Emily Oken
· Professor, Department of Population Medicine Vice Chair and Director of Faculty Development Harvard Pilgrim Health Care Institute Director, Division of Chronic Disease Research Across the LifecourseVerifiedHarvard University · Nutrition
Active 1992–2026
About
Emily Oken is a Professor in the Department of Population Medicine at Harvard Medical School and the Harvard Pilgrim Health Care Institute, as well as in the Department of Nutrition at the Harvard T.H. Chan School of Public Health. She received her medical degree from Harvard Medical School in 1996, completed her internship and residency in internal medicine and pediatrics at the Harvard Combined Program, and completed her fellowship in general internal medicine at Harvard Medical School. She also obtained a Master’s degree in public health from the Harvard School of Public Health. Dr. Oken directs the Division of Chronic Disease Research Across the Lifecourse within the Department of Population Medicine. Her research focuses on the influence of nutrition and other modifiable factors during pregnancy and early childhood on long-term maternal and child health, including cardiometabolic health, cognitive development, asthma, and atopy. She has led studies examining predictors and sequelae of maternal overweight, weight gain, and related conditions such as gestational diabetes mellitus in the peripartum period. Her work on the toxicant risks and nutrient benefits of prenatal fish consumption has influenced national guidelines, emphasizing the overall health effects of fish consumption for mother and baby. She is the Principal Investigator of Project Viva, a US pre-birth cohort study following pregnant women and their children since 1999, and co-leads the assessment of cardio-metabolic, respiratory, and neurocognitive outcomes in children enrolled in the Promotion of Breastfeeding Intervention Trial (PROBIT). Dr. Oken has served on committees to develop maternal nutrition guidelines nationally and internationally. Her dedication to research mentorship and diversity has been recognized through awards including a K24 mid-career development grant from NICHD, the A. Clifford Barger Excellence in Mentoring Award at HMS, and the Harold Amos Faculty Diversity Award. She chairs her departmental diversity committee and serves on the HMS Council of Mentors. Within her department, she is Vice-Chair, Director of Faculty Development, and co-site director for the Harvard General Medicine fellowship. She also co-directs the Clinical Epidemiology and Population Health curriculum for first-year medical students at HMS. Prior to her academic career, she practiced as a primary care physician at the Gretchen and Edward Fish Center for Women’s Health at Brigham and Women’s Hospital.
Research topics
- Medicine
- Internal medicine
- Biology
- Genetics
- Environmental health
- Physiology
- Bioinformatics
- Pediatrics
- Demography
- Obstetrics
- Andrology
- Computer Science
- Gerontology
- Environmental chemistry
- Chemistry
- Statistics
- Surgery
- Psychology
- Nursing
- Psychiatry
- Family medicine
- Geography
- Environmental science
- Psychotherapist
Selected publications
Circulation · 2026-03-24
articleBackground: PFAS are widespread, persistent chemicals that cross the placenta and may affect fetal development. Animal studies suggest prenatal PFAS exposure increases offspring blood pressure (BP); however, epidemiologic evidence is limited and inconsistent. Hypothesis: We hypothesized that prenatal PFAS exposure is associated with higher childhood BP. Methods: We included children aged 3-13 years in the U.S. ECHO Cohort with data on gestational plasma or serum concentrations of PFOA, PFOS, PFHxS, PFNA, PFDA, and MeFOSAA. Children’s BP was obtained from study visits or medical records. We derived age-, sex-, and height-specific BP percentiles according to the 2017 American Academy of Pediatrics Guidelines and defined elevated BP as systolic BP (SBP) or diastolic BP (DBP) ≥90 th percentile. We used multivariable linear and modified Poisson models with generalized estimating equations and repeated BP measures clustered by participant (adjustment variables shown in Figure 1 footnotes ) and addressed missing data using multiple imputation by chained equations. We conducted subgroup analyses by child sex, ethnicity, and race, and we examined trimester-specific associations. Results: Among 2,435 children (50% female, 21% Hispanic, 25% Black), 22% had elevated BP at their last visit at a median age of 7.3 years ( Table 1 ). In adjusted analyses ( Figure 1 ), each doubling of PFOA was associated with a 1.23 (95% CI: 0.02, 2.45) higher SBP percentile, a 0.95 (0.10, 1.79) higher DBP percentile, and 1.07 (1.00, 1.15) times the risk of elevated BP. Each doubling of PFOS and PFNA was associated with a 1.14 (0.01, 2.27) and 0.85 (0.09, 1.61) higher DBP percentile, respectively. The PFOA-SBP association was stronger in males, and associations of PFOA, PFOS, and PFNA with DBP were stronger in females and non-Hispanic children. In trimester-specific analyses ( Figure 2 ), first-trimester PFOA, PFOS, and PFDA were associated with elevated BP; second-trimester PFOA and PFNA were associated with higher SBP percentiles; and third-trimester PFOS and MeFOSAA were associated with higher DBP percentiles. Conclusions: Prenatal exposure to PFOA, PFOS, and PFNA was associated with higher childhood BP. The trimester-specific associations should be interpreted with caution as they may also reflect cohort differences in PFAS profiles. PFAS may contribute to early-life programming of elevated lifelong cardiovascular risk, reinforcing the importance of population-level prevention.
European Heart Journal · 2026-04-07
articleOpen accessBACKGROUND AND AIMS: To elucidate the genetic architecture of blood pressure (BP) and heart rate (HR) during early life and assess their potential relevance to adult health outcomes. METHODS: The largest genome-wide association study (GWAS) meta-analyses to date of childhood systolic BP, diastolic BP, pulse pressure, and mean arterial pressure (n = 28 425) and HR (n = 22 565) were conducted in children of European ancestry aged 4-17 years. Follow-up analyses included comparisons with adult GWAS results, polygenic risk score (PRS) analyses in independent cohorts of diverse ancestries, and a phenome-wide association study in the UK Biobank. RESULTS: Eight genome-wide significant loci were identified for childhood BP (KIAA2013, CACNB2, PLCE1, PAX2, COL4A2, RP11-236L14.1, CFDP1, TPX2) and three loci for childhood HR (CCDC141, ACHE, MYH6); all novel in children but previously reported in adults. Childhood PRSs explained up to 1.6% of BP variance and 5.2% of HR variance among children of European ancestry. Genetic correlations between childhood and adulthood BP traits were moderate (rg = 0.4-0.7), suggesting age-specific genetic effects on BP. In the UK Biobank, higher childhood BP PRS levels were significantly associated with a broad range of adult health outcomes, particularly cardiometabolic outcomes such as hypertension, angina, myocardial infarction, and cardiovascular disease-related mortality. CONCLUSIONS: These findings advance the understanding of the genetic architecture of childhood BP and HR and provide compelling genetic evidence linking childhood BP to a broad spectrum of adult health outcomes-particularly cardiometabolic conditions-which may inform targeted prevention strategies from a young age.
medRxiv · 2026-04-18
articleOpen accessBackground: Extreme-phenotype comparisons allowed the discovery of novel asthma genetic risk loci. However, this approach remains unexplored in epigenome-wide association studies (EWAS). We aimed to identify bulk and cell-specific methylation markers of asthma with severe exacerbations across diverse ancestry groups. Methods: We conducted a meta-EWAS of 739,543 CpGs in whole blood among 1,192 African American and Latino pediatric populations, comparing non-asthmatics and asthma exacerbators. Genome-wide CpGs were followed up for replication in a meta-analysis across 1,516 ethnically diverse participants and in a cross-tissue evaluation of 393 nasal samples. We conducted differentially methylated region (DMRs), cell-type-deconvoluted, and quantitative trait loci analyses (whole-genome sequencing n=1,668; RNA-seq n=1,209). We examined enrichment in traits, pathways, and druggable genes, and analyzed DNAm predictors of plasma proteins and aging. Results: , λ=1.05). We replicated 25 CpGs in blood cells, cross-validated 7 in nasal samples, and detected 42 cell-specific DNAm markers mainly driven by T cells. DNAm at 134 CpGs was associated with gene expression in whole blood, including 118 associations with T-cell receptor genes, and 446 CpGs were regulated by > 1 genetic variant. We found enrichment for previous associations with environmental exposures, immune disorders, immune and inflammatory pathways, and druggable genes by developmental drugs. 21 methylation-predicted plasma proteins, involved in host defense, and one lung aging clock were associated with asthma exacerbations. Conclusions: The first meta-EWAS of extreme asthma phenotypes identified hundreds of novel DNAm markers, suggesting novel methylation biomarkers and candidate drugs for asthma and supporting the role of T cells.
Journal of Autoimmunity · 2025-10-10 · 1 citations
articleOpen accessBACKGROUND: Thyroid peroxidase antibody (TPOAb) positivity is the most important risk factor for hypothyroidism and determines thyroid function follow-up during pregnancy. TPOAb positivity is usually defined by manufacturer cut-offs which typically derived from non-pregnant populations. However, as a state of immune tolerance, pregnancy can affect TPOAb concentrations. To improve the understanding of clinical relevance of TPOAb concentrations during pregnancy, we investigated the association of TPOAbs with maternal thyroid function. METHODS: We performed an individual participant data meta-analysis embedded in the Consortium on Thyroid and Pregnancy. Participants with multiple gestations, pre-existing thyroid disease, thyroid (interfering) medication usage, or conception by in vitro fertilization were excluded. We used mixed effects regression models to assess the association of TPOAb percentiles calculated in each cohort with maternal thyroid function. RESULTS: The study population comprised 62,634 pregnant women from 24 cohorts. As compared to TPOAb percentiles ≤80, there were progressively higher mean thyroid stimulating hormone (TSH) concentrations across TPOAb percentiles ≥89, with corresponding mean differences ranging from +0.11 SD (95 % confidence interval [CI] +0.04 SD, +0.19 SD) at the 89th percentile to +1.04 SD (95 % CI + 0.96 SD, 1.11 SD) at the 100th percentile. Higher TPOAb percentiles were associated with progressively lower mean free thyroxine (FT4) concentrations across TPOAb percentiles ≥91, with corresponding mean differences ranging from -0.08 SD (95 % CI -0.16 SD, -0.01 SD) at the 91st percentile to -0.48 SD (95 % CI -0.56 SD, -0.4 SD) at the 100th percentile. From the 89th TPOAb percentile upwards, there were progressively higher risks of TSH >4.0 mU/L, with absolute risks of 2.4 %, 4.0 %, and 28.1 % in cases of ≤80th, 89th, and 100th TPOAb percentiles, respectively. Higher TPOAb percentiles were also associated with lower thyroidal response to human chorionic gonadotropin stimulation and higher risks of overt and subclinical hypothyroidism. In 19 of the included cohorts, there were 0.4-6.3 % of pregnant women with TPOAb concentrations lower than the positivity cut-offs but larger than or equal to the 89th-percentile concentrations. The associations of TPOAbs with TSH and with FT4 were most apparent during early pregnancy (P for interaction <0.001 for both TSH and FT4). CONCLUSIONS: During pregnancy, TPOAbs were dose-dependently associated with TSH, FT4, and the risk of abnormal thyroid function. With concentrations below currently used positivity cut-offs, TPOAbs could be associated with lower maternal thyroid function, which indicates clinically relevant thyroid autoimmunity. These findings implicates that high normal TPOAb concentrations upon first assessment in pregnancy may warrant active follow-up.
Obesity · 2025-08-26
articleOpen accessOBJECTIVE: To examine the prospective associations of metal mixtures during pregnancy with midlife adiposity and explore metal-folate interactions. METHODS: In 500 participants from Project Viva, we measured six non-essential metals (arsenic, barium, cadmium, cesium, mercury, and lead) and five essential metals (copper, magnesium, manganese, selenium, and zinc) in red blood cells and folate in plasma collected during early pregnancy (mean gestational age: 10.0 weeks; mean age: 32.9 years). We assessed midlife (mean age: 51.2 years) adiposity using BMI and dual-energy X-ray absorptiometry (DXA) measures. We used multivariable-adjusted linear and multinomial logistic regression models to analyze individual exposures and Bayesian kernel machine regression to examine exposure mixtures. RESULTS: Higher arsenic, cesium, and mercury levels were associated with lower midlife DXA percentage fat, total fat mass index, and/or trunk fat mass index, even after adjustments for diet in pregnancy. We observed an antagonistic interaction between folate and arsenic: arsenic was associated with higher obesity risk at lower folate levels but lower obesity risk at higher folate levels. The essential metal mixture tended to be associated with lower midlife BMI and obesity risk. CONCLUSIONS: Higher pregnancy levels of arsenic, cesium, mercury, and the mixture of essential metals were associated with lower midlife adiposity.
Scientific Reports · 2025-08-09 · 1 citations
articleOpen accessNeighborhood and individual-level trauma-related stressors during pregnancy can increase oxidative stress, potentially altering cellular disease pathway biomarkers such as mitochondrial DNA copy number (mtDNAcn) and telomere length (TL). However, the biological mechanisms linking early-life stressors to long-term health outcomes remain understudied. In a subset of Project Viva participants (n = 415-917), we evaluated associations of neighborhood and individual-level stressors with mean relative mtDNAcn and TL measured in first trimester maternal blood and cord blood. Neighborhood stressors during pregnancy were assessed using the Child Opportunity Index (COI) and Social Vulnerability Index (SVI). Trauma-related stressors were measured using the Personal Safety Questionnaire (PSQ), administered mid-pregnancy, and maternal Adverse Childhood Experiences (ACEs), reported during a mid-life follow-up. In multivariable linear regression analysis, residence in a very high versus very low opportunity neighborhood was associated with lower maternal mtDNAcn ([Formula: see text]= - 0.09, 95% confidence interval (CI) - 0.17, - 0.02), while residence in a very high versus very low vulnerability area was associated with higher maternal mtDNAcn ([Formula: see text]= 0.06, 95% CI 0.01, 0.12). Additionally, residence in moderate versus very low opportunity neighborhoods was associated with longer cord blood TL ([Formula: see text]= 0.39, 95% CI 0.0002, 0.78), but associations were attenuated after cell-type adjustment. Our findings suggest that prenatal neighborhood stressors are associated with increased maternal mtDNAcn and neighborhood opportunity is associated with longer fetal TL, indicating possible links to biological pathways related to oxidative stress and cellular aging.
Circulation · 2025-03-11
articleBackground: Pregnancy is a critical period for women’s long-term cardiometabolic health, with women being particularly sensitive to environmental exposures. The effects of heavy metals and essential elements during pregnancy on long-term obesity risk are understudied. Cohort studies and trials suggest that folate may mitigate metal toxicity—a recent AHA Scientific Statement on metals identified this area of research as a critical gap and priority. Objective: 1) To investigate the associations of pregnancy levels of metals and elements with women’s mid-life obesity risk; and 2) to explore whether adequate pregnancy folate mitigates the obesogenic effects of metals. Methods: Project Viva is a pregnancy cohort enrolled in Eastern MA between 1999-2002 (median age: 32.9y). We measured (As, Ba, Cd, Cs, Hg, Pb) and elements (Cu, Mg, Mn, Se, Zn) in red blood cells and folate in plasma collected during the first trimester. At the Mid-Life visit (2017-2021; median age: 51.2y), we measured weight and height and defined obesity as BMI >30 kg/m 2 (reference: ≤30 kg/m 2 ). We examined associations of metals and elements with obesity using modified Poisson regression, adjusting for confounders ( Figure 1 footnote ). We used Bayesian kernel machine regression (BKMR) to assess the mixture effects of all metals, elements, and folate. Results: We followed 500 women (72% White, 11% Black) for a median of 18.1y (range: 17.5-20.8y). Cs and Cu were associated with a lower risk of obesity: per doubling, Cs and Cu were associated with 0.78 (95% CI: 0.63-0.97) and 0.71 (95% CI: 0.50-0.99) times the obesity risk, respectively. Mg, Se, and Zn were also associated with >10% lower obesity risk, though the 95% CIs crossed the null ( Figure 1 ). BKMR results confirmed consistent dose-response associations ( Figure 2 ). Although neither As nor folate was individually associated with obesity, they showed an interaction in association with obesity ( Figure 3 ): at lower folate levels, As was associated with a higher obesity risk, but as folate levels increased, the As-obesity association was attenuated and eventually became inverse. Conclusion: Optimal pregnancy levels of essential elements (e.g., Cu, Se, Mg, Zn) were associated with a lower risk of mid-life obesity, while adequate folate levels may counteract the obesogenic effects of As. Our study advances a research priority in the AHA Scientific Statement, suggesting folate as a potential intervention strategy to mitigate metal-related health effects.
UNC Libraries · 2025-03-02
articleOpen accessThe Lancet Diabetes & Endocrinology · 2025-07-02 · 10 citations
reviewOpen accessPaediatric and Perinatal Epidemiology · 2025-05-01 · 3 citations
articleOpen accessSenior authorABSTRACT Background Limited longitudinal data exist on the associations of infertility with depressive symptoms across the lifecourse. Objectives To investigate how depressive symptoms change across specific life stages (pregnancy, postpartum, and midlife), with a focus on the differences between women with and without a history of infertility before index pregnancy. Methods Women enrolled in Project Viva (1999–2002) during early pregnancy (mean [SD] age 32.5 [4.7] years) completed the Edinburgh Postnatal Depression Scale (EPDS) in mid‐pregnancy (median 27.9 weeks gestation) and at 6 months postpartum, and completed the Patient Health Questionnaire (PHQ‐9) in midlife (2017–2021, 50.9 [5.1] years). We converted EPDS and PHQ‐9 scores to externally standardised T‐scores (mean = 50, SD = 10). We defined infertility before index pregnancy as ≥ 6 cycles to achieve pregnancy if ≥ 35 years of age or ≥ 12 cycles to achieve pregnancy if < 35 years of age, or claims for infertility treatments or prescriptions abstracted from medical records. We performed adjusted linear regression models to examine associations of infertility with depressive symptoms across the three‐time spans (pregnancy‐postpartum, postpartum‐midlife, and pregnancy‐midlife). Results Among 1368 participants, 281 (21%) experienced infertility at index pregnancy. Infertility was associated with a 1.83‐ point increase in depressive symptoms ( T ‐score) between the postpartum period and midlife (adjusted 1.83, 95% confidence interval [CI] 0.00, 3.66). Infertility was unrelated to change in depressive symptoms between pregnancy and postpartum (adjusted 0.02, 95% CI −1.24, 1.28) or pregnancy and midlife (adjusted 1.30, −0.64, 3.23). Conclusions The experience of infertility among parous women is associated with a greater increase in depressive symptoms between the post‐partum period and midlife.
Recent grants
NIH · $9.5M · 2016–2024
Prenatal environmental determinants of health in young adulthood: a lifecourse approach
NIH · $21.9M · 1998–2028
NIH · $2.0M · 2020–2026
A lifecourse approach to women's cardiometabolic and bone health: from fertility to perimenopause
NIH · $80k · 2019–2024
NIH · $4.1M · 2018
Frequent coauthors
- 1444 shared
Sheryl L. Rifas–Shiman
Harvard University
- 918 shared
Marie‐France Hivert
Harvard Pilgrim Health Care
- 913 shared
Leila Beker
Harvard Pilgrim Health Care
- 913 shared
Ekhard E. Ziegler
- 913 shared
Kimberly O’Brien
Cornell University
- 913 shared
Joanne Spahn
Food and Nutrition Service
- 913 shared
Rafael Pérez‐Escamilla
Yale University
- 913 shared
Perrine Nadaud
Awards & honors
- Inducted into the American Society for Clinical Investigatio…
- A. Clifford Barger Excellence in Mentoring Award at HMS
- Mentoring award at the Society for Pediatric and Perinatal E…
- Harold Amos Faculty Diversity Award at HMS
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