Obesity as a predictor of adverse outcome across black and white race

Results from the Shared Equal Access Regional Cancer Hospital (SEARCH) Database

Abstract

BACKGROUND:

Across multiple studies, obesity has been associated with an increased risk of higher grade disease and prostate-specific antigen (PSA) recurrence after radical prostatectomy (RP). Whether these associations vary by race is unknown. In the current study, the authors examined the association between obesity and outcome after RP stratified by race.

METHODS:

A retrospective analysis was performed on 1415 men in the Shared Equal Access Regional Cancer Hospital (SEARCH) database who underwent RP between 1989 and 2008. The association between increased body mass index (BMI) and adverse pathology and biochemical recurrence was examined using multivariate logistic regression and Cox models, respectively. Data were examined stratified by race.

RESULTS:

After adjusting for preoperative clinical characteristics, higher BMI was associated with higher tumor grade (P = .008) and positive surgical margins (P < .001) in white men, and similar but statistically nonsignificant trends were observed in black men. No significant interaction was noted between race and BMI for associations with adverse pathology (P_interaction≥.12). After adjusting for preoperative clinical characteristics, higher BMI was associated with an increased risk of recurrence in both white men (P = .001) and black men (P = .03). After further adjusting for pathologic variables, higher BMI was associated with significantly increased risk of recurrence in white men (P = .002) and black men (P = .01). No significant interactions were observed between race and BMI for predicting biochemical progression adjusting either for preoperative factors (P_interaction = .35) or for preoperative and pathologic features (P_interaction = .47).

CONCLUSIONS:

Obesity was associated with a greater risk of recurrence among both black men and white men. Obesity did not appear to be more or less influential in 1 race than another but, rather, was identified as a risk factor for aggressive cancer regardless of race. Cancer 2009. © 2009 American Cancer Society.

Obesity is a major public health issue and is associated with an increased risk of death from several cancers, including the most common noncutaneous cancer in men—prostate cancer.1 Although the specific biologic processes linking obesity to prostate cancer remain to be elucidated completely, previous studies have demonstrated that obesity is associated with higher grade tumors and poorer outcomes after surgery.2-4

Similar to obese men, black men also are at increased risk for prostate cancer death. Specifically, there are marked racial differences in both prostate cancer incidence and mortality, and black men have the highest risk in the world.5 They also tend to present with more advanced-stage disease than white men.5 The degree to which this is attributable to socioeconomic reasons such as impaired access to healthcare or because of worse tumor biology is debatable.6 Because there is a higher prevalence of obesity among black men with prostate cancer,3 the degree to which excess obesity may explain or contribute to these poorer outcomes among black men is unknown. Likewise, whether obesity is correlated with poor prostate cancer outcomes equally for black men and white men also is unknown.

We propose that obesity holds the same negative consequences regardless of race. To test this hypothesis, we examined the association between body mass index (BMI) and adverse clinical and pathologic characteristics and the risk of biochemical progression after radical prostatectomy (RP) in both black men and white men. To ensure the validity and generalizability of our findings, we used the multicenter, multiethnic Shared Equal Access Regional Cancer Hospital (SEARCH) Database.7 It is important to note that we previously examined the association between obesity and outcome within the SEARCH database and observed that obesity was associated with an increased risk of disease progression.2 However, those analyses were not stratified by race. Given a recent report suggesting that obesity may be a stronger predictor of outcome among black men,8 we re-examined an updated cohort from the SEARCH database to assess this issue.

MATERIALS AND METHODS

Study Population

After obtaining Institutional Review Board approval from each institution to abstract and combine data, we combined data from men who underwent RP at the Veterans Affairs Medical Centers in West Los Angeles, California; Palo Alto, California; Augusta, Georgia; Durham, North Carolina; and Birmingham, Alabama into the SEARCH database.7 This database includes information on patient age at surgery, race, height, weight, clinical stage, grade of cancer on diagnostic biopsies, preoperative prostate-specific antigen (PSA) concentration, surgical specimen pathology (specimen weight, tumor grade, stage, and surgical margin status), and follow-up PSA data. BMI was calculated as weight in kilograms divided by height in meters squared (kg/m²). Patients who received preoperative androgen-deprivation therapy or radiation therapy were excluded. Of the 2320 men within the SEARCH database, we excluded 54 men who were diagnosed from transurethral resection specimens, because this method of diagnosis affects PSA levels; 98 men who had missing PSA values; 191 men who had missing biopsy Gleason scores; 306 who had missing clinical stage data; 155 men who had missing BMI data; and 101 men who were neither black nor white. These exclusions resulted in a study population of 1415 men. Biochemical progression was defined as a single PSA concentration >0.2 ng/mL, 2 concentrations at 0.2 ng/mL, or secondary treatment for an elevated postoperative PSA. Men who received adjuvant treatment for an undetectable PSA were censored as not having recurrent disease at the time of treatment. The prostatectomy specimens were sectioned according to the protocol at each institution.7

Statistical Analysis

We explored differences in the distribution of clinicopathologic characteristics across the BMI groups of normal weight (<25 kg/m²), overweight (25 kg/m² to 29.9 kg/m²), obese (30 kg/m² to 34.9 kg/m²), and moderately and severely obese (≥35 kg/m²) using analysis of variance for continuous variables or the chi-square test for categorical variables. The odds ratio (OR) of the following binary pathologic outcomes was estimated for BMI categories using logistic regression: high-grade disease (Gleason score ≥7), positive surgical margins, extraprostatic extension, and seminal vesicle invasion. Few men had lymph node metastases (n = 20). BMI was entered into all multivariate models as a series of indicator variables for each BMI category. We tested for trend by entering the median BMI of each BMI category as a continuous term into the model and evaluating the coefficient by using the Wald test. We adjusted for preoperative PSA (continuous variable), age at RP (continuous variable), year of surgery (continuous variable), clinical tumor classification (T2/T3 vs T1c), center (categorical variable), and biopsy Gleason score (3 + 4, ≥4 + 3 vs 2-6). Because the data for preoperative PSA were not distributed normally, we examined the data after logarithmic transformation. Data were analyzed both as a whole and separately by race. To test whether the association of obesity with adverse outcome varied by race, we also tested for the interaction between race and BMI strata by including a cross-product term in the multivariate analysis.

The time to biochemical progression was compared among the BMI categories using Kaplan-Meier plots and the log-rank test. To estimate the relative risk of progression associated with obesity, we used a Cox proportional hazards regression model. We ran 2 separate multivariate Cox models to examine whether obesity was associated with biochemical progression and whether this association was independent of any association between obesity and pathologic findings. The first model was adjusted for only preoperative clinical characteristics (age, year of surgery, clinical stage, biopsy Gleason score, center, and preoperative PSA), and the second model was adjusted for preoperative clinical characteristics (except biopsy Gleason score) and pathologic variables (logarithmic transformation of prostate weight, pathologic Gleason score, positive surgical margins, extraprostatic extension, seminal vesicle invasion, and lymph node metastasis). Data were examined as a whole and stratified by race. We tested for an interaction between race and BMI strata as described above.

The point estimates for all crude and age-adjusted models for predicting both the binary pathologic outcomes and the time to progression were similar to the multivariate adjusted point estimates; therefore, only results for the multivariate models are shown. The distribution of all clinicopathologic variables was similar among the SEARCH sites. Therefore, data from all centers were combined for analyses. All statistical analyses were performed using the software package STATA 10.1 (Stata Corp., College Station, Tex).

RESULTS

BMI and Clinicopathologic Characteristics

Black men constituted 47% (n = 662) of the patient population. In univariate analysis, there was no association between BMI and race (chi-square test; P = .49). When stratified by race, higher BMI was associated with more recent year of surgery and younger age in both races, although these associations did not always reach statistical significance (Tables 1 and 2). In white men, higher BMI was associated with lower PSA (P = .05) and larger prostate size (P = .001). Although, in general, the direction of the association between BMI and PSA and prostate size was similar in black men, the association was weaker and was not statistically significant. In white men (P = .02), but not in black men (P = .40), higher BMI was associated with an increased prevalence of positive surgical margins. In both white men and black men, BMI was not related significantly to tumor grade, clinical tumor classification, extraprostatic extension, seminal vesicle invasion, or lymph node involvement.

Table 1. Clinical and Pathologic Features of White Men Undergoing Radical Prostatectomy Stratified by Body Mass Index

Variable	No. of Patients (%)				P*
	Normal Weight, BMI <25 kg/m^2	Overweight, BMI 25 kg/m^2 to 29.9 kg/m^2	Mildly Obese, BMI 30 kg/m^2 to 34.9 kg/m^2	Moderately and Severely Obese, BMI ≥35 kg/m^2
BMI indicates body mass index; SD, standard deviation; PSA, prostate-specific antigen. * P values were determined using the chi-square test except where noted. † This P value was determined using an analysis of variance.
No. of patients	193	349	148	61
Median year of surgery	2000	2001	2002	2003	<.001†
Age: mean±SD, y	62.4±6.3	62.2±6.1	61.9±5.4	60.7±4.9	.22†
PSA, ng/mL					.05†
Median [range]	7.3 [1.5-51.7]	6.7 [0.4-52.4]	7 [0.7-75.4]	6 [0.4-32.4]
Mean±SD	9.7±7.7	8.4±6.5	9.1±9.1	7.6±5.1
Biopsy Gleason sum					.10
2-6	127 (66)	218 (62)	95 (64)	30 (49)
7/3+4	41 (21)	71 (20)	25 (17)	21 (34)
≥4+3	25 (13)	60 (17)	28 (19)	10 (16)
Clinical tumor classification					.84
T1c	86 (45)	159 (46)	72 (49)	30 (49)
T2/T3	107 (55)	190 (54)	76 (51)	31 (51)
Prostate weight, g					.001†
Median [range]	35 [14-115]	40 [9.2-212]	40 [18.0-232.5]	45 [20.3-92]
Mean±SD	39.4±17.2	43.1±19.7	46.7±25.3	46.3±15.7
Pathologic Gleason sum					.06
2-6	86 (45)	146 (42)	50 (34)	16 (27)
7/3+4	65 (34)	120 (35)	64 (43)	23 (38)
≥4+3	40 (21)	80 (23)	34 (23)	21 (35)
Positive surgical margins	76 (40)	144 (42)	75 (51)	35 (59)	.02
Extraprostatic extension	39 (21)	90 (26)	35 (24)	22 (37)	.07
Seminal vesicle invasion	16 (8)	29 (8)	13 (9)	9 (15)	.39
Lymph node involvement	3 (2)	4 (1)	3 (2)	2 (3)	.44

Table 2. Clinical and Pathologic Features of Black Men Undergoing Radical Prostatectomy Stratified by Body Mass Index

Variable	No. of Patients (%)				P*
	Normal Weight, BMI <25 kg/m^2	Overweight, BMI 25 kg/m^2 to 29.9 kg/m^2	Mildly Obese, BMI 30 kg/m^2 to 34.9 kg/m^2	Moderately and Severely Obese, BMI ≥35 kg/m^2
BMI indicates body mass index; SD, standard deviation; PSA, prostate-specific antigen. * P values were determined using the chi-square test except where noted. † P value was determined using an analysis of variance.
No. of patients	162	291	150	59
Median year of surgery	2001	2002	2002	2003	.10†
Age: mean±SD, y	61.5±6.3	60.4±6.6	60.3±7.1	58.5±6.4	.03†
PSA, ng/mL					.61†
Median [range]	7.4 [0.5-42.8]	7.4 [0.5-65]	7.1 [2.1-140]	6.1 [1.1-60.9]
Mean±SD	10.1±7.6	9.3±7.5	10.7±13.4	9.8±9.9
Biopsy Gleason sum
2-6	111 (69)	159 (55)	101 (67)	36 (61)	.07
7 (3+4)	32 (20)	77 (26)	28 (19)	14 (24)
≥4+3	19 (12)	55 (19)	21 (14)	9 (15)
Clinical tumor classification					.12
T1c	95 (59)	176 (60)	105 (70)	40 (68)
T2/T3	67 (41)	115 (40)	45 (30)	19 (32)
Prostate weight, g					.30†
Median [range]	37.8 [10-190]	39 [8.2-201]	40 [12.5-208]	40.8 [15-140]
Mean±SD	42.3±22	44±24.2	46.7±27.3	47±22.6
Pathologic Gleason sum					.46
2-6	67 (42)	104 (36)	50 (34)	19 (33)
7/3+4	64 (40)	119 (41)	72 (49)	28 (48)
≥4+3	29 (18)	66 (23)	26 (18)	11 (19)
Positive surgical margins	68 (43)	117 (41)	67 (46)	30 (53)	.40
Extraprostatic extension	31 (20)	55 (19)	18 (12)	16 (28)	.06
Seminal vesicle invasion	14 (9)	33 (12)	13 (9)	5 (9)	.74
Lymph node involvement	3 (2)	4 (1)	1 (1)	0 (0)	.40

BMI and Risk of Adverse Pathologic Features: Multivariate Analysis

After adjusting for multiple preoperative clinical characteristics, higher BMI was associated significantly with higher pathologic tumor grade (P = .008) and positive surgical margins (P < .001) in white men (Table 3). Although a similar trend was noted among black men, these associations did not achieve statistical significance. Higher BMI was not associated significantly with extraprostatic extension or seminal vesicle invasion in either racial group. In addition, the interaction between race and BMI was not statistically significant for any of these adverse pathologic features (P_interaction≥.12). Because associations between obesity and prostate cancer outcomes theoretically may differ based on the type of surgery performed (ie, retropubic vs laparoscopic), we performed a subanalysis in which the type of surgery was included in the multivariate analysis. When this was done, none of the results changed materially.

Table 3. Odds Ratios and 95% Confidence Intervals of Adverse Pathologic Findings at the Time of Radical Prostatectomy by (BMI) Relative to Normal Weight (BMI <25 kg/m²)*

Adverse Pathologic Finding	White Men			Black Men			PInteraction‡
	OR†	95% CI	P	OR†	95% CI	P
OR indicates odds ratio; 95% CI, 95% confidence interval. * Overweight indicates BMI from 25 kg/m^2 to 29.9 kg/m^2; mild obesity, BMI from 30 kg/m^2 to 34.9 kg/m^2; moderate and severe obesity, BMI ≥35 kg/m^2. † Adjusted for age, biopsy Gleason score, clinical stage, preoperative prostate-specific antigen level, year of surgery, and center. ‡ Pinteraction to study the interaction among the main effects of race and BMI categories by using the cross-product term of the main effects. § P-trend determined using median BMI of each category as a continuous variable.
Pathologic Gleason sum ≥7			.008§			.11§	.47
Overweight	1.17	0.77-1.77		1.14	0.72-1.82
Mild obesity	1.62	0.97-2.70		1.56	0.91-2.68
Moderate and severe obesity	2.35	1.12-4.91		1.48	0.71-3.12
BMI as continuous variable	1.04	1.00-1.08	.03	1.03	0.99-1.07	.14
Positive surgical margins			<.001§			.21§	.12
Overweight	1.29	0.88-1.91		0.91	0.59-1.39
Mild obesity	1.78	1.12-2.83		1.09	0.67-1.79
Moderate and severe obesity	3.24	1.69-6.20		1.52	0.78-2.96
BMI as continuous variable	1.07	1.03-1.10	<.001	1.03	0.99-1.06	.13
Extraprostatic extension			.06§			.81§	.17
Overweight	1.54	0.95-2.49		1.03	0.60-1.77
Mild obesity	1.25	0.69-2.26		0.61	0.31-1.20
Moderate and severe obesity	2.43	1.18-5.02		1.63	0.75-3.52
BMI as continuous variable	1.03	0.99-1.07	.18	0.99	0.95-1.04	.72
Seminal vesicle invasion			.05§			.81§	.27
Overweight	1.17	0.57-2.40		1.31	0.64-2.71
Mild obesity	1.17	0.49-2.82		1.05	0.44-2.48
Moderate and severe obesity	3.38	1.23-9.32		1.29	0.41-4.13
BMI as continuous variable	1.05	0.99-1.12	.10	1.01	0.95-1.07	.73

BMI and Biochemical Disease Progression

Among white men, the mean follow-up was 4 years, and the median follow-up was 3.3 years, during which 222 men (30%) developed recurrent disease. Among black men, the mean follow-up was 3.6 years, and the median follow-up was 2.8 years, during which 230 men (35%) developed recurrent disease. Among all men, black race was associated with a 27% increased risk of PSA progression (hazard ratio, 1.27; 95% confidence interval, 1.06-1.53; P = .01). After adjusting for preoperative clinical characteristics, higher BMI was associated with an increased risk of biochemical recurrence in both white men (P = .001) (Fig. 1) and black men (P = .03) (Fig. 2, Table 4). After further adjusting for multiple pathologic variables, obesity was associated with a significantly increased risk of recurrence in both white men (P = .002) and black men (P = .01). There was no significant interaction between race and BMI for predicting biochemical progression whether adjusting only for preoperative factors (p-interaction = .35) or adjusting for preoperative and pathologic features (P_interaction = .47).

Figure 1. Actuarial 10-year Kaplan-Meier estimates of biochemical recurrence-free survival are shown for white men stratified by body mass index (BMI).

Figure 2. Actuarial 10-year Kaplan-Meier estimates of biochemical recurrence-free survival are shown for black men stratified by body mass index (BMI).

Table 4. Relative Risks and 95% Confidence Intervals of the Time to Biochemical Disease Progression After Radical Prostatectomy by Body Mass Index (BMI) Relative to Normal Weight (BMI <25 kg/m²)

BMI Category*	White Men			Black Men			PInteraction‡
	OR†	95% CI	P	OR†	95% CI	P
OR indicates odds ratio; 95% CI, 95% confidence interval. * Overweight indicates BMI from 25 kg/m^2 to 29.9 kg/m^2; mild obesity, BMI from 30 kg/m^2 to 34.9 kg/m^2; moderate and severe obesity, BMI ≥35 kg/m^2. † Adjusted for age, biopsy Gleason score, clinical stage, preoperative prostate-specific antigen level, year of surgery, and center. ‡ Pinteraction to study the interaction among the main effects of race and BMI categories by using the cross-product term of the main effects. § Ptrend determined using the median BMI of each category as a continuous variable. ∥ Adjusted for age, pathological Gleason score, prostate weight, extracapsular extension, positive surgical margins, seminal vesicale invasion, lymph node involvement, preoperative prostate-specific antigen level, year of surgery, and center.
Adjusting for preoperative clinical characteristics†			.001§			.03§	.35
Overweight	1.54	1.08-2.19		1.14	0.80-1.61
Mild obesity	1.46	0.95-2.22		1.78	1.23-2.59
Moderate and severe obesity	2.91	1.72-4.93		1.19	0.68-2.10
BMI as continuous variable	1.06	1.03-1.09	<.001	1.03	1.00-1.06	.04
Adjusting for clinical and pathologic characteristics∥			.002§			.01§	.47
Overweight	1.60	1.08-2.37		1.23	0.84-1.79
Mild obesity	1.50	0.93-2.39		2.07	1.36-3.15
Moderate and severe obesity	2.73	1.55-4.80		1.30	0.71-2.40
BMI as continuous variable	1.06	1.03-1.10	<.001	1.04	1.01-1.07	.01

DISCUSSION

Previous studies have demonstrated that obesity is associated with an increased risk of adverse pathologic features as well as biochemical progression after RP.2-4 Black men are more likely to be morbidly obese compared with white men,9 and they present with more aggressive tumors and, in general, at a more advanced stage.5 However, whether obesity and race interact such that the combination of black race and obesity creates a particularly aggressive cancer is unknown. We examined whether the association between obesity and adverse outcome after RP varied as a function of race. By using a large, multicenter, equal-access population, we observed that, regardless of race, obesity was associated with an increased risk of biochemical progression after RP. Thus, obesity appears to be related to aggressive disease regardless of race.

The prevalence of obesity has been increasing steadily over the last 20 years; and, currently, 30% of US men are obese.10 In general, the impact of obesity on overall health currently is accepted as a major public health issue. However, the role of obesity in modulating prostate cancer risk and aggressiveness remains hotly debated. Although recent evidence suggests that obesity may be associated with a lower risk of prostate cancer incidence,11-13 there is a consensus that obesity is associated with a higher risk of prostate cancer mortality.1, 12 Moreover, multiple studies, including previous studies from the SEARCH database, have associated a higher BMI with an increased risk of prostate cancer recurrence after RP.2-4

Black men the United States have the highest incidence and mortality from prostate cancer in the world.5 However, data regarding outcomes after RP are conflicting. It has been demonstrated in several large, multi-institutional cohorts that black race is associated with an increased risk of recurrence compared with white race.3, 14 However, data from the SEARCH cohort demonstrated that, after controlling for baseline differences between the races, including PSA, race was not an independent predictor of recurrence, although black men did have a nonsignificantly increased risk of recurrence.7 It is noteworthy that, although the current study indicated no association between race and BMI, many other studies have indicated that black men undergoing prostatectomy were more likely to be obese.3, 15 Also, black men in the general population are more likely to be morbidly obese.9 Therefore, it remains plausible that obesity may contribute to the more aggressive tumor biology of prostate cancer in black men.

Although obesity may contribute to poorer outcomes among black men in general, the currently unanswered question is whether obesity is more influential as a risk factor for aggressive prostate cancer in black men compared with white men. In a recent study, Spangler et al. observed that, among black men, obesity was associated with a significant 5-fold higher risk of recurrence after RP; whereas, among white men, obesity was associated with only a 44% nonsignificant increased risk of recurrence.8 However, that study was limited by the inclusion of only 140 black men, and only 51 of those men were obese. In the current, much larger study of 662 black men, including 209 men who were obese, we did not observe that obesity was more predictive of recurrence after RP among black men than among white men. Rather, the current results indicated that obesity portended a poor prognosis regardless of race. Moreover, the associations between obesity and pathologic findings were more or less similar in both races. We did note that, among white men, obesity was associated with a significantly higher incidence of high-grade tumors and positive surgical margins; whereas, among black men, no significant associations between tumor grade or margin status and BMI were observed. However, the general trends were for more positive margins and more high-grade disease among obese black men, although these trends did not reach statistical significance. Furthermore, there were no significant interactions between race and BMI predicting adverse pathology, suggesting there was no significant difference in the influence of obesity predicting adverse pathologic features between black men and white men. Thus, we are unable to explain the differences between our findings and those of Spangler et al. Whether these stem from differences in patient populations (equal access vs tertiary care), the overall association between race and obesity (not associated in our study, whereas black men were more obese in the study by Spangler et al.), power issues (limited number of obese black men in Spangler et al.), or true differences is unclear and will require further study.

Given the lack of significant interaction between race and obesity for predicting either adverse pathologic features or biochemical progression, it is important to understand the definitive mechanisms through which obesity results in aggressive cancer and poor outcome after surgery, regardless of race. Although these mechanisms have yet to be fully elucidated, a potential mechanism is the alteration of sex hormone levels. Obesity is associated with higher levels of estrogen and lower levels of testosterone. Although the evidence is equivocal for the overall risk of developing prostate cancer, lower levels of testosterone may result in the promotion of aggressive cancers.16, 17 Another possible mechanism may be through the insulin-like growth factor (IGF) axis. Obesity is associated with higher levels of free IGF-1,18 and higher IGF-1 levels are associated positively with an increased risk of several cancers, including prostate cancer.19 Leptin and adiponectin—2 cytokines that are released by the adipose tissue—may form yet another postulated biologic link between obesity and prostate cancer. Leptin is increased in obese men and may be associated with an increased risk of high-grade tumors.20 Conversely, adiponectin levels are related inversely to BMI and may have protective effects.21 However, the evidence for an association between adipokines and prostate cancer risk and aggressiveness is conflicting, and further studies will be required before their exact role is determined. Ultimately, the exact molecular mechanism(s) linking obesity and aggressive prostate cancer remain poorly characterized and are a fertile area for research.

Our study has several limitations. Although there were significant trends of an association between obesity and poor outcomes regardless of race, the risks did not increase steadily as BMI increased. In fact, among black men, the moderately and severely obese group seemed to have a lower risk of recurrence than the mildly obese group. This may have been caused in part by the modest numbers of men in these categories. However, the true importance of this finding is unknown, and we await further studies to explore this issue. The median follow-up in this study was relatively short, and longer follow-up will be needed to confirm these findings. In addition, we assessed biochemical progression as our primary endpoint. However, because early biochemical progression is associated with more definite endpoints, such as metastatic disease and prostate cancer-specific death,22 and is a principal instrument for postsurgical decision making, it is a reasonable intermediate endpoint. This was a retrospective analysis of an RP cohort; therefore, there was a selection bias for early stage disease, and the findings may not be generalizable to patients with more advanced stage disease or to the general population. Finally, the pathologic evaluation was not centralized and, thus, may lead to individual variations in the reporting of pathologic grade and stage, although this should not have been deferential by race or BMI; therefore, its influence on the current findings is unclear.

In conclusion, obesity was associated with a greater risk of recurrence after RP among both white men and black men. Obesity does not appear to be more or less important in 1 race than another but, rather, is a risk factor for aggressive cancer regardless of race.

Conflict of Interest Disclosures

Supported by the Department of Veterans Affairs, National Institutes of Health (NIH) Grant R01CA100938 (to W.J.A.); NIH Specialized Programs of Research Excellence Grant P50 CA92131-01A1 (to W.J.A.); the Georgia Cancer Coalition (to M.K.T.); the Department of Defense, Prostate Cancer Research Program, (to S.J.F. and J.J.); and the American Urological Association Foundation/Astellas Rising Star in Urology Award (to S.J.F.).