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Edward  Giovannucci

Edward Giovannucci

· Associate Professor, Department of Medicine Professor of Nutrition and Epidemiology, Department of Nutrition, Harvard T.H. Chan School of Public Health

Harvard University · Nutrition

Active 1990–2026

h-index267
Citations334.4k
Papers3.6k1046 last 5y
Funding$180.0M
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About

Edward Giovannucci is an Associate Professor in the Department of Medicine and a Professor of Nutrition and Epidemiology at Harvard T.H. Chan School of Public Health. He is affiliated with the Division of Nutrition at Harvard Medical School and is involved in research related to nutrition, epidemiology, and disease prevention. His work encompasses a broad range of topics including obesity, diabetes, cardiovascular health, cancer, microbiome, metabolism, and lifestyle medicine. Dr. Giovannucci's research focuses on understanding the role of nutrition and lifestyle factors in the development and prevention of chronic diseases, contributing to the advancement of clinical and public health strategies.

Research topics

  • Internal medicine
  • Medicine
  • Oncology
  • Biology
  • Gastroenterology
  • Physical therapy
  • Gynecology
  • Demography
  • Genetics
  • Physiology
  • Environmental health
  • Food science
  • Psychology
  • Bioinformatics

Selected publications

  • Abstract PR007: Precision nutrition potentiates radiotherapy in prostate cancer

    Cancer Research · 2026-01-20

    article

    Abstract Background: While curative treatment is achievable for localized prostate cancer (PCa), radiotherapy often fails, with recurrence rates of 20-50%, highlighting need for strategies to improve efficacy and reduce disease progression. Chronic high-saturated fat intake (SFI) accelerates PCa progression but also creates metabolic vulnerabilities, such as obesity-driven tumor glycolysis, that may be exploited. Transiently harnessing and targeting these vulnerabilities through precision nutrition could represent a breakthrough approach. Methods: We investigated chronic and short-term SFI impact on radiotherapy response using the Hi-MYC genetically engineered mouse model, MyC-CaP and TRAMP-C2 murine PCa cell lines, and LuCaP castration-resistant PCa (CRPC) PDX models. Experiments used immunocompetent (FVB, C57BL/6N) and immunodeficient (CB17 SCID, NOD SCID) strains. Clinical relevance was assessed in patient cohort from the Health Professionals Follow-up Study (HPFS) with detailed dietary intake and clinical outcomes. Results: In Hi-MYC prostates, chronic SFI induced a DNA damage response at the transcriptional level and elevated γH2A.X levels compared to control diet (CTD)-fed mice. Critically, short-term SFI (sSFI) was sufficient to induce DNA damage in MyC-CaP tumors allografted into FVB mice. To assess radiosensitization, MyC-CaP tumors grown in immunocompetent mice underwent 10-day sSFI plus radiotherapy, yielding markedly improved responses versus CTD-fed mice. This effect was confirmed using TRAMP-C2 syngeneic model, demonstrating that sSFI-enhanced radiotherapy efficacy is independent of MYC expression and mouse strain. In contrast, sSFI did not enhance radiotherapy efficacy in 15 LuCaP CRPC PDX models grown in immunodeficient CB17 SCID hosts. To determine immune dependency, we repeated the experiments with MyC-CaP and TRAMP-C2 cells in CB17 and NOD SCID mice. Notably, sSFI-mediated radiosensitization was lost in immunodeficient hosts. Immune profiling in FVB mice showed sSFI primed immunity for radiotherapy and reshaped the tumor microenvironment post-treatment. We further examined post-diagnostic fat intake and survival in 3,959 patients with stage T1–T3 PCa from the HPFS with a median follow-up for mortality of 12.8 years. Among those treated with radiotherapy (n = 1,765), replacing 10% of energy intake from carbohydrates with saturated fat was associated with a 34% reduction in PCa-specific mortality (N events 185, Hazard Ratio 0.66, 95% Confidence Interval 0.42–1.04), trending toward statistical significance (p = 0.07; replacement model). No association was observed for cancer-specific mortality in patients undergoing radical prostatectomy (n = 2,194). Conclusion: Our findings demonstrate that sSFI enhances radiotherapy efficacy in preclinical PCa models with an intact immune system and shows translational relevance in clinical cohort. Altogether, precision nutrition (i.e., tailoring diet to treatment modality) may optimize therapeutic outcomes in PCa. Citation Format: Walaa Alahmadi, Tianrui Xu, Maria Celia Fernandez, Yiwen Zhang, Megan Shanahan, Léa Bourguignon, Anna de Polo, Nadia Boufaied, Jiachen Ji, Paolo Chetta, Feryel Azzi, Isabelle Clément, Conner J. Sessions, Holly M. Nguyen, Giorgia Zadra, Francis Rodier, Dominique Trudel, Eva Corey, Julianna Blagih, Edward L. Giovannucci, Lorelei A. Mucci, David P. Labbé. Precision nutrition potentiates radiotherapy in prostate cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Prostate Cancer Research and Treatment; 2026 Jan 20-22; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(2_Suppl):Abstract nr PR007.

  • Postdiagnostic Inflammatory and Insulinemic Diet and Lifestyle Patterns and Risk of Prostate Cancer–specific Mortality in the Health Professionals Follow-up Study

    Cancer Epidemiology Biomarkers & Prevention · 2026-04-27

    article

    BACKGROUND: Few studies have investigated post-diagnostic proinflammatory, hyperinsulinemic, and insulin-resistant dietary and lifestyle patterns in relation to the risk of prostate cancer (PCa)-specific mortality (PCSM). METHODS: In 4,501 men diagnosed with nonmetastatic PCa from the Health Professionals Follow-up Study, we investigated the empirical dietary inflammatory pattern, empirical dietary index for hyperinsulinemia, empirical lifestyle index for hyperinsulinemia, empirical dietary index for insulin resistance, and empirical lifestyle index for insulin resistance in relation to risk of PCSM. Cox proportional hazard models were used to estimate hazard ratios and 95% confidence intervals. RESULTS: Over a median follow-up of 13.3 years starting at time of PCa diagnosis, we identified 281 PCa-specific deaths. None of the indices were statistically significantly associated with risk of PCSM. CONCLUSIONS: Our results do not provide evidence that post-diagnostic dietary and lifestyle patterns that promote inflammation, hyperinsulinemia, or insulin resistance are associated with risk of PCSM. IMPACT: Inflammation and insulin signaling have been implicated in PCa progression, but their associated dietary and lifestyle patterns were not associated with PCa survival in this study sample.

  • Supplementary Figure S1 from Sex-Specific Associations between Adiponectin and Leptin Signaling and Pancreatic Cancer Survival

    2025-11-26

    articleOpen access

    <p>Association between leptin levels and pancreatic cancer mortality using spline regression.</p>

  • Supplementary Table S2 from Elevated Resting Heart Rate Is an Independent Risk Factor for Mortality in Patients with Colorectal Cancer: A Retrospective Cohort Study

    2025-12-01

    articleOpen access

    <p>Supplementary Table S2 shows that patients with an RHR ≥88 bpm had higher risks of all-cause and CRC-specific mortality compared to those with an RHR ≤66 bpm, after excluding patients who had died within 3-month of surgery.</p>

  • Table S2 from Effect Modification by Levels of Sex Hormones in the Association between Adiposity and Cancer Incidence in the UK Biobank

    2025-12-02

    articleOpen access

    <p>Table S2 shows the interaction between hormone levels and adiposity on cancer incidence among never smokers</p>

  • Supplementary Table S3 from Sex-Specific Associations between Adiponectin and Leptin Signaling and Pancreatic Cancer Survival

    2025-11-26

    articleOpen access

    <p>Association between SNPs in the leptin receptor gene and pancreatic cancer mortality by sex</p>

  • Data from Elevated Resting Heart Rate Is an Independent Risk Factor for Mortality in Patients with Colorectal Cancer: A Retrospective Cohort Study

    2025-12-01

    articleOpen access

    <div>AbstractBackground:<p>Although lifestyle factors are associated with resting heart rate (RHR), its association with mortality in patients with colorectal cancer has not been fully understood. Therefore, we sought to determine whether RHR is associated with all-cause and colorectal cancer–specific mortality in patients with stage I to III colorectal cancer.</p>Methods:<p>We included a total of 3,631 patients from the Severance Hospital Colorectal Cancer Registry (Seoul, South Korea) who underwent surgery for stage I to III colorectal cancer. RHR data were collected on the day of surgery. We utilized multivariable Cox proportional hazards models to estimate HRs and 95% confidence intervals (CI) for the association between RHR and all-cause and colorectal cancer–specific mortality.</p>Results:<p>During a median follow-up of 3.0 years, there were 292 all-cause and 177 colorectal cancer–specific deaths. Patients in the highest quintile of RHR [≥88 beats per minute (bpm)] versus patients in the lowest quintile of RHR (≤66 bpm) showed a 3.33-fold increased risk of all-cause mortality (95% CI, 1.85–5.99) and a 2.98-fold increased risk of colorectal cancer–specific mortality (95% CI, 1.72–5.16). For every 10-bpm increase in RHR, there was a 1.44-fold increase in all-cause mortality (95% CI, 1.32–1.58) and a 1.50-fold increase in colorectal cancer–specific mortality (95% CI, 1.33–1.69).</p>Conclusions:<p>Elevated RHR on the day of surgery for colorectal cancer is associated with a higher risk of all-cause/colorectal cancer–specific mortality.</p>Impact:<p>Our data suggest that RHR may serve as a clinically relevant predictor of mortality in patients who undergo surgery for colorectal cancer.</p></div>

  • Supplementary Table S4 from Elevated Resting Heart Rate Is an Independent Risk Factor for Mortality in Patients with Colorectal Cancer: A Retrospective Cohort Study

    2025-12-01

    articleOpen access

    <p>Supplementary Table S4 shows that patients with an RHR ≥88 bpm had higher risks of all-cause and CRC-specific mortality compared to those with an RHR ≤66 bpm, after excluding patients who received neoadjuvant therapy.</p>

  • Figure S1 from Effect Modification by Levels of Sex Hormones in the Association between Adiposity and Cancer Incidence in the UK Biobank

    2025-12-02

    articleOpen access

    <p>Figure S1 shows the exclusions made to the UK Biobank study population to form our analytic population</p>

  • Supplementary Table S3 from Elevated Resting Heart Rate Is an Independent Risk Factor for Mortality in Patients with Colorectal Cancer: A Retrospective Cohort Study

    2025-12-01

    articleOpen access

    <p>Supplementary Table S3 shows that patients with an RHR ≥88 bpm had higher risks of all-cause and CRC-specific mortality compared to those with an RHR ≤66 bpm, after excluding patients with a history of disease.</p>

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