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

Risk of critical congenital heart defects by nuchal translucency norms

Jelliffe-Pawlowski, L. L., Norton, M. E., Shaw, G. M., Baer, R. J., Flessel, M. C., Goldman, S., & Currier, R. J. (2015). American Journal of Obstetrics and Gynecology, 212(4), 518.e1-518.e10. 10.1016/j.ajog.2014.10.1102
Abstract
Abstract
Objective The purpose of this study was to compare the performance of first-trimester nuchal translucency (NT) cutoff of ≥3.5 mm with NT percentiles that were calculated for crown-rump length to identify fetuses with critical congenital heart defects (CCHDs). Study Design This was a population-level study of singleton pregnancies in California with NT measurements performed between 11 and 14 weeks of gestation. Eligible cases were those that resulted in live births from 2009-2010 and had information about the presence or absence of CCHDs available in the hospital discharge records through age 1 year (n = 76,089). Logistic binomial regression methods were used to compare the rate of CCHDs by an NT percentile for crown-rump length and millimeter cutpoints. Results Compared with fetuses with an NT measurement of <90th percentile, fetuses with an NT of ≥99th percentile were >5 times as likely to have a CCHD (1.3% vs 0.2%; relative risk, 5.66; 95% confidence interval, 3.19-10.04) and fetuses with an NT measurement ≥3.5 mm were >12 times as likely to have a CCHD (2.8% vs 0.2%; relative risk, 12.28; 95% confidence interval, 5.11-29.51). NT ≥99th percentile had a sensitivity of 5.8% and a specificity of 98.9% for the detection of CCHDs compared with 2.6% and 99.8% for NT ≥3.5 mm. Conclusion Results show that NT measurements of ≥99th percentile and ≥3.5 mm are not equivalent and that substantial risk for CCHD extends to the less restrictive ≥99th percentile cutpoint. Data suggest that the use of this cutpoint compared with the current standard could double the number of CCHDs that are identified based on NT risk.

Undiagnosed metabolic dysfunction and sudden infant death syndrome - A case-control study

Rosenthal, N. A., Currier, R. J., Baer, R. J., Feuchtbaum, L., & Jelliffe-Pawlowski, L. L. (2015). Paediatric and Perinatal Epidemiology, 29(2), 151-155. 10.1111/ppe.12175
Abstract
Abstract
Background Decades of research has yielded few clues about causes of sudden infant death syndrome (SIDS). While some studies have shown a link to inborn errors of metabolism (IEMs), few have examined the link in a large population-based sample. This population-based case-control study assessed the association between undiagnosed IEMs and SIDS. Methods Children born in California during 2005-08 who died from SIDS were obtained from death records and linked to the newborn screening, birth certificate, and hospital discharge databases. Individuals with known chromosomal and neural tube defects, genetic disorders, and non-singleton births were excluded. Five controls were matched to each case on tandem mass spectrometry testing date and lab code. Rates of undiagnosed IEMs were compared between cases and controls using conditional logistic regression adjusting for known confounding factors. Results After adjusting for known confounding factors, SIDS cases had similar risk of having IEMs as controls (adjusted hazard ratio [HR] 1.3, 95% confidence interval [CI] 0.3, 5.5). Infants who were male, Black, and born preterm had higher risk of SIDS with the highest risk observed for those born preterm [adjusted HR=1.7, 95% CI 1.3, 2.2]. Younger maternal age at delivery, mother being born in the US, parity after current birth >3, and delayed prenatal care were also significantly associated with higher risk of SIDS. Conclusions While many maternal and infant factors are associated with an increased risk of SIDS, there is no evidence that undiagnosed IEMs are associated with increased risk.

Association between maternal characteristics, abnormal serum aneuploidy analytes, and placental abruption

Blumenfeld, Y. J., Baer, R. J., Druzin, M. L., El-Sayed, Y. Y., Lyell, D. J., Faucett, A. M., Shaw, G. M., Currier, R. J., & Jelliffe-Pawlowski, L. L. (2014). American Journal of Obstetrics and Gynecology, 211(2), 144.e1-144.e9. 10.1016/j.ajog.2014.03.027
Abstract
Abstract
Objective The objective of the study was to examine the association between placental abruption, maternal characteristics, and routine first- and second-trimester aneuploidy screening analytes. Study Design The study consisted of an analysis of 1017 women with and 136,898 women without placental abruption who had first- and second-trimester prenatal screening results, linked birth certificate, and hospital discharge records for a live-born singleton. Maternal characteristics and first- and second-trimester aneuploidy screening analytes were analyzed using logistic binomial regression. Results Placental abruption was more frequent among women of Asian race, age older than 34 years, women with chronic and pregnancy-associated hypertension, preeclampsia, preexisting diabetes, previous preterm birth, and interpregnancy interval less than 6 months. First-trimester pregnancy-associated plasma protein-A of the fifth percentile or less, second-trimester alpha fetoprotein of the 95th percentile or greater, unconjugated estriol of the fifth percentile or less, and dimeric inhibin-A of the 95th percentile or greater were associated with placental abruption as well. When logistic models were stratified by the presence or absence of hypertensive disease, only maternal age older than 34 years (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.0-2.0), pregnancy-associated plasma protein-A of the 95th percentile or less (OR, 1.9; 95% CI, 1.2-3.1), and alpha fetoprotein of the 95th percentile or greater (OR, 2.3; 95% CI, 1.4-3.8) remained statistically significantly associated for abruption. Conclusion In this large, population-based cohort study, abnormal maternal aneuploidy serum analyte levels were associated with placental abruption, regardless of the presence of hypertensive disease.

Chromosome abnormalities detected by current prenatal screening and noninvasive prenatal testing

Norton, M. E., Jelliffe-Pawlowski, L. L., & Currier, R. J. (2014). Obstetrics and Gynecology, 124(5), 979-986. 10.1097/AOG.0000000000000452
Abstract
Abstract
OBJECTIVE: To estimate how many additional chromosomal abnormalities can be detected by diagnostic testing compared with noninvasive prenatal testing in a high-risk prenatal population. METHODS: All karyotype results of invasive prenatal testing in singleton pregnancies performed in response to a positive prenatal screen through the California Prenatal Screening Program from April 2009 through December 2012 were examined. Abnormal karyotypes were categorized as to whether the abnormality is detectable by current noninvasive prenatal testing methods. RESULTS: Of 1,324,607 women who had traditional screening during the study period, 68,990 (5.2%) were screen-positive. Of screen-positive women, 26,059 (37.8%) underwent invasive diagnostic testing and 2,993 had an abnormal result (11.5%). Of these, 2,488 (83.1%) were predicted to be detectable with current noninvasive prenatal testing methods, and 506 (16.9%) were considered not currently detectable. Trisomy 21 accounted for 53.2% of the abnormal results (n51,592). Common aneuploidies, detectable by noninvasive prenatal testing, comprised a higher percentage of abnormal results in older women (P<.01). CONCLUSION: For pregnant women with a positive aneuploidy screen who pursued diagnostic testing, 16.9% of chromosome abnormalities are not currently detectable by noninvasive prenatal testing. Undetectable aneuploidies range from relatively mild to those associated with significant disability. This is important information to be considered by patients, health care providers, and screening programs in evaluating the use of traditional screening and invasive prenatal diagnosis compared with noninvasive prenatal testing.

Combined elevated midpregnancy tumor necrosis factor alpha and hyperlipidemia in pregnancies resulting in early preterm birth

Jelliffe-Pawlowski, L. L., Ryckman, K. K., Bedell, B., O’Brodovich, H. M., Gould, J. B., Lyell, D. J., Borowski, K. S., Shaw, G. M., Murray, J. C., & Stevenson, D. K. (2014). American Journal of Obstetrics and Gynecology, 211(2), 141.e1-141.e9. 10.1016/j.ajog.2014.02.019
Abstract
Abstract
Objective The objective of the study was to determine whether pregnancies resulting in early preterm birth (PTB) (<30 weeks) were more likely than term pregnancies to have elevated midtrimester serum tumor necrosis factor alpha (TNF-α) levels combined with lipid patterns suggestive of hyperlipidemia. Study Design In 2 nested case-control samples drawn from California and Iowa cohorts, we examined the frequency of elevated midpregnancy serum TNF-α levels (in the fourth quartile [4Q]) and lipid patterns suggestive of hyperlipidemia (eg, total cholesterol, low-density-lipoproteins, or triglycerides in the 4Q, high-density lipoproteins in the first quartile) (considered independently and by co-occurrence) in pregnancies resulting in early PTB compared with those resulting in term birth (n = 108 in California and n = 734 in Iowa). Odds ratios (ORs) and 95% confidence intervals (CIs) estimated in logistic regression models were used for comparisons. Results Early preterm pregnancies were 2-4 times more likely than term pregnancies to have a TNF-α level in the 4Q co-occurring with indicators of hyperlipidemia (37.5% vs 13.9% in the California sample (adjusted OR, 4.0; 95% CI, 1.1-16.3) and 26.3% vs 14.9% in the Iowa sample (adjusted OR, 2.7; 95% CI, 1.1-6.3). No differences between early preterm and term pregnancies were observed when TNF-α or target lipid abnormalities occurred in isolation. Observed differences were not explicable to any maternal or infant characteristics. Conclusion Pregnancies resulting in early PTB were more likely than term pregnancies to have elevated midpregnancy TNF-α levels in combination with lipid patterns suggestive of hyperlipidemia.

Copy number variation in bronchopulmonary dysplasia

Hoffmann, T. J., Shaw, G. M., Stevenson, D. K., Wang, H., Quaintance, C. C., Oehlert, J., Jelliffe-Pawlowski, L. L., Gould, J. B., Witte, J. S., & O’Brodovich, H. M. (2014, October 1). In American Journal of Medical Genetics, Part A (Vols. 164, Issues 10, pp. 2672-2675). 10.1002/ajmg.a.36659

Early-onset severe preeclampsia by first trimester pregnancy-associated plasma protein A and total human chorionic gonadotropin

Jelliffe-Pawlowski, L. L., Baer, R. J., Currier, R. J., Lyell, D. J., Blumenfeld, Y. J., El-Sayed, Y. Y., Shaw, G. M., & Druzin, M. L. (2014). American Journal of Perinatology, 32(7), 703-711. 10.1055/s-0034-1396697
Abstract
Abstract
Objective This study aims to evaluate the relationship between early-onset severe preeclampsia and first trimester serum levels of pregnancy-associated plasma protein A (PAPP-A) and total human chorionic gonadotropin (hCG). Study Design The association between early-onset severe preeclampsia and abnormal levels of first trimester PAPP-A and total hCG in maternal serum were measured in a sample of singleton pregnancies without chromosomal defects that had integrated prenatal serum screening in 2009 and 2010 (n = 129,488). Logistic binomial regression was used to estimate the relative risk (RR) of early-onset severe preeclampsia in pregnancies with abnormal levels of first trimester PAPP-A or total hCG as compared with controls. Results Regardless of parity, women with low first trimester PAPP-A or high total hCG were at increased risk for early-onset severe preeclampsia. Women with low PAPP-A (multiple of the median [MoM] ≤ the 10th percentile in nulliparous or ≤ the 5th percentile in multiparous) or high total hCG (MoM ≥ the 90th percentile in nulliparous or ≥ the 95th percentile in multiparous) were at more than a threefold increased risk for early-onset severe preeclampsia (RR, 4.2; 95% confidence interval [CI], 3.0-5.9 and RR, 3.3; 95% CI, 2.1-5.2, respectively). Conclusion Routinely collected first trimester measurements of PAPP-A and total hCG provide unique risk information for early-onset severe preeclampsia.

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.