Weight change and prostate cancer incidence and mortality

The relationship between obesity and prostate cancer risk has been studied extensively but with inconsistent findings, particularly for tumor aggressiveness. Few studies have investigated weight change and prostate cancer incidence or mortality. Using the Melbourne Collaborative Cohort Study, which recruited 17,045 men aged between 40 and 69 years at study entry, we investigated associations between reported weight and body mass index (BMI) at age 18 and measured at study entry, height, weight change between age 18 and study entry and prostate cancer incidence and mortality. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression. During follow-up (mean = 15 years) of 16,514 men, we ascertained 1,374 incident prostate cancers of which 410 were classified as aggressive, and 139 deaths from prostate cancer. The incidence of all prostate cancer was not associated with body size or weight change. Weight and BMI at study entry were positively associated with aggressive prostate cancer risk (HR = 1.06, 95% CI: 1.00-1.13 per 5 kg; HR = 1.27, 95% CI: 1.08-1.49 per 5 kg/m(2)) and prostate cancer mortality (HR = 1.12, 95% CI: 1.01-1.23 per 5 kg; HR = 1.49, 95% CI: 1.11-2.00 per 5 kg/m(2)). Weight gain was positively associated with prostate cancer mortality (HR = 1.13, 95% CI: 1.02-1.26 per 5 kg increment); the HR for ≥ kg weight gain between age 18 and study entry compared to <5 kg gain over this period was 1.84, 95% CI: 1.09-3.09. Higher adult weight and BMI increases the risk of aggressive prostate cancer and mortality from prostate cancer. Weight gain during adult life is associated with increased prostate cancer mortality.     

Body mass index and weight change in men with prostate cancer: progression and mortality

Purpose

Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study.

Methods

Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models.

Results

Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03–2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss >5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41–2.66), while a weight gain >5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18–3.16).

Conclusions

Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.     

Obesity and mortality in men with locally advanced prostate cancer: analysis of RTOG 85-31

BACKGROUND: Greater body mass index (BMI) is associated with shorter time to prostate-specific antigen (PSA) failure following radical prostatectomy and radiation therapy (RT). Whether BMI is associated with prostate cancer-specific mortality (PCSM) was investigated in a large randomized trial of men treated with RT and androgen deprivation therapy (ADT) for locally advanced prostate cancer. METHODS: Between 1987 and 1992, 945 eligible men with locally advanced prostate cancer were enrolled in a phase 3 trial (RTOG 85-31) and randomized to RT and immediate goserelin or RT alone followed by goserelin at recurrence. Height and weight data were available at baseline for 788 (83%) subjects. Cox regression analyses were performed to evaluate the relations between BMI and all-cause mortality, PCSM, and nonprostate cancer mortality. Covariates included age, race, treatment arm, history of prostatectomy, nodal involvement, Gleason score, clinical stage, and BMI. RESULTS: The 5-year PCSM rate for men with BMI <25 kg/m(2) was 6.5%, compared with 13.1% and 12.2% in men with BMI > or =25 to <30 and BMI > or =30, respectively (Gray's P = .005). In multivariate analyses, greater BMI was significantly associated with higher PCSM (for BMI > or =25 to <30, hazard ratio [HR] 1.52, 95% confidence interval [CI], 1.02-2.27, P = .04; for BMI > or =30, HR 1.64, 95% CI, 1.01-2.66, P = .04). BMI was not associated with nonprostate cancer or all-cause mortality. CONCLUSIONS: Greater baseline BMI is independently associated with higher PCSM in men with locally advanced prostate cancer. Further studies are warranted to evaluate the mechanism(s) for increased cancer-specific mortality and to assess whether weight loss after prostate cancer diagnosis alters disease course.     

Height, body mass index, and ovarian cancer: a pooled analysis of 12 cohort studies.

BACKGROUND: Although many studies have investigated the association between anthropometry and ovarian cancer risk, results have been inconsistent. METHODS: The associations of height, body mass index (BMI), and ovarian cancer risk were examined in a pooled analysis of primary data from 12 prospective cohort studies from North America and Europe. The study population consisted of 531,583 women among whom 2,036 epithelial ovarian cancer cases were identified. To summarize associations, study-specific relative risks (RR) were estimated using the Cox proportional hazards model and then combined using a random-effects model. RESULTS: Women with height > or =1.70 m had a pooled multivariate RR of 1.38 [95% confidence interval (95% CI), 1.16-1.65] compared with those with height <1.60 m. For the same comparison, multivariate RRs were 1.79 (95% CI, 1.07-3.00) for premenopausal and 1.25 (95% CI, 1.04-1.49) for postmenopausal ovarian cancer (P(interaction) = 0.14). The multivariate RR for women with a BMI > or =30 kg/m(2) was 1.03 (95% CI, 0.86-1.22) compared with women with a BMI from 18.5 to 23 kg/m(2). For the same comparison, multivariate RRs were 1.72 (95% CI, 1.02-2.89) for premenopausal and 1.07 (95% CI, 0.87-1.33) for postmenopausal women (P(interaction) = 0.07). There was no statistically significant heterogeneity between studies with respect to height or BMI. BMI in early adulthood was not associated with ovarian cancer risk. CONCLUSION: Height was associated with an increased ovarian cancer risk, especially in premenopausal women. BMI was not associated with ovarian cancer risk in postmenopausal women but was positively associated with risk in premenopausal women.     

Prospective study of adiposity and weight change in relation to prostate cancer incidence and mortality

BACKGROUND.

Adiposity has been linked inconsistently with prostate cancer, and few studies have evaluated whether such associations vary by disease aggressiveness.

METHODS.

The authors prospectively examined body mass index (BMI) and adult weight change in relation to prostate cancer incidence and mortality in 287,760 men ages 50 years to 71 years at enrollment (1995–1996) in the National Institutes of Health‐AARP Diet and Health Study. At baseline, participants completed questionnaires regarding height, weight, and cancer screening practices, including digital rectal examinations and prostate‐specific antigen tests. Cox regression analysis was used to calculate relative risks (RR) and 95% confidence intervals (95% CIs).

RESULTS.

In total, 9986 incident prostate cancers were identified during 5 years of follow‐up, and 173 prostate cancer deaths were ascertained during 6 years of follow‐up. In multivariate models, higher baseline BMI was associated with significantly reduced total prostate cancer incidence, largely because of the relationship with localized tumors (for men in the highest BMI category [≥40 kg/m²] vs men in the lowest BMI category [<25 kg/m²]: RR, 0.67; 95% CI, 0.50–0.89; P = .0006). Conversely, a significant elevation in prostate cancer mortality was observed at higher BMI levels (BMI <25 kg/m²: RR, 1.0 [referent group]; BMI 25–29.9 kg/m²: RR, 1.25; 95% CI, 0.87–1.80; BMI 30–34.9 kg/m²: RR, 1.46; 95% CI, 0.92–2.33; and BMI ≥35 kg/m²: RR, 2.12; 95% CI, 1.08–4.15; P = .02). Adult weight gain from age 18 years to baseline also was associated positively with fatal prostate cancer (P = .009), but not with incident disease.

CONCLUSIONS.

Although adiposity was not related positively to prostate cancer incidence, higher BMI and adult weight gain increased the risk of dying from prostate cancer. Cancer 2007. Published 2007 by the American Cancer Society.     

Body mass, diabetes and smoking, and endometrial cancer risk: a follow-up study

We examined the relationship of body mass index (BMI), diabetes and smoking to endometrial cancer risk in a cohort of 36 761 Norwegian women during 15.7 years of follow-up. In multivariable analyses of 222 incident cases of endometrial cancer, identified by linkage to the Norwegian Cancer Registry, there was a strong increase in risk with increasing BMI (P-trend <0.001). Compared to the reference (BMI 20-24 kg m(-2)), the adjusted relative risk (RR) was 0.53 (95% confidence interval (CI): 0.19-1.47) for BMI<20 kg m(-2), 4.28 (95% CI: 2.58-7.09) for BMI of 35-39 kg m(-2) and 6.36 (95% CI: 3.08-13.16) for BMI>or=40 kg m(-2). Women with known diabetes at baseline were at three-fold higher risk (RR 3.13, 95% CI: 1.92-5.11) than those without diabetes; women who reported current smoking at baseline were at reduced risk compared to never smokers (RR 0.55, 95% CI: 0.35-0.86). The strong linear positive association of BMI with endometrial cancer risk and a strongly increased risk among women with diabetes suggest that any increase in body mass in the female population will increase endometrial cancer incidence.     

Body mass index and risk of non-Hodgkin's and Hodgkin's lymphoma: a meta-analysis of prospective studies

We conducted a meta-analysis of prospective studies to summarise the epidemiologic evidence regarding the association of body mass index (BMI) with non-Hodgkin's lymphoma (NHL) and Hodgkin's lymphoma (HL) incidence and NHL mortality. Pertinent studies were identified by searching PubMed (1966-May 2011) and the reference lists of retrieved articles. For each study, we estimated a relative risk (RR) for a 5 kg/m(2) increase in BMI. A random-effects model was used to combine the RR estimates from individual studies. The summary RRs for a 5 kg/m(2) increase in BMI were 1.07 (95% confidence intervals (CI), 1.04-1.10) for NHL incidence (16 studies, n=17,291 cases) and 1.14 (95% CI, 1.04-1.26) for NHL mortality (five studies, n=3407 cases). BMI was significantly positively associated with risk of diffuse large B-cell lymphoma (RR, 1.13; 95% CI, 1.02-1.26), but not other NHL subtypes. The difference in risk estimates for subtypes was not statistically significant (P=0.10). There was evidence of a nonlinear association between BMI and HL (P for nonlinearity=0.01) (five studies, n=1557 cases). The summary RRs of HL were 0.97 (95% CI, 0.85-1.12) for overweight and 1.41 (95% CI, 1.14-1.75) for obesity. These results indicate that BMI is positively associated with risk of NHL and HL as well as with NHL mortality.     

Inverse correlation between body mass index and clinical outcomes in men with advanced castration-recurrent prostate cancer

BACKGROUND: Obesity has a variety of adverse health outcomes, but to the authors' knowledge, the effect of obesity on outcome in patients with advanced prostate cancer is not known. For this reason, the correlation between an elevated body mass index (BMI) and clinical outcomes in patients with metastatic, castration-recurrent prostate cancer (CRPC) was evaluated. METHODS: A total of 1226 men with CRPC who were enrolled in 9 prospective clinical trials conducted by the Cancer and Leukemia Group B (CALGB) for the treatment of metastatic disease were considered. Eligible patients had progressive prostate cancer during androgen deprivation therapy (with documented castrate levels of testosterone); an Eastern Cooperative Oncology Group performance status of 0 to 2; and adequate hematologic, renal, and hepatic function. Patients were classified based on BMI as normal (18.5-24.9 kg/m(2)), overweight (25-29.9 kg/m(2)), and mildly to severely obese (> or =30 kg/m(2)). RESULTS: Approximately 24% of the patients had a normal BMI, 43% were overweight, and 33% were mildly to severely obese. On multivariable analysis, BMI was found to be a statistically significant predictor of overall survival and prostate cancer-specific mortality. Compared with men with normal BMIs, the hazard ratios for death for overweight men and mildly to severely obese men were 0.80 (95% confidence interval [95% CI], 0.68-0.93; P = .001) and 0.80 (95% CI, 0.68-0.94; P = .010), respectively. CONCLUSIONS: In patients with metastatic CRPC, obesity (as defined by an elevated BMI) appears to have a protective effect against overall mortality and prostate cancer-specific mortality. Alternatively, a higher BMI may reflect different cancer biology (ie, the lack of cachexia-producing substances). Further studies to gain a more comprehensive understanding of the mechanisms behind these clinical observations are needed.     

Body mass index, weight change, and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort.

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). RESULTS: The association between BMI in 1992 and risk of prostate cancer differed by stage and grade at diagnosis. BMI was inversely associated with risk of nonmetastatic low-grade prostate cancer (RR, 0.84; 95% CI, 0.66-1.06), but BMI was positively associated with risk of nonmetastatic high-grade prostate cancer (RR, 1.22; 95% CI, 0.96-1.55) and risk of metastatic or fatal prostate cancer (RR, 1.54; 95% CI, 1.06-2.23). Compared with weight maintenance, men who lost >11 pounds between 1982 and 1992 were at a decreased risk of nonmetastatic high-grade prostate cancer (RR, 0.58; 95% CI, 0.42-0.79). CONCLUSION: Obesity increases the risk of more aggressive prostate cancer and may decrease either the occurrence or the likelihood of diagnosis of less-aggressive tumors. Men who lose weight may reduce their risk of prostate cancer.     

Body size and composition and prostate cancer risk: systematic review and meta-regression analysis

The evidence that measures of obesity and stature are associated with prostate cancer is weak and inconsistent. We performed a systematic review and meta-analysis of the relationship between body mass index (BMI), height, weight, waist circumference and waist-to-hips ratio (WHR) and the risk of prostate cancer. Study-specific dose-response slopes were obtained, and random effects rate ratios (RRs) were computed from linear meta-regression models. We included 55,521 cases identified among 2,818,767 men from 31 cohort studies, and 13,232 cases and 16,317 controls from 25 case–control studies. The overall RR for BMI was 1.05 per 5 kg/m² increment, 95% CI 1.01–1.08. For studies that reported results by stage of disease, the RRs were stronger for advanced disease (RR 1.12 per 5 kg/m² increment, 95% CI 1.01–1.23) compared with localized disease (RR 0.96 per 5 kg/m² increment, 95% CI 0.89–1.03), p = 0.02. Height was also positively associated with risk (RR 1.05 per 10 cm increment, 95% CI 1.02–1.09), but the evidence was weak for weight (RR 1.01 per 10 kg increment, 95% CI 0.97–1.04), waist circumference (RR 1.03 per 10 cm increment, 95% CI 0.99–1.07), and WHR (RR 1.11 per 0.1 unit increment, 95% CI 0.95–1.30). Stronger associations were observed among cohort studies compared with case–control studies for BMI (p = 0.006), height (p < 0.001) and weight (p = 0.02). This meta-analysis indicates that obesity is weakly associated with an increased risk of prostate cancer (particularly advanced stage tumors). While increased stature may also increase risk, there is little evidence for an association with central obesity.     

The association between metabolic syndrome and the risk of prostate cancer,high-grade prostate cancer,advanced prostate cancer,prostate cancer-specific mortality and biochemical recurrence

Background

Although a previous meta-analysis reported no association between metabolic syndrome (MetS) and prostate cancer risk, a number of studies suggest that MetS may be associated with the aggressiveness and progression of prostate cancer. However, these results have been inconsistent. This systematic review and meta-analysis investigated the nature of this association.

Methods

We systematically searched MEDLINE, EMBASE and bibliographies of retrieved studies up to January 2013 using the keywords “metabolic syndrome” and “prostate cancer”. We assessed relative risks (RRs) of the prostate cancer, several parameters of prostate cancer aggressiveness and progression associated with MetS using 95% confidence intervals (95% CIs).

Results

The literature search produced 547 hits from which 19 papers were extracted for the meta-analysis. In cancer-free population with and without MetS, the combined adjusted RR (95% CI) of prostate cancer risk and prostate cancer-specific mortality in longitudinal cohort studies is 0.96 (0.85 ~ 1.09) and 1.12 (1.02 ~ 1.23) respectively. In the prostate cancer patients with and without MetS, the combined unadjusted OR (95% CI) of high grade Gleason prostate cancer is 1.44 (1.20 ~ 1.72), the OR of advanced prostate cancer is 1.37 (1.12 ~ 1.68) and the OR of biochemical recurrence is 2.06 (1.43 ~ 2.96).

Conclusions

The overall analyses revealed no association between MetS and prostate cancer risk, although men with MetS appear more likely to have high-grade prostate cancer and more advanced disease, were at greater risk of progression after radical prostatectomy and were more likely to suffer prostate cancer-specific death. Further primary studies with adjustment for appropriate confounders and larger, prospective, multicenter investigations are required.     

Anthropometric variables, physical activity, and incidence of ovarian cancer: The Iowa Women's Health Study

BACKGROUND: Reports on the relation between anthropometric variables (height, weight) and physical activity with ovarian cancer have been inconclusive. The objective of the current study was to extend investigation of potential associations in the Iowa Women's Health Study cohort. METHODS: The relation between self-reported anthropometric variables and incident ovarian cancer was studied in a prospective cohort of women ages 55-69 years who were followed for 15 years. Two hundred twenty-three incident cases of epithelial ovarian cancer were identified by linkage to a cancer registry. RESULTS: No association was found overall between ovarian cancer and height, but a positive association was observed for serous ovarian cancers (relative risk [RR], 1.86 for highest quartile vs. lowest quartile; 95% confidence interval [95% CI], 1.06-3.29). Although current body mass index (BMI) was not associated with ovarian cancer, a BMI > or =30 kg/m2 at age 18 years appeared to be associated positively with ovarian cancer (multivariate-adjusted RR, 1.83 for BMI > or =30 kg/m2 vs. BMI <25 kg/m2; 95% CI, 0.90-3.72), and this association was stronger after exclusion of the first 2 years of follow-up (RR, 2.15; 95% CI, 1.05-4.40). In a multivariate analysis, waist-to-hip ratio was associated with ovarian cancer (RR, 1.59 for highest quartile vs. lowest quartile; 95% CI, 1.05-2.40), but a linear dose response was not found. An index that combined the frequency and intensity of leisure-time physical activity was associated positively with ovarian cancer incidence (multivariate-adjusted RR, 1.42 for high activity vs. low activity; 95% CI, 1.03-1.97). This association was particularly strong for frequency of vigorous physical activity (multivariate-adjusted RR, 2.38 for >4 times per week vs. rarely/never; 95% CI, 1.29-4.38). CONCLUSIONS: Anthropometric variables were not major risk factors for ovarian cancer in the cohort studied; however, high BMI in early adulthood and frequent and vigorous physical activity may increase the risk of ovarian cancer among postmenopausal women.     

Weight, weight gain, and survival after breast cancer diagnosis.

PURPOSE: To determine whether weight prior to diagnosis and weight gain after diagnosis are predictive of breast cancer survival. METHODS: Patients included 5,204 Nurses' Health Study participants diagnosed with incident, invasive, nonmetastatic breast cancer between 1976 and 2000; 860 total deaths, 533 breast cancer deaths, and 681 recurrences (defined as secondary lung, brain, bone, or liver cancer, and death from breast cancer) accrued to 2002. We computed the change in body mass index (BMI) from before to the first BMI reported > or = 12 months after the date of diagnosis. Cox proportional hazards models were used to evaluate associations of categories of BMI before diagnosis and of BMI change with time to event. We stratified by smoking, menopausal status, and breast cancer-related variables. RESULTS: In multivariate-adjusted analyses, weight before diagnosis was positively associated with breast cancer recurrence and death, but this was apparent only in never smokers. Similarly, among never-smoking women, those who gained between 0.5 and 2.0 kg/m(2) (median gain, 6.0 lb; relative risk [RR], 1.35; 95% CI, 0.93 to 1.95) or more than 2.0 kg/m(2) (median gain, 17.0 lb; RR, 1.64; 95% CI, 1.07 to 2.51) after diagnosis had an elevated risk of breast cancer death during follow-up (median, 9 years), compared with women who maintained their weight (test for linear trend, P = .03). Associations with weight were stronger in premenopausal than in postmenopausal women. Similar findings were noted for breast cancer recurrence and all-cause mortality. CONCLUSION: Weight and weight gain were related to higher rates of breast cancer recurrence and mortality, but associations were most apparent in never-smoking women.     

Pretreatment prostate-specific antigen velocity is associated with development of distant metastases and prostate cancer mortality in men treated with radiotherapy and androgen-deprivation therapy

BACKGROUND: In men with prostate cancer, pretreatment prostate-specific antigen (PSA) velocity (PSAV) has been demonstrated as a predictor of biochemical and survival outcomes in patients undergoing radical prostatectomy (RP). The utility of pretreatment PSAV in predicting outcomes after radiotherapy (RT), with or without androgen-deprivation therapy (ADT), is less certain. This study was undertaken to determine whether pretreatment PSAV is associated with biochemical disease-free survival, patterns of recurrence, and survival outcomes in men treated with radiation therapy and ADT. METHODS: Two hundred seventy-seven patients with intermediate- and high-risk prostate cancer treated with RT and ADT formed the study cohort. Kaplan-Meier survival estimates and Cox regression analyses were used to evaluate whether PSAV was associated with disease outcomes. RESULTS: The median age of diagnosis was 70 years, and the median follow-up was 6.8 years. Men with a PSAV in the highest quartile tended to have higher risk disease at presentation (P = .028). After adjustment for known prognostic factors and duration of ADT, men who had a PSAV in the highest quartile had an increased risk of distant metastasis (hazard ratio [HR], 4.0; 95% confidence interval [95% CI], 1.61-9.9 [P = .003]) and prostate cancer-specific mortality (HR, 2.75; 95% CI, 1.27-5.95 [P = .01]) compared with men who had a lower PSAV, but had no increase in the risk of local recurrence (P = .76). CONCLUSIONS: A high pretreatment PSAV was associated with distant metastasis and prostate cancer-specific mortality but not with local recurrence. A high pretreatment PSAV may signify the presence of occult metastatic disease. Randomized trials are needed to determine whether more aggressive intervention is required in men who present with high pretreatment PSAV.     

Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States.

Body weight and height have both been associated consistently with postmenopausal breast cancer but less consistently with prostate cancer. The present study examined the relationship between body mass index (BMI), height, and death from prostate cancer in two large American Cancer Society cohorts. Men in the study were selected from the male participants in Cancer Prevention Study I (CPS-I; enrolled in 1959 and followed through 1972) and Cancer Prevention Study II (CPS-II; enrolled in 1982 and followed through 1996). After exclusions, 1,590 prostate cancer deaths remained among 381,638 men in CPS-I and 3,622 deaths among 434,630 men in CPS-II. Cox proportional hazards modeling was used to compute rate ratios (RR) and to adjust for confounders. Prostate cancer mortality rates were significantly higher among obese (BMI, > or =30) than nonobese (BMI, <25) men in both cohorts [adjusted RR, 1.27; 95% confidence interval (CI), 1.04-1.56 in CPS-I; RR, 1.21; 95% CI, 1.07-1.37 in CPS-II]. Prostate cancer mortality rates in the CPS-I cohort were lowest for the shortest men (RR, 0.80; 95% CI, 0.63-1.03 for men <65 inches versus 65-66 inches) and highest for the tallest men (RR, 1.39; 95% CI, 1.11-1.74 for men > or =73 inches tall versus 65-66 inches). Rates remained constant among men 65-72 inches tall. No association between height and prostate cancer mortality was observed in the CPS-II cohort (RR, 1.03; 95% CI, 0.82-1.29 for men > or =75 versus 65-66 inches). These results support the hypothesis that obesity increases risk of prostate cancer mortality. Decreased survival among obese men may be a likely explanation for this association.     

Postdiagnosis body fatness,recreational physical activity,dietary factors and breast cancer prognosis: Global Cancer Update Programme (CUP Global) summary of evidence grading

Based on the Global Cancer Update Programme, formally known as the World Cancer Research Fund/American Institute for Cancer Research Continuous Update Project, we performed systematic reviews and meta-analyses to investigate the association of postdiagnosis body fatness, physical activity and dietary factors with breast cancer prognosis. We searched PubMed and Embase for randomised controlled trials and longitudinal observational studies from inception to 31 October 2021. We calculated summary relative risks (RRs) and 95% confidence intervals (CIs) using random-effects meta-analyses. An independent Expert Panel graded the quality of evidence according to predefined criteria. The evidence on postdiagnosis body fatness and higher all-cause mortality (RR per 5 kg/m² in body mass index: 1.07, 95% CI: 1.05-1.10), breast cancer-specific mortality (RR: 1.10, 95% CI: 1.06-1.14) and second primary breast cancer (RR: 1.14, 95% CI: 1.04-1.26) was graded as strong (likelihood of causality: probable). The evidence for body fatness and breast cancer recurrence and other nonbreast cancer-related mortality was graded as limited (likelihood of causality: limited-suggestive). The evidence on recreational physical activity and lower risk of all-cause (RR per 10 metabolic equivalent of task-hour/week: 0.85, 95% CI: 0.78-0.92) and breast cancer-specific mortality (RR: 0.86, 95% CI: 0.77-0.96) was judged as limited-suggestive. Data on dietary factors was limited, and no conclusions could be reached except for healthy dietary patterns, isoflavone and dietary fibre intake and serum 25(OH)D concentrations that were graded with limited-suggestive evidence for lower risk of the examined outcomes. Our results encourage the development of lifestyle recommendations for breast cancer patients to avoid obesity and be physically active.     

Excess body weight and second primary cancer risk after breast cancer: a systematic review and meta-analysis of prospective studies

Several observational studies have investigated the role of body mass index (BMI) in second primary cancer incidence in women with breast cancer. We conducted a systematic review and meta-analysis of the evidence to assess the strength of this association. PubMed and Embase were searched for observational studies up to May 2012, and the reference lists of studies included in the analysis were examined. Random effects models were used to estimate summary relative risks (RRs) and 95?% confidence intervals (CIs). Thirteen prospective studies, five cohort and eight nested case-control studies, were included. In categorical meta-analyses of BMI, obesity was associated to significantly increased risks of contralateral breast (RR?=?1.37, 95?% CI: 1.20-1.57), breast (RR?=?1.40, 95?% CI: 1.24-1.58), endometrial (RR?=?1.96, 95?% CI: 1.43-2.70), and colorectal (RR?=?1.89, 95?% CI: 1.28-2.79) second primary cancers. For a BMI increase of 5?kg/m(2), dose-response meta-analyses resulted in significantly increased RRs of 1.12 (95?% CI: 1.06-1.20) and 1.14 (95?% CI: 1.07-1.21) for contralateral breast and breast second primary cancers, respectively. The summary RR for endometrial second primary cancers was 1.46 (95?% CI: 1.17-1.83) for a 5-unit increment. This result emphasizes the importance of prevention policies aiming to reduce overweight and obesity prevalence. Clinical trials in breast cancer patients with excess body weight evaluating the effect of normal weight restoration on second primary cancer incidence are needed.     

Obesity is associated with increased risks of prostate cancer metastasis and death after initial cancer diagnosis in middle-aged men

BACKGROUND: Current research is inconclusive regarding the effect of obesity on outcomes after a prostate cancer diagnosis. The objective of this study was to examine associations between obesity and the risks of developing metastasis or prostate cancer-specific mortality in a population-based cohort of men with prostate cancer. METHODS: Seven hundred fifty-two middle-aged men with prostate cancer who were enrolled in a case-control study and remain under long-term follow-up for disease progression and mortality formed the study cohort. Body mass index (BMI) in the year before diagnosis was obtained at the time of initial interview. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) of prostate cancer metastasis and mortality associated with obesity, controlling for age, race, smoking status, Gleason score, stage at diagnosis, diagnostic prostate-specific antigen level, and primary treatment. RESULTS: Obesity (BMI >or=30 kg/m(2)) was associated with a significant increase in prostate cancer mortality (HR, 2.64; 95% CI, 1.18-5.92). Among men who were diagnosed with local- or regional-stage disease, obesity also was associated with an increased risk of developing metastasis (HR, 3.61; 95% CI, 1.73-7.51). Associations generally were consistent across strata defined by Gleason score (2-6 or 7 [3 + 4] vs 7 [4 + 3] or 8-10), stage (local vs regional/distant for mortality), and primary treatment (androgen-deprivation therapy use: yes vs no). CONCLUSIONS: Obesity at the time of diagnosis was associated with increased risks of prostate cancer metastasis and death. The increased risk of prostate cancer death or metastasis associated with obesity largely was independent of key clinical prognostic factors at diagnosis.     

Prospective study of body mass index, height, physical activity and incidence of bladder cancer in US men and women

We evaluated prospectively the association between body mass index (BMI), height, recreational physical activity and the risk of bladder cancer among US adults. Data were used from 2 ongoing cohorts, the Health Professionals Follow-up Study and the Nurses' Health Study, with 3,542,012 years of follow-up and 866 incident bladder cancer cases (men = 507; women = 359) for the anthropometric analysis and 1,890,476 years of follow-up and 706 incident bladder cancer cases (men = 502; women = 204) for the physical activity analysis. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between BMI, height, physical activity and bladder cancer risk adjusting for age, pack-years of cigarette smoking and current smoking. Estimates from each cohort were pooled using a random-effects model. We observed no association between baseline BMI and bladder cancer risk, even when we compared a BMI of > or =30 kg/m(2) to a BMI of 18-22.9 kg/m(2) [pooled multivariate (MV) RR, 1.16; 95% CI: 0.89-1.52]. A weak, but statistically significant, association was observed for the same comparison after excluding bladder cancer cases diagnosed within the first 4 years of follow-up (pooled MV RR, 1.33; 95% CI: 1.01-1.76). Height was not related to bladder cancer risk (pooled MV RR, 0.82; 95% CI: 0.65-1.03, top vs. bottom quintile). Total recreational physical activity also was not associated with the risk of bladder cancer (pooled MV RR, 0.97; 95% CI: 0.77-1.24, top vs. bottom quintile). Our findings do not support a role for BMI, height or physical activity in bladder carcinogenesis.     

Prognostic Value of Hemoglobin in Metastatic Hormone-sensitive Prostate Cancer: A Systematic Review and Meta-analysis

The purpose of this study was to assess the prognostic value of hemoglobin (Hb) in patients with metastatic hormone-sensitive prostate cancer (HSPC). The PUBMED, Web of Science, Cochrane Library, and Scopus databases were searched in December 2019 according to the Preferred Reporting Items for Systematic Review and Meta-analysis statement. Studies were deemed eligible if they compared patients with HSPC with normal and low Hb levels to determine their ability to predict overall survival, cancer-specific survival, progression-free survival, and castration-resistant prostate cancer-free survival. Formal meta-analyses were performed for these outcomes. The systematic review identified 25 studies including 6614 patients; 21 studies comprising 5782 patients were eligible for meta-analysis. Low Hb levels were associated with worse overall survival (pooled hazard ratio [HR], 1.21; 95% confidence interval [CI], 1.15-1.29), cancer-specific survival (pooled HR, 1.46; 95% CI, 1.24-1.72), progression-free survival (pooled HR, 1.21; 95% CI, 1.14-1.28), and castration-resistant prostate cancer-free survival (pooled HR, 1.37; 95% CI: 1.18-1.57). Subgroup analyses revealed that low Hb levels were also associated with poor overall survival in patients with both “high-volume” (pooled HR, 1.49; 95% CI, 1.29-1.72) and “low-volume” HSPC (pooled HR, 1.40; 95% CI, 1.13-1.73). This meta-analysis revealed that low Hb serum levels in patients with metastatic HSPC were associated with increased risks of overall mortality, cancer-specific mortality, disease progression, and biochemical recurrence. Furthermore, Hb levels were independently associated with overall survival in the “high-volume” and “low-volume” HSPC subgroups. Therefore, it might be useful to incorporate Hb testing into prognostic tools for metastatic HSPC.