Obesity increases the risk for high-grade prostate cancer: results from the REDUCE study (original) (raw)
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BACKGROUND: Obesity has been inconsistently linked to prostate cancer, mainly with mortality rather than incidence. Few large-scale studies exist assessing obesity in relation to prostate-specific antigen (PSA)-detected prostate cancer. METHODS: We used cases and stratum-matched controls from the population-based PSA-testing phase of the Prostate testing for cancer and Treatment study to examine the hypothesis that obesity as measured by body mass index (BMI), waist circumference and waist-to-hip ratio (WHR) is associated with increased prostate cancer risk, and with higher tumour stage and grade. In all, 2167 eligible cases and 11 638 randomly selected eligible controls with PSA values were recruited between 2001 and 2008. A maximum of 960 cases and 4156 controls had measurement data, and also complete data on age and family history, and were included in the final analysis. BMI was categorised as o25.0, 25.0 -29.9, X30.0 in kg m À2 . RESULTS: Following adjustment for age and family history of prostate cancer, we found little evidence that BMI was associated with total prostate cancer (odds ratio (OR): 0.83, 95% confidence interval (CI): 0.67, 1.03; highest vs lowest tertile; P-trend 0.1). A weak inverse association was evident for low-grade (OR: 0.76, 95% CI: 0.59, 0.97; highest vs lowest tertile; P-trend 0.045) prostate cancer. We found no association of either waist circumference (OR: 0.94, 95% CI: 0.80, 1.12; highest vs lowest tertile) or waist-to-hip ratio (WHR; OR: 0.93, 95% CI: 0.77, 1.11; highest vs lowest tertile) with total prostate cancer, and in analyses stratified by disease stage (all P-trend40.35) or grade (all P-trend40.16). CONCLUSION: General adiposity, as measured by BMI, was associated with a decreased risk of low-grade PSA-detected prostate cancer. However, effects were small and the confidence intervals had limits very close to one. Abdominal obesity (as measured by WHR/waist circumference) was not associated with PSA-detected prostate cancer.
British journal of cancer, 2011
Obesity has been inconsistently linked to prostate cancer, mainly with mortality rather than incidence. Few large-scale studies exist assessing obesity in relation to prostate-specific antigen (PSA)-detected prostate cancer. We used cases and stratum-matched controls from the population-based PSA-testing phase of the Prostate testing for cancer and Treatment study to examine the hypothesis that obesity as measured by body mass index (BMI), waist circumference and waist-to-hip ratio (WHR) is associated with increased prostate cancer risk, and with higher tumour stage and grade. In all, 2167 eligible cases and 11 638 randomly selected eligible controls with PSA values were recruited between 2001 and 2008. A maximum of 960 cases and 4156 controls had measurement data, and also complete data on age and family history, and were included in the final analysis. BMI was categorised as <25.0, 25.0-29.9, ≥ 30.0 in kg m(-2). Following adjustment for age and family history of prostate cancer...
International Journal of Cancer, 2007
Many investigators suggested that obesity predisposes to adverse prostate cancer characteristics and outcomes. We tested the effect of obesity on the rate of aggressive prostate cancer at either prostate biopsy or radical prostatectomy (RP). Clinical and pathological data were available for 1,814 men. Univariable and multivariable logistic regression models addressed the rate of high grade prostate cancer (HGPCa) at either biopsy or final pathology. Clinical stage, prostate-specific antigen (PSA), percentage of free PSA and prostate volume were the base predictors. All models were fitted with and without body mass index (BMI), which quantified obesity. BMI and its reciprocal (InvBMI) were coded as cubic splines to allow nonlinear effects. Predictive accuracy (PA) was quantified with area under curve estimates, which were subjected to 200 bootstrap resamples to reduce overfit bias. Gains in PA related to the inclusion of BMI were compared using the Mantel-Haenszel test. HGPCa at biopsy was detected in 562 (31%) and HGPCa at RP pathology was present in 931 (51.3%) men. In either univariable or multivariable models predicting HGPCa at biopsy, BMI or InvBMI failed to respectively reach statistical significance or add to multivariable PA (BMI gain 5 0%, p 5 1.0; InvBMI gain 5 20.2%, p 5 0.9). Conversely, in models predicting HGPCa at RP, BMI and InvBMI represented independent predictors but failed to increase PA (BMI gain 5 0.7%, p 5 0.6; InvBMI gain 5 0.5, p 5 0.7%). Obesity does not predispose to more aggressive prostate cancer at biopsy. Similarly, obesity does not change the ability to identify those who may harbor HGPCa at RP. ' 2007 Wiley-Liss, Inc.
Obesity as a risk factor for prostate cancer: A clinical review
Integrative Cancer Science and Therapeutics, 2016
Epidemiological studies have shown a significant association between obesity and several cancers, but the role of obesity in prostate cancer etiology remains elusive. More recent studies somewhat clarify this complex relationship and we sought to review the data linking obesity and prostate cancer to make sense of this conflicting data. To systematically evaluate epidemiologic data available we performed a Google Scholar search with the following keywords: "obesity", "prostate cancer", "obesity and prostate cancer." Recent prospective studies suggest obesity is associated with increased risk of aggressive prostate cancers but with a reduced risk of low-grade tumors. The etiology of the differential effect of obesity on subtypes of prostate cancer is multifactorial, and interactions between hormonal changes including sex steroids, insulin, IGF's and inflammatory mediators have been implicated. It has also been suggested that it is harder to detect prostate cancer in obese men through routine diagnostic approaches. Given the high prevalence of obesity and prostate cancer in the western world, further research to evaluate this complex relationship is warranted. Furthermore, novel approaches may be required to improve disease prostate cancer diagnosis among obese individuals.
Obesity and Prostate Cancer Detection: Insights from Three National Surveys
The American Journal of Medicine, 2010
BACKGROUND: Previous studies suggest that obesity is associated with higher prostate cancer progression and mortality despite an association with lower prostate cancer incidence. This study aims to better understand these apparently inconsistent relationships among obese men by combining evidence from 3 nationally representative cross-sectional surveys. METHODS: We evaluated relationships between obesity and 1) testosterone concentrations in the Third National Health and Nutrition Examination Survey (NHANES III; n ϭ 845); 2) prostate-specific antigen (PSA) in NHANES 2001-2004 (n ϭ 2458); and 3) prostate biopsy rates in the National Health Interview Survey (NHIS 2000; n ϭ 4789) population. Mean testosterone, PSA concentrations, and biopsy rates were computed for Body Mass Index (BMI) categories. RESULTS: Testosterone concentrations were inversely associated with obesity (P-trend Ͻ.0001) in NHANES III. In NHANES 2001-2004, obese (BMI Ͼ35) versus lean (BMI Ͻ25) men were less likely to have PSA concentrations that reached the biopsy threshold of Ͼ4 ng/mL (3% vs 8%; P Ͻ.0001). Among NHIS participants, all BMI groups had similar rates of PSA testing (P ϭ .24). However, among men who had PSA tests, 11% of men with BMI Ͼ30 versus 16% with BMI Ͻ25, achieved a PSA threshold of 4 ng/mL; P ϭ .01. Furthermore, biopsy rates were lower among men with BMI Ͼ30 versus BMI Ͻ25 in NHIS participants (4.6% vs 5.8%; P ϭ .05). CONCLUSIONS: Obesity was associated with lower PSA-driven biopsy rates. These data support further studies to test the hypothesis that obesity affects prostate cancer detection independent of prostate cancer risk by decreasing the PSA-driven biopsy rates.
The uncertain relationship between obesity and prostate cancer: An Italian biopsy cohort analysis
European Journal of Surgical Oncology (EJSO), 2011
The study aims to investigate the relationship between obesity and prostate cancer diagnosis at biopsy. Methods: From 2005 onwards, a consecutive series of patients undergoing 12-core prostate biopsy for PSA value ! 4 ng/ml and/or positive digital rectal examination (DRE) were enrolled. Before the biopsy, patients underwent a physical examination, including height and weight measurement. Obesity was defined as body mass index (BMI) !30 kg/m 2 . Blood samples were drawn from all patients and analyzed for total PSA and testosterone. Results: 885 patients were enrolled with a median age and PSA of 67 years (range 37e95) and 6.4 ng/ml (range 1e30) respectively. Median BMI was 27.1 kg/m 2 (range 18e46.6) with 185 patients classified as obese. 363 patients had cancer at biopsy; 76 were obese. PSA was independently associated with a higher risk of cancer (OR 1.09 per 1 unit PSA, p ¼ 0.01). On multivariate analysis, the BMI was not significantly associated with an increased prostate cancer risk ( p ¼ 0.19). Out of 363 patients with prostate cancer, 154 had a Gleason score 6 (23 were obese) and 209 a Gleason score !7 (53 were obese). Among men with cancer, a higher BMI on univariate ( p ¼ 0.001) and multivariate analysis ( p ¼ 0.005) was associated with high-grade disease (Gleason ! 7). Conclusions: In our single center study and less aggressively screened cohort, obesity is associated with an increased risk of a high-grade Gleason score when prostate cancer is diagnosed at biopsy.
Does obesity modify prostate cancer detection in a European cohort?
2017
Introduction To investigate prostate-specific antigen (PSA) accuracy and digital rectal examination (DRE) accuracy in detecting prostate cancer according to body mass index (BMI) in Spanish men with an indication of the first prostate biopsy. Material and methods We reviewed the clinical and histopathological data of 1,319 patients who underwent transrectal ultrasound-guided prostate needle biopsy. The patients were categorised according to the BMI as follows: <25 kg/m2 (normal weight); 25–29.9 kg/m2 (overweight); and ≥30 kg/m2 (obese). Receiver operator characteristic curves were used to assess PSA accuracy and DRE accuracy by calculating the area under the curve. Results The obesity rate of the cohort was 14%. PSA accuracy for predicting prostate cancer in each BMI category was 0.52, 0.58 and 0.62, respectively (p = 0.01). After stratification by DRE findings, there was no difference in the performance accuracy of PSA in predicting the presence of cancer across BMI groups in ab...
Cancer Epidemiology Biomarkers & Prevention, 2007
Background: Obesity has been associated with aggressive prostate cancer. The extent of this association, which varies by stage and grade, remains unclear. The role of recent weight change had not been previously examined. Methods: We examined body mass index (BMI) and weight change in relation to incident prostate cancer by disease stage and grade at diagnosis among 69,991 men in the Cancer Prevention Study II Nutrition Cohort. Participants provided information on height and weight in 1982, and again at enrollment in 1992. During follow-up through June 30, 2003 (excluding the first 2 years of follow-up), we documented 5,252 incident prostate cancers. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI).
BJU International, 2014
To evaluate the relationship between number of metabolic syndrome (MetS)-like components and prostate cancer diagnosis in a group of men where nearly all biopsies were taken independent of prostate-specific antigen (PSA) level, thus minimising any confounding from how the various MetS-like components may influence PSA levels. Subjects/Patients and Methods We analysed data from 6426 men in the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) study with at least one on-study biopsy. REDUCE compared dutasteride vs placebo on prostate cancer risk among men with an elevated PSA level and negative pre-study biopsy and included two on-study biopsies regardless of PSA level at 2 and 4 years. Available data for MetS-like components included data on diabetes, hypertension, hypercholesterolaemia, and body mass index. The association between number of these MetS-like components and prostate cancer risk and low-grade (Gleason sum <7) or high-grade (Gleason sum >7) vs no prostate cancer was evaluated using logistic regression. Results In all, 2171 men (34%) had one MetS-like component, 724 (11%) had two, and 163 (3%) had three or four. Men with more MetS-like components had lower PSA levels (P = 0.029). One vs no MetS-like components was protective for overall prostate cancer (P = 0.041) and low-grade prostate cancer (P = 0.010). Two (P = 0.69) or three to four (P = 0.15) MetS-like components were not significantly related to prostate cancer. While one MetS-like component was unrelated to high-grade prostate cancer (P = 0.97), two (P = 0.059) or three to four MetS-like components (P = 0.02) were associated with increased high-grade prostate cancer risk, although only the latter was significant. Conclusion When biopsies are largely PSA level independent, men with an initial elevated PSA level and a previous negative biopsy, and multiple MetS-like components were at an increased risk of high-grade prostate cancer, suggesting the link between MetS-like components and high-grade prostate cancer is unrelated to a lowered PSA level.