Saurabh Mehta
· Director, Program in International Nutrition; Janet and Gordon Lankton Professor; Founding Director of the Cornell Joan Klein Jacobs Center for Precision Nutrition and HealthVerifiedCornell University · Nutritional Sciences
Active 1963–2026
About
Professor Saurabh Mehta's research primarily focuses on the intersection of nutrition, micronutrient supplementation, and infectious diseases, particularly HIV/AIDS and tuberculosis. His work extensively explores the effects of vitamins, including vitamin A and vitamin D, on HIV-infected patients, investigating nutritional indicators related to adverse pregnancy outcomes and mother-to-child transmission of HIV. He has contributed to understanding the role of micronutrients in disease progression, anemia, mortality, and morbidity among HIV-infected populations, with a significant emphasis on studies conducted in Tanzania and India. Professor Mehta's research also addresses the impact of nutritional status on treatment outcomes and child health in the context of infectious diseases, including the role of vitamin D in tuberculosis treatment and the effects of zinc supplementation in pediatric pneumonia cases. Additionally, his work extends to the development and application of innovative diagnostic technologies, such as smartphone platforms for quantifying vitamin D levels, demonstrating a commitment to advancing both clinical and technological approaches to global health challenges.
Research topics
- Medicine
- Internal medicine
- Environmental health
- Biology
- Immunology
- Bioinformatics
- Political Science
- Gerontology
- Public administration
- Pathology
- Nursing
- Microbiology
- Physiology
- Risk analysis (engineering)
- Geography
- Pediatrics
- Economics
- Business
- Surgery
- Demography
- Endocrinology
- Obstetrics
- Intensive care medicine
- Economic growth
Selected publications
BMJ Global Health · 2026-05-01
articleOpen accessBACKGROUND: Undernutrition is a leading risk factor for tuberculosis (TB) mortality and poor treatment outcomes. We evaluated the cost-effectiveness of providing in-kind nutritional support to impoverished persons with TB (PWTB) in India. METHODS: We developed a Markov model comparing standard care with a household-level nutritional food-basket intervention. Model parameters were informed from systematic reviews and a recent cluster-randomised study. We estimated TB mortality, disability-adjusted life years (DALYs) and costs from the healthcare perspective. We calculated incremental cost-effectiveness ratios (ICERs), and parameter uncertainty was quantified through deterministic and probabilistic sensitivity analyses. We estimated uncertainty intervals (UIs) with 10 000 Monte Carlo iterations. FINDINGS: Nutritional support was projected to avert 10 470 DALYs per 10 000 PWTB (95% UI 1 775 to 33 255). When scaled to India's 2.8 million annual TB cases, this corresponds to approximately 120 120 TB deaths averted nationwide (95% UI 60 760 to 162 960) under full coverage. The ICER was US$141 per DALY averted (95% UI US$44 to 836). The ICER was most sensitive to the mortality reduction achieved through nutritional support but remained below India's willingness-to-pay threshold (US$550 per DALY averted) as long as the intervention achieved at least a 13% relative reduction in mortality. Nutritional support was cost-effective in 94% of simulations. INTERPRETATION: In-kind nutritional support for PWTB is highly cost-effective and could substantially reduce TB mortality and disengagement from care. Scaling up such interventions could meaningfully improve TB outcomes nationwide and accelerate progress towards the end TB strategy targets.
Clinical Nutrition · 2026-02-10
articleOpen access1st authorCorrespondingBACKGROUND AND AIMS: Biofortification of staple crops with higher concentrations of micronutrients via traditional breeding methods is a sustainable strategy and can possibly complement fortification and other interventions to target micronutrient deficiencies in low resource settings, particularly among populations such as children. We aimed to determine if iron- and zinc-biofortified pearl millet (FeZnPM, Dhanashakti, ICTP-8203Fe)-based complementary feeding improves nutritional status, including iron and zinc biomarkers and growth, in children living in urban slums of Mumbai. METHODS: We conducted a randomized controlled trial of FeZnPM among 223 children aged 12-18 months who were not severely anemic at baseline (hemoglobin ≥9.0 g/dL). Children were randomized to receive either FeZnPM or conventional (non-biofortified) pearl millet (CPM) daily for 9 months. Hemoglobin, serum ferritin, and plasma zinc concentrations as well as growth indicators (length, weight, mid-upper arm circumferences, triceps and subscapular skinfolds) were evaluated at enrollment and throughout the trial. World Health Organization (WHO) anthropometric Z-scores were calculated using WHO growth standards. Primary outcomes were hemoglobin and serum ferritin concentrations, and growth, defined as WHO Z-scores. An intent-to-treat approach was used for analyses. We used the Hodges-Lehmann-Sen test to assess the change in primary outcomes between baseline and the last visit and report corresponding 95 % confidence intervals. RESULTS: At baseline, 49.3 % of children had anemia (hemoglobin <10.5 g/dL) and 59.6 % had iron deficiency (serum ferritin <12 μg/L). Consumption of FeZnPM increased hemoglobin concentration compared to CPM [change over time: 0.10 g/dL (-0.60, 0.90) vs. CPM: -0.15 g/dL (-1.00, 0.40) P = 0.04]. After follow-up, FeZnPM did not increase the concentration of serum ferritin or plasma zincor improve growth, compared to CPM (P > 0.05). Though the trial was not designed to detect this difference, the prevalence of anemia at endpoint was 33.8 % among those consuming FeZnPM, compared to 57.6 % in the CPM group (P = 0.005). CONCLUSIONS: Daily consumption of FeZnPM-based complementary foods improved hemoglobin concentrations and reduced prevalence of anemia in children living in Mumbai's urban slums. However, the intervention did not significantly impact serum ferritin, plasma zincor growth outcomes. TRIAL REGISTRATION: This trial is registered with Clinicaltrials.gov (ID: NCT02233764), and Clinical Trials Registry of India (ID: REF/2014/10/007731).
Clinical Nutrition · 2026-01-21
article1st authorCorrespondingCochrane Database of Systematic Reviews · 2026-02-18 · 2 citations
articleOpen accessBACKGROUND: Malaria is an infectious disease transmitted by female Anopheles mosquitoes, with ongoing transmission in over 80 countries. The malaria parasite requires folate for survival and growth; antifolate antimalarial medications used for prevention and treatment target enzymes in folate metabolism as their mechanism of action. Periconceptional folic acid (synthetic form of folate) supplementation (400 μg/day) is the standard of care for neural tube defect prevention. Concerns have been raised about the potential effects of folic acid (including above the tolerable upper intake level (UL) >1.0 mg/day) in the context of malaria prevention and treatment, including the efficacy of antimalarial medications. Examining the potential impact of folic acid on malaria risk and severity amongst people taking antifolate antimalarial medications may inform public health programmes in malaria-endemic areas. OBJECTIVES: To examine the effects of folic acid supplementation on the risk and severity of malaria infection amongst people taking antifolate antimalarials and living in areas with malaria endemicity. PREVENTION: Amongst uninfected people taking antifolate antimalarial medications for malaria prevention, does folic acid supplementation increase susceptibility or severity of malaria infection? TREATMENT: Amongst people with malaria infection who are being treated with antifolate antimalarial drugs, does folic acid supplementation reduce parasite clearance or increase the risk of treatment failure? SEARCH METHODS: We searched databases including CENTRAL, MEDLINE, Embase, CINAHL, Scopus, and trial registries (September 13, 2024), grey literature, and reference searches to identify additional studies. SELECTION CRITERIA: Randomised trials evaluating the effects of folic acid supplementation (alone or in combination with iron or other vitamins and minerals) amongst individuals taking antifolate antimalarial medications in malaria-endemic areas. DATA COLLECTION AND ANALYSIS: Primary outcomes included uncomplicated malaria or severe malaria, parasite clearance, and treatment failure. Cochrane RoB 2 was used to evaluate the risk of bias. Certainty of evidence was assessed using GRADE for primary outcomes. We performed meta-analyses using random-effects models for all outcomes. MAIN RESULTS: Eight trials with 3486 participants were included: three malaria prevention trials and five malaria treatment trials. Most treatment trials included folic acid doses above the UL (> 1.0 mg/d); one trial included 400 μg per day. Antifolate antimalarials included sulfadoxine-pyrimethamine (SP; five trials), sulfisoxazole plus pyrimethamine (one trial), atovaquone-proguanil (one trial), and proguanil (one trial). Some studies had unclear or high risk of bias due to missing outcome data. Malaria prevention Comparison 1: Folic acid (alone or in combination with other vitamins and minerals) + antifolate antimalarials versus placebo/no folic acid + antifolate antimalarial medications. Data for primary outcomes, uncomplicated and severe malaria, were not reported. One trial reported laboratory parasitaemia; there was little to no difference in malaria parasitaemia amongst pregnant women receiving folic acid (with iron) and antifolate antimalarials compared to iron and antifolate antimalarials (Risk Ratio (RR) 1.21; 95% CI 0.56 to 2.62; P = 0.63; 1 trial, 643 individuals). Comparisons 2-4: No studies reported data for Comparisons 2-4. Malaria treatment Comparison 1: Folic acid (alone or in combination with other vitamins and minerals) + antifolate antimalarial medications versus placebo/no folic acid with antifolate antimalarials. People receiving folic acid (alone or with iron) and antifolate antimalarials were less likely to clear malaria parasites (day 3) compared to individuals who did not receive folic acid (RR 0.89; 95% CI 0.84 to 0.95, 4 trials, 929 individuals, moderate-certainty evidence); and had increased risk of treatment failure on day 7 (RR 2.12; 95% CI 1.41 to 3.19, 4 trials, 1062 individuals, moderate-certainty evidence), day 14 (RR 1.97; 95% CI 1.44 to 2.70, 3 trials; 891 individuals; moderate-certainty evidence), and day 28 (RR 1.35; 95% CI 1.21 to 1.51; 4 trials; 1012 individuals, moderate-certainty evidence). Comparison 2: Folic acid alone + antifolate antimalarials versus placebo/no folic acid + antifolate antimalarial medication. Folic acid supplementation with antifolate antimalarials likely had lower parasite clearance (day 3) (RR 0.87; 95% CI 0.79 to 0.96, 2 trials, 229 individuals, moderate certainty of the evidence), and increased treatment failure (day 7: RR 2.58; 95% CI 0.89 to 7.45; P = 0.08; 2 trials; 344 individuals, moderate-certainty evidence; day 14: RR 4.15; 95% CI 0.92 to 18.65; P = 0.06; 1 trial; 173 individuals, moderate-certainty evidence; and day 28: RR 1.47; 95% CI 0.86 to 2.49; P = 0.16; 2 trials; 294 individuals, moderate-certainty evidence), compared to no folic acid and antifolate antimalarials. Comparison 3: Folic acid with iron + antifolate antimalarial medication versus placebo/no folic acid with iron + antifolate antimalarial medication. People receiving folic acid with iron and antifolate antimalarials were less likely to clear malaria parasites (day 3: RR 0.90; 95% CI 0.83 to 0.98; P = 0.02; 2 trials; 700 individuals, moderate-certainty evidence), and had increased treatment failure (day 7: RR 1.96; 95% CI 1.05 to 3.65; P = 0.03; 2 trials; 718 individuals; day 14: RR 1.90; 95% CI 1.35 to 2.67; 2 trials; 718 individuals; day 28: RR 1.17; 95% CI 0.79 to 1.74; 2 trials; 578 individuals; all moderate-certainty evidence), compared to iron and antifolate antimalarials. Comparison 4: No studies reported data. AUTHORS' CONCLUSIONS: Malaria prevention: None of the included trials reported primary outcomes. Malaria treatment: People who received folic acid supplementation (alone or with iron) and antifolate antimalarial treatment were less likely to clear malaria parasitaemia (day 3), and had increased treatment failure (days 7, 14, 28). Most of the included trials provided folic acid with doses above the tolerable UL (> 1.0 mg). One trial included folic acid at a dose of 400 μg/d (recommended dose for preventing neural tube defects) and showed little to no difference in parasite clearance or treatment failure.
2025-06-03
peer-reviewPLOS Global Public Health · 2025-10-15 · 1 citations
articleOpen accessCorrespondingMycobacterium tuberculosis (Mtb) manipulates host metabolism to gain nutrients and increase virulence. Despite known alterations in metabolism in individuals with pulmonary tuberculosis (PTB) during anti-tuberculosis (TB) treatment, the effect of disease severity on metabolite dynamics in individuals with PTB remains understudied. We examined metabolite dynamics over the course of anti-TB treatment in individuals diagnosed with mild (N = 8; smear grade of 1 + /2+ and mild chest x-ray (CXR) abnormality) or severe drug-sensitive PTB (N = 8; 3 + smear grade and moderate/advanced CXR abnormality) in a pilot proof-of-concept study compared to controls without TB (N = 7). Semi-targeted metabolomic analysis of plasma was performed using tandem liquid chromatography-mass spectrometry and electrospray ionization mass spectrometry at baseline, one month, and six months after treatment initiation. Our analysis revealed disease severity-specific metabolic profiles as well as those unique to controls. Many metabolites specific to mild or severe TB were involved in the glycerophospholipid and sphingolipid pathways. A subset of glycerophospholipids were enriched at baseline, month 1, and at the endpoint in individuals with mild and severe TB, despite anti-TB treatment. Our results highlight the importance of glycerophospholipid and sphingolipid pathways during Mtb infection and treatment, regardless of disease severity, and suggest that Mtb could induce chronic effects on host metabolism even after treatment.
Dengue virus infection in children: Serum lipidomics profiling for biomarker discovery
PLoS neglected tropical diseases · 2025-11-24 · 1 citations
articleOpen accessDengue fever is a significant global health concern, particularly in tropical and subtropical regions, where it disproportionately affects children and adolescents. The disease, caused by the dengue virus (DENV), triggers a complex immune response that leads to metabolic alterations, particularly in lipid metabolism, which plays a key role in inflammation and disease progression. Despite advancements in diagnostic methods, the search for novel biomarkers may support the development of new diagnostic tools for faster patient screening. In this study, we applied a lipidomics approach using liquid chromatography-mass spectrometry to analyze the serum lipid metabolome of children and adolescents infected with DENV (n = 25) compared to controls (n = 15). Multivariate statistics included partial least squares discriminant analysis (PLS-DA) to assess group separation and receiver operating characteristic (ROC) curve analysis to evaluate biomarker performance. The PLS-DA revealed a tendency of separation between groups, with component 5 showing the highest predictive power (Q2 = 0.68345). From this data, 12 metabolites were significantly more abundant in controls, while 3 were more abundant in DENV infected group. ROC curve analysis demonstrated a sensitivity of 80% for the metabolite of m/z 246.265, and a sensitivity of 96% for all metabolites, as a set. The metabolites were attributed to sphingolipids, fatty acids, glycerol lipids, and sterols. Our findings reveal significant lipid metabolic alterations in pediatric dengue fever, highlighting their biomarker potential. This study reinforces the value of lipidomics in dengue research and biomarker discovery, which may contribute to the development of diagnosis tools that will improve patient care.
Cochrane Database of Systematic Reviews · 2025-01-30 · 5 citations
reviewOpen accessSenior authorBACKGROUND: Precision nutrition-based methods develop tailored interventions and/or recommendations accounting for determinants of intra- and inter-individual variation in response to the same diet, compared to current 'one-size-fits-all' population-level approaches. Determinants may include genetics, current dietary habits and eating patterns, circadian rhythms, health status, gut microbiome, socioeconomic and psychosocial characteristics, and physical activity. In this systematic review, we examined the evidence base for the effect of interventions based on precision nutrition approaches on overweight and obesity in children and adolescents to help inform future research and global guidelines. OBJECTIVES: To examine the impact of precision nutrition-based interventions for the management of obesity in children and adolescents in all their diversity. SEARCH METHODS: We searched CENTRAL, MEDLINE, CINAHL, Web of Science Core Collection, BIOSIS Previews, Global Index Medicus (all regions), IBECS, SciELO, PAHO, PAHO IRIS, WHO IRIS, WHOLIS, Bibliomap, and TRoPHI, as well as the WHO ICTRP and ClinicalTrials.gov. We last searched the databases on 23 July 2024. We did not apply any language restrictions. SELECTION CRITERIA: We included randomised or quasi-randomised controlled trials that evaluated precision nutrition-based interventions (accounting for 'omics' such as phenotyping, genotyping, gut microbiome; clinical data, baseline dietary intake, postprandial glucose response, etc., and/or including artificial intelligence such as machine learning methods) compared to general or one-size-fits-all interventions or no intervention in children and adolescents aged 0 to 9 years or 10 to 19 years with overweight or obesity. DATA COLLECTION AND ANALYSIS: Two review authors independently conducted study screening, data extraction, and risk of bias and GRADE assessments. We used fixed-effect analyses. Our outcomes of interest were physical and mental well-being, physical activity, health-related quality of life, obesity-associated disability, and adverse events associated with the interventions as defined or measured by trialists, and weight change (reduction, stabilisation or maintenance). MAIN RESULTS: , 95% CI -0.26 to 6.26; 1 study, 30 participants; very low-certainty evidence) and on weight (MD 11.40 kg, 95% CI -0.47 to 23.27; 1 study, 30 participants; very low-certainty evidence) compared with a one-size-fits-all control intervention. AUTHORS' CONCLUSIONS: Based on data from two small studies with a total of 105 participants, the evidence is very uncertain about the effect of precision nutrition-based interventions on body weight or BMI. This review was limited by the number of available randomised controlled trials in this relatively nascent field. Given these limitations, the two studies do not provide sufficient evidence to adequately inform practice. Future research should report participant outcome data, including outcomes related to mental, emotional, and functional well-being, in addition to biochemical and physical measures, stratified by World Health Organization-defined age groups (children (0 to 9 years), and children and adolescents (10 to 19 years)). Future studies should also report methods related to randomisation, blinding, and compliance, as well as include prespecified analysis plans.
The Lancet Global Health · 2025-03-19 · 16 citations
reviewOpen accessUndernutrition-the leading risk factor for tuberculosis worldwide-is associated with impaired immunity, more extensive disease, delayed sputum conversion, and worse treatment outcomes, including mortality. In this Health Policy, we propose a comprehensive roadmap for integrating nutritional assessment, counselling, and support into tuberculosis treatment as part of person-centred care. At treatment initiation, we recommend standard nutritional assessment with anthropometric measurements and haemoglobin estimation, in addition to macronutrient and micronutrient support alongside nutritional counselling. Weight should be monitored during treatment and lack of weight gain at the end of the intensive phase should prompt an investigation of causes, such as food insecurity, poor treatment adherence, malabsorption, uncontrolled diabetes, or drug resistance. At the end of treatment, we recommend reassessing anthropometric measures to assess nutritional recovery. People with tuberculosis who remain underweight should receive close follow-up to detect early relapse. We call for annual reporting of nutritional metrics by WHO, explicit inclusion of nutritional assessment and care in national strategic plans, domestic or international support of nutritional programmes for people with tuberculosis, increased support for operational research initiatives, and integration of nutritional care into the WHO Multisectoral Accountability Framework at national and regional levels.
SSRN Electronic Journal · 2025-01-01
preprintOpen access
Recent grants
FeverPhone: Point of Care Diagnosis of Acute Febrile Illness using a Mobile Device
NIH · $3.0M · 2020–2022
Frequent coauthors
- 161 shared
Julia L. Finkelstein
Cornell University
- 88 shared
Wafaie Fawzi
Harvard University
- 53 shared
Karim Manji
Muhimbili University of Health and Allied Sciences
- 52 shared
David Erickson
Cornell University
- 49 shared
Taha E. Taha
Johns Hopkins University
- 49 shared
Charles Chasela
- 49 shared
Alicia Young
- 49 shared
Elizabeth R. Brown
Fred Hutch Cancer Center
Education
- 2010
Postdoctoral Training, Nutrition
Harvard School of Public Health
- 2009
Sc.D., Epidemiology, Nutrition
Harvard University
- 2004
S.M., Epidemiology
Harvard University
- 2002
M.B.B.S.
All India Institute of Medical Sciences
Awards & honors
- NIH technology accelerator challenge prize for innovative gl…
- Norman Kretchmer memorial award for nutrition and developmen…
- Rainer Gross Prize for innovations in nutrition and health
- SUNY Chancellor award for scholarship and creative activitie…
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