
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Short Communication |
Departments of 1 Nutrition and 2 Epidemiology, Harvard School of Public Health; and 3 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Requests for reprints: Kana Wu, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Building 2, Boston, MA 02115. Phone: 617-432-1842; Fax: 617-432-2435. E-mail: kana.wu{at}channing.harvard.edu
| Abstract |
|---|
|
|
|---|
| Introduction |
|---|
|
|
|---|
| Materials and Methods |
|---|
|
|
|---|
Case Ascertainment
Men who reported a diagnosis of prostate cancer on their follow-up questionnaires, were contacted and asked for permission to review their medical records. The medical records were reviewed by physicians who extracted information on stage and pathology of the prostate cancer. After excluding cases with stage T1a cancers, a total of 3,002 incident prostate cancer cases with information on stage were identified in our cohort by January 31, 2000. Advanced prostate cancer cases were classified as cancers that had either spread regionally to the seminal vesicle or nearby organs, or were metastatic at diagnosis, or fatal by January 2000.
Assessment of Dietary Patterns
Dietary patterns were identified using the same approach as reported in earlier studies from our cohort (9, 10). We applied the residual method to energy-adjust the factor scores (11).
Statistical Analysis
The Mantel-Haenzel estimator was used to calculate age-adjusted relative risks (RR; ref. 12). We used the Cox proportional hazards model to simultaneously adjust for several potential confounders (13). RRs were adjusted for known and suspected nondietary risk factors for prostate cancer: age, height, smoking, family history of prostate cancer in first-degree relatives, race, history of vasectomy, vigorous exercise, alcohol intake, and body mass index as well as total energy intake. We computed trend tests by using the median of each quintile of dietary pattern as exposure score. Associations were examined using the cumulatively updated dietary pattern scores (i.e., the average of all existing dietary pattern scores calculated from the three FFQs up to the beginning of each follow-up period; ref. 14). Because previous analyses in our cohort have shown that associations between dietary risk factors and risk of prostate cancer might vary by body mass index and age, we also conducted analyses stratified by body mass index and age (6, 7, 15). Interaction tests were done by including a product term with either age (binary variable, <65 versus
65 years) or body mass index (<26 versus
26 kg/m2) and diet pattern score (continuous variable, using median values in each quintile) in the multivariable models. All reported P values were two-sided.
| Results |
|---|
|
|
|---|
|
65 years). Stratification by age indicated no evidence for a protective association between prudent pattern and organ-confined or advanced cancer. Associations between western pattern and organ-confined prostate cancer also did not differ by age (data not shown). Table 3 shows the relative risk of advanced prostate cancer and meat intake and western pattern by age. Among those
65 years of age, we observed a modest but nonsignificant positive association between western pattern scores and risk of advanced prostate cancer.
|
|
26) and western pattern with regard to risk of advanced prostate cancer among older men (Pinteraction = 0.86). We also examined whether the association between western pattern score and advanced prostate cancer risk observed among older men could be explained in part by either red or processed meat intake, two factors previously shown to be associated with advanced prostate cancer risk in this cohort (16). The positive associations between processed meat and advanced prostate cancer seemed to be restricted to older men, whereas the positive associations between red meat and advanced prostate cancer seemed to be restricted to younger men. Adjusting for western pattern did not diminish these associations; if anything, the positive associations between red meat intake and advanced prostate cancer in younger men became slightly stronger. Adding red meat intake to the multivariable models did not appreciably change the association between western pattern and advanced prostate cancer risk in older men, but adding processed meat to the model eliminated the positive association with western pattern and risk of advanced prostate cancer. Neither red meat intake nor processed meat intake were associated with risk of organ-confined prostate cancer (data not shown). When we examined associations between the main contributors for the prudent pattern and risk of prostate cancer, an inverse association between vegetable intake and risk of organ-confined prostate cancer was suggested (highest versus lowest quintile [RR, 0.87; 95% confidence intervals (CI). 0.73-1.03]), but CIs included one. Vegetable intake was not associated with advanced prostate cancer. Fruit intake was neither associated with organ-confined nor advanced prostate cancer (data not shown).
| Discussion |
|---|
|
|
|---|
In addition, we found no evidence for a protective association of a higher prudent pattern score. Epidemiologic studies do not support a substantial effect of fruits on prostate cancer risk. However, some, albeit inconsistent, evidence indicated that higher intake of vegetables such as tomatoes, legumes, and beans may reduce prostate cancer risk (17). In previous analysis in this cohort, we found that higher intake of tomato products, primarily tomato sauce, was associated with lower risk of total and advanced prostate cancer (18). Tomato sauce intake was only weakly correlated with prudent pattern in our cohort (Spearman r = 0.14)
Results from a recent prospective study and a randomized clinical trial also do not support a protective effect of vegetables and fruit intake against prostate cancer risk. In the large European Investigation into Cancer and Nutrition cohort total fruit and vegetable intake was not associated with prostate cancer risk (19). In participants from the Polyp Prevention Trial, a randomized clinical trial, consumption of a low-fat, high-fruit, vegetable, and fiber diet over a period of 4 years did not lower PSA levels over that time period (20).
Red and processed meats are two main contributors to the western pattern. Higher consumption of fat and meat has been associated with higher risk of prostate cancers in some but not all epidemiologic studies (21). In this analysis, the slightly increased risk of advanced prostate cancer with a western pattern among older men did not change considerably after controlling for red meat intake. On the other hand, controlling for processed meat, another major contributor to western pattern, eliminated the suggestive positive associations between western pattern and risk of advanced prostate cancer. The positive associations between intake of processed meat and risk of advanced prostate cancer in older men remained basically unchanged after adjusting for western pattern. Although the rationale of controlling for major components of a specific dietary pattern may be questioned, one of the goals of dietary pattern analysis is to capture associations due to a combination of food items and nutrients, including complex interactions among them, which may be missed by analyses focused on single nutrients, foods, or food groups (3, 22). The fact that the association with advanced prostate cancer was more robust for processed meats than for western pattern suggests either that the causative risk factor is related specifically to processed meats (e.g., through nitrates found in processed meats; ref. 23), or that processed meat captures a correlated dietary factor better than does western pattern with regard to prostate cancer.
To our knowledge, this is by far the largest study that has investigated the association between dietary patterns and prostate cancer risk. Besides the large number of cases, the use of multiple dietary assessments and the long follow-up period (14 years) were major strengths of this study. In addition, we were able to assess subgroups of prostate cancer by stage and age of onset. This study also has some limitations. Subjective decisions had to be made by the investigators with regard to the number of factors to be extracted, types of foods to be grouped together, and labeling of factors. However, results from previously published sensitivity analyses in this cohort showed high reproducibility of those two derived factors (9, 22).
In conclusion, we did not find any evidence for a protective association between prudent and western patterns as identified by factor analysis in our cohort and prostate cancer risk. The lack of association between a western dietary pattern and prostate cancer risk in this study suggests that dietary risk factors for prostate cancer are likely to differ from those for other conditions, such as cardiovascular disease and type 2 diabetes, that have been associated with a western dietary pattern in this cohort (9, 10).
| Footnotes |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 2/ 6/05; revised 9/13/05; accepted 11/ 7/05.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
K. R. Solomon, K. Pelton, K. Boucher, J. Joo, C. Tully, D. Zurakowski, C. P. Schaffner, J. Kim, and M. R. Freeman Ezetimibe Is an Inhibitor of Tumor Angiogenesis Am. J. Pathol., March 1, 2009; 174(3): 1017 - 1026. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. J. Murtola, T. L. J. Tammela, J. Lahtela, and A. Auvinen Antidiabetic Medication and Prostate Cancer Risk: A Population-based Case-Control Study Am. J. Epidemiol., October 15, 2008; 168(8): 925 - 931. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. J. Murtola, T. L.J. Tammela, J. Lahtela, and A. Auvinen Cholesterol-Lowering Drugs and Prostate Cancer Risk: A Population-based Case-Control Study Cancer Epidemiol. Biomarkers Prev., November 1, 2007; 16(11): 2226 - 2232. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. L. Neuhouser, M. J. Barnett, A. R. Kristal, C. B. Ambrosone, I. King, M. Thornquist, and G. Goodman (n-6) PUFA Increase and Dairy Foods Decrease Prostate Cancer Risk in Heavy Smokers J. Nutr., July 1, 2007; 137(7): 1821 - 1827. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Esmaillzadeh, M. Kimiagar, Y. Mehrabi, L. Azadbakht, F. B Hu, and W. C Willett Dietary patterns, insulin resistance, and prevalence of the metabolic syndrome in women Am. J. Clinical Nutrition, March 1, 2007; 85(3): 910 - 918. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |