About

Patricia Ann Cassano holds the position of The Alan D. Mathios Professor in the College of Human Ecology at Cornell University. She is a faculty member in the Department of Nutritional Sciences. Her research focuses on the nutritional genomics of lung phenotypes, nutrition translation and evidence synthesis, and nutrition for precision health. Her work integrates the study of how nutrition interacts with genetic factors affecting lung health, aiming to translate scientific findings into practical nutritional guidance tailored to individual health profiles. Through her expertise, she contributes to advancing the understanding of precision nutrition and its applications in improving health outcomes.

Research topics

• Internal medicine
• Medicine
• Cardiology
• Biology
• Virology
• Genetics

Selected publications

• Effects of Immunomodulatory Fatty Acids on Lung Function Are Mediated Through Smoking-related Differences in DNA Methylation

  American Journal of Respiratory and Critical Care Medicine · 2025-05-01 · 1 citations

  article

  Abstract Rationale: Dietary polyunsaturated fatty acids (PUFAs) found in plant and seed oils and fatty fish have immunomodulatory properties that may influence lung function. Smoking impacts DNA methylation, inflammation, and lung function and may mediate the effects of PUFAs on the lungs. We analyzed omega-3 and omega-6 PUFA biomarker associations with lung function, and investigated whether these associations are mediated through DNA methylation of the AHRR gene, an epigenetic marker of smoking dose and duration. Methods: We evaluated spirometry, AHRR DNA methylation and PUFA biomarker data from 3854 participants in the Genetic Epidemiology of COPD (COPDGene) Study. Infinium MethylationEPIC BeadChip DNAm data was assayed through the NIH NHLBI TOPMed program using peripheral blood leukocyte DNA. Plasma PUFAs were quantified by gas chromatography-mass spectrometry (GC-MS). PUFA associations with FEV1 were estimated using robust linear regression accounting for key lung function covariates. Mediation analyses estimating the average causal effect of PUFAs mediated through AHRR (cg05575921) methylation were performed with the R package ‘mediation’. Results: Higher blood levels of omega-3 PUFAs alpha-linolenic acid (ALA) and eicosapentaenoic acid (EPA) were positively associated with FEV1 while omega-6 PUFA arachidonic acid (AA) was negatively associated with FEV1. Specifically, one standard deviation (SD) higher ALA and EPA were associated with 33.0 (95% confidence interval [CI] 11.2 – 54.8) and 42.4 (95% CI 22.9 – 61.8) ml higher FEV1, while one SD higher AA was associated with 84.3 (95% CI 61.6-107.0) ml lower FEV1. Associations of docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and linoleic acid (LA) with FEV1 were not statistically significant. Mediation analyses revealed significant (p<2E-16) causal mediation through AHRR methylation for EPA and ALA, with the proportion mediated estimated at 0.27 and 0.19 respectively, while there was no statistical evidence (p=0.18) of mediation for AA. In these models, increases in AHRR methylation attributed to one SD higher blood levels of ALA and EPA were associated with 11.6 (95% CI 7.5 – 16.4) and 9.0 (95% CI 5.14 – 13.9) ml higher FEV1. Analyses stratified by smoking status suggest these effects may be realized primarily in former smokers. Conclusions: Omega-3 PUFAs may impact lung function through influences on smoking-associated DNA methylation levels, while the impacts of omega-6 PUFAs may be independent of the epigenetic effects of smoking. These findings shed light on molecular mechanisms underlying intersections of PUFA nutritional status, smoking, and lung function, and highlight a future role for precision nutrition for lung health.

  PublisherDOI

• Associations of Polyunsaturated Fatty Acids With Smoking-Related Epigenetic Alterations

  Current Developments in Nutrition · 2025-05-01

  articleOpen access
  PublisherDOI

• Vitamin D supplementation in pregnant or breastfeeding women or young children for preventing asthma

  Cochrane Database of Systematic Reviews · 2025-08-12 · 4 citations

  reviewOpen accessSenior author

  BACKGROUND: Randomised controlled studies evaluating vitamin D supplementation in pregnancy or early childhood for preventing childhood asthma have yielded inconclusive results. Previous systematic reviews of vitamin D for asthma prevention focused on studies comparing vitamin D to placebo or studies intervening in pregnancy, limiting the body of evidence. OBJECTIVES: Primary: to evaluate the efficacy of any vitamin D supplementation and high-dose vitamin D supplementation in early life, including the prenatal period, for preventing asthma in children. Secondary: to assess the efficacy of vitamin D supplementation: • for preventing asthma in children at risk of vitamin D deficiency at the start of the trial or whose mothers were at risk; • by intervention timing and the cumulative dose administered; • in preventing factors associated with early childhood asthma, including atopic dermatitis, respiratory tract infections, sensitisation to allergens, and airway inflammation. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase, ClinicalTrials.gov, the International Clinical Trials Registry Platform, and the Cochrane Airways and Skin Trial Registers. We checked the reference lists of relevant systematic reviews and meta-analyses. We contacted authors to obtain additional study information as needed. Date of last search: October 2023. SELECTION CRITERIA: We included randomised controlled studies comparing higher versus lower/standard dose vitamin D (≤ 400 international units (IU)/day) or any vitamin D versus placebo/no treatment in generally healthy pregnant or lactating women or children up to five years of age that evaluated childhood asthma, wheeze, atopic dermatitis, airway infections, allergic sensitisation, and airway inflammation. We excluded trials recruiting populations with pre-existing conditions. DATA COLLECTION AND ANALYSIS: We followed standard Cochrane methodological procedures, including using Cochrane's Screen4Me workflow. We considered participants rather than events as the unit of analysis, performed fixed-effect meta-analysis, and reported risk ratios (RRs) or mean differences (MDs) with 95% confidence intervals (CIs) for four comparisons: (1) any vitamin D versus placebo/no supplementation in pregnant or breastfeeding women; (2) any vitamin D versus placebo/no supplementation in infants or children; (3) high versus low/standard dose vitamin D in pregnant or breastfeeding women; (4) high versus low/standard dose vitamin D in infants or children. Our outcomes were: asthma, wheeze, atopic dermatitis, airway infections, allergic sensitisation, airway inflammation, and adverse events. We narratively described results that could not be meta-analysed. We used the Cochrane risk of bias tool (RoB) to assess bias in the studies. We used GRADE to assess the certainty of the evidence. MAIN RESULTS: We included 18 studies involving a total of 10,611 participants, of which 16 contributed data to meta-analyses. Studies were conducted around the world, with most taking place in higher-income countries. The dose and frequency of vitamin D ranged from 200 IU/day to 100,000 IU bolus quarterly, and the duration of supplementation ranged from 28 days to two years. Comparison 1. Any vitamin D versus placebo/no supplementation in pregnant or breastfeeding women (4 studies) Compared to placebo or no supplementation, any vitamin D given to pregnant or breastfeeding women may reduce the risk of early childhood asthma (RR 0.17, 95% CI 0.05 to 0.61; 1 study, 236 participants; low-certainty evidence) and likely has little to no effect on childhood airway infections (RR 1.00, 95% CI 0.97 to 1.04; 3 studies, 1564 participants; moderate-certainty evidence). The evidence is very uncertain for wheeze, atopic dermatitis, allergic sensitisation, airway inflammation, or adverse events. Comparison 2. Any vitamin D versus placebo/no supplementation in infants or children (5 studies) Compared to placebo or no supplementation, any vitamin D given to infants or children may have little to no effect on childhood wheeze (RR 0.89, 95% CI 0.68 to 1.16; 2 studies, 431 participants; low-certainty evidence), atopic dermatitis (RR 1.01, 95% CI 0.80 to 1.28; 2 studies, 448 participants; low-certainty evidence), airway infections (RR 0.92, 95% CI 0.83 to 1.01; 2 studies, 500 participants; low-certainty evidence), allergic sensitisation (RR 2.25, 95% CI 0.60 to 8.50; 1 study, 228 participants; low-certainty evidence), or airway inflammation measured by eosinophil counts (RR 1.06, 95% CI 0.65 to 1.74; 1 study, 226 participants; low-certainty evidence). The evidence is very uncertain for asthma and adverse events. Comparison 3. High versus low/standard dose vitamin D in pregnant or breastfeeding women (4 studies) Compared to low/standard dose, high-dose vitamin D given to pregnant or breastfeeding women likely reduces the risk of childhood wheeze (RR 0.79, 95% CI 0.64 to 0.98; 3 studies, 1439 participants; moderate-certainty evidence), but likely results in little to no difference in childhood asthma, although the direction and magnitude of effect is similar to that for wheeze (RR 0.81, 95% CI 0.63 to 1.04; 2 studies, 1355 participants; moderate-certainty evidence). Compared to low/standard dose, high-dose vitamin D in pregnancy likely has little to no effect on childhood atopic dermatitis (RR 0.91, 95% CI 0.75 to 1.11; 3 studies, 1439 participants; moderate-certainty evidence), airway infections (RR 0.95, 95% CI 0.82 to 1.11; 3 studies, 1441 participants; moderate-certainty evidence), or allergic sensitisation (RR 1.01, 95% CI 0.87 to 1.18; 2 studies, 1110 participants; moderate-certainty evidence). The evidence is very uncertain for adverse events. No studies evaluated airway inflammation. Comparison 4. High versus low/standard dose vitamin D in infants or children (7 studies) Compared to low/standard dose, high-dose vitamin D given to infants or children may slightly reduce airway infections (RR 0.94, 95% CI 0.90 to 0.98; 6 studies, 2385 participants; low-certainty evidence) but may have little to no effect on atopic dermatitis (RR 0.76, 95% CI 0.55 to 1.05; 1 study, 769 participants; low-certainty evidence). The evidence is very uncertain for asthma, wheeze, allergic sensitisation, and adverse events. No studies evaluated airway inflammation. AUTHORS' CONCLUSIONS: Evidence supporting a protective effect of vitamin D supplementation in early life, including the prenatal period, on childhood asthma is limited. Moderate-certainty evidence suggests that high-dose vitamin D in pregnancy likely helps prevent childhood wheeze. Evidence for the effects of vitamin D in early childhood on asthma or wheeze is less certain. Additional high-quality studies, especially in infants and children, are needed to establish with any certainty the effects of vitamin D supplementation on childhood asthma and associated factors.

  PublisherOA PDFDOI

• Multiethnic meta-analysis identifies ancestry-specific and cross-ancestry loci for pulmonary function

  Digital Commons@Becker (Washington University School of Medicine) · 2024-02-07

  articleOpen access

  Nearly 100 loci have been identified for pulmonary function, almost exclusively in studies of European ancestry populations. We extend previous research by meta-analyzing genome-wide association studies of 1000 Genomes imputed variants in relation to pulmonary function in a multiethnic population of 90,715 individuals of European (N = 60,552), African (N = 8429), Asian (N = 9959), and Hispanic/Latino (N = 11,775) ethnicities. We identify over 50 additional loci at genome-wide significance in ancestry-specific or multiethnic meta-analyses. Using recent fine-mapping methods incorporating functional annotation, gene expression, and differences in linkage disequilibrium between ethnicities, we further shed light on potential causal variants and genes at known and newly identified loci. Several of the novel genes encode proteins with predicted or established drug targets, including KCNK2 and CDK12. Our study highlights the utility of multiethnic and integrative genomics approaches to extend existing knowledge of the genetics of lung function and clinical relevance of implicated loci.

  PublisherDOI

• Exploiting meta-analysis of genome-wide interaction with serum 25-hydroxyvitamin D to identify novel genetic loci associated with pulmonary function

  American Journal of Clinical Nutrition · 2024-03-12 · 1 citations

  reviewOpen access

  Higher 25-hydroxyvitamin D (25(OH)D) concentrations in serum has a positive association with pulmonary function. Investigating genome-wide interactions with 25(OH)D may reveal new biological insights into pulmonary function. We aimed to identify novel genetic variants associated with pulmonary function by accounting for 25(OH)D interactions. We included 211,264 participants from the observational United Kingdom Biobank study with pulmonary function tests (PFTs), genome-wide genotypes, and 25(OH)D concentrations from 4 ancestral backgrounds—European, African, East Asian, and South Asian. Among PFTs, we focused on forced expiratory volume in the first second (FEV 1 ) and forced vital capacity (FVC) because both were previously associated with 25(OH)D. We performed genome-wide association study (GWAS) analyses that accounted for variant×25(OH)D interaction using the joint 2 degree-of-freedom (2df) method, stratified by participants’ smoking history and ancestry, and meta-analyzed results. We evaluated interaction effects to determine how variant-PFT associations were modified by 25(OH)D concentrations and conducted pathway enrichment analysis to examine the biological relevance of our findings. Our GWAS meta-analyses, accounting for interaction with 25(OH)D, revealed 30 genetic variants significantly associated with FEV 1 or FVC ( P 2df <5.00×10 -8 ) that were not previously reported for PFT-related traits. These novel variant signals were enriched in lung function-relevant pathways, including the p38 MAPK pathway. Among variants with genome-wide-significant 2df results, smoking-stratified meta-analyses identified 5 variants with 25(OH)D interactions that influenced FEV 1 in both smoking groups (never smokers P 1df interaction <2.65×10 -4 ; ever smokers P 1df interaction <1.71×10 -5 ); rs3130553, rs2894186, rs79277477, and rs3130929 associations were only evident in never smokers, and the rs4678408 association was only found in ever smokers. Genetic variant associations with lung function can be modified by 25(OH)D, and smoking history can further modify variant×25(OH)D interactions. These results expand the known genetic architecture of pulmonary function and add evidence that gene-environment interactions, including with 25(OH)D and smoking, influence lung function.

  PublisherDOI

• Lung function decline in former smokers and low-intensity current smokers: a secondary data analysis of the NHLBI Pooled Cohorts Study

  UNC Libraries · 2024-04-03

  articleOpen access

  Background: Former smokers now outnumber current smokers in many developed countries, and current smokers are smoking fewer cigarettes per day. Some data suggest that lung function decline normalises with smoking cessation; however, mechanistic studies suggest that lung function decline could continue. We hypothesised that former smokers and low-intensity current smokers have accelerated lung function decline compared with never-smokers, including among those without prevalent lung disease. Methods: We used data on six US population-based cohorts included in the NHLBI Pooled Cohort Study. We restricted the sample to participants with valid spirometry at two or more exams. Two cohorts recruited younger adults (≥17 years), two recruited middle-aged and older adults (≥45 years), and two recruited only elderly adults (≥65 years) with examinations done between 1983 and 2014. FEV1 decline in sustained former smokers and current smokers was compared to that of never-smokers by use of mixed models adjusted for sociodemographic and anthropometric factors. Differential FEV1 decline was also evaluated according to duration of smoking cessation and cumulative (number of pack-years) and current (number of cigarettes per day) cigarette consumption. Findings: 25 352 participants (ages 17–93 years) completed 70 228 valid spirometry exams. Over a median follow-up of 7 years (IQR 3–20), FEV1 decline at the median age (57 years) was 31·01 mL per year (95% CI 30·66–31·37) in sustained never-smokers, 34·97 mL per year (34·36–35·57) in former smokers, and 39·92 mL per year (38·92–40·92) in current smokers. With adjustment, former smokers showed an accelerated FEV1 decline of 1·82 mL per year (95% CI 1·24–2·40) compared to never-smokers, which was approximately 20% of the effect estimate for current smokers (9·21 mL per year; 95% CI 8·35–10·08). Compared to never-smokers, accelerated FEV1 decline was observed in former smokers for decades after smoking cessation and in current smokers with low cumulative cigarette consumption (&lt;10 pack-years). With respect to current cigarette consumption, the effect estimate for FEV1 decline in current smokers consuming less than five cigarettes per day (7·65 mL per year; 95% CI 6·21–9·09) was 68% of that in current smokers consuming 30 or more cigarettes per day (11·24 mL per year; 9·86–12·62), and around five times greater than in former smokers (1·57 mL per year; 1·00–2·14). Among participants without prevalent lung disease, associations were attenuated but were consistent with the main results. Interpretation: Former smokers and low-intensity current smokers have accelerated lung function decline compared with never-smokers. These results suggest that all levels of smoking exposure are likely to be associated with lasting and progressive lung damage. Funding: National Institutes of Health, National Heart Lung and Blood Institute, and US Environmental Protection Agency.

  PublisherDOI

• Albuminuria, lung function decline, and risk of incident chronic obstructive pulmonary disease the NHLBI pooled cohorts study

  UNC Libraries · 2024-04-03

  articleOpen access

  Rationale: Chronic lower respiratory diseases (CLRDs), including chronic obstructive pulmonary disease (COPD) and asthma, are the fourth leading cause of death. Prior studies suggest that albuminuria, a biomarker of endothelial injury, is increased in patients with COPD. Objectives: To test whether albuminuria was associated with lung function decline and incident CLRDs. Methods: Six U.S. population–based cohorts were harmonized and pooled. Participants with prevalent clinical lung disease were excluded. Albuminuria (urine albumin-to-creatinine ratio) was measured in spot samples. Lung function was assessed by spirometry. Incident CLRD-related hospitalizations and deaths were classified via adjudication and/or administrative criteria. Mixed and proportional hazards models were used to test individual-level associations adjusted for age, height, weight, sex, race/ethnicity, education, birth year, cohort, smoking status, pack-years of smoking, renal function, hypertension, diabetes, and medications. Measurements and Main Results: Among 10,961 participants with preserved lung function, mean age at albuminuria measurement was 60 years, 51% were never-smokers, median albuminuria was 5.6 mg/g, and mean FEV 1 decline was 31.5 ml/yr. For each SD increase in log-transformed albuminuria, there was 2.81% greater FEV 1 decline (95% confidence interval [CI], 0.86–4.76%; P = 0.0047), 11.02% greater FEV 1 /FVC decline (95% CI, 4.43–17.62%; P = 0.0011), and 15% increased hazard of incident spirometry-defined moderate-to-severe COPD (95% CI, 2–31%, P = 0.0021). Each SD log-transformed albuminuria increased hazards of incident COPD-related hospitalization/mortality by 26% (95% CI, 18–34%, P, 0.0001) among 14,213 participants followed for events. Asthma events were not significantly associated. Associations persisted in participants without current smoking, diabetes, hypertension, or cardiovascular disease. Conclusions: Albuminuria was associated with greater lung function decline, incident spirometry-defined COPD, and incident COPD-related events in a U.S. population–based sample.

  PublisherDOI

• Lung function impairment and risk of incident heart failure: the NHLBI Pooled Cohorts Study

  UNC Libraries · 2024-04-03

  articleOpen access

  Aims: The aim is to evaluate associations of lung function impairment with risk of incident heart failure (HF). Methods and results: Data were pooled across eight US population-based cohorts that enrolled participants from 1987 to 2004. Participants with self-reported baseline cardiovascular disease were excluded. Spirometry was used to define obstructive [forced expiratory volume in 1 <FOR VERIFICATION>s/forced vital capacity (FEV1/FVC) <0.70] or restrictive (FEV1/FVC ≥0.70, FVC <80%) lung physiology. The incident HF was defined as hospitalization or death caused by HF. In a sub-set, HF events were sub-classified as HF with reduced ejection fraction (HFrEF; EF <50%) or preserved EF (HFpEF; EF ≥50%). The Fine-Gray proportional sub-distribution hazards models were adjusted for sociodemographic factors, smoking, and cardiovascular risk factors. In models of incident HF sub-types, HFrEF, HFpEF, and non-HF mortality were treated as competing risks. Among 31 677 adults, there were 3344 incident HF events over a median follow-up of 21.0 years. Of 2066 classifiable HF events, 1030 were classified as HFrEF and 1036 as HFpEF. Obstructive [adjusted hazard ratio (HR) 1.17, 95% confidence interval (CI) 1.07-1.27] and restrictive physiology (adjusted HR 1.43, 95% CI 1.27-1.62) were associated with incident HF. Obstructive and restrictive ventilatory defects were associated with HFpEF but not HFrEF. The magnitude of the association between restrictive physiology and HFpEF was similar to associations with hypertension, diabetes, and smoking. Conclusion: Lung function impairment was associated with increased risk of incident HF, and particularly incident HFpEF, independent of and to a similar extent as major known cardiovascular risk factors.

  PublisherDOI

• A Dyadic Growth Modeling Approach for Examining Associations between Weight Gain and Lung Function Decline

  UNC Libraries · 2024-04-03

  articleOpen access

  The relationship between body weight and lung function is complex. Using a dyadic multilevel linear modeling approach, treating body mass index (BMI; weight (kg)/height (m)2) and lung function as paired, within-person outcomes, we tested the hypothesis that persons with more rapid increase in BMI exhibit more rapid decline in lung function, as measured by forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and their ratio (FEV1:FVC). Models included random intercepts and slopes and adjusted for sociodemographic and smoking-related factors. A sample of 9,115 adults with paired measurements of BMI and lung function taken at ≥3 visits were selected from a pooled set of 5 US population-based cohort studies (1983-2018; mean age at baseline = 46 years; median follow-up, 19 years). At age 46 years, average annual rates of change in BMI, FEV1, FVC, and FEV1:FVC ratio were 0.22 kg/m2/year,-25.50 mL/year,-21.99 mL/year, and-0.24%/year, respectively. Persons with steeper BMI increases had faster declines in FEV1 (r =-0.16) and FVC (r =-0.26) and slower declines in FEV1:FVC ratio (r = 0.11) (all P values < 0.0001). Results were similar in subgroup analyses. Residual correlations were negative (P < 0.0001), suggesting additional interdependence between BMI and lung function. Results show that greater rates of weight gain are associated with greater rates of lung function loss.

  PublisherDOI

• Omega-3 fatty acids and genome-wide interaction analyses reveal DPP10–pulmonary function association

  UNC Libraries · 2024-02-10 · 1 citations

  articleOpen access

  Rationale: Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have anti-inflammatory properties that could benefit adults with comprised pulmonary health. Objective: To investigate n-3 PUFA associations with spirometric measures of pulmonary function tests (PFTs) and determine underlying genetic susceptibility. Methods: Associations of n-3 PUFA biomarkers (a-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid [DPA], and docosahexaenoic acid [DHA]) were evaluated with PFTs (FEV 1 , FVC, and FEV 1 /FVC) in meta-analyses across seven cohorts from the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (N = 16,134 of European or African ancestry). PFT-associated n-3 PUFAs were carried forward to genome-wide interaction analyses in the four largest cohorts (N = 11,962) and replicated in one cohort (N = 1,687). Cohort-specific results were combined using joint 2 degree-of-freedom (2df) meta-analyses of SNP associations and their interactions with n-3 PUFAs Results: DPA and DHA were positively associated with FEV 1 and FVC (P, 0.025), with evidence for effect modification by smoking and by sex. Genome-wide analyses identified a novel association of rs11693320—an intronic DPP10 SNP—with FVC when incorporating an interaction with DHA, and the finding was replicated (P 2df = 9.4 3 10 29 across discovery and replication cohorts). The rs11693320-A allele (frequency, z80%) was associated with lower FVC (P SNP = 2.1 3 10 29 ; b SNP = 2161.0 ml), and the association was attenuated by higher DHA levels (P SNP 3DHA interaction = 2.1 3 10 27 ; b SNP 3DHA interaction = 36.2 ml). Conclusions: We corroborated beneficial effects of n-3 PUFAs on pulmonary function. By modeling genome-wide n-3 PUFA interactions, we identified a novel DPP10 SNP association with FVC that was not detectable in much larger studies ignoring this interaction.

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Recent grants

• NIH Grant R03HL095414

  NIH · $141k · 2011

• NIH Grant R01HL071022

  NIH · $3.1M · 2011

• NIH Grant R29HL045731

  NIH · $538k · 1998

• NIH Grant R03HL066539

  NIH · $159k · 2004

• NUTRITION TRAINING

  NIH · $8.9M · 1976–2027

Frequent coauthors

• George O'connor

  University of Wisconsin–Madison

  87 shared

• Stephanie J. London

  National Institute of Environmental Health Sciences

  84 shared

• Linda Youngman

  University of Oxford

  78 shared

• David Sparrow

  VA Boston Healthcare System

  56 shared

• Martin D. Tobin

  52 shared

• Augusto A. Litonjua

  Golisano Children's Hospital

  48 shared

• Pantel Vokonas

  Boston University

  48 shared

• Josée Dupuis

  Boston University

  47 shared

Labs

• Patricia Ann Cassano LabPI

Education

• Ph.D.

  Cornell University

Awards & honors

• Director of Cornell's PAHO/WHO Collaborating Centre on Nutri…
• Director of the Cochrane US Network Cornell Associate Center…
• Co-Director of the Joan Klein Jacobs Center for Precision Nu…