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Am J Clin Nutr. 2016 Jan;103(1):168-77. doi: 10.3945/ajcn.114.101436. Epub 2015 Nov 25.

Vegetable and fruit consumption and the risk of hormone receptor-defined breast cancer in the EPIC cohort.

Author information

1
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, Netherlands;
2
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, Netherlands; Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom;
3
Section of Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark;
4
Danish Cancer Society Research Center, Copenhagen, Denmark;
5
International Agency for Research on Cancer, Lyon, France;
6
INSERM, Center for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Hormones, and Women's Health Team, Villejuif, France; University Paris Sud, UMRS 1018, Villejuif, France; Gustave Roussy Institute, Villejuif, France;
7
Cancer Epidemiology Centre, Cancer Council of Victoria, Melbourne, Australia; Centre for Epidemiology and Biostatistics, School of Population and Global Health, University of Melbourne, Melbourne, Australia;
8
Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany;
9
Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany;
10
Hellenic Health Foundation, Athens, Greece; Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Goudi, Athens, Greece; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece;
11
Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, Goudi, Athens, Greece; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece; Department of Epidemiology, Harvard School of Public Health, Boston, MA;
12
Hellenic Health Foundation, Athens, Greece; Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece; Department of Epidemiology, Harvard School of Public Health, Boston, MA;
13
Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy;
14
Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy;
15
Dipartimento Di Medicina Clinica E Chirurgia, Federico II University, Naples, Italy;
16
Cancer Registry and Histopathology Unit, Civic-M.P. Arezzo Hospital, ASP Ragusa, Italy;
17
Human Genetic Foundation (HuGeF), Turin, Italy;
18
Department of Community Medicine, School of Health Sciences, University of Tromso, The Arctic University of Norway, Tromso, Norway;
19
Department of Community Medicine, School of Health Sciences, University of Tromso, The Arctic University of Norway, Tromso, Norway; Department of Research, The Cancer Registry of Norway, Oslo, Norway; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Folkhälsan Research Center, Samfundet Folkhälsan, Helsinki, Finland;
20
Public Health Directorate, Asturias, Spain;
21
Unit of Nutrition, Environment, and Cancer, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain;
22
Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs.GRANADA, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain;
23
CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Epidemiology Department, Regional Health Council, Murcia, Spain;
24
CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain; Navarre Public Health Institute, Pamplona, Spain;
25
Public Health Direction and Biodonostia-Ciberesp Basque Regional Health Department, San Sebastian, Spain;
26
Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden;
27
Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden;
28
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom; Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands; Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, Netherlands; Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia;
29
University of Cambridge, Cambridge, United Kingdom; and.
30
Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.
31
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom;
32
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, Netherlands; c.vangils@umcutrecht.nl.

Abstract

BACKGROUND:

The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased steroid hormone receptor-negative breast cancer risk.

OBJECTIVE:

This study aimed to investigate the association between vegetable and fruit intake and steroid hormone receptor-defined breast cancer risk.

DESIGN:

A total of 335,054 female participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were included in this study (mean ± SD age: 50.8 ± 9.8 y). Vegetable and fruit intake was measured by country-specific questionnaires filled out at recruitment between 1992 and 2000 with the use of standardized procedures. Cox proportional hazards models were stratified by age at recruitment and study center and were adjusted for breast cancer risk factors.

RESULTS:

After a median follow-up of 11.5 y (IQR: 10.1-12.3 y), 10,197 incident invasive breast cancers were diagnosed [3479 estrogen and progesterone receptor positive (ER+PR+); 1021 ER and PR negative (ER-PR-)]. Compared with the lowest quintile, the highest quintile of vegetable intake was associated with a lower risk of overall breast cancer (HRquintile 5-quintile 1: 0.87; 95% CI: 0.80, 0.94). Although the inverse association was most apparent for ER-PR- breast cancer (ER-PR-: HRquintile 5-quintile 1: 0.74; 95% CI: 0.57, 0.96; P-trend = 0.03; ER+PR+: HRquintile 5-quintile 1: 0.91; 95% CI: 0.79, 1.05; P-trend = 0.14), the test for heterogeneity by hormone receptor status was not significant (P-heterogeneity = 0.09). Fruit intake was not significantly associated with total and hormone receptor-defined breast cancer risk.

CONCLUSION:

This study supports evidence that a high vegetable intake is associated with lower (mainly hormone receptor-negative) breast cancer risk.

KEYWORDS:

breast cancer; estrogen receptor; fruit; progesterone receptor; vegetables

PMID:
26607934
DOI:
10.3945/ajcn.114.101436
[Indexed for MEDLINE]

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