About

Walter C Willett is Professor of Epidemiology and Nutrition at the Harvard T.H. Chan School of Public Health. He served as Chair of the Department of Nutrition at Harvard T.H. Chan School of Public Health for 25 years. Much of his work has been on the development of methods, using both questionnaire and biochemical approaches, to study the effects of diet on the occurrence of major diseases. He has applied these methods starting in 1980 in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study. Together, these cohorts that include nearly 300,000 men and women with repeated dietary assessments are providing the most detailed information on the long-term health consequences of food choices. Dr. Willett has published over 2,000 research papers, primarily on lifestyle risk factors for heart disease and cancer, and has written the textbook, Nutritional Epidemiology, published by Oxford University Press. He also has four books for the general public. Dr. Willett is the most cited nutritional scientist internationally. He is a member of the National Academy of Medicine and the recipient of many national and international awards for his research.

Research topics

• Medicine
• Internal medicine
• Environmental health
• Gerontology
• Endocrinology
• Biology
• Demography
• Economics
• Sociology
• Computer Science
• Political Science
• Physical therapy
• Food science
• Genetics
• Chemistry
• Nuclear medicine
• Geography
• Family medicine
• Macroeconomics
• Psychology
• Physical medicine and rehabilitation
• Pathology
• Mathematics
• Evolutionary biology

Selected publications

• Supplementary Table 3 from Comparing the Metagenomic Performance of Stools Collected from Custom Cards and 95% Ethanol in Epidemiologic Studies

  2025-08-01

  supplementary-materialsOpen access

  <p>Supplementary Table 3</p>

  PublisherDOI

• The EAT–Lancet Commission on healthy, sustainable, and just food systems

  The Lancet · 2025-10-01 · 235 citations

  reviewOpen access
  PublisherOA PDFDOI

• Data from Loss of PTEN Expression, <i>PIK3CA</i> Mutations, and Breast Cancer Survival in the Nurses’ Health Studies

  2025-11-26

  articleOpen access

  <div>AbstractBackground:<p>The relationships between PTEN loss and/or <i>PIK3CA</i> mutation and breast cancer prognosis remain controversial. We aim to examine the associations in large epidemiologic cohorts.</p>Methods:<p>We followed women with invasive breast cancer from the Nurses’ Health Studies with available data on tumor PTEN expression (<i>n</i> = 4,111) and <i>PIK3CA</i> mutation (<i>n</i> = 2,930). PTEN expression was evaluated by IHC and digitally scored (0%–100%). Pyrosequencing of six hotspot mutations of <i>PIK3CA</i> was performed.</p>Results:<p>We found loss of PTEN expression (≤10%) occurred in 17% of cases, and <i>PIK3CA</i> mutations were detected in 11% of cases. After adjusting for clinical and lifestyle factors, PTEN loss was not associated with worse breast cancer-specific mortality among all samples [HR, 0.85; 95% confidence intervals (CI), 0.71–1.03] or among estrogen receptor (ER)-positive tumors (HR, 0.99; 95% CI, 0.79–1.24). However, among ER-negative tumors, PTEN loss was associated with lower breast cancer-specific mortality (HR, 0.68; 95% CI, 0.48–0.95). <i>PIK3CA</i> mutation was not strongly associated with breast cancer-specific mortality (HR, 0.89; 95% CI, 0.67–1.17). Compared with tumors without PTEN loss and without <i>PIK3CA</i> mutation, those with alterations (<i>n</i> = 540) were not at higher risk (HR, 1.07; 95% CI, 0.86–1.34). However, women with both PTEN loss and <i>PIK3CA</i> mutation (<i>n</i> = 38) were at an increased risk of breast cancer-specific mortality (HR, 1.65; 95% CI, 0.83–3.26).</p>Conclusions:<p>In this large epidemiologic study, the PTEN-mortality association was more pronounced for ER-negative tumors, and the joint PTEN loss and <i>PIK3CA</i> mutation may be associated with worse prognosis.</p>Impact:<p>Further studies with a larger sample of ER-negative tumors are needed to replicate our findings and elucidate underlying mechanisms.</p></div>

  PublisherDOI

• Assessing diet in epidemiologic studies

  Nature Food · 2025-10-14 · 2 citations

  letter1st authorCorresponding
  PublisherDOI

• Supplementary Methods from Comparing the Metagenomic Performance of Stools Collected from Custom Cards and 95% Ethanol in Epidemiologic Studies

  2025-08-01

  preprintOpen access

  <p>Supplementary Methods</p>

  PublisherDOI

• Concern for the validity of short-term dietary crossover trials

  Nature Medicine · 2025-08-22 · 2 citations

  letter
  PublisherDOI

• Long‐Term Adherence to Modifiable Factors and Incident Cardiovascular Disease Among Women With a History of Gestational Diabetes: A Prospective Cohort Study

  Journal of the American Heart Association · 2025-08-05

  articleOpen access

  Background Women with prior gestational diabetes are at increased risk of cardiovascular disease (CVD), but whether and to what extent this risk is modifiable is unknown. Methods NHSII (Nurses' Health Study II) participants (N=4355), who reported a gestational diabetes diagnosis between 1989 and 2001 and were free of type 2 diabetes, CVD, and cancer at baseline were included. Incident CVD included nonfatal myocardial infarction, fatal coronary heart disease, nonfatal/fatal stroke, angiographically confirmed angina, and coronary revascularizations. Modifiable factors were updated every 2 to 4 years. Optimal modifiable factors included body mass index <25.0 kg/m 2 , favorable Alternative Healthy Eating Index‐2010 score (top 40%), ≥150 minutes moderate‐intensity or ≥75 minutes vigorous‐intensity physical activity/week, noncurrent smoking, and moderate alcohol intake (5.0–14.9 g/day). Multivariable‐adjusted Cox models were used to estimate hazard ratios (HR) and 95% CIs with CVD. Results During a median 27.9 years of follow‐up, 188 incident CVD events occurred. Compared with women with zero optimal factors, HR for CVD among women with one, two, three, or four optimal factors was 0.56 (95% CI, 0.22–1.42), 0.40 (95% CI, 0.16–1.02), 0.32 (95% CI, 0.12–0.84), and 0.14 (95% CI, 0.05–0.46), respectively ( P ‐trend<0.0001). There were no incident CVD events in women with all 5 optimal factors. Compared with women with stable modifiable factors, those who increased the number of optimal factors had a lower risk of CVD: 0.30 (95% CI, 0.16–0.55), and those who decreased the number of optimal factors had higher risk: 2.05 (95% CI, 1.28–3.29). Conclusions Long‐term adherence to and improvements in optimal modifiable factors were associated with lower CVD risk after gestational diabetes.

  PublisherDOI

• Ultra-processed Foods and Diet Quality in Association With Long-term Weight Change and Progression to Type 2 Diabetes Among Individuals With a History of Gestational Diabetes Mellitus—A Prospective Study

  Diabetes Care · 2025-08-18

  articleOpen access

  OBJECTIVE: We examined the associations of overall and group-specific ultra-processed food (UPF) consumption with long-term weight change and type 2 diabetes (T2D) progression following gestational diabetes mellitus (GDM)-complicated pregnancies. RESEARCH DESIGN AND METHODS: We included 4,207 women with a history of GDM from the Nurses' Health Study II (1991-2021). UPF intake (servings/day) was assessed via food frequency questionnaires every 4 years and quantified per the NOVA classification. Diet quality was evaluated using the Alternate Healthy Eating Index-2010 (AHEI). Associations between UPF intake changes and weight changes (kg) were assessed using generalized estimating equations (GEE) (n = 3,781). Cox regression models estimated adjusted hazard ratios (HRs) and 95% CIs of habitual UPF intake modeled by time-updated cumulative averages with T2D risk. Joint associations of UPF and AHEI with weight change and T2D risk were examined using the same GEE and Cox regression models, respectively. RESULTS: T2D developed in 1,040 participants. Increased UPF consumption was associated with greater weight gain (P-trend < 0.0001; quartile 1 [Q1] vs. Q4: 0.52 kg vs. 1.65 kg). Habitual UPF consumption was positively associated with T2D risk: adjusted HRs (95% CIs) for Q1 to Q4 were 1.00 (ref), 1.07 (0.87, 1.32), 1.25 (1.03, 1.53), and 1.20 (0.99, 1.46), respectively (P-trend = 0.04). These associations persisted in women with higher AHEI scores. When modeling UPF and AHEI jointly, only women with stable or decreased UPF intake and increased AHEI achieved 4-year weight maintenance. CONCLUSIONS: In women with a history of GDM, UPF consumption was associated with weight gain and higher T2D risk, even among those with higher diet quality.

  PublisherOA PDFDOI

• Abstract 4362202: Combined associations of GLP-1 medications and healthy lifestyle with cardiovascular outcomes among individuals with diabetes: The Million Veteran Program

  Circulation · 2025-11-03

  article

  Background: Incidence of diabetes in the US has more than doubled in the last 20 years, affecting more than 30 million adults. It is unclear what the combined effect of lifestyle habits and GLP-1 receptor agonists (GLP-1 RAs) has on the risk of cardiovascular outcomes. This study aims to assess the independent and combined impact of protective lifestyle factors and GLP-1 RAs on risk of major cardiovascular events (MACE) in a large cohort of US veterans with diabetes. Methods: A prospective cohort study of individuals with type 2 diabetes within the Million Veteran Program with no previous history of myocardial infarction, stroke, cancers or advanced chronic kidney disease. Risk of MACE (i.e., non-fatal stroke, non-fatal myocardial infarction, cardiovascular death) was assessed in the setting of GLP-1 RA usage and healthy lifestyle habits (healthy eating, physically active, not smoking, restful sleep, no to moderate alcohol intake, good stress management, social connection and support, and no opioid addiction) using Cox proportional hazard regression models. Results: A total of 63,656 participants were included in the study with 418,513 person-years of follow-up. The multivariable-adjusted hazard ratio (HR) of MACE was 0.37 (95% confidence interval (CI): 0.24-0.56) comparing participants adhering to all lifestyle habits to those adopting one lifestyle factor or less. When examined individually, all protective lifestyle factors were significantly and independently associated with a lower likelihood of MACE. Multivariable-adjusted HR of MACE was 0.80 (0.71-0.90) comparing users of GLP-1 RA with those not taking GLP-1 RA. The combination of adherence to healthy lifestyle and use of GLP-1 RAs together was associated with a 50% reduction in MACE compared to veterans with a lower adherence to a healthy lifestyle and no GLP-1 RAs usage with standard diabetes care, HR: 0.50 (95% CI: 0.38-0.65). Conclusions: Healthy lifestyle habits in combination with GLP-1 RAs have a greater association than either therapy alone with reduced risk of MACE emphasizing the importance of lifestyle modification with pharmacotherapy.

  PublisherDOI

• Plasma plasmalogen levels and risk of lymph node positive breast cancer

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-15

  articleOpen access

  Lymph node involvement is a key predictor of poor breast cancer prognosis. Systemic lipid alterations can contribute to cancer cell survival in lymph nodes, but their relevance in humans remains unclear. Here, we combine human epidemiologic analyses from the Nurses' Health Study 2 and complementary mechanistic studies in mouse models to investigate how systemic lipid profiles relate to lymph node positive breast cancer. We show that in pre-diagnostic human plasma (n=511), lower levels of phosphatidylethanolamine (PE) and phosphatidylcholine (PC)-enriched plasmalogens are associated with increased risk of lymph node positivity, with stronger associations in samples collected closer to diagnosis. Consistent with the human data, lower levels of PE and PC-enriched plasma plasmalogens are found in mice with nodal involvement. Furthermore, in mice, dietary PUFA depletion reduces lipid oxidation in breast cancer cells in lymph nodes and promotes their survival and metastatic spread. These findings suggest that reduced levels of PE and PC-plasmalogens and decreased PUFA availability creates a lipid environment that enables breast cancer lymph node involvement.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R03TW005773

  NIH · $119k · 2005

• NIH Grant U19CA055075

  NIH · $16.9M · 2013

• NIH Grant K04HL001018

  NIH · $52k · 1986

• Cancer Epidemiology Cohort in Male Health Professionals

  NIH · $11.5M · 2012–2017

• Dietary Etiology of Heart Disease

  NIH · $20.2M · 1985–2030

Frequent coauthors

• Meir J. Stampfer

  The Technological College of Beer Sheva

  2617 shared

• Bernard Rosner

  Harvard University

  2112 shared

• Frank B. Hu

  Brigham and Women's Hospital

  1767 shared

• Edward L. Giovannucci

  Harvard University

  1552 shared

• JoAnn E. Manson

  Brigham and Women's Hospital

  1454 shared

• Eric B. Rimm

  Brigham and Women's Hospital

  1405 shared

• Graham A. Colditz

  Washington University in St. Louis

  1380 shared

• Peter Kraft

  1186 shared

Education

• Ph.D., Nutrition

  Harvard University

  1980

• M.S., Nutrition

  University of California, Berkeley

  1977

• B.S., Nutrition

  University of California, Berkeley

  1975

Awards & honors

• Member of the National Academy of Medicine