JoAnn E Manson

Harvard University, Cambridge, Massachusetts, United States

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Publications (867)9660.7 Total impact

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    ABSTRACT: The first epigenome-wide association study of body-mass index (BMI) identified DNA methylation at a HIF3A locus associated with BMI. We tested the hypothesis that DNA methylation variants might be associated with BMI according to intake of B vitamins. We analyzed the interaction between DNA methylation variants and B vitamins intake on 10-year change in BMI in two large cohorts. We found significant interactions between the DNA methylation-associated HIF3A SNP rs3826795 and intake of B vitamins on 10-year changes in BMI. The association between rs3826795 and BMI changes consistently increased across the tertiles of total vitamin B2 and B12 intake (all P for interaction <0.01). The differences in the BMI changes per increment of minor allele were -0.10 (SE 0.06), -0.01 (SE 0.06), and 0.12 (SE 0.07) within subgroups defined by increasing tertiles of total vitamin B2 intake; and were -0.10 (SE 0.06), -0.01 (SE 0.06), and 0.10 (SE 0.07) within subgroups defined by increasing tertiles of total vitamin B12 intake. In two independent cohorts, a DNA methylation variant in HIF3A was associated with BMI changes through interactions with total or supplemental vitamin B2, vitamin B12 and folate. These findings suggest a potential causal relation between DNA methylation and adiposity. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 05/2015; DOI:10.2337/db15-0264 · 8.47 Impact Factor
  • Frank B Hu, Ambika Satija, JoAnn E Manson
    JAMA The Journal of the American Medical Association 05/2015; DOI:10.1001/jama.2015.5287 · 30.39 Impact Factor
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    ABSTRACT: Adiponectin, an adipocyte-secreted hormone, has insulin-sensitizing characteristics. It remains unclear whether adiponectin may influence colorectal cancer development. To determine whether prediagnostic levels of adiponectin were associated with risk of incident colorectal cancer in the Women's Health Study, we conducted a nested case-control study of 275 colorectal cancer cases and 275 matched controls. Each case was matched to a control by age, ethnicity, fasting status at the time of blood collection, time of day when blood was drawn, and month of blood draw. Multivariable logistic regression with adjustment for colorectal cancer risk factors was used to estimate the odds ratio (OR) and 95 % confidence interval (CI) for risk of colorectal cancer incidence and mortality by adiponectin quartiles based on the control distribution. Median plasma adiponectin level was similar in cases versus controls (6.00 vs. 6.24 μg/mL). In multivariable-adjusted logistic regression models, high plasma adiponectin levels were not significantly associated with risk of colorectal cancer [quartile 4 (Q4) vs. quartile 1 (Q1): OR (95 % CI) 0.86 (0.48-1.56), p trend = 0.63]. These results suggest no appreciable association between plasma adiponectin and risk of colorectal cancer in women. Confirmation of these observations in larger studies is needed.
    Cancer Causes and Control 05/2015; DOI:10.1007/s10552-015-0590-8 · 2.96 Impact Factor
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    ABSTRACT: To examine the effect of an individually tailored, motivationally matched prenatal exercise intervention on gestational diabetes mellitus (GDM) and other measures of glucose intolerance among ethnically diverse prenatal care patients at increased risk for GDM. The Behaviors Affecting Baby and You study randomized eligible women at a mean (standard deviation) of 18.2 (4.1) weeks of gestation to a 12-week individually tailored, motivationally matched exercise intervention or a comparison health and wellness intervention. The goal of the exercise intervention was to achieve the American College of Obstetricians and Gynecologists' guidelines for physical activity during pregnancy. Diagnosis of GDM, impaired glucose tolerance, abnormal glucose screen, and screening glucose values (mg/dL) were abstracted from medical records. A sample size of 352 women (176 per group) was planned to have 80% power to detect reductions in risk of 35% or larger. From July 2007 to December 2012, a total of 251 (86.5%) women completed the intervention; n=124 and 127 in the exercise and comparison interventions, respectively. Based on an intention-to-treat analysis, no statistically significant differences between the intervention groups were observed; the relative odds of GDM in the exercise group was 0.61 (95% confidence interval [CI] 0.28-1.32) as compared with the health and wellness comparison group. Odds ratios for impaired glucose tolerance and abnormal glucose screen were 0.68 (95% CI 0.35-1.34) and 0.86 (95% CI 0.51-1.47), respectively. The intervention had no effect on birth outcomes. In this randomized trial among ethnically diverse pregnant women at increased risk for GDM, we found that a prenatal exercise intervention implemented in the second trimester did not result in a statistically significant reduction in relative odds for GDM, impaired glucose tolerance, or abnormal glucose screen.,, NCT00728377. I.
    Obstetrics and Gynecology 05/2015; 125(5):1195-1204. DOI:10.1097/AOG.0000000000000738 · 4.37 Impact Factor
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    ABSTRACT: Fruit, vegetable, and dietary fiber intake have been associated with lower risk of cardiovascular disease (CVD); however, little is known about their role in obesity prevention. Our goal was to investigate whether intake of fruits, vegetables, and dietary fiber is associated with weight change and the risk of becoming overweight and obese. We studied 18,146 women aged ≥45 y from the Women's Health Study free of CVD and cancer with an initial body mass index (BMI) of 18.5 to <25 kg/m(2). Fruit, vegetable, and dietary fiber intakes were assessed at baseline through a 131-item food-frequency questionnaire, along with obesity-related risk factors. Women self-reported body weight on annual questionnaires. During a mean follow-up of 15.9 y, 8125 women became overweight or obese (BMI ≥25 kg/m(2)). Intakes of total fruits and vegetables, fruits, and dietary fiber were not associated with the longitudinal changes in body weight, whereas higher vegetable intake was associated with greater weight gain (P-trend: 0.02). In multivariable analyses, controlling for total energy intake and physical activity along with other lifestyle, clinical, and dietary factors, women in the highest vs. lowest quintile of fruit intake had an HR of 0.87 (95% CI: 0.80, 0.94; P-trend: 0.01) of becoming overweight or obese. No association was observed for vegetable or dietary fiber intake. The association between fruit intake and risk of becoming overweight or obese was modified by baseline BMI (P-interaction: <0.0001) where the strongest inverse association was observed among women with a BMI <23 kg/m(2) (HR: 0.82; 95% CI: 0.71, 0.94). Our results suggest that greater baseline intake of fruit, but not vegetables or fiber, by middle-aged and older women with a normal BMI at baseline is associated with lower risk of becoming overweight or obese. © 2015 American Society for Nutrition.
    Journal of Nutrition 05/2015; 145(5):960-8. DOI:10.3945/jn.114.199158 · 4.23 Impact Factor
  • Cancer Research 05/2015; 75(9 Supplement):P6-10-04-P6-10-04. DOI:10.1158/1538-7445.SABCS14-P6-10-04 · 9.28 Impact Factor
  • Aruna D Pradhan, JoAnn E Manson
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    ABSTRACT: Despite continued appreciation of the potential role of vitamin D and omega-3 fatty acids in the prevention of cancer and cardiovascular disease (CVD), there remain no completed large-scale, randomized trials of these agents for the primary prevention of cancer or CVD in a population that has not been selected on the basis of elevated risk. The vitamin D and omega-3 trial (VITAL) is a 2×2 factorial randomized, double-blind, placebo-controlled trial of the benefits and risks of vitamin D (vitamin D3 [cholecalciferol], 2000IU/d) and marine omega-3 fatty acids (Omacor(®) fish oil, a 1g/d) in the primary prevention of cancer and CVD among 25,875 men and women, aged ≥50 and ≥55 years, respectively. Randomization began in November 2011 and was completed in March 2014. This report will describe the rationale for the trial and currently available randomized trial data, summarize related ongoing large-scale trials, and provide a brief overview of study design, and an update on randomization milestones, racial/ethnic diversity, biorepository activities, in-depth phenotyping of a subcohort, and ancillary studies. Copyright © 2015. Published by Elsevier Ltd.
    The Journal of steroid biochemistry and molecular biology 04/2015; DOI:10.1016/j.jsbmb.2015.04.006 · 4.05 Impact Factor
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    ABSTRACT: Abdominal obesity is a major risk factor for type 2 diabetes (T2D). We aimed to examine the association between the genetic predisposition to central obesity, assessed by the waist-to-hip ratio (WHR) genetic score, and T2D risk. The current study included 2,591 participants with T2D and 3,052 participants without T2D of European ancestry from the Nurses' Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). Genetic predisposition to central obesity was estimated using a genetic score based on 14 established loci for the WHR. We found that the central obesity genetic score was linearly related to higher T2D risk. Results were similar in the NHS (women) and HPFS (men). In combined results, each point of the central obesity genetic score was associated with an odds ratio (OR) of 1.04 (95% CI, 1.01-1.07) for developing T2D, and the OR was 1.24 (1.03-1.45) when comparing extreme quartiles of the genetic score after multivariate adjustment. The data indicate that genetic predisposition to central obesity is associated with higher T2D risk. This association is mediated by central obesity. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes care 04/2015; DOI:10.2337/dc14-3084 · 8.57 Impact Factor
  • Andrew M Kaunitz, JoAnn E Manson
    Menopause (New York, N.Y.) 04/2015; DOI:10.1097/GME.0000000000000457 · 2.81 Impact Factor
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    ABSTRACT: Results from the Women's Health Initiative (WHI) clinical trials (CT) demonstrated no increase in the risk of lung cancer in postmenopausal women treated with hormone therapy. We conducted a joint analysis of the WHI observational study data and CT data to further explore the association between estrogen and estrogen-related reproductive factors and lung cancer risk. Reproductive history, oral contraceptive (OC) use, and postmenopausal hormone therapy (HT) was evaluated in 160,855 women with known HT exposures. Follow-up for lung cancer was through September 17, 2012; 2,467 incident lung cancer cases were ascertained, with median follow-up of 14 years. For all lung cancers, women with previous use of estrogen plus progestin of < 5 years (HR=0.84; 95% CI 0.71-0.99) were at reduced risk. A limited number of reproductive factors demonstrated associations with risk. There was a trend towards decreased risk with increasing age at menopause (ptrend=0.04) and a trend towards increased risk with increasing number of live births (ptrend=0.03). Reduced risk of non-small cell lung cancer was associated with age 20-29 at first live birth. Risk estimates varied with smoking history, years of HT use and previous bilateral oophorectomy. Indirect measures of estrogen exposure to lung tissue, as used in this study, provide only weak evidence for an association between reproductive history or HT use and risk of lung cancer. More detailed mechanistic studies and evaluation of risk factors in conjunction with ER expression in the lung should continue as a role for estrogen can't be ruled out and may hold potential for prevention and treatment strategies.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 04/2015; DOI:10.1097/JTO.0000000000000558 · 5.80 Impact Factor
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    ABSTRACT: ω3 and ω6 fatty acids (FA) may have divergent effects on the development of obesity. We examined the association of baseline erythrocyte ω3 and ω6 FA composition with body weight change and the risk of becoming overweight or obese in the Women's Health Study (WHS) participants. We identified 534 women who had baseline erythrocyte FA measured and a baseline body mass index (BMI) of 18.5-<25 kg/m(2). Body weight was updated at a total of six time points during follow-up. Weight gain during a mean of 10.4-year follow-up increased with increasing quartiles of baseline erythrocyte cis ω6 FA, ω6/ω3 ratio, and trans FA while decreased with increasing cis ω3 FA. After multivariable adjustment including total energy intake and physical activity, the weight gain (kg) in the highest versus the lowest quartile was 3.08 versus 2.32 for erythrocyte cis ω6 FA (p trend 0.04), 2.07 versus 2.92 for cis ω3 FA (p trend 0.08), 2.93 versus 2.05 for ω6/ω3 ratio (p trend 0.046), and 3.03 versus 2.27 for trans FA (p trend 0.06). Among individual FA, the associations were significant for 18:2ω6, 18:3ω6, and trans 18:1 and marginally significant for 20:3ω6 and trans 18:2. The risk of becoming overweight or obese (defined as BMI ≥25 kg/m(2) at any follow-up time point) increased across increasing ω6/ω3 ratio (multivariable model p trend 0.04). In this prospective study, we found suggestive evidence that erythrocyte cis ω6 FA may be positively associated, and cis ω3 FA inversely associated with weight gain in initially normal-weight women.
    European Journal of Nutrition 03/2015; DOI:10.1007/s00394-015-0889-y · 3.84 Impact Factor
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    ABSTRACT: Observational data on the association between circulating 25(OH)D and colorectal cancer risk are limited in women. To determine whether prediagnostic levels of 25(OH)D were associated with risk of incident colorectal cancer in the Women's Health Study (WHS), we conducted a nested case-control study using 274 colorectal cases and 274 controls. Each case was matched to a control by age, ethnicity, fasting status at the time of blood collection, time of day when blood was drawn, and month of blood draw. Conditional logistic regression was used to estimate the odds ratio (OR) and 95% confidence interval (CI) for colorectal cancer by 25(OH)D quartiles. Mean plasma 25(OH)D was lower in cases versus controls (21.9 vs 23.9 ng/mL, p=0.01). In multivariable-adjusted logistic regression models, plasma 25(OH)D was significantly and inversely associated with odds of colorectal cancer (quartile 4 [Q4] versus quartile 1 [Q1]: OR (95% CI): 0.45 (0.25-0.81), ptrend 0.02). Additionally, we observed a somewhat lower risk of colorectal cancer mortality after adjustment for matching variables, randomization treatment and other risk factors (Q4:Q1 OR[95%CI]: 0.40(0.17-0.97); ptrend 0.05). In this cohort of healthy women, we found a significant inverse association between prediagnostic 25(OH)D levels and risk of incident colorectal cancer, and a borderline significant inverse association between prediagnostic 25(OH)D levels and colorectal cancer mortality. These results support a possible association between plasma 25(OH)D and risk of colorectal cancer in women. Received December 29, 2014. Revision received March 17, 2015. Accepted March 23, 2015.
    Cancer Prevention Research 03/2015; DOI:10.1158/1940-6207.CAPR-14-0470 · 5.27 Impact Factor
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    ABSTRACT: We hypothesized that higher concentrations of LDL particles (LDL-P) and leptin, and lower concentrations of HDL particles (HDL-P), and total and high molecular weight (HMW) adiponectin, would predict incident coronary heart disease (CHD) among severely obese postmenopausal women. In a case-cohort study nested in the Women's Health Initiative Observational Study, we sampled 677 of the 1852 white or black women with body mass index (BMI) ≥40 kg/m(2) and no prevalent cardiovascular disease (CVD), including all 124 cases of incident CHD over mean 5.0 year follow-up. Biomarkers were assayed on stored blood samples. In multivariable-adjusted weighted Cox models, higher baseline levels of total and small LDL-P, and lower levels of total and medium HDL-P, and smaller mean HDL-P size were significantly associated with incident CHD. In contrast, large HDL-P levels were inversely associated with CHD only for women without diabetes, and higher total and HMW adiponectin levels and lower leptin levels were associated with CHD only for women with diabetes. Higher total LDL-P and lower HDL-P were associated with CHD risk independently of confounders including CV risk factors and other lipoprotein measures, with adjusted HR (95%CIs) of 1.55(1.28, 1.88) and (0.70 (0.57, 0.85), respectively, and similar results for medium HDL-P. Higher CHD risk among severely obese postmenopausal women is strongly associated with modifiable concentrations of LDL-P and HDL-P, independent of diabetes, smoking, hypertension, physical activity, BMI and waist circumference. Severely obese postmenopausal women should be considered high risk candidates for lipid lowering therapy.
    03/2015; 120. DOI:10.1016/j.bbacli.2015.03.005
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    ABSTRACT: We examined whether circulating concentrations of sex hormones, including estradiol, testosterone, sex hormone-binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEAS), were associated with alcohol intake or mediated the alcohol-type 2 diabetes (T2D) association. Among women not using hormone replacement therapy and free of baseline cardiovascular disease, cancer, and diabetes in the Women's Health Study, 359 incident cases of T2D and 359 matched controls were chosen during 10 years of follow-up. Frequent alcohol intake (≥1 drink/day) was positively and significantly associated with higher plasma estradiol concentrations in an age-adjusted model (β = 0.14, 95% confidence interval [CI], 0.03, 0.26), compared to rarely/never alcohol intake. After adjusting for additional known covariates, this alcohol-estradiol association remained significant (β = 0.19, 95% CI, 0.07, 0.30). Testosterone (β = 0.13, 95% CI, -0.05, 0.31), SHBG (β = 0.07, 95% CI, -0.07, 0.20), and DHEAS (β = 0.14, 95% CI, -0.04, 0.31) showed positive associations without statistical significance. Estradiol alone or in combination with SHBG appeared to influence the observed protective association between frequent alcohol consumption and T2D risk, with a 12%-21% reduction in odds ratio in the multivariate-adjusted models. Our cross-sectional analysis showed positive associations between alcohol intake and endogenous estradiol concentrations. Our prospective data suggested that baseline concentrations of estradiol, with or without SHBG, might influence the alcohol-T2D association in postmenopausal women.
    Journal of the American College of Nutrition 03/2015; DOI:10.1080/07315724.2014.926163 · 1.68 Impact Factor
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    ABSTRACT: Inflammation may be important in endometrial cancer development. Long-chain ω-3 (n-3) polyunsaturated fatty acids (LCω-3PUFAs) may reduce inflammation and, therefore, reduce cancer risk. Because body mass is associated with both inflammation and endometrial cancer risk, it may modify the association of fat intake on risk. We examined whether intakes of LCω-3PUFAs were associated with endometrial cancer risk overall and stratified by body size and histologic subtype. Women were n = 87,360 participants of the Women's Health Initiative Observational Study and Clinical Trials who were aged 50-79 y, had an intact uterus, and completed a baseline food-frequency questionnaire. After 13 y of follow-up, n = 1253 incident invasive endometrial cancers were identified. Cox regression models were used to estimate HRs and 95% CIs for the association of intakes of individual ω-3 fatty acids and fish with endometrial cancer risk. Intakes of individual LCω-3PUFAs were associated with 15-23% linear reductions in endometrial cancer risk. In women with body mass index (BMI; in kg/m(2)) <25, those in the upper compared with lowest quintiles of total LCω-3PUFA intake (sum of eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids) had significantly reduced endometrial cancer risk (HR: 0.59; 95% CI: 0.40, 0.82; P-trend = 0.001), whereas there was little evidence of an association in overweight or obese women. The reduction in risk observed in normal-weight women was further specific to type I cancers.Conclusions: Long-chain ω-3 intake was associated with reduced endometrial cancer risk only in normal-weight women. Additional studies that used biomarkers of ω-3 intake are needed to more-accurately estimate their effects on endometrial cancer risk. This trial was registered at as NCT00000611. © 2015 American Society for Nutrition.
    American Journal of Clinical Nutrition 03/2015; 101(4). DOI:10.3945/ajcn.114.098988 · 6.92 Impact Factor
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    ABSTRACT: To evaluate the association between statins and breast cancer stage and mortality in the Women's Health Initiative. The study population included 128,675 postmenopausal women aged 50-79 years, out of which there were 7,883 newly diagnosed cases of in situ (19 %), local (61 %)-, regional (19 %)- and distant (1 %)-stage breast cancer and 401 deaths due to breast cancer after an average of 11.5 (SD = 3.7) years of follow-up. Stage was coded using SEER criteria and was stratified into early (in situ and local)- versus late (regional and distant)-stage disease. Information on statins and other risk factors were collected by self- and interviewer-administered questionnaires. Cause of death was based on medical record review. Multivariable-adjusted hazards ratios (HR) and 95 % confidence intervals (CIs) evaluating the relationship between statin use (at baseline only and in a time-dependent manner) and diagnosis of late-stage breast cancer and breast cancer-specific mortality were computed from Cox proportional hazards analyses after adjusting for appropriate confounders. Statins were used by 10,474 women (8 %) at baseline. In the multivariable-adjusted time-dependent model, use of lipophilic statins was associated with a reduction in diagnosis of late-stage breast cancer (HR 0.80, 95 % CI 0.64-0.98, p = 0.035) which was also significant among women with estrogen receptor-positive disease (HR 0.72, 95 % CI 0.56-0.93, p = 0.012). Breast cancer mortality was marginally lower in statin users compared with nonusers (HR 0.59, 95 % CI 0.32-1.06, p = 0.075). Prior statin use is associated with lower breast cancer stage at diagnosis.
    Cancer Causes and Control 03/2015; 26(4). DOI:10.1007/s10552-015-0530-7 · 2.96 Impact Factor
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    ABSTRACT: Objectives To determine whether statin treatment is associated with increased risk of haemorrhagic stroke (HS) in older women. A secondary objective was to evaluate HS risk in users of combined statin and antiplatelet treatment. Design Observational study: secondary data analysis from the Women's Health Initiative (WHI) clinical trials. Setting Women were recruited from 40 participating sites. Participants Cohort of 68 132 women followed through 2005 (parent study) and for an additional 5 years in the extension study. Main outcome measures Statin use was assessed at baseline and at follow-up visits (1, 3, 6 and 9 years). Women brought medications in original containers for inventory. Strokes were ascertained semiannually and centrally adjudicated. Risk of HS by statin use (time-varying covariate, with the ‘no use’ category as the referent) was estimated from Cox proportional hazard regression models adjusted for age (model 1); risk factors for HS (model 2); and possible confounders by indication (model 3). Prespecified subgroup analyses were conducted by use of antiplatelet medications. Results Final models included 67 882 women (mean age, 63±7 years). Over a mean follow-up of 12 years, incidence rates of HS were 6.4/10 000 person-years among statin users and 5.0/10 000 person-years among non-users (p=0.11). The unadjusted risk of HS in statin users was 1.21 (CI 0.96 to 1.53); after adjusting for age and HS risk factors the HR was 0.98 (CI 0.76 to 1.26). Risk of HS was higher among women on statins and antiplatelet agents versus women on antiplatelet medications alone (HR=1.59; CI 1.03 to 2.47); p for interaction=0.011. Conclusions This retrospective analysis did not show an association between statin use and HS risk among older women. HS risk was higher among women taking statins with antiplatelet agents. These findings warrant further investigation, given potential implications for clinical decision-making.
    BMJ Open 02/2015; 5(2):e007075. DOI:10.1136/bmjopen-2014-007075 · 2.06 Impact Factor
  • JoAnn E Manson, Shari S Bassuk
    JAMA The Journal of the American Medical Association 02/2015; 313(13). DOI:10.1001/jama.2015.1353 · 30.39 Impact Factor
  • Gloria Richard-Davis, JoAnn E Manson
    JAMA Internal Medicine 02/2015; 175(4). DOI:10.1001/jamainternmed.2014.8099 · 13.25 Impact Factor
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    ABSTRACT: Objective To test the hypothesis that greater chocolate-candy intake is associated with more weight gain in postmenopausal women.MethodsA prospective cohort study involved 107,243 postmenopausal American women aged 50-79 years (mean = 60.7) at enrollment in the Women's Health Initiative, with 3-year follow-up. Chocolate-candy consumption was assessed by food frequency questionnaire, and body weight was measured. Linear mixed models, adjusted for demographic, socio economic, anthropomorphic, and behavioral variables, were used to test our main hypotheses.ResultsCompared with women who ate a 1 oz (∼28 g) serving of chocolate candy <1 per month, those who ate this amount 1 per month to <1 per week, 1 per week to < 3 per week and ≥3 per week showed greater 3-year prospective weight gains (kg) of 0.76 (95% CI: 0.66, 0.85), 0.95 (0.84, 1.06), and 1.40 (1.27, 1.53), respectively, (P for linear trend<0.0001). Each additional 1 oz/day was associated with a greater 3-year weight gain (kg) of 0.92 (0.80, 1.05). The weight gain in each chocolate-candy intake level increased as BMI increased above the normal range (18.5-25 kg/m2), and was inversely associated with age.Conclusions Greater chocolate-candy intake was associated with greater prospective weight gain in this cohort of postmenopausal women.
    Obesity 02/2015; 23(3). DOI:10.1002/oby.20983 · 4.39 Impact Factor

Publication Stats

72k Citations
9,660.70 Total Impact Points


  • 1994–2015
    • Harvard University
      • Department of Nutrition
      Cambridge, Massachusetts, United States
  • 1991–2015
    • Brigham and Women's Hospital
      • • Division of Preventive Medicine
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 1990–2015
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2014
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
  • 2013
    • University of Washington Seattle
      • Department of Medicine
      Seattle, Washington, United States
    • University of Alabama at Birmingham
      • Department of Epidemiology
      Birmingham, AL, United States
    • The Ohio State University
      Columbus, Ohio, United States
    • McGill University
      • Department of Oncology
      Montréal, Quebec, Canada
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      Torrance, California, United States
  • 2005–2013
    • University of Massachusetts Amherst
      • • Division of Biostatistics and Epidemiology
      • • Department of Public Health
      Amherst Center, Massachusetts, United States
    • German Institute of Human Nutrition
      • Department of Epidemiology
      Potsdam, Brandenburg, Germany
    • University of Pittsburgh
      • Division of General Internal Medicine
      Pittsburgh, PA, United States
  • 2012
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
  • 2011
    • HealthPartners Institute for Education and Research
      Bloomington, Minnesota, United States
    • University of California, San Francisco
      • Department of Obstetrics, Gynecology and Reproductive Sciences
      San Francisco, CA, United States
  • 2000–2011
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, New York, United States
    • University of Alaska Anchorage
      Anchorage, Alaska, United States
  • 2010
    • Medical University of South Carolina
      • Department of Medicine
      Charleston, South Carolina, United States
    • Kaiser Permanente
      Oakland, California, United States
  • 2009
    • John Wayne Cancer Institute
      Santa Monica, California, United States
  • 2005–2009
    • Partners HealthCare
      Boston, Massachusetts, United States
  • 2004–2009
    • Fred Hutchinson Cancer Research Center
      • Division of Public Health Sciences
      Seattle, WA, United States
    • Wake Forest School of Medicine
      • Division of Public Health Sciences
      Winston-Salem, North Carolina, United States
  • 2000–2009
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States
  • 2008
    • University of East Anglia
      • Norwich Medical School
      Norwich, England, United Kingdom
    • Northwestern University
      • Feinberg School of Medicine
      Evanston, IL, United States
  • 2005–2008
    • Beth Israel Deaconess Medical Center
      • Division of Endocrinology, Diabetes and Metabolism
      Boston, Massachusetts, United States
  • 2007
    • University of California, Los Angeles
      • Department of Epidemiology
      Los Angeles, CA, United States
  • 2006–2007
    • George Washington University
      • Department of Medicine
      Washington, Washington, D.C., United States
    • 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
  • 2005–2007
    • Florida Atlantic University
      • Department of Biomedical Science
      Boca Raton, Florida, United States
  • 2004–2006
    • Massachusetts General Hospital
      • Department of Medicine
      Boston, Massachusetts, United States
    • Columbia University
      New York, New York, United States
  • 2004–2005
    • University of California, San Diego
      • Department of Family and Preventive Medicine
      San Diego, CA, United States
    • Simmons College
      • Program in Nutrition and Dietetics
      Boston, Massachusetts, United States
  • 2003
    • University of Iowa
      Iowa City, Iowa, United States
    • Vancouver General Hospital
      Vancouver, British Columbia, Canada
    • Boston Children's Hospital
      Boston, Massachusetts, United States
  • 2002
    • University of Zurich
      • Internal Medicine Unit
      Zürich, ZH, Switzerland
    • Boston University
      Boston, Massachusetts, United States
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
  • 1996
    • William Penn University
      Filadelfia, Pennsylvania, United States