JoAnn E Manson

University of Minnesota Duluth, Duluth, Minnesota, United States

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Publications (743)7026.34 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: -Vitamin D supplementation may be an inexpensive intervention to reduce heart failure (HF) incidence. However, there are insufficient data to support this hypothesis. This study evaluates whether vitamin D plus calcium (CaD) supplementation is associated with lower rates of HF in post-menopausal women and whether the effects differ between those at high versus low risk for HF.
    Circulation Heart Failure 11/2014; · 6.68 Impact Factor
  • Robert A Wild, JoAnn E Manson
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    ABSTRACT: Identifying appropriate candidates for menopausal hormone therapy (HT) is challenging given the complex profile of risks and benefits associated with treatment. Most professional societies agree that HT should not be used for chronic disease prevention. Recent findings from the Women's Health Initiative and other randomized trials suggest that a woman's age, proximity to menopause, underlying cardiovascular risk factor status, and various biological characteristics may modify health outcomes with HT. An emerging body of evidence suggests that it may be possible to assess individual risk and therefore better predict who is more likely to have favorable outcomes versus adverse effects when taking HT. Thus, once a woman is identified as a potential candidate for HT due to moderate-to-severe menopausal symptoms or other indications, risk stratification may be an important tool for minimizing patient risk. This individualized approach holds great promise for improving the safety of HT. We review here the evidence for this approach, focusing on vascular health because of limited data on other outcomes. The ultimate goal of this research is to develop a personalized risk/benefit prediction model to be used when a woman seeks therapy for symptom management. Patient centered outcomes including quality of life and sense of well-being should also be incorporated and will directly impact the benefit: risk ratio and compliance. Additional research on hormone dose, formulation, and route of delivery will be important for improving this model.
    Seminars in Reproductive Medicine 11/2014; 32(6):433-437. · 3.21 Impact Factor
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    ABSTRACT: Background Although N-terminal pro–B-type natriuretic peptide (NT-proBNP) has a strong relationship with incident cardiovascular disease (CVD), few studies have examined whether NT-proBNP adds to risk prediction algorithms, particularly in women. Objectives This study sought to evaluate the relationship between NT-proBNP and incident CVD in women. Methods Using a prospective case-cohort within the WHI (Women’s Health Initiative) observational study, we selected 1,821 incident cases of CVD (746 myocardial infarctions, 754 ischemic strokes, 160 hemorrhagic strokes, and 161 other cardiovascular [CV] deaths) and a randomly selected reference cohort of 1,992 women without CVD at baseline. Results Median levels of NT-proBNP were higher at study entry among incident cases (120.3 ng/l [interquartile range (IQR): 68.1 to 219.5 ng/l]) than among control subjects (100.4 ng/l [IQR: 59.7 to 172.6 ng/l]; p < 0.0001). Women in the highest quartile of NT-proBNP (≥140.8 ng/l) were at 53% increased risk of CVD versus those in the lowest quartile after adjusting for traditional risk factors (1.53 [95% confidence interval (CI): 1.21 to 1.94]; p for trend <0.0001). Similar associations were observed after adjustment for Reynolds Risk Score covariables (1.53 [95% CI: 1.20 to 1.95]; p for trend <0.0001); the association remained in separate analyses of CV death (2.66 [95% CI: 1.48 to 4.81]; p for trend <0.0001), myocardial infarction (1.39 [95% CI: 1.02 to 1.88]; p for trend = 0.008), and stroke (1.60 [95% CI: 1.22 to 2.11]; p for trend <0.0001). When added to traditional risk covariables, NT-proBNP improved the c-statistic (0.765 to 0.774; p = 0.0003), categorical net reclassification (0.08; p < 0.0001), and integrated discrimination (0.0105; p < 0.0001). Similar results were observed when NT-proBNP was added to the Reynolds Risk Score. Conclusions In this multiethnic cohort of women with numerous CV events, NT-proBNP modestly improved measures of CVD risk prediction.
    Journal of the American College of Cardiology 10/2014; 64(17):1789–1797. · 14.09 Impact Factor
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    ABSTRACT: Background The impact of a healthy lifestyle on risk of heart failure (HF) is not well known. Objectives The objectives of this study were to evaluate the effect of a combination of lifestyle factors on incident HF and to further investigate whether weighting each lifestyle factor has additional impact. Methods Participants were 84,537 post-menopausal women from the WHI (Women’s Health Initiative) observational study, free of self-reported HF at baseline. A healthy lifestyle score (HL score) was created wherein women received 1 point for each healthy criterion met: high-scoring Alternative Healthy Eating Index, physically active, healthy body mass index, and currently not smoking. A weighted score (wHL score) was also created in which each lifestyle factor was weighted according to its independent magnitude of effect on HF. The incidence of hospitalized HF was determined by trained adjudicators using standardized methodology. Results There were 1,826 HF cases over a mean follow-up of 11 years. HL score was strongly associated with risk of HF (multivariable-adjusted hazard ratio [HR] [95% confidence interval (CI)] 0.49 [95% CI: 0.38 to 0.62], 0.36 [95% CI: 0.28 to 0.46], 0.24 [95% CI: 0.19 to 0.31], and 0.23 [95% CI: 0.17 to 0.30] for HL score of 1, 2, 3, and 4 vs. 0, respectively). The HL score and wHL score were similarly associated with HF risk (HR: 0.46 [95% CI: 0.41 to 0.52] for HL score; HR: 0.48 [95% CI: 0.42 to 0.55] for wHL score, comparing the highest tertile to the lowest). The HL score was also strongly associated with HF risk among women without antecedent coronary heart disease, diabetes, or hypertension. Conclusions An increasingly healthy lifestyle was associated with decreasing HF risk among post-menopausal women, even in the absence of antecedent coronary heart disease, hypertension, and diabetes. Weighting the lifestyle factors had minimal impact.
    Journal of the American College of Cardiology 10/2014; 64(17):1777–1785. · 14.09 Impact Factor
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    ABSTRACT: Determine effects of low-dose estradiol and low-dose venlafaxine on self-reported sleep measures in menopausal women with hot flashes.
    Sleep 10/2014; · 5.10 Impact Factor
  • Menopause (New York, N.Y.) 10/2014; · 3.08 Impact Factor
  • Shilpa N Bhupathiraju, JoAnn E Manson
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    ABSTRACT: Objective: This review provides a comprehensive overview of the most recent findings from the Women's Health Initiative (WHI) hormone therapy (HT) trials and highlights the role of age and other clinical risk factors in risk stratification.Methods: We review the findings on cardiovascular disease, cancer outcomes, all-cause mortality, and other major endpoints in the two WHI HT trials (conjugated equine estrogens [CEE: 0.625 mg/d] with or without medroxyprogesterone acetate [MPA: 2.5 mg/d]).Results: The hazard ratio (HR) for coronary heart disease (CHD) was 1.18 (95% confidence interval (CI): 0.95-1.45) in the CEE+MPA trial and 0.94 (95% CI: 0.78-1.14) in the CEE-alone trial. In both HT trials, there was an increased risk of stroke and deep vein thrombosis, and a lower risk of hip fractures and diabetes. The HT regimens had divergent effects on breast cancer. CEE+MPA increased breast cancer risk (cumulative HR=1.28, 95% CI: 1.11-1.48) while CEE-alone had a protective effect (cumulative HR=0.79, 95% CI: 0.65-0.97). The absolute risks of HT were low in younger women (ages 50-59) and those who were within 10 years of menopause onset. Further, for CHD, the risks were elevated for women with metabolic syndrome or high LDL-C concentrations, but not in women without these risk factors. Factor V Leiden genotype was associated with elevated risk of venous thromboembolism on HT.Conclusion: HT has a complex pattern of benefits and risks. Women in early menopause have low absolute risks of chronic disease outcomes on HT. Use of HT for management of menopausal symptoms remains appropriate, and risk stratification will help to identify women in whom benefits would be expected to outweigh risks.
    10/2014;
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    ABSTRACT: Background: The Women's Health Initiative (WHI) low fat (20% kcal) diet modification (DM) trial (1993-2005) demonstrated a non-significant reduction in breast cancer, a nominally significant reduction in ovarian cancer and no effect on other cancers (mean 8.3 years intervention). Consent to non-intervention follow-up was 83% (n=37,858). This analysis was designed to assess post-intervention cancer risk in women randomized to the low-fat diet (40%) versus usual diet comparison (60%). Methods: Randomized, controlled low fat diet intervention for prevention of breast and colorectal cancers conducted in 48,835 postmenopausal U.S. women, aged 50-79 years at 40 U.S. sites. Outcomes included total invasive cancer, breast and colorectal cancer, cancer-specific and overall mortality. Results: There were no intervention effects on invasive breast 1.08 (0.94, 1.24) or colorectal cancer, other cancers, cancer-specific or overall mortality during the post-intervention period or the combined intervention and follow-up periods. For invasive breast cancer, the HRs were 0.92 (0.84, 1.01) during intervention, during the post-intervention period, and 0.97 (0.89, 1.05) during cumulative follow up. A reduced risk for estrogen receptor positive/progesterone receptor negative tumors was demonstrated during follow-up. Women with higher baseline fat intake (quartile), point estimates of breast cancer risk were HR-0.76; 0.62, 0.92 during intervention versus HR-1.11; 0.84, 1.4 during post-intervention follow-up (p-diff=.03). Conclusions: Dietary fat intake rose post-intervention in intervention women; no long-term reduction in cancer risk or mortality was shown in the WHI DM trial. Impact: Dietary advisement to reduce fat for cancer prevention after menopause generally was not supported by the WHI DM trial.
    09/2014;
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    ABSTRACT: Background Statins increase the risk of new-onset type 2 diabetes mellitus. We aimed to assess whether this increase in risk is a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the intended drug target. Methods We used single nucleotide polymorphisms in the HMGCR gene, rs17238484 (for the main analysis) and rs12916 (for a subsidiary analysis) as proxies for HMGCR inhibition by statins. We examined associations of these variants with plasma lipid, glucose, and insulin concentrations; bodyweight; waist circumference; and prevalent and incident type 2 diabetes. Study-specific effect estimates per copy of each LDL-lowering allele were pooled by meta-analysis. These findings were compared with a meta-analysis of new-onset type 2 diabetes and bodyweight change data from randomised trials of statin drugs. The effects of statins in each randomised trial were assessed using meta-analysis. Findings Data were available for up to 223 463 individuals from 43 genetic studies. Each additional rs17238484-G allele was associated with a mean 0·06 mmol/L (95% CI 0·05–0·07) lower LDL cholesterol and higher body weight (0·30 kg, 0·18–0·43), waist circumference (0·32 cm, 0·16–0·47), plasma insulin concentration (1·62%, 0·53–2·72), and plasma glucose concentration (0·23%, 0·02–0·44). The rs12916 SNP had similar effects on LDL cholesterol, bodyweight, and waist circumference. The rs17238484-G allele seemed to be associated with higher risk of type 2 diabetes (odds ratio [OR] per allele 1·02, 95% CI 1·00–1·05); the rs12916-T allele association was consistent (1·06, 1·03–1·09). In 129 170 individuals in randomised trials, statins lowered LDL cholesterol by 0·92 mmol/L (95% CI 0·18–1·67) at 1-year of follow-up, increased bodyweight by 0·24 kg (95% CI 0·10–0·38 in all trials; 0·33 kg, 95% CI 0·24–0·42 in placebo or standard care controlled trials and −0·15 kg, 95% CI −0·39 to 0·08 in intensive-dose vs moderate-dose trials) at a mean of 4·2 years (range 1·9–6·7) of follow-up, and increased the odds of new-onset type 2 diabetes (OR 1·12, 95% CI 1·06–1·18 in all trials; 1·11, 95% CI 1·03–1·20 in placebo or standard care controlled trials and 1·12, 95% CI 1·04–1·22 in intensive-dose vs moderate dose trials). Interpretation The increased risk of type 2 diabetes noted with statins is at least partially explained by HMGCR inhibition. Funding The funding sources are cited at the end of the paper.
    The Lancet. 09/2014;
  • Michal L Melamed, JoAnn E Manson
    Nature Reviews Endocrinology 08/2014; · 11.03 Impact Factor
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    ABSTRACT: -Healthy levels of lifestyle factors can reduce risk of CVD. However, except for smoking status, often considered a traditional risk factor, their effect on cardiovascular risk prediction is unclear.
    Circulation 08/2014; · 15.20 Impact Factor
  • Menopause (New York, N.Y.) 08/2014; · 3.08 Impact Factor
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    ABSTRACT: Objective: Prior studies of the association between physical activity and hypertensive disorders of pregnancy have been conflicting; the majority focused on leisure-time activity only, did not use physical activity questionnaires validated for pregnancy, and were conducted in primarily non-Hispanic white populations. Methods: We prospectively evaluated this association among 1240 Hispanic women in Proyecto Buena Salud. The Pregnancy Physical Activity Questionnaire, validated for use in pregnancy, was used to assess pre- and early pregnancy sports/exercise, household/caregiving, occupational and transportation activity. Diagnoses of hypertensive disorders of pregnancy were based on medical record abstraction and confirmed by the study obstetrician. Results: A total of 49 women (4.0%) were diagnosed with a hypertensive disorder of pregnancy, including 32 women (2.6%) with pre-eclampsia. In age-adjusted analyses, high levels of early pregnancy household/caregiving activity were associated with reduced risk of total hypertensive disorders (OR = 0.4, 95% CI 0.1-0.9) and pre-eclampsia (OR = 0.3, 95% CI 0.1-0.9) relative to low levels; however, these findings were no longer statistically significant in multivariable models. Pre-pregnancy activity and pattern of activity from pre- to early-pregnancy were not significantly associated with risk. Finally, sedentary behavior was not significantly associated with hypertensive disorders. Conclusion: Findings from this prospective study of Hispanic women were consistent with those of prior prospective cohorts indicating that physical activity prior to and during early pregnancy does not significantly reduce risk of hypertensive disorders of pregnancy.
    Hypertension in pregnancy. 08/2014;
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    ABSTRACT: Abstract Background: Previous studies have suggested that violence victimization is prevalent among women with premenstrual syndrome (PMS). However, it is unclear whether early life abuse contributes directly to PMS or whether associations are explained by the high prevalence of PMS risk factors including smoking and obesity among women reporting childhood abuse. Methods: We have assessed the relation of early life abuse and the incidence of moderate-to-severe PMS in a study nested within the prospective Nurses' Health Study 2. Participants were aged 27-44 years and free from PMS at baseline, including 1,018 cases developing PMS over 14 years and 2,277 comparison women experiencing minimal menstrual symptoms. History of early life emotional, physical, and sexual abuse was self-reported in 2001. Results: After adjustment for obesity, smoking, and other factors, emotional abuse was strongly related to PMS (pTrend<0.0001); women reporting the highest level of emotional abuse had 2.6 times the risk of PMS as those reporting no emotional abuse (95% confidence interval, 1.7-3.9). Women reporting severe childhood physical abuse had an odds ratio of 2.1 (95% confidence interval, 1.5-2.9; pTrend<0.001) compared with those reporting no physical abuse. Sexual abuse was less strongly associated with risk. Adjustment for childhood social support minimally affected findings. Conclusions: Findings from this large prospective study suggest that early life emotional and physical abuse increase the risk of PMS in the middle-to-late reproductive years. The persistence of associations after control for potential confounders and mediators supports the hypothesis that early life abuse is importantly related to PMS.
    Journal of women's health (2002). 08/2014;
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    ABSTRACT: Background: We aimed to determine the association between self-reported birth weight and incident cancer in the Women's Health Initiative Observational Study cohort, a large multiethnic cohort of postmenopausal women. Methods: 65,850 women reported their birth weight by category (<6lbs, 6-7lbs 15oz, 8-9lbs 15oz, and ≥10lbs). All self-reported, incident cancers were adjudicated by study staff. We used Cox proportional hazards regression to estimate crude and adjusted hazard ratios (aHR) for associations between birth weight and: (1) all cancer sites combined, (2) gynecologic cancers, and (3) several site-specific cancer sites. Results: After adjustments, birth weight was positively associated with the risk of lung cancer (p=0.01), and colon cancer (p=0.04). An inverse trend was observed between birth weight and risk for leukemia (p=0.04). A significant trend was not observed with breast cancer risk (p=0.67); however, women born weighing ≥10lbs were less likely to develop breast cancer compared to women born between 6lbs-7lbs 15oz (aHR 0.77, 95% CI 0.63, 0.94). Conclusion: Birth weight category appears to be significantly associated with the risk of any postmenopausal incident cancer, though the direction of the association varies by cancer type.
    Cancer Epidemiology 08/2014; · 4.33 Impact Factor
  • Chrisandra L Shufelt, JoAnn E Manson
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    ABSTRACT: The 2013 American College of Cardiology/American Heart Association guidelines on the treatment of cholesterol recommend therapy for patients with 1) known cardiovascular disease (CVD); 2) low-density lipoprotein cholesterol (LDL-C) of 190 mg/dL or higher; 3) type 1 or type 2 diabetes mellitus and LDL-C between 70 mg/dL and 189 mg/dL (for ages 40-75); and 4) LDL-C between 70 mg/dL and 189 mg/dL and an estimated 10-year cardiovascular risk ≥7.5% (for ages 40-75), using their new risk calculator. Although statin therapy is indicated for women at elevated risk of CVD, safety concerns related to glucose elevations and myalgias may outweigh benefits for women at low absolute risk of CVD.
    Menopause (New York, N.Y.) 08/2014; 21(8):896-898. · 3.08 Impact Factor
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    ABSTRACT: Whether menopausal hormone therapy (MHT) protects against cardiovascular disease (CVD) remains unclear.
    Annals of internal medicine 07/2014; · 13.98 Impact Factor
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    ABSTRACT: Poor diet quality is thought to be a leading risk factor for years of life lost. We examined how scores on 4 commonly used diet quality indices-the Healthy Eating Index 2010 (HEI), the Alternative Healthy Eating Index 2010 (AHEI), the Alternate Mediterranean Diet (aMED), and the Dietary Approaches to Stop Hypertension (DASH)-are related to the risks of death from all causes, cardiovascular disease (CVD), and cancer among postmenopausal women. Our prospective cohort study included 63,805 participants in the Women's Health Initiative Observational Study (from 1993-2010) who completed a food frequency questionnaire at enrollment. Cox proportional hazards models were fit using person-years as the underlying time metric. We estimated multivariate hazard ratios and 95% confidence intervals for death associated with increasing quintiles of diet quality index scores. During 12.9 years of follow-up, 5,692 deaths occurred, including 1,483 from CVD and 2,384 from cancer. Across indices and after adjustment for multiple covariates, having better diet quality (as assessed by HEI, AHEI, aMED, and DASH scores) was associated with statistically significant 18%-26% lower all-cause and CVD mortality risk. Higher HEI, aMED, and DASH (but not AHEI) scores were associated with a statistically significant 20%-23% lower risk of cancer death. These results suggest that postmenopausal women consuming a diet in line with a priori diet quality indices have a lower risk of death from chronic disease.
    American journal of epidemiology. 07/2014;
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    ABSTRACT: Total energy consumption and activity-related energy expenditure (AREE) estimates that have been calibrated using biomarkers to correct for measurement error were simultaneously associated with the risks of cardiovascular disease, cancer, and diabetes among postmenopausal women who were enrolled in the Women's Health Initiative at 40 US clinical centers and followed from 1994 to the present. Calibrated energy consumption was found to be positively related, and AREE inversely related, to the risks of various cardiovascular diseases, cancers, and diabetes. These associations were not evident in most corresponding analyses that did not correct for measurement error. However, an important analytical caveat relates to the role of body mass index (BMI) (weight (kg)/height (m)(2)). In the calibrated variable analyses, BMI was regarded, along with self-reported data, as a source of information on energy consumption and physical activity, and BMI was otherwise excluded from the disease risk models. This approach cannot be fully justified with available data, and the analyses herein imply a need for improved dietary and physical activity assessment methods and for longitudinal self-reported and biomarker data to test and relax modeling assumptions. Estimated hazard ratios for 20% increases in total energy consumption and AREE, respectively, were as follows: 1.49 (95% confidence interval: 1.18, 1.88) and 0.80 (95% confidence interval: 0.69, 0.92) for total cardiovascular disease; 1.43 (95% confidence interval: 1.17, 1.73) and 0.84 (95% confidence interval: 0.73, 0.96) for total invasive cancer; and 4.17 (95% confidence interval: 2.68, 6.49) and 0.60 (95% confidence interval: 0.44, 0.83) for diabetes.
    American journal of epidemiology. 07/2014;
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    ABSTRACT: Recent posttrial analysis of a completed randomized trial found an increased risk of prostate cancer among healthy men taking high-dose vitamin E supplements. Trials that examined the effect of vitamin C supplements on cancer risk are few.OBJECTIVE: We examined whether vitamin E or vitamin C supplementation affects the risk of cancer events during posttrial follow-up of the Physicians' Health Study II.DESIGN: Beginning in 1997, a total of 14,641 US male physicians aged ≥50 y were randomly assigned to receive 400 IU of vitamin E every other day, 500 mg of vitamin C daily, or their respective placebos. The vitamin E and vitamin C treatment ended in 2007, and observational follow-up continued through June 2011.RESULTS: This study included an additional 356 cases of incident prostate cancer and 771 total cancers that developed during a mean (maximum) of 2.8 (3.8) y of posttrial observation. During an overall mean of 10.3 (13.8) y, there were a total of 1373 incident prostate cancers and 2669 total cancers documented. In comparison with placebo, vitamin E supplementation had no effect on the incidence of prostate cancer (HR: 0.99; 95% CI: 0.89, 1.10) or total cancers (HR: 1.02; 95% CI: 0.95, 1.10). There was also no effect of vitamin C supplementation on total cancers (HR: 1.02; 95% CI: 0.94, 1.10) or incident prostate cancer (HR: 1.03; 95% CI: 0.93, 1.15). Neither vitamin E nor vitamin C supplementation had effects on other site-specific cancers overall. Stratification by known cancer risk factors, history of cancer, other randomized treatment, and follow-up time showed no significant interactions.Conclusion: In this large-scale randomized trial in men, vitamin E and C supplementation had no immediate or long-term effects on the risk of total cancers, prostate cancer, or other site-specific cancers. This trial was registered at clinicaltrials.gov as NCT00270647.
    American Journal of Clinical Nutrition 07/2014; · 6.50 Impact Factor

Publication Stats

43k Citations
7,026.34 Total Impact Points

Institutions

  • 2012–2014
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
    • Brown University
      • Department of Epidemiology
      Providence, RI, United States
    • University of Southern California
      • Department of Preventive Medicine
      Los Angeles, CA, United States
    • Medical College of Wisconsin
      • Department of Psychiatry and Behavioral Medicine
      Milwaukee, WI, United States
    • Columbia University
      New York City, New York, United States
    • University of Massachusetts Medical School
      • Division of Preventive and Behavioral Medicine
      Worcester, MA, United States
  • 1999–2014
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, Massachusetts, United States
  • 1997–2014
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • University of Alabama at Birmingham
      • Department of Epidemiology
      Birmingham, AL, United States
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States
  • 2011–2013
    • Stanford University
      • • Department of Medicine
      • • Department of Dermatology
      Palo Alto, CA, United States
    • University of California, San Francisco
      • Department of Obstetrics, Gynecology and Reproductive Sciences
      San Francisco, CA, United States
    • Washington Hospital Center
      Washington, Washington, D.C., United States
    • Pennsylvania State University
      • Department of Nutritional Sciences
      University Park, MD, United States
    • Rutgers, The State University of New Jersey
      • Department of Nutritional Sciences
      New Brunswick, NJ, United States
  • 2007–2013
    • National Heart, Lung, and Blood Institute
      Maryland, United States
    • Isfahan University of Medical Sciences
      • Epidemiology and Biostatistics Department
      Eşfahān, Ostan-e Esfahan, Iran
  • 2005–2013
    • University of Pittsburgh
      • • Department of Epidemiology
      • • Division of General Internal Medicine
      • • Department of Medicine
      Pittsburgh, Pennsylvania, United States
    • Hennepin County Medical Center
      Minneapolis, Minnesota, United States
  • 2011–2012
    • Alpert Medical School - Brown University
      Providence, Rhode Island, United States
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
  • 2008–2012
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, NY, United States
    • Northwestern University
      • Feinberg School of Medicine
      Evanston, IL, United States
    • University of East Anglia
      • Norwich Medical School
      Norwich, England, United Kingdom
    • University of North Carolina at Chapel Hill
      • Department of Epidemiology
      Chapel Hill, NC, United States
    • The University of Tennessee Health Science Center
      • Department of Preventive Medicine
      Memphis, TN, United States
    • Thomas Jefferson University
      Philadelphia, Pennsylvania, United States
  • 2007–2012
    • CSU Mentor
      Long Beach, California, United States
  • 2005–2012
    • University of Massachusetts Amherst
      • • Division of Biostatistics and Epidemiology
      • • Department of Public Health
      Amherst Center, MA, United States
    • University of California, Los Angeles
      • • Department of Medicine
      • • Department of Epidemiology
      Los Angeles, CA, United States
  • 2003–2012
    • Fred Hutchinson Cancer Research Center
      • Division of Public Health Sciences
      Seattle, WA, United States
    • Boston Children's Hospital
      Boston, Massachusetts, United States
    • Vancouver General Hospital
      Vancouver, British Columbia, Canada
  • 2002–2012
    • Harvard University
      • • Department of Nutrition
      • • Department of Epidemiology
      Cambridge, Massachusetts, United States
    • University of Zurich
      • Internal Medicine Unit
      Zürich, ZH, Switzerland
  • 2009–2011
    • Drexel University
      • Department of Epidemiology and Biostatistics
      Philadelphia, PA, United States
  • 2004–2011
    • University of California, San Diego
      • Department of Family and Preventive Medicine
      San Diego, California, United States
  • 2002–2011
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 2010
    • Kaiser Permanente
      Oakland, California, United States
    • University of Virginia
      • Division of Endocrinology and Metabolism
      Charlottesville, VA, United States
    • Harbor-UCLA Medical Center
      Torrance, California, United States
  • 2009–2010
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      Torrance, California, United States
  • 2007–2010
    • George Washington University
      • Department of Medicine
      Washington, Washington, D.C., United States
  • 2006–2010
    • Tufts Medical Center
      • Division of Endocrinology, Diabetes and Metabolism
      Boston, Massachusetts, United States
    • University at Buffalo, The State University of New York
      • Department of Social and Preventive Medicine
      Buffalo, NY, United States
    • Ben-Gurion University of the Negev
      Be'er Sheva`, Southern District, Israel
  • 2008–2009
    • John Wayne Cancer Institute
      Santa Monica, California, United States
  • 2004–2009
    • Massachusetts General Hospital
      • • Reproductive Endocrine Unit
      • • Department of Medicine
      Boston, MA, United States
    • Simmons College
      Boston, Massachusetts, United States
  • 2003–2009
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States
  • 2005–2008
    • Beth Israel Deaconess Medical Center
      • • Division of Endocrinology, Diabetes and Metabolism
      • • Department of Medicine
      Boston, Massachusetts, United States
    • German Institute of Human Nutrition
      • Department of Epidemiology
      Potsdam, Brandenburg, Germany
  • 2005–2006
    • MedStar Health Research Institute
      Maryland, United States