Rowan T Chlebowski

Torrance Memorial Medical Center, Torrance, California, United States

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Publications (337)3103.78 Total impact

  • Rowan T Chlebowski
    The Lancet Oncology 12/2014; · 25.12 Impact Factor
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    ABSTRACT: A body shape index (ABSI) has been proposed as a possible improvement over waist circumference (WC) as a marker of abdominal adiposity because it removes the correlation of WC with body mass index (BMI) and with height. We assessed the association of ABSI with four obesity-related cancers compared to that of other anthropometric measures of adiposity. We used data from the Women's Health Initiative, a large cohort of postmenopausal women, recruited between 1993 and 1998 and followed until September 2013, to assess the associations of ABSI and other anthropometric measures with risk of cancers of the breast, endometrium, colorectum, and kidney. The four comparison anthropometric measures were BMI, WC, waist circumference-to-height ratio (WHtR), and waist-hip ratio (WHR). Over a median of 12.7 years of follow-up, among 143,901 women, we identified 7,039 invasive breast cancers, 1,157 endometrial cancers, 1,908 colorectal cancers, and 376 kidney cancers. We used Cox proportional hazards models to estimate the association of quintiles of the five measures with risk of the four cancers. Unlike the other anthropometric indices, ABSI was not associated with increased risk of breast or endometrial cancer. BMI and WC were comparable as predictors of breast and endometrial cancer, and these associations were unchanged after mutual adjustment. For colorectal and kidney cancers, ABSI was a significant predictor comparable to BMI; however, WC showed the strongest association with colorectal cancer, and WC, WHtR, and WHR all showed stronger associations with kidney cancer. In contrast to other anthropometric measures, ABSI showed no association with risk of breast or endometrial cancer and was more weakly associated with risk of colorectal and kidney cancers compared to more established measures of central adiposity.
    Cancer causes & control : CCC. 11/2014;
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    ABSTRACT: Positive associations between dog ownership and physical activity in older adults have been previously reported. The objective of this study was to examine cross-sectional associations between dog ownership and physical activity measures in a well-characterized, diverse sample of postmenopausal women. Analyses included 36,984 dog owners (mean age: 61.5years), and 115,645 non-dog owners (mean age: 63.9years) enrolled in a clinical trial or the observational study of the Women's Health Initiative between 1993 and 1998. Logistic regression models were used to test for associations between dog ownership and physical activity, adjusted for potential confounders. Owning a dog was associated with a higher likelihood of walking ≥150min/wk (Odds Ratio, 1.14; 95% Confidence Interval, 1.10-1.17) and a lower likelihood of being sedentary ≥8h/day (Odds Ratio, 0.86; 95% Confidence Interval, 0.83-0.89) as compared to not owning a dog. However, dog owners were less likely to meet ≥7.5MET-h/wk of total physical activity as compared to non-dog owners (Odds Ratio, 1.03; 95% Confidence Interval, 1.00-1.07). Dog ownership is associated with increased physical activity in older women, particularly among women living alone. Health promotion efforts aimed at older adults should highlight the benefits of regular dog walking for both dog owners and non-dog owners. Copyright © 2014 Elsevier Inc. All rights reserved.
    Preventive medicine. 11/2014; 70C:33-38.
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    ABSTRACT: Lung cancer is the leading cause of worldwide cancer deaths. While smoking is its leading risk factor, few prospective cohort studies have reported on the association of lung cancer with both active and passive smoking. This study aimed to determine the relationship between lung cancer incidence with both active and passive smoking (childhood, adult at home, and at work).
    Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 10/2014;
  • Rowan T Chlebowski, Kathy Pan
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    ABSTRACT: To the Editor: In a planned subgroup analysis of the Tamoxifen and Exemestane Trial (TEXT) and the Suppression of Ovarian Function Trial (SOFT) reported by Pagani et al. (July 10 issue),(1) an interaction between human epidermal growth factor receptor 2 (HER2) status and treatment is shown (see Fig. S1 in the Supplementary Appendix, available with the full text of the article at NEJM.org), with apparently no benefit of exemestane plus ovarian suppression versus tamoxifen plus ovarian suppression in patients with HER2-positive tumors. This finding is unexpected considering that HER2 status is prognostic but not predictive of the efficacy of aromatase . . .
    New England Journal of Medicine 10/2014; 371(14):1357-1359. · 54.42 Impact Factor
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    ABSTRACT: Rates of obesity have increased significantly over the last three decades in the United States and globally. In addition to contributing to heart disease and diabetes, obesity is a major unrecognized risk factor for cancer. Obesity is associated with worsened prognosis after cancer diagnosis and also negatively affects the delivery of systemic therapy, contributes to morbidity of cancer treatment, and may raise the risk of second malignancies and comorbidities. Research shows that the time after a cancer diagnosis can serve as a teachable moment to motivate individuals to adopt risk-reducing behaviors. For this reason, the oncology care team-the providers with whom a patient has the closest relationships in the critical period after a cancer diagnosis-is in a unique position to help patients lose weight and make other healthy lifestyle changes. The American Society of Clinical Oncology is committed to reducing the impact of obesity on cancer and has established a multipronged initiative to accomplish this goal by 1) increasing education and awareness of the evidence linking obesity and cancer; 2) providing tools and resources to help oncology providers address obesity with their patients; 3) building and fostering a robust research agenda to better understand the pathophysiology of energy balance alterations, evaluate the impact of behavior change on cancer outcomes, and determine the best methods to help cancer survivors make effective and useful changes in lifestyle behaviors; and 4) advocating for policy and systems change to address societal factors contributing to obesity and improve access to weight management services for patients with cancer.
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 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;
  • Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 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
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    ABSTRACT: Background:A growing body of evidence suggests that diabetes is a risk factor for endometrial cancer incidence. However, most of these studies used case-control study designs and did not adjust for obesity, an established risk factor for endometrial cancer. In addition, few epidemiological studies have examined the association between diabetes treatment and endometrial cancer risk. The objective of this study was to assess the relationships among diabetes, diabetes treatment and endometrial cancer risk in postmenopausal women participating in the Women's Health Initiative (WHI).Methods:A total of 88 107 postmenopausal women aged 50-79 years who were free of cancer and had no hysterectomy at baseline were followed until date of endometrial cancer diagnosis, death, hysterectomy or loss to follow-up, whichever came first. Endometrial cancers were confirmed by central medical record and pathology report review. Multivariate Cox proportional hazards regression models were used to estimate hazard ratios (HRs) (95% confidence interval (CI)) for diagnosis of diabetes and metformin treatment as risk factors for endometrial cancer.Results:Over a mean of 11 years of follow-up, 1241 endometrial cancers developed. In the primary analysis that focused on prevalent diabetes at enrolment, compared with women without diabetes, women with self-reported diabetes, and the subset of women with treated diabetes, had significantly higher risk of endometrial cancer without adjusting for BMI (HR=1.44, 95% CI: 1.13-1.85 for diabetes, HR=1.57, 95% CI: 1.19-2.07 for treated diabetes). However after adjusting for BMI, the associations between diabetes, diabetes treatment, diabetes duration and the risk of endometrial cancer became non-significant. Elevated risk was noted when considering combining diabetes diagnosed at baseline and during follow-up as time-dependent exposure (HR=1.31, 95% CI: 1.08-1.59) even after adjusting for BMI. No significant association was observed between metformin use and endometrial cancer risk.Conclusions:Our results suggest that the relationship observed in previous research between diabetes and endometrial cancer incidence may be largely confounded by body weight, although some modest independent elevated risk remains.British Journal of Cancer advance online publication, 22 July 2014; doi:10.1038/bjc.2014.407 www.bjcancer.com.
    British journal of cancer. 07/2014;
  • Rowan T Chlebowski, Garnet L Anderson
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    ABSTRACT: Menopausal hormone therapy with estrogen plus progestin or estrogen alone (for women with prior hysterectomy) is still used by millions of women for climacteric symptom management throughout the world. Until 2002, hormone therapy influence on cancer risk and other chronic diseases was determined through observational study reports. Since then, results from the Women's Health Initiative randomized, placebo-controlled hormone therapy trials have substantially changed concepts regarding estrogen plus progestin and estrogen alone influence on the most common cancers in postmenopausal women. In these trials, estrogen plus progestin significantly increased breast cancer incidence and deaths from breast cancer, significantly increased deaths from lung cancer, significantly decreased endometrial cancer, and did not have a clinically significant influence on colorectal cancer. In contrast, estrogen alone use in women with prior hysterectomy significantly reduced breast cancer incidence and deaths from breast cancer without significant influence on colorectal cancer or lung cancer. These complex results are discussed in the context of known potential mediating mechanisms of action involved in interactionwith steroid hormone receptors.
    Steroids 06/2014; · 2.80 Impact Factor
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    ABSTRACT: The findings of the Women's Health Initiative (WHI) estrogen plus progestin (E+P) trial led to a substantial reduction in use of combined hormone therapy (cHT) among postmenopausal women in the United States. The economic effect of this shift has not been evaluated relative to the trial's $260 million cost (2012 U.S. dollars). To estimate the economic return from the WHI E+P trial. Decision model to simulate health outcomes for a "WHI scenario" with observed cHT use and a "no-WHI scenario" with cHT use extrapolated from the pretrial period. Primary analyses of WHI outcomes, peer-reviewed literature, and government sources. Postmenopausal women in the United States, aged 50 to 79 years, who did not have a hysterectomy. 2003 to 2012. Payer. Combined hormone therapy. Disease incidence, expenditure, quality-adjusted life-years, and net economic return. The WHI scenario resulted in 4.3 million fewer cHT users, 126 000 fewer breast cancer cases, 76 000 fewer cardiovascular disease cases, 263 000 more fractures, 145 000 more quality-adjusted life-years, and expenditure savings of $35.2 billion. The corresponding net economic return of the trial was $37.1 billion ($140 per dollar invested in the trial) at a willingness-to-pay level of $100 000 per quality-adjusted life-year. The 95% CI for the net economic return of the trial was $23.1 to $51.2 billion. No evaluation of indirect costs or outcomes beyond 2012. The WHI E+P trial made high-value use of public funds with a substantial return on investment. These results can contribute to discussions about the role of public funding for large, prospective trials with high potential for public health effects. National Heart, Lung, and Blood Institute.
    Annals of internal medicine 05/2014; 160(9):594-602. · 13.98 Impact Factor
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    ABSTRACT: Exemestane, a steroidal aromatase inhibitor, reduced invasive breast cancer incidence by 65% among 4,560 postmenopausal women randomly assigned to exemestane (25 mg per day) compared with placebo in the National Cancer Institute of Canada (NCIC) Clinical Trials Group MAP.3 (Mammary Prevention 3) trial, but effects on quality of life (QOL) were not fully described. Menopause-specific and health-related QOL were assessed by using the four Menopause-Specific Quality of Life Questionnaire (MENQOL) domains and the eight Medical Outcomes Study Short Form Health Survey (SF-36) scales at baseline, 6 months, and yearly thereafter. MENQOL questionnaire completion was high (88% to 98%) in both groups at each follow-up visit. Change scores for each MENQOL and SF-36 scale, calculated at each assessment time relative to baseline, were compared by using the Wilcoxon rank-sum test. Clinically important worsened QOL was defined as a MENQOL change score increase of more than 0.5 (of 8) points and an SF-36 change score decrease of more than 5 (of 100) points from baseline. Exemestane had small negative effects on women's self-reported vasomotor symptoms, sexual symptoms, and pain, which occurred mainly in the first 6 months to 2 years after random assignment. However, these changes represented only a small excess number of women being given exemestane with clinically important worsening of QOL at one time or another; specifically, 8% more in the vasomotor domain and 4% more each in the sexual domain and for pain. No other between-group differences were observed. Overall, slightly more women in the exemestane arm (32%) than in the placebo arm (28%) discontinued assigned treatment. Exemestane given for prevention has limited negative impact on menopause-specific and health-related QOL in healthy postmenopausal women at risk for breast cancer.
    Journal of Clinical Oncology 04/2014; · 18.04 Impact Factor
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    ABSTRACT: Background Ovarian cancer is often diagnosed at late stages and consequently the 5-year survival rate is only 44%. However, there is limited knowledge of the association of modifiable lifestyle factors, such as physical activity and obesity on mortality among women diagnosed with ovarian cancer. The purpose of our study was to prospectively investigate the association of (1) measured body mass index (BMI), and (2) self-reported physical activity with ovarian cancer-specific and all-cause mortality in postmenopausal women enrolled in the Women's Health Initiative (WHI). Methods Participants were 600 women diagnosed with primary ovarian cancer subsequent to enrollment in WHI. Exposure data, including measured height and weight and reported physical activity from recreation and walking, used in this analysis were ascertained at the baseline visit for the WHI. Cox proportional hazard regression was used to examine the associations between BMI, physical activity and mortality endpoints. Results Vigorous-intensity physical activity was associated with a 26% lower risk of ovarian cancer specific-mortality (HR = 0.74; 95% CI: 0.56–0.98) and a 24% lower risk of all-cause mortality (HR = 0.76; 95% CI: 0.58–0.98) compared to no vigorous-intensity physical activity. BMI was not associated with mortality. Conclusions Participating in vigorous-intensity physical activity, assessed prior to ovarian cancer diagnosis, appears to be associated with a lower risk of ovarian cancer mortality.
    Gynecologic Oncology 04/2014; 133(1):4–10. · 3.93 Impact Factor
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    ABSTRACT: Paradoxically, a breast cancer risk reduction with conjugated equine estrogens (CEE) and a risk elevation with CEE plus medroxyprogesterone acetate (CEE + MPA) were observed in the Women's Health Initiative (WHI) randomized controlled trials. The effects of hormone therapy on serum sex hormone levels, and on the association between baseline sex hormones and disease risk, may help explain these divergent breast cancer findings. Serum sex hormone concentrations were measured for 348 breast cancer cases in the CEE + MPA trial and for 235 cases in the CEE trial along with corresponding pair-matched controls, nested within the WHI trials of healthy postmenopausal women. Association and mediation analyses, to examine the extent to which sex hormone levels and changes can explain the breast cancer findings, were conducted using logistic regression. Following CEE treatment, breast cancer risk was associated with higher concentrations of baseline serum estrogens, and with lower concentrations of sex hormone binding globulin. However, following CEE + MPA, there was no association of breast cancer risk with baseline sex hormone levels. The sex hormone changes from baseline to year 1 provided an explanation for much of the reduced breast cancer risk with CEE. Specifically, the treatment odds ratio (95% confidence interval) increased from 0.71 (0.43, 1.15) to 0.92 (0.41, 2.09) when the year 1 measures were included in the logistic regression analysis. In comparison, the CEE + MPA odds ratio was essentially unchanged when these year 1 measures were included. Breast cancer risk remains low following CEE use among women having favorable baseline sex hormone profiles, but CEE + MPA evidently produces a breast cancer risk for all women similar to that for women having an unfavorable baseline sex hormone profile. These patterns could reflect breast ductal epithelial cell stimulation by CEE + MPA that is substantially avoided with CEE, in conjunction with relatively more favorable effects of either regimen following a sustained period of estrogen deprivation. These findings may have implications for other hormone therapy formulations and routes of delivery.Trial registration: clinicaltrials.gov identifier: NCT00000611.
    Breast cancer research: BCR 03/2014; 16(2):R30. · 5.87 Impact Factor
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    ABSTRACT: In vitro and animal data suggest cadmium, a heavy metal that contaminates some foods and tobacco plants, is an estrogenic endocrine disruptor. Elevated estrogen exposure is associated with breast, endometrial, and ovarian cancer risk. Examine the association between dietary cadmium intake and risk of these cancers in the large, well-characterized Women's Health Initiative (WHI). 155,069 postmenopausal women, age 50-79, enrolled in the WHI clinical trials or observational study participated in this study. We estimated dietary cadmium consumption by combining baseline food frequency questionnaire responses with US Food and Drug Administration data on food cadmium content. Participants reported incident invasive breast, endometrial, or ovarian cancer and WHI centrally adjudicated all cases through August 2009. We applied Cox regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) for each cancer, comparing quintiles of energy-adjusted dietary cadmium intake. Over an average of 10.5 years, 6,658 invasive breast cancers, 1,198 endometrial cancers, and 735 ovarian cancers were reported. We observed no statistically significant associations between dietary cadmium and risk of any of these cancers after adjustment for potential confounders including total dietary energy intake. Results did not differ in any sub-group of women examined. We found little evidence that dietary cadmium is a risk factor for breast, endometrial, or ovarian cancers in postmenopausal women. Misclassification in dietary cadmium assessment may have attenuated observed associations.
    Environmental Health Perspectives 03/2014; · 7.26 Impact Factor
  • Joann E Manson, Rowan T Chlebowski, Aaron K Aragaki
    JAMA The Journal of the American Medical Association 01/2014; 311(4):417-8. · 29.98 Impact Factor
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    ABSTRACT: Healthy lifestyle behaviors are recommended to reduce cancer risk and overall mortality. Adherence to cancer-preventive health behaviors and subsequent cancer risk has not been evaluated in a diverse sample of postmenopausal women. We examined the association between the American Cancer Society (ACS) Nutrition and Physical Activity Cancer Prevention Guidelines score and risk of incident cancer, cancer-specific mortality, and all-cause mortality in 65,838 postmenopausal women enrolled in the Women's Health Initiative Observational Study. ACS guidelines scores (0-8 points) were determined from a combined measure of diet, physical activity, body mass index (current and at age 18 years), and alcohol consumption. After a mean follow-up of 12.6 years, 8,632 incident cancers and 2,356 cancer deaths were identified. The highest ACS guidelines scores compared with the lowest were associated with a 17% lower risk of any cancer [HR, 0.83; 95% confidence interval (CI), 0.75-0.92], 22% lower risk of breast cancer (HR, 0.78; 95% CI, 0.67-0.92), 52% lower risk of colorectal cancer (HR, 0.48; 95% CI, 0.32-0.73), 27% lower risk of all-cause mortality, and 20% lower risk of cancer-specific mortality (HR, 0.80; 95% CI, 0.71-0.90). Associations with lower cancer incidence and mortality were generally strongest among Asian, black, and Hispanic women and weakest among non-Hispanic whites. Behaviors concordant with Nutrition and Physical Activity Cancer Prevention Guidelines were associated with lower risk of total, breast, and colorectal cancers and lower cancer-specific mortality in postmenopausal women. Cancer Prev Res; 7(1); 42-53. ©2014 AACR.
    Cancer Prevention Research 01/2014; 7(1):42-53. · 4.89 Impact Factor
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    ABSTRACT: In a recent article, Sarrel et al.(1) assert that estrogen avoidance since 2002 has caused tens of thousands of premature deaths among posthysterectomy women aged 50 to 59 years in the United States. They fault Women's Health Initiative (WHI) investigators for inadequate efforts to communicate the benefits of unopposed estrogen and to contrast (unopposed) estrogen findings from those for estrogen plus progestin in reporting on the WHI randomized controlled trials.(2-5) (Am J Public Health. Published online ahead of print October 17, 2013: e1. doi:10.2105/AJPH.2013.301604).
    American Journal of Public Health 10/2013; · 3.93 Impact Factor
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    ABSTRACT: Abstract Background: Clinical outcomes of the Women's Health Initiative (WHI) calcium plus vitamin D supplementation trial have been reported during 7.0 years of active intervention. We now report outcomes 4.9 years after the intervention stopped and cumulative findings. Methods: Postmenopausal women (N=36,282) were randomized; postintervention follow-up continued among 29,862 (86%) of surviving participants. Primary outcomes were hip fracture and colorectal cancer. Breast cancer, all cancers, cardiovascular disease (CVD), and total mortality were predetermined major study outcomes. Results: Hip fracture incidence was comparable in the supplement and the placebo groups, postintervention hazard ratio (HR)=0.95, 95% confidence interval (95% CI: 0.78, 1.15) and overall HR=0.91 (95% CI: 0.79, 1.05). Overall, colorectal cancer incidence did not differ between randomization groups, HR=0.95 (95% CI: 0.80, 1.13). Throughout, there also was no difference in invasive breast cancer, CVD, and all-cause mortality between groups. In subgroup analyses, the invasive breast cancer effect varied by baseline vitamin D intake (p=0.03 for interaction). Women with vitamin D intakes >600 IU/d, had an increased risk of invasive breast cancer, HR=1.28 (95% CI; 1.03, 1.60). Over the entire study period, in post hoc analyses, the incidence of vertebral fractures, HR=0.87 (95% CI: 0.76, 0.98) and in situ breast cancers, HR=0.82 (95% CI: 0.68, 0.99) were lower among women randomized to supplementation. Conclusion: After an average of 11 years, calcium and vitamin D supplementation did not decrease hip fracture or colorectal cancer incidence. Exploratory analyses found lower vertebral fracture and in situ breast cancer incidence in the supplement users. There was no effect on CVD or all-cause mortality.
    Journal of Women's Health 10/2013; · 1.90 Impact Factor

Publication Stats

13k Citations
3,103.78 Total Impact Points

Institutions

  • 2014
    • Torrance Memorial Medical Center
      Torrance, California, United States
  • 2001–2014
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      • Department of Medicine
      Torrance, California, United States
  • 1981–2014
    • University of California, Los Angeles
      • • Jonsson Comprehensive Cancer Center
      • • Department of Medicine
      • • Division of Hematology and Medical Oncology
      Los Angeles, California, United States
  • 2013
    • University of Alabama at Birmingham
      • Department of Epidemiology
      Birmingham, AL, United States
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2006–2013
    • University of Pittsburgh
      • Department of Epidemiology
      Pittsburgh, Pennsylvania, United States
    • University at Buffalo, The State University of New York
      • Department of Social and Preventive Medicine
      Buffalo, NY, United States
  • 2002–2013
    • Fred Hutchinson Cancer Research Center
      • Division of Public Health Sciences
      Seattle, WA, United States
  • 1979–2013
    • Harbor-UCLA Medical Center
      • Department of Pediatrics
      Torrance, California, United States
  • 2012
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • CSU Mentor
      Long Beach, California, United States
    • University of New England (USA)
      • College of Osteopathic Medicine
      Biddeford, ME, United States
  • 2010–2012
    • University of Massachusetts Amherst
      • Division of Biostatistics and Epidemiology
      Amherst Center, MA, United States
  • 2007–2012
    • Albert Einstein College of Medicine
      • Department of Epidemiology & Population Health
      New York City, NY, United States
    • County of Los Angeles Public Health
      Los Angeles, California, United States
  • 2011
    • Yale University
      • Department of Chronic Disease Epidemiology
      New Haven, CT, United States
    • Karmanos Cancer Institute
      Detroit, Michigan, United States
    • University of Nevada School of Medicine
      Reno, Nevada, United States
  • 2006–2011
    • Stanford University
      • • Department of Dermatology
      • • Department of Medicine
      Stanford, CA, United States
  • 2008
    • The University of Arizona
      • Division of Epidemiology and Biostatistics
      Tucson, AZ, United States
    • University of North Carolina at Chapel Hill
      • Department of Epidemiology
      Chapel Hill, NC, United States
    • University of California, San Francisco
      • Department of Physiological Nursing
      San Francisco, CA, United States
    • Yeshiva University
      • Department of Epidemiology & Population Health
      New York City, New York, United States
    • Maine Medical Center
      Portland, Maine, United States
  • 2005
    • Lifespan
      Providence, Rhode Island, United States
  • 2003
    • The Ohio State University
      Columbus, Ohio, United States
    • University of South Carolina
      • Department of Epidemiology & Biostatistics
      Columbia, SC, United States
  • 1999
    • American Society of Clinical Oncology
      Alexandria, Virginia, United States
  • 1996
    • Virginia Commonwealth University
      Richmond, Virginia, United States
  • 1987
    • Children's Hospital Los Angeles
      • Division of Hospital Medicine
      Los Angeles, California, United States
  • 1982
    • University of Southern California
      • Department of Medicine
      Los Angeles, California, United States