INTENSIVE LIFESTYLE CHANGES MAY AFFECT THE PROGRESSION OF PROSTATE CANCER
ABSTRACT
Purpose
Men with prostate cancer are often advised to make changes in diet and lifestyle, although the impact of these changes has not been well documented. Therefore, we evaluated the effects of comprehensive lifestyle changes on prostate specific antigen (PSA), treatment trends and serum stimulated LNCaP cell growth in men with early, biopsy proven prostate cancer after 1 year.
Materials and Methods
Patient recruitment was limited to men who had chosen not to undergo any conventional treatment, which provided an unusual opportunity to have a nonintervention randomized control group to avoid the confounding effects of interventions such as radiation, surgery or androgen deprivation therapy. A total of 93 volunteers with serum PSA 4 to 10 ng/ml and cancer Gleason scores less than 7 were randomly assigned to an experimental group that was asked to make comprehensive lifestyle changes or to a usual care control group.
Results
None of the experimental group patients but 6 control patients underwent conventional treatment due to an increase in PSA and/or progression of disease on magnetic resonance imaging. PSA decreased 4% in the experimental group but increased 6% in the control group (p = 0.016). The growth of LNCaP prostate cancer cells (American Type Culture Collection, Manassas, Virginia) was inhibited almost 8 times more by serum from the experimental than from the control group (70% vs 9%, p <0.001). Changes in serum PSA and also in LNCaP cell growth were significantly associated with the degree of change in diet and lifestyle.
Conclusions
Intensive lifestyle changes may affect the progression of early, low grade prostate cancer in men. Further studies and longer term followup are warranted.
From the Departments of Urology (PRC) and Medicine (DO) and Preventive Medicine Research Institute (DO, RM, EBP, CJR, SDE, LC, PM, DJM, JDF, JW, GW), University of California-San Francisco, San Francisco and Departments of Physiological Science (RJB, THN) and Urology (WJA), University of California-Los Angeles, Los Angeles, California, Department of Urologic Oncology, Memorial Sloan-Kettering Cancer Center (WRF and AMD), New York and Department of Statistics, State University of New York at Stony Brook (NRM), Stony Brook, New York, and Windber Research Institute (FNJ), Johnstown, Pennsylvania
Correspondence: Preventive Medicine Research Institute, University of California-San Francisco, 900 Bridgeway, Sausalito, California 94965.
Submitted for publication September 9, 2004.
Study received University of California-San Francisco Committee on Human Research institutional review board approval.
Supported by Department of Defense Uniformed Services University Grant MDA905–99–1–0003 via the Henry M. Jackson Foundation Grant 600–06971000–236, The Prostate Cancer Foundation, National Institutes of Health 5P50CA089520–02 University of California-San Francisco Prostate Cancer Specialized Program of Research Excellence, Bucksbaum Family Foundation, Ellison Foundation, Fisher Foundation, Gallin Foundation, Highmark, Inc., Koch Foundation, Resnick Foundation, Safeway Foundation, Wachner Foundation, Walton Family Foundation and Wynn Foundation.
No supporting agencies were involved in the design or conduct of the study, in the collection, analysis or interpretation of the data, or in the preparation, review or approval of the manuscript.
† Financial interest and/or other relationship with Random House and Harper-Collins.
‡ Financial interest and/or other relationship with TAP Pharmaceutical Products, AstraZeneca, Pfizer and National Institutes of Health.
ABSTRACT