l0)' The CPS was setup to identify antepartum and subsequent events that affectchildren's morbidity. mortality, and development' It prospec'tively followed the course of58 957 children from before birthto aje 7 y in l2 medical school-affiliated hospitals in differentregions of the United States between 1959 and l966 Data fromz ioO oftne 58 957 childrcn could not be analyzed because theirmothers delivered at a non-CPS hospital. leaving 56 857 avail-able lor the current analyses. These children were the productsof 55 665 singleton gestations and 598 pregnancies that pro-duced twins^ The CPS recorded events ofgestation, labor, de-livery, and neonatal periods as well as children's subsequentgroMh and psychomotor and sensory development' Detaiteddescriptions of the sampling methods, definitions' and studyprocedures have been published (8-10). Data from the CPS arestill being analyzed because they are the largest set o[prospec-tive information ever gathered to study pregnancy and its out'come. The current anatyses locus on the relationship olrelativematernal pregravid body weight to pregnancy outcome'Quetelet's index [pregravid weight (kg)/ht (m'?)] was used tomeasure relative weieht (?), Maternal heights were obtained bymeasurement and maternal pregravid weights by interview atthe first clinic visit for antenatal medical care. Mothers wel:edivided into four categories according to Quetelet's index val-ues: < 20 (thin), 20-24 (normal), 25-30 (mildly overweight)'and > 30 (obese). Those in the 25-30 category presumably in-cluded women who had a large lean body mass flor height inaddition to those who were slightly obese, and that is whywomen in this category were designated as slightly overweightrather than slightly obese. Maternal pregnancy risk factors ana-lyzed included age, parity, cigarette smoking' weight gain' thepresence or absence of diabetes mellitus, and hypertensive dis-orders. Age groups analyzed as potentially high risk were teen'agers (10-18 y) and advanced age (35-50 v) (8). The diabetesrietlitus category included both women who developed the dis-

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    I From the Depanment of Pathology' MS Hershey Medical Center'Pennsylvania State University College of Medicine, Hershey' PA'

    : Addres reprint requesls to RL Naeye. MS Hershey Medical Cen-ter. Pennsylvania State University College ol Medicine, Hershcy' PAl 7033.

    Received July 3, 1989.Accepted for publication September 20. I 989.

    ..tm J Clin,\,rrrr !990:52:273-9. Pnnted in USA. rO 1990 Amencan Society forClinical Nutntton 273

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