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

Metabolic heritability at birth: Implications for chronic disease research

Ryckman, K. K., Smith, C. J., Jelliffe-Pawlowski, L. L., Momany, A. M., Berberich, S. L., & Murray, J. C. (2014). Human Genetics, 133(8), 1049-1057. 10.1007/s00439-014-1450-4
Abstract
Abstract
Recent genome-wide association studies of the adult human metabolome have identified genetic variants associated with relative levels of several acylcarnitines, which are important clinical correlates for chronic conditions such as type 2 diabetes and obesity. We have previously shown that these same metabolite levels are highly heritable at birth; however, no studies to our knowledge have examined genetic associations with these metabolites measured at birth. Here, we examine, in 743 newborns, 58 single nucleotide polymorphisms (SNPs) in 11 candidate genes previously associated with differing relative levels of short-chain acylcarnitines in adults. Six SNPs (rs2066938, rs3916, rs3794215, rs555404, rs558314, rs1799958) in the short-chain acyl-CoA dehydrogenase gene (ACADS) were associated with neonatal C4 levels. Most significant was the G allele of rs2066938, which was associated with significantly higher levels of C4 (P = 1.5 × 10-29). This SNP explains 25 % of the variation in neonatal C4 levels, which is similar to the variation previously reported in adult C4 levels. There were also significant (P < 1 × 10-4) associations between neonatal levels of C5-OH and SNPs in the solute carrier family 22 genes (SLC22A4 and SLC22A5) and the 3-methylcrotonyl-CoA carboxylase 1 gene (MCCC1). We have replicated, in newborns, SNP associations between metabolic traits and the ACADS and SLC22A4 genes observed in adults. This research has important implications not only for the identification of rare inborn errors of metabolism but also for personalized medicine and early detection of later life risks for chronic conditions.

Obstetric, perinatal, and fetal outcomes in pregnancies with false-positive integrated screening results

Baer, R. J., Currier, R. J., Norton, M. E., Flessel, M. C., Goldman, S., Towner, D., & Jelliffe-Pawlowski, L. L. (2014). Obstetrics and Gynecology, 123(3), 603-609. 10.1097/AOG.0000000000000145
Abstract
Abstract
OBJECTIVE:: To assess the risk of adverse obstetric, perinatal, and fetal outcomes for pregnant women participating in prenatal sequential integrated screening through the California Prenatal Screening Program who had a false-positive screening result. METHODS:: Women who underwent first-and second-trimester prenatal integrated screening plus nuchal translucency measurement with outcome information available were included. Fetuses and neonates with chromosomal or neural tube defects were excluded. We compared the risk of adverse outcomes for all women with a positive screening result compared with a 10% random sample of women with a negative screening result. Logistic binomial regression was used to compare adverse outcomes in screen-positive compared with screen-negative women. RESULTS:: We identified 9,051 screen-positive and 30,928 screen-negative pregnancies with outcome information available. Compared with screen-negative pregnancies, screen-positive women were more likely to be diagnosed with preeclampsia, placenta previa, or abruption (7.6% screen-positive, 3.8% screen-negative; relative risk 1.7, 95% confidence interval [CI] 1.6-1.8) or experience fetal loss before 20 weeks of gestation (1.9% screen-positive, 0.2% screen-negative; relative risk 3.5, 95% CI 3.2-3.8). Women with positive results for more than one screened condition were at substantially greater risk of fetal and neonatal mortality (relative risks 33.6-156.7, 95% CIs 21.8-194.4). CONCLUSION:: Among pregnancies without chromosomal or neural tube defects, prenatal sequential integrated screening provides information regarding risk across a variety of adverse pregnancy outcomes. LEVEL OF EVIDENCE:: II

Population-based biomarker screening and the development of severe preeclampsia in California

Taché, V., Baer, R. J., Currier, R. J., Li, C. S., Towner, D., Waetjen, L. E., & Jelliffe-Pawlowski, L. L. (2014). American Journal of Obstetrics and Gynecology, 211(4), 377.e1-377.e8. 10.1016/j.ajog.2014.03.026
Abstract
Abstract
Objective The purpose of this study was to examine the relationship between second-trimester maternal serum biomarkers and the development of early- and late-onset severe preeclampsia in euploid pregnancies. Study Design Included were 136,139 pregnancies that obtained second-trimester prenatal screening through the California Prenatal Screening Program with live births in 2006-2008. We identified severe preeclampsia diagnoses from hospital discharge records. We used log binomial regression to examine the association between abnormal second-trimester maternal serum biomarkers and the development of severe preeclampsia.Results Approximately 0.9% of all women (n = 1208) in our sample experienced severe preeclampsia; 329 women at <34 weeks' gestation and 879 women ≥34 weeks' gestation. High levels of alpha fetoprotein (AFP), human chorionic gonadotropin, inhibin (multiple of the median, ≥95th percentile), and low unconjugated estriol (multiple of the median, ≤5th percentile), were associated with severe preeclampsia (relative risk, 2.5-11.7). Biomarkers were more predictive of early-onset severe preeclampsia (relative risk, 3.8-11.7). One in 9.5 pregnancies with combined high AFP, inhibin, and low unconjugated estriol levels experienced severe early-onset preeclampsia compared with 1 in 680.5 pregnancies without any abnormal biomarkers.Conclusion The risk of the development of severe preeclampsia increases for women with high second-trimester AFP, human chorionic gonadotropin, inhibin, and/or low unconjugated estriol; this is especially true for early-onset severe preeclampsia. When abnormal biomarkers co-occur, risk dramatically increases. Although the screening value of second-trimester biomarkers is low, abnormal biomarkers, especially when occurring in combination, appear to indicate placental dysfunction that is associated with the development of severe preeclampsia.

Risk of selected structural abnormalities in infants after increased nuchal translucency measurement

Baer, R. J., Norton, M. E., Shaw, G. M., Flessel, M. C., Goldman, S., Currier, R. J., & Jelliffe-Pawlowski, L. L. (2014). American Journal of Obstetrics and Gynecology, 211(6), 675.e1-675.e19. 10.1016/j.ajog.2014.06.025
Abstract
Abstract
OBJECTIVE: We sought to examine the association between increased first-trimester fetal nuchal translucency (NT) measurement and major noncardiac structural birth defects in euploid infants. STUDY DESIGN: Included were 75,899 singleton infants without aneuploidy or critical congenital heart defects born in California in 2009 through 2010 with NT measured between 11-14 weeks of gestation. Logistic binomial regression was employed to estimate relative risks (RRs) and 95% confidence intervals (CIs) for occurrence of birth defects in infants with an increased NT measurement (by percentile at crown-rump length [CRL] and by ≥3.5 mm compared to those with measurements <90th percentile for CRL). RESULTS: When considered by CRL adjusted percentile and by measurement ≥3.5 mm, infants with a NT ≥95th percentile were at risk of having ≥1 major structural birth defects (any defect, RR, 1.6; 95% CI, 1.3-1.9; multiple defects, RR, 2.1; 95% CI, 1.3-3.4). Infants with a NT measurement ≥95th percentile were at particularly high risk for pulmonary, gastrointestinal, genitourinary, and musculoskeletal anomalies (RR, 1.6-2.7; 95% CI, 1.1-5.4). CONCLUSION: Our findings demonstrate that risks of major pulmonary, gastrointestinal, genitourinary, and musculoskeletal structural birth defects exist for NT measurements ≥95th percentile. The ≥3-fold risks were observed for congenital hydrocephalus; agenesis, hypoplasia, and dysplasia of the lung; atresia and stenosis of the small intestine; osteodystrophies; and diaphragm anomalies.

Association of early-preterm birth with abnormal levels of routinely collected first- and second-trimester biomarkers

Jelliffe-Pawlowski, L. L., Shaw, G. M., Currier, R. J., Stevenson, D. K., Baer, R. J., O’Brodovich, H. M., & Gould, J. B. (2013). American Journal of Obstetrics and Gynecology, 208(6), 492.e1-492.e11. 10.1016/j.ajog.2013.02.012
Abstract
Abstract
Objective: The purpose of this study was to examine the relationship between typically measured prenatal screening biomarkers and early-preterm birth in euploid pregnancies. Study Design: The study included 345 early-preterm cases (<30 weeks of gestation) and 1725 control subjects who were drawn from a population-based sample of California pregnancies who had both first- and second-trimester screening results. Logistic regression analyses were used to compare patterns of biomarkers in cases and control subjects and to develop predictive models. Replicability of the biomarker early-preterm relationships that was revealed by the models was evaluated by examination of the frequency and associated adjusted relative risks (RRs) for early-preterm birth and for preterm birth in general (<37 weeks of gestation) in pregnancies with identified abnormal markers compared with pregnancies without these markers in a subsequent independent California cohort of screened pregnancies (n = 76,588). Results: The final model for early-preterm birth included first-trimester pregnancy-associated plasma protein A in the ≤5th percentile, second-trimester alpha-fetoprotein in the ≥95th percentile, and second-trimester inhibin in the ≥95th percentile (odds ratios, 2.3-3.6). In general, pregnancies in the subsequent cohort with a biomarker pattern that were found to be associated with early-preterm delivery in the first sample were at an increased risk for early-preterm birth and preterm birth in general (<37 weeks of gestation; adjusted RR, 1.6-27.4). Pregnancies with ≥2 biomarker abnormalities were at particularly increased risk (adjusted RR, 3.6-27.4). Conclusion: When considered across cohorts and in combination, abnormalities in routinely collected biomarkers reveal predictable risks for early-preterm birth.

A genome-wide association study (GWAS) for bronchopulmonary dysplasia

Wang, H., Julien, K. R., Stevenson, D. K., Hoffmann, T. J., Witte, J. S., Lazzeroni, L. C., Krasnow, M. A., Quaintance, C. C., Oehlert, J. W., Jelliffe-Pawlowski, L. L., Gould, J. B., Shaw, G. M., & O’Brodovich, H. M. (2013). Pediatrics, 132(2), 290-297. 10.1542/peds.2013-0533
Abstract
Abstract
OBJECTIVE: Twin studies suggest that heritability of moderate-severe bronchopulmonary dysplasia (BPD) is 53% to 79%, we conducted a genome-wide association study (GWAS) to identify genetic variants associated with the risk for BPD. METHODS: The discovery GWAS was completed on 1726 very low birth weight infants (gestational age = 250-296/7 weeks) who had a minimum of 3 days of intermittent positive pressure ventilation and were in the hospital at 36 weeks' postmenstrual age. At 36 weeks' postmenstrual age, moderate-severe BPD cases (n = 899) were defined as requiring continuous supplemental oxygen, whereas controls (n = 827) inhaled room air. An additional 795 comparable infants (371 cases, 424 controls) were a replication population. Genomic DNA from case and control newborn screening bloodspots was used for the GWAS. The replication study interrogated single-nucleotide polymorphisms (SNPs) identified in the discovery GWAS and those within the HumanExome beadchip. RESULTS: Genotyping using genomic DNA was successful. We did not identify SNPs associated with BPD at the genome-wide significance level (5 3 1028) and no SNP identified in previous studies reached statistical significance (Bonferroni-corrected P value threshold .0018). Pathway analyses were not informative. CONCLUSIONS: We did not identify genomic loci or pathways that account for the previously described heritability for BPD. Potential explanations include causal mutations that are genetic variants and were not assayed or are mapped to many distributed loci, inadequate sample size, race ethnicity of our study population, or case-control differences investigated are not attributable to underlying common genetic variation. Pediatrics 2013;132:290-297

High Quality Genome-Wide Genotyping from Archived Dried Blood Spots without DNA Amplification

St. Julien, K. R., Jelliffe-Pawlowski, L. L., Shaw, G. M., Stevenson, D. K., O’Brodovich, H. M., & Krasnow, M. A. (2013). PloS One, 8(5). 10.1371/journal.pone.0064710
Abstract
Abstract
Spots of blood are routinely collected from newborn babies onto filter paper called Guthrie cards and used to screen for metabolic and genetic disorders. The archived dried blood spots are an important and precious resource for genomic research. Whole genome amplification of dried blood spot DNA has been used to provide DNA for genome-wide SNP genotyping. Here we describe a 96 well format procedure to extract DNA from a portion of a dried blood spot that provides sufficient unamplified genomic DNA for genome-wide single nucleotide polymorphism (SNP) genotyping. We show that SNP genotyping of the unamplified DNA is more robust than genotyping amplified dried blood spot DNA, is comparable in cost, and can be done with thousands of samples. This procedure can be used for genome-wide association studies and other large-scale genomic analyses that require robust, high-accuracy genotyping of dried blood spot DNA.

Risk of bronchopulmonary dysplasia by second-trimester maternal serum levels of α-fetoprotein, human chorionic gonadotropin, and unconjugated estriol

Jelliffe-Pawlowski, L. L., Shaw, G. M., Stevenson, D. K., Oehlert, J. W., Quaintance, C., Santos, A. J., Baer, R. J., Currier, R. J., O’Brodovich, H. M., & Gould, J. B. (2012). Pediatric Research, 71(4), 399-406. 10.1038/pr.2011.73
Abstract
Abstract
INTRODUCTION: Although maternal serum α-fetoprotein (AFP), human chorionic gonandotropin (hCG), and estriol play important roles in immunomodulation and immunoregulation during pregnancy, their relationship with the development of bronchopulmonary dysplasia (BPD) in young infants is unknown despite BPD being associated with pre-and postnatal inflammatory factors. RESULTS: We found that these serum biomarkers were associated with an increased risk of BPD. Risks were especially high when AFP and/or hCG levels were above the 95th percentile and/or when unconjugated estriol (uE3) levels were below the 5th percentile (relative risks (RRs) 3.1-6.7). Risks increased substantially when two or more biomarker risks were present (RRs 9.9-75.9). DISCUSSION: Data suggested that pregnancies that had a biomarker risk and yielded an offspring with BPD were more likely to have other factors present that suggested early intrauterine fetal adaptation to stress, including maternal hypertension and asymmetric growth restriction. METHODS: The objective of this population-based study was to examine whether second-trimester levels of AFP, hCG, and uE3 were associated with an increased risk of BPD.

Second trimester serum predictors of congenital heart defects in pregnancies without chromosomal or neural tube defects

Jelliffe-Pawlowski, L., Baer, R., Moon-Grady, A. J., & Currier, R. J. (2011). Prenatal Diagnosis, 31(5), 466-472. 10.1002/pd.2720
Abstract
Abstract
Objective: To compare euploid pregnancies with congenital heart defects (CHDs) to similar pregnancies without CHDs on typically collected second trimester biomarker measurements. Method: Second trimester serum levels of alpha-fetoprotein (AFP), human chorionic gonadotrophin (hCG), and unconjugated estriol were compared for 306 CHD cases and 1224 no-CHD controls drawn from a sample of singleton pregnancies without chromosomal or neural tube defects (NTDs). Logistic regression models were built comparing biomarkers for cases and controls. Results: Regardless of the severity of defect, CHD cases were more likely to have unusually high AFP and/or hCG levels and/or unusually low hCG and/or uE3 levels [odds ratio (OR) 1.8-2.4, 95% confidence intervals (CIs) 1.2-4.0]. Cases with critical CHDs were more than twice as likely to have an AFP multiple of the median (MoM) ≥ the 95th percentile and/or an hCG and/uE3 MoM ≤ the 5th percentile (OR 2.1-3.9, 95% CIs 1.1-7.8). Conclusion: Abnormal levels of specific second trimester maternal serum biomarkers indicated an increased risk for CHDs among this sample of low risk pregnancies. Our data suggest that future efforts aimed at improving CHD detection in low risk pregnancies may benefit from considering serum biomarkers.

Second trimester serum predictors of preterm birth in a population-based sample of low-risk pregnancies

Jelliffe-Pawlowski, L. L., Baer, R. J., & Currier, R. J. (2010). Prenatal Diagnosis, 30(8), 727-733. 10.1002/pd.2489
Abstract
Abstract
Objective: To examine the relationship between typically collected second trimester maternal serum biomarkers and preterm birth among pregnancies without intrauterine-growth-retardation or other specific risk factors. Methods: Included were 102 861 singleton pregnancies without specific risks that resulted in the live birth of an infant of normal birth weight for gestational age without aneuploidy or a neural tube defect. Logistic binomial regression analyses were used to estimate the relative risk (RR) of giving birth preterm among pregnancies with an abnormal level of alpha-fetoprotein (AFP), human chorionic gonatotropin (hCG), and/or unconjugated estriol (uE3) compared to pregnancies with normal biomarker levels. Results: When compared to pregnancies with normal levels of AFP, hCG, and uE3, pregnancies with elevated levels of any biomarker [multiple of the median (MoM) ≥2.0] were at an increased risk for preterm birth regardless of preterm grouping (RRs 1.3-5.4). Risks for preterm birth tended to increase substantially when at least two biomarkers were elevated (RRs 2.2-18.7). Conclusion: The results suggest that second trimester maternal serum biomarkers may help identify pregnancies at increased risk for preterm birth when no other identified risks are present. Data indicates that biomarkers may be particularly predictive of early preterm birth.