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Exercise Preserves Physical Function in Prostate Cancer Patients with Bone Metastases.
Galvão, DA, Taaffe, DR, Spry, N, Cormie, P, Joseph, D, Chambers, SK, Chee, R, Peddle-McIntyre, CJ, Hart, NH, Baumann, FT, et al
Medicine and science in sports and exercise. 2018;50(3):393-399
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Existing research indicates cancer patients with bone metastases should not participate in exercise due to potential risks to the skeletal system. However, current oncology guidelines suggest that all cancer patients should avoid inactivity, including those with bone metastases. The purpose of this study is to determine the safety and efficacy of exercise among 57 prostate cancer patients with bone metastases. Participants were randomised to either participate in exercise or receive usual care for three months. Exercise consisted of supervised aerobic activity, resistance training and stretching three days a week. Overall health status and physical function was measured by self-reported questionnaire. This study found self-reported physical functioning and lower muscle strength was improved significantly in the exercise group. There were no difference in bone pain between groups, and no adverse events occurred. Based on these results, the authors conclude exercise is safe and can help improve physical functioning among prostate cancer patients with bone metastasis.
Abstract
PURPOSE The presence of bone metastases has excluded participation of cancer patients in exercise interventions and is a relative contraindication to supervised exercise in the community setting because of concerns of fragility fracture. We examined the efficacy and safety of a modular multimodal exercise program in prostate cancer patients with bone metastases. METHODS Between 2012 and 2015, 57 prostate cancer patients (70.0 ± 8.4 yr; body mass index, 28.7 ± 4.0 kg·m) with bone metastases (pelvis, 75.4%; femur, 40.4%; rib/thoracic spine, 66.7%; lumbar spine, 43.9%; humerus, 24.6%; other sites, 70.2%) were randomized to multimodal supervised aerobic, resistance, and flexibility exercises undertaken thrice weekly (EX; n = 28) or usual care (CON; n = 29) for 3 months. Physical function subscale of the Medical Outcomes Study Short-Form 36 was the primary end point as an indicator of patient-rated physical functioning. Secondary end points included objective measures of physical function, lower body muscle strength, body composition, and fatigue. Safety was assessed by recording the incidence and severity of any adverse events, skeletal complications, and bone pain throughout the intervention. RESULTS There was a significant difference between groups for self-reported physical functioning (3.2 points; 95% confidence interval, 0.4-6.0 points; P = 0.028) and lower body muscle strength (6.6 kg; 95% confidence interval, 0.6-12.7; P = 0.033) at 3 months favoring EX. However, there was no difference between groups for lean mass (P = 0.584), fat mass (P = 0.598), or fatigue (P = 0.964). There were no exercise-related adverse events or skeletal fractures and no differences in bone pain between EX and CON (P = 0.507). CONCLUSIONS Multimodal modular exercise in prostate cancer patients with bone metastases led to self-reported improvements in physical function and objectively measured lower body muscle strength with no skeletal complications or increased bone pain. TRIAL REGISTRATION ACTRN12611001158954.
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Coffee, tea and decaffeinated coffee in relation to hepatocellular carcinoma in a European population: multicentre, prospective cohort study.
Bamia, C, Lagiou, P, Jenab, M, Trichopoulou, A, Fedirko, V, Aleksandrova, K, Pischon, T, Overvad, K, Olsen, A, Tjønneland, A, et al
International journal of cancer. 2015;136(8):1899-908
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The most investigated risk factors for Hepatocellular carcinoma (HCC) (Liver cancer) are alcohol, diet and obesity. This cohort study looks at tea and coffee (caffeinated and decaffeinated) consumption with HCC risk using data from the European Prospective Investigation into Cancer and nutrition study (EPIC). The EPIC study recruited 521,000 apparently healthy participants, aged 25-70 years, from 10 European countries between 1992 and 2000. Their diets were assessed by questionnaire alongside biometric data and other lifestyle factors. The researchers were able to identify 201 HCC cases among 486,799 men/women, after a median follow-up of 11 years. Some data had to be excluded based on cultural tea and coffee drinking habits (particularly lack of data from certain nationalities). There was coffee data from 163,672 participants drinking an overall median of 354 ml/d among men and 290 ml/d among women. The results found that increased coffee intake in participants in the highest compared to the lowest quintile had a lower HCC risk by 72%. There was no significant data for decaffeinated coffee. Tea drinkers represented just 66% of the total cohort and median intakes were 107 ml/d for men and 190 ml/d for women. Tea intake was also inversely associated with HCC incidence with 60% lower HCC risk. The study concludes that intakes of coffee and, to a lesser extent, tea are associated with lower HCC incidence. The incidence of HCC in participants was low so further studies are necessary.
Abstract
Inverse associations of coffee and/or tea in relation to hepatocellular carcinoma (HCC) risk have been consistently identified in studies conducted mostly in Asia where consumption patterns of such beverages differ from Europe. In the European Prospective Investigation into Cancer and nutrition (EPIC), we identified 201 HCC cases among 486,799 men/women, after a median follow-up of 11 years. We calculated adjusted hazard ratios (HRs) for HCC incidence in relation to quintiles/categories of coffee/tea intakes. We found that increased coffee and tea intakes were consistently associated with lower HCC risk. The inverse associations were substantial, monotonic and statistically significant. Coffee consumers in the highest compared to the lowest quintile had lower HCC risk by 72% [HR: 0.28; 95% confidence intervals (CIs): 0.16-0.50, p-trend < 0.001]. The corresponding association of tea with HCC risk was 0.41 (95% CI: 0.22-0.78, p-trend = 0.003). There was no compelling evidence of heterogeneity of these associations across strata of important HCC risk factors, including hepatitis B or hepatitis C status (available in a nested case-control study). The inverse, monotonic associations of coffee intake with HCC were apparent for caffeinated (p-trend = 0.009), but not decaffeinated (p-trend = 0.45) coffee for which, however, data were available for a fraction of subjects. Results from this multicentre, European cohort study strengthen the existing evidence regarding the inverse association between coffee/tea and HCC risk. Given the apparent lack of heterogeneity of these associations by HCC risk factors and that coffee/tea are universal exposures, our results could have important implications for high HCC risk subjects.
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Lycopene and Risk of Prostate Cancer: A Systematic Review and Meta-Analysis.
Chen, P, Zhang, W, Wang, X, Zhao, K, Negi, DS, Zhuo, L, Qi, M, Wang, X, Zhang, X
Medicine. 2015;94(33):e1260
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Lycopene is an antioxidant agent derived from tomatoes, with possible anti-cancer properties including inhibiting growth factors, promoting cell apoptosis, and preventing carcinogenesis. This 2014 meta-analysis reviewed 26 studies and a total of 17,517 prostate patients to see if dose-dependent lycopene supplementation reduced the incidence of prostate cancer compared to 563,299 controls. Prostate cancer (PCa) is the second most common cancer, and a cause of mortality in men. General lycopene intake, via supplementation, showed a slight trend in reducing risk factors for prostate cancer but it was only significant when data from one study was removed to improve the data quality. However, dose-dependent analysis showed that each 5 mg/day increase in lycopene decreased the risk ratio. A higher lycopene consumption of 9 to 21 mg/d was inversely associated with a reduced risk of PCa. High circulating plasma levels of lycopene between 2.17 and 85mg/dL was linearly inversed with PCa risk. Interestingly sub-group analysis of important confounders such as age, family history, energy intake, BMI did not differ considerably between studies. The data was collected from food questionnaires so there may be slight limitations of reporting between the various studies. The study concludes that lycopene may reduce the risk of prostate cancer, but more studies are required to understand the mechanism.
Abstract
Prostate cancer (PCa) is a common illness for aging males. Lycopene has been identified as an antioxidant agent with potential anticancer properties. Studies investigating the relation between lycopene and PCa risk have produced inconsistent results. This study aims to determine dietary lycopene consumption/circulating concentration and any potential dose-response associations with the risk of PCa. Eligible studies published in English up to April 10, 2014, were searched and identified from Pubmed, Sciencedirect Online, Wiley online library databases and hand searching. The STATA (version 12.0) was applied to process the dose-response meta-analysis. Random effects models were used to calculate pooled relative risks (RRs) and 95% confidence intervals (CIs) and to incorporate variation between studies. The linear and nonlinear dose-response relations were evaluated with data from categories of lycopene consumption/circulating concentrations. Twenty-six studies were included with 17,517 cases of PCa reported from 563,299 participants. Although inverse association between lycopene consumption and PCa risk was not found in all studies, there was a trend that with higher lycopene intake, there was reduced incidence of PCa (P = 0.078). Removal of one Chinese study in sensitivity analysis, or recalculation using data from only high-quality studies for subgroup analysis, indicated that higher lycopene consumption significantly lowered PCa risk. Furthermore, our dose-response meta-analysis demonstrated that higher lycopene consumption was linearly associated with a reduced risk of PCa with a threshold between 9 and 21 mg/day. Consistently, higher circulating lycopene levels significantly reduced the risk of PCa. Interestingly, the concentration of circulating lycopene between 2.17 and 85 μg/dL was linearly inversed with PCa risk whereas there was no linear association >85 μg/dL. In addition, greater efficacy for the circulating lycopene concentration on preventing PCa was found for studies with high quality, follow-up >10 years and where results were adjusted by the age or the body mass index. In conclusion, our novel data demonstrates that higher lycopene consumption/circulating concentration is associated with a lower risk of PCa. However, further studies are required to determine the mechanism by which lycopene reduces the risk of PCa and if there are other factors in tomato products that might potentially decrease PCa risk and progression.
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Fish consumption and markers of colorectal cancer risk: a multicenter randomized controlled trial.
Pot, GK, Majsak-Newman, G, Geelen, A, Harvey, LJ, Nagengast, FM, Witteman, BJ, van de Meeberg, PC, Timmer, R, Tan, A, Wahab, PJ, et al
The American journal of clinical nutrition. 2009;90(2):354-61
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Colorectal cancer (CC) risk is strongly related to dietary habits, with 65–75% of the incidence of CC attributed to dietary factors. This RCT studied the effects of fish consumption on markers of CC risk. 242 patients, either at high risk of developing CC or with a healthy bowel, were randomly assigned to 3 groups - 2 portions of oily fish per week, 2 portions of lean fish per week, or a control group who received dietary advice only for 6 months. 216 patients completed the trail. No statistically significant effect on CC risk markers was found between the fish groups and controls at 6 months. These results did not support the hypothesis that additional fish consumption over a 6-month period changes the number of colonic precancerous cells. The authors call for further studies to include non-fish eaters to further test their hypothesis.
Abstract
BACKGROUND Diet is a major factor in the etiology of colorectal cancer, with high fish consumption possibly decreasing colorectal cancer risk, as was shown in several observational studies. To date, no intervention trials have examined the possible beneficial effects of fish intake on colorectal cancer risk. OBJECTIVE The objective was to investigate the effects of a 6-mo intervention with oil-rich or lean fish on apoptosis and mitosis within the colonic crypt. DESIGN In a multicenter, randomized, controlled intervention trial, patients with colorectal polyps, inactive ulcerative colitis, or no macroscopic signs of disease were recruited (n = 242) and randomly allocated to receive dietary advice plus either 300 g oil-rich fish (salmon) per week (n = 82), 300 g lean fish (cod) per week (n = 78), or only dietary advice (DA) (n = 82). Apoptosis and mitosis were measured in colonic biopsy samples collected before and after intervention (n = 213). RESULTS The total number of apoptotic cells per crypt did not increase in the salmon or cod group: -0.10 (95% CI: -0.36, 0.16) and -0.06 (95% CI: -0.32, 0.20), respectively, compared with the DA group. The total number of mitotic cells per crypt decreased nonsignificantly in the salmon group (-0.87; 95% CI: -2.41, 0.68) and in the cod group (-1.04; 95% CI: -2.62, 0.53) compared with the DA group. Furthermore, the distribution of mitosis within the crypt did not significantly change in either group. CONCLUSION An increase in the consumption of either oil-rich or lean fish to 2 portions weekly over 6 mo does not markedly change apoptotic and mitotic rates in the colonic mucosa. This trial was registered at www.clinicaltrials.gov as NCT00145015.