Laura Jelliffe-Pawlowski

Faculty

Jelliffe-Pawlowski Headsot

Laura Jelliffe-Pawlowski

MS PhD

1 212 998 9020

433 First Ave
New York, NY 10010
United States

Laura Jelliffe-Pawlowski, PhD, MS, is a Professor. Prof. Jelliffe-Pawlowski’s research interests focus on understanding and addressing the drivers and consequences of adverse pregnancy outcomes with a special emphasis on preterm birth and associated racial/ethnic and socioeconomic inequities. Her work is highly transdisciplinary and looks at the interplay of biomolecular, social, and policy factors in observed patterns and outcomes. Her teaching and mentorship activities reflect this transdisciplinary approach with an emphasis on motivating the translation of research findings into action.

 

Prof. Jelliffe-Pawlowski leads a number of statewide, national, and international research efforts funded by the National Institutes of Health, the Bill and Melinda Gates Foundation, the March of Dimes, the State of California, and other entities. These includes, notably, the “Healthy Outcomes of Pregnancy for Everyone (HOPE)” consortium and study which focuses on understanding the experience of pregnant people and their infants pre- and post-COVID 19 pandemic. HOPE examines how biomolecular, social, and community factors affect the well-being and outcomes of mothers and infants and includes enrollment during pregnancy with outcome follow-up to 18-months after birth. Other ongoing projects include, for example, the NIH funded “Prediction Of Maturity, Morbidity, and Mortality in PreTerm Infants (PROMPT)”, study which focuses on examining the metabolic profiles of newborns with early preterm birth and associated outcomes, the “Transforming Health and Reducing PerInatal Anxiety through Virtual Engagement (THRIVE)”, randomized control trial (RCT), funded by the State of California which examines whether digital cognitive behavior therapy delivered by mobile app can assist in reducing anxiety symptoms in pregnant people and also examines participant acceptability of the application. Ongoing efforts also include leading the “California Prediction of Poor Outcomes of Pregnancy (CPPOP)” cohort study which focuses on investigating multi-omic drivers of preterm birth. The study interrogates biomolecular signals associated with preterm birth and includes full genome sequencing and mid-pregnancy biomolecular signaling related to metabolic, immune, stress, and placental function in hundreds of pregnancies with and without preterm birth. 

 

Prior to her joining NYU Meyers, Prof. Jelliffe-Pawlowski was a Professor of Epidemiology & Biostatistics, Chief of the Division of Lifecourse Epidemiology, a Professor in the Institute of Global Health Sciences, and Director of Discovery and Precision Health for the UCSF California Preterm Birth Initiative in the University of California San Francisco (UCSF) School of Medicine. She has a lifetime appointment as an Emeritus Professor of Epidemiology & Biostatistics in the UCSF School of Medicine and continues to work closely with the new Center for Birth Equity at UCSF. Prior to her appointment at UCSF, she was a leader at the Genetic Disease Screening Program within the California Department of Public Health. 

 

Prof. Jelliffe-Pawlowski efforts have been highlighted in numerous academic and lay articles including in the New York Times, in WIRED Magazine, in the Atlantic, on CNN, and on MSNBC. In 2023, she was recognized by Forbes Magazine as one of the top 50 over 50 Innovators in the United States. She is also a Phase I and Phase II Bill and Melinda Gates Foundation Grand Challenges awardee for her work in the United States and Uganda which focused on the development and validation of newborn metabolic profile as a novel measure of gestational age in infants.

BA, Psychology, University of California Los Angeles
MS, Child Development, University of California Davis
PhD, Human Development, University of California Davis

Preterm Birth

Forbes 50 over 50 awardee in Innovation (2023)
Delegate, African Academy of Sciences (2016)
Governor Brown Appointee for the California Department of Public Health, Interagency Coordinating Council on Early Intervention
Awardee, Bill and Melinda Bates Foundation, Gates Grand Challenges Phase I and II

Identification of second trimester screen positive pregnancies at increased risk for congenital heart defects

Jelliffe-Pawlowski, L. L., Walton-Haynes, L., & Currier, R. J. (2009). Prenatal Diagnosis, 29(6), 570-577. 10.1002/pd.2239
Abstract
Abstract
Objective: To examine whether second trimester biomarkers could be used to identify screen positive pregnancies at increased risk for congenital heart defects (CHDs) and measure the effect of using different biomarker cut points on the detection of CHDs and on the performance of predictive models. Methods: Included were 19,402 pregnancies without chromosomal defects, which were screen positive for Down syndrome or other birth defects based on maternal serum measurements of alpha-fetoprotein (AFP), human chorionic gonadotrophin (hCG), and unconjugated estriol (uE3). Logistic regression models were built that compared biomarkers for CHD cases compared to controls. Results: CHD cases were more likely to be screen positive for trisomy-18, to have a nuchal fold (NF) ≥5 mm, and/or to have an hCG multiple of the median (MoM) ≥95th percentile in models that considered screen positive grouping. In models that did not consider screen positive grouping, cases were more likely to have a NF ≥5 mm, an AFP MoM ≤10th percentile, an hCG MoM ≤25th percentile, and/or an hCG MoM ≥75th percentile. Conclusion: Along with NF, second trimester maternal serum biomarkers may be useful indicators for fetal and newborn evaluation for CHDs in screen positive pregnancies without identified chromosomal defects.

Triple-marker prenatal screening program for chromosomal defects

Kazerouni, N. N., Cunier, B., Malm, L., Riggle, S., Hodgkinson, C., Smith, S., Tempelis, C., Lorey, F., Davis, A., Jelliffe-Pawlowski, L., Walton-Haynes, L., & Roberson, M. (2009). Obstetrics and Gynecology, 114(1), 50-58. 10.1097/AOG.0b013e3181a9479e
Abstract
Abstract
OBJECTIVE: To examine screening performance of California's triple-marker screening program, using data from a statewide registry for chromosomal defects. METHODS: This study included 752,686 women who received a screening risk and had an expected date of delivery between July 2005 and the end of June 2007. Follow-up diagnostic services for screen-positive women were performed at state-approved centers. Data on diagnostic outcomes from these visits were entered into the California Chromosomal Defect Registry (CCDR). Other CCDR sources include mandatory reporting by all cytogenetic laboratories and hospitals and outcome data forms submitted by prenatal care providers. RESULTS: The observed detection rate for Down syndrome (N = 1,217) was 77.4%. It varied significantly by gestational dating method and maternal age. The rates for women aged younger than 35 years and 35 years and older were 62.4% and 94.0%, respectively. The detection rates were 81.3% for ultrasound-dated pregnancies and 67.5% for last menstrual period-dated pregnancies. For Turner syndrome, trisomy 18, triploidy, and trisomy 13, the detection rates were 79.4%, 82.5%, 98.1%, and 36.0%, respectively. The positive rate for Down syndrome was 5.4%. Of women with a Down syndrome fetus who were screen positive, only 49.5% opted for amniocentesis. Of women who obtained results from amniocentesis indicating a Down syndrome fetus, 61.4% had an elective termination, 26.2% had a live birth, 4.5% had a death or miscarriage, and 7.9% had an unknown outcome. CONCLUSION: The observed performance of this large triple-marker screening program exceeds generally predicted detection rates for Down syndrome. This study methodology will be used to measure the performance of subsequent screening enhancements.

Using second trimester ultrasound and maternal serum biomarker data to help detect congenital heart defects in pregnancies with positive triple-marker screening results

Jelliffe-Pawlowski, L. L., Walton-Haynes, L., & Currier, R. J. (2008). American Journal of Medical Genetics, Part A, 146(19), 2455-2467. 10.1002/ajmg.a.32513
Abstract
Abstract
Congenital heart defects (CHDs) are the most common of all birth defects. For many newborns with a CHD, prenatal versus postnatal detection is associated with substantially decreased morbidity and mortality risks. Although technological advances in fetal echocardiography have led to an increased capacity to detect CHDs prenatally, pregnancies without an identified risk factor are not routinely screened. With the aim of identifying pregnancies at increased risk for CHDs, this study examined the relationship between CHDs and typically collected second trimester biomarker data collected on a large population-based sample of singleton pregnancies with one or more second trimester screen positive result for Down syndrome, trisomy 18 (T-18), Smith-Lemli-Opitz syndrome (SLOS), or a neural tube defect (NTD). Where possible, logistic models for cases and controls were built and potential referral models were tested among study subsamples with information on the presence or absence of CHDs reported pre- and perinatally. When considered in combination, screen positive for T-18, screen positive for SLOS, nuchal fold measurement ≥ 5 mm, and/or having an adjusted hCG multiple of the median ≥ the 95th centile detected 42.7% of all pregnancies with a CHD in the combined subsample (where co-occurrence with chromosomal defects was not considered) and detected 29.7% of all pregnancies with a CHD in the no-chromosomal defect subsample. A nuchal fold measurement ≥ 5 mm detected 18.2% of those with a CHD in the Down syndrome subsample and an adjusted hCG multiple of the median (MoM) ≤ 5th centile detected 92.9% of those with a CHD in the T-18 subsample.

Infant C677T MTHFR polymorphism and severe mental retardation

Shaw, G. M., Jelliffe-Pawlowski, L., Nelson, V., Zhu, H., Harris, J. A., & Finnell, R. H. (2007). Birth Defects Research Part A - Clinical and Molecular Teratology, 79(1), 24-26. 10.1002/bdra.20321
Abstract
Abstract
BACKGROUND: We investigated whether infants with homozygous genotype TT of the MTHFR gene were at increased risk of severe mental retardation. METHODS: One hundred children with severe mental retardation (cases) were investigated from a large geographic-based study of infants born in California in 1992-1993. Cases were compared to 743 randomly selected nonmalformed control infants born in California during 1987-1991. DNA was extracted from newborn screening filter papers. Cases and controls were genotyped TT if homozygous for the MTHFR C677T allele, CT if heterozygous for the C677T allele, and CC if homozygous for the C677 (wild type) allele. RESULTS: Overall, case and control infants had similar percentages of TT and CT genotypes. Percentages between cases and controls differed somewhat across race/ethnic groups. Elevated ORs of 1.9 (95% CI: 0.7-5.0) and 2.6 (95% CI: 1.1-5.8) were observed for the TT and CT genotypes, respectively, among Hispanic children. Observed results were not substantially altered for analyses that removed 41 case children who also had structural birth defects. CONCLUSIONS: Folate-related mechanisms are important to investigate for etiologies of birth defects, and such lines of inquiry may be revealing for mental retardation given the relationships between mental retardation and birth defects and potential relationships between folate, DNA methylation, and mental retardation.

Effect of magnitude and timing of maternal pregnancy blood lead (Pb) levels on birth outcomes

Jelliffe-Pawlowski, L. L., Miles, S. Q., Courtney, J. G., Materna, B., & Charlton, V. (2006). Journal of Perinatology, 26(3), 154-162. 10.1038/sj.jp.7211453
Abstract
Abstract
Objective: Associations between magnitude and timing of maternal pregnancy blood lead (Pb) levels (BLLs), birth weight, and total days of gestation were examined, as well as associations with related clinical diagnoses of low birth weight (LBW), preterm, and small-for-gestational-age (SGA) birth. Study Design: Among a sample of 262 mother-infant pairs studied retrospectively, one-way analysis of variance and regression statistics were used to measure the relationship between level of maternal pregnancy BLLs and birth outcomes while controlling for key maternal and newborn factors. Results: Women with maximum pregnancy BLLs (max-PBLLs) ≥10 μ/dl tended to give birth earlier and their babies were at substantially increased risk for preterm and SGA birth. By holding other explanatory factors constant, each unit increase in max-PBLL above 10≥ μ/dl was found to be associated with a decrease of -0.3 in total days of gestation. Compared to women with lower levels, women with max-PBLLs 10≥ μ/dl were at a threefold increased risk for preterm birth (adjusted OR = 3.2, 95% CI 1.2-7.4) and more than a fourfold increased risk for having an SGA infant (adjusted OR = 4.2, 1.3-13.9). Second trimester maximum BLLs 10≥ μ/dl were associated with a steep decrease in total days of gestation (a decrease of -1.0 days per each unit increase above 10≥ μ/dl). Conclusions: These data provide evidence of the adverse effects of maternal pregnancy BLLs, particularly when levels are 10≥ μ/dl. Prenatal Pb exposure at these levels was associated with significant decreases in total days of gestation and an increased risk of preterm and SGA birth.

Risks for severe mental retardation occurring in isolation and with other developmental disabilities

Jelliffe-Pawlowski, L. L., Shaw, G. M., Nelson, V., & Harris, J. A. (2005). American Journal of Medical Genetics, 136(2), 152-157. 10.1002/ajmg.a.30801
Abstract
Abstract
Individual and maternal characteristics as potential risk factors for having severe mental retardation (SMR) occurring with and without cerebral palsy (CP), epilepsy, or a pervasive developmental disorder (PDD) were explored among a cohort of 119,404 children without Down syndrome born in the California Central Valley in 1992 and 1993. Unadjusted and adjusted relative risks (RRs) and their 95% confidence intervals (CIs) based on the Poisson distribution were used to estimate the risks associated with each individual and maternal factor studied for each SMR diagnostic category. The most notable increased risks for SMR occurring in isolation or with CP or epilepsy was for children born low-birth-weight or preterm who were at a substantially increased risk (RRs 2.6-9.9). In contrast, the risk of SMR occurring with a PDD was the greatest among males compared to females (RR = 3.4, 95% CI 1.5, 7.9), Blacks compared to Whites (RR = 5.1, 95% CI 1.7, 15.5), and Asians compared to Whites (RR = 3.9, 95% CI 1.3, 12.0). Etiologic heterogeneity when SMR occurs with a PDD was suggested.

Neurodevelopmental outcome at 8 months and 4 years among infants born full-term small-for-gestational-age

Jelliffe-Pawlowski, L. L., & Hansen, R. L. (2004). Journal of Perinatology, 24(8), 505-514. 10.1038/sj.jp.7211111
Abstract
Abstract
Objectives: To examine the association between intrauterine growth restriction and neurodevelopmental outcome among full-term small-for-gestational-age (SGAT) infants at 8 months and 4 years of age. Study Design: Growth parameters at birth and test scores on measures of neurodevelopmental function for 3922 children born SGAT were compared with those of 29,369 children born appropriately grown-for-gestational-age term from similar economic backgrounds. Additional within-SGAT/economic group comparisons were made for 1684 SGAT infants with symmetric undergrowth at birth and 2034 SGAT infants with asymmetric undergrowth at birth. Results: Regardless of socioeconomic background, infants born SGAT were found to be at significantly increased risk for neurodevelopmental difficulties at 8 months and at 4 years of age. Few within SGAT/socioeconomic group differences in neurodevelopmental outcome appeared to be associated with specific pattern of growth restriction at birth. Conclusions: The present findings provide further evidence of the individual and public health impact of SGAT birth.

Risk of mental retardation among children born with birth defects

Jelliffe-Pawlowski, L. L., Shaw, G. M., Nelson, V., & Harris, J. A. (2003). Archives of Pediatrics and Adolescent Medicine, 157(6), 545-550. 10.1001/archpedi.157.6.545
Abstract
Abstract
Background: A paucity of epidemiologic research exists concerning the co-occurrence of birth defects and mental retardation (MR). Study of this co-occurrence may yield important clues about the causes of both. Objective: To examine the co-occurrence of birth defects and MR, taking into consideration the type of birth defect, level of MR, co-occurrence of MR with other developmental disabilities, and individual and maternal factors. Design: A retrospective cohort study of infants born in the California Central Valley with and without a structural birth defect by 1 year of age, and with or without MR by 7 to 9 years of age. Setting and Participants: One-year survivors (N = 119556) born in nonmilitary hospitals in 8 California counties between January 1, 1992, and December 31, 1993, for whom information about birth defects was recorded within the first year of life. Main Outcome Measure: Diagnosis of MR by age 7 years considered as being mild or severe and as occurring without other developmental disabilities (isolated MR) or as occurring with other developmental disabilities, including cerebral palsy, epilepsy, or a pervasive developmental disorder. Results: Children with birth defects were nearly 27 times more likely to have MR by 7 years of age compared with children without a diagnosed birth defect regardless of type of defect (prevalence ratio, 26.8; 95% confidence interval, 22.7-31.7). Among those with birth defects, children with Down syndrome (prevalence ratio, 211.7; 95% confidence interval, 171.3-261.5) and children with sex chromosomal defects (prevalence ratio, 57.4; 95% confidence interval, 23.7-138.6) were at the highest risk for MR. Children with nonchromosomal defects, including central nervous system defects and all types of organ and system defects, were at substantially increased risk for all levels of MR. Risks of MR among children with Down syndrome and nonchromosomal defects were not substantially altered when adjusted for individual and maternal factors. Conclusions: Children with chromosomal and other structural birth defects are at a substantially increased risk for having MR by 7 years of age compared with children born without a birth defect. Children with birth defects are at an especially increased risk for having severe MR and MR occurring independently of other developmental disabilities.

Neuropeptides and neurotrophins in neonatal blood of children with autism or mental retardation

Nelson, K. B., Grether, J. K., Croen, L. A., Dambrosia, J. M., Dickens, B. F., Jelliffe, L. L., Hansen, R. L., & Phillips, T. M. (2001). Annals of Neurology, 49(5), 597-606. 10.1002/ana.1024
Abstract
Abstract
There has been little exploration of major biologic regulators of cerebral development in autism. In archived neonatal blood of children with autistic spectrum disorders (n = 69), mental retardation without autism (n = 60), or cerebral palsy (CP, n = 63) and of control children (n = 54), we used recycling immunoaffinity chromatography to measure the neuropeptides substance P (SP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP), and the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5). Neonatal concentrations of VIP, CGRP, BDNF, and NT4/5 were higher (ANOVA, all p values < 0.0001 by Scheffe test for pairwise differences) in children in the autistic spectrum and in those with mental retardation without autism than in control children. In 99% of children with autism and 97% with mental retardation, levels of at least one of these substances exceeded those of all control children. Concentrations were similar in subgroups of the autistic spectrum (core syndrome with or without mental retardation, other autistic spectrum disorders with or without mental retardation) and in the presence or absence of a history of regression. Among children with mental retardation, concentrations did not differ by severity or known cause (n = 11, including 4 with Down syndrome). Concentrations of measured substances were similar in children with CP as compared with control subjects. SP, PACAP, NGF, and NT3 were not different by diagnostic group. No measured analyte distinguished children with autism from children with mental retardation alone. In autism and in a heterogeneous group of disorders of cognitive function, overexpression of certain neuropeptides and neurotrophins was observed in peripheral blood drawn in the first days of life.